Textbook of Interventional Cardiovascular Pharmacology - part 10 pps

Combination therapy
Combination therapy with a thrombolytic agent and
GPIIb/IIIa inhibitor has been studied in acute MI. Various
randomized trials (TAMI-8, IMPACT, INTRO AMI, TIMI-14,
SPEED, GUSTO V) in the coronary literature have shown
that combination therapy reduced thrombolysis time and
permitted a reduction of thrombolytic doses by 25% to 50%
of the normal dose. This is explained by the fact that thrombus
is composed of both fibrin and platelets. Thrombolytics only
address the fibrin component of acute thrombus.
Furthermore, thrombolytics may actually activate platelets
directly resulting in additional thrombus formation.
Therefore, the addition of GPIIb/ IIIa inhibition facilitates the
efficiency of the thrombolytic agent. It is also known that
GPIIb/IIIa inhibition alone can actually dissolve platelet rich
clot (41,42,43).
There are several small studies examining this concept of
thrombolytic infusion with GPIIb/IIIa inhibition to reduce lytic
infusion time and improve efficacy as summarized below. This
concept is not universally proven in these studies. A larger
randomized trail is needed to examine this concept before a
clinical practice recommendation can be made.
Tepes et al. reported the first clinical experience with abcix-
imab and urokinase combination therapy in the peripheral
circulation (44). Schweizer et al. used abciximab and rt-PA
versus rt-PA with ASA in an 84 patient trial and found a
significantly shorter duration of thrombolytic infusion was
required to achieve lytic success in the combination group as
well as improved clinical endpoints of less re-hospitalization,
re-intervention, and amputation compared to ASA and
heparin (45).

Duda et al. prospectively studied 70 patients in the
PROMPT trial of UK and abciximab versus UK alone. The
trial showed the combination therapy resulted in a decreased
infusion time, improved amputation free survival, and
improved open surgery free survival at 90 days (46).
Interestingly, a post hoc economic analysis of the PROMPT
trial found an economic benefit to combination therapy at 90
days based on endpoints of amputation free survival, survival
without open surgery, lack of major amputation and lack of
major complications. The extra cost of abciximab was more
than offset by the decreased costs through improved patient
outcomes (47).
Yoon et al. retrospectively compared the clinical outcomes
of 17 patients who received eptifibatide and rt-PA to an age-
matched group of patients who received only rt-PA. The
study demonstrated a significantly decreased thrombolytic
dose in the combination group (9.0 ϩ/– 4.4 mg vs. 38.9 ϩ/–
30.7 mg) (48). Syed et al. reported that intra-arterial eptifi-
batide infusion with reteplase can be successful in restoring
blood flow in the presence of chronic arterial thrombus (49).
With combination therapy using reteplase and abciximab, a
prospective double center study of 50 patients was reported
by Drescher et al (50). Recently, however, the 74 patient
RELAX trial comparing reteplase and abciximab combination
therapy to reteplase monotherapy found no significant differ-
ence in safety and efficacy in all major clinical end points
(death, amputation, PTA/stent, surgical revascularization).
The trial did demonstrate a decreased rate of distal embolic
event in the combination group (51).
Very limited clinical data is available for tenecteplase and

eptifibatide combination therapy. A small 16 patient study did
show feasibility of combining these agents with positive
efficacy and safety (52). However, there was a negative safety
correlation with the use of abciximab with tenecteplase in a
recent 37 patient study (53).
A 60 patient study comparing treatment with abciximab
and rt-PA to treatment with tirofiban with rt-PA found no
difference in bleeding complications, re-hospitalization, re-
intervention, or amputation rate. The duration of lysis was
only slightly shorter in the abciximab group but this was not
clinically relevant (149.7 ϩ 18 vs. 139.3 ϩ31.3 min) (54).
The 50 patient APART trial recently compared reteplase plus
abciximab or urokinase plus abciximab and found overall no
significant differences except a decreased thrombolysis time in
the urokinase and abciximab group (120 min vs. 200 min,
p ϭ 0.001) (55).
References
1 McLean J. The thromboplastic action of cephalin. Am J Physiol
1916; 41:250–257.
2 Johnson EA, Mulloy B. The molecular weight range of mucosal
heparin preparations. Carbohydr Res 1976; 51:119–127.
3 Rosenberg RD, Lam L. Correlation between structure and
function of heparin. Proc Natl Acad Sci USA 1979;
76:1218–1222.
4 Hirsh J, Warkentin TE, Shaughnessy SG, et al. Heparin and
low-molecular-weight heparin: mechanisms of action, phar-
macokinetics, dosing, monitoring, efficacy, and safety. Chest
2001; 119(1 suppl):64S–94S.
5 Weitz JI, Crowther M: Direct thrombin inhibitors. Thromb
Res 2002; 106:V275–V284.

6 Hirsh j, Anand SS, Halperin JL, Fuster V. Guide to Anticoagulant
therapy: heparin. Circulation 2001; 103:2994–3018.
7 Levine MN, Raskob G, Landefeld S, Kearon C. Hemorrhagic
complications of anticoagulant treatment. Chest 2001; 119(1
suppl):108S–121S.
8 Wester JP, de Valk HW, Nieuwenhuis HK, et al. Risk factors for
bleeding during treatment of acute venous thromboembolism.
Thromb Haemost 1996; 76:682–688.
9 Gupta AK, Kovacs MJ, Sauder DN. Heparin-induced throm-
bocytopenia. Ann Pharmacotherapy 1998; 32:55–59.
10 Weitz JI, Crowther M: Direct thrombin inhibitors. Thromb
Res 2002; 106:V275–284.
11 Wiggins BS, Spinler S, Wittkowsky AK, Stringer KA.
Bivalirudin. a direct thrombin inhibitor for percutaneous
transluminal coronary angioplasty. Pharmacotherapy 2002;
22:1007–1018.
580 Anticoagulants in peripheral vascular interventions
1180 Chap49 3/14/07 5:00 PM Page 580
12 Bates SM, Weitz JI. Direct thrombin inhibitors for treatment of
arterial thrombosis: Potential differences between bivalirudin
and hirudin. Am J Cardiol 1998; 82:12–18.
13 Direct thrombin inhibitors in acute coronary syndromes:
Principal results of a meta-analysis based on individual patients’
data. Lancet 2002; 359:294–302.
14 Bittl JA, Strony J, Brinker JA, et al. Treatment with bivalirudin
(Hirulog) as compared with heparin during coronary angio-
plasty for unstable or postinfarction angina. Hirulog Angioplasty
Study Investigators. N Engl J Med 1995; 333:764–769.
15 Lincoff AM, Bittl JA, Harrington RA, et al. and for the
REPLACE-2 Investigators. bivalirudin and provisional glycopro-

tein IIb/IIIa blockade compared with heparin and planned
glycoprotein IIb/IIIa blockade during percutaneous coronary
intervention: REPLACE-2 randomized trial. JAMA 2003;
289:853–863.
16 Alle D, Hall P, Shammas N, et al. The Angiomax peripheral
procedure registry of vascular events trial (APPROVE):
In hospital and 30-day results. J Invas Cardiol 2004;
16:651–656.
17 Eres A. Use of bivalirudin as the foundation anticoagulant
during percutaneous peripheral interventions. J Invas Cardiol
2006; 18:125–128.
18 Allie D, Lirtzman M, Watt DH, et al. Bivalirudin as a foundation
anticoagulant in peripheral vascular disease: a safe and feasible
alternative for renal and iliac interventions. J Invasive Cardiol
2003; 15:334–342.
19 Shammas N, Lemke J, Dippel E et al. Bivalirudin in peripheral
vascular interventions: A single center experience. J Invas
Cardiol 2003; 15:401–404.
20 Comerota AJ, Rao AK, Throm RC, et al. A prospective,
randomized, blinded, and placebo-controlled trial of intraoper-
ative intraarterial urokinase infusion during lower extremity
revascularization: Regional and systemic effects. Ann Surg
1993; 218:534.
21 Varadi A, Patthy L. Location of plasminogen-binding sites in
human fibrin(ogen). Biochemistry 1983; 22:2240–2246.
22 Ouriel K, Shortell C, DeWeese J, et al. A comparison of throm-
bolytic therapy with operative revascularization in the initial
treatment of acute peripheral arterial ischemia. J Vasc Surg 1994;
19:1021.
23 Ouriel K, Veith FJ, Sasahara AA, et al. Thrombolysis or periph-

eral artery surgery: phase 1 results. J Vasc Surg 1996; 23:64–75.
24 Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinant
urokinase with vascular surgery as initial treatment for acute
arterial occlusion of the legs. N Engl J Med 1998;
338:1105–1111.
25 Goldhaber SZ, Kessler CM, Heit J, et al. Randomized
controlled trial of recombinant tissue plasminogen activator
versus urokinase in the treatment of acute pulmonary
embolism. Lancet 1988; 2:293–298.
26 The Stile Investigators. Results of a prospective randomized
trial evaluating surgery versus thrombolysis for ischemia of the
lower extremity. Ann Surg 1994; 220:251–268.
27 Ouriel K, Katzen B, Mewissen M, et al. Reteplase in the treat-
ment of peripheral arterial and venous occlusions: a pilot study.
J Vasc Interv Radiol 2000; 11(7):849–854.
28 Castaneda F, Swischuk JL, Li R, Young K, Smouse B, Brady T.
Declining-dose study of reteplase treatment for lower extremity
arterial occlusions. J Vasc Interv Radiol 2002; 13(11):1093–1098.
References 581
29 Kiproff PM, Yammine K, Potts JM, et al. Reteplase infusion in
the treatment of acute lower extremity occlusions. J Thromb
Thrombolysis 13:75–79, 2002.
30 McCluskey ER, Refino CJ, Zioncheck TF, et al. Tenecteplase:
Biochemistry, pharmacology, and clinical experience. In
Sasahara AA, Loscalzo J (eds): New Therapeutic Agents in
Thrombosis and Thrombolysis, 2nd ed. New York: Marcel
Dekker, 2003:501–511.
31 Razavi MK, Wong H, Kee ST, Sze DY, Semba CP, Dake MD.
Initial clinical results of tenecteplase (TNK) in catheter-directed
thrombolytic therapy. J Endovasc Ther 2002; 9(5):593–598.

32 Burkart DJ, Borsa JJ, Anthony JP, Thurlo SR. Thrombolysis of
occluded peripheral arteries and veins with tenecteplase: a
pilot study. J Vasc Interv Radiol 2002; 13(11):1099–1102.
33 Dasgupta H, Blankenship JC, Wood GC, Frey CM, Demko SL,
Menapace FJ. Thrombocytopenia complicating treatment with
intravenous glycoprotein IIb/IIIa receptor inhibitors: a pooled
analysis. Am Heart J 2000; 140(2):206–211.
34 Scarborough RM, Kleiman NS, Phillips DR. Platelet glycopro-
tein IIb/IIIa antagonists. What are the relevant issues
concerning their pharmacology and clinical use? Circulation
1999; 100(4):437–444.
35 Ansel GM, Silver MJ, Botti CF Jr, et al. Functional and clinical
outcomes of nitinol stenting with and without abciximab for
complex superficial femoral artery disease: a randomized trial.
Catheter Cardiovasc Interv 2006; 67(2):288–297.
36 Dorffler-Melly J, Mahler F, Do DD, Triller J, Baumgartner I.
Adjunctive abciximab improves patency and functional
outcome in endovascular treatment of femoropopliteal occlu-
sions: initial experience. Radiology 2005; 237(3):1103–1119.
37 Rocha-Singh KJ, Rutherford J. Glycoprotein IIb-IIIa receptor
inhibition with eptifibatide in percutaneous intervention for
symptomatic peripheral vascular disease: the circulate pilot
trial. Catheter Cardiovasc Interv 2005; 66(4):470–473.
38 Shammas NW, Dippel EJ, Lemke JH, et al. Eptifibatide in
peripheral vascular interventions: results of the Integrilin
Reduces Inflammation in Peripheral Vascular Interventions
(INFLAME) trial. J Invasive Cardiol 2006 18(1):6–12.
39 Merlini PA, Rossi M, Menozzi A, et al. Thrombocytopenia
caused by abciximab or tirofiban and its association with clini-
cal outcome in patients undergoing coronary stenting.

Circulation 2004; 109(18):2203–2206. Epub 2004 Apr 26.
40 Allie DE, Hebert CJ, Lirtzman MD, et al. A safety and feasibility
report of combined direct thrombin and GP IIb/IIIa inhibition
with bivalirudin and tirofiban in peripheral vascular disease
intervention: treating critical limb ischemia like acute coronary
syndrome. J Invasive Cardiol 2005; 17(8):427–432.
41 Gold HK, Garabedian HD, Dinsmore RE, et al. Restoration of
coronary flow in myocardial infarction by intravenous chimeric
7E3 antibody without exogenous plasminogen activators.
Observations in animals and humans. Circulation 1997;
95(7):1755–1759.
42 Rerkpattanapipat P, Kotler MN, Yazdanfar S. Images in
cardiovascular medicine. Rapid dissolution of massive
intracoronary thrombosis with platelet glycoprotein IIb/IIIa
receptor inhibitor. Circulation 1999; 99(22):2965. No abstract
available.
43 Berkompas DC. Abciximab combined with angioplasty in a
patient with renal artery stent subacute thrombosis. Cathet
Cardiovasc Diagn 1998; 45(3):272–274.
1180 Chap49 3/14/07 5:00 PM Page 581
44 Tepe G, Duda SH, Erley CM, Schott U, Huppert PE, Claussen
CD. [The adjuvant use of the monoclonal antibody c7E3 Fab
in peripheral arterial thrombolysis] Rofo 1997;
166(3):254–257. German.
45 Schweizer J, Kirch W, Koch R, Muller A, Hellner G, Forkmann
L. Short- and long-term results of abciximab versus aspirin in
conjunction with thrombolysis for patients with peripheral
occlusive arterial disease and arterial thrombosis. Angiology
2000; 51(11):913–923.
46 Duda SH, Tepe G, Luz O, et al. Peripheral artery occlusion:

treatment with abciximab plus urokinase versus with urokinase
alone—a randomized pilot trial (the PROMPT Study). Platelet
receptor antibodies in order to manage peripheral artery
thrombosis. radiology 2001; 221(3):689–696.
47 Duda SH, Tepe G, Luz O, et al. Peripheral artery occlusion:
treatment with abciximab plus urokinase versus with urokinase
alone–a randomized pilot trial (the PROMPT Study).
platelet receptor antibodies in order to manage peripheral
artery thrombosis. Radiology 2001; 221(3):689–696.
48 Yoon HC, Miller FJ Jr. Using a peptide inhibitor of the glyco-
protein IIb/IIIa platelet receptor: initial experience in patients
with acute peripheral arterial occlusions. AJR Am J Roentgenol
2002; 178(3):617–622.
49 Syed, MI, Shaikh, A. Combination thrombolysis/GPIIbIIIa
inhibition in chronic peripheral thrombosis- A case report.
New Deve- lopments in Vascular Disease. Vol 1, (4) Spring
2003: 12–17.
50 Drescher P, McGuckin J, Rilling WS, Crain MR. Catheter-
directed thrombolytic therapy in peripheral artery occlusions:
combining reteplase and abciximab. AJR Am J Roentgenol
2003; 180(5):1385–1391.
51 Ouriel K, Castaneda F, McNamara T, et al. Reteplase
monotherapy and reteplase/abciximab combination therapy in
peripheral arterial occlusive disease: results from the RELAX
trial. J Vasc Interv Radiol 2004; 15(3):229–238.
52 Burkart DJ, Borsa JJ, Anthony JP, Thurlo SR. Thrombolysis of
acute peripheral arterial and venous occlusions with
tenecteplase and eptifibatide: a pilot study.
582 Anticoagulants in peripheral vascular interventions
1180 Chap49 3/14/07 5:00 PM Page 582

Introduction
Fifteen years ago, the only option for patients with large
abdominal aortic aneurysms (AAA) that required either elec-
tive or emergent repair was an open surgical approach using
a transperitoneal or retroperitoneal incision. Now with the
advent of endovascular approaches to aortic diseases, many
patients, especially those in the high-risk groups, have a mini-
mally invasive option to permit repair of aortic aneurysms,
dissections, pseudoaneurysms, and ruptures.
The endovascular procedure is most frequently used to
treat infrarenal AAAs that are a leading cause of death in the
older population. As our population ages, we will encounter
AAAs more frequently than ever before. An aneurysm is
defined by a size greater than 5 cm or 2.5 times the normal
diameter of the native artery. Most aneurysms begin below
the renal arteries and end close to the iliac bifurcation. More
complicated AAAs exist involving the suprarenal aorta and
visceral vessels and extending into the iliac arteries. The preva-
lence of AAAs is 3% to 10% for patients older than 50 years
(1). They occur more frequently in men and reach a peak inci-
dence close to the age of 80 years. AAA rupture is associated
with an 80% to 90% mortality rate and therefore the focus of
AAA treatment is on intervening before the aneurysm
ruptures; elective repair has mortality rate of less than 5%.
The first endovascular repair of an AAA in a human was
performed by Parodi in 1991. He made an endograft by
combining a prosthetic vascular graft with expandable Palmaz
stents (2). Since this milestone, the field has undergone
immense growth and has benefited from many technologic
advances that have permitted a wider application of this treat-

ment modality. The patient population that has benefited most
has been the population at high risk for open surgical repair.
These patients have severe comorbidities including and not
limited to old age, renal, heart, and pulmonary diseases.
Endovascular aneurysm repair (EVAR) of AAAs, results in a
quick recovery, can be done under local anesthesia and has
fewer systemic complications than open surgical repair. The
goal of this chapter is to describe patient and aneurysm
selection factors, the procedure and endografts, review clini-
cal trials, outcomes and complications and address some of
the controversial and challenging areas of EVAR with a view
to the future.
Patient selection factors
Abdominal aortic aneurysms can present as an incidental asymp-
tomatic finding on imaging or with symptoms, most prominently,
back and abdominal pain. The asymptomatic aneurysms can be
detected during routine physical examination but are more likely
found during workup for other complaints or as part of a screen-
ing program for patients who are at high risk for developing AAAs
(positive family or personal history of aneurysms). Intervention is
indicated for symptomatic aneurysms regardless of size, and
asymptomatic aneurysms with a size greater than 5 cm in diam-
eter or with an increase in size greater than 10% per year as
these groups have the greatest chance of rupture. Controversy
exists as to when to intervene in females with aneurysms less
than 5 cm diameter. Given smaller native aorta in this group, the
aneurysmal dilatation can be greater than 2.5 times the diameter
of the native aorta and less than 5 cm in diameter. Given the
smaller native aorta in this group, the aneurysmat dilatation can
be greater than 2.5 times the diameter of the native aorta and

less than 5 cm in diameter. This smaller size of aneurysm may
put the patient at equivalent risk of rupture.
There are patient selection factors for EVAR of AAAs that
set this procedure apart from open repair. The durability of
the open repair is well known and has been demonstrated in
multiple clinical studies. EVAR on the other hand requires
routine and frequent follow-up with ultrasound examination
and or CT scans to evaluate the repair for the development
of complications that require secondary interventions. The
patient must be able to commit to this follow-up routine in
order to be eligible for the procedure. In general, patients
who are young with few comorbidites are still advised to
undergo open surgical repair because of the demonstrated
50
Repair of AAAs
Alexandra A. MacLean and Barry T. Katzen
1180 Chap50 3/14/07 11:49 AM Page 583
longevity of the repair and ease of follow-up. EVAR has
become the procedure of choice for patients at high risk for
open repair given an older age and other morbidities (3).
Aneurysm assessment
The aneurysm and aorta are assessed with a 3D reconstruc-
tion CT scan or aortography with a calibrated catheter
(Table 1, Fig. 1). The fitness of the femoral arteries is evalu-
ated as the access route. They should be greater than 7 mm
in diameter and free from extensive atherosclerotic or
stenotic disease.
The anatomy of the proximal neck is important; the length
of aneurysm free aorta from the most caudal renal artery to
the beginning of aneurysmal dilatation must be at least 15 mm

to permit adequate seal of the device to a segment of normal
aorta. In addition, the angulation of the neck is ideally less than
60°. The placement of an endovascular device is not possible
when the neck is too large. The size limitation comes from
the need to have device sizes that can be packaged into
sheaths deliverable through the femoral artery. The shape of
the neck is described as tapered, reverse tapered, or straight,
with the latter being ideal.
The distal landing zone is evaluated for the location of the
hypogastric artery and presence of iliac aneurysms. Once again,
an area adequate for seal of the device to the iliac artery is
located, usually 20 mm in length. If a common iliac aneurysm
precludes landing the device proximal to the takeoff of the
hypogastric artery, then the patient’s circulation is evaluated for
preoperative embolization of the hypogastric artery. This will
permit the device to land distal to the hypogastric artery and
backflow from this artery is eliminated by the embolization.
The visceral vessels are evaluated for patency because the
required coverage of the inferior mesenteric artery mandates
that blood supply to the viscera be adequate from other
sources (celiac and superior mesenteric arteries). With expe-
rience, some of these contraindications can be overcome
with suprarenal attachment devices, additional cuffs, and
limbs, but for the nascent EVAR physician the contraindica-
tions should be acknowledged and adherence to the
fundamental principles of endovascular device implantation
will permit good outcomes.
EVAR technology
Endograft design is derived directly from the traditional grafts
used in open aortic surgery. The endograft body comes in

one piece (unibody) or as a bifurcated graft (Fig. 2). The
unibody endograft is designed to land into one of the iliac
arteries, thereby necessitating contralateral iliac occlusion and
a femoro-femoral bypass graft. Most of the procedures
carried out today use a bifurcated graft that comes with
extensions into the limbs and additional cuffs. This design
provides greater flexibility for matching the device to the
particular aneurysm features. The early endografts were
unsupported throughout the body with stents at the proximal
and distal ends. Today, the endografts have a metal skeleton
throughout the graft providing a supported structure. The
metal skeleton is covered with a fabric [polyester or polyte-
trafluoroethylene (PTFE)]. To prevent slippage of the
endograft, it is secured either by radial force or additional
hooks and barbs. The majority of the endografts are designed
to fixate and seal to a 15 mm segment of normal infrarenal
native aorta. The device is deployed with either a self-
expanding or balloon-expanding mechanism.
584 Repair of AAAs
CT scan assessment for EVAR eligibility
Proximal neck: diameter, length, angle,
Presence or absence of thrombus
Distal landing zone: diameter and length
Iliac arteries: presence of aneurysms and occlusive disease
Access arteries (common, external and femoral arteries):
Diameter, presence of occlusive disease
Contraindications for EVAR
Short proximal neck
Thrombus presence in proximal landing zone
Conical proximal neck

Greater than 120° angulation of the proximal neck
Critical inferior mesenteric artery
Significant iliac occlusive disease
Tortuosity of iliac vessels
Abbreviation
: EVAR, endovascular aneurysm repair.
Table 1 Assessment and contraindications
Figure 1
(
Left
) Angiogram of infrarenal abdominal aortic aneurysms (AAA)
with marker catheter in place; (
Right
) 3D CT reconstruction of
an infrarenal AAA.
1180 Chap50 3/14/07 11:49 AM Page 584
The many permutations of these features have led to the
generation of multiple devices employing a variety of concepts
and approaches ( Table 2). Two devices are no longer available
(Ancure and Vanguard/Stentor) but are mentioned because
some patients had these implanted and these may be encoun-
tered in the clinical setting. Four devices are currently FDA
approved for commercial use in the United States (AneuRx,
Excluder, Zenith, and PowerLink); the other devices are in
clinical trials or in use in Europe.
With multiple devices available and increased clinical and
technical experiences, it is apparent that each device has its own
advantages and disadvantages. The best results can come from
optimizing the type of endograft to specific anatomy of a given
patient. This is less important in patients with ‘ideal’ anatomic

features, but when features such as neck angulation, calcification,
access tortuosity are encountered, one device may to superior
to another for dealing with the challenging anatomy. On some
occasions supraprenal attachment may be necessary and desir-
able, in others infrarenal fixation may be sufficient.
The procedure: start to finish
Once the patient is selected and the appropriate device is in
hand to deal with the particular aneurysm morphology, the
patient is brought into the interventional or operating room
suite for the procedure. The procedure is now performed by
interventional radiologists, cardiologists, and vascular surgeons
with the patient under general, regional, or local anesthesia
(4). The femoral arteries are accessed by either open surgical
incisions or percutaneously. An aortogram is performed to
locate the renal and hypogastric arteries. The main body is
then inserted through either femoral arteriotomy but the
largest and most disease free femoral artery is preferred. The
patient is anticoagulated as at this point in the procedure blood
flow to the legs is interrupted by the size of the sheath; heparin
or a direct thrombin inhibitor (e.g., bivalirudin) may be used
(5). The location of the renal arteries with respect to the top
of the endograft is reassessed. The endograft is then deployed.
Next the limbs are inserted through each groin into the
respective leg of the endograft. Once again the location of
the hypogastric arteries is verified before the limbs are landed
just proximal to their orifices or distally if the hypogastric
was embolized preoperatively. A completion angiogram is
performed and examined for the development of complica-
tions, especially Type I endoleaks. If further intervention is
required, it is done at this point. Finally, the groins are closed

either with sutures or with the aid of one of many percuta-
neous closure devices. The distal pulses are examined and
documented for further vascular monitoring.
Endograft challenges
Ruptured aneurysm
A ruptured AAA is a devastating event with an overall mortality
rate of greater than 90% and 40% to 70% of those patients
who make it to the hospital alive die (1). An endovascular
approach to ruptured aneurysms has been developed and
involves the rapid deployment of a proximal occlusion balloon
through the brachial artery to sit in the descending thoracic
aorta. Some of the key maneuvers include permissive hypoten-
sion, placement of the brachial wire under local anesthesia,
performance of a diagnostic angiogram, and of course, readi-
ness for conversion to an open procedure if necessary (6,7).
The patients who undergo endovascular repair have to be
stable enough to have a CT scan performed preoperatively. In
one study, the thirty day mortality rate was 10.8% for this
approach and the late conversion rate was 9% and was attrib-
uted to mainly infection issues and device migration (8). Survival
was 89.1% at one year and 69.9% at four years. This was
compared with a thirty-day mortality rate of 35% for patients
undergoing open repair of ruptures.
Difficult neck
The difficult neck comes in a variety of types: angulated, coni-
cal, stenotic (Fig. 3). The angulated neck makes wire passage
challenging, but this can be overcome with the use of flexible
sheaths and if necessary brachial artery insertion of the initial
wire for retrieval from the femoral artery. In addition, the
angulation often straightens during endograft placement and

Endograft challenges 585
Available or in trials/development
AneuRx (Medtronic, Santa Rosa, CA, U.S.A.)
Excluder (W.L. Gore, Flagstaff, AZ, U.S.A.)
Zenith (Cook Inc., Bloomington, IN, U.S.A.)
PowerLink (Endologix, Irvine, CA, U.S.A.)
Talent (Medtronic, Santa Rosa, CA, U.S.A.)
Fortron (Cordis Corp., Johnson and Johnson,
Miami, FL, U.S.A.)
Lifepath (Edwards Lifesciences, Irvine, CA, U.S.A.)
Quantum (Cordis Corp., Johnson and Johnson, Miami, FL)
Enovus (Trivascular, Santa Rosa, CA, U.S.A.)
No longer available
Ancure (Guidant Corp., Indianapolis, IN, U.S.A.)
Vanguard/Stentor (Boston Scientific Corp., Natick,
MA, U.S.A.)
Table 2 Endo devices
1180 Chap50 3/14/07 11:49 AM Page 585
therefore the ability to judge the exact postprocedure
location of the graft is difficult, especially with respect to the
renal arteries.
The conical neck can be viewed as a cone with an increas-
ing diameter from the renals to the aneurysm sac. This neck
is a challenge for endograft sizing and achievement of graft
seal to nonaneurysmal aorta. The first issue is often dealt with
by decreasing the amount of the usual graft oversizing from
the normal 20% to 10% to 15%; this reduces stretching the
narrower portion of the conical neck. Endografts that require
balloon expansion, as opposed to radial force, may facilitate
graft seal when dealing with the conical neck.

The third type of challenging neck is the stenotic neck.
Once again, the issue centers on the importance of sizing the
graft correctly. If the graft is oversized for the stenotic portion,
graft infolding may occur. On the other hand, if the graft is
undersized, then the neck may seal but the remainder of the
repair does not fit properly, leading to endoleak and possible
graft migration.
Difficult iliac arteries
Access to the aorta is usually obtained through the femoral
arteries, either by percutaneous methods or by surgical
exposure. The presence of tortuous or atherosclerotic
iliac arteries makes the insertion of wires and sheaths through
the arteriotomy difficult and potentially risky (Fig. 3). CT
scan imaging techniques often do not adequately show iliac
artery anatomy. Even arteriography cannot reliably measure
areas of stenosis. 3D CT scan reconstructions with the
ability to insert a virtual sheath help tackle the challenge of
preoperative imaging and measuring of iliac arteries.
Sometimes it is necessary to access the brachial artery to
pass the initial wire into the femoral artery (9) or access
the iliac artery or aorta through a retroperitoneal incision
with the addition of a conduit to facilitate endograft
insertion (10).
Small iliac arteries are encountered in 8% of the popula-
tion and most are found in women (II). Some arteries can be
dilated but not without risk of dissection and rupture.
Therefore, a patient with an external iliac artery smaller than
7 mm should undergo either open repair or have the endo-
graft inserted through the larger common iliac artery or aorta.
Stenotic iliac arteries can also be dilated but with the same

risks of dissection and rupture. Aneurysmal iliac disease is a
challenging anatomical feature especially for adequate endo-
graft distal landing and sealing and may require coverage of
the hypogastric artery.
EVAR complications
One of the distinguishing differences between EVAR and
open repair is the higher rate of graft related complications
with EVAR (12). Some occur during or soon after the proce-
dure whereas others are only noticed during the graft
surveillance period (Table 3). Reporting standards have been
established to permit comparison of complications (13). The
analysis of the Lifeline Registry (2664 EVAR cases and 334
open surgical cases) showed that the thirty-day operative
mortality rates for the two groups were similar at 1.7% for
EVAR and 1.4% for open surgical. The freedom from rupture
was also similar for the two groups at one year: 99.8% and
100% and there was no difference in AAA-related death rates
(14). Greenhalgh in the report from the EVAR 1 trial noted
that complication rate was 41% for EVAR patients and 9% for
open surgical patients within four years of the procedure (15).
The aneurysm-related death rate was 4% for EVAR patients
and 7% for open surgical patients. The all-cause mortality
rates were similar for the two groups (28%).
586 Repair of AAAs
Figure 2
Abdominal aortic aneurysms bifurcated supported stent graft
(Excluder, Gore).
Figure 3
(
Left

) Angulated proximal aortic neck; (
Right
) tortuous iliac
arteries.
1180 Chap50 3/14/07 11:49 AM Page 586
EVAR complications 587
Early
Type I proximal and distal endoleaks
Type IV endoleak
Device related complications
Inability to deploy stent
Arterial complications
Systemic complications
Cardiac
Cerebral
Pulmonary
Renal
Access site and lower limb complications
Bleeding, hematoma, false aneurysm
Arterial thrombosis
Death
Conversion
Rupture
Late
Endoleaks: I (a, b), II, III
Aneurysm growth greater than or equal to 8 mm
Late AAA-related death
Death
Conversion
Rupture

Classification of endoleaks
Attachment site leaks
Proximal end of endograft
Distal end of endograft
Iliac occluder (plug)
Branch leaks (without attachment site connection
Simple or to-and-fro (from only one patent branch)
Complex or flow-through (with two or
more patent branches)
Graft defect
Junctional leak or modular disconnect
Fabric disruption (midgraft hole)
Minor (Ͻ2 mm; e.g., suture holes)
Major (Ն2 mm)
Graft wall (fabric) porosity (Ͻ30 days after graft
placement)
Table 3 Complications
Access complications
Access problems occur with either the percutaneous
approach or open surgical approach to the vessels for endo-
graft insertion. The femoral artery may be injured and require
immediate repair with a patch or replacement of a segment.
In addition, distal thrombosis may occur from the blockage
of the flow into the lower extremities by the sheath and
inadequate anticoagulation. This highlights the importance of
noting the preoperative pulse examination, so that the post-
operative findings can be correctly interpreted. As with
any groin procedure, lymph leaks, wound infections and
hematomas can occur and vary from the benign
that resolves to the serious that requires further intervention

(re-exploration, evacuation, muscle flaps, etc.).
Device problems
Device design evolves to remedy problems associated
with structural integrity. There have been reports of
fabric erosion (16), hook fractures (17), and component
separation (18).
Surgical conversion
Primary surgical conversion occurs within the first postopera-
tive 30 days and secondary surgical conversion occurs any
time after that. In an examination of the EUROSTAR
(European Collaborators on Stent/graft Techniques for aortic
Aneurysm Repair) registry, 2.6% of the 1871 patients
required conversion and in 38 patients this occurred in the
first postoperative month (primary conversion) (19). Eleven
patients underwent open surgical repair during a mean
follow-up period of eight months (secondary conversion) and
rupture was the most frequent reason for this. Kong et al.
examined secondary conversion for the 594 patients in the
Excluder clinical trials and noted that 2.7% of the patients
underwent late open conversion; no conversions occurred in
the first year after the procedure. Freedom from conversion
was 96.7% at forty-eight months postoperative. The major
indication noted was the development of endotension in the
absence of a demonstrable endoleak.
Endoleaks
Endoleaks are a major concern for those engaged in EVAR
(Table 3, Fig. 4). This phenomenon describes the continua-
tion of blood flow into the extragraft portion of the aneurysm
(20). Endoleaks are related to the graft itself or other factors
such as the presence of large patent lumbar arteries (21). The

presence of an endoleak increases the chance of rupture.
Diagnostic imaging plays an important role in the detection
of endoleaks: intraprocedural angiograms, surveillance CT
scans, or duplex ultrasounds.
The management of endoleaks varies according to the type:
type I and III endoleaks should be addressed expediently, and
type IV endoleaks usually resolve. The treatment algorithm for
1180 Chap50 3/14/07 11:49 AM Page 587
type II endoleaks is not straightforward as these endoleaks may
resolve on their own over time. If a type I endoleak is noted on
the completion angiogram, a stent-graft cuff or extension is
immediately placed to facilitate better seal. A similar treatment
plan is undertaken if the type I endoleak is noted in the post-
operative period. Type II endoleaks can be followed and
intervention planned if the endoleak does not resolve; some
physicians suggest a follow-up CT scan at six months and if the
endoleak is present, then the patent artery is either embolized
or surgically ligated. Other physicians will only treat type II
endoleaks if it is accompanied with sac enlargement. Gelfand
et al. examined the clinical significance of type II endoleaks by
analyzing data from 10 EVAR trials (22). The authors found
that approximately half of the endoleaks disappeared within
12 months. This paper delineated situations when type II
endoleak intervention is warranted: AAA sac enlargement after
six months, increased sac pressure (Ͼ20% of systolic BP),
presence of leak greater than 12 months after procedure.
Endograft limb occlusion
This is an infrequently encountered problem, occurring in less
than 5% of patients, but its morbidity is serious leading to
extremity loss (23). Small limb diameter and graft extension

to the external iliac artery, as opposed to the common iliac, is
a risk factor for the development of limb occlusion. Fifty
percent of the thromboses occurred within 30 days of the
procedure and almost 70% required intervention: surgical
(femorofemoral, axillary-femoral, axillary-bifemoral bypasses)
and/or endoluminal techniques (rheolytic and pharmacologic
thrombolysis).
Graft kinks
Stent-graft kinks are more often seen when unsupported
endografts are used (24). This complication occurred in 3.7%
of the patients in the EUROSTAR registry and was associated
with type I and III endoleaks, graft stenosis, graft limb throm-
bosis, graft migration, and conversion to open repair (25). In
addition, women with angulated AAA necks were atmost risk
for stent-graft kink. This problem is usually managed with
stenting of the kink.
Sac enlargement
The AneuRx clinical trial was analyzed by Zarins to describe
the phenomenon of aneurysm sac enlargement (26). Twelve
percent of the patients experienced aneurysm sac enlarge-
ment and these patients were older and usually had an
endoleak. When patients with endoleaks were analyzed,
17% had sac enlargement whereas only 2% of patients with-
out endoleaks had the same finding. Elevated pressure within
the aneurysm sac, also known as endotension, has been
reported as one mechanism that is responsible for sac
enlargement (27). This finding is documented when the intra-
aneurysm pressure is measured during follow-up
angiography. Endotension can exist without an endoleak.
Device migration

The AneuRx trial has also been analyzed to determine the
frequency of stent migration and identify risk factors (21,28).
Ninety-four of 1119 patients had evidence of stent migration
that occurred a mean of 30 months after EVAR. Low initial
deployment, below the renals, and short proximal fixation
length are the identifiable risk factors. In this study, 68% of the
patients required no treatment whereas 23 patients had
extender modules placed and seven patients underwent
surgical conversion. Surgical conversion was examined in a
single center study of 640 patients by Verzini (29). This group
found that early conversion (within 30 days) was performed
in nine patients and late conversion was carried out in 29. At
588 Repair of AAAs
Figure 4
Type IA endoleak noted on completion angiogram.
1180 Chap50 3/14/07 11:49 AM Page 588
six years after EVAR the risk of undergoing a conversion was
9%. A study by Tonnessen et al. examined device migration
at mid- and long-term timepoints with the AneuRx and
Zentih endografts (30). The AneuRx device had a significantly
higher incidence of migration than the Zenith device. At three
and four years out from the procedure, the migration rate
was 22% and 28%, respectively, for AneuRx and only 2.4%
for Zenith. In addition, a greater proportion of the migrated
AneuRx endografts had dilated necks compared with the
nonmigrated AneuRx endografts. One of the conclusions was
that devices with active fixation design (e.g., Zenith) may be
protective against migration. Also, a significant proportion of
patients with endograft migration required intervention and
so this one again highlights the importance of long-term

surveillance.
Extremity and visceral ischemia
Ischemia to the viscera and extremities can also occur and the
signs can be subtle (decreased pulses, mild abdominal pain,
buttock claudication) or alarmingly obvious (lower extremity
mottling, severe abdominal pain, elevated creatinine phos-
phokinase levels, or gastrointestinal bleeding) (31). Lower
extremity ischemia can result from problems at the femoral
access site (dissection, atheroembolization) or from issues
with the endograft (limb occlusion, kinking). The former often
requires surgical intervention whereas the latter can be
managed by interventional techniques like placing additional
stents. The endograft covers the inferior mesenteric artery
and if the remainder of the visceral and hypogastric circulation
is poor or compromised can lead to colonic ischemia. In addi-
tion, spinal cord ischemia can manifest in paresis or paralyis
due to the coverage of intercostals arteries; this complication
is rare but serious.
Surveillance
The recommended surveillance routine is for a CT scan at 1,
6, and 12 months and annually thereafter. If an endoleak is
detected, the frequency of the scans increases to every six
months until resolution of the endoleak is detected.
Investigators have compared duplex ultrasound with CT scan
for surveillance and found that CT scan is superior for endoleak
detection (32). Since endoleaks are an important complication
with therapeutic implications, CT scans should be used rather
than duplex examination for repair surveillance.
MRI has been investigated as a useful way to follow these
patients. It has advantages over CT scan surveillance because

it does not put renal function at risk in this older population. It
should especially be entertained in patients with preexisting
renal insufficiency (33). Endograft surveillance methods now
include the use of an implanted sensor to measure sac
pressure to assess for the development of endotension
(34,35). The advances in EVAR technology have been accom-
panied by a greater understanding of the basic science of
aneurysmal disease and cross-fertilization has occurred. For
example, Curci has been studying the relationship between
the secretion of matrix metalloproteinases (MMPs) and AAAs
(36). He has measured increased levels in the aneurysmal
rather than the normal arterial wall. This finding led physicians
to develop a new method for endograft surveillance: the lack
of a decrease in MMP-3 and MMP-9 levels should alert the
physician to possibility of a failing endograft repair (37).
Advances in the basic science of aneurysm disease are helping
us better manage this disease.
EVAR outcomes and trial
results
Examination of outcomes of endovascular AAA repair comes
from mainly two sources: databases and clinical trials.
Eurostar registry
The EUROSTAR Registry was started in 1996 and has contin-
ued to provide a substantial amount of data especially for
outcome analyses. Data come from 135 vascular centers in
Europe (38–40).
Outcomes in patients greater than or equal to eighty years
old have been analyzed and compared to those less than 80
years (41). The octogenarians more frequently had heart,
kidney, and lung disease preoperatively and a greater propor-

tion was deemed not fit for surgery compared with the
younger group of patients. The thirty-day and in-house
mortality rate for octogenarians was significantly higher than
the younger group: 5% versus 2%. In addition, this group of
patients had higher device-related and systemic complication
rates. Finally, aneurysm related and all cause mortality rates
were significantly higher for this older group of patients.
Dream trial
The Dream trial examined outcomes two years following
open or endovascular repair of AAAs (42). The cumulative
survival rates for the two groups were similar: 89.6% (open),
89.7% (endovascular). There was no significant difference in
aneurysm related mortality. The study concluded that the
early advantage of EVAR is no longer present after one year
following intervention.
EVAR outcomes and trial results 589
1180 Chap50 3/14/07 11:49 AM Page 589
EVAR 1 and 2 trials
Results of the EVAR trial 1 were recently published and
describe the outcomes of 543 patients who were anatomi-
cally suitable for EVAR and fit for open repair but ultimately
underwent EVAR and 539 patients who had open repair (15).
The authors found that EVAR is more expensive, had a higher
number of complications and reinterventions but it resulted in
a 3% better aneurysm survival rate. The EVAR trial 2 then
examined those patients who were unfit for open repair and
underwent either EVAR or no intervention (43). The 30-day
operative mortality rate in the EVAR group was 9% and in the
no intervention group the rupture rate was nine per 100
person years. There was no significant difference in either

aneurysm-related mortality or all-cause mortality.
EVAR future directions and
controversies
The future of EVAR is not fully determined; many questions
remain unanswered. Some help will come from the results of
ongoing clinical trials. The impact of endotension and the
viability of pressure monitoring will become clearer once
more intragraft sensor data becomes available. In addition,
the utility of fenestrated transrenal endografts is an area of
great interest. We will soon see if this is a solution to short
proximal aortic necks and suprarenal aneurysms (44). With
this new technology and low mortality rate physicians are
investigating whether we should be treating smaller
aneurysms and clinical trials are being conducted to address
this issue (45,46). As the design of EVAR devices evolves and
our facility using them improves, the one thing that will not
change is the importance of appropriate patient selection.
References
1 Rutherfor RB, ed. Vascular Surgery, 6th ed. Amsterdam,
Netherlands: Elsevier, 2005.
2 Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft
implantation for abdominal aortic aneurysms. Ann Vasc Surg
1991; 5(6):491–499.
3 Hua HT, Cambria RP, Chuang SK, et al. Early outcomes of
endovascular versus open abdominal aortic aneurysm repair in
the National Surgical Quality Improvement Program-Private
Sector (NSQIP-PS). J Vasc Surg 2005; 41(3):382–389.
4 Parra JR, Crabtree T, McLafferty RB, et al. Anesthesia tech-
nique and outcomes of endovascular aneurysm repair. Ann
Vasc Surg 2005; 19(1):123–129.

5 Katzen BT, Ardid MI, MacLean AA, et al. Bivalirudin as an anti-
coagulation agent: safety and efficacy in peripheral interventions.
J Vasc Interv Radiol 2005; 16(9):1183–1187; quiz 7.
6 Lee WA, Hirneise CM, Tayyarah M, et al. Impact of endovas-
cular repair on early outcomes of ruptured abdominal aortic
aneurysms. J Vasc Surg 2004; 40(2):211–215.
7 Ohki T, Veith FJ. Endovascular therapy for ruptured abdominal
aortic aneurysms. Adv Surg 2001; 35:131–151.
8 Hechelhammer L, Lachat ML, Wildermuth S, et al. Midterm
outcome of endovascular repair of ruptured abdominal aortic
aneurysms. J Vasc Surg 2005; 41(5):752–757.
9 Criado FJ, Wilson EP, Abul-Khoudoud O, et al. Brachial artery
catheterization to facilitate endovascular grafting of abdominal
aortic aneurysm: safety and rationale. J Vasc Surg 2000;
32(6):1137–1141.
10 Carpenter JP. Delivery of endovascular grafts by direct sheath
placement into the aorta or iliac arteries. Ann Vasc Surg 2002;
16(6):787–790.
11 Wolf YG, Arko FR, Hill BB, et al. Gender differences in
endovascular abdominal aortic aneurysm repair with the
AneuRx stent graft. J Vasc Surg 2002; 35(5):882–886.
12 Elkouri S, Gloviczki P, McKusick MA, et al. Perioperative
complications and early outcome after endovascular and open
surgical repair of abdominal aortic aneurysms. J Vasc Surg
2004; 39(3):497–505.
13 Chaikof EL, Blankensteijn JD, Harris PL, et al. Reporting stan-
dards for endovascular aortic aneurysm repair. J Vasc Surg
2002; 35(5):1048–1060.
14 Lifeline registry of endovascular aneurysm repair: long-term
primary outcome measures. J Vasc Surg 2005; 42(1):1–10.

15 Greenhalgh RM, Brown LC, Kwong GP, et al. Endovascular
aneurysm repair versus open repair in patients with abdominal
aortic aneurysm (EVAR trial 1): randomised controlled trial.
Lancet 2005; 365(9478):2179–2186.
16 Teutelink A, van der Laan MJ, Milner R, et al. Fabric tears as a
new cause of type III endoleak with Ancure endograft. J Vasc
Surg 2003; 38(4):843–846.
17 Najibi S, Steinberg J, Katzen BT, et al. Detection of isolated hook
fractures 36 months after implantation of the Ancure endograft:
a cautionary note. J Vasc Surg 2001; 34(2): 353–356.
18 Maleux G, Rousseau H, Otal P, et al. Modular component
separation and reperfusion of abdominal aortic aneurysm sac
after endovascular repair of the abdominal aortic aneurysm: a
case report. J Vasc Surg 1998; 28(2):349–352.
19 Cuypers PW, Laheij RJ, Buth J. Which factors increase the risk
of conversion to open surgery following endovascular abdom-
inal aortic aneurysm repair? The EUROSTAR collaborators.
Eur J Vasc Endovasc Surg 2000; 20(2):183–189.
20 White GH, Yu W, May J. Endoleak—a proposed new termi-
nology to describe incomplete aneurysm exclusion by an
endoluminal graft. J Endovasc Surg 1996; 3(1):124–125.
21 Veith FJ, Baum RA, Ohki T, et al. Nature and significance of
endoleaks and endotension: summary of opinions expressed at
an international conference. J Vasc Surg 2002; 35(5):1029–1035.
22 Gelfand DV, White GH, Wilson SE. Clinical significance of type
II endoleak after endovascular repair of abdominal aortic
aneurysm. Ann Vasc Surg 2006; 20(1):69–74.
23 Carroccio A, Faries PL, Morrissey NJ, et al. Predicting iliac limb
occlusions after bifurcated aortic stent grafting: anatomic and
device-related causes. J Vasc Surg 2002; 36(4):679–684.

24 Carpenter JP, Neschis DG, Fairman RM, et al. Failure of
endovascular abdominal aortic aneurysm graft limbs. J Vasc
Surg 2001; 33(2):296–302; discussion 3.
590 Repair of AAAs
1180 Chap50 3/14/07 11:49 AM Page 590
25 Fransen GA, Desgranges P, Laheij RJ, et al. Frequency, predictive
factors, and consequences of stent-graft kink following endovas-
cular AAA repair. J Endovasc Ther 2003; 10(5): 913–918.
26 Zarins CK, Bloch DA, Crabtree T, et al. Aneurysm enlarge-
ment following endovascular aneurysm repair: AneuRx clinical
trial. J Vasc Surg 2004; 39(1):109–117.
27 Lin PH, Bush RL, Katzman JB, et al. Delayed aortic aneurysm
enlargement due to endotension after endovascular abdominal
aortic aneurysm repair. J Vasc Surg 2003; 38(4):840–842.
28 Zarins CK, Bloch DA, Crabtree T, et al. Stent graft migration
after endovascular aneurysm repair: importance of proximal
fixation. J Vasc Surg 2003; 38(6):1264–1272; discussion 72.
29 Verzini F, Cao P, De Rango P, et al. Conversion to open repair
after endografting for abdominal aortic aneurysm: causes,
incidence and results. Eur J Vasc Endovasc Surg 2006;
31(2):136–142.
30 Tonnessen BH, Sternbergh WC, 3rd, Money SR. Mid- and
long-term device migration after endovascular abdominal
aortic aneurysm repair: a comparison of AneuRx and
Zenith endografts. J Vasc Surg 2005; 42(3):392–400;
discussion-1.
31 Maldonado TS, Rockman CB, Riles E, et al. Ischemic compli-
cations after endovascular abdominal aortic aneurysm repair.
J Vasc Surg 2004; 40(4):703–709; discussion 9–10.
32 Raman KG, Missig-Carroll N, Richardson T, et al. Color-flow

duplex ultrasound scan versus computed tomographic scan in
the surveillance of endovascular aneurysm repair. J Vasc Surg
2003; 38(4):645–651.
33 Engellau L, Albrechtsson U, Hojgard S, et al. Costs in follow-
up of endovascularly repaired abdominal aortic aneurysms.
Magnetic resonance imaging with MR angiography versus
EUROSTAR protocols. Int Angiol 2003; 22(1):36–42.
34 Baum RA, Carpenter JP, Cope C, et al. Aneurysm sac pressure
measurements after endovascular repair of abdominal aortic
aneurysms. J Vasc Surg 2001; 33(1):32–41.
35 Ellozy SH, Carroccio A, Lookstein RA, et al. First experience in
human beings with a permanently implantable intrasac pressure
transducer for monitoring endovascular repair of abdominal
aortic aneurysms. J Vasc Surg 2004; 40(3): 405–412.
36 Curci JA, Thompson RW. Adaptive cellular immunity in aortic
aneurysms: cause, consequence, or context? J Clin Invest
2004; 114(2):168–171.
37 Sangiorgi G, D’Averio R, Mauriello A, et al. Plasma levels of
metalloproteinases-3 and -9 as markers of successful abdomi-
nal aortic aneurysm exclusion after endovascular graft
treatment. Circulation 2001; 104(12 suppl 1):I288–1295.
38 Berg P, Kaufmann D, van Marrewijk CJ, et al. Spinal cord
ischaemia after stent-graft treatment for infra-renal abdominal
aortic aneurysms. Analysis of the Eurostar database. Eur J Vasc
Endovasc Surg 2001; 22(4):342–347.
39 Fransen GA, Vallabhaneni SR Sr, van Marrewijk CJ, et al.
Rupture of infra-renal aortic aneurysm after endovascular
repair: a series from EUROSTAR registry. Eur J Vasc Endovasc
Surg 2003; 26(5):487–493.
40 Peppelenbosch N, Buth J, Harris PL, et al. Diameter of

abdominal aortic aneurysm and outcome of endovascular
aneurysm repair: does size matter? A report from
EUROSTAR. J Vasc Surg 2004; 39(2):288–297.
41 Lange C, Leurs LJ, Buth J, et al. Endovascular repair of abdom-
inal aortic aneurysm in octogenarians: an analysis based
on EUROSTAR data. J Vasc Surg 2005; 42(4):624–630;
discussion 30.
42 Blankensteijn JD, de Jong SE, Prinssen M, et al. Two-year
outcomes after conventional or endovascular repair of abdomi-
nal aortic aneurysms. N Engl J Med 2005; 352(23):2398–2405.
43 Endovascular aneurysm repair and outcome in patients unfit
for open repair of abdominal aortic aneurysm (EVAR trial 2):
randomised controlled trial. Lancet 2005; 365(9478):
2187–2192.
44 Verhoeven EL, Prins TR, Tielliu IF, et al. Treatment of short-necked
infrarenal aortic aneurysms with fenestrated stent-grafts: short-
term results. Eur J Vasc Endovasc Surg 2004; 27(5): 477–483.
45 Cao P. Comparison of surveillance vs Aortic Endografting
for Small Aneurysm Repair (CAESAR) trial: study design
and progress. Eur J Vasc Endovasc Surg 2005; 30(3):245–251.
46 Zarins CK, Crabtree T, Arko FR, et al. Endovascular repair or
surveillance of patients with small AAA. Eur J Vasc Endovasc
Surg 2005; 29(5):496–503; discussion 4.
References 591
1180 Chap50 3/14/07 11:49 AM Page 591
1180 Chap50 3/14/07 11:49 AM Page 592
Transcatheter ablation of
septal hypertrophy
Approximately 25% of all patients with hypertrophic
cardiomyopathy (HCM) have latent left ventricular outflow

obstruction with an intraventricular gradient (1). Pathophysiologic
features are asymmetric hypertrophy of the septum and a
systolic anterior movement of the anterior leaflet. Medical
treatment includes betablockers, and calcium antagonists of
the verapamil type. Approximately 5–10% of the patients
with outflow obstruction are refractory to such negative
inotropic therapy (2). Positive inotropic drugs such as digitalis
or sympathomimetics are strictly contraindicated. In the pres-
ence of atrial fibrillation, anticoagulation therapy should be
started. Since endocarditis is more common in patients with
HCM because of turbulence in the left ventricle, prophylactic
antibiotics should be administered for periods
of potential bacteraemia.
Subvalvular myectomy has a reported success of more
than 90% with a mortality rate of less than 2%, but this ther-
apy is not applicable to every patient. Transcatheter ablation
of septal hypertrophy has been performed since 1994 as a
reasonable option for obstructive HCM patients. An increas-
ing number of reports claim efficacy comparable to that of the
surgical approach (3).
Patients with a high risk of surgical morbidity and mortality
and those who suffer from pharmacologic side effects under
conservative treatment should be considered for tran-
scatheter alcohol ablation. NYHA classification, left ventricular
gradient, and a septal thickness exceeding 16 mm are indica-
tions for intervention. NYHA or CCS class II patients with a
minimum resting gradient of 50 mmHg are candidates for
this procedure as well as class III and IV patients with a rest-
ing gradient of more than 30 mmHg or a provoked gradient
greater than 60 mmHg (4,5).

The initial stage of the procedure entails measurement of
the peak to peak intraventricular gradient at rest. Induced
extrasystolic beats can unmask a potentially higher gradient.
Stepwise application (until a heart rate of about 110 bpm is
achieved) of isoproterenol 200 mcg in 50 cc of saline can be
used to increase the pressure gradient in sedated patients.
Following administration of heparin, the target vessel for alco-
hol dilution is probed by catheter. The target vessel is almost
always the first septal branch of the left anterior descending
artery. Balloon inflation isolates the vessel, occluding blood
flow. Retrograde leakage of alcohol back into the left anterior
descending has to be avoided. An echo contrast study is
performed to confirm effective occlusion and thus obviate this
complication. Intravenous analgesia should be administered
before alcohol injection to diminish chest pain.
Slow application of 0.2–1.5 mL of alcohol through the
inflated balloon catheter induces necrosis of the myocardium,
which is seen as an obvious contrast enhancement on
echocardiography. If the gradient post instillation of alcohol
remains above 30 mmHg, the balloon may be positioned
more proximally in the vessel or a second septal perforating
artery may be treated in the same way.
In some cases, tissue edema of the affected myocardium
may temporarily increase the outflow gradient during the
early days of follow-up. During subsequent months remodel-
ing of the outflow tract is usually observed, resulting in a
progressive reduction in gradient. Several studies have docu-
mented the efficacy of alcohol septal ablation (6Ϫ8),
demonstrating improvement in functional class and exercise
capacity.

Possible complications include massive myocardial infarc-
tion due to retrograde flow around the occlusion balloon,
complete heart block, ventricular fibrillation, stroke, dissec-
tion of the left anterior descending artery, and right coronary
artery thrombosis. Though high grade atrioventricular block-
age occurs relatively frequently, procedural mortality rate is
low (0–4%) and severe complications are rare and often
avoidable (7Ϫ10).
Creatinine kinase levels should be assessed frequently
during the stay in the coronary care unit and may rise up to
1500 U/ l. After the procedure there may be some risk
51
Interventions for structural heart disease
Ralph Hein, Neil Wilson, and Horst Sievert
1180 Chap51 3/14/07 11:49 AM Page 593
of thrombus formation in the area of ablation. Some opera-
tors prescribe aspirin (100 mg/day, p.o.) for four weeks
postinterventionally.
LAA occlusion
The left atrial appendage (LAA) is a muscular cavity discharging
into the left atrium. It is the prevalent location for intracardiac
thrombus (11). If atrial fibrillation cannot be eliminated with
medical therapy or an ablation procedure then life-long anti-
coagulation is necessary. Usually patients with chronic atrial
fibrillation are anticoagulated with coumadin type drugs. Many
patients however have contraindications to anticoagulation like
intracerebral aneurysms, hemorrhagic diathesis, gastrointesti-
nal lesions, and liver dysfunction. For such patients
interventional closure of the LAA may be a therapeutic alter-
native, and has been performed now for almost five years.

There are currently three devices under investigation:
1. PLAATO device (ev3, Inc., Plymouth, MN)
2. Amplatzer occluder (AGA Medical Corporation, Golden
Valley, MN)
3. Watchman device (Atritech, Inc., Minneapolis, MN)
1. The PLAATO device (Fig. 1) was the first device to be
implanted in a human LAA in August 2001. Its nitinol framework
features a tissue-anchoring system on the struts to maintain the
correct position once deployed. The orifice of the LAA is sealed
by a nonthrombogenic polytetrafluoroethylene membrane
excluding the appendage from the blood circulation and allow-
ing tissue adhesion.
The morphology and diameter of the appendage are very
variable; hence, detailed preinterventional imaging with trans-
esophageal echocardiography (TEE) and angiography is
important. Thrombus in the appendage is obviously a strict
contraindication to the procedure and should be excluded by
transesophageal echo before attempting closure. The orifice
diameter of the appendage should range between 13 and
27 mm to achieve a stable device position.
To access the LAA transseptal puncture is necessary.
Angiography is performed for further morphologic measure-
ments. The PLAATO system is engaged via a delivery catheter
and unfolded in the appendage. Compression of 10% is
mandatory and at least two rows of anchors should be
engaged into the surrounding tissue.
In July 2005, the PLAATO Feasibility Study reported good
implantation results with this device with an acceptable
complication rate (12).
For premedication aspirin 300 mg twice a day 48 hours prior

to the procedure and a loading dose of clopidogrel 300 mg (or
ticlopidine 250 mg) is recommended. Endocarditis prophylaxis
with a first generation cephalosporin (e.g., cefuroxime, 1, 5 g,
i.v.) should be administered before and after intervention. After
transseptal puncture, 10,000 units of heparin are administered.
An activated clotting time of 200–300 seconds is desirable.
Postprocedure, clopidogrel (75 mg/day, p.o.) and endo-
carditis prophylaxis for the first six months is suggested. Aspirin
(300–325 mg/day, p.o.) should be prescribed indefinitely.
2. A variety of Amplatzer devices are applicable for LAA
occlusion including the atrial and ventricular septal defect
devices, the patent foramen ovale devices, the patent ductus
arteriosus devices, and other arteriovenous fistulae devices.
A special fabric-free LAA plug is currently under investigation
(Fig. 2).
The characteristic feature of all Amplatzer devices is the niti-
nol wire mesh. There are two possible methods of
implantation. Either the device is placed entirely into the
appendage or the distal disc is expanded in the neck and the
proximal disc in the left atrium. The risk of residual shunting
around the device is increased when it is totally inserted into
the LAA with no part protruding into the atrium. The
Amplatzer occluder series holds the widest spectrum of
device sizes (4 to 40 mm). The device is attached to a delivery
cable and can simply be opened or recollapsed into the deliv-
ery catheter. Release is by unscrewing the device after first
testing stability with simple traction.
Intravenous antibiotics are given before and after the
procedure. Five thousand to ten thousand units of heparin
should be administered after transseptal puncture. Aspirin

(100–300 mg/day, p.o.) and clopidogrel (75 mg/day, p.o.) is
prescribed for the following six months as well as endocardi-
tis prophylaxis. A TEE is performed at six months. If the LAA
is completely occluded, no further anticoagulation is required.
594 Interventions for structural heart disease
Figure 1
PLAATO left atrial appendage device.
1180 Chap51 3/14/07 11:49 AM Page 594
Intravenous antibiotics are given before and after the
procedure. Endocarditis prophylaxis is recommended for six
months. Coumadin type drugs should be administered at
least for 45 days after the Watchman implantation procedure
with an INR between two and three in combination with
100 mg aspirin. When complete endothelialization is likely
with no or only little flow through the device, coumadin can
be discontinued and clopidogrel 75 mg/day is given until six
months follow-up examination. In the absence of thrombus
or flow in the appendage at TEE at six months, clopidogrel is
stopped and aspirin therapy 100 mg/day is continued indefi-
nitely. If thrombus formation is seen, obviously coumadin
therapy is restarted.
Valvuloplasty
Percutaneous valvuloplasty was introduced during the early
1980s as a method for treatment of stenotic valves (14).
Since then, with the improvement in wire and balloon tech-
nology and expertise, it is the method of choice for almost all
patients with severe pulmonary stenosis and for younger
patients with congenital noncalcified aortic valve stenosis.
Mitral balloon valvuloplasty is widely applicable and efficacious
in postrheumatic mitral stenosis. Tricuspid valvuloplasty is

rarely performed as severe rheumatic stenosis of this valve is
rarely seen.
Pulmonary stenosis
Congenital abnormalities of pulmonary valve morphology
including fused valve commissures, unicuspid and bicuspid
valves, leaflet thickening, or valve dysplasia may occur in
isolation or combination to cause narrowing of the valve.
Without treatment, chronic right ventricular hypertension
leads to severe hypertrophy and ultimately right ventricular
failure, tricuspid regurgitation, and atrial and ventricular
tachyarrhythmias.
The first report of percutaneous balloon dilation of a
pulmonary valve was published in 1982 (14). Today the tran-
scatheter approach has largely replaced surgical valvulotomy
for pure stenosis. Surgery is only necessary when balloon
dilatation was not successful or other heart abnormalities
demand an open heart procedure.
Exercise intolerance and dyspnea are the predominant
symptom. Doppler systolic gradient on echocardiography of
50 mmHg or more is generally accepted as a clear indication
for intervention, accepting that invasive gradients measured in
a sedated or anesthetized patient are likely to be less than the
Doppler gradient for reasons of timing and a reduced cardiac
output. After puncture of the femoral vein, a multipurpose
catheter is used to document right ventricular and pulmonary
Pulmonary stenosis 595
Figure 2
Amplatzer left atrial appendage plug.
Aspirin therapy should be continued to prevent thrombus
formation outside the LAA.

3. The Watchman implant (Fig. 3) is the latest device to be
used for occlusion of the LAA.
The nitinol frame structure incorporates a permeable
160 micron PET filter on the proximal face of the device to
encourage endothelialization. Fixation barbs on the surface
anchor the device to the LAA wall. The filter is released distal
to the LAA ostium. Clinical experience is limited with this
device (13).
Figure 3
Watchman left atrial appendage device.
1180 Chap51 3/14/07 11:49 AM Page 595
artery pressures, with a pullback across the pulmonary valve
to measure the peak-to-peak systolic gradient. A right ventricu-
lar angiogram is performed in an right anterior oblique (RAO)
and/or lateral projection to localize the valve and to measure
the size of the valve annulus. A multipurpose catheter is then
advanced to one of the branch pulmonary arteries and an
exchange length guidewire positioned in a distal branch. An
appropriate sized balloon catheter is advanced into the right
ventricle and positioned across the pulmonary valve. The
balloon diameter should measure about 1.2–1.5 times the
size of the valve annulus. Balloon inflation is performed until
the waist is abolished, signaling effective disruption of the
stenotic valve leaflets. After dilation, the pressure gradient
across the valve is measured; a reduction to less than half the
predilation gradient is accepted as an effective result.
However, some patients, especially those with the more
severe obstruction, display a “reactive” infundibular dynamic
obstruction after valvuloplasty. In this case, the initial fall in
gradient may seem disappointing, but providing the operator

is confident that an appropriate sized balloon was used, the
gradient will fall further in the weeks following valvuloplasty as
the right ventricular hypertrophy regresses.
Complications reported with this type of intervention are
rare. Rupture of the annulus is reported. The tricuspid valve
may also be damaged if a large diameter balloon catheter has
been passed inadvertently through the tricuspid valve chor-
dae. After inflation, the balloon is relatively bulky and as it is
removed the tricuspid valve apparatus may be disrupted
causing regurgitation. A procedure-associated death rate of
0.24% and a major complication rate of 0.35% were found
in a large study comprising 822 balloon pulmonary valvulo-
plasty procedures (15).
Aortic stenosis
The commonest cause of stenosis in patients below 60 years
of age is a congenitally bicuspid aortic valve with fused
commissures and/or dysplastic leaflets. Over time calcification
and fibrosis may cause the valve to become rigid and obstruc-
tive. Coexisting regurgitation of these valves is common.
The number of patients with a rheumatic type of stenosis
has decreased in recent years. Rheumatic valve disease
causes fusion and thickening of the commissures, which in
turn accelerates calcification and fibrosis.
A third type of stenosis of a degenerative nature occurs in
patients above 70 years of age in whom the commissures
stay separated but the valve excursion is impeded at the base
of the leaflets. Clinical symptoms may include syncope, dysp-
nea, or angina. Advanced stages of this disease can cause
heart failure and sudden death.
Surgery has been the preferred option for patients with

severe stenosis. The options are either a commissurotomy or,
in patients with significant regurgitation or severe calcification,
valve replacement or a pulmonary autograft procedure, the
Ross operation.
After successful experience with pulmonary balloon valvu-
loplasty, aortic balloon valvuloplasty has gained acceptance
(16Ϫ18). The aim of aortic valvuloplasty is to reduce the
transvalvular gradient to a subintervention level. An efficacious
result is generally accepted as a pressure gradient less than
50 mmHg and an increase in valve area of 100%. The acute
results of dilation are comparable to pulmonary procedures
though the complication rate is considerably higher. Aortic
regurgitation, embolic events, arrhythmias, and progressive
heart failure have all been reported during intervention or
follow-up. Recurrent stenosis is the highest among patients
with severe calcification (19), which has been addressed by
the development of transcutaneous valve replacement (for
further information see the section “valve replacement”).
Mitral stenosis
Mitral stenosis is seen typically as a consequence of chronic
rheumatic fever. Isolated congenital mitral stenosis is very rare
and not suitable for balloon valvuloplasty. Clinical symptoms
depend on the degree of obstruction. Dyspnea, atrial fibrilla-
tion, embolic events, pulmonary edema, and right heart
decompensation may occur and are all indications for treat-
ment. Surgery and catheter intervention provide similar
results. Balloon valvuloplasty produces best results in patients
with little or no calcification of the mitral leaflets (20Ϫ23).
Since the first steps in transluminal balloon dilation of mitral
valves in 1982 (24) numerous techniques have been

described. One method is to access the left atrium with a
transseptal puncture from the venous side (antegrade).
Another way is to advance the catheter via the aorta into the
left ventricle and perform the valvulotomy from the arterial
side (retrograde). The use of two dilation balloons introduced
via the transseptal approach is a common technique
described by Bonhoeffer using a monorail-type system over
a single guidewire (25).
Minor degrees of mitral regurgitation are relatively
common after valvuloplasty of the mitral valve. More severe
regurgitation requiring early surgical repair or replacement
may also occur. Restenosis is seen after both surgical and
interventional valvuloplasty on the mitral valve in longer-term
follow-up (26,27). The valve area usually increases approxi-
mately from 1 to 1.8Ϫ2.2 cm
2
(28).
Tricuspid stenosis
Isolated tricuspid stenosis is very rare and almost always asso-
ciated with chronic rheumatic fever. Techniques to dilate this
valve are based on those for mitral dilation.
596 Interventions for structural heart disease
1180 Chap51 3/14/07 11:49 AM Page 596
During all valvuloplasty interventions antibiotics (e.g.,
cefuroxime, 1, 5 g, i.v.) are administered. Patients allergic to
penicillin should receive vancomycin 1 g intravenously. Most
physicians perform transcatheter valvuloplasty in the fasting
state under mild sedation. Substances that are frequently
used are meperidine, promethazine, and chlorpromazine,
given intramuscularly or intermittent doses of midazolam

(0.05 to 0.1 mg/kg, i.v.) and/or fentanyl (0.5 to 1.0 µg/kg, i.v.).
Some operators also apply ketamine or general anesthesia for
all interventional cases.
Following transseptal left heart catheterization, systemic
anticoagulation is achieved by the intravenous administration
of 100 U/kg of heparin.
Mitral valve repair
Transcutaneous mitral valve repair has been developed for
patients with significant valve regurgitation. A frequent etiology
of regurgitation is myocardial infarction causing ventricular dila-
tion, rupture of chordae, or dysfunctional papillary muscles.
Additionally mitral valve prolapse, dilated cardiomyopathy, or
rheumatic/bacterial endocarditis can result in a regurgitant
mitral valve. Chronic regurgitation is tolerated by many patients
for quite a long time but eventually symptoms of dyspnea,
palpitations, edema, and severe arrhythmias emerge.
Indications for surgical intervention include regurgitation
with NYHA III–IV symptoms or NHYA ϾII with atrial fibrilla-
tion refractory to conservative treatment. Several surgical
techniques are effective. The “Alfieri stitch” or “edge to edge”
technique is of interest because one of the percutaneous
mitral valve repair techniques is based on an equivalent prin-
ciple (29,30). Currently two methods for transcatheter mitral
valve repair are investigated in clinical trials:
1. Edge-to-edge repair
2. Transcatheter annuloplasty
1. In 1991, the surgical variant of the edge-to-edge repair
technique was first tried in patients that were not suitable for
complex mitral valve repair (29). This procedure is still
performed with the intention of sewing together part of the

free edges of the anterior and posterior valve leaflets in such
a way as to construct a double orifice valve to decrease
regurgitation.
The edge-to-edge transcatheter mitral valve repair system
consists of a steerable guide catheter and a steerable clip or
suture delivery system. From a venous approach, a transsep-
tal puncture is employed to access the left atrium. The
delivery system is maneuvered through the mitral valve into
the left ventricle and aligned perpendicular to the line of valve
coaptation. The EVEREST I trial featured first data on tran-
scatheter mitral repair with this technique using a clip (31). In
89% the implantation procedure was successful reducing
mitral regurgitation in 67% of the patients to levels under II°.
However, 25% of these patients required surgery within two
months after the intervention.
2. The concept of percutaneous transvenous mitral annulo-
plasty is to place a relatively stiff rod or stent into the coronary
sinus (CS) to achieve a configuration change of the dilated
mitral annulus. This procedure is feasible due to the fact that
the posterior mitral annulus is separated from the CS and
great cardiac vein (GCV) only by a thin band of atrial muscle
and connective tissue. Preinterventional assessment of the
anatomical relationships between the CS and mitral annulus
by magnetic resonance imaging, CT scan, or 3D echocardio-
graphy is helpful for this procedure. The rod is positioned
under fluoroscopic guidance through the CS and GCV to an
appropriate position. By straightening the venous vessels, the
posterior leaflet converges to the anterior leaflet thereby
reducing regurgitation. A new CS probe, which applies heat
energy to the mitral annulus, is being developed to denatur-

ize collagen fibers in the adjacent mitral annulus producing a
shrinkage effect that decreases the valve dilation, potentially
reducing regurgitation. Perforation and tamponade, coronary
occlusion, sinus thrombosis, or device migration are all
potential complications of this procedure. Short- and mid-
term follow-up results are expected (32,33).
With annuloplasty procedures heparin and endocarditis
prophylaxis should be administered before the procedures.
When the edge-to-edge technique is performed, heparin
should not be administered until the transseptal puncture has
been performed. Regular follow-up examination, anticoagu-
lation, and endocarditis prophylaxis are recommended after
mitral repair procedures.
Valve replacement
Currently transcatheter replacement of heart valves is limited
to the aortic and pulmonary valves.
Hywel Davies reported of temporarily treatment of aortic
regurgitation with a parachute valve mounted onto a catheter
tip in 1965 (34). Twenty-seven years later Andersen and his
colleagues described the first experience with a bioprosthetic
valve attached to a wire-based stent and mounted on a balloon
valvuloplasty catheter (35). In 2002, Alain Cribier performed
the first transcatheter valve implantation in an elderly patient
with inoperable aortic stenosis using a prototype of a stent-
mounted, pericardial, tricuspid aortic valve (36).
Approaching the aortic valve with a catheter can be
achieved via the venous (antegrade, transseptal) or the arter-
ial routes (retrograde) (37,38). The delivery assembly is
positioned within the diseased native valve. Before expansion
of the valve mounted balloon rapid pacing (Ͼ200 beats/min)

is performed to lower stroke volume during the implantation
sequence. The balloon is inflated fixing the stented valve to
the implantation site. Immediately after balloon deflation
Valve replacement 597
1180 Chap51 3/14/07 11:49 AM Page 597
pacing is discontinued and the balloon removed leaving the
valve in position. Reported complications in this group of
patients with very high comorbidity are renal failure, pericar-
dial tamponade, stroke, injury to the mitral valve and atrial
septum, paravalvular regurgitation, valve migration and
cardiogenic shock.
Residual regurgitation after reparative surgery of congenital
heart disease is the most frequent indication for pulmonary
valve replacement. Bonhoeffer reported early results in 2000
(39,40). Since then, over 100 patients have undergone this
procedure. Extensive diagnostic imaging is performed before
pulmonary valve implantation to delineate anatomy, and
quantify the regurgitation and right ventricular function. The
pulmonary valve is a bovine jugular vein valve mounted within
a platinum iridium stent. It is advanced on a double-balloon
delivery system via the femoral vein into the right atrium,
through the tricuspid valve and into the right ventricular
outflow tract.
Once the correct position of the valve-stent assembly is
identified angiographically, the inner and outer balloons are
inflated sequentially, and subsequently deflated and removed.
Occasionally, it is necessary to perform further deployment of
the valve using a high pressure, noncompliant balloon system.
The procedures may be performed under local anesthesia
and mild sedation or general anesthesia with heparin antico-

agulation. Aspirin (160 mg, p.o.) and a loading dose of
clopidogrel (300 mg, p.o.) are administered 24 hours before
intervention for the aortic valve. Antibiotics (e.g., first genera-
tion cephalosporin, i.v.) are given before the procedure and
continued for 48 hours. After the procedure aspirin is contin-
ued for three to six months.
Post-surgical and post-
myocardial infarction
ventricular septal defect
The vast majority of ventricular septal defects (VSD) are congen-
ital. Acquired VSDs are almost always a consequence of septal
rupture following myocardial infarction, traumatic VSDs as a
consequence of sharp or blunt chest trauma are exceptionally
rare. Typically the post myocardial infarction ventricular septal
defect (PMIVSD) occurs within the first week after the event
(41). In the current era of thrombolysis about 0.2% of patients
develop a VSD as a result of septal necrosis. Medical manage-
ment of these patients is limited and carries a 30-day mortality
of 94% compared with 47% who were treated surgically (42).
A residual VSD following surgical closure occurs in 10% to
40% of patients depending on its location (43). Selected patients
are suitable for a transcatheter approach. Interventional closure
of selected muscular VSD has been possible for some years
using the Rashkind (44) and subsequent generation devices
(Clamshell, CardioSEAL). Currently the Amplatzer muscular,
membranous, and the new perimembranous device (Fig. 4) are
by far the most widely applied. The CardioSEAL-STARflex
occluder or Nit-Occlud Coils may also be used for this purpose.
Before intervention clinical condition often warrants intra-
aortic balloon pump and revascularization or stenting of the

infarct-related artery. For VSD closure either the transvenous
or the transarterial approach can be used to access the
defect. Commonly an arteriovenous circuit is established.
This increases wire stability and thus facilitates positioning of
the delivery sheath. The appropriate device size is selected
and positioned within the defect. Care is taken that the device
does not impinge on important related structures such as the
aortic, mitral, and tricuspid valves. The morphology of the
post infarction VSDs is complex thus residual shunting is often
seen and mortality remains high. While the procedure may
be life saving in some circumstances, procedural failure and
residual flow are commoner than with congenital defects (for
further information on congenital VSD closure see chap. 62).
Post infarction patients need to be treated with long-term
antiplatelet therapy. Aspirin (100 mg/day, p.o.) reduces the
mortality rate within one year post infarction by 15% and the
risk for reinfarction by 30%. Additionally, clopidogrel
(75 mg/day, p.o.) may be administered. Supplementary clopi-
dogrel therapy for at least nine months also improves
prognosis (45). The risk of thrombus formation in the affected
myocardium is high. Anticoagulation for three months with a
target INR of 2.0–3.0 is recommended by some operators.
Patent foramen ovale
Persistence of patent foramen ovale (PFO) into adulthood
carries a risk of paradoxical embolization. This risk is accentuated
598 Interventions for structural heart disease
Figure 4
Amplatzer post myocardial infarction ventricular septar defects
(VSD) occluder.
1180 Chap51 3/14/07 11:49 AM Page 598

if the PFO is associated with an atrial septal aneurysm (46).
Therapeutic options to prevent embolism are a lifelong applica-
tion of anticoagulant drugs, surgical closure, or catheter
intervention. Despite efficacious new generation antiplatelet and
anticoagulation drugs there is nevertheless a risk of recurrent
embolic events. Additionally, 2–5% of the patients on anticoag-
ulant drugs will encounter significant bleeding complications
per year (47).
Surgery for PFO closure lowers the rate of cerebrovascular
events per year and carries a mortality of less than 1%, but is
associated with significant morbidity. Transcatheter closure of
PFO is a standard technique for many interventional cardiolo-
gists. Low morbidity, efficacy approaching 100% at follow-up,
and the avoidance of scar, make transcatheter closure the
procedure of choice. All double disc devices (see later) are
introduced via the femoral vein and advanced within a delivery
catheter through the PFO into the left atrium. Here the distal
disc of the occluder is released and carefully withdrawn to the
left side of the atrial septum. The proximal disc is deployed on
the right side of the septum. Effective positioning is confirmed
on fluoroscopy and transesophageal or intracardiac echo and
the device subsequently released from its delivery system.
Following devices are either standard PFO devices or
constitute emerging methods for PFO closure:
1. Amplatzer PFO occluder (AGA Medical Corporation,
Golden Valley, MN)
2. Helex occluder (W.L. Gore & Associates, Flagstaff, AZ)
3. Premere occluder (St Jude Medical, Maple Grove, MN)
4. CardioSEAL-STARflex occluder (NMT Medical, Inc.,
Boston, MA)

5. BioSTAR (NMT Medical, Inc., Boston, MA)
6. PFX Closure System (Cierra, Inc., Redwood City, CA)
1. The Amplatzer occluder (Fig. 5) is probably the most
widely used device in this indication. This double disc device
consists of self-expandable nitinol wire mesh. Both discs contain
patches of polyester fabric for enhanced defect occlusion.
Compared to other Amplatzer devices, the PFO occluder
features a thinner connection waist and is available in sizes of 18,
25, and 35 mm. Most frequently the 18 and 25 mm devices are
implanted, but the 35 mm occasionally is useful in patients with
a large ASA.
Before insertion the device needs to be evacuated from air
by expanding and refolding the wire mesh in saline. Once
accomplished, the device is loaded into the delivery catheter
and percutaneously introduced. Self-expansion of the left and
right atrial discs is achieved by pushing the delivery cable and
retrieving the catheter stepwise. After checking for proper
device position and configuration, the device is released.
2. The Helex device differs from the common double
umbrella concept (Fig. 6). Expanded polytetrafluoroethylene
(ePTFE) patch material is bonded to a single strand of nitinol
wire. When fully constituted the device conforms in a circular
fashion with two discs held together by an integrated eyelet
mechanism. This mechanism also provides visibility under
fluoroscopy and ensures flat alignment of the discs to the left
and right aspects of the atrial septum. Due to its round edges,
ePTFE material and the fine nitinol wire, this device has a low
rate of complications. The device remains elongated in a linear
form when loaded in the catheter and forms 1
1

/
4
turns on
each side of the septum after deployment. A security suture is
attached to the proximal eyelet allowing device retrieval even
after release.
3. The Premere PFO occluder (Fig. 7) is another self-
expanding double disc device specifically designed for PFO
closure. The right-sided anchor is constructed of nitinol
between two layers of knitted polyester fabric connected by
a flexible polyester braided tether to the left atrial anchor. The
left atrial anchor consists of four radiating arms without poly-
ester layers to improve tissue absorption and to minimize
thrombus formation. Since the distance between the anchors
Patent foramen ovale 599
Figure 5
Amplatzer PFO occluder.
Figure 6
Helex PFO occluder.
1180 Chap51 3/14/07 11:49 AM Page 599
adapts to the tunnel length, this device is suitable for long-
tunnel type PFOs. Until the abovementioned tether is cut,
the anchors are fully retrievable. This device was first used in
November 2003.
4. The CardioSEAL occluder features eight wire spring
arms that form two rectangular discs. Each disc is covered with
a knitted polyester patch. The CardioSEAL-STARflex septal
repair system (Fig. 8) is an advanced version, which has nitinol
coil microsprings connecting the opposing arms of the left and
right atrial discs. These springs enable self-centering of the

device to obtain improved adjustment to the septal anatomy.
5. The BioSTAR occluder (Fig. 9) evolved from the
CardioSEAL-STARflex design. It is a prototype of a bioactive
device that uses tissue-engineered collagen matrix derived
from the submucosal layer of the porcine small intestine
(Organogenesis Inc., Canton, MA) as its “fabric”. The device
is 90% absorbable and has a very low profile encouraging
tissue overgrowth and decreased thrombogenicity. The
BioSTAR occluder features drug eluting capabilities for
heparin or growth factors. This device is currently in clinical
trials.
6. The PFX Closure system (Fig. 10) does not involve the
implantation of a device. The method of action involves the
sealing of the flap valve of the foramen ovale to the atrial
septum. The distal end of the catheter consists of an electrode
composed of a metallic wire framework and covered by an
elastomeric vacuum housing. A retractable outer sleeve
confines the electrode from the surrounding blood. The
system is introduced transvenously and positioned in the right
atrium. The electrode is guided toward the overlapping
septum primum and secundum. Both parts of the atrial
septum are engaged by inducing a vacuum within the elas-
tomeric housing. After confirming the position of the electrode
by TEE or ICE, a monopolar radiofrequency energy impulse is
triggered, welding the tissues of septum primum and septum
secundum together. This procedure was first performed
in 2005 and is currently under procedural and technical
evaluation (48).
It has become recognized that PFO device closure not
only significantly decreases the incidence of paradoxical

embolism (47), but can also reduce the incidence of migraine
in susceptible patients. Fifty-five percent of patients with aura
and 62% of those without aura experienced a reduction of
600 Interventions for structural heart disease
Figure 7
Premere PFO occluder.
Figure 8
CardioSEAL-STARflex device.
Figure 9
BioSTAR persistence of patient foramenovale (PFO) occluder.
1180 Chap51 3/14/07 11:49 AM Page 600
headache frequency after PFO closure (49). The MIST study
() found out that PFO closure
might achieve a mean reduction in headache burden of 50
hours per month. In this study, 42% of the patients with
migraine experienced a 50% reduction in headache.
Reported major procedural and post procedural complica-
tions include frame fracture, device embolization, or the need
for surgical retrieval. Depending on the operator experience,
the method and the morphology of the PFO, the procedure
time constitutes approximately 20–40 minutes. The hospital
stay is rarely more than a single overnight stay; many patients
undergo PFO closure as a day case procedure.
Before intervention heparin is administered (100 U/kg) in
addition to endocarditis prophylaxis (e.g., cefuroxime, 1,5 g,
i.v.). Endocarditis prophylaxis is repeated after the procedure.
Aspirin (100 mg, p.d.) and clopidogrel (75 mg/day, p.o.) are
prescribed for six months after implantation. The incidence of
thrombus formation varies between devices (50). If thrombus
is seen during follow-up, coumadin therapy should be

commenced.
References
1 Maron MS, Olivotto I, Betocchi S, et al. Effect of left ventricu-
lar outflow tract obstruction on clinical outcome in
hypertrophic cardiomyopathy. N Engl J Med 2003; 348:
295–303.
2 Maron BJ, Bonow RO, Cannon RO III, et al. Hypertrophic
cardiomyopathy. Interrelations of clinical manifestations,
pathophysiology, and therapy (2). N Engl J Med 1987; 316
(14):844–852. Review.
3 Gietzen FH, Leuner CJ, Obergassel L, et al. Role of transcoro-
nary ablation of septal hypertrophy in patients with
hypertrophic cardiomyopathy, New York Heart Association
functional class III or IV, and outflow obstruction only under
provocable conditions. Circulation 2002; 106:454–459.
4 Maron BJ, McKenna WJ, Danielson GK, et al. Task Force on
Clinical Expert Consensus Documents. American College of
Cardiology; Committee for Practice Guidelines. European
Society of Cardiology. American College of Cardiology/
European Society of Cardiology clinical expert consensus
document on hypertrophic cardiomyopathy. A report of the
American College of Cardiology Foundation Task Force on
Clinical Expert Consensus Documents and the European
Society of Cardiology Committee for Practice Guidelines.
J Am Coll Cardiol 2003; 42:1687–1713.
5 Seggewiss H. Medical therapy versus interventional therapy in
hypertropic obstructive cardiomyopathy. Curr Control Trials
Cardiovasc Med 2000; 1:115–119.
6 Kim JJ, Lee CW, Park SW, et al. Improvement in exercise
capacity and exercise blood pressure response after

transcoronary alcohol ablation therapy of septal hypertrophy
in hypertrophic cardiomyopathy. Am J Cardiol 1999; 83(8):
1220–1223.
7 Knight C, Kurbaan AS, Seggewiss H, et al. Nonsurgical septal
reduction for hypertrophic obstructive cardiomyopathy:
outcome in the first series of patients. Circulation 1997;
95(8):2075–2081.
8 Gietzen FH, Leuner CJ, Raute-Kreinsen U, et al. Acute and
long-term results after transcoronary ablation of septal hyper-
trophy (TASH). Catheter interventional treatment for
hypertrophic obstructive cardiomyopathy. Eur Heart J 1999;
20(18):1342–1354.
9 Lakkis NM, Nagueh SF, Dunn JK, et al. Nonsurgical septal reduc-
tion therapy for hypertrophic obstructive cardiomyopathy:
one-year follow-up. J Am Coll Cardiol 2000; 36:852–855.
10 Kuhn H, Seggewiss H, Gietzen FH, et al. Catheter-based ther-
apy for hypertrophic obstructive cardiomyopathy. First
in-hospital outcome analysis of the German TASH Registry.
Z Kardiol 2004; 93:23–31.
11 Blackshear JL, Odell JA. Appendage obliteration to reduce
stroke in cardiac surgical patients with atrial fibrillation.
Ann Thorac Surg 1996; 61:755–759.
12 Ostermayer SH, Reisman M, Kramer PH, et al. Percutaneous
left atrial appendage transcatheter occlusion (PLAATO system)
to prevent stroke in high-risk patients with non-rheumatic
atrial fibrillation: Results from the international multi-center
feasibility trials. J Am Coll Cardiol 2005; 46(1):9–14.
13 Sick P, Ulrich M, Muth G, et al. Universität Leipzig, Herzzentrum
GmbH, Leipzig; Herzzentrum Siegburg; Krankenhaus der
Barmherzigen Brüderk, Trier. Erste klinische Erfahrungen mit

dem WATCHMAN® Verschlußsystem für das linke Vorhofohr
zur Verhinderung thromboembolischer Komplikationen bei
Patienten mit nicht valvulärem Vorhofflimmern. Z Kardiol 2005;
94(Suppl 1). Abstract V241.
14 Kan JS, White RI Jr, Mitchell SE, et al. Percutaneous balloon
valvuloplasty: a new method for treating congenital pulmonary-
valve stenosis. N Engl J Med 1982; 307(9):540–542.
15 Stanger P, Cassidy SC, Girod DA, et al. Balloon pulmonary valvu-
loplasty: results of the valvuloplasty and angioplasty of congenital
anomalies registry. Am J Cardiol 1990; 65(11): 775–783.
16 Lababidi Z, Wu JR, Walls JT. Percutaneous balloon aortic valvulo-
plasty: results in 23 patients. Am J Cardiol 1984; 53(1):194–197.
17 Cribier A, Savin T, Saoudi N, et al. Percutaneous transluminal
valvuloplasty of acquired aortic stenosis in elderly patients: an
alternative to valve replacement? Lancet 1986; 1(8472): 63–67.
References 601
Figure 10
PFX electrode.
1180 Chap51 3/14/07 11:49 AM Page 601
18 Sievert H, Kaltenbach M, Bussmann WD, et al. Percutaneous
valvuloplasty of the aortic valve in adults. Dtsch Med
Wochenschr 1986; 111(13):504–506. German.
19 Otto CM, Mickel MC, Kennedy JW, et al. Three-year outcome
after balloon aortic valvuloplasty. Insights into prognosis of
valvular aortic stenosis. Circulation 1994; 89(2):642–650.
20 Lock JE, Khalilullah M, Shrivastava S, et al. Percutaneous
catheter commissurotomy in rheumatic mitral stenosis. N Engl
J Med 1985; 313(24):1515–1518.
21 Al Zaibag M, Ribeiro PA, Al Kasab S, et al. Percutaneous
double-balloon mitral valvotomy for rheumatic mitral-valve

stenosis. Lancet 1986; 1(8484):757–761.
22 Reyes VP, Raju BS, Wynne J, et al. Percutaneous balloon valvu-
loplasty compared with open surgical commissurotomy for
mitral stenosis. N Engl J Med 1994; 331(15):961–967.
23 Sievert H, Kober G, Bussmann WD, et al. Catheter valvulo-
plasty in mitral valve stenosis. Dtsch Med Wochenschr 1989;
114(7):248–252. German.
24 Inoue K, Owaki T, Nakamura T, et al. Clinical application of
transvenous mitral commissurotomy by a new balloon
catheter. J Thorac Cardiovasc Surg 1984; 87(3):394–402.
25 Bonhoeffer P, Esteves C, Casal U, et al. Percutaneous mitral
valve dilatation with the Multi-Track System. Catheter
Cardiovasc Interv 1999; 48(2):178–183.
26 Block PC, Palacios IF, Block EH, et al. Late (two year) follow-
up after percutaneous mitral balloon valvotomy. Am J Cardiol
1992; 69:537–541.
27 Hung JS, Chern MS, Wu JJ, et al. Short and long-term results
of catheter balloon percutaneous transvenous mitral commis-
surotomy. Am J Cardiol 1991; 67:854–862.
28 Ribeiro PA, al Zaibag M, Abdullah M. Pulmonary artery pres-
sure and pulmonary vascular resistance before and after mitral
balloon valvotomy in 100 patients with severe mitral valve
stenosis. Am Heart J 1993; 125(4):1110–1114.
29 Maisano F, Torracca L, Oppizzi M, et al. The edge-to-edge
technique: a simplified method to correct mitral insufficiency.
Eur J Cardiothorac Surg 1998; 13:240–245.
30 Alfieri O, Maisano F, De Bonis M, et al. The double-orifice
technique in mitral valve repair: a simple solution for complex
problems. J Thorac Cardiovasc Surg 2001; 122:674–681.
31 Feldman T, Wasserman HS, Herrmann HC, et al. Percutaneous

mitral valve repair using the edge-to-edge technique: six-
month results of the EVEREST Phase I Clinical Trial. J Am Coll
Cardiol 2005; 46:2134–2140.
32 Liddicoat JR, Mac Neill BD, Gillinov AM, et al. Percutaneous
mitral valve repair: a feasibility study in an ovine model of acute
ischemic mitral regurgitation. Catheter Cardiovasc Interv
2003; 60:410–416.
33 Maniu CV, Patel JB, Reuter DG, et al. Acute and chronic reduc-
tion of functional mitral regurgitation in experimental heart
failure by percutaneous mitral annuloplasty. J Am Coll Cardiol
2004; 44:1652–1661.
34 Davies H. Catheter mounted valve for temporary relief of
aortic insufficiency. Lancet 1965; 1:250.
35 Andersen HR, Knudsen LL, Hasenkam JM. Transluminal implan-
tation of artificial heart valves. Description of a new expandable
aortic valve and initial results with implantation by catheter tech-
nique in closed chest pigs. Eur Heart J 1992; 13(5):704–708.
36 Cribier A, Eltchaninoff H, Bash A, et al. Percutaneous tran-
scatheter implantation of an aortic valve prosthesis for calcific
aortic stenosis: first human case description. Circulation 2002;
106(24):3006–3008.
37 Cribier A, Eltchaninoff H, Tron C, et al. Early experience with
percutaneous transcatheter implantation of heart valve prosthe-
sis for the treatment of end-stage inoperable patients with calcific
aortic stenosis. J Am Coll Cardiol 2004; 43(4):698–703.
38 Webb JG, Chandavimol M, Thompson CR, et al.
Percutaneous aortic valve implantation retrograde from the
femoral artery. Circulation 2006; 113(6):842–850.
39 Bonhoeffer P, Boudjemline Y, Saliba Z et al. Transcatheter
implantation of a bovine valve in pulmonary position. A lamb

study. Circulation 2000; 102:813–816.
40 Bonhoeffer P, Boudjemline Y, Saliba Z et al. Percutaneous
replacement of pulmonary valve in a right-ventricle to
pulmonary-artery prosthetic conduit with valve dysfunction.
Lancet 2000; 356:1403–1405.
41 Topaz O, Taylor AL. Interventricular septal rupture complicating
acute myocardial infarction: from pathophysiologic features to
the role of invasive and noninvasive diagnostic modalities in
current management. Am J Med 1992; 93(6):683–688. Review.
42 Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors,
angiographic patterns, and outcomes in patients with ventricu-
lar septal defect complicating acute myocardial infarction.
GUSTO-I (Global Utilization of Streptokinase and TPA for
Occluded Coronary Arteries) Trial Investigators. Circulation
2000; 101(1):27–32.
43 Killen DA, Piehler JM, Borkon AM, et al. Early repair of postin-
farction ventricular septal rupture. Ann Thorac Surg 1997;
63(1):138–142.
44 Lock JE, Block PC, McKay RG, et al. Transcatheter closure of
ventricular septal defects. Circulation 1988; 78:361–368.
45 Fox KA, Mehta SR, Peters R, et al. Clopidogrel in Unstable
angina to prevent Recurrent ischemic Events Trial. Benefits and
risks of the combination of clopidogrel and aspirin in patients
undergoing surgical revascularization for non-ST-elevation
acute coronary syndrome: the Clopidogrel in Unstable angina
to prevent Recurrent ischemic Events (CURE) Trial.
Circulation 2004; 110(10):1202–1208.
46 Mas JL, Arquizan C, Lamy C. Patent Foramen Ovale and Atrial
Septal Aneurysm Study Group: recurrent cerebrovascular
events associated with patent foramen ovale, atrial septal

aneurysm or both. N Eng J Med 2001; 345:1740–1746.
47 Khairy P, O’Donnell CP, Landzberg MJ. Transcatheter closure
versus medical therapy of patent foramen ovale and presumed
paradoxical thromboemboli: a systematic review. Ann Intern
Med 2003; 139(9):753–760.
48 Skowasch M, Hein R, Buescheck F, et al. Non-Implant Closure
of Patent Foramen Ovale: First-in-Man Results. Am J Cardiol
2005; 96(suppl 7A):101H.
49 Schwerzmann M, Wiher S, Nedeltchev K, et al. Percutaneous
closure of patent foramen ovale reduces the frequency of
migraine attacks. Neurology 2004; 62(8):1399–1401.
50 Krumsdorf U, Ostermayer S, Billinger K, et al. Incidence and
clinical course of thrombus formation on atrial septal defect
and patient foramen ovale closure devices in 1,000 consecu-
tive patients. J Am Coll Cardiol 2004; 43(2):302–309. Review.
602 Interventions for structural heart disease
1180 Chap51 3/14/07 11:49 AM Page 602
Hypertrophic cardiomyopathy, a primary myocardial
disorder of sacromeric proteins with an autosomal dominant
pattern of inheritance is characterized by asymmetric hyper-
trophy of the septum with or without dynamic obstruction of
the outflow tract (1,2). The prevalence in the general popu-
lation is estimated as 1:500 and it is the most common
monogenic cardiac disorder. Annual mortality in an unse-
lected population is reported to be about 1% to 2%, and
sudden death is the most common cause. Sudden death is
assumed to be due to idiopathic ventricular arrhythmias, but
hemodynamic factors and myocardial ischemia may be
involved as well.
Hemodynamics

The most characteristic hemodynamic feature of hyper-
trophic cardiomyopathy is the dynamic intraventricular
pressure gradient (3). Obstruction to left ventricular ejection
occurs in the left ventricular outflow tract due to the contrac-
tion of the basal aspect of an asymmetrically hypertrophied
interventricular septum resulting in a subaortic pressure gradi-
ent. As the ventricle contracts the subaortic flow velocity
increases. The acceleration of blood flow through the
narrowed outflow tract causes a pressure drop that draws the
anterior leaflet of the mitral valve towards the ventricular
septum due to a Venturi effect, exacerbating the outflow
obstruction and contributing to mitral incompetence.
Outflow obstruction is a dynamic phenomenon. Patients with
hypertrophic cardiomyopathy may not have a systolic pres-
sure gradient at rest but can have one provoked with the
Valsava maneuver or an extrasystole. There is a variability and
heterogeneity of hemodynamics among affected patients and
even within the same patient over time.
The dynamic outflow obstruction leads to the characteris-
tic spike-and-dome arterial pressure waveform seen most
evidently in the proximal aorta (Fig. 1). The early spike is due
to a rapid ventricular ejection from the hypercontractile
myocardium, and the pressure dip and subsequent doming of
the pulse reflect the dynamic outflow obstruction. This is seen
following conditions that increase the dynamic gradient, such
as an extrasystole, the Valsalva maneuver, or administration of
beta-adrenergic agonists or vasodilators. The narrowing in
pulse pressure of the spike-and-dome arterial waveform
following an extra-systole is known as the Brockenbrough-
Braunwald sign. Associated diastolic dysfunction is common

with increased diastolic filling pressure evident in the contour
of the left ventricular diastolic pressure tracing.
Treatment options
The treatment strategy in patients with severe symptoms
unresponsive to maximum medical management and a signif-
icant outflow tract obstruction is the reduction of the
myocardial septum either by surgery or alcohol ablation (4–6).
Surgery
Surgical myectomy involves incision into and resection of
small portions of the hypertrophied septum resulting in a
significant reduction or abolition of intramyocardial gradients
and reduction in mitral incompetence. Patients report a signif-
icant reduction in disabling symptoms and improvement in
exercise capacity, and the benefit is usually sustained. The
complications are few and the postoperative mortality is
52
Pharmacologic use of ethanol for myocardial
septal ablation
George D. Dangas, Edwin Lee, and Jeffrey W. Moses
1180 Chap52 3/14/07 11:50 AM Page 603
1–3% when myectomy are performed by experienced
surgeons in a comprehensive care setting. Long-term survival
in patients with obstructive hypertrophic cardiomyopathy and
severe symptoms postsurgical myectomy was equivalent to
that of the general population (7). Surgical myectomy patients
had reduced all cause mortality and sudden cardiac death
compared to nonoperated obstructive hypertrophic
cardiomyopathy patients (7), suggesting that myectomy may
reduce mortality risk in severely symptomatic patients with
obstructive hypertrophic cardiomyopathy.

Septal Ablation
Septal alcohol ablation, first reported in 1995 (4), has evolved
to become a relatively common procedure with Ͼ4000
patients having been treated. This procedure consists of
injecting absolute alcohol into a septal perforator to create
necrosis and permanent myocardial infarction (MI) in the
proximal septum. Subsequent intramyocardial scarring (8)
leads to progressive left ventricular wall thinning, restricted
septal excursion, enlargement of the outflow tract and
consequent reduction in obstruction and mitral regurgitation,
thus mimicking the remodeling that results from surgical
myectomy.
Selection of patients
Selection of patients for septal ablation includes those with
severe symptoms (i.e., New York Heart Association functional
class III or IV) despite appropriately adjusted medical therapy,
with a documented resting left ventricular outflow tract gradi-
ent Ͼ30mmHg or a provocable gradient Ն60mmHg and
septal thickness of at least 18 mm. Patients at high risk of surgi-
cal morbidity or mortality, including patients of advanced age or
with insufficient motivation for surgery, and those with other
important comorbidities or other conditions that will likely limit
long-term survival are candidates for septal ablation (Table 1).
Patients who have not obtained a satisfactory result after
surgical myectomy may also be candidates for septal ablation.
Selected patients with advanced function class II with obstruc-
tive symptoms that interfere with their occupation may also
be candidates for intervention.
Patients with the non-obstructive form of hypetrophic
cardiomyopathy should not undergo septal ablation. Patients

with congential anomalies of the mitral valve apparatus, asso-
ciated heart lesions (e.g., advanced multivessel coronary
artery disease) requiring surgical correction, unfavorable distri-
bution of septal hypertrophy with mild proximal thickening,
basal septal wall thickness Ͻ18mm, or anatomically unsuitable
septal perforators should not be candidates for septal ablation.
604 Pharmacologic use of ethanol for myocardial septal ablation
Figure 1
Demonstration of the typical hemodynamic evaluation of hypertrophic cardiomyopathy. Equipment used: single end-hole pigtail catheter, a
femoral arterial sheath at least one size larger than the catheter, and two pressure transducers (one at the femoral sheath side port and the
other at the pigtail catheter). The catheter is initially seated beyond the stenosis and a pressure gradient is documented, as well as the
spike-and-dome configuration during systolic ventricular pressure rise can be observed while the arterial systolic pressure upstroke is steep
(
single black arrow
). While the catheter is pulled back, the gradient essentially disappears while the catheter is still inside the left ventricular
cavity as documented by the diastolic part of the pressure curve. Finally, the catheter is pulled outside the ventricle and the two transducers
document essentially identical pressures (small differences are due to the aortic to femoral pressure wave potentiation). This pullback
maneuver is pathognomonic for subaortic obstruction and needs to be performed very slowly and taking special care to avoid provoking a
series of ventricular extra-systoles that will obviate the above-described evaluation.
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