Ebook Practical cardiovascular medicine: Part 1

Practical Cardiovascular
Medicine


Practical Cardiovascular
Medicine

Elias B. Hanna, MD

Associate Professor of Medicine
Associate Program Director of Cardiovascular Disease Fellowship
Associate Program Director of Interventional Cardiology Fellowship
Louisiana State University School of Medicine
University Medical Center
New Orleans, Louisiana, USA


This edition first published 2017
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Library of Congress Cataloging‐in‐Publication Data
Names: Hanna, Elias B., author.
Title: Practical cardiovascular medicine / Elias B. Hanna.
Description: Chichester, West Sussex ; Hoboken, NJ : John Wiley & Sons Inc., 2017. |
Includes bibliographical references and index.
Identifiers: LCCN 2016055802| ISBN 9781119233367 (pbk.) | ISBN 9781119233497 (epub)
Subjects: | MESH: Cardiovascular Diseases
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Set in 8.5/10.5pt Frutiger Light by SPi Global, Pondicherry, India

10 9 8 7 6 5 4 3 2 1

To my mother Marie, my sister Eliana, and my beautiful niece Clara and nephew Marc‐Elias,
the constant light in my life
To my mentors and my fellows, and to all those who share my love for cardiology


Contents

Preface, xix
Abbreviations, xx
PART 1.  Coronary Artery Disease, 1
1.  Non‐ST‐Segment Elevation Acute Coronary Syndrome, 1
I. Types of acute coronary syndrome (ACS),  1
II. Mechanisms of ACS,  2
III. ECG, cardiac biomarkers, and echocardiography in ACS,  3
IV. Approach to chest pain, likelihood of ACS, risk stratification of ACS,  4
V.Management of high‐risk NSTE‐ACS,  6
VI. General procedural management after coronary angiography: PCI, CABG, or medical therapy only,  9
VII. Management of low‐risk NSTE‐ACS and low‐probability NSTE‐ACS,  11
VIII. Discharge medications,  11
IX. Prognosis, 12
Appendix 1.  Complex angiographic disease, moderate disease,  13
Appendix 2.  Women and ACS, elderly patients and ACS, CKD,  14
Appendix 3.  Bleeding, transfusion, prior warfarin therapy, gastrointestinal bleed,  15
Appendix 4.  Antiplatelet and anticoagulant therapy,  16
Appendix 5.  Differences between plaque rupture, plaque erosion, and spontaneous coronary dissection,  19
Appendix 6.  Harmful effects of NSAIDs and cyclooxygenase‐2 inhibitors in CAD,  19
Questions and answers,  19
References, 25

2. ST‐Segment Elevation Myocardial Infarction, 30
1.  Definition, reperfusion, and general management,  31
I. Definition, 31
II. Timing of reperfusion,  31
III. ECG phases of STEMI,  32
IV. STEMI diagnostic tips and clinical vignettes,  32
V.Specific case of new or presumably new LBBB,  33
VI. Reperfusion strategies: fibrinolytics, primary PCI, and combined fibrinolytics–PCI,  34
VII. Coronary angiography and PCI later than 24 hours after presentation: role of stress testing,  37
VIII. Angiographic findings, PCI, and cellular reperfusion; multivessel disease in STEMI,  38
IX. Antithrombotic therapies in STEMI,  39
X. Other acute therapies,  40
XI. Risk stratification,  41
XII. LV remodeling and infarct expansion after MI,  41
XIII. Discharge, EF improvement, ICD,  41
2. STEMI complications, 42
I. Cardiogenic shock,  42
II. Mechanical complications,  45
III. Recurrent infarction and ischemia,  47
IV. Tachyarrhythmias, 47
V.Bradyarrhythmias, bundle branch blocks, fascicular blocks,  49
VI. LV aneurysm and LV pseudoaneurysm,  50
VII. Pericardial complications,  51
VIII. LV thrombus and thromboembolic complications,  51
IX. Early and late mortality after STEMI,  52
Appendix 1.  Out‐of‐hospital cardiac arrest: role of early coronary angiography and therapeutic hypothermia,  52
Questions and answers,  54
References, 59
3. Stable CAD and Approach to Chronic Chest Pain, 65
I. Causes of angina; pathophysiology of coronary flow,  65

II. Diagnostic approach,  66
vii


viii  Contents

III. Silent myocardial ischemia,  68
IV. Medical therapy: antiplatelet therapy to prevent cardiovascular events,  70
V.Medical therapy: antianginal therapy,  70
VI. Medical therapy: treatment of risk factors,  72
VII. Indications for revascularization,  72
VIII. CABG, 73
IX. PCI, 73
X. PCI vs. medical therapy,  74
XI. PCI vs. CABG in multivessel disease,  75
XII. High‐surgical‐risk patients,  76
XIII. Role of complete functional revascularization,  76
XIV. Hybrid CABG–PCI,  77
XV. Enhanced external counterpulsation (EECP),  77
XVI. Mortality in CAD,  77
Appendix 1. Note on outcomes with various surgical grafts,  77
Appendix 2. Coronary vasospasm (variant angina, Prinzmetal angina),  79
Appendix 3. Women with chest pain and normal coronary arteries,  81
Appendix 4. Myocardial bridging,  81
Appendix 5. Coronary collaterals, chronic total occlusion,  82
Appendix 6. Hibernation, stunning, ischemic preconditioning,  82
Questions and answers,  83
References, 87

PART 2.  Heart Failure (Chronic and Acute Heart Failure, Specific Cardiomyopathies,

and Pathophysiology), 93
4. Heart Failure, 93
Definition, types, causes, and diagnosis of heart failure,  94
1.  Definition and types of heart failure,  94
I. Heart failure is diagnosed clinically, not by echocardiography,  94
II. After HF is defined clinically, echocardiography is used to differentiate the three major types of HF,  95
III. Two additional types of HF,  96
2.  Causes of heart failure,  97
I. Systolic HF (or HF with reduced EF),  97
II. HF with preserved EF,  98
III. Right HF,  100
3. Diagnostic tests, 100
I. Echocardiography, 100
II. BNP, 100
III. ECG, 101
IV. Coronary angiography and other ischemic workup,  101
V.Diastolic stress testing,  102
VI. Endomyocardial biopsy,  102
VII. Cardiac MRI,  102
Chronic treatment of heart failure,  102
1.  Treatment of systolic heart failure,  102
I. Treat the underlying etiology,  102
II. Value of revascularization in ischemic cardiomyopathy: STICH trial,  102
III. Subsets of patients who are likely to benefit from revascularization: role of viability testing and ischemic testing,  103
IV. Drugs that affect survival,  105
V.Specifics of drugs that affect survival,  106
VI. Drugs that improve symptoms and morbidity,  110
VII. Devices, 112
VIII. Other therapeutic measures,  113
IX. Prognosis, 113

2. Treatment of HFpEF, 114
Acute heart failure and acutely decompensated heart failure,  115
I. Triggers of acute decompensation,  116
II. Profiles of acute HF: congestion without low cardiac output, congestion with low cardiac output,  116
III. Treatment of acute HF: diagnosis and treatment of triggers,  117
IV. Treatment of acute HF: diuretics, cardiorenal syndrome, aggressive decongestion, ultrafiltration,  118
V.Treatment of acute HF: vasodilators,  121
VI. Treatment of acute HF: IV inotropic agents (dobutamine, milrinone, dopamine),  122


Contents  ix

VII. In‐hospital and pre‐discharge use of ACE‐Is and β‐blockers, 122
VIII. Treatment of acute HF: O2, non‐invasive ventilatory support (CPAP, BiPAP), intubation,  123
IX. Summary: keys to the treatment of acute HF,  123
X. Discharge, 124
XI. Inability of severe HF to tolerate vasodilatation or hemodialysis,  124
XII. Outpatient monitoring of HF and prevention of hospitalization,  124
Appendix 1. Management of isolated or predominant RV failure,  125
Questions and answers,  127
References, 135
5. Additional Heart Failure Topics, 142
1. Specific cardiomyopathies, 142
I. Specific dilated cardiomyopathies,  142
II. Specific infiltrative restrictive cardiomyopathies,  145
2.  Advanced heart failure: heart transplant and ventricular assist devices (VADs),  146
I. Stages of HF,  146
II. Cardiac transplantation,  146
III. Left ventricular assist devices (LVADs),  147
3.  Pathophysiology of heart failure and hemodynamic aspects,  149

I. LV diastolic pressure in normal conditions and in HF (whether systolic or diastolic),  149
II. Definition of afterload,  149
III. Cardiac output, relation to preload and afterload,  150
IV. LV pressure–volume relationship in systolic versus diastolic failure: therapeutic implications,  151
V.Decompensated LV failure: role of heart rate,  152
VI. Mechanisms of exercise intolerance in HF,  153
VII. Pressure–volume (PV) loops (advanced reading),  153
VIII. Additional features of HF with preserved EF,  153
IX. High‐output HF,  154
References, 155
PART 3.  Valvular Disorders, 157
6. Valvular Disorders, 157
1. Mitral regurgitation, 158
I. Mechanisms of mitral regurgitation,  158
II. Specifics of various causes of mitral regurgitation,  158
III. Assessment of MR severity,  164
IV. Natural history and pathophysiology of organic MR,  164
V.Treatment of organic (primary) MR,  165
VI. Treatment of secondary MR (ischemic and non‐ischemic functional MR),  166
VII. Treatment of acute severe MR related to acute MI,  167
VIII. Percutaneous mitral valve repair using the Mitraclip device,  167
2. Mitral stenosis, 167
I. Etiology and natural history,  167
II. Diagnosis, 168
III. Treatment, 171
3. Aortic insufficiency, 173
I. Etiology, 173
II. Pathophysiology and hemodynamics,  174
III. Diagnosis, 176
IV. Natural history and symptoms,  176

V.Treatment, 176
4. Aortic stenosis, 178
I. Etiology, 178
II. Laboratory diagnosis and severity,  179
III. Low‐gradient AS with aortic valve area (AVA) ≤1 cm2 and low EF <50%,  181
IV. Low‐gradient AS with aortic valve area (AVA) ≤ 1 cm2 but normal EF (paradoxical
low‐flow/low‐gradient severe AS),  181
V.Pressure recovery phenomenon,  182
VI. Symptoms, 183
VII. Natural history,  183
VIII. AS should be differentiated from subvalvular and supravalvular AS in children
or young adults,  183
IX. Treatment, 184


x  Contents

5.  Tricuspid regurgitation and stenosis,  186
I. Etiology of tricuspid regurgitation (TR),  186
II. Natural history of TR,  187
III. Treatment of TR,  187
IV. Tricuspid stenosis (TS),  187
6.  Pulmonic stenosis and regurgitation,  187
I. Pulmonic stenosis (PS),  187
II. Pulmonic regurgitation (PR),  188
7.  Mixed valvular disease; radiation heart disease,  188
I. Mixed single‐valve disease,  188
II. Multiple valvular involvement (combined stenosis or regurgitation of two different valves),  188
III. Radiation heart disease,  189
8. Prosthetic valves, 189

I. Bioprosthesis, 189
II. Mechanical valve: bileaflet tilting disk (St. Jude) or single‐leaflet tilting disk (e.g., Medtronic‐Hall),  190
III. Determinants of valve degeneration and valve thrombosis; anticoagulation guidelines,  190
IV. Particular cases: women who wish to become pregnant and dialysis patients,  191
V.Echocardiographic follow‐up of prosthetic valves,  191
VI. Complications, 191
9.  Auscultation and summary ideas,  193
I. Auscultation and other physical findings,  193
II. General ideas and workup,  196
Questions and answers,  197
References, 206
PART 4.  Hypertrophic Cardiomyopathy, 211
7. Hypertrophic Cardiomyopathy, 211
I. Definition and features of HCM,  211
II. Natural history and mortality,  213
III. Symptoms and ECG,  214
IV. Exam, 214
V.Invasive hemodynamic findings,  214
VI. Echocardiographic findings,  214
VII. Provocative maneuvers,  216
VIII. Genetic testing for diagnosis; screening of first‐degree relatives,  216
IX. Differential diagnosis of LVOT obstruction,  216
X. Differential diagnosis of severe LV hypertrophy,  218
XI. Treatment of symptoms,  218
XII. Treatment: sudden cardiac death risk assessment and ICD therapy,  220
Questions and answers,  221
References, 222
PART 5.  Arrhythmias and Electrophysiology, 225
8. Approach to Narrow and Wide QRS Complex Tachyarrhythmias, 225
I. The unstable patient (shock, acute pulmonary edema),  225

II. Initial approach to any tachycardia,  225
III. Approach to narrow QRS complex tachycardias,  226
IV. Approach to wide QRS complex tachycardias,  227
V.Features characteristic of VT, as opposed to SVT with aberrancy,  228
VI. Features characteristic of SVT with pre‐excitation,  232
VII. Role of adenosine in establishing a diagnosis,  233
VIII. Differential diagnosis of a wide complex tachycardia on a one‐lead telemetry or Holter monitor strip,  234
IX. Various notes,  234
X. General management of SVT,  234
XI. Non‐tachycardic wide complex rhythms,  235
Questions and answers: Practice ECGs of wide complex tachycardias,  235
Further reading,  241
9. Ventricular Arrhythmias: Types and Management, Sudden Cardiac Death, 242
I. Premature ventricular complexes,  242
II. Ventricular tachycardia (VT),  243
III. Polymorphic ventricular tachycardia,  246


Contents  xi

IV. Congenital long QT syndrome (LQT),  248
V.Indications for ICD implantation,  249
VI. Specific VTs that should be considered in the absence of obvious heart disease,  251
VII. Causes of sudden cardiac death (SCD),  253
Questions and answers,  254
References, 256
Further reading,  257
10. Atrial Fibrillation, 258
I. Predisposing factors,  258
II. Types of AF,  259

III. General therapy of AF,  259
IV. Management of a patient who acutely presents with symptomatic AF,  261
V.Peri‐cardioversion management and long‐term management after the acute presentation,  262
VI. Decisions about long‐term anticoagulation, role of clopidogrel, role of triple therapy,  262
VII. Special situation: atrial fibrillation and heart failure,  264
VIII. Special situation: atrial fibrillation with borderline blood pressure,  265
Appendix 1. Antiarrhythmic drug therapy (indications and examples),  265
Appendix 2. Catheter ablation of atrial fibrillation, surgical ablation, AV nodal ablation,  267
Appendix 3. INR follow‐up in patients receiving warfarin; new anticoagulants,  268
Appendix 4. Bridging anticoagulation in patients undergoing procedures and receiving warfarin,  270
Appendix 5. Management of elevated INR values,  270
Appendix 6. A common special situation: AF and symptomatic pauses (sinus or AF pauses) or bradycardia,  271
Appendix 7. DC cardioversion in patients with a slow ventricular response,  271
Appendix 8. AF occurring post‐cardiac surgery and AF related to acute transient triggers,  271
Appendix 9. Brief asymptomatic runs of AF seen on telemetry or device interrogation,  272
Questions and answers,  272
References, 274
Further reading,  277
11. Atrial Flutter and Atrial Tachycardia,  278
I. Atrial flutter,  278
II. Focal atrial tachycardia,  281
III. Multifocal atrial tachycardia (MAT) (or chaotic atrial tachycardia),  284
IV. Ectopic atrial rhythm,  285
Questions and answers,  285
References, 287
Further reading,  287
12. Atrioventricular Nodal Reentrant Tachycardia, Atrioventricular Reciprocating Tachycardia,
Wolff–Parkinson–White Syndrome, and Junctional Rhythms, 288
I. Sinus tachycardia,  288
II. Atrioventricular nodal reentrant tachycardia (AVNRT),  288

III. Atrioventricular reciprocating tachycardia (AVRT) and Wolff–Parkinson–White (WPW) syndrome,  291
IV. Junctional escape rhythm and accelerated junctional rhythm (or non‐paroxysmal junctional tachycardia),  299
Questions and answers,  301
Further reading,  302
13.Bradyarrhythmias, 304
I. AV block,  304
II. Sinus bradyarrhythmias,  312
III. Bundle branch blocks, bifascicular and trifascicular block,  315
Questions and answers,  317
References, 319
14. Permanent Pacemaker and Implantable Cardioverter Defibrillator, 320
I. Indications for permanent pacemaker implantation,  320
II. Types of cardiac rhythm devices,  320
III. Pacemaker intervals,  324
IV. Leads, 327
V.Systematic PM/ICD interrogation using the programmer,  328
VI. Pacemaker troubleshooting,  329
VII. Perioperative management of PM and ICD (during any surgery),  333


xii  Contents

VIII. Differential diagnosis and management of the patient who presents with ICD shock(s),  333
IX. Evidence and guidelines supporting various pacing devices,  334
Questions and answers: Cases of PM troubleshooting,  338
References, 344
15. Basic Electrophysiologic Study, 346
I. General concepts; intracardiac electrograms,  346
II. AV conduction abnormalities,  346
III. Sinus node assessment,  348

IV. Ventricular vs. supraventricular tachycardia,  348
V.Dual AV nodal pathways,  348
VI. AVNRT, 349
VII. Accessory pathway, orthodromic AVRT, antidromic AVRT,  349
VIII. Atrial flutter,  351
IX. Inducible VT,  352
X. Mapping for ablation,  353
Further reading,  357
16. Action Potential Features and Propagation: Mechanisms of Arrhythmias,
Antiarrhythmic Drugs, 358
I. Action potential,  358
II. Action potential propagation and mechanisms of arrhythmias,  358
III. General mechanism of action of antiarrhythmic agents,  361
IV. Modulated receptor hypothesis and use dependence,  363
V.Concept of concealed conduction,  364
VI. Specific examples of drugs,  364
VII. Amiodarone toxicity,  365
VIII. Effect on pacing thresholds and defibrillation thresholds,  365
Further reading,  365
PART 6.  Pericardial Disorders, 367
7. Pericardial Disorders, 367
1
1. Acute pericarditis, 368
I. Causes of acute pericarditis,  368
II. History and physical findings,  368
III. ECG findings,  368
IV. Echocardiography, 368
V.Myopericarditis and perimyocarditis,  369
VI. Treatment, 369
2. Tamponade, 370

I. Definition, 370
II. Pathophysiology and hemodynamics,  370
III. Diagnosis: tamponade is a clinical diagnosis, not an echocardiographic diagnosis,  371
IV. Echocardiographic findings supporting the hemodynamic compromise of tamponade,  371
V.Role of hemodynamic evaluation,  372
VI. Special circumstances: low‐pressure tamponade, tamponade with absent pulsus paradoxus, regional tamponade,  372
VII. Effusive–constrictive pericarditis,  373
VIII. Treatment of tamponade,  373
3. Pericardial effusion, 373
I. Causes of a pericardial effusion with or without tamponade,  373
II. Management of asymptomatic effusions and role of pericardiocentesis,  374
III. Note on postoperative pericardial effusions (after cardiac surgery),  375
IV. Note on uremic pericardial effusion,  376
4. Constrictive pericarditis, 376
I. Causes, 377
II. Pathophysiology and hemodynamics,  377
III. Hemodynamic findings in constrictive pericarditis and differential diagnosis of constrictive pericarditis:
restrictive cardiomyopathy, decompensated RV failure, COPD,  379
IV. Practical performance of a hemodynamic study when constrictive pericarditis is suspected,  381
V.Echocardiographic features of constrictive pericarditis, and differentiation between constrictive pericarditis
and restrictive cardiomyopathy,  381
VI. Physical exam, ECG findings, BNP, pericardial thickness (CT/MRI),  382
VII. Transient constrictive pericarditis,  383
VIII. Treatment, 383


Contents  xiii

Questions and answers,  384
References, 386

Further reading,  387
PART 7.  Congenital Heart Disease, 389
18. Congenital Heart Disease, 389
1.  Acyanotic congenital heart disease,  389
I. Atrial septal defect (ASD),  389
II. Patent foramen ovale (PFO),  393
III. Ventricular septal defect (VSD),  394
IV. Patent ductus arteriosus (PDA),  396
V.Coarctation of the aorta,  397
VI. Other anomalies,  397
2.  Cyanotic congenital heart disease,  398
I. Pulmonary hypertension secondary to shunt,  398
II. Tetralogy of Fallot,  399
III. Ebstein anomaly,  401
3.  More complex cyanotic congenital heart disease and shunt procedures,  401
I. Functionally single ventricle and Fontan procedure,  401
II. Transposition of great arteries (TGA),  403
III. Other anomalies,  404
Questions and answers,  404
References, 407
PART 8.  Peripheral Arterial Disease, 409
19. Peripheral Arterial Disease, 409
1.  Lower extremity peripheral arterial disease,  409
I. Clinical tips,  410
II. Clinical classification of PAD: critical limb ischemia, acute limb ischemia, atheroembolization,  411
III. Diagnosis of PAD,  413
IV. Medical therapy of PAD,  414
V.Revascularization for PAD,  414
VI. Notes on the technical aspects of surgical and percutaneous therapies,  416
VII. Management of acute limb ischemia,  418

VIII. Management of lower extremity ulcers,  418
2. Carotid disease, 418
I. Assessment of carotid stenosis,  418
II. Medical therapy of carotid stenosis,  419
III. Revascularization of asymptomatic carotid stenosis,  419
IV. Revascularization of symptomatic carotid stenosis,  419
V.Main risks of CEA and carotid stenting,  420
VI. CEA versus carotid stenting,  420
VII. Carotid disease in a patient undergoing CABG,  420
VIII. Subtotal and total carotid occlusions,  420
3.  Renal artery stenosis,  421
I. Forms of renal artery stenosis,  421
II. Screening and indications to revascularize renal artery stenosis,  421
III. Notes, 422
Questions and answers,  422
References, 425
0. Aortic Diseases, 428
2
I. Aortic dissection,  428
II. Thoracic aortic aneurysm,  432
III. Abdominal aortic aneurysm,  436
References, 437
PART 9.  Other Cardiovascular Disease States, 439
1. Pulmonary Embolism and Deep Vein Thrombosis, 439
2
1. Pulmonary embolism, 439
I. Presentation of pulmonary embolism (PE) and risk factors,  439
II. Probability of PE,  440

xiv  Contents

III. Initial workup,  440
IV. Specific PE workup,  440
V.Submassive PE, pulmonary hypertension, and thrombolysis,  442
VI. PE and chronic pulmonary hypertension,  443
VII. Acute treatment of PE,  443
VIII. Duration of anticoagulation,  444
IX. Thrombophilias, 445
X. PE prognosis,  445
2.  Deep vein thrombosis,  445
I. Types, 445
II. Diagnosis, 445
III. Treatment, 446
3.  Immune heparin‐induced thrombocytopenia,  446
I. Incidence, 446
II. Diagnosis, 446
III. Treatment, 446
Questions and answers,  447
References, 447
2. Shock and Fluid Responsiveness, 449
2
1. Shock, 449
I. Shock definition and mechanisms,  449
II. Goals of shock treatment,  450
III. Immediate management of any shock,  450
2. Fluid responsiveness, 452
Appendix. Hemodynamic equations, transfusion, and miscellaneous concepts,  454
References, 455
3.Hypertension, 456

2
1. Hypertension, 456
I. Stages of hypertension,  456
II. Causes of HTN,  456
III. Treatment of HTN: goals of therapy,  458
IV. Treatment of HTN: timing, first‐line drugs, compelling indications for specific drugs,  458
V.Resistant HTN,  459
VI. Peripheral vs. central aortic pressure: therapeutic implications,  460
VII. Antihypertensive drugs,  460
VIII. Other considerations in therapy,  464
2.  Hypertensive urgencies and emergencies,  465
I. Definitions, 465
II. Treatment of hypertensive emergencies,  465
III. Treatment of hypertensive urgencies,  466
IV. Causes and workup,  467
V.Specific situations,  467
Questions and answers,  467
References, 469
4. Dyslipidemia, 472
2
I. Indications for therapy,  472
II. Notes on LDL, HDL, and triglycerides,  473
III. Drugs: LDL‐lowering drugs,  473
IV. Drugs: TG/HDL‐treating drugs and lifestyle modification,  474
V.Metabolic syndrome,  475
VI. Diabetes, 475
VII. Elevated hs‐CRP (high‐sensitivity C‐reactive protein test) ≥2 mg/l,  475
VIII. Chronic kidney disease (CKD),  475
IX. Causes of dyslipidemia to consider,  475
X. Side effects of specific drugs: muscle and liver intolerance with statins, fibrates,

and niacin, 475
Questions and answers,  476
References, 477


Contents  xv

25. Pulmonary Hypertension, 479
I. Definition, 479
II. Categories of PH,  479
III. Two tips in the evaluation of PH,  481
IV. Hypoxemia in patients with PH,  481
V.Diagnosis: echocardiography; right and left heart catheterization,  481
VI. Treatment, 482
Questions and answers,  484
References, 486
26.Syncope, 488
I. Neurally mediated syncope (reflex syncope),  488
II. Orthostatic hypotension,  489
III. Cardiac syncope,  490
IV. Other causes of syncope,  490
V.Syncope mimic: seizure,  490
VI. Clinical clues,  491
VII. Diagnostic evaluation of syncope,  491
VIII. Tilt table testing,  494
IX. Indications for hospitalization,  494
X. Treatment of neurally mediated syncope,  495
Questions and answers,  495
References, 497
7. Chest Pain, Dyspnea, Palpitations, 499

2
1. Chest pain, 499
I. Causes, 499
II. Features, 500
III. Management of chronic chest pain,  501
IV. Management of acute chest pain,  501
2. Acute dyspnea, 502
I. Causes, 502
II. Notes, 503
III. Management, 503
3. Palpitations, 504
I. Causes, 504
II. Diagnosis, 504
References, 505
28. Infective Endocarditis and Cardiac Rhythm Device Infections, 507
1. Infective endocarditis, 507
I. Clinical diagnosis,  507
II. Echocardiography: timing and indications,  507
III. Organisms, 508
IV. Morphology, 508
V.Anatomical complications,  508
VI. Indications for valvular surgery and special situations,  508
2.  Cardiac rhythm device infections,  511
I. Organisms and mechanisms of infection,  511
II. Diagnosis, 511
III. Diagnosis in patients with bacteremia but no local or TEE signs of infection,  511
IV. Management, 511
References, 513
29. Preoperative Cardiac Evaluation, 514
I. Steps in preoperative evaluation,  515

II. Surgical risk: surgery’s risk and patient’s risk,  515
III. CARP and DECREASE V trials,  516
IV. Only the highest‐risk coronary patients require revascularization preoperatively,  516
V.Preoperative percutaneous revascularization,  516


xvi  Contents

VI. Surgery that needs to be performed soon after stent placement,  517
VII. Preoperative β‐blocker therapy,  517
VIII. Other interventions that improve outcomes,  517
IX. Severe valvular disease,  517
X. Perioperative hypertension,  518
XI. Preoperative management of patients with pacemakers or ICDs,  518
Questions and answers,  518
References, 519
0. Miscellaneous Cardiac Topics: Cardiac Masses and Tumors, Pregnancy, HIV and Heart Disease,
3
Cocaine and the Heart, Chemotherapy and Heart Disease, Chest X‐Ray, 521
1. Cardiac masses, 522
I. Differential diagnosis of a cardiac mass,  522
II. Cardiac tumors; focus on atrial myxoma,  522
2.  Pregnancy and heart disease,  523
I. High‐risk cardiac conditions during which pregnancy is better avoided,  524
II. Cardiac conditions that are usually well tolerated during pregnancy, but in which careful cardiac evaluation
and clinical and echo follow‐up are warranted  524
III. Cardiac indications for cesarean section,  525
IV. Mechanical prosthetic valves in pregnancy: anticoagulation management,  525
V.Peripartum cardiomyopathy (PPCM),  525
VI. Cardiovascular drugs during pregnancy,  526

VII. Arrhythmias during pregnancy,  526
VIII. MI and pregnancy,  526
IX. Hypertension and pregnancy,  527
3.  HIV and heart disease,  527
I. Pericardial disease,  527
II. HIV cardiomyopathy,  527
III. Pulmonary hypertension (PH),  527
IV. CAD, 527
4. Cocaine and the heart, 527
I. Myocardial ischemia,  527
II. Other cardiac complications of cocaine,  528
5.  Chemotherapy and heart disease,  528
I. Cardiomyopathy, 528
II. Myocardial ischemia,  529
6. Chest X‐ray, 529
I. Chest X‐ray in heart failure,  529
II. Various forms of cardiomegaly,  530
III. Left atrial enlargement; aortic dilatation,  531
IV. Lateral chest X‐ray,  532
V.Chest X‐ray in congenital heart disease,  532
Questions and answers,  532
References, 534
PART 10.  Cardiac Tests: Electrocardiography, Echocardiography, and Stress Testing, 537
1.Electrocardiography, 537
3
I. Overview of ECG leads and QRS morphology,  537
II. Stepwise approach to ECG interpretation,  540
III. Rhythm and rate,  541
IV. QRS axis in the limb leads and normal QRS progression in the precordial leads,  543
V.P wave: analyze P wave in leads II and V1 for atrial enlargement, and analyze

PR interval,  544
VI. Height of QRS: LVH, RVH,  546
VII. Width of QRS. Conduction abnormalities: bundle brunch blocks,  548
VIII. Conduction abnormalities: fascicular blocks,  551
IX. Low QRS voltage and electrical alternans,  553
X. Assessment of ischemia and infarction: Q waves,  554
XI. Assessment of ischemia: ST‐segment depression and T‐wave inversion,  557
XII. Assessment of ischemia: differential diagnosis of ST‐segment elevation,  567
XIII. Assessment of ischemia: large or tall T wave,  573
XIV. QT analysis and U wave,  574
XV. Electrolyte abnormalities, digitalis effect and digitalis toxicity, hypothermia, PE, poor precordial 
R‐wave progression,  577


Contents  xvii

XVI. Approach to tachyarrhythmias,  582
XVII. Approach to bradyarrhythmias: AV block,  585
XVIII. Abnormal automatic rhythms that are not tachycardic,  587
XIX. Electrode misplacement,  588
Appendix 1.  Supplement on STEMI and Q‐wave MI: phases and localization,  589
Appendix 2.  Spread of electrical depolarization in various disease states using vector illustration,  594
Questions and answers,  595
References, 598
Further reading,  601
2.Echocardiography, 602
3
1. General echocardiography, 602
I. The five major echocardiographic views and the myocardial wall segments,  602
II. Global echo assessment of cardiac function and structure,  602

III. Doppler: mainly assesses blood flow direction (→ regurgitation), timing, and velocity,  612
IV. Summary of features characterizing severe valvular regurgitation and stenosis,  623
V.M‐mode echocardiography is derived from 2D echo,  624
VI. Pericardial effusion,  624
VII. Echocardiographic determination of LV filling pressure and diastolic function,  628
VIII. Additional echocardiographic hemodynamics,  630
IX. Prosthetic valves,  634
X. Brief note on Doppler physics and echo artifacts,  637
2.  Transesophageal echocardiography (TEE) views,  639
Further reading,  648
33. Stress Testing, Nuclear Imaging, Coronary CT Angiography, 649
I. Indications for stress testing,  649
II. Contraindications to all stress testing modalities,  650
III. Stress testing modalities,  650
IV. Results, 651
Appendix 1. Mechanisms of various stress modalities,  656
Appendix 2. Nuclear stress imaging,  657
Appendix 3. Coronary CT angiography,  660
References, 663
Further reading,  664
PART 11.  Cardiac Tests: Invasive Coronary and Cardiac Procedures, 665
34. Angiographic Views: Coronary Arteries and Grafts, Left Ventricle, Aorta, Coronary Anomalies,
Peripheral Arteries, Carotid Arteries, 665
I. Right coronary artery,  665
II. Left coronary artery,  666
III. Coronary angiography views. Recognize the angle of a view: LAO vs. RAO, cranial vs. caudal,  667
IV. Coronary angiography views. General ideas: cranial vs. caudal views,  667
V.Coronary angiography views. General ideas: foreshortening and identifying branches,  670
VI. Left coronary views,  670
VII. Right coronary views,  679

VIII. Improve the angiographic view in case of vessel overlap or foreshortening: effects of changing
the angulation, effects of respiration, and vertical vs. horizontal heart,  681
IX. Saphenous venous graft views,  682
X. LIMA‐to‐LAD or LIMA‐to‐diagonal views,  684
XI. Left ventriculography,  685
XII. Aortography for assessment of aortic insufficiency,  688
XIII. Coronary anomalies,  688
XIV. Lower extremity angiography,  691
XV. Carotid angiography,  696
Questions and answers,  697
Further reading,  699
35. Cardiac Catheterization Techniques, Tips, and Tricks, 700
I. View for the engagement of the native coronary arteries: RAO vs. LAO,  700
II. Design of the Judkins and Amplatz catheters,  700
III. Engagement of the RCA,  700
IV. How to gauge the level of the RCA origin in relation to the aortic valve level,  703
V.What is the most common cause of failure to engage the RCA? What is the next step?,  704


xviii  Contents

VI. JR4 catheter engages the conus branch. What is the next step?,  704
VII. Left coronary artery engagement: general tips,  704
VIII. Management of a JL catheter that is sub‐selectively engaged in the LAD or LCx,  706
IX. Specific maneuvers for the Amplatz left catheter,  706
X. If you feel that no torque is getting transmitted, what is the next step?,  706
XI. Appropriate guide catheters for left coronary interventions,  706
XII. Appropriate guide catheters for RCA interventions,  708
XIII. Selective engagement of SVGs: general tips,  709
XIV. Specific torque maneuvers for engaging the SVGs,  709

XV. Appropriate catheters for engaging SVGs,  711
XVI. Engagement of the left internal mammary artery graft,  712
XVII. Left ventricular catheterization,  713
XVIII. Engagement of anomalous coronary arteries,  714
XIX. Specific tips for coronary engagement using a radial approach,  714
XX. Damping and ventricularization of the aortic waveform upon coronary engagement,  717
XXI. Technique of right heart catheterization,  718
6.Hemodynamics, 720
3
I. Right heart catheter,  720
II. Overview of pressure tracings: differences between atrial, ventricular, and arterial tracings,  720
III. RA pressure abnormalities,  720
IV. Pulmonary capillary wedge pressure (PCWP) abnormalities,  720
V.LVEDP, 725
VI. Cardiac output and vascular resistances,  726
VII. Shunt evaluation,  727
VIII. Valvular disorders: overview of pressure gradients and valve area calculation,  729
IX. Dynamic LVOT obstruction,  733
X. Pericardial disorders: tamponade and constrictive pericarditis,  735
XI. Exercise hemodynamics,  736
Appendix 1. Advanced hemodynamic calculation: a case of shunt with pulmonary hypertension,  737
Questions and answers: Additional hemodynamic cases,  738
References, 740
7. Intracoronary Imaging, 741
3
1.  Intravascular ultrasound (IVUS),  741
I. Image basics,  741
II. Plaque types,  744
III. Basic IVUS measurements,  746
IV. Interpretation of how a severe stenosis may look mild angiographically, yet severe by IVUS;

significance of lesion haziness,  748
V.Endpoints of stenting,  748
VI. Assessment of lesion significance by IVUS,  748
VII. Assessment of left main by IVUS,  749
2.  Optical coherence tomography (OCT),  749
References, 751
Further reading,  751
38. Percutaneous Coronary Interventions and Complications, Intra‐Aortic Balloon Pump,
Ventricular Assist Devices, and Fractional Flow Reserve, 752
I. Major coronary interventional devices,  752
II. Stent thrombosis, restenosis, and neoatherosclerosis,  754
III. Peri‐PCI antithrombotic therapy,  756
IV. Complex lesion subsets,  756
V.Sheath management,  757
VI. Post‐PCI mortality and coronary complications,  758
VII. Femoral access complications,  760
VIII. Renal, stroke, and atheroembolic complications,  761
IX. Intra‐aortic balloon pump (IABP) or intra‐aortic balloon counterpulsation,  762
X. Percutaneous LV assist device: Impella and TandemHeart,  765
XI. Extracorporeal membrane oxygenation (ECMO),  767
XII. Fractional flow reserve (FFR),  767
Questions and answers,  770
Further reading,  773
Index, 775


Preface

You should learn solely in order to create. For willing is creating.
Friedrich Nietzsche, Thus Spoke Zarathustra

Work without ceasing. If you remember in the night, “I have not done what I ought to have done,” rise up at once and do it. Believe
to the end, even if all men went astray and you were left the only one faithful.
Fyodor Dostoevsky, The Brothers Karamazov
Practical Cardiovascular Medicine is a comprehensive yet practical review of all fields of cardiovascular medicine. It addresses various cardiac
diseases and presentations using both pathophysiology and clinical evidence, and expands from basic concepts to advanced ones. It should
therefore prove useful to experienced physicians as well as trainees. In fact, there is a particular emphasis on the knowledge gaps of cardiologists and cardiology fellows. Organizing fellowship conferences and working with cardiology and interventional cardiology fellows has
helped me perceive common deficiencies and focus on them.
Colleagues who read the book will find that it provides them with an in‐depth understanding that translates into better patient management. My aim has also been to improve on pre‐existing knowledge of pathophysiology and clinical trials. The book follows a comprehensive yet easy, practical, and illustrated flow. To facilitate learning, bottom‐line approaches are consistently provided throughout the 38
chapters. There is an extra emphasis on concepts that are frequently misunderstood by practitioners.
Throughout, I have tried to answer daily, practical questions that may not be addressed in any other book. Even classic topics, such as
ST‐segment elevation myocardial infarction, heart failure, arrhythmias, atrial fibrillation, cardiac catheterization, or electrocardiography are
discussed from a different, fresh, and contemporary viewpoint. The book is comprehensive, and many of its chapters could even stand
alone as separate books.
In order to consolidate the understanding of complex topics, review questions with detailed answers are provided at the end of clinical
chapters, mainly in a clinical vignette format (approximately 400 questions overall). The book will serve cardiologists and cardiology fellows,
but will also be valuable to internists, internal medicine residents, and all professionals caring for patients with cardiovascular disease. I have
written this book in an effort to embrace the magic and evolving depths of cardiovascular diseases. It is written with love, and with the
hope of improving patients’ outcomes.
Elias B. Hanna
August 2016

xix


Abbreviations

3Dthree‐dimensional
AAD
antiarrhythmic drug
AAA

abdominal aortic aneurysm
ABI
ankle–brachial index
ACC
American College of Cardiology
ACCP
American College of Chest Physicians
ACE‐I
angiotensin converting enzyme inhibitor
ACS
acute coronary syndrome
ACT
activated clotting time
ADHF
acutely decompensated heart failure
ADP
adenosine diphosphate
AF
atrial fibrillation
Aflutter
atrial flutter
American Heart Association
AHA
AI
aortic insufficiency
AIVR
accelerated idioventricular rhythm
AM
acute marginal
ANA

antinuclear antibodies
Aoaorta
AoV
aortic valve
AP
accessory pathway
AP
anteroposterior view
angiotensin‐II receptor blocker
ARB
acute respiratory distress syndrome
ARDS
ARVC
arrhythmogenic right ventricular cardiomyopathy
arrhythmogenic right ventricular dysplasia
ARVD
AS
aortic stenosis
ASD
atrial septal defect
AT
anterior tibial artery
AT
atrial tachycardia
AT1 receptor type receptor of angiotensin 2
AT2 receptor type 2 receptor of angiotensin 2
antithrombin IIII
AT III
AVatrioventricular
AV block

atrioventricular block
AVA
aortic valve area
atrioventricular nodal reentrant tachycardia
AVNRT
aortic valve replacement
AVR
atrioventricular reciprocating tachycardia
AVRT
BBB
bundle branch block
BiPAP
bilevel positive airway pressure
BiVbiventricular
biVAD
biventricular assist device
BMS
bare‐metal stent
BNP
brain natriuretic peptide
BP
blood pressure
bpm
beats per minutes
BSA
body surface area
BUN
blood urea nitrogen
Cacalcium
CABG

coronary artery bypass grafting
CAD
coronary artery disease
CBC
complete blood count
CCB
calcium channel blockers
CEA
carotid endarterectomy
CIA
common iliac artery
xx


Abbreviations  xxi

CK
creatine kinase
CK‐MB
creatine kinase MB
chronic kidney disease
CKD
congestive heart failure
CHF
cardiac output
CO
chronic obstructive pulmonary disease
COPD
continuous positive airway pressure
CPAP

C‐reactive protein test
CRP
cardiac resynchronization therapy
CRT
computed tomography
CT
CTA
computed tomography angiography
CTI
cavotricuspid isthmus
CTO
chronic total occlusion
chronic thromboembolic pulmonary hypertension
CTPH
central venous pressure
CVP
continuous wave Doppler
CW
CYP 450
cytochrome P450
chest X‐ray
CXR
DAD
delayed afterdepolarization
diastolic blood pressure
DBP
DC cardioversion R‐wave synchronized direct‐current cardioversion
dilated cardiomyopathy
DCM
drug‐eluting stent

DES
dihydropyridine (calcium channel blocker)
DHP
dP/dt
delta pressure/delta time (sharpness of rise in pressure over time)
direct thrombin inhibitor
DTI
Duke treadmill score
DTS
deep vein thrombosis
DVT
early afterdepolarization
EAD
ECGelectrocardiogram
echoechocardiogram
extracorporeal membrane oxygenation
ECMO
emergency department
ED
ejection fraction
EF
EIA
external iliac artery
EPelectrophysiological
effective regurgitant orifice
ERO
European Society of Cardiology
ESC
erythrocyte sedimentation rate
ESR

end‐stage renal disease
ESRD
fractional flow reserve
FFR
FiO2
fraction of inspired oxygen
fibromuscular dysplasia
FMD
GFR
glomerular filtration rate
GIgastrointestinal
glycoprotein IIb–IIIa inhibitor
GPI
Hbhemoglobin
glycosylated hemoglobin
HbA1c
HCM
hypertrophic cardiomyopathy
HCTZhydrochlorothiazide
high‐density lipoprotein
HDL
heart failure
HF
HFpEF
heart failure with preserved ejection fraction
heart failure with reduced ejection fraction
HFrEF
HIT
heparin‐induced thrombocytopenia
Human immunodeficiency virus

HIV
HOCM
hypertrophic obstructive cardiomyopathy
HR
heart rate
hs‐CRP
high sensitivity C‐reactive protein test
HTNhypertension
IABP
intra‐aortic balloon pump
ICD
implantable cardioverter defibrillator
ICU
intensive care unit


xxii  Abbreviations

INR
international normalized ratio
IV
intravenous or intravenously
IVC
inferior vena cava
IVC‐
isovolumic contraction
IVCT
isovolumic contraction time
IVR
isovolumic relaxation

isovolumic relaxation time
IVRT
intravascular ultrasound
IVUS
JVD
jugular venous distension
JVP
jugular venous pressure
Kpotassium
LA
left atrium
LAA
left atrial appendage
LAFB
left anterior fascicular block
LAD
left anterior descending artery
LAO
left anterior oblique
LBBB
left bundle branch block
LCx
left circumflex coronary artery
low‐density lipoprotein
LDL
left heart catheterization and coronary angiogram
LHC
LIMA
left internal mammary artery
left lower sternal border

LLSB
left main
LM
low‐molecular‐weight heparin
LMWH
LPFB
left posterior fascicular blockLUSB left upper sternal border
left ventricle or left ventricular
LV
LVAD
left ventricular assist device
left ventricular end‐diastolic diameter
LVEDD
LVEDP
left ventricular end‐diastolic pressure
left ventricular ejection fraction
LVEF
LVESD
left ventricular end‐systolic diameter
left ventricular hypertrophy
LVH
left ventricular outflow tract
LVOT
mean arterial pressure
MAP
multifocal atrial tachycardia
MAT
metabolic equivalent of task
MET
mph

miles per hour
myocardial infarction
MI
mitral regurgitation
MR
magnetic resonance angiography
MRA
magnetic resonance imaging
MRI
mitral stenosis
MS
MV
mitral valve
MV O2
mixed venous oxygen saturation
mitral valve area
MVA
MVP
mitral valve prolapse
MVR
mitral valve replacement
Nasodium
NO
nitric oxide
non‐steroidal anti‐inflammatory drug
NSAID
NSTEMI
non‐ST‐segment elevation myocardial infarction
non‐sustained ventricular tachycardia
NSVT

NT pro‐BNP amino‐terminal pro‐brain natriuretic peptide
NTGnitroglycerin
NYHA
New York Heart Association
optical coherence tomography
OCT
OM
obtuse marginal branch of the left circumflex
Ppressure
PA
pulmonary arterial or pulmonary artery
PA O2
pulmonary arterial oxygen saturation
PAC
premature atrial complex
PaCO2
partial pressure of carbon dioxide in arterial blood
PAD
peripheral arterial disease


Abbreviations  xxiii

PAH
pulmonary arterial hypertension
PAI
plasminogen activator inhibitor
PaO2
arterial oxygen pressure
PaO2

alveolar oxygen pressure
PCI
percutaneous coronary intervention
PCSK9 Proprotein convertase subtilisin/kexin type 9
pulmonary capillary wedge pressure
PCWP
patent ductus arteriosus
PDA
PDA
posterior descending artery branch of the right coronary artery or left circumflex
pulmonary embolism
PE
PEA
pulseless electrical activity
PET
positron emission tomography
patent foramen ovale
PFO
PFT
pulmonary function testing
PH
pulmonary hypertension
PHT
pressure half‐time
proximal isovelocity surface area
PISA
permanent junctional reciprocating tachycardia
PJRT
posterolateral ventricular branches of the right coronary artery or left circumflex
PLB

PMpacemaker
percutaneous mitral balloon valvuloplasty
PMBV
pacemaker‐mediated tachycardia
PMT
paroxysmal nocturnal dyspnea
PND
POTS
postural orthostatic tachycardia syndrome
purified protein derivative for Mycobacterium tuberculosis
PPD
proton pump inhibitor
PPI
patient/prosthesis mismatch
PPM
PR
pulmonic regurgitation
pulmonic stenosis
PS
PT
posterior tibial artery
partial thromboplastin time
PTT
PV loop pressure–volume loop
PV O2
pulmonary venous oxygen saturation
PVARP post‐ventricular atrial refractory period
PVC
premature ventricular complex
pulmonary vascular resistance

PVR
PW
pulsed wave Doppler
pulmonary blood flow
Qp
Qs
systemic blood flow
corrected QT interval
QTc
RA
right atrium
renin‐angiotensin‐aldosterone system
RAAS
RAO
right anterior oblique
RAS
renal artery stenosis
RBBB
right bundle branch block
right coronary arteryRHC
right heart catheterization
RCA
RIMA
right internal mammary artery
rPAreteplase
rpm
revolutions per minute
r‐tPA
recombinant tissue plasminogen activator
right upper sternal border

RUSB
RV
right ventricle/ventricular
RVAD
right ventricular assist device
RVEDP right ventricular end‐diastolic pressure
right ventricular hypertrophy
RVH
RVOT
right ventricular outflow tract
SAsinoatrial
SA O2
systemic arterial oxygen saturation
SAM
systolic anterior motion
SaO2
arterial oxygen saturation
SBE
subacute bacterial endocarditis
SBP
systolic blood pressure
SCD
sudden cardiac death


xxiv  Abbreviations

SIRS
systemic inflammatory response syndrome
SFA

superficial femoral artery
SNRT
sinus node reentrant tachycardia
single photon emission computed tomography (nuclear imaging)
SPECT
SQsubcutaneously
ST‐segment elevation myocardial infarction
STEMI
Society of Thoracic Surgeons
STS
SV
stroke volume
superior vena cava
SVC
SVG
saphenous venous graft
SvO2
mixed venous oxygen saturation
SVR
systemic vascular resistance
supraventricular tachycardia
SVT
thoracic aortic aneurysm
TAA
TdP
torsades de pointes
TEE
transesophageal echocardiogram
transposition of great arteries
TGA

transient ischemic attack
TIA
TID
transient ischemic dilatation
TR
tricuspid regurgitation
thyroid stimulating hormone
TSH
transthoracic echocardiogram
TTE
unstable angina
UA
unfractionated heparin
UFH
VAD
ventricular assist device
V/Q scan lung ventilation/perfusion scan
VF
ventricular fibrillation
very‐low‐density lipoprotein
VLDL
velocity of propagation
Vp
ventricular septal defect
VSD
VSR
ventricular septal rupture
ventricular tachycardia
VT
velocity‐time integral

VTI
WPWWolff–Parkinson–White


Part 1  Coronary Artery Disease
1 

Non‐ST‐Segment Elevation Acute Coronary Syndrome

I.  Types of acute coronary syndrome (ACS)  1
II.  Mechanisms of ACS  2
III.  ECG, cardiac biomarkers, and echocardiography in ACS  3
IV.  Approach to chest pain, likelihood of ACS, risk stratification of ACS  4
V. Management of high‐risk NSTE‐ACS  6
VI.  General procedural management after coronary angiography: PCI, CABG, or medical therapy only  9
VII.  Management of low‐risk NSTE‐ACS and low‐probability NSTE‐ACS  11
VIII.  Discharge medications  11
IX.  Prognosis 12
Appendix 1. Complex angiographic disease, moderate disease  13
Appendix 2. Women and ACS, elderly patients and ACS, CKD  14
Appendix 3. Bleeding, transfusion, prior warfarin therapy, gastrointestinal bleed  15
Appendix 4. Antiplatelet and anticoagulant therapy  16
Appendix 5. Differences between plaque rupture, plaque erosion, and spontaneous coronary dissection  19
Appendix 6. Harmful effects of NSAIDs and cyclooxygenase‐2 inhibitors in CAD  19
Questions and answers  19

I.  Types of acute coronary syndrome (ACS)
A.  Unstable angina
Unstable angina is defined as any of the following clinical presentations, with or without ECG evidence of ischemia and with a normal
troponin:

• Crescendo angina: angina that increases in frequency, intensity, or duration, often requiring a more frequent use of nitroglycerin
• New‐onset (<2 months) severe angina, occurring during normal activities performed at a normal pace
• Rest angina
• Angina occurring within 2 weeks after a myocardial infarction (post‐infarction angina)
B.  Non‐ST‐segment elevation myocardial infarction (NSTEMI)
A rise in troponin, per se, is diagnostic of myocardial necrosis but is not sufficient to define myocardial infarction (MI), which is myocardial
necrosis secondary to myocardial ischemia. Additional clinical, ECG, or echocardiographic evidence of ischemia is needed to define MI.
In fact, MI is defined as a troponin elevation above the 99th percentile of the reference limit (~0.03 ng/ml, depending on the assay)
with a rise and/or fall pattern, along with any one of the following four features: (i) angina; (ii) ST‐T abnormalities, new LBBB, or new Q
waves on ECG; (iii) new wall motion abnormality on imaging; (iv) intracoronary thrombus on angiography.1 NSTEMI is defined as MI without persistent (>20 min) ST‐segment elevation.
Isolated myocardial necrosis is common in critically ill patients and manifests as a troponin rise, sometimes with a rise and fall pattern, but frequently no other MI features. Also, troponin I usually remains <1 ng/ml in the absence of underlying CAD.2,3

Practical Cardiovascular Medicine, First Edition. Elias B. Hanna.
© 2017 John Wiley & Sons Ltd. Published 2017 by John Wiley & Sons Ltd.

1


2  Part 1.  Coronary Artery Disease

A rise or fall in troponin is necessary to define MI. A fluctuating troponin or a mild, chronically elevated but stable troponin may be
seen in chronic heart failure, myocarditis, severe left ventricular hypertrophy, or advanced kidney disease. While having a prognostic value,
this stable troponin rise is not diagnostic of MI. Different cutoffs have been used to define a relevant troponin change, but, in general, a
troponin that rises above the 99th percentile with a rise or fall of >50–80% is characteristic of MI (ACC guidelines use a less specific cutoff
of 20%; 50–80% cutoff is more applicable to low troponin levels <0.1 ng/ml).4
C.  ST‐segment elevation myocardial infarction (STEMI)
STEMI is defined as a combination of ischemic symptoms and persistent, ischemic ST‐segment elevation.1,5 For practical purposes, ischemic
symptoms with ongoing ST‐segment elevation of any duration are considered STEMI and treated as such. The diagnosis may be retrospectively changed to NSTEMI if ST elevation quickly resolves without reperfusion therapy, in <20 minutes.
Unstable angina and NSTEMI are grouped together as non‐ST‐segment elevation ACS (NSTE‐ACS). However, it must be noted
that unstable angina has a much better prognosis than NSTEMI, and particularly that many patients labeled as unstable angina do

not actually have ACS.6 In fact, in the current era of highly sensitive troponin assays, a true ACS is often accompanied
by a troponin rise. Unstable angina is, thus, a “vanishing” entity.7

II.  Mechanisms of ACS
A. True ACS is usually due to plaque rupture or erosion that promotes platelet aggregation (spontaneous or type 1 MI). This
is followed by thrombus formation and microembolization of platelet aggregates. In NSTEMI, the thrombus is most often a platelet‐rich
non‐occlusive thrombus. This contrasts with STEMI, which is due to an occlusive thrombus rich in platelets and fibrin. Also, NSTEMI usually
has greater collateral flow to the infarct zone than STEMI.
As a result of the diffuse inflammation and alteration of platelet aggregability, multiple plaque ruptures are seen in ~30–80% of ACS
cases, although only one is usually considered the culprit in ACS.8 This shows the importance of medical therapy to “cool down” the diffuse
process, and explains the high risk of ACS recurrence within the following year even if the culprit plaque is stented.8
Occasionally, a ruptured plaque or, more commonly, an eroded plaque may lead to microembolization of platelets and thrombi and
impaired coronary flow without any residual, angiographically significant lesion or thrombus.
B. Secondary unstable angina and NSTEMI (type 2 MI). In this case, ischemia is related to severely increased O2 demands (demand/
supply mismatch). The patient may have underlying CAD but the coronary plaques are stable without acute rupture or thrombosis.
Conversely, the patient may not have any underlying CAD, in which case troponin I usually remains <0.5–1 ng/ml.2,3 Acute antithrombotic
therapy is not warranted.
In the absence of clinical or ECG features of MI, the troponin rise is not even called MI.

Cardiac causes of secondary unstable angina/NSTEMI include: severe hypertension, acute HF, aortic stenosis/hypertrophic cardiomyopathy,
tachyarrhythmias. Non‐cardiac causes of secondary unstable angina/NSTEMI include: gastrointestinal bleed, severe anemia, hypoxia, sepsis.
While acute HF often leads to troponin elevation, ACS with severe diffuse ischemia may lead to acute HF, and in fact 30% of acute HF
presentations are triggered by ACS.9 HF presentation associated with crescendo angina, ischemic ST changes, or severe troponin rise
(>0.5–1 ng/ml) should be considered ACS until CAD is addressed with a coronary angiogram.
Acute bleed, severe anemia, or tachyarrhythmia destabilizes a stable angina. Treating the anemia or the arrhythmia is a first priority in
these patients, taking precedence over treating CAD.

While acute, malignant hypertension may lead to secondary ACS and troponin rise, ACS with severe angina may lead to
hypertension (catecholamine surge). In ACS, hypertension drastically improves with angina relief and nitroglycerin, whereas
in malignant hypertension, hypertension is persistent and difficult to control despite multiple antihypertensive therapies,

nitroglycerin only having a minor effect. Nitroglycerin has a mild and transient antihypertensive effect, and thus a sustained
drop in BP with nitroglycerin often implies that hypertension was secondary to ACS.

C.  Coronary vasospasm
It was initially hypothesized by Prinzmetal and then demonstrated in a large series that vasospasm and vasospastic angina (Prinzmetal)
often occur in patients with significant CAD at the site of a significant atherosclerotic obstruction.10,11 In one series, 90% of patients with
vasospastic angina had significant, single‐ or multivessel CAD. Most frequently, CAD was not only significant but unstable.12 In fact, a
ruptured plaque is frequently accompanied by vasospasm, as the activated platelets and leukocytes release vasoconstrictors. About 20%
of these patients with underlying CAD go on to develop a large MI, while >25% develop severe ventricular arrhythmias or paroxysmal AV
block with syncope.