Clinical biochemistry of cardiovascular

CLINICAL OF BIOCHEMISTRY
Assignment: CARDIOVASCULAR DISEASE
Student’s name : Dang Quynh Nhu
Student’s ID : BTBCIU19059
Instructor : Dr. Hoang Le Son
I.

INTRODUCTION

The cardiovascular system, also known as the
circulatory system, is made up of the heart and
blood vessels (arteries, arterioles, capillaries,
venules and veins). When it works properly, blood
circulation maintains tissue perfusion, supplying
substrates for cellular metabolism and removing
excretory products. It also allows hormones to be
transferred from their origin organs to their target
tissues, protects against infection by facilitating the
flow of white cells and cytokines, and supports
haemostasis by delivering platelets and clotting
factors to injured tissue, among other critical
activities.
The human circulatory system is an organ system that distributes blood to and from every
region of the body via vessels, giving nutrients and oxygen while removing waste products such as
carbon dioxide. The blood is pumped through a closed tubular system by a muscular heart. The
pulmonary and systemic circuits are made up of arterial, capillary, and venous components.
The self-activating characteristic of specific cardiac cells, which ordinarily generate an
orderly contraction of the heart chambers, is critical in this function. Smooth muscle cells in blood
arteries are regulated by a number of signal molecules and play a vital role in blood pressure
regulation and oxygen/nutrient distribution. Diseases of these blood vessels, particularly
hypertension and atherosclerosis, are responsible for much of the illness and death in the developed

world.
Heart
The average adult human heart is around 13 by 9 by 6 cm (5 by 3.5 by 2.5 inches), weighs
approximately 10.5 ounces, and is somewhat larger than a clenched fist (300 grams). It has a conelike shape, with the wide base pointing upward and right and the tip pointing downward and left. It


is located above the diaphragm in the thoracic cavity of the chest, behind the sternum of the
breastbone, in front of the esophagus, descending aorta, trachea, and lungs (the muscular partition
between the chest and abdominal cavities). The heart is roughly two-thirds of the way to the left of
the midline.

II.

CARDIAC MUSCLE STRUCTURE AND FUNCTION
Cardiac muscle is distinct from skeletal and smooth muscle in various ways:
1. More mitochondria enable for ongoing high-level adenosine triphosphate (ATP) generation,
allowing for continued operation without tiredness. Anaerobic respiration can give enough
energy for contraction to persist during periods of low oxygen.
2. The primary energy source is lipids [fatty acids and triglycerides (60%)], followed by carbs
(35%), amino acids, and ketone bodies (5%).
3. Has fewer but larger T tubules and intercalated discs, which allow for the rapid and
synchronized propagation of action potentials between adjacent cells, allowing for coordinated
cardiac muscle contraction.
4. The electrical signal of the action potential is converted into mechanical work of contraction
by the fast release and re-uptake of intracellular calcium reserves.

III.

BLOOD FLOW OF THE HUMAN HEART

1. Anemic blood that has been evacuated from the body returns to the right atrium (upper right
chamber) via the inferior and superior vena cava veins.
2. The tricuspid valve (lower right chamber) allows blood to enter the right ventricle.
3. Blood is pushed from the right ventricle out the major pulmonary artery via the pulmonary
valve.
4. The blood is subsequently pumped into the lungs via the left and right pulmonary arteries.
Breathing causes the body to absorb oxygen while expelling carbon dioxide. As a result, the
blood now contains an abundance of oxygen.
5. The blood is returned to the heart via four pulmonary veins, where it enters the left atrium
(upper left chamber).
6. The mitral valve (lower left chamber) allows blood to enter the left ventricle.
7. Through the aortic valve, blood is pushed from the left ventricle into the "aorta," a major
artery.


IV.

BLOOD VESSELS

Blood vessels, which include arteries, veins, and capillaries, serve as a conduit for blood to be
delivered to and from every tissue in the human body, delivering oxygen and nutrition while
removing carbon dioxide and waste.
Arteries and veins are made up of three layers of cells and/or polysaccharide matrix,
connective and elastic tissues, and smooth muscle cells, as well as their own system of blood vessels
(vasa vasorum) and nerves that feed and regulate their structure and, thus, activity. Capillaries, which
are responsible for the actual transfer of molecules between the blood and the cells, are typically
composed of a single layer of cells joined by connective tissue.
Vasoconstriction is generally caused by peptide hormones like vasopressin, angiotensin II,
and endothelin, or by neurological transmitter molecules like epinephrine.
Epinephrine can also elicit vasodilatation and/or vasoconstriction via a2- and b2-receptors,

respectively, and increased heart rate and contractile force via b1-receptors, all via the Gi or Gs,
adenylyl cyclase/cAMP messenger system.
Vasodilation is caused by chemicals like nitric oxide (NO), which diffuses across the plasma
membrane of blood vessel cells and binds to a soluble guanylate cyclase. This enzyme generates
cGMP, which activates protein kinase G, resulting in the dephosphorylation and inactivation of
smooth muscle myosin molecules via MLCK inactivation.
Despite the fact that the average lifetime of NO in the body is only a few seconds, its
pharmacological effects are seen in medications such as sublingual nitroglycerin for chest pain via
decreased cardiac workload, treatment of neonatal patients with pulmonary hypertension in an
intensive care setting, and even modern erectile disorder drugs (e.g., sildenafil/ Viagra), which
prolong the lifetime of cGMP and, thus, vasodilation of vessels in the penis.

V.

Intermediate-density lipoprotein (IDL) and LDL

Following multiple rounds of LPL action, apo C and apo E (not shown) are transported back
to HDL from the diminishing VLDL. This leads in the development of an IDL including apo B100
and some of the remaining apo E. IDL, like HDL and chylomicron remnants, can be removed from
the liver via the apo E receptor (genetic defects in the apo E ligand or its receptor elicit type III
hyperlipidemia, in which IDL, chylomicron remnants, and HDL are elevated).
LDL is formed using cholesteryl esters from either the liver (endogenous) or chylomicron
leftovers after further hydrolysis of triacylglycerol in IDL by LPL and transfer of the remaining apo
E to HDL (exogenous). VLDLs lose surface area as their triacylglycerols are digested, eventually
reducing them to cholesteryl ester-enriched LDL.
LDL's principal role is to transport cholesterol to peripheral tissues. LDL receptors, which are
responsible for this absorption, are coupled with clathrin-coated pits on these cells' plasma


membranes and identify apo B100 (Figure 16-8). LDL particles and receptors are then endocytosed

into numerous tissues, including the liver.
The receptors and clathrin mostly recycle back to the plasma membrane. Most of the LDL
(70%) binds to receptors on liver hepatocytes. The remainder of the LDL associates with receptors
on peripheral cells. Lipoprotein disorders in which LDL receptors, or their capacity to bind the apo
B100 ligand, are defective, result in an increased level of cholesterol in LDL remaining in
circulation, causing hypercholesterolemia and atherosclerosis.
HDL
HDL, a discoidal particle generated in the liver and secreted into plasma, aids in this function
by acting as a cholesterol scavenger and promoting the transfer of cholesterol from the periphery to
the liver for conversion to bile acids and eventual elimination (Figure 16-8). This cholesterolremoving ability is what earns HDL the title of "good" cholesterol carrier.
Lecithin, cholesterol ester, lecithin cholesterol
acyl transferase (LCAT), apo A1, apo C, and apo E are
all found in mature HDL particles. Cholesterol efflux
regulatory protein (CERP), an ATP-binding protein
transporter, facilitates the acquisition of cholesterol by
circulating HDL from peripheral cells. CERP is
activated by apo A1 and flips unesterified cholesterol
and lecithin to the cell membrane's outer layer. CERP
then distributes free cholesterol and lecithin to HDL as
substrates for LCAT. Apo A1 also activates LCAT in
developing HDL and acts as a ligand for a cell surface
receptor on peripheral cells.
LCAT catalysis produces cholesterol esters, which migrate to the core of nascent HDL for
eventual transport back to the liver. "Reverse cholesterol transport" refers to the complete process of
LCAT extraction of cell cholesterol and incorporation into HDL for liver clearance. Another
important role of HDL is to act as a storage site for apo A1, apo C, and apo E. Transfer of apo C is
necessary for chylomicron and VLDL metabolism, whereas transfer of apo E is required for
clearance of chylomicron remnants, IDLs, and HDLs. As a result, HDL contributes to both external
and endogenous lipid transport mechanisms.
VI.

CARDIOVASCULAR DISORDER

Cardiovascular disease
Cardiovascular disease (CVD) is defined as
disease of the heart and blood vessels (usually
always arteries) supplying any organ. The heart
(coronary artery disease), the brain (cerebrovascular
disease), and the limbs are the most usually affected
organs by arterial disease (peripheral arterial
disease). Renovascular disease is a major contributor
to chronic renal disease and hypertension.
Because atherosclerosis is by far the most
common cause of cardiovascular disease in
developed countries, the term 'cardiovascular
disease' is commonly used and perceived to mean
'atherosclerotic disease,' the term 'coronary artery disease' or 'coronary heart disease' to mean
atherosclerosis of the coronary arteries, and 'cerebrovascular disease' to mean atherosclerosis of the
cerebral vasculature.
Coronary artery atherosclerosis causes a reduction in blood supply to the myocardium, often
known as ischaemia. When this reaches a critical point, the heart muscles die, resulting in


a'myocardial infarction' (MI), which is frequently, but not always, accompanied by diagnostic
abnormalities on the electrocardiogram (ECG).
Atherosclerosis
Chronic atherosclerosis leads to hardening of the plaque by calcium as well as thickening and
stiffening (arteriosclerosis) of the affected arterial
walls. The exact mechanism of the formation of a
plaque is still under investigation, but current opinion

is
that the initial step involves oxidation of LDL,
probably by the enzymatic action of lipoproteinassociated phospholipase A2. These oxidized LDL
particles are more readily taken up by macrophages
that
can invade endothelial cells in the wall of an artery that
are
themselves damaged by oxidation.
The injury initiates an immune response by
macrophages, which bind to the area via the protein
vascular cell adhesion molecule-1 and vainly attempt to
remove the oxidized LDL molecules. Platelets are also
recruited to the site of injury and attempt to cover the
area. The accumulation of oxidized LDL and the
monocytes/ macrophages attempting to ingest it is
known as a fatty streak— continued inflammation and
growth of the fatty streak leads to an atheroma of the
arterial wall.
As the immune response continues the monocytes/ macrophages die, releasing inflammatory
factors such as IL-1 and tumor necrosis factor-a. More white blood cells, including T-lymphocytes
and mast cells, are recruited with continued inflammation of the arterial wall. The continued
inflammation also impacts smooth muscle cells, both leading to increased numbers and movement
toward the growing plaque, adding to its size and composition.
Congenital heart disease
Congenital (present at birth) heart disease
is caused by faulty cardiac development. A
septal defect is a hole in the septum, the wall
that separates the left and right sides of the
heart. The hole could be in the interatrial
septum or the interventricular septum.

These flaws allow blood to flow from one
side of the heart to the other, reducing the heart's
pumping function significantly. When a blood
channel termed the ductus arteriosus, which is
present in the fetus, fails to close after birth, the
condition is known as patent ductus arteriosus.
The ductus arteriosus connects the pulmonary
trunk to the aorta. It permits blood to bypass the
lungs by traveling from the pulmonary trunk to
the aorta. Because the lungs do not function
before birth, this is natural.
If the ductus arteriosus fails to shut after birth, blood flows from the aorta to the pulmonary
trunk in the opposite way. As a result, blood flows through the lungs at a higher pressure, damaging
them. Furthermore, the amount of work required by the left ventricle to maintain normal systemic
blood pressure rises.


Heart failure
Heart failure (HF) is characterized by the inability of the heart to fill with (diastolic HF) or
eject (systolic HF) blood, or both. Congestive heart failure refers to pulmonary congestion produced
by back pressure generated by the left ventricle's failure to move blood around the body. Ischaemic
heart disease is by far the most prevalent cause, however it can also be caused by any structural or
functional cardiac pathology, such as valvular heart disease, hypertension, or viral cardiomyopathy.
Although chronic heart failure might be relatively asymptomatic, dyspnea is the most
common symptom. In its early phases. Acute life-threatening pulmonary oedema may also occur as
a medical emergency. There is a wide range of severity. Between these two extremes, symptomatic
heart failure is a rather typical reason for emergency room visits.
Heart failure has an overall frequency of about 2%, but it is significantly greater in the
elderly, affecting up to 15% of people over the age of 85. Its incidence is expected to rise as the
population ages. It affects men more than women at all ages. The illness worsens over time, and

people with heart failure have a lower life expectancy and a lower quality of life. In the United
Kingdom, more than 40% of patients die within 18 months of being diagnosed.

VII.

DIAGNOSTIC TESTS FOR CARDIOVASCULAR DESEASE

Electrocardiogram (ECG or EKG) (ECG or EKG). An electrocardiogram (ECG) is a
rapid and painless examination that records electrical signals in the heart. It can detect whether the
heart is beating too quickly or too slowly.
Holter recording. A Holter monitor is a portable ECG device that is worn for a day or more
to record the activity of the heart during daily activities. This test can detect irregular heartbeats that
a standard ECG cannot.
Echocardiogram. This noninvasive scan creates detailed images of the heart in action using
sound waves. It depicts how blood flows through the heart and its valves. An echocardiography can
assist in determining whether a valve is constricted or leaking.
Stress testing or exercise tests. These tests frequently entail walking on a treadmill or riding
a stationary bike while having the heart rate monitored. Exercise testing can indicate how the heart
responds to physical activity and whether or not symptoms of heart disease arise during exercise. If
you are unable to exercise, you may be prescribed medication.
Catheterization of the heart. This test can detect cardiac artery blockages. A catheter is a
long, thin, flexible tube that is placed into a blood artery, typically in the groin or wrist, and guided
to the heart. Dye is delivered to arteries in the heart via the catheter. The dye makes the arteries
more visible on X-ray images acquired during the exam.
CT scan of the heart (cardiac). You recline on a table within a doughnut-shaped machine
for a heart CT scan. Inside the machine, an X-ray tube spins around your body, collecting images of
your heart and chest.


Magnetic resonance imaging (MRI) of the heart (cardiac). A cardiac MRI creates

comprehensive images of the heart by using a magnetic field and computer-generated radio waves.
VIII. TREATMENT
The therapy of heart illness is determined by the source and type of heart injury.
Healthy lifestyle behaviors, such as eating a low-fat, low-salt diet, obtaining regular exercise and
adequate sleep, and not smoking, are critical components of treatment.
Medications: If lifestyle changes alone are ineffective in controlling heart disease symptoms
and preventing complications, medicines may be required. The drug utilized is determined by the
type of heart disease.
Surgery or other medical treatments: Some persons suffering from heart disease may require
a treatment or surgery. The sort of operation or surgery will be determined by the type of heart
disease and the extent of heart damage.
IX.

LIFESTYLE AND HOME REMERDIES

Heart complaint can be bettered — or indeed averted — by making certain life changes. The
following changes are recommended to ameliorate heart health
Do not bomb. Smoking is a major threat factor for heart complaint, especially
atherosclerosis. Quitting is the stylish way to reduce the threat of heart complaint and
itscomplications. However, talk to your provider, If you need help quitting.
Eat healthy foods. Eat plenitude of fruits, vegetables and whole grains. Limit sugar, swab
and impregnated fats.
Control blood pressure. unbridled high blood pressure increases the threat of serious health
problems. Get your blood pressure checked at least every two times if you are 18
andolder.However, you may need more-frequent checks, If you have threat factors for heart
complaint or are over age 40. Ask your health care provider what blood pressure reading is stylish
for you.
Get a cholesterol test. Ask your provider for a birth cholesterol test when you are in your
20s and also at least every 4 to 6 times. You may need to start testing earlier if high cholesterol is in
your family. You may need more-frequent checks if your test results are not in a desirable range or

you have threat factors for heart complaint.
Managediabetes. However, tight blood sugar control can help reduce the threat of heart
complaint, If you have diabetes. Exercise. Physical exertion helps you achieve and maintain a
healthy weight. Regular exercise helps control diabetes, high cholesterol and high blood pressure all
threat factors for heart complaint. With your provider's OK, aim for 30 to 60 twinkles of physical
exertion most days of the week. Talk to your health care provider about the quantum and type of
exercise that is stylish for you. Maintain a healthy weight. Being fat increases the threat of heart
complaint. Talk with your care provider to set realistic pretensions for body mass indicator( BMI)
and weight.
Manage stress. Find ways to help reduce emotional stress. Getting further exercise,
rehearsing awareness and connecting with others in support groups are some ways to reduce and
managestress. However, talk to your provider about strategies to help, If you have anxiety or
depression.
Exercise good hygiene. Regularly wash your hands and encounter and floss your teeth to
keep yourself healthy.
Exercise good sleep habits. Poor sleep may increase the threat of heart complaint and other
habitual conditions. Grown-ups should aim to get 7 to 9 hours of sleep daily. kiddies frequently
need further. Go to bed and wake at the same time every day, including onweekends.However, talk
to your provider about strategies that might help, If you have trouble sleeping.
X.

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