1. What is the mechanisms of cardiovascular dysfunction?

(311 – Rakshita) (312 – Aashish Bharti)

-There are six principal mechanisms of cardiovascular dysfunction.

Failure of the pump. In the most common situation, the cardiac muscle contracts
weakly and the chambers cannot empty properly—so-called systolic dysfunction.
In some cases, the muscle cannot relax sufficiently to permit ventricular filling,
resulting in diastolic dysfunction.
• Obstruction to flow. Lesions that prevent valve opening (e.g., calcific aortic valve
stenosis) or cause increased ventricular chamber pressures (e.g., systemic
hypertension or aortic coarctation) can overwork the myocardium,
which has to pump against the obstruction.
• Regurgitant flow. Valve lesions that allow backward flow of blood create
conditions that add increased volume workload to the affected chambers with each
contraction, (e.g., left ventricle in aortic regurgitation; left atrium and left ventricle
in mitral regurgitation).
• Shunted flow. Defects (congenital or acquired) that divert blood inappropriately
from one chamber to another, or from one vessel to another, lead to pressure and
volume overloads.
• Disorders of cardiac conduction. Uncoordinated cardiac impulses or blocked
conduction pathways can cause arrhythmias that reduce contraction frequency or
diminish effective cardiac output.
• Rupture of the heart or major vessel. Loss of circulatory continuity (e.g., gunshot
wound through the thoracic aorta) leads to exsanguination, hypotensive shock, and
death.

2. Heart failure. What is it? Causes. Classification.

(311 – Pooja Bhat) (312 – Rithika)
Heart failure generally is referred to as congestive heart failure (CHF). CHF is the
common end point for many forms of cardiac disease and typically is a progressive
condition that carries an extremely poor prognosis. Most cases of heart failure are
due to systolic dysfunction—inadequate myocardial contractile function,
characteristically a consequence of ischemic heart disease or hypertension.
Alternatively, CHF also can result from diastolic dysfunction—inability of the
heart to adequately relax and fill, such as in massive left ventricular hypertrophy,
myocardial fibrosis, amyloid deposition, or constrictive pericarditis. Finally, heart
failure also can be caused by valve dysfunction (e.g., due to endocarditis) or can
occur in normal hearts suddenly burdened with an abnormal load (e.g., with fluid
or pressure overload).
CHF occurs when the heart cannot generate sufficient output to meet the metabolic
demands of the tissues—or can only do so at higher-than-normal filling pressures;
in a minority of cases, heart failure can be a consequence of greatly increased
tissue demands, as in hyperthyroidism, or poor oxygen carrying capacity as in
anemia (high-output failure). CHF onset can be abrupt, as in the setting of a large
myocardial infarct or acute valve dysfunction. In many cases, however, CHF
develops gradually and insidiously owing to the cumulative effects of chronic work
overload or progressive loss of myocardium.
In CHF, the failing heart can no longer efficiently pump the blood delivered to it by
the venous circulation. The result is an increased end-diastolic ventricular volume,
leading to increased end-diastolic pressures and, finally, elevated venous pressures.
Thus, inadequate cardiac output—called forward failure—is almost always
accompanied by increased congestion of the venous circulation— that is,
backward failure. As a consequence, although the root problem in CHF typically is
deficient cardiac function, virtually every other organ is eventually affected by
some combination of forward and backward failure. Compensatory hypertrophy
comes at a cost to the myocyte. The oxygen requirements of hypertrophic
myocardium are amplified owing to increased myocardial cell mass. Because the
myocardial capillary bed does not expand in step with the increased myocardial
oxygen demands, the myocardium becomes vulnerable to ischemic injury.

3. Left-sided heart failure.

(311– Reddy Manoj) (312 – Rithika)
Heart failure can affect predominantly the left or the rightside of the heart or
may involve both sides. The most common causes of left-sided cardiac failure
are ischemic heart disease (IHD), systemic hypertension, mitral or aortic valve
disease (Stenosis or regurgitation), and primary diseases of the myocardium
(e.g., amyloidosis). The morphologic and clinical effects of left-sided CHF stem
from diminished systemic perfusion and the elevated back-pressures within the
pulmonary circulation.
Clinical Features:
Dyspnea (shortness of breath) on exertion is usually the earliest and most
significant symptom of left-sided heart failure; cough also is common as a
consequence of fluid transudation into air spaces. As failure progresses, patients
experience dyspnea when recumbent (orthopnea); this occurs because the
supine position increases venous return from the lower extremities and also
elevates the diaphragm. Orthopnea typically is relieved by sitting or standing,
so patients usually sleep in a semiseated position.
Paroxysmal nocturnal dyspnea is a particularly dramatic form of breathlessness,
awakening patients from sleep with extreme dyspnea bordering on feelings of
suffocation. Systemically, diminished cardiac output leads to decreased renal
perfusion that in turn triggers the reninangiotension-aldosterone axis, increasing
intravascular volume and pressures. Unfortunately, these compensatory effects
exacerbate the pulmonary edema.
With further reduction in renal perfusion, prerenal azotemia may supervene,
with impaired excretion of nitrogenous wastes and increasing metabolic
derangement. In severe
CHF, diminished cerebral perfusion can manifest as hypoxic encephalopathy
with irritability, diminished cognition, and restlessness that can progress to
stupor and coma.
Clinical manifestatios (summarized):
dyspnea caused by pulmonary congestion (edema)
orthopnea as blood is redistributed from the legs to the central circulation
when the patient lies down at night
paroxysmal nocturnal dyspnea due to the reabsorption of interstitial fluid
when lying down and reduced sympathetic stimulation while sleeping
fatigue associated with reduced oxygenation and a lack of activity
cough associated with pulmonary congestion
crackles due to pulmonary congestion
hemoptysis resulting from bleeding veins in the bronchial system caused by
venous distention
point of maximal impulse displaced toward the left anterior axillary line
caused by left ventricular hypertrophy
tachycardia due to sympathetic stimulation
cool, pale skin resulting from peripheral vasoconstriction
restlessness and confusion due to reduced cardiac output
4. Right-sided heart failure.
(311 – Mohammad Asif) (312 – Simi Lal Aishwaria)
Right heart failure usually is the consequence of left-sided heart failure, since
any pressure increase in the pulmonary circulation inevitably produces an
increased burden on the right side of the heart. Isolated right-sided heart failure
also can occur in a few diseases. The most common of these is severe
pulmonary hypertension, resulting in right-sided heart pathology termed cor
pulmonale. In cor pulmonale, myocardial hypertrophy and dilation generally
are confined to the right ventricle and atrium, although bulging of the
ventricular septum to the left can cause left ventricular dysfunction. Isolated
right-sided failure also can occur in patients with primary pulmonic or tricuspid
valve disease, or congenital heart disease, such as with left-to-right shunts
causing chronic volume and pressure overloads. The major morphologic and
clinical effects of pure rightsided heart failure differ from those of left-sided
heart failure in that engorgement of the systemic and portal venous systems
typically is pronounced and pulmonary congestion is minimal.
Causes (summarized):
Severe pneumonia
Pulmonary embolus
Pulmonary hypertension (increased pulmonary venous pressure – pulmonary
hypertension – right ventricular hypertrophy - RSHF)
Stenosis or regurgitation of the tricuspid or pulmonic valves
Right ventricular infarction
Cardiomyopathy (right-sided backflow that result in venous congestion)
Persistent left–sided failure (poor emptying of the LA - increased pulmonary
venous pressure – pulmonary hypertension – right ventricular hypertrophy -
RSHF)

Clinical Features
Unlike left-sided heart failure, pure right-sided heart failure typically is
associated with very few respiratory symptoms. Instead, the clinical
manifestations are related to systemic and portal venous congestion, including
hepatic and splenic enlargement, peripheral edema, pleural effusion,
and ascites. Venous congestion and hypoxia of the kidneys and brain due to
right heart failure can produce deficits comparable to those caused by the
hypoperfusion caused by left heart failure.
Of note, in most cases of chronic cardiac decompensation, patients present with
biventricular CHF, encompassing the clinical syndromes of both right-sided
and left-sided heart failure. As congestive heart failure progresses, patients may
 become frankly cyanotic and acidotic, as a consequence of decreased tissue
perfusion resulting from both diminished forward flow and increasing
retrograde congestion.
Clinical manifestatios (summarized):
elevated jugular venous distention due to venous congestion
hepatomegaly secondary to venous congestion
right upper quadrant pain caused by liver engorgement
anorexia, fullness, and nausea may be caused by congestion of the liver and
intestines
nocturia as fluid is redistributed at night
weight gain due to the retention of sodium and water
edema associated with fluid volume excess
ascites or anasarca caused by fluid retention
5. CONGENITAL HEART DISEASE
(311 - Ankita) (311 – Jailal Seena Jyothilakshmi)

6. Cardiogenic shock
(311 – Dileep) (312 – Raam Kumar)
Cardiogenic shock implies failure of the heart to pump blood normally.
In cardiogenic shock, the left ventricle can't maintain an adequate cardiac
output
Causes:
 myocardial infarction (most common cause)
 heart failure
 cardiomyopathy
 arrhythmias
 pericardial tamponade
 tension pneumothorax
 pulmonary embolism
Compensatory mechanisms increase heart rate, strengthen myocardial
contractions, promote sodium and water retention, and cause selective
vasoconstriction.
There are three basic stages of cardiogenic shock:
 compensatory
 progressive
 irreversible or refractory
An initial compensatory stage, during which reflex compensatory
mechanisms are activated and vital organ perfusion is maintained.
When arterial pressure and tissue perfusion are reduced,
 compensatory mechanisms are activated
 to maintain perfusion to the heart and brain.
The carotid sinus and aortic arch
 sense a drop in blood pressure,
 epinephrine and norepinephrine are secreted
 to increase peripheral resistance, blood pressure, and myocardial
contractility.
The kidney activates the renin–angiotensin–aldosterone system,
 causing vasoconstriction
 and sodium and water retention,
 leading to increased blood volume and venous return.
In the compensatory stage of shock, signs and symptoms may include:
Tachycardia and bounding pulse due to sympathetic stimulation
Restlessness and irritability related to cerebral hypoxia
Tachypnea to compensate for hypoxia
Reduced urinary output secondary to vasoconstriction
Cool, pale skin associated with vasoconstriction
Warm, dry skin in septic shock due to vasodilation

A progressive stage, characterized by tissue hypoperfusion and onset of

worsening circulatory and metabolic derangement, including acidosis.
This stage of shock
 begins as compensatory mechanisms
 fail to maintain cardiac output.
Tissues become hypoxic
 because of poor perfusion.
As cells switch to anaerobic metabolism,
 lactic acid builds up,
 producing metabolic acidosis.
In the progressive stage of shock, signs and symptoms may include:
Tachycardia and bounding pulse due to sympathetic stimulation
Restlessness and irritability related to cerebral hypoxia
Tachypnea to compensate for hypoxia
Reduced urinary output secondary to vasoconstriction
Cool, pale skin associated with vasoconstriction
Warm, dry skin in septic shock due to vasodilation
An irreversible stage, in which cellular and tissue injury is so severe that even
if the hemodynamic defects are corrected, survival is not possible.
As the shock syndrome progresses,
 permanent organ damage occur
 as compensatory mechanisms
 can no longer maintain cardiac output.
Perfusion to the coronary arteries is reduced,
 causing myocardial depression
Reduced perfusion damages cell membranes,
 lysosomal enzymes are released,
 and energy stores are depleted,
 possibly leading to cell death.
Eventually, circulatory and respiratory failure occurs.
Death is inevitable.
Unconsciousness and absent reflexes caused by
 reduced cerebral perfusion,
 acid–base imbalance,
 or electrolyte abnormalities
Rapidly falling blood pressure
 as decompensation occurs
Weak pulse caused by reduced cardiac output
Slow, shallow or Cheyne–Stokes respirations
 secondary to respiratory center depression
Anuria related to renal failure

Possible complications of shock include:

 acute respiratory distress syndrome
 acute tubular necrosis
 disseminated intravascular coagulation (DIC)
 cerebral hypoxia
 death

7. Ischemic heart disease (IHD). Causes. Tipes.

(311 – Monika ) (312 – Sulubadh Kumar)

Since cardiac myocytes generate energy almost exclusively through

mitochondrial oxidative phosphorylation, cardiac function is strictly dependent
upon the continuous flow of oxygenated blood through the coronary arteries.
Ischemic heart disease (IHD) is a broad term encompassing several
 closely related syndromes caused by myocardial ischemia—an imbalance
between cardiac blood supply (perfusion) and myocardial oxygen and
nutritional requirements.
The term ischemic heart disease refers to inadequate perfusion of the
myocardium.
In more than 90% of cases, IHD is a consequence of reduced coronary blood
flow secondary to obstructive atherosclerotic vascular disease. Thus, unless
otherwise specified, IHD usually is synonymous with coronary artery disease
(CAD).
Less frequently, IHD can result from increased demand
(e.g., with increased heart rate or hypertension); diminished
blood volume (e.g., with hypotension or shock); diminished
oxygenation (e.g., due to pneumonia or CHF); or diminished
oxygen-carrying capacity (e.g., due to anemia or carbon monoxide
poisoning).
The manifestations of IHD are a direct consequence of the insufficient blood
supply to the heart. The clinical presentation may include one or more of the
following cardiac syndromes:
• Angina pectoris (literally, “chest pain”): Ischemia induces pain but is
insufficient to cause myocyte death. Angina can be stable (occurring
predictably at certain levels of exertion), can be caused by vessel spasm
(Prinzmetal angina), or can be unstable (occurring with progressively
less exertion or even at rest).
• Acute myocardial infarction (MI): The severity or duration of ischemia is
sufficient to cause cardiomyocyte death.
• Chronic IHD with CHF (congestive heart failure): Progressive cardiac
decompensation after acute MI, or secondary to accumulated small ischemic
insults, eventually precipitates mechanical pump failure.
• Sudden cardiac death (SCD): This can occur as a consequence of tissue
damage from MI, but most commonly results from a lethal arrhythmia without
myocyte necrosis.
The term acute coronary syndrome is applied to any of the three catastrophic
manifestations of IHD—unstable angina, acute MI, and SCD.

8. Angina pectoris.
(311 – Venkatesh Yashwanth) (312 – Farhan)

Angina pectoris is an intermittent chest pain caused by transient, reversible

myocardial ischemia. The pain probably is a consequence of the ischemia-
induced release of adenosine, bradykinin, and other molecules that stimulate the
autonomic afferents. Three variants are recognized:
  Typical or stable angina is predictable episodic chest pain
associated with particular levels of exertion or some other increased demand
(e.g., tachycardia). The pain is classically described as a crushing or squeezing
substernal sensation, that can radiate down the left arm or to the left jaw
(referred pain). The pain usually is relieved by rest (reducing demand) or by
drugs such as nitroglycerin, a vasodilator that increases coronary perfusion.
 Prinzmetal or variant angina occurs at rest and is caused by coronary artery
spasm. Although such spasms typically occur on or near existing atherosclerotic
plaques, completely normal vessel can be affected. Prinzmetal angina typically
responds promptly to vasodilators such as nitroglycerin and calcium channel
blockers.
 Unstable angina (also called crescendo angina) is characterized
by increasingly frequent pain, precipitated by progressively less exertion or
even occurring at rest. Unstable angina is associated with plaque disruption
and superimposed thrombosis, distal embolization of the thrombus, and/or
vasospasm; it is often the harbinger of MI, caused by complete vascular
occlusion.

9. Myocardial infarction.
(311– Babu Therkat Androwe Geoyd) (312 – Satveer)
Death of a segment of myocardium due to prolonged ischemia, usually due to
obstruction of a coronary artery lasting longer than 30 to 45 minutes.
Coronary Artery Occlusion. In a typical MI, the following sequence of
events takes place:
• An atheromatous plaque is suddenly disrupted by intraplaque hemorrhage or
mechanical forces, exposing subendothelial collagen and necrotic plaque
contents to the blood.
• Platelets adhere, aggregate, and are activated, releasingthromboxane A2,
adenosine diphosphate (ADP), and serotonin—causing further platelet
aggregation and vasospasm.
• Activation of coagulation by exposure of tissue factor and other mechanisms
adds to the growing thrombus.
• Within minutes, the thrombus can evolve to completely occlude the coronary
artery lumen.
Myocardial Response to Ischemia. Loss of the myocardial blood supply leads
to profound functional, biochemical, and morphologic consequences. Within
seconds of vascular obstruction, aerobic glycolysis ceases, leading to a drop in
adenosine triphosphate (ATP) and accumulation of potentially noxious
metabolites (e.g., lactic acid) in the cardiac myocytes. The functional
consequence is a rapid loss of contractility, which occurs within a minute or so
of the onset of ischemia. Ultrastructural changes (including myofibrillar
relaxation, glycogen depletion, cell and mitochondrial swelling) also become
rapidly apparent. These early changes are potentially reversible. Only severe
ischemia lasting at least 20 to 40 minutes causes irreversible damage and
myocyte death leading to coagulation necrosis. With longer periods of
ischemia, vessel injury ensues, leading to microvascular thrombosis.
Myocardial ischemia also contributes to arrhythmias, probably by causing
electrical instability (irritability) of ischemic regions of the heart.
Predisposing risk factors include:
• Positive family history
• Gender men and postmenopausal women are more susceptible to MI than
premenopausal women
• Hypertension
• Smoking
• Elevated serum triglyceride, total cholesterol, and low–density lipoprotein
levels
• Obesity
• Excessive intake of saturated fats
• Sedentary lifestyle
• Aging
The following signs and symptoms may occur:
Persistent, crushing substernal chest pain
 that may radiate to the left arm, jaw, neck, or shoulder blades
 caused by reduced oxygen supply to the myocardial cells;
Blood pressure and pulse initially elevated
 as a result of sympathetic nervous system activation.
 If cardiac output is reduced, blood pressure may fall.
Cool extremities, perspiration, anxiety, and restlessness
 due to the release of catecholamines
Fatigue and weakness
 caused by reduced perfusion to skeletal muscles
Nausea and vomiting
 as a result of reflex stimulation of vomiting centers by pain fibers
Shortness of breath and crackles reflecting heart failure
Low–grade temperature due to the inflammatory response
Complications of MI include:
• Arrhythmias (ventricular fibrillation or heart block of impulse)
• Cardiogenic shock
• Heart failure causing pulmonary edema
• Pericarditis
• Dressler’s syndrome Dressler’s syndrome associated with pericarditis,
pleurisy, and pneumonitis (1 day and several weeks after infarction) due to
hypersensitivity response to tissue necrosis.
 • Mural thrombi causing cerebral or pulmonary emboli
• Myocardial rupture with tamponade
•
10. Hypertension.
(311 – Bee Sana) (312 – Manish Gitala)
Elevated systemic blood pressure
 systolic pressure >140 mm Hg
 or diastolic pressure >90 mm Hg.
Hypertension occurs as two major types:
essential (primary) hypertension, the most common (90-95 %)
secondary hypertension, which results from renal disease or another
identifiable cause.
Risk factors for primary hypertension include:
 family history
 advancing age
 obesity
 tobacco use
 high intake of sodium
 high intake of saturated fat
 excessive alcohol consumption
 sedentary lifestyle
 stress
 diabetes mellitus

Mechanisms of Essential Hypertension

Although the specific triggers are unknown, it appears that both altered renal
sodium handling and increased vascular resistance contribute to essential
hypertension.
• Reduced renal sodium excretion in the presence of normal arterial pressure
probably is a key pathogenic feature; indeed, this is a common etiologic factor in
most forms of hypertension. Decreased sodium excretion causes an obligatory
increase in fluid volume and increased cardiac output, thereby elevating blood
pressure. At the new higher blood pressure, the kidneys excrete additional sodium.
Thus, a new steady state of sodium excretion is achieved, but at the expense of an
elevated blood pressure.
• Increased vascular resistance may stem from vasoconstriction or structural
changes in vessel walls. These are not necessarily independent factors, as chronic
vasoconstriction may result in permanent thickening of the walls of affected
vessels.
• Genetic factors play an important role in determining blood pressure, as shown
by familial clustering of hypertension and by studies of monozygotic and dizygotic
twins.
Hypertension has been linked to specific angiotensinogen polymorphisms and
angiotensin II receptor variants; polymorphisms of the renin-angiotensin system
also may contribute to the known racial differences in blood pressure regulation.
Susceptibility genes for essential hypertension in the larger population are
currently unknown but probably include those that govern renal sodium handling,
pressors, and smooth muscle cell growth.
• Environmental factors, such as stress, obesity, smoking, physical inactivity, and
high levels of salt consumption, modify the impact of genetic determinants.
Evidence linking dietary sodium intake with the prevalence of hypertension in
different population groups is particularly strong.
Summarize:
• Hypertension is a common disorder affecting 25% of the population; it is a
major risk factor for atherosclerosis, congestive heart failure, and renal failure.
• Essential hypertension represents 95% of cases and is a complex, multifactorial
disorder, involving both environmental influences and genetic polymorphisms that
may influence sodium resorption, aldosterone pathways, and the renin–angiotensin
system.
• Hypertension occasionally is caused by single-gene disorders or is secondary to
diseases of the kidney, adrenal, or other endocrine organs.

11. Secondary hypertension.

(311 – Gouri Mohammad Sahil) (312 – Rajan Nithin Raj)
Causes of secondary hypertension
Coarctation of the aorta (congenital localized constriction in the diameter of
the aorta, that’s why vascular resistance for the blood flow will be increased,
and it will increase blood pressure)
Renal artery stenosis and renal parenchymal disease (in a response to
ischemia kidneys released renin, renin-angiotensin-aldosteron system activated
and it will increased blood pressure by the increase reabsorbtion of water and
sodium in the kidneys tubules)
 Brain tumor and head injury (stimulation of sympathetic NS)
Pheochromocytoma (is a benign tumor of the adrenal medulla that secretes
epinephrine and norepinephrine)
Cushing's syndrome (increased cortisol levels raise BP by increasing renal
sodium retention, angiotensin II levels)
Hyperaldosteronism (also will increse renal sodium and water retention,
angiotensin II levels and vasoconstriction.
Oral contraceptives, cocaine (vasospasm)
Pregnancy–induced hypertension (toxemia of pregnancy, damage of the kidney
blood vessels)
Excessive alcohol consumption (has tendency to elevate BP)

12. Signs, symptoms and complication of hypertension.

(311 – Akshay Ravi Mantha) (312 – Govindasamy Guna)
Hypertension not only accelerates atherogenesis but also causes degenerative
changes in the walls of large and mediumsized arteries that can lead to aortic
dissection and cerebrovascular hemorrhage. Two forms of small blood vessel
disease are hypertension-related: hyaline arteriolosclerosis
and hyperplastic arteriolosclerosis. Hyaline arteriolosclerosis is associated with
benign hypertension. In the kidneys, the arteriolar narrowing caused by hyaline
arteriosclerosis leads to diffuse vascular compromise and nephrosclerosis
(glomerular scarring). The same lesions also are common in diabetic
microangiopathy; in this disorder, the underlying etiology is
hyperglycemiaassociated endothelial cell dysfunction.
Hyperplastic arteriolosclerosis is more typical of severe hypertension. Vessels
exhibit “onionskin,” concentric, laminated thickening of arteriolar walls and
luminal narrowing. The laminations consist of smooth muscle cells and
thickened, reduplicated basement membrane. In malignant hypertension these
changes are accompanied by fibrinoid deposits and vessel wall necrosis
(necrotizing arteriolitis), which are particularly prominent in the kidney.

Signs, symptoms
• Elevated blood pressure
• Occipital headache may worsen on rising in the morning as a result
of increased intracranial pressure;
• Nausea and vomiting
• Epistaxis possibly due to vascular involvement bruits
 • Dizziness, confusion, and fatigue caused by decreased tissue
perfusion
• Blurry vision as a result of damage to the retina
• Nocturia caused by an increase in blood flow to the kidneys and an
increase in glomerular filtration
• Edema caused by increased capillary hydrostatic pressure.

Complications of hypertension include:

 hypertensive crisis
 dissecting aortic aneurysm
 CAD (сcoronary artery disease)
 angina, MI, heart failure, arrhythmias, and sudden death
 cerebrovascular accident
 retinopathy
 hypertensive encephalopathy
 renal failure

13. Atherosclerosis
(311 – Reddy Amruth ) (312 –Singh Bhupinder)
Arteriosclerosis is also known as “hardening”
 or sclerosis of the arteries
 and characterized by fibrosis, lipid deposition and chronic inflammation.
Affects large and medium–sized arteries
 Lesions comprise fatty streaks, fibrolipid plaques and complicated lesions
Risk factors include increasing age, male gender, hypertension, smoking and
diabetes
Associated with
 increased levels of LDL–cholesterol, Lp(a)
 and reduced levels of HDL–cholesterol
Major cause of organ ischemia (e.g. myocardial infarction)

Atherosclerosis is produced by the following pathogenic events:

Endothelial injury, which causes increased vascular permeability, leukocyte
adhesion, and thrombosis
Accumulation of lipoproteins (mainly LDL) in the vessel wall
Monocyte adhesion to the endothelium, followed by migration into the intima
and transformation into macrophages and foam cells
Platelet adhesion Factor release from activated platelets, macrophages, and
vascular wall cells, inducing smooth muscle cell recruitment
Smooth muscle cell proliferation and ECM production
Lipid accumulation both extracellularly and within cells
(macrophages and smooth muscle cells)

Consequences of atherosclerotic disease

Myocardial infarction (heart attack),
cerebral infarction (stroke),
aortic aneurysms,
and peripheral vascular disease (gangrene of the legs) are the major
consequences of atherosclerosis.