6

Heart diseases
LM 202
Dr. Hassan Kofahi
Heart failure (HF)
• Often referred to as congestive heart failure (CHF).
• HF occurs when the heart cannot generate sufficient output to meet
the metabolic demands of the body.
• HF is a common end point for many cardiac diseases.
• HF is a progressive condition with a poor prognosis.
• Approximately, 50% of CHF patients die within 5 years following the diagnosis.
• In HF, both forward and backward failure co-exist
• Forward failure: inadequate cardiac output, leads to hypoperfusion of the
organs.
• Backward failure: inadequate blood return to the heart, leads to congestion and
edema.
 Forward Vs backward failure
Heart failure
Backward failure Forward failure
Failure to return enough Failure to pump enough
blood from the venous blood out into the
circulation arteries

Blood backs-up in Reduced amount of

the venous Inadequate blood return Inadequate cardiac output blood flowing to
circulation, the tissues and
increasing venous organs
pressure and leading (hypoperfusion)
to congestion and
edema
HF: Pathogenesis
• HF may result from systolic
dysfunction or diastolic
dysfunction.
• Systolic dysfunction: inadequate
contractile function of the heart.
• Usually occurs as a consequence of
ischemic heart disease or hypertension.
• Diastolic dysfunction: inability of the
heart to adequately relax and fill.
• Can be caused by massive ventricular
hypertrophy (due to hypertension) or
myocardial fibrosis.
Heart failure (HF)
• The onset of heart failure can be sudden or gradual:
• Sudden onset occurs as a result of a large myocardial infarct or acute valve
dysfunction.
• Gradual onset occurs mainly in hypertension due to the cumulative effects of
chronic work overload and progressive loss of myocardium.
• HF can affect:
• The left ventricle of the heart  Left-sided HF
• The right ventricle of the heart  Right-sided HF
• Both ventricles  Biventricular HF
Left-sided HF often causes right-sided HF
Left-sided heart failure
• Most common causes are:
• Ischemic heart disease (IHD)
• Systemic hypertension
• Mitral or aortic valve disease
• Left-sided HF results in
• Diminished systemic perfusion (forward)
• Congestion and elevated pressure in the pulmonary circulation (backward)
• Clinical manifestations:
• Pulmonary edema, which leads to the following symptoms:
- Dyspnea (difficulty in breathing)
- Orthopnea (Dyspnea that occurs when lying flat)
- Crackles (rales)
- Paroxysmal nocturnal dyspnea: a severe form of dyspnea that awakens patients from sleep.
• Hypoperfusion activates the the renin-angiotensin-aldosterone system, increasing
blood volume and blood pressure, which further exacerbate pulmonary edema.
• Other symptoms include enlargement of the heart, tachycardia, azotemia and, in
severe cases, hypoxic encephalopathy.
Left-sided heart failure
Congestion Edema

Failure

Hypoperfusion
Right-sided heart failure
• Causes:
• In most of the cases, right-sided HF occurs as a consequence of
left-sided HF. JVD
• High pressure in the pulmonary circulation, due to left-sided HF, results
in an increased burden on the right side of the heart leading to its
failure.
• Isolated right-sided HF (not caused by left-sided HF) may occur
due intrinsic lung diseases, and it is often referred to as
cor pulmonale.
Pitting edema
• Clinical manifestations:
• Pure right-sided HF leads to congestion in the systemic and portal
circulation.
• Symptoms:
• Hepatospleenomegaly: liver and spleen enlargement. May progress to
cirrhosis in severe long standing right-sided HF.
• Jugular venous distention (JVD)
• Pitting edema in the lower extremities
Ascites
• Ascites
Right-sided heart failure

Failure

Edema Congestion
Ischemic Heart Disease (IHD)
• IHD is a broad term describes several syndromes caused by myocardial
ischemia,
• i.e., when the cardiac blood supply (perfusion) is less than the myocardial oxygen
and nutritional requirements.
• IHD is a leading cause of mortality in the world.
• In more than 90% of cases, IHD is a consequence of a coronary artery
disease (i.e., reduced blood flow in the coronary arteries secondary to
atherosclerosis).
• The remaining 10% of IHD cases are caused by:
• Increased demand (due to increased heart rate or hypertension)
• Diminished blood volume (due to hypotension or shock)
• Diminished oxygenation (due to pneumonia or HF)
• Diminished oxygen-carrying capacity (due to anemia or carbon monoxide poisoning).
IHD: Clinical manifestations
• The clinical presentation of IHD may include one or more of the
following cardiac syndromes:
• Angina pectoris
• Myocardial infarction
• Chronic IHD with CHF
• Sudden cardiac death (SCD)
Angina pectoris
• Is a chest pain caused by transient, reversible myocardial ischemia.
• A crushing or squeezing substernal sensation that often radiates down the left arm
or to the left jaw.
• The pain results from the ischemia-induced release of molecules (such as bradykinin)
that stimulate the autonomic nerves.
• Types of angina:
• Typical (stable) angina
• Predictable episodes of pain that is associated with a particular level of exertion or stress.
• Caused by stenosis (narrowing) of coronary arteries to > 70%.
• Can be relieved by rest or medication (nitroglycerine, a vasodilator).
• Prinzmetal (variant) angina
• Episodes of pain that do not correlate with exertion, can happen anytime including at rest.
• Results from coronary artery spasm.
• Unstable angina
• Occur with progressively less exertion or even at rest.
• Associated with acute atherosclerotic plaque changes and superimposed thrombosis or
embolization.
• May progress to myocardial infarction.
Myocardial Infarction (MI)
• Commonly known as “heart attack”.
• MI is the necrosis of heart muscle cells resulting from ischemia.
• The major underlying cause of MI is atherosclerosis.
• Epidemiology:
• Leading cause of death.
• The risk increases with age.
• Men are more at risk than women.
• Women’s risk increases after menopause.
MI: Pathogenesis
• Most of MIs (90%) are caused by acute thrombosis within coronary
arteries.
• Thrombosis is initiated by the rupture or erosion of a preexisting
atherosclerotic plaque.
• The thrombus occlude the coronary artery, leading to infarction of the perfused
myocardium.
• The following events take place:
1. Erosion or rupture of an atherosclerotic plaque
2. Platelets adhere, aggregate and become activated
3. Coagulation cascade is activated
4. Within minutes, the thrombus can completely occlude the coronary artery.
• The remaining MI cases (10%) are caused by vasospasm, embolism
and other causes.
Myocardial response to ischemia
• Immediately after the occlusion of a coronary artery, aerobic
metabolism in the myocardium stops, leading to a reduction in ATP
and an increase in lactic acid.
• This leads to rapid loss of contractility occurring within a minute of the
onset of ischemia.
• These changes are reversible.
• Irreversible injury (necrosis) occurs only after 20-40 minutes of
ischemia.
• If blood is restored before irreversible injury, the myocardium can be
preserved.
• Necrosis occurs first in the subendocardial zone and, with time,
expands to involve the full wall thickness of the heart. Why?
•  Because the subendocardial zone is the last area to receive blood
delivered by the epicardial coronary arteries, and also because it is
exposed to relatively high intramural pressures, which act to impede the
inflow of blood.
Patterns of MI
• Transmural infarct:
• also called ST-segment elevated MIs (STEMIs).
• Involves the full thickness of the heart wall.
• Caused by a permanent and complete occlusion of coronary arteries due to an
intracoronary thrombus, usually associated with an ulcerated atherosclerotic plaque.
• Subendocardial Infarcts:
• Also called non–ST-segment elevated MIs (NSTEMIs).
• Limited to the inner third of the heart
• Caused by
• Transient or partial occlusion of coronary arteries (stenosis)
• Transient decreases in oxygen delivery (as with hypotension, anemia, or pneumonia)
• High oxygen demand (as with tachycardia or hypertension).
• Microscopic infarcts:
• Occur as a result of small intramural vessel occlusions.
• May not show any diagnostic changes in the ECG.
MI: Clinical features
• Symptoms:
• Severe crushing substernal pain that radiates to the left arm, nick, jaw and
epigastrium.
• The pain lasts longer than angina and is not relieved by rest or medication.
• Rapid and weak pulse
• Sweeting, nausea, and dyspnea
• MI is diagnosed by:
• Physical examination
• Electrocardiogram (ECG)
• Blood tests: Troponin I, Troponin T, creatinine kinase (CK-MB).
Consequences and Complications of MI
• 1/3 of out-of-hospital transmural MI cases die within one hour of symptoms
onset before they reach the hospital.
• Transmural MIs (STEMIs) has higher mortality rate than Subendocardial Infarcts (NSTEMIs).
• Usually, death occurs due to lethal arrhythmia and sudden cardiac death (will be discussed
later).
• If they survive the acute attack, ¾ of MI patients experience complications, these
include:
• Systolic dysfunction and HF: in most of the cases, MI causes a certain degree of left
ventricular failure.
• Cadiogenic shock occur if >40% of the left ventricle is damaged.
• Papillary muscle rupture and dysfunction impairs the normal functions of the valves.
• Myocardial rupture: A rare complication (1%-5% of the cases). Fatal.
• Arrhythmias: MIs lead to myocardial irritability and conduction disturbances that can cause
sudden death.
• Mural thrombus (see chapter 4)
• Ventricular aneurysm.
A) Anterior free wall myocardial rupture (arrow). (B) Ventricular septal rupture (arrow). (C)
Papillary muscle rupture. (D) left ventricular aneurysm (arrow).
Chronic ischemic heart disease (Chronic IHD)
• Also called ischemic cardiomyopathy
• Chronic IHD is a progressive heart failure secondary to ischemic
myocardial damage.
• Causes:
• In most of the cases, chronic IHD occurs in patients with previous MI.
• Chronic IHD appears when the compensatory mechanisms of the residual myocardium
begins to fail.
• In the remaining cases, chronic IHD occurs secondary to severe coronary
artery disease (severe stenosis) that leads to a gradual loss of the myocardial
functions.
Sudden cardiac death (SCD)
• Is an unexpected death due to lethal arrhythmias.
Arrhythmias: abnormal heart rhythm (abnormal rate or irregular rhythm)
• Caused by disorganized electrical activity in the heart.
• Many arrhythmias are harmless, but some are lethal and cause SCD.
• The most common lethal arrhythmia is ventricular fibrillation in which, the
ventricles quiver (vibrate) instead of the normal functional organized contractions.
• Coronary artery atherosclerosis is the leading cause of SCD.
• In most of SCD cases, coronary artery atherosclerosis causes SCD without MI (i.e.,
SCD is the first manifestation of IHD).
• In younger victims of SCD, non-atherosclerotic causes are more common,
including the following:
• Hereditary or acquired abnormalities of the cardiac conduction system
• Congenital coronary arterial abnormalities
• Myocardial hypertrophy
SCD: Clinical features
• Before SCD: Warning symptom occur in 50% of the cases prior to SCD. These
include:
• Chest pain
• Shortness of breath
• Dizziness
• Vomiting
• In the remaining 50%, SCD is not preceded by any warning symptoms
• After cardiac arrest: signs
• No pulse
• No breathing
• Loss of consciousness
• Emergency treatment
• Cardiopulmonary resuscitation (CPR)
• Defibrillation
Hypertensive Heart Disease (HHD)
• HHD is a consequence of the increased demands placed on the heart
by hypertension.
• Results in ventricular hypertrophy.
• Myocyte hypertrophy is a compensatory adaptation to pressure
overload.
• Mostly affects the left side of the heart as a result of systemic
hypertension.
• Pulmonary hypertension can cause a HHD of the right side of the
heart.
Systemic (left sided) HHD
• Diagnosis of Systemic HHD is based on the following criteria
• History of hypertension
• Hypertrophy of the left side of the heart
• Systemic HHD is usually asymptomatic
• Possible outcomes of systemic HHD
• Depending on the severity of the condition, the underlying cause of hypertension
and the adequacy of control of hypertension, HHD patients will have one of the
following outcomes:
• No clinically significant effects and the patient lives a normal life
• The patient may develop IHD
• The patient may develop HF
• The patient may suffer renal damage or cerebrovascular stroke
• The patient might die by sudden cardiac death
Pulmonary Hypertensive Heart Disease-
Cor Pulmonale
• Cor pulmonale is characterized by a right
ventricular hypertrophy and dilation, and it is
frequently accompanied by right-sided heart
failure.
• Cor pulmonale is generally a result of pulmonary
hypertension.
• Pulmonary hypertension is caused by disorders of
the lung parenchyma or pulmonary vasculature.
• e.g., COPD (will be discussed in chapter 8).
• e.g., pulmonary embolism
By definition, right-sided HF that is caused by left-
sided HF is not cor pulmonale.
Rheumatic fever
• An acute, immunologically mediated, multisystem inflammatory
disease.
• Occurs after an infection with group A β-hemolytic streptococcus
(which usually causes bacterial pharyngitis).
• Occurs in 3% of streptococcal infections.
• Rheumatic heart disease is the cardiac manifestation of rheumatic
fever.
• Associated with inflammation of the heart.
• Inflammation and scarring of the valves is the most clinically-significant
outcome.
Rheumatic fever: Pathogenesis
• Rheumatic fever is caused by antibodies directed against group A
streptococcus antigens.
• These antibodies cross-react with host myocardial antigens.
• Binding of these antibodies to antigens in the myocardium or cardiac
valves induces inflammation.
• The inflammation causes injury to the myocardium and cardiac
valves.
Rheumatic fever: Clinical features
• Mainly, affects the children.
• The symptoms appear 2-3 weeks after the infection.
• Symptoms:
• Fever
• Migratory polyarthritis (i.e., migratory inflammation of multiple joints).
• Pericardial friction rubs (an extra sound detected by auscultation)
• Arrhythmias
• In severe cases, may cause cardiac dilation and HF.
• Less than 1% of patients die of acute rheumatic fever.