The Heart
DR KHALID WISSAMPathology Department
Mosul Medical college
Lec 1
The Heart
— Heart weight varies with body weight and height, (250-320gm in females, 300-360g in males)— Thickness of right ventricle is 0.3-0.5cm and of left ventricle is 1.3-1.5cm
—Increases in heart weight or ventricular thickness above these normal limits indicates hypertrophy, and an enlarged chamber size implies dilation, and both result in cardiomegaly
—— Epicardial coronary arteries, (left anterior descending, left circumflex, right)
— Intramural are vessels that penetrate the myocardium
Mechanisms of cardiac dysfunction
Pump failureOutflow obstruction.
Shunted flow.
Flow regurgitation.
Conductive failure
Disruption of the continuity of the circulatory system
HEART FAILUREcongestive heart failure (CHF)
Definition:
Inability of the heart to pump blood at a rate needed by tissues for normal metabolism.
Causes of heart failure
Failure of myocardial contractility : (systolic dysfunction)
ischemic injury
pressure overload
volume overload
dilated cardiomyopathy
Inability of the heart to relax or expand: (diastolic dysfunction)
myocardial abnormality (hypertrophy, fibrosis, amyloidosis)
pericardial abnormality (constrictive pericarditis )
Inadequate cardiac output— called forward failure—is almost always accompanied by increased congestion of the venous circulation—that is, backward failure.
— Left ventricular hypertrophy
Left-Sided Heart Failure
Causes:-Ischemic heart disease
-Systemic hypertension
-Aortic and mitral valvular diseases
-Non-ischemic myocardial diseases
Pathological changes
Heart. The gross cardiac findings depend on the underlying disease process.
The left ventricle is usually hypertrophied and can be dilated with left atrial enlargement, which is associated with an increased incidence of atrial fibrillation.
The microscopic changes in heart consisting of myocyte hypertrophy with interstitial fibrosis.
Lung. congestion and edema. The breakdown of red cells and hemoglobin leads to the appearance of hemosiderin-laden alveolar macrophages—so-called heart failure cells —that reflect previous episodes of pulmonary edema.
RIGHT-SIDED HEART FAILURE
Causes:-Secondary to left-sided failure
-Chronic pulmonary hypertension (cor pulmonale)
Organ changes in Rt side HF:
liver, congestive hepatomegaly (nutmeg liver) > cardiac cirrhosis
spleen, congestive splenomegaly and ascites (portal hypertension)
kidneys, congestion
bowels, congestion
pleural cavity, effusion
pericardial sac, effusion
systemic, edema > anasarca
ISCHEMIC HEART DISEASE (IHD)
A group of closely related syndromes due to imbalance between (perfusion) and demand of the heart for oxygenated blood.Ischemia comprises:
-insufficiency of oxygen.
-reduced availability of nutrients.
-inadequate removal of metabolites.
IHD is the leading cause of death in most parts of the world
> 90% of cases, IHD is a consequence of reduced coronary blood flow secondary to obstructive atherosclerotic vascular disease.
ISCHEMIC HEART DISEASE (IHD)
IHD Include:
1 -Myocardial infarction ( MI)
2 -Angina pectoris
3 -Chronic ischemic heart disease
4 -Sudden cardiac death (SCD)
The term acute coronary syndrome is applied to any of the three catastrophic manifestations of IHD— unstable angina, acute MI, and SCD.
Sequential progression of coronary artery lesions to acute coronary syndromes
ANGINA PECTORISParoxysmal and recurrent attacks of substernal or chest discomfort (as constricting, squeezing, choking or knife- like), caused by transient (15seconds- 15minutes) myocardial ischemia that is insufficient to induce myocyte necrosis.
3 over-lapping patterns:
1- Stable (typical)
2- Prinzmetal variant
3 - Unstable or crescendo
Stable Angina (typical)
Most common form of anginaCaused by an imbalance in coronary perfusion (due to chronic stenosing coronary atherosclerosis) relative to myocardial demand , such as that produced by physical activity, emotional excitement or psychological stress.
Relieved by rest or vasodilators (nitroglycerin).
Prinzmetal Angina or variant angina
Uncommon
Is due to coronary artery spasm.
Responds to vasodilators
Unstable Angina ( Crescendo)
. Frequent, prolonged (>20 min), or severe angina or chest discomfort , precipitated by progressively lower levels of physical activity or even occurring at rest
. Associated with plaque disruption with superimposed partial thrombosis, distal embolization &/or vasospasm
. It is often the harbinger of MI, caused by complete vascular occlusion
MYOCARDIAL INFARCTION
“Heart Attack” is the necrosis of cardiac muscle due to prolonged severe ischemia.
The major underlying cause of IHD is atherosclerosis;
Acute plaque change>total thrombotic occlusion>death of cardiac muscle
Nearly 10% occur in people under 40 years and 45% occur in people under 65 years
Males > females
Pathogenesis of MI
- Coronary arterial occlusion (90%)Sudden change in the morphology of an atheromatous plaque( hemorrhage, ulceration,…) > Platelets adhesion, aggregation, activation > Vasospasm > Activation of extrinsic pathway of coagulation > Thrombosis.
Progression of myocardial necrosis following coronary artery occlusion
Gross:Infarcts <12 hrs are usually not apparent grossly, can be demonstrated by solution (triphenyltetrazolium chloride)
Infarct older than 12-24 hrs appears red/ blue ( stagnant blood), progressively becomes yellow/tan
By 3-7 days is rimmed by hyperemia / central yellow tan
Over weeks scar will develop
Light microscopy:
4-24 hrs beginning & ongoing coagulative necrosis
1-3 days Coagulative necrosis & acute inflammation
3-7 days beginning phagocytosis of macrophages
1-2 weeks granulation tissue peaking
> 2 months dense collagenous scar
Transmural myocardial infarction, staining by tripheniletetrazolium chloride: pale zone due to loss of dehydrogenases
Myocardial infarction, 1 day, 3-4 days, 7-10 days, granulation tissue, scar
Clinical features of MI
Patient has chest pain, rapid weak pulse, dyspnea, profuse sweating, nausea- Painless MI: diabetic neuropathy / elderly
- Diagnosis depends on:
Typical symptoms
Biochemical evidence
ECG changes
Factors associated with poor prognosis
- Advanced age - Female gender
- Diabetes mellitus - Previous MI
Laboratory diagnosis
Depends on measuring leaky cellular substances1- Myoglobin
2- Cardiac troponins T and I
3 - Creatine kinase (MB fraction)
4- Dehydrogenase enzyme
5- lactate dehydrogenase.
The best are troponins T and I, both rise at 2-4 hrs and peak at 48 hrs, and remain elevated for 7-10 days
Complications after Acute MI
Contractile dysfunctions & pump failure
- Papillary muscle dysfunction
Arrhythmias
Pericarditis & Dressler syndrome
Infarction of right ventricle
Mural thrombus
Myocardial rupture (Lt vent. Or septal)
Ventricular aneurysm
Progressive late heart failure