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DISEASES OF THE HEART. MYOCARDIUM & PERICARDIUM. Dr Eman MS Muhammad. Coronary circulation. Blood supply of the heart: Generating energy almost exclusively by the oxidation of substrates, the heart relies heavily on an adequate flow of oxygenated blood through the coronary arteries.
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DISEASES OF THE HEART MYOCARDIUM & PERICARDIUM Dr Eman MS Muhammad
Blood supply of the heart: • Generating energy almost exclusively by the oxidation of substrates, the heart relies heavily on an adequate flow of oxygenated blood through the coronary arteries. • With origin from the aorta immediately distal to the aortic valve, the coronary arteries consists of 5-10 cm long, 2-4 mm diameter, arise. • They run along the external surface of the heart and are called epicardial coronary arteries. • Whereas, the smaller vessels that penetrate the myocardium are the intramural arteries.
The three major epicardial coronaries are: • The left anterior descending artery (LAD). • The left circumflex artery (LCX). • Both arising as branches from the bifurcation of the left (main) coronary artery. • The right coronary artery (RCA). • Branches of LAD are called diagonal and septal perforates. • Branches of LCX are obtuse marginals.
Most coronary blood flow to the myocardium occurs during diastole, when the microcirculation is not compressed by myocardial contraction. • The LAD supplies most of the apex of the heart, the anterior wall of the left ventricle, and the anterior two thirds of the ventricular septum. • LCX peruses the lateral wall of the LV. • RCA supplies the right ventricular free wall, and the posterobasal wall of the LV and the posterior third of the ventricular septum.
ISCHAEMIC HEART DISEASE • General consideration and causal factors: • Ischemic heart diseases (IHD or CHD): are the leading cause of death in most industrialized countries. • Myocardial ischemia basically results from imbalance between myocardial oxygen supply and the demand of cardiac muscle.
This imbalance results from: • ↓ Coronary blood flow (90%): the most important factor, it is caused by: • Atherosclerosis + vasospasm + thrombosis • Other less common causes e.g. • Embolism from the aortic valve • Coronary artery spasm • Dissecting aneurysm • Polyartritisnodosa • Syphylitic aortic incompetence
Calcific aortic stenosis ↓ blood volume with systemic hypotension, shock Cocaine-induced vasospasm ↑ myocardial demand exceeding vascular supply in case of e.g. Severe exercise and tachycardia Hypertension and cardiac hypertrophy Vavular lesions of the heart Coarctation of the aorta and LV hypertrophy
Decreased oxygen carrying capacity of the blood e.g. Severe anemia Advanced lung diseases, as in severe pneumonias Congenital cyanotic heart diseases Congestive heart failure Carbon monoxide poisoning Cigarette smoking
Death rates from IHD ↑ with age; after the age of 40. • IHD affects men earlier. • Sex: ♂: ♀ = 4-6:1, but the incidence ↑ in women after menopause. • Death rates are higher in men than in women • Race: both black and white are affected equally. • As atherosclerosis (AS) of coronary artery is the main pathogenic factor so, predisposing (risk) factors of IHD are those of AS. • Long-term regular exercise and ↓alcohol intake → protection against IHD.
Depending on the onset, duration and severity of O2 deficit, 4 general ischemic syndromes are recognized: • Angina pectoris. • Chronic ischemia. • Myocardial infarction. • Sudden cardiac death.
Angina Pectoris • Angina is an episodic chest pain of variable severity often described as gripping, compressing or crushing. • It is due to transient reversible myocardial ischemia and is caused by an imbalance between myocardial oxygen supply and demand. • The pain is usually retro-sternal and may radiate to the neck and jaw or to the upper aspect of either or both arms and hands.
Attacks are brought on by factors which increase the work of the heart and includes; physical activity, exposure to cold, emotional stress, or heavy meal. • Ischemia induces release of adenosine, bradykinin that stimulate autonomic afferents → pain. • It is usually relieved by rest and/or vasodilators. • Ischemia, however, does not always give pain and up to 70% of ischemic episodes are silent. • Prognosis depends on the severity of ischemia by ECG exercise testing, left ventricular function, and the number of vessels involved.
Variants of angina are: • Typical Stable Angina: • This is the commonest form of angina and many sufferers live for over 30 years. • It is due to progressive stenosing coronary artery by atheroma. • It is precipitated by exertion, emotional stress, and is relieved by rest or sublingual nitroglycerin. • Pain is classically described as a crushing or squeezing substernal sensation that radiate down the left arm or to the left jaw.
Variant Angina “Prinzmetal’s angina”: • In this form the attacks of pain are not related to exercise and can occur at rest. • It is caused by spasm of large or medium-sized coronary arteries, often at or near the site of atheromatous narrowing. • In 15% of cases, however, the coronary arteries appear normal. The mechanisms of vasospasm are not known. • Prinzmetal angina typically respond promptly to vasodilators as nitroglycerin and calcium channel blockers.
Unstable Angina (cresendo angina): • This clinical pattern may supervene in previously stable angina, or may commence de novo. • There is a sudden increase in the severity and duration of episodes of chest pain which begin to occur more frequently and often at rest. • The pathogenesis is similar to that of acute myocardial infarction. • It is associated with plaque disruption and superimposed thrombus, distal embolization of the thrombus and/or vasospasm. • In some patients it may progress to MI or sudden death.
Chronic ischemic heart diseases It is progressive heart failure secondary to ischemic myocardial damage. In most cases there is history of previous MI. It occurs late in life.
Gross: LV hypertrophy and dilatation, discrete areas of grey white scarring from previous healed infarcts. There is moderate to severe atherosclerosis of the coronary arteries, sometimes with total occlusion. Microscopic: Thisinclude myocardial hypertrophy, diffuse subendocardial vacuolization and fibrosis from previous infarction.
Myocardial Infarction • It is commonly referred to as “heart attack”. • It is necrosis of heart muscle resulting from sudden severe myocardial ischemia. • The mortality of acute myocardial infarction (MI) is approximately 30-35%, with 50% of these deaths occurring within an hour of onset from ventricular fibrillation (VF). • The survivors suffer from variable degrees of impaired cardiac function, including cardiac failure, arrhythmias and thrombo-emolism.
Although atrial infarction occurs in 20% of cases, the ventricular myocardium is predominantly affected. Risk factors are the same as those of atherosclerosis.
There are two forms of MI: • Regional MI: • It represents 90% of cases. • Most of which are transmural and affect the myocardium lying within the region supplied by a major coronary artery, which is almost always occluded by thrombus in an area of atherosclerotic narrowing.
Subendocardial MI: • It represents 10% of cases, affecting the inner half or two thirds of the ventricular wall throughout most or all of its circumference. • In such cases the major coronary arteries are severely atheromatous, but recent occlusion by thrombus is unusual. • Arrhythmia is common, thus being dangerous.
Some describes a third variant of MI named: Microscopic infarcts: occur in the setting of small vessel occlusions. They can occur in cases of vasculitis, embolization of valve vegetations, or mural thrombi, or vessel spasm due to elevated catecholamines either endogenous (e.g., pheochromocytoma or severe stress), or exogenous (e.g., cocaine).
Regional MI: • They vary greatly in size, but most are at least 2 cm across, and many are much larger. • The frequency of involvement of the coronary arteries and the distribution of infarction is: • LAD (40-50% of cases): the infarct is anterior extending from the apex, up to anterior wall of the LV, often involving the anterior part of the inter-ventricular septum, and adjacent anterior wall of the RV.
RCA (30-40% of cases): The infarct is inferior (posterior) extending from the apex, up to inferior wall of the LV, often involving the adjacent parts of the inter-ventricular septum, and the inferior (posterior) wall of the RV. • LCX (15% of cases): the infarct involves the lateral wall of the LV.
MI is commonly caused by thrombosis of the left main coronary artery or much less commonly two main coronary arteries. • The extent of infarction depends on the site of occlusion (proximal or distal within the artery), and on the presence of collateral circulation. • Gradual atheromatous narrowing of a major branch may result in opening of the collateral vessels, so that when it is finally occluded by thrombus, only a small infarct is produced.
Pathogenesis: • Three of the acute clinical events in IHD, unstable angina, MI, and sudden death, usually result from cracking or ulceration of an underlying atheromatous plaque. The sequence is: • Fissuring, cracking or rupture of a plaque which has a lipid pool. • Acute enlargement of the plaque with thrombosis of the lumen. • Occlusion of the lumen. • Penetration of vessels into the plaque.
The role of thrombotic occlusion of coronary artery occurs in 90% 0f MI. • Vasospasm may contribute to the occlusion, but the predominant cause is thrombus formation. • Spontaneous relieve of vasospasm and activation of the fibrinolytic system will relieve the occlusion. • Thrombi may occur at areas of endothelial damage over a severe atheromatousstenosis.
Fissuring or ulceration of a plaque is thought to be the mechanisms which initiates the sequence of events in MI. • Healing of fissuring and thrombosis may be a factor in growth of the plaque. • The precipitating cause of severe fissuring leading to occlusion is unknown. • Shear stresses at the site of plague, increased blood pressure, and local vasospasm have all been implicated.
Once thrombus has formed the following sequences are possible: • Spontaneous lysis. • Platelet embolisationwhich may aggravate the ischemia distal to the occlusion. • Continued thrombus formation progressing to local occlusion and propagation of the thrombus distally and proximally.
Platelet activation at the site of thrombus formation result in the release of vaso-active factors such as thromboxane, possibly inducing vasospasm. • Coronary artery thrombus is a dynamic progressive process and factors which determine the clinical syndromes and final outcome are complex.
Myocardial response to ischemia: Loss of myocardial blood supply leads to profound functional, biochemical and morphological consequences as: A drop in ATP and and accumulation of potentially noxious metabolitis (e.g., lactic acid) in cardiac myocytes. Necrotic myocardial cells release enzymes which are helpful in diagnosing MI; cytokeratin (CK) and its specific cardiac isoform CK-MB, lactic dehydrogenase (LD); its LDH-5 iso-enzyme and myocardial protein Troponin-1 (c-Tn1).
A rapid loss of contractility which occurs within a minute of the onset of ischemia. It also contribute to arrhythmia probably by causing electrical instability (irritability) of the ischemic but not the infarcted area of the heart. Only severe ischemia lasting 20-40 minutes causes irreversible injury and myocyte death. MI reaches its full size in 3-6 hours, intervension during this time can limit the final extent of necrosis.
Morbid anatomy: • Initially the necrotic muscle appears grossly and microscopically normal. • Myocardial necrosis can not be recognized in patients dying less than 6-8 hours after the onset. • The first change visible at autopsy are blotchy pallor and congestion, followed in 24-48 hours by palpable softening. • The color usually changes to grey-brown and then to yellow-grey. • Hemorrhages then appear at the margins.
After few days the infarct becomes more sharply defined by the development of red zone of granulation tissue at the margins. • Removal of dead myocardium precedes gradually. • There may be a fibrinous or hemorrhagic pericarditis which may be generalized or localized to the area of infarction. • On the inner aspect of the infarct, the endocardium and a thin layer of underlying myocardium remains viable, nourished by blood from the lumen. • In patients surviving for several days, mural thrombus is often formed on the endocardial surface.
Microscopically: • The infarcted muscle shows the changes of coagulative necrosis. • After about 8 hours it is infiltrated by PNL, and after a few days digestion by macrophages and organization can be seen at the margins. • The dead muscles is replaced by a fibrous scar over the next 6-8 weeks. • Hypertrophy of the non infarcted myocardium occurs and the chamber enlarges to compensate for the decrease in contractility caused by the infarct, thus maintaining the stroke volume. • In 25-30% of transmural regional infarct, stretching of the infarcted zone occurs, this may lead to aneurysmal formation.
Micrograph of a coronary artery with the most common form of coronary artery disease (atherosclerosis) and marked luminal narrowing. Masson's trichrome.
Size and rate of development of MI depend on: The size and distribution of the affected vessel. The rate of development and duration of occlusion. Metabolic demands of the myocardium (affected by blood pressure and heart rate). Extent of collateral circulation.
Clinical feature and course: • The dominant symptom of MI is severe retrosternal pain, that does not relived by rest or vasodilators and persists for at least one or several hours. • It is usually accompanied by nausea, vomiting, sweating, weakness and prostration. • These early features are usually dramatic, but there is a spectrum of severity of symptoms. • In some cases MI is “silent”with little or no pain or constitutional symptoms.
