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الكلية كلية طب الاسنان
القسم العلوم الاساسية
المرحلة 3
أستاذ المادة علي زكي ناجي الاسدي
5/31/2011 8:10:42 AM
ischemic heart disease
ihd is the generic designation for a group of closely related syndromes resulting from myocardial ischemia. ihd can be divided into four syndromes:
1.mi(myocardial infarction)
2.angina pectoris.
3.chronic ischemic heart disease with heart failure
4.sudden cardiac death
epidemiology. ihd in its various forms is the leading cause of death for both men and women in the united states and other industrialized nations. the overall death rate from ihd has fallen due to the followings :
(1) prevention achieved by modification of determinants of risk, such as smoking, elevated blood cholesterol, hypertension, and a change in life style
(2) therapeutic advances, including new medications, coronary care units, thrombolysis for mi, percutaneous transluminal coronary angioplasty (ptca), intravascular stents, coronary bypass surgery, and improved control of arrhythmias. pathogenesis. ihd syndromes developed due to diminished coronary perfusion relative to myocardial demand, due to a fixed atherosclerotic narrowing of the coronary arteries, intraluminal thrombosis overlying a disrupted atherosclerotic plaque, platelet aggregation, and vasospasm.
role of vasoconstriction.
vasoconstriction at sites of atheroma is stimulated by
(1) circulating adrenergic agonist.
(2) locally released platelet contents.
(3) impaired secretion of endothelial cell relaxing factors (e.g., nitric oxide)
(4) mediators released from perivascular inflammatory cells (mast cells).
angina pectoris
angina pectoris characterized by recurrent attacks of substernal or precordial chest discomfort (variously described as constricting, squeezing, or knifelike) caused by transient (15 seconds to 15 minutes) myocardial ischemia. there are three overlapping patterns of angina pectoris:
(1) stable or typical angina.
(2) prinzmetal or variant angina.
(3) unstable or crescendo angina.
stable angina: the most common form and therefore called typical angina pectoris, appears to be caused by the reduction of coronary perfusion to a critical level by chronic stenosing coronary atherosclerosis this make the heart vulnerable to further ischemia whenever there is increased demand, such as that produced by physical activity, emotional excitement, or any other cause of increased cardiac workload.
typical angina pectoris is usually relieved by rest (thereby decreasing demand) or nitroglycerin, a strong vasodilator
prinzmetal variant angina: an uncommon pattern of episodic angina that occurs at rest and has been documented to be due to coronary artery spasm. although individuals with this form of angina may well have significant coronary atherosclerosis, the anginal attacks are unrelated to physical activity, heart rate, or blood pressure.
prinzmetal angina generally responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers.
unstable angina: refers to a pattern of pain that occurs with progressively increasing frequency, is precipitated with progressively less effort, often occurs at rest, and tends to be of more prolonged duration.
in most patients, unstable angina is induced by disruption of an atherosclerotic plaque with superimposed partial (mural) thrombosis and possibly embolization. this syndrome is sometimes referred to as pre-infarction angina.
myocardial infarction (m.i.): mi, also known as heart attack, is the most important form of ihd and alone is the leading cause of death in the united states and industrialized nations. about 1.5 million individuals in the united states suffer an acute mi every year, and approximately one third of them die.
types of (m.i.)
1-transmural infarction. most myocardial infarcts are transmural, in which the ischemic necrosis involves the full or nearly full thickness of the ventricular wall in the distribution of a single coronary artery. this pattern of infarction is usually associated with chronic coronary atherosclerosis, acute plaque change, and superimposed, completely obstructive thrombosis.
2- subendocardial infarct. constitutes an area of ischemic necrosis limited to the inner one third or at most one half of the ventricular wall.
the subendocardial zone is normally the least well-perfused region of myocardium and therefore most vulnerable to any reduction in coronary flow. in the majority of subendocardial infarcts, there is diffuse stenosing coronary atherosclerosis and reduction of coronary flow but neither plaque disruption nor superimposed thrombosis.
subendocardial infarcts, however, can also result from sufficiently prolonged and severe reduction in systemic blood pressure, as in shock in cases of hypotension, resulting subendocardial infarcts are usually circumferential rather than limited to the distribution of a single major coronary artery.
incidence and risk factors.
the risk factors for atherosclerosis, the major underlying cause of ihd in general, mi may occur at any age, but the frequency rises progressively with increasing age and when predispositions to atherosclerosis are present, such as hypertension, cigarette smoking, diabetes mellitus, genetic hypercholesterolemia. throughout life, men are at significantly greater risk of mi than women, the differential progressively declining with advancing age.
the decrease of estrogen after menopause can permit rapid development of coronary heart disease among women.
pathogenesis. the ischemia result from (coronary arterial occlusion), and this result from the followings:
1-severe coronary atherosclerosis
2-acute atheromatous plaque change (such as rupture), superimposed platelet activation, thrombosis.
3-vasospasm in addition, either increased myocardial demand (as with hypertrophy or tachycardia) or hemodynamic compromise (as with a droping in blood pressure) can worsen the situation. collateral circulation may provide perfusion to ischemic zones from a relatively unobstructed branch of the coronary tree, bypassing the point of obstruction and protecting against the effects of an acute coronary occlusion.
morphological changes of m.i.
1- gross appearance of m.i. affected areas of the heart undergo a progressive coagulative necrosis, followed by inflammation and repair. the appearance of an infarct at autopsy depends on the duration of survival of the patient after mi. myocardial infarcts fewer than 12 hours old are usually unapparent on gross examination. it is often possible, however, to highlight the area of necrosis that first becomes apparent after 2 to 3 hours by immersion of tissue slices in a solution of triphenyltetrazolium chloride. by 12 to 24 hours, the lesion can be identified in routinely fixed gross slices owing to a red-blue color. progressively, the infarct becomes a more sharply defined, yellow-tan, some that softened area (with inflammatory cells) that by 10 days to 2 weeks is rimmed by a hyperemic zone of highly vascularized granulation tissue. over the succeeding weeks, the injured region evolves to a fibrous scar.
2- microscopical appearance of m.i. the typical microscopic changes of coagulative necrosis become detectable variably in the first 4 to 12 hours. the necrotic muscle elicits acute inflammation (typically most prominent at 2 to 3 days). macrophages remove the necrotic myocytes (most pronounced at 5 to 10 days).highly vascularized granulation tissue (most prominent at 2 to 4 weeks), which progressively becomes less vascularized and more fibrous, once a lesion is completely healed, it is impossible to distinguish its age (i.e., an 8-week-old lesion and a 10-year-old lesion can look similar clinical features. patients with mi have rapid, weak pulse with dyspnea due to impaired contractility of the myocardium that accompanied by pulmonary congestion and edema. in about 10 to 15% of mi patients, the onset is entirely asymptomatic, and the disease is discovered only later by ecg changes. such silent mis are particularly common in patients with underlying diabetes mellitus and in elderly patients.
laboratory evaluation is based on measurement of release into the circulation of intracellular macromolecules that leak out of fatally damaged myocardial cells through a compromised sarcolemmal membrane .
complications of myocardial infarction.
1-contractile dysfunction: myocardial infarcts produce abnormalities in left ventricular function approximately proportional to their size. most often, there is some degree of left ventricular failure with hypotension, pulmonary vascular congestion, and transudation into the interstitial pulmonary spaces, which may progress to pulmonary edema with respiratory embarrassment. 2-severe pump failure (cardiogenic shock), which occurs in 10 to 15% of patients after acute mi, generally indicates a large infarct (often greater than 40% of the left ventricle). cardiogenic shock has a nearly 70% mortality rate and accounts for two thirds of in-hospital deaths.
3-arrhythmias: many patients have conduction disturbances or myocardial irritability after mi, which undoubtedly is responsible for many of the sudden deaths. mi-associated arrhythmias include sinus bradycardia or tachycardia, ventricular premature contractions or ventricular tachycardia, ventricular fibrillation, or asystole. owing to the location of portions of the av conduction system (bundle of his) in the inferoseptal myocardium, infarcts of this region may also be associated with heart block. prompt intervention by mobile and hospital coronary care units has succeeded in controlling potentially lethal arrhythmias in many patients.
4-myocardial rupture: the cardiac rupture syndromes result from the mechanical weakening that occurs in necrotic and subsequently inflamed myocardium and include:
(1) rupture of the ventricular free wall (most commonly), with haemopericardium and cardiac tamponade and usually fatal.
(2) rupture of the ventricular septum leading to a left-to-right shunt.
(3) papillary muscle rupture resulting in the acute onset of severe mitral regurgitation.
4-pericarditis: a fibrinous pericarditis usually develops about the second or third day after a transmural infarct and usually resolves over time
5-mural thrombus: with any infarct, the combination of a local myocardial abnormality in contractility (causing stasis) with endocardial damage (causing a thrombogenic surface) can foster mural thrombosis and potentially thromboembolism.
6-ventricular aneurysm: this is a late complication that most commonly results from a large transmural anteroseptal infarct that heals into a large region of thin scar tissue.
7-papillary muscle dysfunction: postinfarct mitral regurgitation is most commonly due to early ischemic dysfunction of a papillary muscle.
valvular heart disease valvular involvement by disease causes stenosis, insufficiency (regurgitation), or both. stenosis is the failure of a valve to open completely, while insufficiency, regurgitation, or incompetence, in contrast, results from failure of a valve to close completely, thereby allowing reversed flow. these abnormalities can be either pure, when only stenosis or regurgitation is present, or mixed, when both stenosis and regurgitation coexist in the same valve. abnormalities of flow often produce abnormal heart sounds known as murmurs.
rheumatic fever and rheumatic heart disease
rheumatic fever is an acute, immunologically mediated, multisystem inflammatory disease that occurs a few weeks after an episode of group a (beta -hemolytic) streptococcal pharyngitis and often involves the heart. acute rheumatic carditis, which complicates the active phase of rheumatic fever, may progress to chronic valvular deformities. rheumatic fever does not follow infections by other strains of streptococci at other sites, such as the skin. the incidence and mortality rate of rheumatic fever have declined remarkably in many parts of the world over the past 30 years owing to improved socioeconomic conditions, rapid diagnosis and treatment of streptococcal pharyngitis, and an unexplained decrease in the virulence of group a streptococci. nevertheless, in third world countries and in many crowded, economically depressed urban areas in the western world, rheumatic fever remains an important public health problem. fortunately, rheumatic fever occurs in only about 3% of patients with group a streptococcal pharyngitis. after an initial attack, however, there is increased vulnerability to reactivation of the disease with subsequent pharyngeal infections.
rheumatic fever is characterized by a constellation of findings that includes as major manifestations:
1) migratory polyarthritis of the large joints.
2) carditis.
3) subcutaneous nodules.
4) erythema marginatum of the skin, and
5) sydenham chorea a neurologic disorder with involuntary purposeless, rapid movements.
the most important consequence of rheumatic fever is chronic rheumatic heart disease, characterized principally by deforming fibrotic valvular disease (particularly mitral stenosis), which can produce permanent dysfunction and severe, sometimes fatal, cardiac dysfunction decades later.
morphology. during acute rheumatic fever, focal inflammatory lesions are found in various sites. they are most distinctive within the heart where they are called aschoff bodies. they constitute foci of fibrinoid degeneration surrounded by lymphocytes (primarily t cells), occasional plasma cells, and plump macrophages called anitschkow cells (pathognomonic for rheumatic fever). these distinctive cells have abundant cytoplasm and central round-to-ovoid nuclei. some of the larger altered histiocytes become multinucleated to form aschoff giant cells.
during acute rheumatic fever, diffuse inflammation and aschoff bodies may be found in any of the three layers of the heart pericardium, myocardium, or endocardium hence a pancarditis. in the pericardium, they are accompanied by a fibrinous or serofibrinous pericardial exudate, described as a bread-and-butter pericarditis, which generally resolves without sequelae.
the myocardial involvement myocarditis takes the form of scattered aschoff bodies within the interstitial connective tissue, often perivascular. concomitant involvement of the endocardium and the left-sided valves by inflammatory foci typically comprises fibrinoid necrosis within the cusps or along the tendinous cords on which sit small (1 to 2 mm) vegetations—verrucae along the lines of closure.
these irregular, warty projections probably result from the precipitation of fibrin at sites of erosion related to underlying inflammation and fibrinoid degeneration. these acute valvular changes cause little disturbance in cardiac function. chronic rheumatic heart disease is characterized by organization of the acute inflammation and subsequent deforming fibrosis. in particular, the valvular leaflets become thickened and retracted, causing permanent deformity. in chronic disease, the mitral valve is virtually always deformed, but involvement of another valve, such as the aortic, may be the most clinically important in some cases. the cardinal anatomic changes of the mitral (or tricuspid) valve are leaflet thickening shortening, thickening, and fusion of the tendinous cords. microscopically, there is diffuse fibrosis and often neovascularization that obliterate the originally layered and a vascular leaflet architecture. aschoff bodies are replaced by fibrous scar diagnostic forms are rarely seen in surgical specimens or autopsy tissue from patients with chronic rheumatic heart disease at extended intervals after acute rheumatic fever. rheumatic heart disease is the most frequent cause of mitral stenosis (99% of cases). pathogenesis. acute rheumatic fever is a hypersensitivity reaction induced by group a streptococci., but the exact pathogenesis remains uncertain. it is proposed that antibodies directed against the m proteins of certain strains of streptococci cross-react with tissue glycoproteins in the heart, joints, and other tissues.
the onset of symptoms usually 2 to 3 weeks after infection and the absence of streptococci from the lesions support the concept that rheumatic fever results from an immune response against the offending bacteria. because the nature of cross-reacting antigens has been difficult to define, it has also been suggested that the streptococcal infection evokes an autoimmune response against self-antigens. because only a minority of infected patients develop rheumatic fever, it is suspected that genetic susceptibility regulates the hypersensitivity reaction. the chronic sequelae result from progressive fibrosis because of both healing of the acute inflammatory lesions and the turbulence i induced by ongoing valvular deformities
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
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