Ischemic heart disease_Myocardial infarction_

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  • Angina pectoris (literally chest pain), wherein the ischemia causes pain but is insufficient to lead to death of myocardium; as we will discuss, angina may be stable (occurring reliably after certain levels of exertion), may be due to vessel spasm (variant angina or Prinzmetal angina), or may be unstable (occurring with progressively less exertion or even at rest).
  • Ischemic heart disease_Myocardial infarction_

    1. 1. Ischemic Heart Disease Myocardial Infarction Robinson Joseph DPT-student 3rd year 1
    2. 2. 2
    3. 3. IHD cont… • Coronary Artery Disease (CAD). IHD is also frequently called coronary artery disease (CAD). • The clinical manifestations of IHD are a direct consequence of insufficient blood supply to the heart. 3
    4. 4. There are four basic clinical syndromes of IHD: I. Angina pectoris (literally chest pain), wherein the ischemia causes pain but is insufficient to lead to death of myocardium; II. Acute myocardial infarction (MI), wherein the severity or duration of ischemia is enough to cause cardiac muscle death. III. Chronic IHD refers to progressive cardiac decomposition (heart failure) following MI. IV. Sudden cardiac death (SCD), can result from a lethal arrhythmia following myocardial ischemia. 4
    5. 5. Pathogenesis • In most cases IHD occurs because of inadequate coronary perfusion relative to myocardial demand. This may result from a combination of pre-existing ("fixed") atherosclerotic occlusion of coronary arteries and new superimposed thrombosis and/or vasospasm 5
    6. 6. 6
    7. 7. Myocardial Infarction 7
    8. 8. Myocardial Infarction • MI, popularly called heart attack, is necrosis of heart muscle resulting from ischemia. • The major underlying cause of IHD is atherosclerosis. • The frequency of MIs rises progressively with increasing age and presence of other risk factors such as  hypertension,  smoking,  and diabetes. 8
    9. 9. Myocardial Infarction Cont… • Approximately 10% of MIs occur in people younger than 40 years, and 45% occur in people younger than age 65. Blacks and whites are equally affected. • Men are at significantly greater risk than women, although the gap progressively narrows with age. • In general, women are remarkably protected against MI during their reproductive years. Nevertheless, menopause-and presumably declining estrogen production-is associated with exacerbation of coronary atherosclerosis. 9
    10. 10. Pathogenesis • Although any form of coronary artery occlusion can cause acute MI, angiographic studies demonstrate that most MIs are caused by acute coronary artery thrombosis. • In most cases, disruption of an atherosclerotic plaque results in the formation of thrombus. Vasospasm and/or platelet aggregation can contribute but are infrequently the sole cause of an occlusion. • Sometimes, particularly with infarcts limited to the innermost (subendocardial) myocardium, thrombi may be absent. In these cases, severe diffuse coronary atherosclerosis significantly limits coronary vessel perfusion, and a prolonged period of increased demand (e.g., due to tachycardia or hypertension) may be sufficient to cause necrosis of myocytes most distal to the epicardial vessels. 10
    11. 11. Coronary Artery Occlusion • In a typical MI, the following sequence of events transpires: • There is a sudden disruption of an atheromatous plaque -for example, intraplaque hemorrhage, erosion or ulceration, or rupture or fissuring-exposing subendothelial collagen and necrotic plaque contents.Platelets adhere, aggregate, become activated, and release potent secondary aggregators including thromboxane A2, adenosine. • Vasospasm is stimulated by platelet aggregation and mediator release. • Other mediators activate the extrinsic pathway of coagulation, adding to the bulk of the thrombus.Within minutes the thrombus can evolve to completely occlude the coronary lumen of the coronary vessel. 11
    12. 12. Myocardial Response to Ischemia • • • • Coronary artery obstruction blocks the myocardial blood supply, leading to profound functional, biochemical, and morphologic consequences. Within seconds of vascular obstruction, cardiac myocyte aerobic glycolysis ceases, leading to inadequate production of adenosinetriphosphate (ATP) and accumulation of potentially noxious breakdown products (e.g., lactic acid). The functional consequence is a striking loss of contractility, occurring within a minute or so of the onset of ischemia. Ultrastructural changes including myofibrillar relaxation, glycogen depletion, and cell and mitochondrial swelling also become rapidly apparent. However, these early changes are potentially reversible, and myocardial cell death is not immediate. Only severe ischemia lasting at least 20 to 40 minutes causes irreversible injury and myocyte death. 12
    13. 13. The final location, size, and specific morphologic features of an acute MI depend on: • • • • • • Location, severity, rate of development of the coronary occlusion Size of the vascular bed perfused by the obstructed vessels Duration of the occlusion Metabolic demands of the myocardium (affected, e.g., by blood pressure and heart rate). • Extent of collateral supply. 13
    14. 14. Clinical Features • • • • • An MI is usually heralded by severe, crushing substernal chest pain or discomfort that can radiate to the neck, jaw, epigastrium, or left arm. In contrast to the pain of angina pectoris, the pain of an MI typically lasts from 20 minutes to several hours and is not significantly relieved by or rest. In a substantial minority of patients (10% to 15%) MIs can be entirely asymptomatic. Such "silent" infarcts are particularly common in patients with underlying diabetes mellitus (with peripheral neuropathies) and in the elderly. With MIs the pulse is generally rapid and weak, and patients can be diaphoretic and nauseated particularly with posterior-wall MIs. Dyspnea is common and is caused by impaired myocardial contractility and dysfunction of the mitral valve apparatus, with resultant pulmonary congestion and edema. Electrocardiographic abnormalities are important markers of MIs; Laboratory evaluation of MI is based on measuring the blood levels of intracellular macromolecules that leak out of injured myocardial cells through damaged cell membranes. 14
    15. 15. Consequences and Complications of MI • Unfortunately, half of the deaths associated with acute MI occur in individuals who never reach the hospital; such patients generally die within 1 hour of symptom onset-usually as a result of arrhythmias. The variables associated with a poor prognosis include  advanced age,  female gender,  diabetes mellitus,  and previous MI. 15
    16. 16. Figure 11-12 Complications of MI. A-C, Cardiac rupture. A, Anterior myocardial rupture in an acute infarct (arrow). B, Rupture of the ventricular septum (arrow). C, Complete rupture of a necrotic papillary muscle. D, Fibrinous pericarditis, showing a dark, roughened epicardial surface overlying an acute infarct. E, Early expansion of anteroapical infarct with wall thinning (arrow) and mural thrombus. F, Large apical left ventricular aneurysm (arrow). (A-E, From Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles. Philadelphia, WB Saunders, 1989. F, Courtesy of Dr. William D. Edwards, Mayo Clinic, Rochester, Minnesota.) 16
    17. 17. • The risk of developing complications and the prognosis after MI depend on i. infarct size ii. site, and iii. fractional thickness of the myocardial wall that is damaged. 17
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