Myocardial infarction A heart attack or acute myocardial infarction (MI) occurs when one of the arteries that supplies the heart muscle becomes blocked. Blockage may be caused by spasm of the artery or by atherosclerosis with acute clot formation. The blockage results in damaged tissue and a permanent loss of contraction of this portion of the heart muscle.
<ul><li>Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance of oxygen supply and demand. </li></ul><ul><li> CLASSIFICATION </li></ul><ul><li>Transmural: :( Q –wave infarction) : most infartcts are transmural involve the full thickness of ventricular wall in the distribution of single coronary artery. </li></ul><ul><li>These infracts are caused by ch atherosclerosis, acute plaque changes b y occlusive thrombi and less commonly thromboemboli or vasospasm. </li></ul>
<ul><li>2. Subendocardial: these infarcts involve inner one third to one half of ventricular wall as subendo cardial zone is less perfused area of myocardial zone. The infarcts are caused by hypoperfusion of myocardium and not by coronary occlusion. These occur in hypotensive shock, and by typical ECG findings these are so called non Q wave infar </li></ul><ul><li>Less common causes of MI: </li></ul><ul><li>vasculitis PAN and kawasaki disease. </li></ul><ul><li>Cocain use </li></ul><ul><li>Embolization of plaque material </li></ul><ul><li>Thrombosis syndrome </li></ul>
<ul><li>PATHOGENESIS: </li></ul><ul><li>Occlusion is typically seen in the proximal 2 cm of the left anterior descending and left circumflex arteries and in the proximal and distal thirds of the right coronary artery. </li></ul><ul><li>Rupture of the lipid-rich atheromatous plaque, intraplaque hemorrhage, and intraluminal thrombus are three pathological hallmarks most commonly recognized in the infarct-related coronary artery at the site of acute myocardial infarction. </li></ul><ul><li>Role of the platelet-derived mediators (e.g. TXA2, serotonin, ADP, & PDGF that promote thrombosis and vasoconstriction occur. </li></ul>
<ul><li>Diminished availability of those natural endogenous substances that inhibit platelet aggregation, such as EDRF, tissue plasminogen activator, and PGI2. </li></ul><ul><li>Vasospsm is stimulated by mediators release from platelets. </li></ul><ul><li>Tissue factor activates the coagulation pathway. </li></ul><ul><li>Thrombus occlude the lumen of vessel. </li></ul><ul><li>Ischemia with out detection of coronary thrombosis due to vaculitis </li></ul>
These serial sections of a coronary artery demonstrate grossly the appearance of lumenal narrowing with atherosclerosis.
<ul><li>Grossly :Before 6 to 12 hours: No visible lesion is seen. </li></ul><ul><li>By 18 to 24 hours: Infarct area becomes pale to cyanotic & swollen. </li></ul><ul><li>In the first week: The infarct area becomes progressively more sharply defined, yellow and softened. </li></ul><ul><li>By the 7 to 10 days, circumference of the infarct area becomes hyperemic, and progressively expands. </li></ul><ul><li>By the 6 weeks, fibrous scar is well established. </li></ul>
myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct ) after occlusion (1) of a branch of the left coronary artery(LCA, right coronar
This is an acute myocardial infarction in the septum. After several days, there is a yellowish center with necrosis and inflammation surrounded by a hyperemic border.
This is an acute myocardial infarction of the anterior left ventricular free wall and septum in cross section. Note that the infarction is nearly transmural. There is a yellowish center with necrosis and inflammation surrounded by a hyperemic borde
When the infarction is 3 to 5 days old, the necrosis and inflammation are most extensive, and the myocardium is the softest, so that transmural infarctions may be complicated by rupture. A papillary muscle may rupture as well to produce sudden valvular insufficiency. Rupture through the septum results in a left-to-right shunt and right heart failure.
Gross morphologic changes evolve over time as follows : Time from Onset Gross Morphologic Finding 18 - 24 Hours Pallor of myocardium 24 - 72 Hours Pallor with some hyperemia 3 - 7 Days Hyperemic border with central yellowing 10 - 21 Days Maximally yellow and soft with vascular margins 7 weeks White fibrosis
This is normal myocardium. There are cross striations and central nuclei. Pale pink intercalated disks are also present.
<ul><li>Microscopic features: </li></ul><ul><li>Within 1 hour of ischemic injury, there is intercellular edema and “wavy fibers” may be present at the periphery of the infarct. These are noncontrctile dead fibers, stretched by the adjacent viable contracting myocytes </li></ul><ul><li> Electron microscopy shows reversible changes (swelling of mitochondria & endoplasmic reticulum and relaxation of myofibrils). </li></ul><ul><li>Histochemically, there is loss of oxidative enzyme & fall of glycogen. </li></ul><ul><li>In 12 to 72 hours , there is infiltration of neutrophils with progressive coagulative necrosis of myocytes. Dead myocytes become hypereosinophilic with loss of nuclei. </li></ul><ul><li> </li></ul>
This is an early acute myocardial infarction. (<iday) Note the prominent pink contraction bands.
1-2 daysThis is an early acute myocardial infarction. There is increasing loss of cross striations, and some contraction bands are also seen, and the nuclei are undergoing karyolysis. Some neutrophils are beginning to infiltrate the myocardium.
1-2days This is an acute myocardial infarction. There is loss of cross striations, and the nuclei are not present. There is extensive hemorrhage here at the border of the infarction, which accounts for the grossly apparent hyperemic border.
3-4 days This is an acute myocardial infarction of several days' duration. There is a more extensive neutrophilic infiltrate along with the prominent necrosis and hemorrhage.
<ul><li>Between 3 and 7 days after onset, dead myocytes begin to disintegrate and are removed by macrophages and enzyme proteolysis. There is proliferation of fibroblasts with formation of granulation tissue, which progressively replaces necrotic tissue. </li></ul><ul><li>After 6 weeks , healing is complete by fibrosis. </li></ul><ul><li>Contraction band necrosis : Contraction band necrosis, characterized by hypereosinophilic transverse bands of precipitated myofibrils in dead myocytes is usually seen at the edge of an infarct or with reperfusion (e.g. with thrombolytic therapy). </li></ul><ul><li>Reperfusion of an infarct: Reperfusion of an infarct is also associated with more hemorrhage, less acute inflammation, less limitation of the acute inflammation to the periphery in the first few days, reactive stromal cells, more macrophage infiltration earlier and a more patchy distribution of necrosis, especially around the periphery. </li></ul><ul><li> </li></ul><ul><li> </li></ul>
2-3 wks Toward the end of the first week, healing of the infarction becomes more prominent, with capillaries, fibroblasts, and macrophages filled with hemosiderin. The granulation tissue seen here is most prominent from 2 to 3 weeks following onset of infarction.
weeks –years After a couple of weeks, healing is well under way, and there is more extensive collagen deposition.
wks –yrs The remote myocardial infarction is evidenced by a collagenous scar seen here in a subendocardial location.
Microscopic morphologic changes evolve over time as follows: Time from Onset Microscopic Morphologic Finding 1 - 3 Hours Wavy myocardial fibers 2 - 3 Hours Staining defect with tetrazolium or basic fuchsin dye 4 - 12 Hours Coagulation necrosis with loss of cross striations, contraction bands, edema, hemorrhage, and early neutrophilic infiltrate 18 - 24 Hours Continuing coagulation necrosis, pyknosis of nuclei, and marginal contraction bands 24 - 72 Hours Total loss of nuclei and striations along with heavy neutrophilic infiltrate 3 - 7 Days Macrophage and mononuclear infiltration begin, fibrovascular response begins 10 - 21 Days Fibrovascular response with prominent granulation tissue 7 Weeks Fibrosis
Symptoms of a possible heart attack include chest pain and pain that radiates down the shoulder and arm. Some people (the elderly, people with diabetes, and women) may have little or no chest pain. Or, they may experience unusual symptoms (shortness of breath, fatigue, weakness). Women are more likely than men to have symptoms of nausea, vomiting, back or jaw pain, and shortness of breath with chest pain.
<ul><li>Clinical features: Chest pain- 20-30% does not cause chest pain, common in patients with diabetes mellitus, hypertension, & in elderly patients. </li></ul><ul><li>2. Nausea, diaphoresis and dyspnea. </li></ul><ul><li>Fate of the patient: hospitalized patients (where angiography, echocardiography and perfusion scintigraphy are available) usual fate are: </li></ul><ul><li>i) About 25 % of patients dye of cardiogenic shock or fatal arrythmia. </li></ul><ul><li>ii) Patients who survive the acute phase may develop: </li></ul>
<ul><li>Congestive heart failure </li></ul><ul><li>- Cardiac arrythmia </li></ul><ul><li>- Left ventricular failure with pulmonary edema. </li></ul><ul><li>- Rupture of ventricular wall, interventricular septum and papillary muscle </li></ul><ul><li>- Thromboembolism. </li></ul><ul><li> iii) 10-20% patients recover with no complication . </li></ul><ul><li> iv) Early restoration of blood flow by thrombolysis or balloon angioplasty provides better prognosis. </li></ul><ul><li> </li></ul>
Screening and Diagnosis Stress Test measures blood supply to heart Coronary Angiography specific shows coronaries Narrowing in Sites of Electro- cardiogram measures electrical impulses
<ul><li>Diagnosis:It is based on symptoms, electrocardiographic change and serum elevation of myocardial enzymes (creatine kinase-MB isoenzyme) or other proteins (troponin I, troponin T or myoglobin), that leak out of dead cells. </li></ul><ul><li>The classic EKG findings: ST segment elevation, followed by T wave inversion and Q waves, are associated with transmural infarction. ST segment depression and T wave inversion are associated with subendocardial infarction. </li></ul>
<ul><li>The laboratory diagnosis of myocardial infarction: 1) This has been based on elevation of creatine phosphokinase (CPK), with an MB fraction >5% of the total CPK or a relative index >3 (if the MB The elevation of CPK begins around 8 hours after the onset of infarction, peaks around 18 hours and ends around 48 hours . </li></ul><ul><li>2) The late diagnosis of myocardial infarction can be based on elevation of lactate dehydrogenase (LDH), with an LDH-1 fraction >40% of the total LDH or LDH-1/LDH-2 ratio >1, because this peaks around 5 days. </li></ul>
<ul><li>3) Recently, the early and late diagnosis of acute myocardial infarction has been based on elevated serum levels of cardiac troponin. This elevation begins around 4 hours after the onset of infarction and lasts longer than LDH; this test has a sensitivity similar to CPK-MB fraction and better than LDH. </li></ul><ul><li>For the diagnosis of acute myocardial infarction even earlier than detectable by troponin levels, myoglobin can be tested. </li></ul><ul><li>Elevated levels of myoglobin can be detected </li></ul>
<ul><li>around 2 hours after the onset of infarction, but this has only about 60% specificity for the heart. </li></ul><ul><li>A new type of test being evaluated for the diagnosis of acute myocardial infarction is CPK MB isoform assay, which has a 96% sensitivity and 93% specificity for infarction within 6 hours of onset of chest pain. </li></ul><ul><li>The combination of CPK MB and troponin testing can have even higher sensitivity and is used for the purpose of "ruling out" myocardial infarction. </li></ul>
<ul><li>Complications : It depends on the size , location duration of the lesion. </li></ul><ul><li>With in minutes to 3 days of onset: </li></ul><ul><li>1. Arrythmias :75-95% i) ventricular fibrillation ; ii) block of A-V bundles and its branches causing acute heart failure. </li></ul><ul><li>2. Cardiogenic shock 10-15%(usually in large infarct) causing acute heart failure. </li></ul><ul><li>3. Thrombotic complication- 15-40% mural thrombus over infarct area or Atrial thrombus, causing embolism to brain, kidney etc. </li></ul><ul><li>4. Rupture of heart. </li></ul>
<ul><li>3-14 days: </li></ul><ul><li>Large infarct: There is softening of dead muscle (myomalacia cordis) leading to rupture & death. </li></ul><ul><li>Site of rupture is ventricular wall, papillary muscle & interventricular septum. </li></ul><ul><li>5. Acute fibrinous or hemorrhagic pericarditis - over infarct area. </li></ul><ul><li>After weeks or months: </li></ul><ul><li>6. Chronic heart failure </li></ul><ul><li>7. Cardiac aneurysm, which may rupture producing hemopericardium and death. </li></ul>
Myocardial Rupture Myocardial aneurysm with thrombosis inside.
Rupture (at the arrow) into the pericardial sac can produce a life-threatening cardiac tamponade, as seen here. The septum may also rupture.
Rupture of papillary muscle…..mitral incompetence.
Left ventricular aneurysm containing mural thrombus A complication of infarction is aneurysm formation, which is the bulge seen here in the left ventricular wall. Note the very thin white wall of the aneurysm toward the apex.
The myocytes here are hypertrophied, marked by the large, dark nuclei, and there is interstitial fibrosis. This is an example of cardiomyopathy. In this case, long-standing, severe occlusive atherosclerosis led to "ischemic" cardiomyopathy.
<ul><li>6- Dressler’s syndrome </li></ul><ul><li>Is complication of transmural MI </li></ul><ul><li>-an autoimmune disorder resulting from damage of the myocardium </li></ul><ul><li>-antibodies developed against protein release from necrotic myocardial cells </li></ul><ul><li>-autoimmune pericarditis, pericardial friction rub and pleurisy. </li></ul>
<ul><li>Blood tests: used to evaluate kidney and thyroid function as well as to check cholesterol levels and the presence of anemia. </li></ul><ul><li>Chest X-ray: shows the size of heart and whether there is fluid build up around the heart and lungs. </li></ul><ul><li>Echocardiogram: shows a graphic outline of the heart’s movement </li></ul><ul><li>Ejection fraction (EF): determines how well heart pumps with each beat. </li></ul>Other Tests
1) Stenting <ul><li>a stent is introduced into a blood vessel on a balloon catheter and advanced into the blocked area of the artery </li></ul><ul><li>the balloon is then inflated and causes the stent to expand until it fits the inner wall of the vessel, conforming to contours as needed </li></ul><ul><li>the balloon is then deflated and drawn back </li></ul><ul><li>The stent stays in place permanently, holding the vessel open and improving the flow of blood. </li></ul>
2) Angioplasty <ul><li>a balloon catheter is passed through the guiding catheter to the area near the narrowing. A guide wire inside the balloon catheter is then advanced through the artery until the tip is beyond the narrowing. </li></ul><ul><li>the angioplasty catheter is moved over the guide wire until the balloon is within the narrowed segment. </li></ul><ul><li>balloon is inflated, compressing the plaque against the artery wall </li></ul><ul><li>once plaque has been compressed and the artery has been sufficiently opened, the balloon catheter will be deflated and removed. </li></ul>
3) Bypass surgery <ul><li>healthy blood vessel is removed from leg, arm or chest </li></ul><ul><li>blood vessel is used to create new blood flow path in your heart </li></ul><ul><li>the “bypass graft” enables blood to reach your heart by flowing </li></ul>around (bypassing) the blocked portion of the diseased artery. The increased blood flow reduces angina and the risk of heart attack.
Prevention <ul><li>Get regular medical checkups. </li></ul><ul><li>Control your blood pressure. </li></ul><ul><li>Check your cholesterol. </li></ul><ul><li>Don’t smoke. </li></ul><ul><li>Exercise regularly. </li></ul><ul><li>Maintain a healthy weight. </li></ul><ul><li>Eat a heart-healthy diet. </li></ul><ul><li>Manage stress. </li></ul>