Acute myocardial infarction continues to be a major public health problem and is one of the most common diagnosis occurring in hospitalized patients. Mortality with Acute Infarction isapproximately 30 per cent, with more than half of the deaths occurring before hospitalization.Although survival following hospitalization has improved over the last two decades, risk of excess mortality and recurrent non-fatal MI, still persists in patients who recover.
Despite, the major health challenge presented by Coronary Heart Disease and Acute Myocardial Infarction, substantial progress has been made over the past 30 yrs. Mortality and morbidity due to coronary artery disease are on the decline.Improvements in primary prevention, therapy and secondary prevention are believed to have contributed to this decline. Progress has resulted from improved understanding of the pathophysiolgy in acute myocardial infarction. Drug therapy continues to be an integral part of the treatment of patients with acute myocardial infarction. But despite the gratifying success of all modalities of therapy for acute myocardial infarction, several observations indicate that considerable room for improvement exists.
Pathophysiology
Vast majority of myocardial infarctions result from occlusion of coronary artery due to thrombus propagating from a ruptured atheromatous plaque. Atheromatous plaques are of two types vulnerable and stable plaques. The vulnerable plaque typically has substantial lipid core and a thin fibrous cap. In contrast stable plaque has a relatively thick fibrous cap protecting the thin lipid core from contact with the blood. Clinical data suggest that stable plaques more often show luminal narrowing detectable by angiography than do vulnerable plaques.Mechanisms responsible for the conversion of Chronic Coronary Heart
Despite, the major health challenge presented by Coronary Heart Disease and Acute Myocardial Infarction, substantial progress has been made over the past 30 yrs. Mortality and morbidity due to coronary artery disease are on the decline.Improvements in primary prevention, therapy and secondary prevention are believed to have contributed to this decline. Progress has resulted from improved understanding of the pathophysiolgy in acute myocardial infarction. Drug therapy continues to be an integral part of the treatment of patients with acute myocardial infarction. But despite the gratifying success of all modalities of therapy for acute myocardial infarction, several observations indicate that considerable room for improvement exists.
Pathophysiology
Vast majority of myocardial infarctions result from occlusion of coronary artery due to thrombus propagating from a ruptured atheromatous plaque. Atheromatous plaques are of two types vulnerable and stable plaques. The vulnerable plaque typically has substantial lipid core and a thin fibrous cap. In contrast stable plaque has a relatively thick fibrous cap protecting the thin lipid core from contact with the blood. Clinical data suggest that stable plaques more often show luminal narrowing detectable by angiography than do vulnerable plaques.Mechanisms responsible for the conversion of Chronic Coronary Heart
Disease to Acute Coronary Syndromes involves:
• Endothelial injury usually at sites of atherosclerotic plaques or plaque fissuring or ulceration.
• This results in exposure of potent thrombogenic stimuli within the plaque and subendothelium of the vessel to be exposed to circulating platelets.
• Platelet adhesion, aggregation and fibrin formation takes place. Also activation of selected mediators occurs.
• Endothelial injury usually at sites of atherosclerotic plaques or plaque fissuring or ulceration.
• This results in exposure of potent thrombogenic stimuli within the plaque and subendothelium of the vessel to be exposed to circulating platelets.
• Platelet adhesion, aggregation and fibrin formation takes place. Also activation of selected mediators occurs.
This results in mechanical obstruction of the narrowed artery. The relative absence of prostacyclin (PGI2), tissue plasminogen activator (TPA) and Endothelin derived relaxation factor (EDRF) (NO) at sites of endothelial injury contribute to the development of thrombosis,vasocontriction and neointimal proliferation.
There is also evidence that in atherosclerotic plaques prone to rupture, there is increased rate of formation of melalloprotienase enzymes such as collagenase, gelatinase, stromelysins that degrade components of the protective matrix. These protienases may be elaborated by activated macrophages and mast cells which accumulate in high concentration at the site of atheroma.There are also T- lymphocytes in atheromatous plaque which secretes cytokine inerferone gamma (INF-γ) that inhibits the ability of vascular smooth muscles to form interstitial collagen.A number of physiological parameters such as systolic BP, heart rate, blood viscosity, endogenous tissue plasminogen activator, plasminogen activation inhibitor – I (PAI-I) levels,plasma cortisol levels and plasma epinephrine levels also influence the conversion of chronic stable coronary artery disease to ACS.
Thus rupture of atheromatous plaque and platelet thrombus formation are the common pathophysiological substrate of ACS that range from UA through non- ST elevation and ST elevation AMI.
Plaque Rupture
ompletely occlusive thrombus Less obstructive thrombus
Non-STEMI UA
Transmural MI
The thrombus is non-occlusive in 80 per cent of patients with UA and is composed primarily of platelets. The pathophysiology of non-Q wave MI is very similar to that of UA. It involves plaque fissuring with formation of mural intra luminal thrombus in most (75 per cent) patients. In the other 25 per cent of the subjects the thrombus is occlusive, but distal myocardium remains perfused by collaterals. The primary distinction between non-Q-wave MI and UA is the elevated level of cardiac enzymes associated with non-Q MI indicative of myocardial necrosis.Fixed and persistent blockage of a coronary artery by a combination of ruptured atherosclerotic plaque and superimposed intraluminal platelet rich thrombus leads to Acute Q-wave MI.The thrombus associated with Q-wave MI is occlusive in 80 per cent of patients and has a high content of trapped red blood cells. Diagnostic features of a Q-wave MI involves increased level of myocardial enzymes as well as ST-segment elevation and development of abnormal Q-waves.
Ventricular Remodeling
Ventricular remodeling is a descriptive term for the biologic adaptability of the cardiac chambers to adjust their size and configuration or ‘remodel’ in response to long-term alteration in haemodynamic loading. The remodeling that occurs after AMI differs from the normal adaptive response, as well as the response to pathophysiologic loading conditions in that the initial inciting event in post MI remodeling is an abrupt loss of contractile tissue. This loss of myocytes leads to thinning and elongation of the infarct containing segment-infarct expansion. This creates abnormalities in wall stress that promote ventricular enlargement. Patients who exhibit infarct expansion early in their clinical course are at much greater risk for later complications such as heart failure and death. Post MI remodeling is a heterogenous and regional process. It is distinct from other conditions producing remodeling in that it is not a gradual response to supra-normal systemic workloads, but rather is an attempt to restore pump function of the actually damaged
ventricle.
Stunning
Stunning is a acute reversible LV dysfunction following reperfusion of an occluded vessel or transient ischaemia due to any cause. It may occur following exercise induced ischaemia and coronary spasm. Myocardial stunning is an important feature of unstable angina. The severity of stunning is always greater in the subendocardial layers of the LV wall. The duration of ischaemia is a second important factor.
Hibernation
Hibernation is a chronic reversible LV dysfunction due to chronic coronary artery disease. It recovers following revascularisation. Radionuclide imaging techniques, positron emission tonography and stress echocardiography are capable of assessing myocardial perfusion and viability and are helpful in determining whether myocardial dysfunction is due to necrosis or hibernation. It is important to diagnosis hibernation because successful restoration of flow will lead to improvement in LV function.
Clinical Presentation
Onset of MI may be at any time of the day or night, but a higher frequency of onset occurs in the morning within a few hours of awakening. Triggers such as physical exercise, emotional stress,medical and surgical illness can play a role in triggering an acute event. But in roughly one half of cases no precipitating factors appears to be present prior to MI.
Pain is the most common presenting complaint in patients with myocardial Infarction.
• Pain is usually retrosternal in location spreading to both sides of the anterior chest with prediliction for the left side.
• In about 30 per cent pain radiates down the ulnar aspect of the left wrist, hand and fingers.
• Pain is deep and visceral lasting more than 30 mts.
• It is typically described as constricting, oppressing or compressing.
• Often complaints of a sensation of heavy weight or squeezing in the chest.
• Less common sites of radiations include the epigastrium, back, lower jaw and neck.
• The pain in MI may radiate as high as the occipital area but not below the umbilicus.
• The pain is often associated with weakness, sweating, nausea, vomiting, giddiness and anxiety.
Unusual Presentation
Although pain is the most common presenting complaint, 15-20 per cent of MI are painless. The incidence of painless infarcts are greater in women, diabetics and with increasing age.Other unusual presentations are in the form of pulmonary oedema, marked weakness, syncope, a confusional state, appearence of an arrhythmia, evidence of peripheral embolism or merely an unexplained drop in arterial pressure.
Physical Examination
Most patients are restless and in profound distress. They massage or clutch their chest and often describe their pain with a clenched fist held against the sternum (the “Levine sign” named after Dr. Samuel A. Levine). Pallor is common and is often associated with perspiration and coolness of the extremities. Heart rate may vary from marked bradycardia to a rapid regular or irregular tachycardia depending on the underlying rhythm. Patients in cardiogenic shock by definition have systolic BP below 90 mm of Hg and evidence of end organ hypoperfusion. JVP is normal in majority of patients with Anterior MI. The ‘a’ wave may be prominent in patients with pulmonary hypertension secondary to LVF or reduced compliance. RV Infarction often results in marked Jugular venous distensions. JVP is elevated in patients with cardiogenic shock.In 1967 killip proposed a prognostic classification based on the presence and severity of rales
detected in patients presenting with AMI.
Class I–Patients are free of rales and third heart sound.
Class II – Patients have rales but only to a mild to moderate degree (< 50 per cent of lung fields) and may or may not have S3.
Class III – Patients have rales in more than half of each lung field and frequently have pulmonary oedma.
Class IV – Patients are in cardiogenic shock.
Precordial Examination
Despite severe symptoms, findings on examination of the heart may be unremarkable. S4 is common. S3 occurs in the presence of LV systolic dysfunction. Dyskinetic segment may be palpable as an abnormal, paradoxic pulsation in the 3rd, 4th or 5th interspace to the left of sternum. Systolic murmurs transient or persistent are commonly audible in patients with AMI and generally result from mitral regurgitation secondary to dysfunction of mitral valve apparatus,rupture of interventricular septum or tricuspid regurgitation caused by right ventricular failure.Pericardial friction rub is audible in 6-30 per cent of all patients with AMI and is higher in patients with transmural infarction.
Onset of MI may be at any time of the day or night, but a higher frequency of onset occurs in the morning within a few hours of awakening. Triggers such as physical exercise, emotional stress,medical and surgical illness can play a role in triggering an acute event. But in roughly one half of cases no precipitating factors appears to be present prior to MI.
Pain is the most common presenting complaint in patients with myocardial Infarction.
• Pain is usually retrosternal in location spreading to both sides of the anterior chest with prediliction for the left side.
• In about 30 per cent pain radiates down the ulnar aspect of the left wrist, hand and fingers.
• Pain is deep and visceral lasting more than 30 mts.
• It is typically described as constricting, oppressing or compressing.
• Often complaints of a sensation of heavy weight or squeezing in the chest.
• Less common sites of radiations include the epigastrium, back, lower jaw and neck.
• The pain in MI may radiate as high as the occipital area but not below the umbilicus.
• The pain is often associated with weakness, sweating, nausea, vomiting, giddiness and anxiety.
Unusual Presentation
Although pain is the most common presenting complaint, 15-20 per cent of MI are painless. The incidence of painless infarcts are greater in women, diabetics and with increasing age.Other unusual presentations are in the form of pulmonary oedema, marked weakness, syncope, a confusional state, appearence of an arrhythmia, evidence of peripheral embolism or merely an unexplained drop in arterial pressure.
Physical Examination
Most patients are restless and in profound distress. They massage or clutch their chest and often describe their pain with a clenched fist held against the sternum (the “Levine sign” named after Dr. Samuel A. Levine). Pallor is common and is often associated with perspiration and coolness of the extremities. Heart rate may vary from marked bradycardia to a rapid regular or irregular tachycardia depending on the underlying rhythm. Patients in cardiogenic shock by definition have systolic BP below 90 mm of Hg and evidence of end organ hypoperfusion. JVP is normal in majority of patients with Anterior MI. The ‘a’ wave may be prominent in patients with pulmonary hypertension secondary to LVF or reduced compliance. RV Infarction often results in marked Jugular venous distensions. JVP is elevated in patients with cardiogenic shock.In 1967 killip proposed a prognostic classification based on the presence and severity of rales
detected in patients presenting with AMI.
Class I–Patients are free of rales and third heart sound.
Class II – Patients have rales but only to a mild to moderate degree (< 50 per cent of lung fields) and may or may not have S3.
Class III – Patients have rales in more than half of each lung field and frequently have pulmonary oedma.
Class IV – Patients are in cardiogenic shock.
Precordial Examination
Despite severe symptoms, findings on examination of the heart may be unremarkable. S4 is common. S3 occurs in the presence of LV systolic dysfunction. Dyskinetic segment may be palpable as an abnormal, paradoxic pulsation in the 3rd, 4th or 5th interspace to the left of sternum. Systolic murmurs transient or persistent are commonly audible in patients with AMI and generally result from mitral regurgitation secondary to dysfunction of mitral valve apparatus,rupture of interventricular septum or tricuspid regurgitation caused by right ventricular failure.Pericardial friction rub is audible in 6-30 per cent of all patients with AMI and is higher in patients with transmural infarction.
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