Myocardial infarction , acute

Myocardial infarction is caused by acute thrombotic occlusion of a coronary artery (A). Therapeutic interventions aim to restore blood flow in the occluded vessel in order to reduce infarct size or to rescue ischemic myocardial tissue. 

In the area perfused by the affected vessel, inadequate supply of oxygen and glucose impairs the function of heart muscle contractile force declines. In the great majority of cases, the left ventricle (anterior or posterior wall) is involved. 

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

The success of infarct therapy critically depends on the length of time between the onset of the attack and the start of treatment Whereas some therapeutic measures are indicated only after the diagnosis is confirmed, others necessitate prior exclusion of contraindications or can be instituted only in specially equipped facilities. Without exception, however, prompt action is imperative. Thus, a staggered treatment schedule has proven useful. 

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The dmg is effective in the treatment of ventricular arrhythmias, especially those following acute myocardial infarctions (1,2,22). 

A third study (85) enrolled 7825 hypertensive patients (55% males and 45% females) having diastoHc blood pressures (DBP) of 99—104 mm Hg (13—14 Pa) there were no placebo controls. Forty-six percent of the patients were assigned to SC antihypertensive dmg therapy, ie, step 1, chlorthaUdone step 2, reserpine [50-55-5] or methyldopa [555-30-6], and step 3, hydralazine [86-54-4]. Fifty-four percent of the patients were assigned to the usual care (UC) sources in the community. Significant reductions in DBP and in cardiovascular and noncardiovascular deaths were noted in both groups. In the SC group, deaths from ischemic heart disease increased 9%, and deaths from coronary heart disease (CHD) and acute myocardial infarctions were reduced 20 and 46%, respectively. 

In a more extensive international trial, 17,187 patients were treated intravenously with streptokinase alone, aspirin alone, a combination of streptokinase and aspirin, or placebo (78). Streptokinase and aspirin were equally effective in treating acute myocardial infarction, each decreasing mortahty by 25% their combination further reduced mortahty by 42%. A significant reduction in mortahty was seen even in those patients treated up to 24 hours after the onset of symptoms. 

Compared to streptokinase, urokinase has been less extensively studied because of its high cost, ie, about 10 times that of a comparable treatment with streptokinase. In addition to the indications described for streptokinase, urokinase is indicated for use in patients with prior streptokinase treatment, or prior Streptococcal infection. Urokinase is commonly used at a loading dose of 4400 units /kg, with a maintenance intravenous infusion dose of 4400 units/kg/h for thromboses other than acute myocardial infarction. In the latter case, a much larger dose, ie, 0.5—2.0 million units/h or a bolus dose of 1.0 million units followed by a 60-min infusion with 1.0 million units, has been found optimal (106). An intracoronary dose of 2000 units/min for two hours was used in one comparative study with intracoronary streptokinase (107). In this study, urokinase exhibited efficacy equivalent to streptokinase with fewer side effects. Other studies with intracoronary urokinase have adrninistered doses ranging from 2,000 to 24,000 units/min with a reperfusion efficacy of 60—89% (108—112). In another urokinase trial, 2.0 million units were adrninistered intravenously, resulting in a thrombolytic efficacy of 60% (113). Effectiveness in terms of reduction in mortaUty rate has not been deterrnined because of the small number of patients studied. 

GPIIb/IIIa antagonists have to be administered parenterally. They are currently used prophylactically during intracoronary interventions such as percutaneous transluminal revascularization with balloon angioplasty or intracoronary stenting, as well as to treat acute coronary syndromes like unstable angina and acute myocardial infarction. The main complications... 

Acute coronary syndromes most often result from a physical disruption of the fibrous cap, either frank cap fracture or superficial endothelial erosion, allowing the blood to make contact with the thrombogenic material in the lipid core or the subendothelial region of the intima. This contact initiates the formation of a thrombus, which can lead to a sudden and dramatic blockade of blood flow through the affected artery. If the thrombus is nonocclusive or transient, it may either be clinically silent or manifest as symptoms characteristic of unstable angina. Importantly, if collateral vessels have previously formed, for example, due to chronic ischemia produced by multi vessel disease, even total occlusion of one coronary artery may not lead to an acute myocardial infarction. 

Occurs when the volume of extracellular fluid is significantly diminished. Examples include hemorrhage, fluid loss caused by burns, diarrhea, vomiting, or excess diuresis Occurs when the heart is unable to deliver an adequate cardiac output to maintain perfusion to the vital organs. Examples include as the result of an acute myocardial infarction, ventricular arrhythmias, congestive heart failure (CHF), or severe cardiomyopathy. 

The nitrates are used cautiously in patients witii severe hepatic or renal disease, severe head trauma, acute myocardial infarction (MI), hypotiiyroidism, and during pregnancy (Pregnancy Category C, except for amyl nitrate) or lactation. 

Systemic anaphylaxis in man is frequently accompanied by electrocardiographic alterations ischemic ST waves, arrhythmias and atrial fibrillation [6-11]. Anaphylactic reactions after insect stings can lead to coronary spasm or acute myocardial infarction [12, 13]. Myocardial infarction can also occur as a consequence of idiopathic... 

Krumholz HM, Pasternak RC, Weinstein MC, et al. Cost effectiveness of thrombolytic therapy with streptokinase in elderly patients with suspected acute myocardial infarction. N Engl J Med 1992 327 7-13. 

Data from Webb J, Thompson C Thrombolysis for acute myocardial infarction. Can Fam Physician 1992 38 1415. 

The LD-1 is less than 30% of total LD in normal serum, whereas in patients with an acute myocardial infarction it is between 50-90% of total LD activity. The ratio of LD-l/LD-2 is usually greater than one in acute myocardial infarction (37). 

The only other condition which causes (MB) to appear in serum is muscular dystrophy. The MB isoenzyme appears in the serum of the patient with acute myocardial infarction within 6 hours and remains elevated for approximately 48-60 hours. 

Wagner et. al (46) studied 376 patients to evaluate the importance of identification of the myocardial-specific MB isoenzyme in the diagnosis of acute myocardial infarction. An attempt was made to determine the incidence of falsely positive (mb). No acute infarction was diagnosed in all patients in whom neither total CK nor the isoenzymes of LD indicated myocardial necrosis. Incidence of falsely negative (MB) was zero in 33 patients. They concluded that determination of the isoenzymes of CK provides both a sensitive and specific indication of acute myocardial infarction. 

Ronttinen, A. and Somer, H. Specificity of seriim creatine kinse isoenzymes in diagnosis of acute myocardial infarction. Br. Med. J. (1973), 1, 386-389. 

It is important to obtain a baseline EKG and cardiac enzymes to evaluate the possibility of an acute myocardial infarction. The short-term (2-4 weeks) stroke risk after acute myocardial infarction (AMI) is 2.5%. Stroke is usually an early (within 14 days) complication of AMI and is more common in anterior wall (4—12%) than in inferior wall infarction (1%). Approximately 40% of patients with an anterior wall myocardial infarction develop left ventricular thrombus. 

Tavani, A. et al., Beta-carotene intake and risk of nonfatal acute myocardial infarction in women, Eur. J. Epidemiol, 13, 631, 1997. 

Kardinaal, A.E. et al.. Association between beta-carotene and acute myocardial infarction depends on polyunsaturated fatty acid status the EURAMIC study (European Study on Antioxidants, Myocardial Infarction, and Cancer of the Breast), Arterioscler. Thromb. Vase. Biol, 15, 726, 1995. 

Pasternak, R.C., Braunwald, E. and Sobel, B.E. (1988). Acute Myocardial Infarction Heart Disease . W.B. Saunders, Philadelphia. 

One eritical factor that has been neglected in considering mechanisms of cardiac fatalities is the timeframe for various types of toxicities. For example, a majority of cocaine-related fatalities and near fatalities reported from emergency rooms are attributed to one or more types of cardiac ischemic or hypertensive episodes (Isner et al. 1986). Thus, these studies may discount the cocaine-induced arrhythmias and conduction defects as important direct causes of fatalities. Yet, if coroner reports are used as data sources (Virmani et al. 1988 Wetli and Wright 1979 Mittleman and Wetli 1984), there are great numbers of deaths in which pulmonary effusion and lack of evidence for coronary occlusion, acute myocardial infarction, or... 

Ascher, E.K. Stauffer, J-C.E. and Gaasch, W.H. Coronary artery spasm, cardiac arrest, transient electrocardiographic Q waves and stunned myocardium in cocaine-associated acute myocardial infarction. 

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