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Myocardial Infarction

Acute myocardial infarction (AMI) is the leading cause of death in the United States. In 1993, there were more than 1.5 million cases of AMI in the United States, and almost 500,000 associated deaths. Forty-six percent of AMIs occurred in those younger than 65 years. AMI most commonly occurs from a sudden thrombotic occlusion at the site of a ruptured or fissured atherosclerotic plaque.

Early identification of AMI, prevention of evolving infarction, and, if possible, restoration of coronary perfusion improves outcomes in patients with AMI. A 1987 study of 205,000 AMIs demonstrated significant improvements.

With these clinical issues in clear focus, this issue provides an overview of current diagnostic and therapeutic approaches to AMI. The objective is to provide a systematic approach to patient assessment, to identify the clinical advantages of newer enzymatic tests for confirming the diagnosis of acute coronary ischemia, and to review in detail the mortality reduction techniques - including pharmacotherapeutic and invasive procedures - supported by evidentiary clinical trials. Finally, a clinical algorithm outlining outcome-enhancing strategies for this life-threatening heart attack.

Overview of Clinical Principles

Diagnostic Criteria. In 1983, the World Health Organization (WHO) outlined the components necessary to establish the definitive diagnosis of acute myocardial infarction (AMI). This triad consists of chest pain.

Table 1. Killip Classification

Class I

No clinical heart failure, <5% mortality

Class II

Bales bilaterally in up to 50% of lung fields, isolated S3, good prognosis

Class III

Rales in all lung fields, acute mitral regurgitation, aggressive management required

Class IV

Cardiogenic shock: stuporous, systolic BP <90, decreased urine output, pulmonary edema and cold clammy skin, mortality near 80%

 

Electrocardiogram (ECG). Although the ECG is highly specific for diagnosis of AMI, the initial ECG reveals diagnostic ST elevations in only 40% of patients who eventually have a confirmed AMI.

Laboratory Markers: Diagnostic and Prognostic Indications

General Principles. Enzyme markers are routinely used for the detection and management of AMI. Serum markers enhance the sensitivity for early detection of myocardial necrosis and ischemia as compared to the ECG. They also help determine the time of cardiac injury, especially when used in combination.

Guidelines for Mortality Reduction: Non-thrombolytic Agents

The goal of management in AMI is to prevent evolution of infarction, reduce myocardial necrosis, minimize complications, and ultimately reduce short- and long-term mortality.

Nitroglycerin. Sublingual nitroglycerin (NTG) may improve ischemic chest pain but can also cause headaches. Initially, give up to three doses of 0.4 mg sublingual NTG every five minutes.

Aspirin. The benefits of aspirin therapy for reducing mortality after MI and in the setting of unstable angina.

Beta Blockade. Beta blockers have been shown to decrease mortality and to reduce infarct size in several clinical trials. The ISIS-1 and the MIAMI trial are the most important than showing benefits from this intervention. In ISIS-l, 16,027 patients were randomized to receive IV atenolol or placebo. There was a significant, relative decrease in mortality rates (3.89% mortality rate in the drug group vs. 4.57% placebo) in the first week.

Heparin. Although heparin is commonly used for management of chest pain, there is still some skepticism.

ACE Inhibitors. Both the ISIS-4 trial and the GISSI-3 trial have shown increased survival in patients with AMI who are given an oral ACE inhibitor within the first 24 hours. In the GISSI-3 trial, which consisted of 19,394 patients, patients were randomized to lisinopril or placebo for six weeks after AMI.

Magnesium. Intravenous magnesium was shown to be beneficial in the L1MIT-2 study of 2316 patients.

Thrombolytics: Mortality-Reducing Options

Introduction. Plasmin is the complex that facilitates lysis of a coronary thrombus that precipitates AMI. Thrombolytic therapy enhances the conversion ofplasminogen to plasmin, thereby inducing clot lysis. Plasminogen is an inactive proteolytic enzyme that is found in plasma and bound to fibrin in thrombi.

Streptokinase. Streptokinase (SK) is produced from b-hemolytic Streptococci cultures. Intravenous SK acts on inactive plasminogen to produce the active enzyme plasmin. This, in tum, leads to fibrin lysis and thrombus.

Tissue Plasminogen Activator. The first reported clinical use oftPA was in 19847 Tissue plasminogen activator is a naturally occurring enzyme found in vascular endothelial cells. This agent converts plasminogen.

APSAC. Anisoylated plasminogen streptokinase activator complex (APSAC) also activates plasminogen molecules to lyse fibrin. Similar to SK in this respect, APSAC is antigenic.

Reteplase. Reteplase (r-PA) is a non-glycosylated deletion mutant of wild-type tPA. Reteplase is administered as a double bolus infusion of 10 megaunits (10 U) 30 minutes apart. Outcomes data from the large GUSTO-III.

Percutaneous Coronary Angioplasty (PTCA). One of the most important debates in emergency medicine is whether pharmacologic therapy (thrombolysis) or mechanical therapy (PTCA) is the preferred strategy.