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Diagnosis of Acute Myocardial Infarction
Background
Myocardial infarction is a life-threatening cardiovascular disease which is featured by the necrosis of myocardium (muscles present in the wall of the heart). The disease is primarily caused due to insufficient supply of blood and oxygen to the myocardium. The insufficient blood flow results from the formation of emboli, thrombus or constriction of the coronary blood vessels. Atherosclerosis and arteriosclerosis are the major risk factors for the coronary constriction or vascular spasm. Myocardial infarction is diagnosed by different subjective and objective measures. However, the criteria for diagnosis are associated with the stage of MI and the presence of comorbid disorders. Hypertension or sustained elevated blood pressure is the major risk factor for MI. On the other hand, obesity and diabetes mellitus are two major comorbid conditions that increase the risk of MI. The symptoms of MI include chest pain, flushing, fatigue and respiratory distress. In advanced stages, death may result from ventricular fibrillation. MI is managed through surgical and pharmacological interventions (Alpert 1335-1341).
The surgical interventions for MI include angioplasty and stent implantation. On the other hand, pharmacological interventions include thrombolytic and anticoagulant agents. Angioplasty refers to the surgical removal of thrombus from coronary blood vessels.

Stent implantation refers to the dilatation of the coronary blood vessels by surgical devices (stents). Anticoagulants like aspirin are used as a prophylactic medication for reducing the chances of MI or aggravation of MI. Thrombolytic agents like heparin are used to dissolute the thrombus. On the other hand, sublingual nitrates are also used to dilate the coronary blood vessels for improving blood flow to the myocardium. However, sublingual nitrates are non-specific and act on all coronary blood vessels. This leads to the “coronary steal” effect. This means that blood flows more through the unobstructed coronary blood vessels than the obstructed vessels. Hence, the myocardium beyond the obstructed blood vessels continues to remain hypoxic. As a result, the MI gets aggravated. Based on the clinical features and complications it is important to appropriately diagnose and manage MI (Alpert 1335-1341). The present article focuses on different diagnostic tools that are used to diagnose acute myocardial infarction (AMI).
Acute Myocardial Infarction: Issues and Concerns
Timely and appropriate diagnosis of AMI is extremely essential for ensuring positive health outcomes for patients. AMI is featured by high mortality rates within the first hour of its clinical presentation. The major symptom of AMI is severe chest pain. The pain is severe, diffuse, retrosternal and radiating. The pain radiates to the arms or from the jaws right up to the umbilicus. The pain does not subside with the administration of sublingual nitrates or NSAIDs (like aspirin). Retrosternal burning sensation and eructation is quite common. AMI is often associated with vomiting, sweating, and breathlessness. As a result, the symptoms of MI are often mistaken as hyperacidity. On the other hand, almost 15% to 20% of AMI are painless. Painless AMI is witnessed in elderly individuals and individuals suffering from diabetes mellitus (Lee & Goldman 1187-1195).
Classification of Myocardial Infarction
Myocardial infarction is broadly classified into five types. The classification is based on the circumstance in which it happens. The different types of MI are:
Type-1 MI: It is a spontaneous MI featured by ischemia. The ischemia results from primary coronary events like plaque erosion/rupture or fissuring.
Type-2 MI: This MI is caused secondary to the ischemic episode. The MI results from increased oxygen demand or deficit in oxygen supply. Such MI is witnessed in conditions like coronary artery spasm, arrhythmias, hypotension, coronary embolism, hypertension, and anemia.
Type-3 MI: This type of Mi is featured by sudden cardiac death. The cardiac death results from cardiac arrest with certain symptoms of myocardial ischemia.
Type-4: This type of MI results secondary to interventional procedures like stent thrombosis or angioplasty.
Type-5: This type of MI results during CABG (Lee & Goldman 1187-1195).
Diagnosis of acute myocardial infarction
Electrocardiography
ECG is the most common diagnostic tool for acute MI. The T waves are tall, and there is the marked elevation of the S-T segment. These features are prominent within minutes after onset of pain associated with acute MI. The Q waves are delayed, and this effect is manifested after 6 hrs of onset of AMI. The Q waves indicate severe necrosis of the myocardium. On the other hand, after one day to one week of onset of acute MI, the nature of T waves and S-T segment elevation changes. The T waves become inverted, and the S-T segment becomes more convex. This change indicates that the time taken for repolarization is shorter due to a damaged myocardium. Arrhythmias are also noted during the initial stages of MI. The mere presence of MI does not have any prognostic value. Hence, localization of MI is extremely essential. Myocardial infarction may be localized in the anterior wall or the inferior wall (Pope, Aufderheide & Ruthazer 1163-1170). The differential diagnoses of both are as follows:
Anterior Wall MI: ST segment elevation is usually diagnosed prominently in the unipolar chest leads (V4 to V6 leads).ST segment elevation in V2 to V6 indicates LAD proximal to the first diagonal branch. On the other hand, ST segment depression in augmented limb leads (aVL) indicates LAD distal to the first diagonal branch (Pope 1163-1170).
Inferior Wall MI: ST segment elevation is mainly witnessed in lead III compared to lead II. It indicates occlusion of the right coronary arteries. If the ST segment elevation featured in lead III coincides with ST segment elevation in VI lead, it indicates occlusion that occurs proximal to the acute marginal branch. On the other hand, if the ST segment elevation is mainly witnessed in lead II compared to lead I it denotes occlusion of the left coronary arteries. Such elevations are also supported by ST segment elevations in leads V5, V6, Lead I and aVL (Ozdemir, Altunkeser & Icli 19-26).
Echocardiography (EKG)
EKG is useful during active chest pain. The absence of motion abnormalities in the left ventricular wall during active chest pain excludes the possibility of acute MI. On the other hand, motion abnormalities in the left or right ventricular wall signify acute MI. EKG helps to confirm the non-diagnostic features of acute chest pain. Moreover, EKG is also helpful for estimating the risk of myocardial damage and for specifying the size of the infarct after reperfusion injury. EKG also helps to rule out other causes of chest pain (like aortic dissection, cor pulmonale, and pericarditis) which are often confused with acute MI. For analyzing regional wall motions, the American Society of Echocardiography has recommended a 16-segment/17-segment model with an addition of the apical cap. A scoring system has been developed by ASE for grading regional wall motion (Kushner, Hand & Sidney 2205-2241). The grading system is represented in Table 1.
Score Regional Wall Motion Echocardial motion Estimated Wall Thickening
1 Normal motion Normal Greater than 30% (Normal)
2 Hypokinetic Reduced Lesser than 30% (reduced)
3 Akinesis (loss of motion) absent Absent
4 Dyskinesis outward thinning
5 Aneurysms Diastolic deformity Absent or thinning
Table 1: Grading system of regional wall motion (Source: ASE)
Biochemical markers
Cardiac biomarkers have been conventionally used for diagnosing acute MI. However, such biomarkers are also used to diagnose Non-STEMI and episodes of unstable angina. Elevation of Creatinine Kinase (CK) isoenzymes (specifically type MB) is elevated in acute MI. Elevated levels of CK signifies myocardial necrosis. Serum myoglobin levels are also enhanced, but it is not a specific biomarker of myocardial damage. On the other hand, cardiac-specific troponins (like I and T) can differentiate between myocardial damage or damage to the skeletal muscles. During acute MI, the serum levels of cardiac-specific troponins (like I and T) are 20 times higher than their reference range (Ozdemir et al., 19-26). Increased WBC count is also an indicator for acute MI. The elevation is mainly witnessed within first 2 hours after initiation of chest pain. The count reaches a peak within two to four days after infarction. However, the WBC count returns to normal within 1 week after onset of acute chest pain (Lee & Goldman 1187-1195).
Discussion and Conclusion
Acute Myocardial Infarction is a serious cardiovascular disorder that is often accompanied by cardiac arrest or death. Appropriate and timely management of acute MI is strongly associated with the accurate and timely diagnosis. Different subjective and objective diagnostic tools are implemented for diagnosing MI. These diagnostic tools are effective in diagnosing and localizing acute MI. However, different diagnostic tests should be conducted to confirm or exclude the possibilities of acute MI. Appropriate diagnosis may improve the prognosis of acute MI.
Works Cited
Alpert, J, Thygesen, K, Jaffe, A, & Harvey D (2008). The universal definition of myocardial
infarction: a consensus document. Heart 2008;94: 1335–1341
Kushner F, Hand M, Sidney C.. Focused Updates: ACC/AHA Guidelines for the
Management of Patients With ST-Elevation Myocardial Infarction J Am Coll Cardiol
2009; 54: 2205-2241.
Lee TH, & Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med
2000; 342,1187-1195
Ozdemir K, Altunkeser BB, Icli A. New parameters in identification of right
ventricular myocardial infarction and proximal right coronary lesion. Chest 2003;
124,19-26.
Pope JH, Aufderheide TP, Ruthazer R. Missed diagnoses of acute cardiac ischemia in
the emergency department. N Engl J Med 2000;342:1163-1170.