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The diagnosis of myocardial infarction is made by integrating the history of the presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage). A coronary angiogram allows to visualize narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.
A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed on admittance to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of a myocardial infarction and are sometimes performed in equivocal cases. Technetium and thallium can be used in nuclear medicine to visualize areas of reduced blood flow and tissue viability, respectively. Technetium is used in a MUGA scan.
[edit] Diagnostic criteria
WHO criteria have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:
1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers such as creatine kinase, troponin I, and lactate dehydrogenase isozymes specific for the heart.
The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression or coronary intervention are diagnostic of MI.
Physical examination
The general appearance of patients may vary according to the experienced symptoms; the patient may be comfortable, or restless and in severe distress with an increased respiratory rate. A cool and pale skin is common and points to vasoconstriction. Some patients have low-grade fever (38–39 °C). Blood pressure may be elevated or decreased, and the pulse can be become irregular.
If heart failure ensues, elevated jugular venous pressure and hepatojugular reflux, or swelling of the legs due to peripheral edema may be found on inspection. Rarely, a cardiac bulge with a pace different from the pulse rhythm can be felt on precordial examination. Various abnormalities can be found on auscultation, such as a third and fourth heart sound, systolic murmurs, paradoxical splitting of the second heart sound, a pericardial friction rub and rales over the lung.
Electrocardiogram
The primary purpose of the electrocardiogram is to detect ischemia or acute coronary injury in broad, symptomatic emergency department populations. However, the standard 12 lead ECG has several limitations. An ECG represents a brief sample in time. Because unstable ischemic syndromes have rapidly changing supply versus demand characteristics, a single ECG may not accurately represent the entire picture. It is therefore desirable to obtain serial 12 lead ECGs, particularly if the first ECG is obtained during a pain-free episode. Alternatively, many emergency departments and chest pain centers use computers capable of continuous ST segment monitoring. It should also be appreciated that the standard 12 lead ECG does not directly examine the right ventricle, and does a relatively poor job of examining the posterior basal and lateral walls of the left ventricle. In particular, acute myocardial infarction in the distribution of the circumflex artery is likely to produce a nondiagnostic ECG. The use of non-standard ECG leads like right-sided lead V4R and posterior leads V7, V8, and V9 may improve sensitivity for right ventricular and posterior myocardial infarction. In spite of these limitations, the 12 lead ECG stands at the center of risk stratification for the patient with suspected acute myocardial infarction. Mistakes in interpretation are relatively common, and the failure to identify high risk features has a negative effect on the quality of patient care. The 12 lead ECG is used to classify patients into one of three groups:
1. those with ST segment elevation or new bundle branch block (suspicious for acute injury and a possible candidate for acute reperfusion therapy with thrombolytics or primary PCI),
2. those with ST segment depression or T wave inversion (suspicious for ischemia), and
3. those with a so-called non-diagnostic or normal ECG.
A normal ECG does not rule out acute myocardial infarction. Sometimes the earliest presentation of acute myocardial infarction is the hyperacute T wave, which is treated the same as ST segment elevation. In practice this is rarely seen, because it only exists for 2-30 minutes after the onset of infarction. Hyperacute T waves need to be distinguished from the peaked T waves associated with hyperkalemia. The current guidelines for the ECG diagnosis of acute myocardial infarction require at least 1 mm (0.1 mV) of ST segment elevation in 2 or more anatomically contiguous leads. This criterion is problematic, however, as acute myocardial infarction is not the most common cause of ST segment elevation in chest pain patients. In addition, over 90% of healthy men have at least 1 mm (0.1 mV) of ST segment elevation in at least one precordial lead. The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, benign early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm.
Left bundle branch block and pacing can interfere with the electrocardiographic diagnosis of acute myocadial infarction. The GUSTO investigators Sgarbossa et al. developed a set of criteria for identifying acute myocardial infarction in the presence of left bundle branch block and paced rhythm. They include concordant ST segment elevation > 1 mm (0.1 mV), discordant ST segment elevation > 5 mm (0.5 mV), and concordant ST segment depression in the left precordial leads. The presence of reciprocal changes on the 12 lead ECG may help distinguish true acute myocardial infarction from the mimics of acute myocardial infarction. The contour of the ST segment may also be helpful, with a straight or upwardly convex (non-concave) ST segment favoring the diagnosis of acute myocardial infarction.
The constellation of leads with ST segment elevation enables the clinician to identify what area of the heart is injured, which in turn helps predict the so-called culprit artery.
Wall Affected Leads Showing ST Segment Elevation Leads Showing Reciprocal ST Segment Depression Suspected Culprit Artery
Septal V1, V2 None Left Anterior Descending (LAD)
Anterior V3, V4 None Left Anterior Descending (LAD)
Anteroseptal V1, V2, V3, V4 None Left Anterior Descending (LAD)
Anterolateral V3, V4, V5, V6, I, aVL II, III, aVF Left Anterior Descending (LAD), Circumflex (LCX), or Obtuse Marginal
Extensive anterior (Sometimes called Anteroseptal with Lateral extension) V1,V2,V3, V4, V5, V6, I, aVL II, III, aVF Left main coronary artery (LCA)
Inferior II, III, aVF I, aVL Right Coronary Artery (RCA) or Circumflex (LCX)
Lateral I, aVL, V5, V6 II, III, aVF Circumflex (LCX) or Obtuse Marginal
Posterior (Usually associated with Inferior or Lateral but can be isolated) V7, V8, V9 V1,V2,V3, V4 Posterior Descending (PDA) (branch of the RCA or Circumflex (LCX))
Right ventricular (Usually associated with Inferior) II, III, aVF, V1, V4R I, aVL Right Coronary Artery (RCA)
As the myocardial infarction evolves, there may be loss of R wave height and development of pathological Q waves. T wave inversion may persist for months or even permanently following acute myocardial infarction. Typically, however, the T wave recovers, leaving a pathological Q wave as the only remaining evidence that an acute myocardial infarction has occurred.
Cardiac markers
Main article: Cardiac marker
Cardiac markers or cardiac enzymes are proteins from cardiac tissue found in the blood. These proteins are released into the bloodstream when damage to the heart occurs, as in the case of a myocardial infarction. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. Then it was found that disproportional elevation of the MB subtype of the enzyme creatine kinase (CK) was very specific for myocardial injury. Current guidelines are generally in favor of troponin sub-units I or T, which are very specific for the heart muscle and are thought to rise before permanent injury develops. Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future.
The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24 hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.
Angiography
In difficult cases or in situations where intervention to restore blood flow is appropriate, coronary angiography can be performed. A catheter is inserted into an artery (usually the femoral artery) and pushed to the vessels supplying the heart. Obstructed or narrowed arteries can be identified, and angioplasty applied as a therapeutic measure (see below). Angioplasty requires extensive skill, especially in emergency settings, and may not always be available out of hours. It is commonly performed by interventional cardiologists.
Histopathology
Histopathological examination of the heart may reveal infarction at autopsy. Under the microscope, myocardial infarction presents as a circumscribed area of ischemic, coagulative necrosis (cell death). On gross examination, the infarct is not identifiable within the first 12 hours.
Although earlier changes can be discerned using electron microscopy, one of the earliest changes under a normal microscope are so-called wavy fibers. Subsequently, the myocyte cytoplasm becomes more eosinophilic (pink) and the cells lose their transversal striations, with typical changes and eventually loss of the cell nucleus. The interstitium at the margin of the infarcted area is initially infiltrated with neutrophils, then with lymphocytes and macrophages, who phagocytose ("eat") the myocyte debris. The necrotic area is surrounded and progressively invaded by granulation tissue, which will replace the infarct with a fibrous (collagenous) scar (which are typical steps in wound healing). The interstitial space (the space between cells outside of blood vessels) may be infiltrated with red blood cells.
These features can be recognized in cases where the perfusion was not restored; reperfused infarcts can have other hallmarks, such as contraction band necrosis.
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