Investigations

ECG is an important diagnostic tool in the diagnosis of Acute Myocardial infarction. Myocardial infarction results in myocardial necrosis, injury and ischaemia. Severe acute ischaemia lowers theresting membrane potential and shortens the duration of action potential. Such changes cause a voltage gradient between normal and ischaemic zones. These so-called currents of injury are

represented on the surface ECG by deviation of ST-segment.

When acute ischaemia is transmural, ST-T vector is usually shifted in the direction of outer (epicardial) layers producing ST elevation and sometimes in the earliest stages of ishaemia tall,positive T-waves called hyperacute T-waves over the ischaemic zone. With ischaemia confined primarily to the subendocardium, ST vector typically shifts toward the subendocardium and ventricular cavity so that overlying (e.g. anterior precardial) leads show ST-segment depression (with ST elevation in lead a VR).

Evolutionary changes in ECG are typical of myocardial ischaemia. Myocardial infarction evolves through four easily recognizable electrographic phases.

1) Hyperacute

2) Acute

3) Subacute

4) Chronic stabilized

In the hyperacute phase, the earliest manifestation of an acute infarction is straightening of the normal upward concavity of the ST-T-segment

In acute phase ST-T-segment becomes elevated and ST-T-segment slopes upward. Also the amplitude of T-wave is usually increased.

In subacute phase abnormal Q-waves representing myocardial necrosis appear. In the fully evolved phase the ST-T-segments begins to diminish in amplitude and become coved upwards and blends into the symmetrically inverted T-waves. During the chronic phase there is resolution of ST-T-waves with the only residual change being abnormal Q-waves.

ECG leads are helpful in localizing the site of Q-wave infarction.

ECG wave with anterior Q wave infraction

ECG wave with inferior Q wave infraction

Severe anterior wall ischaemia

Site of Infarction                                      ECG Leads

1) Anterior wall                    one or more of precordial leads (V1-V6), I, aVL

2) Antero septal                                          V1-V3

3) Lateral or apical                                    V4-V6

4) Inferior                                                   II, III,   avF

RV Infarction

Isolated RV infarction is a rarely recognized phenomenon. RV Myocardial infarction (RVMI) should be strongly suspected if in the clinical setting of Acute Inferior Wall MI (IWMI), there is ST segment elevations of 1mm or more in lead V1 and V4 R or any one of the extra right precordial leads (V4R-V6R). In most studies lead V4R was found to be the most sensititive of all-extra right precordial leads. ST-T-segment which is higher in lead V4R than in leads V1-V3 offers highest specificity in diagnosis. When there is ST-T segment elevation in lead V1 with ST-T-segment depression in lead V2-a discordant relationship, it also suggests the presence of RV infarction. A diagnosis of RV infarction should only be entertained if there is concomitant electrographic evidence of IWMI or Infero-Posterior myocardial Infarction.

Posterior Wall MI

Posterior myocardial infarction occurs in the posterior left ventricular wall. An isolated true posterior wall infarction is quite uncommon. It is usually associated with inferior or lateral infarction.ECG changes of a true posterior infarction are seen as mirror image representations in lead V1 to V3.Perloff described the criteria for a true posterior infarction as follows: R-waves of 40 ms in lead V1 and in contiguous right precordial leads with upright T-waves. In the acute phase ST-segment depression and R/S Ratio equal to or greater than 1 in leads V1 and V2 are diagnostic.Usually there are associated changes in inferior and lateral leads.Atrial Infarction Usually reflected in PR-segment elevation or depression and P-wave abnormalities. It is frequently associated with supraventricular arrhythmias.

Serum Enzymes
Following MI large quantities of enzymes are released into the blood from necrotic heart muscle. The rate of liberation of specific enzymes are of diagnostic importance.

Creatine Kinase (CK)

CK is a 85-kDa enzyme found in all striated muscles. There are three isoenzymes of CK: CK-MM is the predominant form in striated muscle.CK-MB, most common in the heart; and CK-BB, most common in brain but also found in gut and kidney. Sensitivity for acute MI is > 90 per cent by 6hrs. Total CK may be falsely elevated in many pathologic conditions like muscle diseases, alcohol intoxication, Diabetes Mellitus,skeletal muscle trauma, vigorous exercise, convulsions, intramusclar injection and pulmonary embolisms. Hence it is a relatively nonspecific marker.

CK-MB

In the bloodstream CK-MB exists predominantly in equilibrium between two forms, the tissue form (MB2) and the circulating seroconverted form (MB1). As cardiac muscle cells die, MB2 is converted to MB1 by carboxypeptidase enzyme. An absolute level of MB2 > 1U/L and MB2/MB1 ratio of > 1.5 are highly sensitive markers of myocardial necrosis. The ratio of CK-MB mass of about 2.5 per cent CK activity is indicative of myocardial rather than skeletal source of the CK MB elevation. In addition to AMI secondary to coronary obstruction, other forms of injury to cardiac muscle such as those resulting from myocarditis, cardiac catheterization, shock and cardiac surgery may also produce elevated serum CK-MB levels.

Normally, Baseline CK-MB activity is 2-4 IU/L. For a reliable diagnosis of MI, it should increase above 9-10 IU/L. Plasma CK-MB activity of reliable diagnostic sensitivity is reached with in 12-16 hrs of onset of symptoms. Maximal levels are reached between 14-36hrs with a return to normal levels occurring after 48-72 hrs.

Cardiac Specific Troponins

Two new diagnostic cardiac markers have been introduced-Troponin T and Troponin I, which are part of the sarcomere complex.Troponin T has a molecular weight of 38,000 and Troponin I 23,000. Cardiac troponin I has 31 aminoacids which are not present in the skeletal forms. The recognition site of the antibody used in the assay is in the cardiac specific region, which makes the test very specific as a marker for myocardial injury. Cardiac Troponin I and Cardiac troponin T are not normally detected in the blood. Cardiac Troponin T has 11 aminoacids not present in the skeletal forms and hence it is also specific. It has similar sensitivity to troponin I but somewhat less specificity.

Troponin I and Troponin T are released into the plasma so that a reliable diagnostic sensitivity is reached by 12-16 hrs and maximal activity is reached by 24-36 hrs. The levels return to normal within 10-12 days.Myoblobin It is a low molecular weight heme protein found in cardiac and skeletal muscle. It is is not cardiac specific but released more rapidly from infarcted myocardium than CK-MB. It is detected as early as 2 hrs after MI and remains increased for at least 7-12 hrs.

Enzymatic Criteria for the Diagnosis of Myocardial Infarction

— Serial increase, then decrease of plasma MB-CK, with a change > 25 per cent between any two values.

— MB-CK >10-13 U/L or 75 per cent total CK activity.

— Increase in MB-CK activity > 50 per cent between any two samples, separated by at least 4 hrs. If only single is samples available MB-CK elevation > two fold.

— Beyond 75 hrs, an elevation of Troponin T or I or LDH-1 > LDH-2.

Serum Lipids

Total cholesterol and HDL remain at or near baseline values during the 24-48 hrs after the acute event, but fall precipitously after that and later values are therefore, unreliable after the first 24 hours.

Hematological Manifestations
WBC count elevates within 2 hrs after chest pain and reaches a peak 2-4 days following infarction. It returns to normal within a week. ESR rises to a peak on the 4th-5th day of infarction.

Chest X-ray

Provides very important information in the assessment of myocardial infarction. Points to look into are (signs of left ventricular failure) cardiothoracic ratio to detect cardiomegaly, ventricular aneurysms, pericardial effusion, etc.

Echocardiography

It can be of importance in patients with acute MI. Abnormalities of wall motion are almost universally present. Estimation of left ventricular function is relatively accurate and can be useful prognostically. It may be particularly useful in the diagnosis of RV infarction, ventricular aneurysm, pericardial effusion and left ventricular thrombus. Additionally Doppler echocardiography is useful in the detection of a ventricular septal defect and mitral regurgitation.