Myocardial Infarction and Its Symptoms | Cardiovascular Disease

In myocardial infarction (MI) there is necrosis of cardiac muscle due to inadequate coronary circulation. Sudden death may occur when obstruction to coronary flow is precarious. Most deaths occurring within 24 hours of the onset of attack are due to ventricular fibrillation.

Anatomy of Coronary Arteries:

There are three main sources of coronary arterial blood supply:

(1) The anterior descending branch of left coronary artery

(2) Circumflex branch of left coronary artery

(3) Right coronary artery.

The areas supplied by these arteries have their EC.G. characteristics easily recognised.

(1) Anteroseptal

(2) Anterolateral

(3) Inferior wall or posterior

S.A. node and A.V. node are usually perfused through branches of right coronary artery. E.C.G. mapping can also be done by special techniques. Coronary angiography has now become a perfected technique in specialised centres and which can clearly reveal diseased vessels so that proper therapeutic measures can be selected.

Pathogenesis:

Coronary occlusion occurs due to atherosclerosis of the coronary vessels in 90% of instances but coronary insufficiency can also be due to syphilitic narrowing of coronary ostium, embolic or inflammatory lesions. Thrombotic lesion in the atheromatous vessels may or may not be present. Emboli may come from vegetations on the mitral or aortic valve (infective endocarditis) or from left auricular thrombus. Polyarteritis nodosa is a very rare cause. The ultimate result of a major occlusion is myocardial infarction.

Myocardial infarction pathologically means that there is microscopic and macroscopic damage to cardiac muscle, due to lack of oxygen supply. The cardiac muscle however may not become necrotic immediately or within a few hours. Detectable histological changes take about six hours to develop. So if the patient suddenly dies of coronary occlusion, due to severe atherosclerosis, myocardial necrosis may not be pathologically detected at autopsy.

If however patient dies after 24 hours or more, the cardiac muscles look pale, yellowish and later haemorrhagic.

Hence the relationship of atherosclerosis, thrombus formation and embolic lesions to myocardial infarction may be apparently clear but what triggers the episode is not yet well understood. Instances are recorded that patients dying of road accidents or due to war casualties may show severe atherosclerosis, while there has been no history of angina pectoris during life-time.

Pathologists during medico-legal autopsies have demonstrated presence of scars of infarction in heart muscles in persons, who never complained of anginal pain in life.

In tropics and developing countries, under-weight people with low fat diet as well as having normal cholesterol levels also develop myocardial infarction. Data on their lipid profile are inadequate in developing countries. Hence much more studies are required before we can specify how a so-called heart attack is precipitated. Most attacks occur at night or early in the morning or while in the toilet but rarely during physical exertion.

Symptoms:

Occurrence of MI is signalled by precordial pain in most cases though rarely it may be painless especially in very old people or diabetics.

Pain similar to anginal distribution may occur in 80% of cases. The degree of severity may vary. In old people painless MI may occur and the symptom may be only a fainting episode. Diabetic patients may sometimes develop myocardial infarction quite silently or without much pain.

Pain of angina pectoris is usually relieved with rest or rest plus glyceryl trinitrate (GNT), but once MI is established, GNT does not relieve pain but it may sometimes be more harmful causing further fall of B.P. which may be already low due to shock. GNT may be useful in the state of coronary insufficiency (pre-infarction angina) but once infarction has occurred it may cause “steal phenomena” and not resolve the infarction. In coronary artery spasm, it is undoubtedly of great value. Long-term therapy, high dose therapy, low dose therapy with beta-blockers are all recommended.

There may be evidence of L.V.F. without much frank physical signs. Careful assessment, however, may reveal evidence of orthopnoea and radiograph taken in bed may show perihilar congestion.S3 and S4, gallop rhythm can be heard and even a systolic thrust may be palpable over left parasternal area (left ventricular wall dysfunction).

Pericardial rub may occur in some cases after 24 to 48 hours. There may also be some low grade fever within 24 hours which returns to normal within five days.

Various presenting symptoms with or without chest pain are due to vasomotor instability, e.g.:

(1) Sudden orthopnoea

(2) Fainting

(3) Tachycardia, bradycardia or irregular action or heart (dysrhythmias)

(4) Cold sweats with cold extremities following dyspnoea

(5) Symptoms of upper abdominal discomfort which may be attributed to ‘gas’ in stomach by the patients.

Clinical Findings:

In angina pectoris, physical signs are usually lacking. Hypertension may be associated.

In coronary insufficiency, clinical features vary considerably; chest pain may be associated, with tachycardia, bradycardia or some arrhythmias; B.P. may rise or fall.

In MI the signs may be plentiful. Usually there is tachycardia, pulse rate reaching over 120 pm or there may be bradycardia, various types of heart block, severe hypotension, signs of shock, collapse, even unconsciousness. Stoke-Adam’s syndrome may occur. Gallop rhythm may be heard proclaiming left ventricular dysfunction.

In many instances, patients initially may not have severe symptoms. They may attribute the local discomfort to gas, due to indigestion or rheumatism. The pain is often felt as pressure or load on the chest or some kind of compression across the anterior chest wall.

The clinical picture of a classical acute attack may be as follows:

(1) Sudden onset of acute anterior wall chest pain with or without radiation to the periphery.

(2) Sweating and cold extremities.

(3) Rapid pulse rate.

(4) Ectopic beats tachy-, or brady-arrythmias

(5) Signs or L.V.F.

Sudden death may occur in severe AMI within a few minutes, which is usually due to ventricular fibrillation.

Diagnosis:

The diagnosis is chiefly clinical, as E.C.G. changes may occur later on, after some hours and serum enzyme changes proclaiming myocardial injury are also not immediates. Anticipation is very important. The clinical judgment is the sine que non of early diagnosis and the ‘G.P.’ (family physician) is the supreme commander to decide the treatment, at home or hospital. Immediate hospitalisation in rural setting is not usually possible.

If E.C.G. is taken during pain of angina pectoris, ST-T changes or depression of S.T. segment may be noted, ECG taken soon after an attack of angina may or may not show any abnormality.

In acute MI, ECG changes occur within a few hours but almost always, characteristic changes are seen within 24 to 36 hours of infarction.

ECG Changes in Acute Myocardial Infarction:

(1) Extensive Anterior Wall Infarction:

(Left coronary artery occlusion)

Q waves in leads I, II, AVL, V₁ to V₆ with ST elevation.

(2) Anteroseptal Infarction:

(Anterior descending branch of left coronary occluded) Q in leads I, AVL, V₂ to V₄ with ST elevation.  

(3) Anterolateral Infarction:

Q in leads I, AVL, V₄ to V₆ with ST elevation.

(4) Inferior Wall Infarction:

(Right coronary artery occlusion)

Q in leads II, II & AVF with S.T. elevation.

As the damaged myocardium heals the Q waves regress elevated ST segment reverse and finally T-waves become inverted in the opposite direction. ECG may gradually improve but rarely becomes entirely normal.

The earliest change may be elevation of ST segment in some leads depending on the site of infarction, which are later on followed by T-waves inversion. If the infarction is transmural Q waves appear. Otherwise, if the whole thickness of muscle is not involved, Q waves may not appear but the R-wave amplitudes may be low.

The important points to note are:

(1) Elevated S.T. segments, in leads facing area of damage and reciprocal S.T. depression in opposite leads. ST elevation is due to the ‘current of injury’.

(2) Inversion of T-waves.

(3) Appearances of deep and wide Q-waves in appropriate leads, which indicates through and through infarction in this area of myocardium.

(4) S.T. segment elevation gradually becomes normal in a few days or weeks but sometimes may remain elevated for a long time or even permanently (possible aneurysm of the heart).

Anatomically the following points are important. Left coronary involvement may present as follows depending on the area of damage:

(1) Antero septal V₁ to V₃

(2) Antero lateral V₅ to V₇

(3) Anterior wall V₁ to V₅

(4) High lateral I, AVL

Right coronary artery:

(1) Inferior wall – II, III, AVF

(2) Posterior wall – V₁ & V₂ — very tall T waves

The important points to note are:

(1) Elevated S.T. segments, in leads facing areas of initial damage and reciprocal ST depression in opposite leads. Pathological Q waves proclaim presence of myocardial necrosis when only ST changes are present without Q waves appears, it suggests that there is coronary occlusion without real pathological necrosis. Highly peaked tall T waves are also suspicious in this clinical setting.

(2) Inversion of T-waves.

(3) Appearances, of deep and wide Q-waves in appropriate leads.

(4) ST segment elevation gradually becomes normal in a few days or weeks but sometimes, may remain elevated for a long time or even permanently. Persistent elevation of ST-segment denotes myocardial dyskinesia but not necessarily dilatation.

Investigations:

(1) Blood examination within 24 and 48 hours may show leucocytosis with raised E.S.R. Serum bilirubin may show a little elevation sometimes.

(2) Urine may show excess of urobilinogen in the early stage.

(3) Serum enzymes are also elevated within 24 to 48 hours.

(4) Serum enzymes are also elevated within 24 to 48 hours. Three types of enzymes are noted to rise within a few hours of attack. These enzymes are liberated from damaged myocardial cells.

Serum Enzyme Levels:

Myocardial enzymes are released from myocardial cells after myocardial necrosis has occurred.

Three enzymes are usually measured i.e. SGOT, CPK and LDH.

In this part of the world facilities of SGOT estimation are commonly available, while CPK and LDH are often more useful, provided its enzymes are measured and serial observations are made.

SGOT — (Serum Aspartate Transaminase):

This enzyme starts rising from 6 to 24 hours after the onset of infarction and reaches its peak in 24 to 48 hours to return to normal within three to five days.

SGOT is also present in the liver and lungs, so some elevation of SGOT may also occur in pulmonary infarction and hepatocellular injury. The test is easily done in most laboratories and hence a reliable test for cardiac infarction in proper clinical setting.

CPK (or CK):

Creatine phospho-Kinase has three plasma isoenzymes, MM, MB and BB. Elevated MB-CPK activity is almost specific of myocardial infarction. It is elevated within 4 to 6 hours and reaches its peak in 12 to 48 hours and returns to normal level within 36 to 48 hours. The value of rising MB-CPK level between 24 and 36 hours of chest pain is highly specific. It also gives some idea of the extent of myocardial damage. Hence becoming more popular among cardiologists.

These enzymes can be measured in serum within 12 hours of chest pain and reaches its peak in 24 to 48 hours.

These enzymes, however, remain high even up to one to two weeks. The value of elevated LDH level is less specific because these enzymes are also present in RBC, brain, kidney, and gastric tissues. However, LDH₁/LDH₂ ratio of greater than 1.0 is suggestive of myocardial injury.

Serial estimations are valuable.

However, none of these tests are useful within first 3 to 4 hours after the heart attack, which is the most critical period after the attack. Even typical ECG changes may not occur soon after the attack; hence clinical diagnosis still remains the most valuable method. These sophisticated and expensive enzyme tests are not of much use to our rural patients.

The clinical diagnosis should not be difficult when typical features are present along with abnormal ECG findings. But in some cases diagnosis may be difficult in the most critical stage i.e. within first one to three hours of infarction. ECG change may not be always present and serum enzyme levels take time to be elevated and results also are not available at once. The clinician’s role is therefore supreme.

Hence careful and critical evaluation of symptomatology and history is essential. Perforation of peptic ulcer and acute pancreatitis are the two most difficult problems.

In a large general hospital of Calcutta with 1500 beds about 500 to 600 cases are usually admitted annually. Most large hospitals have 6 to 8 beds in a CCU; hence it is not possible to admit all cases in C.C.U.

Management:

Rest & Nursing Care:

When attack is severe, patient must be kept in bed and should receive continuous nursing care if possible in a C.C.U.

There is always some risk during transporting patient from the place of occurrence to hospital but proper supervision of treatment is hardly possible at home, except, in special circumstances It the patient is in shock he should be kept in bed without a pillow in supine position but if there is L.V.F., he should be supported by a back rest at about 40° to 45° angle with oxygen line The number of days of bed-rest depends on the seriousness of the attack. It may be a few days to two or three weeks depending on clinical situation, complications and E.C.G. findings.

Some patients often do not tolerate morphine and pethidine so well and suffer from nausea and vomiting. Pethidine with Phenergan may be helpful.

Relief of Pain:

Morphine or pethidine are the best drugs to relieve pain. It is best to give 10 to 15 mg of morphine sulphate or 50 to 100 mg of pethidine slowly I.V. depending on body weight and severity of the pain.

Nitrites which are always helpful in angina pectoris do not relieve pain if infarction has occurred. Rather if too much nitrite is taken by the patient, there may be fall of B.P., hypoperfusion of myocardium and possible development of arrhythmias. “Occasionally in des­peration, patients consume large quantities of nitrites over a short period of time producing hypotension and sometimes syncope” (Oxford Textbook of Medicine 13.175, 1983) However if the patient is in I.C.U. and if there is no hypotension, GNT may be tried sublingual or by I.V. route, to find out if any useful result can be derived.

Treatment of cardiogenic shock is an extremely difficult problem in general practice.

For proper assessments is essential to assess the cardiovascular status by monitoring the following factors:

(1) State of consciousness and clinical data e.g. B. P., pulmonary congestion, pulse rate, arrhythmias, gallop, renal function (urine output) and metabolic acidosis.

(2) B.P. record can only be correctly in measured by direct arterial needle as routine clinical method can be fallacious.

(3) Oxygen, CO₂ level and pH should be measured but in any case oxygen inhalation must be ensured.

(4) Central venous pressure (C.V.P.) should be measured. The best method is to measure pulmonary wedge pressure (P.W.P.) by Swan-Ganz balloon catheter. If the P.W.P. is high, patient has volume overload and will require diuretics and inotropic drugs and if it is lower than normal (14 to 18 mm Hg), I.V. fluids should be given.

(5) If no such facilities are available and if hypovolaemia is clinically suspected, 5% glucose I.V. drip can be started and after infusing 200 to 300 ml, clinical condition is watched. If pulmonary congestion or breathlessness increases stop the I.V. drip and start diuretics and watch renal function.

(6) Vasopressor agents e.g. noradrenaline and mephentermine were used in the past. The modern opinion is going against it. It is argued that in cardiogenic shock there is already existing severe vasoconstriction and these drugs may be harmful.

Dopamine however is considered useful as it has inotropic effect on the myocardium and appears to improve cardiac output. It also has renal vasodilating action but constrictor action on muscular and cutaneous vessels. Hence it is recommended to infuse 200 mg of dopamine (5 ml ampoule) in a bottle of 5% dextrose to be given as I.V; drip at the rate of 20 to 40 drops per minute and carefully watch the effect.

If a pressor agent e.g. noradrenaline or mephentermine is used on a short-term basis when dopamine is not available, it should not be given as bolus-dose. Put 2-4 mg. of noradrenaline in a bottle of 5% glucose saline and ensure flow rate of 10-15 µg/min. As it produces intense vasoconstriction it should better be avoided in cardiogenic shock.

Mephentermine sulphate 15 to 30 mg I.M. may tide over a desperate situation in rural setting and slow I.V. drug containing 150 mg of mephentermine in bottle of 5% glucose has saved many lives in the past although cardio­logists working in ICU need not use these two drugs. It is reported that these drugs may increase the infarct size also.

But it is also true that we have salvaged many patients in severe cardiogenic shock using one of these two drugs before Dopamine was available. These drugs were also reinforced with I.V. hydrocortisone in dosage of 200 mg bolus dose and then in I.V. drip up to 400 to 600 mg in first 24 hours.

There are also controversies in the use of steroids in cardiogenic shock but I will recommend its use in shocked patient of myocardial infarction in above dosage as I have salvaged many dying patients by using this drug.

Embolic Manifestation:

Sudden pulmonary embolism is a very important cause of unexpected death due to a thrombus coming from clots in deep leg veins. Systemic arterial embolism from an intracardiac mural thrombus is not so common. The risk of embolism remains for two to three weeks, i.e. as long as the patient is in bed, receiving sedatives and tranquilisers.

Leg movement and light physiotherapy are helpful in initial stages. Deep vein thrombus in legs can be detected early, by checking tenderness in calf-muscles every day. Calf muscles must be checked daily for any evidence of deep tenderness (Hoffman’s sign for phlebothrombosis).

Acute left ventricular failure is another important complication and this is often manifested by sudden development of dyspnoea due to pulmonary congestion. Gallop rhythm and pulsus alternans are warning signs. Left ventricular failure may ultimately result is congestive heart failure recognised by enlarged tender liver and peripheral oedema. In a lying patient sacral region should be examined for oedema. The legs should also be daily inspected for oedema.

Pericarditis:

Presence of pericardial rub over precordium proclaims pericarditis. This is often easily heard if the patient can sit up and lean forward. It may occur within a few days of heart attack or after a few weeks there may be associated pleurisy (Dresslar’s syndrome). It usually responds to analgesics but rarely corticosteroids are required especially where pleuro-pericarditis is present.

Left Ventricular Aneurysm:

When myocardial infarction is through and through and if considerable area is involved the firbrous tissue formed in the infarcted area may distend to form an aneurysmal dilatation. If it causes left ventricular failure, surgery should be considered. Overall mortality is still about 15%.

Mitral Regurgitation:

Mitral valve prolapse may occur due to damaged papillary muscles. Mild cases can be treated with diuretics while severe cases should be surgically managed by mitral valve replacement.

Cardiac Rupture:

The damaged myocardium may suddenly rupture causing sudden death. Other injuries due to infarction may cause rupture of the I.V. septum resulting in pansystolic murmur as in VSD. Pansystolic murmur may also occur due to rupture and papillary muscle resulting in mitral regurgitation.

Other Complications:

Other less acute complications are muscular wasting as well periarthritis, particularly of the shoulder-joint (Frozen shoulder).

Anxiety neurosis and depression state (melancholia) are sometimes quite troublesome. Attention to patient s mental rehabilitation is as important as cardiovascular rehabilitation.

Proper physiotherapy from the beginning usually prevents frozen shoulder or arthritic problems. Once frozen shoulder develops it is a difficult problem to tackle. Physiotherapy, ultrasonic heat and sometimes intra-articular steroids may be required.

First-Aid Management Acute Attack:

1. Set up an IV drip of 5% glucose solution, if not already done.

2. Oxygen administration should be started.

3. Connect the patient to the scope (if available) and read the ECG to come to a diagnosis about the site of the myocardial infarction, the state of cardiac rhythm, presence of the arrhythmias etc. Inform your senior.

4. Inj. morphine 10-15 mg I.M. for relief of pain, if not already given and then repeat this as and when considered essential. Pethidine also can be given in dosage of 50 to 100 mg. either pethidine or morphine can be combined with Phenergan 2.5 mg to ensure relief of pain as well as sedation. Those steps can be done even in coronary care ambulance including oxygen administration.

5. A thorough clinical examination should be done with the particular emphasis on the state of shock, CHF and arrhythmia.

6. Charts for the pulse. B.P., temperature, respiration should be meticulously maintained.

7. Chart for the intake/output of fluid and the drugs administered should be maintained.

8. Inj. Hydrocortisone or Dexamethasone may be useful in some cases, who are in shock.

9. Anticoagulants should be considered in all severe cases of myocardial infarction if there is no contraindication. Give Inj. Heparin 7500 units I.V. and then repeat 5000 units I.V. six hourly BT-CT should be done before giving the next dosage so that the adjustment can be done Heparin should be continued for 48 hours. Tab. Sinthrom (4mg) – start with four tablets stat then give two tablets on the second day and again two tablets on the third day. Prothrombin time should be done daily to adjust the dosage of Sinthrom. Vitamin K and Protamin should be available for emergency.

10. Introduction of intracoronary streptokinase is another new method in making attempts to revascularize the ischaemic heart.

11. Infarctectomy is too heroic with very limited success.

12. Rupture of heart is always fatal but rarely slow leak may result in formation of pseudoaneurysm. The aneurysm can however be diagnosed by echocardiography and may be surgically excised in rare cases.