Drug Therapy in Myocardial Infarction

DRUG THERAPY IN MYOCARDIAL INFARCTION

Myocardial infarction (MI) is ischaemic necrosis of a portion of the myocardium due to sudden occlusion of a branch of coronary artery. An acute thrombus at the site of atherosclerotic obstruction is the usual cause. About ¼ patients die before therapy can be instituted. The remaining are best treated in specialized coronary care units with continuous monitoring of the haemodynamic parameters and ECG to guide the selection of drugs and dosage. Those who receive such facility can be greatly benefitted by drug therapy, which according to individual needs is directed to:

Pain, Anxiety And Apprehension

Opioid analgesics (morphine/pethidine), diazepam administered parenterally.

Oxygenation

By O₂ inhalation and assisted respiration, if needed.

Maintenance Of Blood Volume, Tissue Perfusion And Microcirculation

Slow i.v. infusion of saline/low molecular weight dextran (avoid volume overload).

Correction Of Acidosis

Due to lactic acid production—sod. bicarbonate by i.v. infusion.

Prevention And Treatment Of Arrhythmias

Prophylactic i.v. infusion of a β blocker (unless contraindicated) as soon as the MI patient is seen and its continuation orally for a few days has been shown to reduce the incidence of arrhythmias and mortality. β blockers used early in evolving MI can reduce the infarct size (myocardial salvage) and subsequent complications.

Tachyarrhythmias may be treated with lidocaine, procainamide or other antiarrhythmics. Routine prophylactic lidocaine infusion is not recommended now. Bradycardia and heart block may be managed with atropine or electrical pacing.

Pump Failure

The objective is to increase c.o. and/or decrease filling pressure without unduly increasing cardiac work or reducing BP. Drugs used for this purpose are:

(a) Furosemide: indicated if pulmonary wedge pressure is > 20 mm Hg. It decreases cardiac preload.

(b) Vasodilators: venous or combined dilator is selected according to the monitored haemodynamic parameters. Drugs like GTN (i.v.), or nitroprusside have been mainly used (see Ch. No. 40).

(c) Inotropic agents: dopamine or dobutamine (rarely digoxin if AF present) may be needed to augment the pumping action of heart and tide over the crisis.

Prevention Of Thrombus Extension, Embolism, Venous Thrombosis

Aspirin (162–325 mg) should be given for chewing and swallowing as soon as MI is suspected (if not already being taken on a regular basis). This is continued at 80–160 mg/day. Anticoagulants (heparin followed by oral anticoagulants) are used primarily to prevent deep vein thrombosis (risk due to bed rest) and pulmonary/systemic arterial embolism. Its value in checking coronary artery thrombus extension is uncertain. Any benefit is shortterm; anticoagulants are not prescribed on long-term basis now (see Ch. No. 44).

Thrombolysis And Reperfusion

Fibrinolytic agents, i.e. plasminogen activators—streptokinase/urokinase/alteplase to achieve reperfusion of the infarcted area (see Ch. No. 44). Unless thrombolysis can be started within 1–2 hours of MI symptom onset, primary percutaneous coronary intervention (PCI) with stenting is now the preferred revascularization procedure, wherever available.

Prevention Of Remodeling And Subsequent CHF

ACE inhibitors/ARBs are of proven efficacy and afford long-term survival benefit (see Ch. No. 36).

Prevention Of Future Attacks

Platelet inhibitors—aspirin or clopidogrel given on long-term basis are routinely prescribed (see Ch. No. 44).

β blockers—reduce risk of reinfarction, CHF and mortality. All patients not having any contraindication are put on a β blocker for at least 2 years.

Control of hyperlipidaemia—dietary substitution with unsaturated fats, hypolipidemic drugs especially statins (see Ch. No. 45).