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.
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).
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