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Rajesh Parikh

Family Physician, Gamdevi, Mumbai.

In recent time, many new drugs have been introduced in the field of cardiology. However their use remains restricted in the hands of a family physician due to inadequate knowledge about their advantages over the already established drugs. Salient features of some frequently used drugs (by a family physician) is given below.


A. ACE Inhibitors

Mechanism of action

They are competitive inhibitors of angiotensin converting enzyme and prevent the conversion of angiotensin I to angiotensin II. Due to this

a. There is arteriolar dilatation which causes fall in systemic vascular resistance, BP and after load.

b. Reduction in aldosterone secretion which increases sodium excretion and potassium retention.

c. Inhibition in bradykinin degradation resulting into increase in level of bradykinin. Bradykinin stimulates vasodilator prostaglandin which has protective effect on the endothelium.


1. Hypertension - in all grades of hypertension but particularly in young and persons with high renin states like:

• Hypertension due to oral contraceptive pills.

• Coarctation of aorta.

• Hypertension with heart failure.

• Hypertensive diabetic patient as they are effective in reducing micro proteinuria as they reduce protein leakage and prolong the life of the nephrons.

2. Heart failure - for amelioration of symptoms specially when used with diuretics and digitalis. The therapy should be started with a smallest dose.

3. Acute myocardial infarction - an indirect anti anginal effect by lessening the after load. In post infarction patient, there is a favourable ventricular remodeling, decrease in the incidence of heart failure and rate of hospitalisation.

4. Aortic regurgitation - to reduce the after load.

5. Diabetic nephropathy.

Contra - indications

1. Bilateral renal artery stenosis or renal artery stenosis in a solitary kidney.

2. Significant aortic stenosis.

3. Hypertrophic and restrictive cardiomyopathy and constrictive pericarditis.

4. Severe renal failure (creatinine > 2.3 mg).

5. Pre-existing neutropenia and hypotension.

6. Pregnancy and lactation.

Adverse effects

1. Hypotension specially in heart failure patient treated along with diuretics.

2. Renal failure when there is a unilateral tight renal artery stenosis.

3. Cough-dry, ticklish, irritating, non productive cough due to increase sensitivity of the cough reflex and increase bradykinin formation.

4. Hyperkalaemia - Either due to renal failure or concomitant use of potassium sparing diuretics or potassium supplements.

5. Loss of taste sensation or metallic and sour taste.

6. Angioedema - due to increased level of bradykinin

7. Rash - pruritic in nature, typically maculo- papular on arms and legs.

8. Oedema of gastrointestinal tract leading to recurrent abdominal pain, distension, vomiting, diarrhoea and ascites.

Special precaution; profound drop in blood pressure during initial dose specially in volume or salt depleted patients.

Drug interaction

Increases lithium and potassium levels.

Hypotensive effect increased by diuretics.

Non steroidal anti-inflammatory drugs may reduce its effect.

Newer drugs in this group are


Advantage over enalapril : 1. Truly once a day anti-hypertensive, 2. Does not undergo hepatic metabolism hence does not change by hepatic dysfunction. Thus specially useful when several agents are being administered as there is no risk of hepatic pharmacokinetic interaction.

Available as 2.5, 5, 10 mg tablets.

Dose; Hypertension : start with 2.5 mg initially and increase to 5-20 mg once daily.

Pharmacokinetics; onset : 2-4 hours. Peak effect : 4-8 hours. Duration; 24-30 hours.


•Available as 1.25, 2.5, 5 mg tablets

Dose : 1.25 mg initially to maximum of 7.5 mg. The dose is reduced in renal dysfunction.

• Pharmaco kinetics : Onset peak effect 6 hours. Duration of action; 24 hours.

Mainly useful in early post-infarct heart failure.


Available as 2.5, 5 and 10 mg tablets

Dose : Heart failure: start with 2.5 mg with close check on blood pressure. With normal BP increase it to 2.5 mg twice daily to maximum of 7.5 - 10 mg. twice daily. Hypertension: usually from 2.5 mg to 10 mg. to maximum of 15 mg. In schedule of 10 mg morning and 5 mg in the evening. Increased dose required in hepatic dysfunction.

Pharmacokinetics: onset: Peak effect : after 5 hours. 1/2 life: 11 hours.


Mechanism of action

Blocks the angiotensin II receptor AT1 which causes effective blockade of renin angiotensin system.

•Available; 25, 50 mg tablets.

Dose; 50-100 mg once daily.


1. Since it blocks at the receptor site more effectively for the control of left ventricular failure and remodelling in post infarction state.

2. No bradykinin mediated side effects like cough and angio-edema.


Absence of beneficial action of bradykinin like renal vasodilation and endothelial protection (mainly important in treatment of heart failure).

B. Alpha Blockers

Mechanism of action

Competitive blockade of vascular post synaptic alpha 1 adrenergic receptors and thereby causing peripheral vasodilation.


Moderate and severe hypertension as an adjuvant therapy in patients with disturbance of blood lipid profile as it may reduce cholesterol. Benign prostatic hypertrophy with obstructive symptoms.

Contra indication

Pregnancy, syncope with nitrates, cardiac failure due to mechanical obstruction.

Adverse effects

First dose syncope - decrease the dose of diuretic before starting. Postural hypotension, dizziness, tachycardia and palpitation. Nausea, diarrhoea, fluid retention.

Rarely acute psychosis or depression.


False positive results may occur in screening test for pheochromocytoma.

Positive anti nuclear antibody (ANA) test.

Since it has substantial hepatic metabolism need for caution in patient with liver disease.

The important drugs in this groups are :


•Available : scored tablets of 1, 2, 5 mg

Dose: start with .5 mg at night if no syncope 12 hours later give. .5-1 mg twice daily for 1 week progressing to three times.

Maintenance: 2 mg three times.

• Pharmacokinetics : 1/2 life 3/4 hours but hypertensive effect lasts for 10 hours. 1/2 life increased in renal failure.


•Available : 1,2,4,8 mg tablets

Dose : 1 mg Daily for 1 week and then 2-4 mg


Mechanism of action

1. Calcium ions play a vital role in the contraction of cardiac, smooth and skeletal muscles and these compounds inhibit entry of calcium into the cells by blocking voltage dependant calcium in myocardium and arteries.


a. No action on sino atrial and atrio ventricular nodes; (nifedipine, amlodipine, felodipine etc.)

b. Additional action on sino atrial and atrio ventricular nodes : (verapamil and diltiazime).

a. Agents with no effect on nodal tissue :



1. Hypertension

2. Ischaemic heart disease : reduces ST-T changes and symptomatic angina.


1. Patients with heart failure or known poor left ventricular contractibility.

2. Significant aortic stenosis as it can lead to pulmonary oedema.

Adverse effects

1. Dizziness, headache and burning sensation

2. Upper gastrointestinal upset and constipation.

3. Depression, psychosis and blurred vision.

4. Arthritis and muscle cramps.

5. Ankle oedema (women > men).

Drug interactions

1. Decreases blood levels of quinidine.

2. Increases hypotensive effects of prazocin.
Available as 2.5, 5, and 10 mg tablets

Dose : Initial dose of 2.5 mg to maximum of 10 mg once daily. Decrease the dose in elderly, peak level; 6-12 hours. 1/2 life 35-50 hours.

b. Agents having effect on nodal tissue:


Pharmacological action

It binds to the alpha 1 sub unit of calcium channel and mainly acts on av node to stop re entry pathway. It decreases sinus rate, decreases myocardial contraction and causes peripheral vasodilation resulting into substantial reduction in myocardial oxygen demand. It thus has a negative inotropic action.


1. Stable angina mainly when beta blockers can not be used

2. Angina due to coronary artery spasm or

3. Unstable angina with beta blockers and nitrates

4. Non Q wave infarct.


1. Bradycardia, hypotension and heart failure.

2. Increased PR interval, 2nd or 3rd degree heart block.

3. Sick sinus syndrome.

4. Pregnancy and lactation.

Adverse effects

1. Headache, dizziness and flushing may occur.

2. Sedation, mania and psychosis.

3. Rash, oedema and constipation.

4. Reversible acute hepatic injury shown by increased liver enzymes.

5. Myopathy with increased creatinine kinase.

6. Acute renal failure.

Drug interactions

Amiodarone : sinus arrest and hypotension

Digoxin : increase in blood levels.

Cimetidine, cycloserine, carbamezapine.

Beta blockers.

•Available as 30, 60, 90, 120 mg tablets and in sustained release form.

Dose : Initially 30-60 mg three times daily before meals. Increasing to a maximum of 240 mg. Slow release preparations require only twice daily administration.

• Pharmacokinetics : Onset : 30 minutes. Peak effect : 1-2 hours 1/2 life: 4 hours hence dosage required 6-8 hours.


Mechanism of action

It lengthens the effective refractory period by prolonging the action potential in the cardiac muscle including accessory pathways. This causes consistent lengthening of QT interval. Decreases sinus, atrial and atrioventricular function and depresses conduction in myocardium and bundle of His-Purkinje fibres. It causes little or no myocardial depression.


Prophylactic control of life threatening ventricular and supraventricular tachyarrhythmia, specially post infarct. Also for prevention of recurrence of paroxysmal atrial fibrillation or flutter. W-P-W syndrome.

Adverse effects

1. Corneal micro deposits of yellow brown granules. It does not affect the vision and is reversible on withdrawal.

2. Skin rash - photosensitivity, permanent greyish blue discolouration.

3. Bradycardia - use with care in sick sinus syndrome.

4. Pulmonary infilteration and fibrosis - monitored by periodic pulmonary function test mainly diffusion capacity. Pneumonia should be suspected if there is progressive shortness of breath or cough.

5. Hyper or hypo thyroidism - monitoring of tri iodo thyronine concentration every 6 months may give early warning of drug related thyrotoxicosis.

6. Gastro intestinal symptoms like anorexia, nausea, abdominal pain and increase in transaminases.

7. Hallucination, proximal muscle weakness, peripheral neuropathy and other neurological symptoms like headache, insomnia, ataxia and tremors.

Drug interaction

It increases plasma digoxin concentration and the action of theophylline and phenytoin, increases in QT interval with quinidine and procainamide, increases prothrombin time and bleeding in patient on warfarin.


Drugs like sotalol, disopyramide, procainamide, tricyclic antidepressants and phenothiazines which increase QT interval should not be combined. Potassium sparing diuretics should also be avoided.

Available : 200 mg tablets, 150 mg ampoules.

Dose : Oral: 200 mg three times a day as a loading dose, reduce by 200 mg every week till maintenance of 200 mg, or less according to the requirement.

Pharmaco kinetics : peak level after 6-8 hours. Large volume of distribution hence loading dose required. 1/2 life:30-100 days.



They are an advance over dinitrate because they eliminate variable hepatic metabolism.

Mechanism of action

1. Bind to nitrate receptors in vascular smooth muscle wall and causes relaxation and dilatation of large coronary arteries and arterioles to redistribute blood flow along collateral channels and from epi to endocardial region.

2. Relieve coronary spasm at epicardial sites.

3. Increases venous capacitance causing pooling of blood in the peripheral veins, decrease venous return and reduces mechanical stress on myocardial wall and oxygen demand. This also results in reduction of pre load.


1. Prevention of angina - due to veno dilatation and relief of coronary vasoconstriction.

2. Congestive cardiac failure due to unloading effects.

Adverse effects

Headache - reduced on repeated administration.

Tachyphylaxis - reduced by giving nitrate free period replacing it with either beta blockers or calcium channel blockers. Transient episodes of giddiness, weakness and other symptoms of cerebral ischaemia due to postural hypotension.

Drug rash and sleep disturbances.

Contra indication

Absolute : Angina caused by hypertrophic obstructive cardio myopathy.

Acute inferior infarct with right ventricular involvement.

Relative : Cor pulmonale with arterial hypoxaemia

Pericarditis and tight mitral stenosis.

Drug interaction

Sulphhydryl containing compounds, propranolol.

Dose : isosorbide-5-mononitrate; 20 mg twice daily 7 hours apart to be swallowed whole.

Imdur : 60-120 mg once daily to maximum of 240 mg.


Mechanism of action

It reverses metabolic consequences of myocardial ischaemia like reduction of intracellular acidosis, myocardial fatty acid metabolism and neutrophil infilteration, (reduces creatinine phosphokinase and protects against oxygen free radical - induced membrane damage. By reducing fatty acid metabolism) it thus stimulates glucose metabolism and protects heart against harmful effects of ischaemia. It also has a direct protective effect in patients undergoing coronary angioplasty.


Symptomatic relief and functional improvement in angina pectoris either singly or as an adjuvant therapy, in those patients not sufficiently controlled by nitrates, beta blockers or calcium antagonist.

Dose : 40-60 mg in 2-3 divided doses with meals.

Caution : Avoid during pregnancy and breast feeding.

Adverse effects

Mild gastrointestinal disorders such as gastric burning, fatigue, dizziness or muscular cramps.


Mechanism of action

It is a K+ channel activator and acts by increasing membrane conduction to K+ ions, which causes arterial and veno dilatation and decreases pre and after load. It thus increases coronary blood flow and increases perfusion of post stenotic regions of myocardium.


In prevention and treatment of angina either as monotherapy or in combination.

Available : 5-10 mg tablets

Dose : 10 mg twice daily and increase according to response, 30 mg as maintenance.

Contra indication

Pregnancy and lactation, cardiogenic shock, left ventricular failure with pulmonary oedema, hypo volaemia and hypotension.

Adverse action

Headache, bradycardia and dizziness, asthenia due to vasodilatation.


Included here because they can really help in prevention of cardiac disease.


Mechanism of action

Competitive inhibition of HMG Co A, a key enzyme in the biosynthesis of cholesterol in hepatocytes and thus lowers cholesterol, LDL and triglycerides. This in turn slows the progression of diffuse and focal coronary atherosclerosis.


Primary non-familial hypercholesterolaemia. It reduces atherosclerotic lesions, occurrence of myocardial infarction and stabilises atheromatous plaque thus reduces risk of mortality, decreases risk in patient undergoing myocardial re-vascularisation. Addition of cholestyramine resin doubles the cholesterol reducing capacity.

Contra indication

Hepatic dysfunction, concomitant use of nicotinic acid or fibrates, cyclosporins and other cytotoxic drugs, erythromycin. Porphyria, women of child bearing age and lactation.

Adverse effects

It increases hepatic transaminases hence monitoring required every 4 months. Myositis with rhabdomyolysis leading to renal damage sp. with cyclorine. Myalgia with or without elevation of CPK enzyme. Headache, constipation, flatulence, dyspepsia, alopecia and pancreatitis.

Drug combinations

Increases level of warfarin and digoxin, avoid with fibrinoids, nicotinic acid, cyclosporin, erythromycin. Synergistic action with cholestyramine LDL-cholesterol level falls faster.

Available : 5, 10, 20 mg tablets.

Dose : Initial dose: 10 mg once daily in the evening before meals and increased to 40 mg. According to serum levels.


    1. Cardiac drug therapy 4th edition by M. Gabriel Khan - Prism India Publication.
    2. Drugs for the heart 4th edition by Lionel H Opie - Prism India Publication.
    3. Adis Drug evaluation Trimetazidine.

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