Here is a list of sixteen drugs that are mostly used for curing heart diseases.
Drug # 1. Oxyfedrine:
This drug increases coronary micro-circulation, reduces the oxygen demand of the heart, improves left ventricular function, normalises availability and utilisation of energy. It is contraindicated in aortic regurgitation, aortic stenosis and pregnancy. It can produce temporary loss of taste.
Dose:
Available in tablet, oral drops and injection forms, Tablets 8 mg.-2 tab. thrice daily before food.
Drops:
10 mg. per ml. acts more quickly given sublingually (10 ml. vials.)
Injection:
4 mg. per 2 ml; 2 ml. amp should be given in a drip in post M.I. states.
Recently doubts have been expressed whether it is that effective.
Drug # 2. Phenylamine Lactate:
This drug dampens excessive sympathetic drive, has calcium transport inhibiting property, mild central sedative action and a mild coronary vasodilatation. Because of its first property (dampening excessive sympathetic drive) it is particularly useful in patients who face many stress situations in their everyday life and are hyper-reactors.
This drug should always be used with another coronary dilator e.g. nitrates. It is contraindicated in the presence of conduction defects, in the presence of C.C.F., liver and kidney disease.
Dose:
Dragees 60 mg. given two or three times a day. Rarely higher dose of 120 mg. tds may be necessary, to be reduced to two or three tablets daily.
Drug # 3. Nefidipine:
This is a dihydropyridine derivative which acts in angina pectoris by its calcium-entry-blocking effect to myocardial tissue.
Dose:
5 mg. x TDS upto 20 mg. TDS. To enhance effect it can be given sublingual by breaking the capsule in the mouth.
Adverse Effects:
Headache (usually passes off gradually after some time), dizziness, hypotension, tachycardia, fatigue, oedema, or allergic rash.
Drug # 4. Dipyridamole:
The drug increases coronary blood flow by reducing coronary vascular resistance. In recent years it has been found that increased adhesiveness of platelets and increase in the viscosity of blood play significant role in the pathogenesis of I.H.D. Dypyridamole reduces platelet adhesiveness and is very useful in the long-term treatment of angina pectoris, diabetes with I.H.D. and hypercholesteremia. It is also given in combination with aspirin.
Dose:
Available in 25 mg. and 100 mg. tablets. 30-300 mg. daily before food.
Side-Effects:
Bradycardia, hypotension, heart block, constipation and C.C.F.
Drug # 5. SuIphin-Pyrazone:
Attention to this drug was first drawn in 1965 when investigators observed that patients being treated for gout had fewer heart attacks than the general population.
The trials were started in 1975 in big hospitals in U.S.A. and Canada. In 1978 it was confirmed that sulphin-pyrazone indeed prevents further attacks and has a very significant role to play l, prevention of sudden death in the first year after an attack of ML It is contraindicated in peptic ulcer, in patients who are on salicylate therapy and in aspinn-induced asthma.
Dose:
One capsule (200 mg) four times a day.
Available in strips of 10 tablets and bottle containing 50 tablets.
Treatment of variant angina or Prinzmetal’s angina:
(Coronary Spasm)
In recent years considerable interest has been drawn on this subject. The condition was first described by Prinzmetal in 1957.
These patients have the following characteristics:
(1) The pain occurs at rest – may disappear on exercise.
(2) Nitrates may not relieve the pain as it always does in classic angina
(3) There is ST elevation in ECG during the attack instead of depression. The ECG may be normal.
(4) Risk of sudden death is more if the spasm occurs in right coronary artery (sinus node artery).
Drug # 6. Sinus Tachycardia:
It is a very common condition. There are many causes: physiological, cardiac and extracardiac. It occurs in connection with heart disease in (a) Cardiac failure, (b) Rheumatic fever and rheumatic heart disease, (c) Subacute bacterial endocarditis and (d) Myocardial Infarction.
Drugs used in sinus tachycardia are:
(i) Digoxin:
Initial dose is 0.25 mg. TDS or B.D.
(ii) B – Blockers; Propranolol:
80 to 240 mg daily orally, in divided doses. It is contraindicated in cardiac failure and dysrhythmias arising in the atrium.
Atrial Premature Beats:
(Atrial Ectopic Beats)
It arises from the discharge of an ectopic focus anywhere in right or left atrium for no apparent reason. Occasionally they are produced in anoxia and low serum potassium.
The importance of atrial ectopics is that, they are very often a prelude to persistent dysrythmias e.g. atrial flutter and fibrillation.
Treatment:
No specific treatment required except correction of electrolyte disturbance and anoxia.
Drug # 7. Physical Maneuvers:
The attack in many cases can be terminated by pressure on carotid sinus which lies at the level of upper border of thyroid cartilage or by soft pressure on eyeball, drinking ice cold water, putting the head between the knees and Valsalva maneuver (forcible expiration against a closed glottis). The author prefers massaging the carotid sinus as in his experience it has been almost always successful. Sometimes patients learn how to terminate the attack. If the above methods fail, drug treatment is required.
The following drugs are useful:
(1) Digoxin is still the drug of choice — 0.5 mg 8 hourly by mouth or 1 mg I.V. in 10 ml dextrose solution. For obvious reasons digoxin is contraindicated in digitalis toxicity.
(2) β-Blockers — Propranolol can be given.
Dose of propranolol: 10 mg I. V. is most effective. It can also be given orally 80 mg initially, followed by 40 mg 8 hourly.
(3) Verapamil — is also useful, especially in tachycardias where there is preexcitation phenomenon, l.V. ampoules are available in 2 ml containing 5 mg of verapamil can be given as an l.V. drip – 5-10 mg hourly.
40 mg tablets are available, dose same as Propranolol.
Caution — Should not be given along with β – blockers.
All these three drugs mentioned above reduce the ventricular rate, but the atrial arrhythmia continues. The atrial arrhythmia can be converted to sinus rhythm by
(a) Quinidine: 5-10 mg daily.
(b) Disopyramide: 200 – 300 mg daily
(c) β- Blockers.
In refractory cases, D-C counter-shock should be given before which all the drugs must be withdrawn for at least twenty-four hours, otherwise there is danger of precipitating fatal ventricular fibrillation.
Paroxysmal Atrial Tachycardia with 2: 1 AV Block (PATB). This condition most often is precipitated by digitalis intoxication and is aggravated by low potassium.
Treatment:
The drug of choice is propranolol I.V. or orally, (dose mentioned before) and supplement of potassium. D. C. counter—shock is absolutely contraindicated.
Drug # 8. Atrial Flutter:
This dysrhythmia is due to atria discharging in a coordinated manner at rate of about 250-350 per minute. There is varying degree of A.V. block from 1: 1 to 4: 1. If the ventricular rate is rapid the patient gets symptoms. The danger of this condition is that, if ventricles beat 1: 1 ratio there is severe haemodynamic impairment.
(i) Carotid sinus pressure may abruptly change 1: 1 to 2: 1, 3: 1 or even 4: 1 AV block and bring down the ventricular rate.
(ii) D.C. counter-shock is very effective, low energy 50W/second is required. No anaesthetic is required, 10 mg of I.V. diazepam will be sufficient.
(iii) Digoxin — I.V. route or oral route.
(iv) Propranolol — I.V. or oral route.
(v) Disopyramide: Available in 100 mg and 150 mg tablets
Dose – 200 to 300 mg daily.
Long-Term Treatment of Atrial Flutters:
Atrial flutter is on exasperating dysrhythmia as it has a strong tendency to recur, particularly after closure of atrial septal defect. The following drugs are recommended for long-term treatment.
(a) Disopyramide — Loading dose 300 mg later W0 to 200 mg X six hourly.
(b) Quinidine sulphate available in 200 mg tablets, 200 mg three times a day. Quinidine phenyl ethyl barbiturate — 100 mg tab. three times a day can be given.
(c) Digoxin is also useful but quinidine is preferable. Digoxin in post-operation Atrial Flutter.
Drug # 9. Procainamide (Class IA):
Action:
Procainamide resembles quinidine but QT prolongation is less. It may be used intravenously.
Rapid renal elimination occurs (half-life 3.5 hrs.). Effective blood level is 4-10 µg/ML. Plasma metabolisms – acetylation converts it to N-acetyl procainamide (half-life 6-8 hrs.).
Use:
Effective is prevention of ventricular arrhythmias early after myocardial infarction. It is often effective when lidocaine fails.
Contra-Indication:
Shock, heart failure, myasthenia gravis, renal failure and heart block.
Side Effects:
1. Fall of BP when used by IV route
2. Heart block
3. Vagolytic effect — may exaggerate post occlusion ventricular-arrhythmias. It is can worsen myasthenia gravis.
4. Rash, fever, arthralgia, lupus like syndrome, and agranulocytosis.
Drug # 10. Newer Antiarrhythmic Agents:
Disopyramide (Class IA) — It is a quinidine like drug.
Action:
Like quinidine. Potent anticholinergic and negative inotropic action; increases peripheral resistance. Increases refractoriness of accessory AV Pathways.
Indications:
1. As quinidine. Controls ventricular tachyarrhythmias.
2. Reduces recurrence of arrhythmia after D.C. cardioversion.
3. Effective against atrial arrhythmias complicating WPW syndrome as it depresses conduction via bundle of Kent. It is less effective against other atrial arrhythmias.
4. Arrhythmias complicating mitral valve prolapse.
It is not metabolised in liver.
Half-life 8 hrs but prolonged in renal failure, and acute myocardial infarction. Blood level 2—6 mg.ml (Toxic over mg/ml)
Dosage:
Intravenously — 2mg/kg/5min (Max. 150 mg— upto 300 mg/1st hour).
Then 0.4 mg/kg
Oral – 300 mg loading dose – then 100-200 mg 6 hourly.
Side Effects:
Hypotension, heart failure, tachycardia (Torsades de Pointes). Sinus node depression, coronary vaso-constriction, QRS widening and anti-cholinergic effects. Avoid loading dose if there is cardiomegaly.
Drug # 11. Aprindine (Class 1B):
Use:
Against VPC and VT (specially digitalis toxicity). Effective in SVT, WPW Syndrome, drug resistant ventricular arrhythmias associated with mitral valve prolapse. Prevents recurrence of AF.
Pharmacokinetics:
Blood level 1 to 3 mg/L Metabolised in liver.
Toxicity:
Polymorphic VT can occur. It has negative inotropic properties. Other adverse effects include tremor, nervousness, dizziness, ataxia, seizure, psychosis, agranulocytosis, cholestatic jaundice.
Dosage:
Intravenously 150-250 mg/5 min. total 750 mg/3 hrs. followed by 0.5—1.0 mg/min. or divided doses).
Drug # 12. Encainide (Class 1C):
Action:
Reduces conduction velocity in specialised tissue. Increases AV conduction time and QRS duration. No effect on action potential duration or refractoriness. Effective against experimental atrial arrhythmias, sometimes VPC and recurrent VT. Therapeutic plasma concentration 1-56 ng/ml. Toxic level – 135-570 ng/ml.
Toxicity:
May cause or aggravate polymorphic VT (not necessarily with prolonged QT interval).
Side effects:
Ataxia, diplopia, dizziness, tremor, headache.
Drug # 13. Flecainide Acetate (Class 1C):
Action – Slow and conduction increases refractoriness in slow and fast response tissues. Effects — Suppresses VPC and non-sustained VT.
Therapeutic Plasma Level:
0.3 to 1.4 mg/L.
Administration:
I.V. loading dose 1 mg/kg body wt./5 min. Additional boluses 0.5 mg/kg every 30 min. Total dose – 2.0 mg/kg.
Oral dose – 200-600 mg/day – given in two divided doses.
Toxicity:
Blurred vision, abnormal taste, flushing, tinnitus, sleepiness, paresthesias, increased serum alkaline phosphatase.
Drug # 14. Beta Adrenergic Receptor Antagonists (Class II):
Propranolol:
Competitively blocks effects of catecholamines on the heart. Indirectly reduces slow inward current that contributes to action potential. Exerts direct membrane stabilising effect in high dose.
Anti-Arrhythmic Effects:
Propranolol is effective against
1. Atrial tachyarrhythmias
2. AV nodal reentrant tachycardia
3. AV reentrant tachycardia using accessory AV pathway
4. Ventricular premature beats
5. Exercise provoked ventricular tachycardia
6. Torsades de Pointes (with prolonged QT)
7. Arrhythmias of digitalis toxicity
8. Reduces risk of sudden death in first year after acute myocardial infarction.
Dosage:
Inravenously 0.1 to 0.2 mg/kg body wt. given @ 1-2 mg every 3-5 min. Oral administration — 40 mg to 1 gm — daily in 2 to 4 divided doses.
Toxicity:
CVS — negative inotropy, sinus bradycardia, AV nodal block; circulatory collapse, peripheral vasospasm Extracardiac effects — nausea, vomiting, bronchospasm, diarrhoea, fatigue, insomnia, nightmares, impotence.
Precaution:
Avoid its use in diabetes unless there is an overriding indication.
Newer:
Adrenergic receptor antagonists
Selective β Blockers:
Metoprolol, Atenolol, Acebutol
Less Lipophilic β Blockers:
Atenolol, Nadolol, Timolol
Drug # 15. Amiodarone (Class III):
Action:
1. Increases ERP by prolonged action potential duration
2. Coronary and peripheral vasodilator
3. Calcium channel antagonist.
Uses:
1. Atrial flutter-fibrillation in WPW syndrome
2. Life threatening ventricular tachyarrhythmias. Recurrent cardiac arrest.
3. Paroxysmal atrial fibrillation or flutter. Paroxysmal supraventricular tachycardia
4. Maintains sinus rhythm after cardioversion of atrial fibrillation
5. AV nodal reentrant tachycardia
6. AV reentrant tachycardia using accessory AV pathway.
Pharmacokinetics:
Half-life — 15 to 105 days.
A loading dose is required — peak effect: may take weeks. Contains iodine; inhibits conversion of T4 to T3. Not excreted by kidneys.
Dosage:
Intravenous 5 mg/Kg/5 min. then infusion @ 25 mg/hr. Oral — Loading dose 1200 — 1600 mg daily for 7—14 days. Maintenance dose 200-800 mg once daily.
Contraindication:
SA block, AV block.
Drug Interaction:
Digoxin, quinidine, procaine amide (increased blood level), coumarin (bleeding tendency).
Side-Effects:
Corneal microdeposits (whorl-like pigmentation, cornea verticillata), halovi- sion, photo-sensitivity, slate-gray or bluish skin discolouration, proximal muscle, weakness, peripheral neuropathy tremor, impaired memory, insomnia, pulmonary infiltrates, hyper or hypothyroidism. Torsades de pointes, VF, hypotension, constipation, nausea, vomiting.
Drug # 16. Bretylium Tosylate (Class III)
Action and indication:
1. VF refractory to lidocaine and multiple D.C. shocks
2. Resistant ventricular arrhythmias (may take 20-40 minutes)
3. Causes hypotension
4. Adrenergic neurone blocking properties.
Pharmacokinetics:
No liver metabolism. Half-life 7.5 hours
Toxicity:
Nausea, vomiting, parotid pain, postural hypotension, worsening of arrhythmia.
Contra-Indication:
Digitalis toxicity.
Dose:
Intravenous 5 to 10 mg/kg. D.C. shock may be applied if required.
Maintenance dose 5 -10 mg/kg IV every 6 to 8 hours or infusion @ 1-2 mg/min.