RECENT STUDIES HAVE DEMONSTRATED THAT ELIMINATING "VPCS" WITH AVAILABLE ANTIARRHYTHMIC DRUGS INCREASES THE RISK OF DEATH TO THE PATIENT WITHOUT PROVIDING ANY MEASURABLE BENEFIT.
Medical Care: Deciding when to treat VPCs is difficult because not all patients with VPCs are at risk of sudden death and treatment is associated with risk. The approach to VPCs depends on the frequency of VPCs, attributable symptoms, the presence or absence of underlying structural heart disease, and the estimated risk of sudden cardiac death.
" Absence of significant structural heart disease (eg, normal ventricular function, no coronary or valvular heart disease)
o Asymptomatic VPCs require no therapy.
o For symptomatic VPCs, recommended treatment usually involves patient education and reassurance, avoidance of aggravating factors (eg, stress, caffeine-containing products), and anxiolytic drugs if education and avoidance of aggravating factors are ineffective. Beta-blockers and nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) can be used to treat symptomatic patients. Beta-blockers with intrinsic sympathomimetic activity may be particularly helpful. The use of antiarrhythmic therapy is not generally recommended and is only used to prevent symptoms. The risk of the drug (including the risk of arrhythmic death from proarrhythmia) must be weighed against the benefits of VPC suppression.
In patients who are symptomatic on Beta-blockers and/or calcium channel blockers, consider cautious use of Amiodarone. The role of newer class III antiarrythmic like dofetilide and azimilide for VPCs is unclear at present.
" Presence of underlying heart disease (eg, VPCs in patients post-MI)
o Various strategies, both invasive and noninvasive, predict prognosis in patients with VPCs post-MI.
o The most powerful combination of noninvasive prognostic variables that identify patients in whom invasive strategies are suitable includes the presence of 2 or more of the following variables, (1) LV EF less than 0.40, (2) ventricular late potentials (on signal-averaged ECG), and (3) repetitive VPCs.
" Supportive management
o Treatment should include limiting transient ischemia.
o Optimal treatment for congestive heart failure (CHF), CAD, or both should be instituted.
o Maintain electrolyte balance.
o Blood pressure control should be obtained because LV hypertrophy is associated with increased VPCs.
Surgical Care: Patients deemed to be at high risk of sudden cardiac death may benefit from implantable cardioverter defibrillator (ICD) implantation.
Diet: Recommendations depend on the underlying cardiac disease; avoidance of caffeine, nicotine, and alcohol may reduce the frequency of VPCs.
DRUG TREATMENT :
Acute management :- Treatment steps for VPC include looking for and correcting the reversible causes (eg, hypoxia, hypokalemia, hypomagnesemia).
Long-term treatment :- The long-term treatment of VPCs is highly controversial. Class I drugs affect fast sodium channels; they are classified into A, B, and C groups according to effects on phase 0 of the action potential, repolarization, and conduction.
Class IA drugs (eg, procainamide, quinidine, disopyramide) are moderately effective but have proarrhythmic effects. Procainamide is associated with a high incidence of allergic reactions, and quinidine is poorly tolerated due to adverse effects.
Class IB drugs (eg, mexiletine) may have less proarrhythmic effect (although one post-MI trial showed higher mortality for mexiletine than placebo) than class I antiarrhythmic drugs. They have a high incidence of adverse noncardiac effects. These drugs may show reasonable efficacy in some patients.
Class IC drugs (eg, flecainide, propafenone) are effective for reducing ventricular ectopy and are relatively well tolerated in patients with normal or minimally reduced LV function and no ischemic heart disease. They are not recommended in patients with ischemic heart disease because of the adverse outcome observed in the Cardiac Arrhythmia Suppression Trial (CAST). In CAST II, moricizine demonstrated neither benefits nor adverse effects long term, but, in the early use of the drug, increased mortality on moricizine occurred.
Class II drugs (beta-blockers) are the drugs of choice in patients who are symptomatic but do not have structural heart disease. Also, class II drugs are considered the first choice of therapy for patients with underlying heart disease, even if their EF is reduced.
Drug of choice in patients with VPC postmyocardial infarction :- Class III drugs (eg, amiodarone, sotalol) are approved for use only in life-threatening arrhythmia. Recent data suggest that amiodarone is safe post-MI for patients with VPCs, even though they do not reduce the risk of death.
Class IV drugs (calcium channel blockers), in general, have no role in the treatment of VPCs. However, occasionally these drugs may suppress triggered automaticity or idiopathic VPCs.
Currently, no evidence supports treatment of asymptomatic VPCs after MI with medication other than beta-blockers. Treatment considerations include symptoms caused by VPC, other prognostic variables (ie, presence or absence and type of structural heart disease, CAD, and LV dysfunction), and adverse effects (specifically proarrhythmic effects of medications).
Clinical trials have suggested that type I antiarrhythmic agents and racemic sotalol increase mortality in patients post-MI. Amiodarone may have no adverse effect on mortality in this setting.
DRUG TREATMENT :
1. ANTIARRHYTHMIC AGENTS :
- METOPROLOL
- AMIODARONE : IF STRUCTURAL HEART DISEASE
- SOTALOL : IF STRUCTURAL HEART DISEASE
- ANXIOLYTICS
CONTRAINDICATIONS :
- CLASS I-C DRUGS ARE CONTRAINDICATED, AND ALL CLASS I DRUGS ARE PROBABLY INADVISABLE IN ISCHAEMIC HEART DISEASE