Traditionally it is thought that sympathoadrenergic system activation is compensatory in heart failure. This is true in acute heart failure. But in chronic heart failure, sympathoadrenergic system becomes counter productive and maladaptive. It increases the afterload and myocardial cell necrosis as well down regulation of beta receptors. This is why betablockers have been considered in the treatment of chronic heart failure. Studies have shown that if you treat 100 patients with heart failure, it will prevent 4 deaths and 4 hospitalisations. Carvedilol, bisoprolol and metoprolol succinate have been shown to improve the survival in heart failure in various studies, but bucindolol failed to do so in the BEST trial. Even though COMET trial showed superiority of carvedilol over metoprolol tartarate, there were several criticisms about the methodology of the trial questioning whether it was a fair comparison. Metoporolol tartarate was a short acting preparation compared to the metoprolol succinate extended release preparation which was shown to be useful in heart failure earlier. Hence the superiority of carvedilolol over metoporlol in heart failure is not yet fully accepted. Betablockers are indicated in all patients with symptomatic heart failure. But they have to be started only only when they are stable and not on inotropic support or intravenous diuretics.

What is the role for devices in heart failure management?

All patients need optimal pharmacological therapy and life style modifications. But in a small subset, there is a definite role for devices. Ventricular tachycardia in a scar of old myocardial infarction may necessitate the implantation of an implantable cardioverter defibrillator (ICD). Hypotensive ventricular tachycardia in heart failure is an important cause for sudden cardiac death (SCD) as it can degenerate into ventricular fibrillation in a short time. Those who have survived a SCD are those at a higher risk of recurrence and benefit maximum with an ICD implantation. ICD improves the life expectancy by 6 years in these high risk individuals.

Intraventricular dyssynchrony in the presence of severe left ventricular dysfunction is an important indication for cardiac resynchronization therapy (CRT). Delay between the contractions of the septum and the lateral left ventricular wall causes reduced left ventricular stroke volume. The important surrogate of ventricular dyssynchrony is an increased QRS duration. In CRT, septum and lateral left ventricular wall contracts simultaneously producing improvement in the left ventricular stroke volume. This is achieved by pacing the lateral wall of the left ventricle through a coronary vein along with right ventricular endocardial pacing. CRT improves the symptomatic status and survival of heart failure patients with left ventricular dyssynchrony. But still there is a 30% non-responder rate of patients who do not respond to CRT.

What is the implication of Starlings law of the heart?

It is the volume of the heart which determines the force of contraction. Increase in muscle fibre length increases the force of contraction upto a certain level. Beyond this level, further increase in the volume of the heart produces deterioration of cardiac output. 2.2 microns is the critical sarcomere length at which there is optimal force of contraction, due to good overlap of actin and myosin filaments.

Heart failure is a clinical syndrome due to abnormal left ventricular function characterized by systemic or pulmonary venous congestion. Heart failure is classified into systolic and diastolic heart failure as follows:

Systolic heart failure: ejection fraction (EF) less than 40%.

Diastolic heart failure: EF > 40%. Normal systolic function has to be documented by echocardiography within 24 hours of onset of symptoms of heart failure. Ideally, elevated filling pressure as a cause of symptoms has to be demonstrated. Diastolic heart failure has a good prognosis.

What is the cardiorenal model of heart failure? 

Renal retention of salt and water resulting in fluid overload, systemic and pulmonary venous congestion is proposed as one of the mechanisms of pathophysiology of heart failure. This pathophysiology can explain the response to diuretics.

What is ventricular remodeling?

Ventricular remodeling is the change in shape and size of left ventricle, usually following myocardial infarction. The two components are infarct expansion and dilatation of the rest of the ventricle.

What is myocardial stunning?

Myocardial stunning is reversible left ventricular function which persists for some time after relief of myocardial ischemia by thrombolysis or revascularization in acute myocardial infarction.

What is myocardial hibernation?

Myocardial hibernation is reversible left ventricular dysfunction which occurs in a chronically ischemic myocardium, which improves after revascularization.