PHARMACOLOGICAL MANAGEMENT OF HEART FAILURE

Pharmacological Management of Heart Failure using Digoxin

Pharmacological Management of Heart Failure

Abstract

Congestive heart failure is a progressive disease with significant morbidity and mortality. Despite advances in the avoidance and treatment of cardiovascular diseases, the incidence and prevalence of congestive heart failure have increased in latest years. Contributing factors encompass increased survival in patients with coronary artery disease (especially myocardial infarction), an aging population and significant advances in the command of other potentially lethal diseases. New and existing agents, encompassing angiotensin-converting enzyme inhibitors, beta blockers and, more lately, spironolactone, are being used increasingly to extend life in patients with heart failure. Although digoxin has been used to treat heart failure for more than 200 years, its function in patients with congestive heart failure and sinus tempo is still debatable. Over the past decade, digoxin has obtained improved attention because of acknowledgement of its neurohormonal result and the successful use of smaller dosages. In latest trials, digoxin has been shown to decrease morbidity associated with congestive heart failure but to have no demonstrable result on survival. The goal of digoxin therapy in patients with congestive heart failure is to advance quality of life by decreasing symptoms and stopping hospitalizations.

Medical Review

Congestive heart failure has been identified as a syndrome of anatomic, functional and biologic alterations that interact simultaneously in a convoluted manner over a extended period. Initially, this syndrome was examined predominantly as a difficulty of salt and water keeping caused by abnormalities of renal body-fluid flow. Over time, although, physicians began to identify that congestive heart failure was associated with decreased cardiac yield and excessive peripheral vasoconstriction. Recognition of this association supplied the rationale for the use of inotropic agents and intravenously administered vasodilators to advance cardiac output.

Despite these therapeutic developments, it became apparent that at some issue, congestive heart failure would progress unaligned of the patient's hemodynamic status. Thus, the neurohormonal form evolved. According to this form, heart failure progresses as a result of overexpression of biologically active molecules that use harmful effects on the heart and circulation.(Grauer, 2007)

 

Discussion

Following an initial catalogue happening that results in a down turn of ventricular contractility, most patients remain asymptomatic or minimally symptomatic for some time. The initial happening may be abrupt, such as a myocardial infarction, or it may have a gradual onset, as in the case of hypertension or capacity overload.(Hardman, 2004) The catalogue happening may also be a hereditary status such as a genetic cardiomyopathy.

Many compensatory mechanisms, encompassing the sympathetic nervous system and salt- and water-retaining systems, become activated in the setting of a depressed cardiac output. The compensatory systems can maintain left ventricular function for days to months.(Grauer, 2007) However, when patients become openly symptomatic, they start to know-how a striking increase in morbidity and mortality. The transition to symptomatic heart failure is accompanied by farther activation of the neurohormonal system, encompassing the sympathetic nervous system and a series of adaptive changes in the myocardium, collectively mentioned to as "left ventricular ...