Chronic heart failure: an overview of conventional treatment versus novel approaches.
Chronic heart failure (CHF) is a leading cause of hospitalization and is associated with a poor prognosis, although in the past decade substantial progress has been made in understanding the pathophysiology and therapy of CHF with reduced left ventricular (LV) ejection fraction. Use of angiotensin-converting-enzyme inhibitors and angiotensin-receptor antagonists either individually or in combination, certain beta-receptor blockers, and judicious use of aldosterone antagonists, has reduced hospital admission rates and mortality from CHF with reduced LV ejection fraction. More clinical trials are needed, however, particularly in patients with CHF and preserved LV ejection fraction. In patients who remain symptomatic despite medical therapy, and who have long QRS intervals (>0.12 s) and markedly reduced LV ejection fraction, the value of cardiac resynchronization therapy with a biventricular pacemaker has now been demonstrated. Yet, morbidity and mortality remain high, indicating a major need for further improvement. Novel therapies include medical management with statins, vasopressin antagonists, erythropoietin, oxypurinol and levosimendan, which improve vascular and myocardial function and reduce fluid overload, in addition to surgical approaches, which reduce LV remodeling. These routes might not, however, suffice in patients with CHF and LV dysfunction. Prevention of apoptosis and particularly regeneration of cardiac muscle would represent a shift of the current paradigm. Stem-cell-based therapies are rapidly evolving, and while basic science is needed to optimize these strategies, medium-sized clinical studies could help to verify the beneficial effects on LV function. In this review, we discuss current treatment methods and new strategies to improve treatment of CHF.
Landmesser
Ulf
U
Abteilung Kardiologie und Angiologie, Medizinische Hochschule Hannover, Hannover, Germany.
Drexler
Helmut
H
D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D017209:Apoptosis / Q000187:drug effects; D002301:Cardiac Glycosides / Q000627:therapeutic use; D004921:Erythropoietin / Q000627:therapeutic use; D006333:Heart Failure / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D018384:Oxidative Stress; D010138:Pacemaker, Artificial; D013148:Spironolactone / Q000627:therapeutic use; D013318:Stroke Volume; D013777:Tetrazoles / Q000627:therapeutic use; D014633:Valine / Q000031:analogs & derivatives / Q000627:therapeutic use; D000068756:Valsartan; D018487:Ventricular Dysfunction, Left / Q000209:etiology; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
D047228:Angiotensin II Type 1 Receptor Blockers; D002301:Cardiac Glycosides; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000451:Mineralocorticoid Receptor Antagonists; D013777:Tetrazoles; D004921:Erythropoietin; D013148:Spironolactone; D000068756:Valsartan; D014633:Valine