Abstract
Heart failure is a clinically complex syndrome that results due to the failure of the ventricles to function as pump and oxygenate end organs. The repercussions of inadequate perfusion are seen in the form of sympathetic overactivation and third spacing, leading to clinical signs of increased blood pressure, dyspnea, fatigue, palpitations, etc. This article provided a brief overview of the clinical syndrome of heart failure; its epidemiology, risk factors, symptoms, and staging; and the mechanisms involved in disease progression. This article also described several landmark trials in heart failure that tested the efficacy of first-line drugs such as beta-blockers, angiotensin receptor blockers, angiotensin-converting enzyme inhibitors, and the latest drugs in the field of heart failure: angiotensin receptor neprilysin inhibitors. Most studies described in this article were guideline-setting trials that revolutionized the practice of medicine and cardiology.
Highlights
BackgroundHeart failure (HF) is a complex, heterogeneous clinical syndrome that develops due to structural, functional, or physiologic abnormality of the heart, leading to a gradual and progressive failure of the ventricles to fill and to pump blood [1]
The results showed the candesartan group exhibited 33% cardiovascular deaths or hospitalizations vs. 40% in the placebo group, hazard ratio 0.77 [95% CI 0.67-0.89]; p=0.0004
This study explored the benefit of adding angiotensin receptor blockers (ARBs) to the treatment regimen among patients with HF with preserved EF (HFpEF)
Summary
Heart failure (HF) is a complex, heterogeneous clinical syndrome that develops due to structural, functional, or physiologic abnormality of the heart, leading to a gradual and progressive failure of the ventricles to fill and to pump blood [1]. Intricate changes are seen in the serum sodium levels and the extracellular fluid volume composition via the activation of aldosterone, a mineralocorticoid hormone that promotes sodium and water retention, thereby resulting in hypertension, a primary risk factor for potentiating HF [5,14] This physio-pathological pathway has been studied to a great level, including at the molecular level of changes brought about through RAAS on sodium-potassium channels, cardiac calcium regulation, and the influence of RAAS on gene expression, etc. The study's primary outcome measured all-cause mortality, which was found to be 0.072 vs 0.11 per patient-year (risk reduction 0.34; 95% CI 0.19-0.47; p=0.00009), metoprolol subjects compared to placebo subjects respectively. At this time, it was evident that in patients with well-controlled HF, BBs demonstrated excellent efficacy in reducing mortality rates and hospitalizations secondary to HF. Carvedilol (n=1156) or placebo (n=1133) with an initial dose of 3.125 mg taken twice every day for two weeks, which was increased at progressive, two-week intervals unless otherwise required, first to 6.25 mg, to 12.5 mg, and to a target dose of 25 mg twice every day
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