Best of heart failure

18 clear reasons, and they are stem. Recently, the advent inhibitor (ARNI) sacubi- rmacologic approach that al endopeptidase enzyme concomitantly blocks the ith valsartan). of ARNI with ACEI to rtality and Morbidity in tudy [ 31 ], a double-blind, patients with Class II–IV tion of 40% or less were itril/valsartan (at a dose of ectively) or enalapril (at a rimary outcome of death rt failure rehospitalization ARNI arm (21.8%) com- 01). Cardiovascular death % CI, 0.71; 0.89)) and risk n by 21% (HR 0.79 (95% lity was reduced by 16% HR 0.84 (95% CI, 0.76; y stopped because of the en compared to ACEI. ere reported in more than study, and these included gh, dizziness, and renal dema was also higher in pared to enalapril (0.5% in the black population). be encountered more fre- double-blind period of by a single-blind run-in ed if they could not toler- I. en tested in CHF patients . These include endothelin agents, and growth hor- terventions that modulate he neprilysin enzyme (in only proven treatment to patients with congestive t in treating patients with bradine, an HCN channel n normal sinus rhythm and or on maximum tolerable was tested in The Systolic inhibitor ivabradine Trial 505 patients with chronic bradine versus placebo on t. Patients had to be in rt rate of more or equal ss or equal 35%, and have N. W. Shammas 458 favorable effect on survival, whereas ICD reduced overall mortality by 23% at 45.5 months mean follow-up [ 132 ]. In addition, the COMPANION [ 131 ] trial showed that ICD therapy can reduce death by 36% ( p = 0.003) in patients with advanced heart failure due to ischemic or nonischemic cardiomyopathy and a QRS ≥ 120 ms when compared to optimal medical therapy. The Multicenter Automatic Defibrillator Implantation Trial II (MADIT-II) randomized 1232 patients with EF ≤ 30% to ICD or conventional medi- cal therapy. Death was the primary endpoint, and the aver- age follow-up was 20 months. The mortality rates were 19.8% in the conventional therapy group and 14.2% in the defibrillator group (hazard ratio for the risk of death in the ICD group was 0.69, p = 0.016) [ 133 ]. A long-term follow- up study from MADIT-II showed that the probability of sur- vival after successful therapy with an ICD for ventricular fibrillation or tachycardia was 80% at 1 year [ 134 ]. The MADIT-II also indicated that benefit from ICD therapy is similar among all the different heart failure subgroups [ 71 ]. Currently the MADIT-CRT is ongoing and is testing whether CRT-D will reduce the risk of mortality in patients with reduced EF ( ≤ 30%) and prolonged QRS ≥ 130 ms and NYH Class I–II [ 135 ]. 24.4.12 Miscellaneous Therapy CHF patients need to be instructed on dietary salt restriction (2 g sodium/day), fluid restriction, daily weight monitoring, smoking cessation, regular exercise, avoidance of alcohol intake, and aggressive treatment of high blood pressure and dyslipidemia. Aggressive treatment of sleep apnea is also indicated [ 136 ]. In general CHF patients need to avoid non- steroidal anti-inflammatory drugs (NSAIDS), most calcium channel blockers, and antiarrhythmic agents. Finally, exer- cise testing and enrolment in an exercise structured program are advised in these patients. 24.4.13 Management of the ACC/AHA Stage D Congestive Heart Failure Patient Acutely decompensated CHF patients with severe left ven- tricular dysfunction require intense pharmacologic and mechanical management. Patients with advanced decompen- sated failure have a poor short-term prognosis. In the Initiation Management Pre-discharge Assessment of Carvedilol Heart Failure (IMPACT-HF) registry [ 137 ], mortality and rehospi- talization rate was 31% at 60-day follow-up. Positive inotropic agents such as dopamine and milrinone might be utilized for palliative reasons because they improve symptoms and increase functional capacity, but they could worsen arrhythmias and possibly increase the risk of mortal- ity [ 138 , 139 ]. In a randomized trial of milrinone versus pla- cebo in 951 patients with decompensated CHF, milrinone caused more sustained hypotension and atrial arrhythmias compared to placebo with no positive impact on mortality [ 140 ]. An analysis from the Acute Decompensated Heart Failure National Registry (ADHERE), a large retrospective registry of patients with acute decompensated CHF, patients who received milrinone and dobutamine had a higher in- hospital mortality than those who received nitroglycerin and nesiritide. Both nesiritide and nitroglycerin had similar in- hospital mortality [ 141 ]. Current ACC/AHA Guidelines consider the use of inter- mittent positive inotropic agents for the management of decompensated heart failure as a Class III indication, indi- cating that their use should be discouraged. Data on IV nesiritide suggest that this drug is effective in lowering wedge pressure and improving patient’s symptoms [ 142 ]. In the Vasodilatation in the Management of Acute CHF (VMAC) trial, 489 inpatients with decompensated CHF were enrolled in a randomized trial of nesiritide versus nitroglycerin or placebo for 3 h followed by nesiritide or nitroglycerin for 24 h. The primary and secondary outcomes of the study are pulmonary capillary wedge pressure (PCWP) at 3 and 24 h, respectively. IV nesiritide was administered as a bolus of 2 μ g/kg followed by continuous infusion of 0.01 μ g/kg/min. At 3 h, dyspnea improved with nesiritide compared with placebo ( p = 0.03), but there was no differ- ence compared to nitroglycerin. At 24 h, the reduction in PCWP was greater in the nesiritide group ( − 8.2 mmHg) than the nitroglycerin group ( − 6.3 mmHg) with a modest improvement in clinical status (VMAC investigators). In VMAC, there was no significant difference between nesirit- ide and nitroglycerin subjects in 6-month mortality. The hemodynamic benefits and safety of nesiritide in patients with acutely decompensated CHF are maintained in patients receiving chronic beta blockers [ 143 ]. In the Prospective Randomized Evaluation of Cardiac EctopywithDobutamine or Natrecor Therapy (PRECEDENT), 255 patients were randomized to dobutamine or nesiritide in N. W. Shammas