The relatively low efficacy of ACE-inhibitors in the treatment of heart failure in women after estrogen loss may be due to their inability to reach the intracellular sites at which angiotensin (Ang) II is generated and/or the existence of cell-specific mechanisms in which ACE is not the essential processing pathway for Ang II formation.
Whereas the results are not conclusive, there may be a significant interaction between ACE genotype and response to ACE inhibitors in patients with heart failure.
One half of patients with HF had been prescribed angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and 39% evidence-based β-blockers.
Prescription of recommended HF drugs was low: 42.6% (629) used Angiotensin Converting Enzyme Inhibitors (ACEI) or Angiotensin Receptor Blockers (ARBs), 48.0% (709) β-blockers, and 21.9% (324) ACEI or ARB with β-blockers, even in reduced LVEF.
Prophylactic ACE inhibitor does not attenuate development of LV dysfunction or heart failure in patients receiving anthracycline chemotherapy ± trastuzumab.
Recently, the addition of neprilysin inhibition to angiotensin receptor blockade has been shown to be even more effective than angiotensin-converting enzyme inhibition alone in heart failure with reduced ejection fraction, marking an important new milestone in heart failure treatment.
The great variety of cardiovascular effects mediated by these vasoactive peptides and the efficacy of ACE inhibitors in the treatment of hypertension and heart failure emphasize the prominent role of ACE in the cardiovascular system.
The PARADIGM-HF (Prospective Comparison of ARNI With an ACE-Inhibitor to Determine Impact on Global Mortality and Morbidity in Heart Failure) trial randomly assigned 8399 patients with chronic HF, New York Heart Association class II to IV symptoms, and a left ventricular EF of 40% or less to treatment with enalapril 10 mg twice daily or sacubitril/valsartan 97/103 mg twice daily (previously known as LCZ696 [200 mg twice daily]) in addition to guideline-directed medical therapy.
Angiotensin-converting enzyme inhibitors were more protective in the advancement and/or hospitalization of the hypertensive patient for heart failure than angiotensin receptor blockers.
The target of the current study was to examine the possible cardioprotective effect of telmisartan (Tel), an angiotensin II type 1 receptor (AT1R) blocker, compared with that of captopril (Cap), an angiotensin converting enzyme (ACE) inhibitor, in ameliorating PRG-induced HF in rats by assessing morphometric, echocardiographic and histopathological parameters.
Several polymorphisms that have supporting molecular and clinical data in the heart failure literature are reviewed, among them the beta1-adrenergic receptor variant Arg389Gly and the angiotensin converting enzyme gene insertion/deletion polymorphism.
Although the first-in-class ARNi sacubitril/valsartan (LCZ696) reduced mortality and morbidity in heart failure (HF) with reduced ejection fraction (EF) compared to angiotensin converting enzyme inhibitor (ACEi), mechanistic data on ARNi are scarce.
Using the 2008-2012 IBM MarketScan Commercial database, we followed 26,439 individuals aged 18-64 years with newly diagnosed HF and calculated their adherence (using the proportion of days covered (PDC) algorithm) to the five guideline-recommended medication categories: angiotensin-converting enzyme inhibitors/angiotensin-receptor blockers; beta blockers; aldosterone receptor antagonists; hydralazine; and isosorbide dinitrate.
Multivariate analysis revealed that several variables (including gender, hypertension, renal dysfunction, TIMI flow grade post-PCI < 3, and treatment administered after PCI with betablockers and angiotensin-converting enzyme inhibitors) had per se a significant influence on the occurrence of [death or hospitalization for heart failure] at 1 year.
At discharge, women less frequently received ACE inhibitors (189 [81.1%] vs. 702 [85.8%], p=0.045) and presented more major adverse events (death, bleeding, infection, myocardial infarction, stent thrombosis or heart failure) during the first month after discharge (10.5% vs. 4.5%, p<0.001) and higher long-term mortality (hazard ratio [HR] 1.6, 95% CI 1.1-2.2).
Most estimates revealed no effectiveness differences between classes; however, thiazide or thiazide-like diuretics showed better primary effectiveness than angiotensin-converting enzyme inhibitors: acute myocardial infarction (HR 0·84, 95% CI 0·75-0·95), hospitalisation for heart failure (0·83, 0·74-0·95), and stroke (0·83, 0·74-0·95) risk while on initial treatment.
There is currently no consensus on the effect of treatment with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), on the prognosis of patients with heart failure and preserved ejection fraction (HFpEF).
Angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blockers (ARB) were administered in 68.9% of HF discharged patients, beta-blockers in 84.8%, mineralocorticoid receptor antagonist (MRA) in 57.9%, diuretics in 85.9%, and digoxin in 23%.
Angiotensin-converting enzyme (ACE) inhibitors (ACEis) are beneficial in patients with heart failure, yet their role after heart transplantation (HTx) remains ambiguous.
The HF pharmacogenetic literature is still in its very early stages, but there are promising candidate genetic variants that may identify which HF patients are most likely to benefit from beta-blockers and ACE inhibitors and patients that may require additional therapies.
ACE inhibitors are recognised as being highly effective therapy for hypertension and cardiac insufficiency, and have a more beneficial effect on survival rate than expected on the basis of known mechanisms of action.
A 445-patient subset received at least 1 GDMT (angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, or beta-blocker) at baseline; these patients had 33% lower HF hospitalization rates (HR: 0.67; 95% CI: 0.54 to 0.82; p = 0.0002) and 47% lower mortality (HR: 0.63; 95% CI: 0.41 to 0.96, p = 0.0293) than controls.