Common genetic variants reported to be associated with BNP levels were not associated with a relevant risk of heart failure in our population-based cohort.
IL-6 concentration in the plasma of <i>TNFα</i> A-allele carriers at months 1 and 12 after CABG was higher in the HF group compared to the non-HF group (1 month after CABG: 5.3 ± 3.4 vs. 3.1 ± 2.9, p<0.05; 12 months after CABG: 4.2 ± 3,9 vs. 1.4 ± 1.2, p<0.01, respectively).
The Prospective comparison of Angiotensin Receptor-neprilysin inhibitor (ARNI) with Angiotensin converting enzyme inhibitor (ACEI) to Determine Impact on Global Mortality and morbidity in Heart Failure (HF) trial (PARADIGM-HF) showed that adding a neprilysin inhibitor (sacubitril) to a renin-angiotensin system blocker (and other standard therapy) reduced morbidity and mortality in ambulatory patients with chronic HF with reduced ejection fraction (HFrEF).
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.
The comparison of prognosis⁻predictivity of a single measurement of plasma NT-pro BNP in different follow-up periods in acute HF patients has been less studied.
Although angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) have been recommended for patients with heart failure, their clinical and prognostic impact in the very acute phase of acute heart failure (AHF) is unclear, mainly because data on their safety and efficacy are lacking.
To investigate the possible effects of telmisartan and losartan on cardiac function in adriamycin (ADR)-induced heart failure in rats, and to explore the changes in plasma level of angiotensin-(1-7)[Ang-(1-7)] and myocardial expression of angiotensin II type 1/2 receptors (AT(1)R / AT(2)R) and Mas receptor caused by the two drugs.
These are the first data to demonstrate that cardiac overexpression of ET-1 is sufficient to cause increased expression of inflammatory cytokines and an inflammatory cardiomyopathy leading to heart failure and death.
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.
We compared the effects of sudden stretch to SFR as well as to twitch and Ca2+ transient characteristics in rat myocardium with monocrotaline-induced heart failure with those in normal rat myocardium without and with inhibition of angiotensin II type-1 (AT1) receptors.
Expression of constitutive NOS isoforms in heart exhibits wide variability in HF patients, but this variability was not related to aetiology, disease severity, concomitant pathologies or drug regimes.
However, increased ACE/ACE2 ratios may induce angiotensin II over-activation and accelerate cardiac remodeling in patients with moderate to severe heart failure.
The observation that ATP2A2rs1860561 gene variant associated with lower risk of life-threatening arrhythmia in HF patients suggests that selected calcium gene variants may modify the risk of SD even within the complex and polygenic pathological condition of HF.
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.