Search

Objective: The aim of this study was to conduct a systematic review and meta-analysis to investigate the effect of the premorbid use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers (ACEI/ARB) on short-term mortality in patients with sepsis.Data Sources: Embase, the Cochrane Central Register of Controlled Trials, and MEDLINE were searched for studies based on the below eligibility criteria. The protocol was registered at the PROSPERO (CRD42022309129).Study Selection: Eligibility criteria were as follows: (1) randomized controlled trials, cohort studies, cross-sectional studies, (2) patients with sepsis aged ≥16 years, and (3) received premorbid ACEI/ARB, or not.Data Extraction: The patient and study characteristics and outcomes were extracted. All analyses were presented with the use of random-effects models. The primary outcome was short-term mortality defined as ≤30-day, in-hospital, or intensive care unit (ICU)- mortality. The secondary outcome was acute kidney injury (AKI).Data Synthesis: Fifteen studies (N = 96,159) met the eligibility criteria. Of these, eleven studies (N = 40,360) reported unadjusted short-term mortalities. The pooled odds ratio (OR) of short-term mortality with the premorbid use of ACEI/ARB was as follows: OR, 0.86; 95% confidence interval (CI), 0.67 to 1.11; P = 0.24, I2 = 88%. Five studies reported an adjusted OR of short-term mortality with the premorbid use of ACEI/ARB as follows: OR, 0.74; 95%CI, 0.59 to 0.93; P < 0.01, I2 = 93%. Seven studies reported the pooled adjusted OR of AKI with the premorbid use of ACEI/ARB as follows: OR: 1.57, 95%CI: 1.26-1.96, p < 0.01, I2 = 69%.Conclusion: In this meta-analysis, the premorbid ACEI/ARB was associated with significantly lower short-term mortality in patients with sepsis despite the significantly higher risk of AKI. [ABSTRACT FROM AUTHOR]

Angiotensin-converting enzyme inhibitors (ACEi) and angiotensin-receptor blockers (ARB) have shown antiarrhythmic effects that are useful as part of the upstream therapy for atrial fibrillation (AF), both for primary and secondary prevention. Nevertheless, the potential prognosis value of these drugs in terms of mortality and major cardiovascular events is unclear, especially in older population with AF. Scientific evidence is scarce in this population and shows contradictory results. The aim of this study was to assess the potential benefit of ACEi and ARB in terms of mortality and major cardiovascular outcomes (hospitalization for heart failure, acute myocardial infarction and stroke) in older patients with AF, based on a real-world data analysis. Observational: analysis of a retrospective registry. The study included 9365 patients of 75 years or older diagnosed with AF, from CardioCHUVI-AF_75 registry: ClinicalTrials.gov Identifier: NCT04364516. Date of registration: November 26, 2018. We performed propensity score matching techniques to obtain 2 comparable groups of 3601 patients with and without ACEi or ARB treatment. We compared survival and cardiovascular outcomes in both groups of patients using Cox proportional hazards models. We did not find significant differences in terms of survival between using or not using ACEi or ARB for the older population (hazard ratio for mortality: 0.959, 95% confidence interval 0.872–1.054). There were no significant differences regarding cardiovascular major events between the 2 groups. Treatment with ACEi or ARB did not improve outcomes in terms of survival and cardiovascular events in older patients with AF. These results should prompt the conduct of randomized clinical trials specifically in the older AF patient population to robustly address this issue. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this prospective, randomized study was to evaluate the effects of telmisartan, compared with the calcium-channel blocker amlodipine, on endothelial function after coronary drug-eluting stent (DES) implantation in hypertensive patients. Background: DES implantation impairs local endothelial function, which may be associated with future cardiovascular events. Telmisartan, which has unique peroxisome proliferator-activated-receptor-gamma–mediated effects in addition to its renin-angiotensin system–inhibition effects, has favorable effects on endothelial function. Methods: Fifty-one hypertensive patients with coronary artery stenosis but without coronary artery spasm, treated with a sirolimus-eluting stent, were randomly assigned to either the telmisartan (25 cases) or amlodipine (26 cases) treatment groups. At baseline and at 3 months after DES implantation, endothelium-dependent and -independent vasomotion were evaluated by quantitative coronary angiography under the condition of medication withdrawal. The mean luminal diameter of a 20-mm coronary segment, beginning 5 mm distal to the stent, was measured before and after infusion of intracoronary acetylcholine (10−7, 10−6 mol/l) and then again after infusion of nitroglycerin. Results: Blood pressure was comparable between groups at baseline and after 3 months. Vasoconstriction after acetylcholine infusion at 3 months (impaired endothelial function) was less pronounced in the telmisartan group than in the amlodipine group (p < 0.0001), although there was no significant difference between the 2 groups before DES implantation. The response to nitroglycerin did not differ between groups before or at 3 months after DES implantation. Conclusions: Telmisartan, compared with amlodipine, significantly ameliorated endothelial dysfunction after DES implantation in terms of vasoconstriction induced by acetylcholine. [Copyright &y& Elsevier]

Abstract: Background: Myocardial fibrosis and dysfunction can be detected in the early phases of organ damage associated with hypertension. Valsartan, an angiotensin-II receptor blocker, is efficacious in lowering blood pressure (BP) and reducing left ventricular mass in patients with hypertension. Levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and procollagen type I carboxy-terminal propeptide (PICP) are correlated with organ damage in patients with overt congestive heart failure; however, few data are available in patients with hypertension. Objective: The aim of this study was to assess the effects of 12 months of valsartan treatment on echocardiographic measures and indices of organ damage (NT-proBNP and PICP) in newly diagnosed patients with hypertension. Methods: This was a prospective, open-label, single-center, exploratory study. Patients with newly diagnosed, previously untreated hypertension were treated for 12 months with valsartan 160 mg/d and compared with an equal number of healthy, untreated control subjects. Baseline and follow-up visits at 3, 6, and 12 months included physical examination, systolic BP (SBP) and diastolic BP (DBP) measurements, ECG, echocardiography, and NT-proBNP and PICP determination. Results: A total of 20 patients (mean [SD] age, 48.05 [7.29] years) were enrolled and compared with 20 healthy controls (age, 49-6 [6.95] years). Compared with baseline, valsartan was associated with reduced BP in the group with hypertension after 12 months of treatment (mean SBP, 150.05 [11.15] vs 120.00 [8.43] mm Hg, P < 0.001; DBP, 97.80 [8.36] vs 79-50 [4.26] mm Hg, P < 0.001). Compared with the control group, at baseline, the group with hypertension had significantly higher mean left ventricular mass index (LVMI) (119.88 [22.86] vs 87.31 [15.77] g/m2; P < 0.001), relative wall thickness (thickness/radius [h/r] ratio: 0.45 [0.08] vs 0.35 [0.07]; P = 0.001), and NT-proBNP (50.00 [32.01] vs 25.47 [9.69] pg/dL; P = 0.002). PICP was higher, but the difference was not statistically significant (46.10 [15.69] vs 37.50 [7.20] μg/L). After 12 months, treatment with valsartan was associated with significant reductions in all measured parameters compared with baseline (LVMI, 106.51 [17.12] g/m2, P = 0.004; h/r, 0.41 [0.07], P = 0.026; NT-proBNP, 22.55 [13.52] pg/dL, P = 0.001; PICP, 35.20 [9–19] μg/L, P < 0.008). At 12 months, patients with hypertension treated with valsartan achieved NT-proBNP and PICP levels not statistically different from those of the healthy controls (NT-proBNP, 22.55 [13–52] vs 25.24 [8.43] pg/dL; PICP, 35.20 [9.19] vs 36.90 [6.41] μg/L). Conclusion: Patients treated with valsartan for 12 months had significant reductions in BP, LVMI, and indices of subclinical organ damage (NT-proBNP and PICP) compared with baseline. [Copyright &y& Elsevier]

Abstract: Background:: The Losartan Intervention For Endpoint reduction (LIFE) study was a randomized, doubleblind trial that compared the effects of losartan-based treatment with those of atenolol-based treatment on cardiovascular disease (CVD)-related morbidity and mortality in 9193 patients with hypertension and left-ventricular hypertrophy (LVH). Compared with atenolol, losartan reduced the combined risk for CVD-related morbidity and mortality by 13% (P = 0.021), and reduced the risk for stroke by 25% (P = 0.001), with comparable blood pressure control in both trial arms. Objective:: The aim of this study was to analyze the cost-effectiveness of losartan compared with atenolol in the treatment of stroke from the Dutch health care perspective. Methods:: Utilization of losartan and atenolol within the trial period (mean, 4.8 years) and an estimation of direct medical costs of stroke for The Netherlands were combined with estimates of reduction in life expectancy through stroke. Medication costs and stroke incidence during 5.5 years of patient follow-up were estimated separately, adjusted for the baseline degree of LVH and Framingham risk score. To estimate lifetime stroke costs, the cumulative incidence of stroke was multiplied by the lifetime direct medical costs attributable to stroke. All costs are in 2006 Dutch prices and discounted following the former (4% costs and effects) and new Dutch guideline (4% costs, 1.5% effects) for conducting pharmacoeconomic analyses. Results:: With 4% discounting, prevention of stroke was associated with a gain of 3.7 life-years. As a consequence, losartan treatment was associated with 0.059 life-year gained (LYG) per patient treated with losartan. Losartan reduced stroke-related costs by 1076 (US $1349) per patient. After inclusion of study medication cost, net cost per patient was 51 ($64) higher for losartan than atenolol. The net cost per LYG was 864 ($1083), which is below the Dutch pharmacoeconomic threshold of 20,000/LYG (−$25,000/LYG) for accepting interventions. The corresponding probability of a cost-effectiveness ratio below this Dutch threshold was 0.95. Discounting money and health following the new Dutch guideline resulted in an even more favorable cost-effectiveness for losartan. Conclusions:: Results from the present analysis suggest that, in The Netherlands, treatment with losartan compared with atenolol may well be a cost-effective intervention based on the reduced risk for stroke observed in the LIFE trial. [Copyright &y& Elsevier]