ResultSeven trial, sixof them was randomized clinical trial ,one cohort study. That enrolled 960participants were included in the present systematic review, the mean durationof follow-up of 9.1+_3.
0 months. The Characteristics of the included studiesare summarized in Table , Spironolactone was used in five of the included trials, whereas eplerenone wasused in 2 studies ,3 studies were conducted in a double-blind fashion comparingspironolactone against placebo , onestudy was conducted in a double-blind comparingeplerenone against placebo . All 7 studies included baseline and follow-upechocardiographic examination of study participants. Spironolactone in patients with HFpEF Spironolactone was used in five of the included trials, whereas eplerenone wasused in 2 studies ,3 studies were conducted in a double-blind fashion comparingspironolactone against placebo , 1 A perfect adherence was notified in both groups, high K level anddecrease resting BP were Couse the full dose not to be taken in 10% of theparticipants. Equal numbers of participants were receiving spironolactone andplacebo and followed for 4 months. Adverse events were seen in 23 pt. equallydistributed between the tow groups. Chest pain, SOB, syncope, hypotension wasthe most common.
No significant different in quality of life, LV structure andfunction and arterial function. 2 Of 251 patients screened from November 2011 to February 2015, 150 weresuitable for randomization to spironolactone or placebo. A total of 19 subjects(13%) discontinued study participation before the 6-month follow-up visit andwere not considered in the analysis. There were no differences between botharms in the proportion of patients graded according to the severity of LVdiastolic dysfunction . In comparison with placebo, treatment withspironolactone significantly improved peak VO2, the spironolactone arm alsoshowed favorable changes in metabolic equivalents, exercise time, OUES,anaerobic threshold, and RER at followup Peak heart rate at exercise and heartrate reserve significantly increased at follow-up in the spironolactone group.No changes were found in maximal exertional BP. Although resting systolic (p ¼0.02) and diastolic BP (p ¼ 0.
05) decreased from baseline to follow-up withspironolactone, these changes were not significant compared with placebo. Nosignificant alterations were noted at follow-up in circulating BNP andgalectin-3 in both study arms. Significant improvement with spironolactone (ascompared with placebo) was found in subgroupsabove and below an RER of 1 (the achievement of which was used to definemaximum effort), with the effect size being medium at RER >1 and large atRER3>. Adverse events during follow-up were rare , Spironolactone wasassociated with a small increase in serum potassium. There were no significantdifferences in all patient characteristics presented in between the groups ofenrollees with complete and incomplete follow-up. 3 There were 19 patients withhigh and 15 with low aldosterone levels.
There were no significant differencesin age, sex, race, body mass index, clinic and 24-h ambulatory BP levels,duration of HTN and number of antihypertensive medications in high- versusnormal-aldosterone patient groups. There was no significant change in anystudied parameter of diastolic function with spironolactone treatment at 3 or 6months of follow-up , except that peak early-diastolic longitudinal strain ratein the normal aldosterone group was significantly decreased at 6 monthscompared to baseline. Notably, the LV ejection fraction was preserved in bothhighand normal-aldosterone groups. There were no significant changes in LVejection fraction with time due to spironolactone therapy. As previously reported by our group,12 there were significant reductionsin LVMI (g m?2 ) at 3 and 6 months of follow-up during spironolactone treatmentin both the high-aldosterone group (80 ± 4 (baseline), 67 ± 3 (3 months), 63 ±3 (6 months)) and the normal-aldosterone group (81 ± 4 (baseline), 73 ± 3 (3months), 71 ± 3 (6 months)); all comparisons Po0.001 versus baseline .4 From January 1, 2005to December 31, 2009, 6022 patients with hypertension visited our hospital(department of inpatient or outpatient). We included a total of 1610 patientswith hypertension, LVH and suspected LV diastolic dysfunction, in which 68patients have medical records of spironolactone prescription, while 1542patients without spironolactone treatment.
The final study population comprised65 patients with spironolactone therapy and 1542 patients withoutspironolactone therapy. After propensity score matching, a total of 65 patientsreceiving spironolactone and 130 patients without spironolactone treatment wereenrolled.E/E? significantly declined in the spironolactone group (change frombaseline: 0.6 ± 0.7, P b 0.001) and non-spironolactone group (change frombaseline: 0.
3 ± 0.7, P b 0.001). And the change of E/E? was much more prominentin the spironolactone group (P = 0.005). After a median follow-up of 7.4 years,the new onset symptomatic HFpEF occurred in 3 patients (4.6%) of thespironolactone group and 21 patients (16.
2%) of the non-spironolactone group (P= 0.021). After 5-year follow-up, For multivariate regression analysis,variables with P b 0.10 (age, LVMI, E/E?, beta-blocker prescription, ACEI/ARBexposure and spironolactone treatment) from univariate regression analysis wereentered into the multivariate logistic regression model. The result showed thatspironolactone exposure (OR 0.177, 95% CI: 0.
045–0.687, P = 0.012) wasassociated with a reduced risk of new onset of symptomatic HFpEF, and theelevation of LVMI (OR 1.053, 95% CI: 1.011– 1.097, P = 0.
012) or E/E? (OR1.280, 95% CI: 1.015–1.615, P = 0.
037) was associated with a high risk of newonset of symptomatic HFpEF.Eplerenone In patients with HFpEFOf the 198 patients screened, 150 were excluded, of which 28 patientsrefused to participate or appeared unable to adhere to the study procedures and122 met at least 1 exclusion criterion including significant comorbidities (n 527), Forty-eight patients were enrolled in the open label period and assignedto receive eplerenone 25 mg daily for 2 weeks. Two patients developed serumpotassium levels O 5 mEq/L. Although the 6MWD improved significantly frombaseline in both groups, there was no significant difference in the change in6MWD between the eplerenone and placebo arms.
There was also no significantdifference in change in NYHA class between groups at week 26. there were nosignificant differences by treatment group in change from baseline to week 26 inleft ventricular size, wall thickness and mass, or in left atrial volume orDoppler mitral inflow measurements. p. In addition, there was no significantdifference in the change in early diastolic annular velocity, E0 in theeplerenone group (0.8 6 1.99 cm/s) compared to the placebo group (0.11 6 1.
86c/sec; P 5 .12). A total of 42 patients (21 per group; mean age,63.5 ± 9.1 years; 37 male, mean bodymass index 27.
1 ± 3.5 kg/m2) were included in the study. No adverse effectswere noted during the duration of the study. Consistency of the measurement wasverified using endothelium-independent vasodilatation after glyceryltrinitrate, which showed no significant differences. There was no significantdifference in the number of circulating EPCs after treatment with eplerenonecompared with placebo also , no significant differences in platelet adhesionwere seen between eplerenone and placebo