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ABSTRACT: OBJECTIVE: Lowering systolic blood pressure (BP) (SBP) by 10 mmHg or diastolic BP by 5 mmHg using any of the main classes of BP lowering drugs reduces stroke by about a third. The objective of the present study is to determine whether there is a limit to the extent to which BP should be lowered. METHODS: From the individual 17 primary-prevention trials of single drug therapy included in a recent meta-analysis, we abstracted reductions in SBP (SBP reduction in the treatment group minus that in the control group [mmHg]) and data regarding incidence of stroke to generate relative risks (RRs). We performed "flexible" (not "linear") unrestricted maximum likelihood meta-regression, using fractional polynomials, of the reduction in SBP on the risk of stroke. RESULTS: The best-fitting model offered a gain in deviance of 5.71 with respect to the reference linear model, according to the expected inverse J-shaped (nadir at a 13.7-mmHg reduction in SBP) dose-response relation between reductions in SBP and logarithmic RRs for stroke. CONCLUSIONS: More than 13.7-mmHg SBP reduction with single drug therapy could produce no longer additional reduction in the risk of stroke in a primary-prevention setting.
High Blood Pressure & Cardiovascular Prevention 05/2013;
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ABSTRACT: AIMS: The antiarrhythmic effect of triple-site biventricular stimulation (Tri-V) is poorly understood. This study aims to evaluate the effect of cardiac resynchronization therapy (CRT) on ventricular arrhythmia (VA) with Tri-V using a single right ventricular (RV) and double left ventricular (LV) lead.METHODS AND RESULTS: Over a period of 3.5 years, 58 consecutive patients with New York Heart Association class II-IV heart failure, an LV ejection fraction of ≤0.35, and a QRS interval of ≥120 ms were enrolled. Acute haemodynamic responses to dual-site biventricular stimulation (Bi-V) and Tri-V were evaluated by assigning patients to a Bi-V or Tri-V group. Electrocardiogram parameters [QT interval, JT interval, and transmural dispersion of repolarization (TDR)] were measured over time after CRT. Spontaneous VA detected by telemetry was reviewed and confirmed. During a mean follow-up of 481 days after implantation, VA occurred in 2 of 22 patients in the Tri-V group and 14 of 36 patients in Bi-V group. Triple-site biventricular stimulation was thus associated with a decreased VA risk (P = 0.044). Multivariate Cox analysis showed that Tri-V pacing prevented arrhythmic events as compared with Bi-V pacing (hazard ratio, 0.13; 95% confidence interval, 0.029-0.610; P = 0.009). Ventricular repolarization indices at 6 months were significantly shortened in Tri-V compared with Bi-V (QTc, -23.6 vs. -14.1%, P = 0.008; JTc, -21.4 vs. -7.7%, P = 0.005; TDRc, -39.9 vs. -17.0%, P < 0.001).CONCLUSION: Compared with Bi-V, Tri-V reduced VA during long-term follow-up. Improvements in repolarization parameters may result in antiarrhythmic effects.
Europace 05/2013; · 1.98 Impact Factor
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ABSTRACT: In addition to their high-intensity effects on the reduction in low-density lipoprotein (LDL) levels, rosuvastatin and atorvastatin would be expected to also reduce small dense LDL (sdLDL) levels. To determine which reduces sdLDL levels more, we performed the first meta-analysis and meta-regression of randomized head-to-head trials of rosuvastatin versus atorvastatin therapy. MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through April 2012. Eligible studies were prospective, randomized controlled trials of rosuvastatin versus atorvastatin therapy reporting final sdLDL (directly measured or calculated) levels as an outcome. For each study, data regarding final sdLDL levels in both the rosuvastatin and atorvastatin groups were used to generate mean differences (MD) and 95 % confidence intervals (CI). Meta-regression analysis was performed to determine whether the effects of rosuvastatin therapy were modulated by the prespecified factors. Of 159 potentially relevant articles screened initially, 28 reports of randomized trials enrolling a total of 7802 patients were included. Pooled analysis suggested a significant reduction in final sdLDL levels among patients randomized to rosuvastatin versus atorvastatin therapy (MD, -1.56 mg/dl; 95 % CI, -2.30 to -0.83 mg/dl; P < 0.0001). The meta-regression coefficients were statistically significant for the baseline LDL/sdLDL level and the difference in LDL changes between the two groups. In conclusion, rosuvastatin rather than atorvastatin therapy is likely more effective in reduction of sdLDL levels. It should be further investigated whether the reduction in sdLDL levels implies overt clinical benefits of rosuvastatin over atorvastatin.
Heart and Vessels 05/2013; · 2.05 Impact Factor
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ABSTRACT: Telmisartan has been proposed to be a promising cardiometabolic sartan due to its unique peroxisome proliferator-activated receptor-gamma-inducing property. To determine whether telmisartan improves metabolic parameters in metabolic syndrome, we perform the first meta-analysis of randomized controlled trials (RCTs). MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through September 2012 using PubMed and OVID. Eligible studies were RCTs of telmisartan therapy enrolling individuals with metabolic syndrome and reporting metabolic parameters as outcomes. Of 31 potentially relevant articles screened initially, 10 reports of RCTs, enrolling a total of 546 patients with metabolic syndrome, were identified and included. Pooled analysis suggested significant reductions in % changes of fasting glucose (standardized mean difference, -0.51; 95% confidence interval [CI], -0.96 to -0.06; P = .03), insulin (-0.23; 95% CI, -0.40 to -0.06; P = .008), glycosylated hemoglobin (-0.26; 95% CI, -0.44 to -0.08; P = .005), and homeostasis model assessment index (-0.22; 95% CI -0.39 to -0.05; P = .01); and a significant increase in % changes of adiponectin (0.75; 95% CI, 0.40 to 1.09; P < .0001) among patients with metabolic syndrome randomized to telmisartan versus control therapy. Telmisartan therapy appears to significantly improve metabolic parameters in patients with metabolic syndrome.
Journal of the American Society of Hypertension (JASH) 03/2013;
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International journal of cardiology 02/2013; · 7.08 Impact Factor
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International journal of cardiology 02/2013; · 7.08 Impact Factor
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ABSTRACT: A previous meta-analysis of six randomized head-to-head trials suggests that the blood pressure (BP)-lowering capabilities of telmisartan may be comparable to those of valsartan. We performed an updated meta-analysis of telmisartan vs. valsartan therapy for the reduction of BP in hypertensive patients. MEDLINE, EMBASE and the Cochrane Central Register of Controlled Trials were searched through August 2012 using web-based search engines (PubMed, OVID). Eligible studies were prospective randomized controlled trials examining telmisartan vs. valsartan therapy and reporting clinic BP as an outcome. For each study, the data regarding changes from baseline to final clinic systolic BP (SBP) and diastolic BP (DBP) in both the telmisartan and valsartan groups were used to generate mean differences (MDs) and 95% confidence intervals (CIs). Of the 62 potentially relevant articles initially screened, 17 reports about prospective randomized controlled clinical trials of telmisartan vs. valsartan therapy, including a total of 5422 patients with hypertension, were identified and included. Pooled analysis suggested significant differences in BP reductions among the patients randomized to telmisartan vs. valsartan therapy (MD for SBP, -2.04 mm Hg; 95% CI, -2.80 to -1.28 mm Hg; P<0.00001; MD for DBP, -1.08 mm Hg; 95% CI, -1.55 to -0.62 mm Hg; P<0.00001). When data from the monotherapy and combination therapy (with hydrochlorothiazide) trials were pooled separately, telmisartan therapy was associated with a statistically significant difference in BP reductions relative to valsartan therapy in both the monotherapy and combination therapy groups. In conclusion, telmisartan therapy appears to reduce BP more than valsartan therapy in patients with hypertension.Hypertension Research advance online publication, 24 January 2013; doi:10.1038/hr.2012.233.
Hypertension Research 01/2013; · 2.58 Impact Factor
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ABSTRACT: A recent meta-analysis of randomized head-to-head trials suggests that therapy with telmisartan, an angiotensin II receptor blocker (ARB) and partial agonist of peroxisome proliferator-activated receptor-gamma, may increase adiponectin levels more strongly than other ARB therapies. Therefore, telmisartan would be expected to reduce interleukin-6 (IL-6) or tumor necrosis factor-alpha (TNF-α). To determine whether telmisartan reduces IL-6 or TNF-α, we performed the first meta-analysis of randomized controlled trials of telmisartan therapy. MEDLINE, EMBASE and the Cochrane Central Register of Controlled Trials were searched through November 2011. Eligible studies were prospective randomized controlled trials of telmisartan vs. unrestricted control therapy reporting IL-6 or TNF-α levels as an outcome. For each study, data regarding percent changes from baseline to final IL-6 or TNF-α levels in both the telmisartan and control groups were used to generate standardized mean differences (SMDs) and 95% confidence intervals (CIs). Nine reports of randomized trials enrolling a total of 645 patients were identified. Pooled analysis of seven and five trials demonstrated a statistically significant reduction in percent changes of IL-6 (fixed-effects SMD, -0.385; 95% CI, -0.581 to -0.189; P<0.001; P for heterogeneity=0.073) and TNF-α levels (random-effects SMD, -0.627; 95% CI, -0.945 to -0.308; P<0.001; P for heterogeneity=0.029) with telmisartan relative to control therapy, respectively. In conclusion, based on a meta-analysis of nine randomized controlled trials, telmisartan therapy is likely effective in reducing IL-6 and TNF-α levels.Hypertension Research advance online publication, 13 December 2012; doi:10.1038/hr.2012.196.
Hypertension Research 12/2012; · 2.58 Impact Factor
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International journal of cardiology 12/2012; · 7.08 Impact Factor
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International journal of cardiology 11/2012; · 7.08 Impact Factor
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International journal of cardiology 11/2012; · 7.08 Impact Factor
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International journal of cardiology 11/2012; · 7.08 Impact Factor
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International journal of cardiology 10/2012; · 7.08 Impact Factor
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International journal of cardiology 10/2012; · 7.08 Impact Factor
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Surgical Endoscopy 06/2012; · 4.01 Impact Factor
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International journal of cardiology 06/2012; 159(3):230-3. · 7.08 Impact Factor
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International journal of cardiology 05/2012; 159(2):150-4. · 7.08 Impact Factor
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International journal of cardiology 05/2012; 159(1):69-72. · 7.08 Impact Factor
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International journal of cardiology 05/2012; 158(2):285-9. · 7.08 Impact Factor
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International journal of cardiology 05/2012; 158(3):435-8. · 7.08 Impact Factor
