Losartan and amlodipine on myocardial structure and function: a prospective, randomized, clinical trial

Fogari, Roberto; Mugellini, Amedeo; Destro, Maurizio; Corradi, Luca; Lazzari, Pierangelo; Zoppi, Annalisa; Preti, Paola; Derosa, Giuseppe

doi:10.1111/j.1464-5491.2011.03383.x

Cited by 22 publications

(9 citation statements)

References 35 publications

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“…There was observed a significant reduction in values of interventricular septum, PWT, LV diastolic internal diameter, and LVMI in both losartan group and amlodipine group. Indexed LV mass reduced in both groups by 6 months; effects of reducing LVMI in losartan study group was found to be more effective than amlodipine study group, which was more comparable with the results of Fogari et al's study [20] (Table 5). …”

Section: Rutuparna Et Alsupporting

confidence: 81%

Assesment of Clinical Effectiveness of Losartan and Amlodipine in Hypertensive Patient With Left Ventricular Hypertrophy

Hameed

Rutuparna

Merin

et al. 2017

Asian J Pharm Clin Res

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Objective: Hypertension is an important worldwide public health challenge because of its high frequency and concomitant risks of cardiovascular and kidney diseases. Left ventricular hypertrophy (LVH) is defined as an increase in the mass of the LV, which can be secondary to an increase in wall thickness, an increase in cavity size, or both. Relevant study reported that LVH is one of the major and independent risk factors for coronary artery disease, heart failure, serious dysrhythmias, and sudden death. Thus, regression of LVH is a primary pharmacologic objective. The objective of this study is to assess the effectiveness of losartan and amlodipine in regression of LVH and to monitor the adverse effects of these drugs on monotherapy. The study also focused to estimate the clinical effectiveness of specified drugs in lowering hypertension. Methods:The study conducted was retrospective, prospective, comparative study extended over 1 year on 28 patients based on inclusion and exclusion criteria.Results: Both these drugs cause regression of LVH with a decrease in LV mass index value; it is seen that amlodipine is better in controlling elevated blood pressure (BP), especially diastolic BP. In statistical analysis, regression of LVH was found to be correlated with reduction of BP. Conclusion:Incidence of adverse effect was found to be prominent in amlodipine group. Thus, losartan was found to be better in regressing LVH than amlodipine.

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Section: Rutuparna Et Alsupporting

confidence: 81%

Assesment of Clinical Effectiveness of Losartan and Amlodipine in Hypertensive Patient With Left Ventricular Hypertrophy

Hameed

Rutuparna

Merin

et al. 2017

Asian J Pharm Clin Res

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“…A total of 28 RCTs 13 – 40 with 2403 hypertensive patients were identified for inclusion from 6042 relevant publications. The flow of selecting studies for the meta-analysis was shown in Figure 1 .…”

Section: Resultsmentioning

confidence: 99%

“…Sample size of the studies ranged from 24 to 411 participants, totaling 2403 participants. 13 – 40 The average age ranged from 43.8 to 66.7 years, and men accounted for 23.7% to 100% in each study. The range of mean SBP at baseline was 144 to 189 mmHg, whereas the range of mean DBP was 86 to 106 mmHg.…”

Section: Resultsmentioning

confidence: 99%

Independent Influence of Overweight and Obesity on the Regression of Left Ventricular Hypertrophy in Hypertensive Patients

Zhang

Huang²,

Chen

et al. 2014

Medicine

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Overweight and obesity are associated with adverse cardiovascular outcomes. However, the role of overweight and obesity in left ventricular hypertrophy (LVH) of hypertensive patients is controversial. The aim of the current meta-analysis was to evaluate the influence of overweight and obesity on LVH regression in the hypertensive population.Twenty-eight randomized controlled trials comprising 2403 hypertensive patients (mean age range: 43.8–66.7 years) were identified. Three groups were divided according to body mass index: normal weight, overweight, and obesity groups.Compared with the normal-weight group, LVH regression in the overweight and obesity groups was more obvious with less reduction of systolic blood pressure after antihypertensive therapies (P < 0.001). The renin–angiotensin system inhibitor was the most effective in regressing LVH in overweight and obese hypertensive patients (19.27 g/m2, 95% confidence interval [15.25, 23.29], P < 0.001), followed by β-blockers, calcium channel blockers, and diuretics. In the stratified analysis based on blood pressure measurement methods and age, more significant LVH regression was found in 24-h ambulatory blood pressure monitoring (ABPM) group and in relatively young patients (40–60 years’ old) group (P < 0.01).Overweight and obesity are independent risk factors for LVH in hypertensive patients. Intervention at an early age and monitoring by ABPM may facilitate therapy-induced LVH regression in overweight and obese hypertensive patients.

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“…Selectivity for nuclear GRK5 activity may also explain discrepancies in the success of current HF treatments targeting Gq-coupled GPCRs. For example, AT 1 R antagonists (ARBs) such as Losartan, demonstrate efficacy in reversing cardiac hypertrophy in humans [56], [57]. Although the effects of ARBs are thought to be at least partly due to decreased blood pressure and cardiac load, patients treated with Losartan have attenuated hypertrophy accompanied by reduced cardiac fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Nuclear Translocation of Cardiac G Protein-Coupled Receptor Kinase 5 Downstream of Select Gq-Activating Hypertrophic Ligands Is a Calmodulin-Dependent Process

et al. 2013

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G protein-Coupled Receptors (GPCRs) kinases (GRKs) play a crucial role in regulating cardiac hypertrophy. Recent data from our lab has shown that, following ventricular pressure overload, GRK5, a primary cardiac GRK, facilitates maladaptive myocyte growth via novel nuclear localization. In the nucleus, GRK5’s newly discovered kinase activity on histone deacetylase 5 induces hypertrophic gene transcription. The mechanisms governing the nuclear targeting of GRK5 are unknown. We report here that GRK5 nuclear accumulation is dependent on Ca2+/calmodulin (CaM) binding to a specific site within the amino terminus of GRK5 and this interaction occurs after selective activation of hypertrophic Gq-coupled receptors. Stimulation of myocytes with phenylephrine or angiotensinII causes GRK5 to leave the sarcolemmal membrane and accumulate in the nucleus, while the endothelin-1 does not cause nuclear GRK5 localization. A mutation within the amino-terminus of GRK5 negating CaM binding attenuates GRK5 movement from the sarcolemma to the nucleus and, importantly, overexpression of this mutant does not facilitate cardiac hypertrophy and related gene transcription in vitro and in vivo. Our data reveal that CaM binding to GRK5 is a physiologically relevant event that is absolutely required for nuclear GRK5 localization downstream of hypertrophic stimuli, thus facilitating GRK5-dependent regulation of maladaptive hypertrophy.

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Losartan and amlodipine on myocardial structure and function: a prospective, randomized, clinical trial

Abstract: Losartan provided a greater attenuation of left ventricular hypertrophy than amlodipine, seemingly as a result of a greater reduction of myocardial fibrosis.

Cited by 22 publications

References 35 publications

Assesment of Clinical Effectiveness of Losartan and Amlodipine in Hypertensive Patient With Left Ventricular Hypertrophy

Assesment of Clinical Effectiveness of Losartan and Amlodipine in Hypertensive Patient With Left Ventricular Hypertrophy

Independent Influence of Overweight and Obesity on the Regression of Left Ventricular Hypertrophy in Hypertensive Patients

Nuclear Translocation of Cardiac G Protein-Coupled Receptor Kinase 5 Downstream of Select Gq-Activating Hypertrophic Ligands Is a Calmodulin-Dependent Process

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