The Effect of Losartan and Amlodipine on Left Ventricular Diastolic Function and Atherosclerosis in Japanese Patients with Mild-to-Moderate Hypertension (J-ELAN) study

Abstract

This study was a prospective, randomized, open, blinded endpoint study to assess the effects of angiotensin II type 1 receptor blocker, losartan, compared with calcium channel blocker, amlodipine, on left ventricular (LV) diastolic function and atherosclerosis of the carotid artery in Japanese patients with mild-to-moderate hypertension, LV hypertrophy, diastolic dysfunction and preserved systolic function. Fifty-seven patients were randomly assigned to losartan-or amlodipine-based treatment groups and were followed up for 18 months. Blood pressure was similarly reduced by both regimens. Losartan shortened the transmitral E-wave deceleration time, and amlodipine reduced LV mass index; however, there was no significant difference in the percent changes of these indices between the two groups. Mean carotid intima-media thickness (mean IMT) as well as plaque score significantly increased in the amlodipine-based regimen (pre: 1.05 ± 0.26 mm, follow-up: 1.23 ± 0.33 mm, P¼0.0015), but not in the losartan-based regimen (pre: 1.08 ± 0.35 mm, follow-up: 1.16 ± 0.52 mm, P¼non-significant). The percent increase in mean IMT in the amlodipine-based regimen tended to be large compared with the losartan-based regimen (amlodipine: 19.8 ± 23.7%, losartan: 6.9 ± 23.3%, P¼0.06). Under similar reduction of blood pressure, losartan is likely effective in protecting the progression of atherosclerosis of the carotid artery compared with amlodipine. Losartan may improve LV diastolic function, and amlodipine may attenuate LV hypertrophy; however, this study cannot make consecutive remarks about the superiority of either treatment regimen in the effects on cardiac function and geometry. This study has been registered at

Association between long-term prescription of aldosterone antagonist and the progression of heart failure with preserved ejection fraction in hypertensive patients

“…Meanwhile, LV diastolic function and hypertrophy were also ameliorated in the non-spironolactone group compared with baseline, which might be attributed to extensively prescribed ACEI/ARB, calcium blockers and beta-blockers in our enrolled patients. Both ACEI/ARB and calcium blockers are effective in decreasing LVH and improving LV diastolic function [13][14][15]. Our previous study showed that long-term beta-blocker exposure was associated with protective effects in terms of LV diastolic dysfunction and LVH in patients with hypertension [5].…”

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

“…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.…”

The potential therapeutic use of renin–angiotensin system inhibitors in the treatment of inflammatory diseases

“…Yamamoto et al compared the effects of losartan and amlodipine, a calcium channel blocker, on atherosclerosis of the carotid artery in Japanese patients with mild-to-moderate hypertension, left ventricular hypertrophy and diastolic dysfunction. Under similar reduction of blood pressure, losartan was more effective than amlodipine in protecting the progression of atherosclerosis(Yamamoto et al, 2011). In another study on 116 patients with acute myocardial infarction (AMI), additional ARB (5 mg of valsartan twice daily) therapy had minimal impact on the progression of coronary atherosclerosis as compared with an ACE inhibitor (3 mg of captopril three times daily) alone(Yano et al, 2012).…”