Synergistic effect of amlodipine and atorvastatin on blood pressure, left ventricular remodeling, and C-reactive protein in hypertensive patients with primary hypercholesterolemia

Abstract

Our aim in this study was to investigate the changes of serum high-sensitive C-reactive protein (hs-CRP) and uric acid (UA), and evaluate the synergistic effect of amlodipine and atorvastatin on blood pressure and left ventricular remodeling in hypertensive patients with primary hypercholesterolemia. One hundred and twenty-six hypertensive patients with hypercholesterolemia were randomized into amlodipine group (10 mg/day, group A, n = 65) and amlodipine (10 mg/day) plus atorvastatin group (20 mg/day, group B, n = 61), treated for 4 months continuously. Serum concentrations of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, hs-CRP, and UA were determined, and blood pressure of both groups was examined before and after treatment. Left ventricular posterior wall thickness and interventricular spectum thickness were measured by echocardiography, and left ventricular mass index (LVMI) was calculated. After 4-months of treatment with atorvastatin, serum concentrations of total cholesterol, low-density lipoprotein cholesterol, triglycerides, hs-CRP, and UA were significantly decreased in group B (P < 0.05, P < 0.01), while serum concentrations of high-density lipoprotein cholesterol was elevated (P < 0.05). Meanwhile, systolic blood pressure and diastolic blood pressure were reduced in both groups (P < 0.05), and blood pressure in group B was markedly lower than that in group A after treatment (P < 0.05). Compared with that before treatment, LVMI in both groups decreased (P < 0.05), to a significantly lower degree in group B than in group A (P < 0.05). Atorvastatin can decrease serum concentrations of hs-CRP and UA. The amlodipine-atorvastatin combination markedly reduces blood pressure and reverses left ventricular hypertrophy more than amlodipine monotherapy. The positive effect suggests that in hypertensive and hypercholesterolemic patients, the combination of amlodipine and atorvastatin could be the treatment of choice.

Atorvastatin Prevents Left Ventricular Remodeling in Spontaneously Hypertensive Rats

“…13) In vivo studies revealed that atorvastatin inhibited LV remodeling in spontaneously hypertensive rats (SHRs) through the induction of cardiomyocyte apoptosis; up-regulation of myocardial P27 protein expression; down-regulation of PKD/MEF2D activation; and decreasing blood pressure, serum uric acid concentration, and myocardial angiotensin II concentration. 6,[14][15][16] The effects of atorvastatin on myocardial CTGF expression in SHRs are not clear. SHRs develop high blood pressure and LV hypertrophy at an early age, and are a commonly used model of essential hypertension in humans.…”

“…The apoptosis rate in myocardiocytes in the SHR-DW group was reduced, whereas 12-week treatment with atorvastatin induced myocardiocyte apoptosis accompanied by alleviated LV remodeling. This indicated that in SHRs aged [8][9][10][11][12][13][14][15][16][17][18][19][20] weeks, reduced apoptosis in myocardiocytes was involved in the development of LV remodeling, and that the effects of atorvastatin on apoptosis may be applicable only to SHRs of this age. Studies on myocardiocyte apoptosis and the effects of atorvastatin on this parameter in SHRs older than 20 weeks should be carried out.…”

Left ventricular remodelling in asymptomatic HIV infection on chronic HAART: comparison between hypertensive and normotensive subjects with and without HIV infection

“…First, we selected subjects never treated with antihypertensive drugs or statins, in order to avoid the possible influence of these treatments LV characteristics and metabolic profile. [31][32][33][34] Second, we matched the 4 groups by age, sex and BMI, all factors known to influence LV characteristics; moreover, we matched HIV þ and HIVÀ subjects also by smoking habit, since smoking …”

Clinical Prognostic Significance of Plasma Cystatin C Levels among Patients With Acute Coronary Syndrome

“…The incidence of coronary artery disease (CAD) is occurring much more frequently. Cardiovascular disease is characterized by a complex multifactorial pathophysiology, 1 which involves extracellular matrix (ECM) degradation and vascular wall remodeling. Positive arterial remodeling (compensatory enlargement) is more often observed in lesions of patients who have acute coronary syndromes (ACS) or vulnerable (rupture-prone) plaques.…”