Why the study?
Does cilnidipine improve ambulatory blood pressure and suppress cardiac hypertrophy compared to control CCBs in hypertensive CKD patients on renin-angiotensin system inhibitors?
Does cilnidipine improve ambulatory blood pressure and suppress cardiac hypertrophy compared to control CCBs in hypertensive CKD patients on renin-angiotensin system inhibitors?
In hypertensive patients with CKD, adding cilnidipine to renin-angiotensin system inhibitors improves ambulatory BP and reduces left ventricular mass index compared to other CCBs.
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Supports cilnidipine over other CCBs to regress LV mass in hypertensive CKD on RAS inhibitors; extends RCT evidence for differential CCB effects.
Ambulatory blood pressure (BP) and heart rate (HR) profile are proposed to be related to renal deterioration and cardiovascular complication in hypertension and chronic kidney disease (CKD). In this study, we examined the beneficial effects cilnidipine, a unique L/N-type calcium channel blocker (CCB), in addition to renin-angiotensin system inhibitors, on ambulatory BP and HR profile, as well as cardiorenal function in hypertensive CKD patients. Forty-five patients were randomly assigned to the cilnidipine replacement group (n = 21) or the control CCBs group (n = 24) during a 24-week active treatment period. Although clinical BP values were similar in the cilnidipine and control CCBs groups after the treatment period, the results of ambulatory BP monitoring showed that the 24-h and daytime systolic BP levels in the cilnidipine group were significantly lower compared with the control group after the study. Furthermore, the left ventricular mass index (LVMI) was significantly decreased in the cilnidipine group compared to the control group after the study (LVMI, 135.3 ± 26.4 versus 181.2 ± 88.4, p = 0.031), with a significant difference in the changes in the LVMI between the cilnidipine and control groups (change in LVMI, -12.4 ± 23.7 versus 26.2 ± 64.4, p = 0.007). These results indicate that cilnidipine is beneficial for the suppression of pathological cardiac remodeling, at least partly, via a superior improving effect on ambulatory BP profile compared with control CCBs in hypertensive CKD patients.
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Kanaoka et al. (2013) studied this question.
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