Differential Effects of Nifedipine and Co-Amilozide on the Progression of Early Carotid Wall Changes

Simon, Alain; Gariepy, Jérôme; Moyse, Dominique; Levenson, Jaime

doi:10.1161/01.cir.103.24.2949

Cited by 177 publications

(98 citation statements)

References 16 publications

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“…30 Moreover, most long-term studies relating BP to CCA-IMT on antihypertensive agents have shown that changes in CCA-IMT should not be evaluated in absolute values, but rather in terms of lesser progression of wall thickness with time. 32 Thus, it is safe to assume that the significant association we observed between PP and CCA-IMT does not reflect a direct cause-effect relationship but rather the presence of a common denominator increasing arterial wall thickness and arterial stiffness.…”

Section: Interpretation Of Resultsmentioning

confidence: 70%

Association between pulse pressure, carotid intima–media thickness and carotid and/or iliofemoral plaque in hypertensive patients

Kesri

Safar

et al. 2004

J Hum Hypertens

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Increased common carotid artery intima-media thickness (CCA-IMT) and carotid and/or iliofemoral (C/IF) plaque are frequent in subjects treated for hypertension, but their association with pulse pressure (PP) has rarely been studied. Using ultrasound techniques, CCA-IMT and C/IF plaques were studied in 323 hypertensive subjects, who were classified into four groups according to the adequacy of blood pressure (BP) control (systolic BP (SBP) o140 mmHg and diastolic BP (DBP) o90 mmHg) and PP (high or low). After adjustment for confounding variables, an increase in CCA-IMT was the only factor significantly and independently associated with high PP, irrespective of the effectiveness of blood pressure control and of antihypertensive drug treatment. CCA-IMT correlated with age, PP, waist-to-hip ratio, tobacco consumption, and heart rate. C/IF plaques correlated with age, tobacco consumption, diabetes mellitus, and dyslipidaemia. To conclude, even with SBPo140 mmHg and DBPo90 mmHg on treatment, hypertensive subjects may have increased CCA-IMT values and C/IF plaque. Four cardiovascular risk factors seem to be involved in these alterations, namely tobacco consumption, dyslipidaemia, diabetes and increased PP. Only the latter factor does not have a standardized effective treatment.

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Section: Interpretation Of Resultsmentioning

confidence: 70%

Association between pulse pressure, carotid intima–media thickness and carotid and/or iliofemoral plaque in hypertensive patients

Kesri

Safar

et al. 2004

J Hum Hypertens

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“…In the LIFE study, the prevalence of LV hypertrophy decreased from 70% at baseline to 23% over 5 years of antihypertensive treatment, and such regression in LV mass was associated with reduced relative risks of CVD events 28. In other clinical trials, antihypertensive treatment was associated with benign structural remodeling of the common carotid artery 29, 30. Higher BP values were also associated with indices of early kidney damage 27, 31.…”

Section: Discussionmentioning

confidence: 98%

Residual Cardiovascular Risk in Individuals on Blood Pressure–Lowering Treatment

Lieb

Enserro

Sullivan

et al. 2015

JAHA

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BackgroundHypertensive individuals on blood pressure (BP)–lowering treatment with BP in the normal or high‐normal range have higher cardiovascular risk than untreated persons with usual BP in the same range. This residual risk (relative and absolute) is not well quantified and may be attributable in part to the higher burden of subclinical disease in treated individuals.Methods and ResultsWe assigned 3024 Framingham Offspring Cohort participants to 5 categories based on systolic BP (SBP) and diastolic BP (DBP) and use of BP‐lowering treatment: (1) untreated SBP/DBP <120/80 mm Hg; (2) untreated SBP/DB ≥120/80 to <140/90 mm Hg; (3) treated SBP/DBP <140/90 mm Hg; (4) untreated SBP/DBP ≥140/90 mm Hg; and (5) treated SBP/DBP ≥140/90 mm Hg. A composite subclinical disease score was constructed, including information on left ventricular hypertrophy, systolic dysfunction, carotid ultrasound abnormality, peripheral artery disease, and microalbuminuria. The prevalence of subclinical disease rose across BP groups, as did the event rates for incident cardiovascular disease (449 events, median follow‐up of 11 years; group 1, 0.65 event per 100 person‐years; group 5, 3.20 events per 100 person‐years; P<0.0001 for trend). On multivariable adjustment, treated hypertensives in groups 3 and 5 had 50% (95% CI 13% to 99%) and 28% (95% CI −6% to 73%) higher hazards, respectively, of developing cardiovascular disease compared with their untreated counterparts with similar levels of BP (groups 1 and 2 and group 4, respectively). The increased risk of cardiovascular disease in treated hypertensives was attributable in part to greater subclinical disease burden.ConclusionsTreated hypertensives have higher subclinical cardiovascular disease burden, which partly explains their higher cardiovascular disease risk compared with untreated persons with similar BP levels.

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“…The regression effect of the calcium channel blocker for more significant lesions is consistent with the post hoc analysis of the PREVENT trial. 3 6 showed that nifedipine decreased the IMT, the PRE-VENT study 7 demonstrated that amlodipine decreased IMT, and the ELSA study 8 suggested that lacidipine slowed down progression of carotid IMT. For ACE inhibitors, the Study to Evaluate Carotid Ultrasound Changes in Patients Treated with Ramipril and Vitamin E (SECURE) 9 and the Plague Hypertension Lipid Lowering Italian Study (PHYLLIS) 10 showed that ACE inhibitors decreased IMT of the carotid bifurcation and internal carotid artery, whereas the PART-2 Collaborative Research Study 11 demonstrated no suppressive effects of the same drug on IMT of the common carotid artery.…”

Section: Discussionmentioning

confidence: 99%

“…13 Although most of these effects require a much higher dose than usual clinical doses, it has been reported recently that some calcium channel blockers can suppress atherosclerosis even at clinical doses. 3,6,7,8 ACE inhibitors, on the other hand, have been reported to suppress atherosclerosis progression in various processes by inhibiting angiotensin II formation and bradykinin degradation. 14 In the present study, no significant differences were found in the achieved blood pressure levels and the degree of their reduction between the 2 groups.…”

Section: Discussionmentioning

confidence: 99%

Quantitative Coronary Angiogram Analysis

et al. 2005

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Abstract-This study was performed to compare the effects of nifedipine retard and angiotensin-converting enzyme (ACE) inhibitors on the progression of coronary atherosclerosis by means of quantitative coronary angiogram. Coronary angiogram was performed before the start of the study and during the 3-year treatment period. This study was conducted on the assumption that possible coronary vasodilation, which may be caused by nifedipine, was excluded by administration of sufficient isosorbide dinitrate. The changes from the baseline in the minimum lumen diameter of the coronary artery in all measured segments were negligible in the nifedipine group (ϩ0.02Ϯ0.27 mm; Pϭ0.543), whereas they were significantly reduced in the ACE inhibitor group (Ϫ0.12Ϯ0.27 mm; PϽ0.001), with a significant difference observed between the groups (Pϭ0.002). The number of progressors in the nifedipine group was significantly lower than that in the ACE inhibitor group (Pϭ0.019), and there was also a significant difference between the groups in the number of patients in whom Ն1 lesion developed after treatment (Pϭ0.040). However, the changes of minimum lumen diameter stratified by baseline percent diameter stenosis demonstrated that progression of coronary atherosclerosis was suppressed in the nifedipine group for lesions with a percent diameter stenosis of Յ40 but was suppressed in both groups for those with a percent diameter stenosis of Ն41. This study suggests that nifedipine retard and ACE inhibitors may be effective in suppression of progression of coronary atherosclerosis, and that nifedipine in particular may be effective for mild to moderate stenosis. Key Words: nifedipine Ⅲ angiotensin-converting enzyme Ⅲ atherosclerosis W e previously conducted the Japan Multicenter Investigation for Cardiovascular Diseases-B (JMIC-B) study and reported that the effects of nifedipine retard on cardiovascular events in patients with hypertension complicated by coronary artery disease were similar to those of angiotensinconverting enzyme (ACE) inhibitors. 1 In this article, we report the results from the JMIC-B side arm study, in which the effects of nifedipine retard on the progression of coronary atherosclerosis were compared with those of ACE inhibitors using quantitative coronary angiogram (QCA) of the cardiovascular measurement system. Methods Quantitative Coronary AngiogramThe JMIC-B side arm study was conducted using patients enrolled in the JMIC-B main study. The institutional ethical committee at each participating hospital approved the study, and all patients gave written informed consent to participate. The detailed procedure of patient recruitment is stated in the article on the main study and is omitted here. 1 Follow-up films were taken 36 months after the start of treatment. When cardiac events occurring during treatment resulted in percutaneous coronary intervention (PCI), the follow-up was terminated at this time point, and the films taken immediately before PCI were used for evaluation. The routine dose of isosorbide dinitrate adm...

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Differential Effects of Nifedipine and Co-Amilozide on the Progression of Early Carotid Wall Changes

Abstract: A difference in early carotid wall changes is shown between 2 equally effective antihypertensive treatments.

Cited by 177 publications

References 16 publications

Association between pulse pressure, carotid intima–media thickness and carotid and/or iliofemoral plaque in hypertensive patients

Association between pulse pressure, carotid intima–media thickness and carotid and/or iliofemoral plaque in hypertensive patients

Residual Cardiovascular Risk in Individuals on Blood Pressure–Lowering Treatment

Quantitative Coronary Angiogram Analysis

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