Developments in Cardiovascular Medicine

1993

DOI: 10.1007/978-94-011-1854-5_15

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The impact of the calcium antagonist nifedipine on the angiographic progression of coronary artery disease: Results of the INTACT (international nifedipine trial on antiatherosclerotic therapy)

Paul R. Lichtlen¹,

W. Rafflenbeul²,

et al.

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Introduction3

Treatment Of Hypertension With Ca Channel Blockers1

Patients With Iddm1

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Cited by 66 publications

(73 citation statements)

References 22 publications

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“…Several clinical trials in the general population have suggested a therapeutic or prophylactic effect of Ca channel blockers (CCB) on the progression of the atherosclerotic process (35)(36)(37). In the PREVENT study, the CCB amlodipine was found to reduce intimal medial thickness in type 2 diabetes (37).…”

Section: Treatment Of Hypertension With Ca Channel Blockersmentioning

confidence: 99%

Reducing the Burden of Cardiovascular Calcification in Patients with Chronic Kidney Disease

¹

2005

Journal of the American Society of Nephrology

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Patients with chronic kidney disease (CKD) have a higher burden of atherosclerotic coronary artery disease compared with age-and gender-matched individuals with normal renal function. Cardiovascular calcification (CVC), a marker of atherosclerosis, is also more prevalent in these patients and is associated with serious clinical consequences. The pathogenesis of CVC is complex and includes factors that promote calcification and others that inhibit calcification. Thus, multiple therapeutic interventions should be used simultaneously to reduce the burden of calcification in patients with CKD. Thus far, interventional attempts have focused on curtailing the effects of factors that promote calcification such as management of known traditional factors for atherosclerotic coronary artery disease and on adopting specific approaches to normalize mineral metabolism, deliver adequate dialysis, and control serum cholesterol level. By contrast, interventions that may bolster the effects of inhibitors of calcification have not yet been studied well but are beginning to attract attention. Ideally, the goal of interventions is not only to slow or halt progression of calcification but also to reverse pre-existing calcification. Whether this goal is achievable is not currently known. This review examines the potential of various therapeutic interventions in reducing the CVC burden in patients with CKD. Moreover, the review is intended to stimulate more research in this area because the efficacy of these interventions has not been examined in controlled clinical trials.

“…Several clinical trials in the general population have suggested a therapeutic or prophylactic effect of Ca channel blockers (CCB) on the progression of the atherosclerotic process (35)(36)(37). In the PREVENT study, the CCB amlodipine was found to reduce intimal medial thickness in type 2 diabetes (37).…”

Section: Treatment Of Hypertension With Ca Channel Blockersmentioning

confidence: 99%

Reducing the Burden of Cardiovascular Calcification in Patients with Chronic Kidney Disease

¹

2005

Journal of the American Society of Nephrology

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Patients with chronic kidney disease (CKD) have a higher burden of atherosclerotic coronary artery disease compared with age-and gender-matched individuals with normal renal function. Cardiovascular calcification (CVC), a marker of atherosclerosis, is also more prevalent in these patients and is associated with serious clinical consequences. The pathogenesis of CVC is complex and includes factors that promote calcification and others that inhibit calcification. Thus, multiple therapeutic interventions should be used simultaneously to reduce the burden of calcification in patients with CKD. Thus far, interventional attempts have focused on curtailing the effects of factors that promote calcification such as management of known traditional factors for atherosclerotic coronary artery disease and on adopting specific approaches to normalize mineral metabolism, deliver adequate dialysis, and control serum cholesterol level. By contrast, interventions that may bolster the effects of inhibitors of calcification have not yet been studied well but are beginning to attract attention. Ideally, the goal of interventions is not only to slow or halt progression of calcification but also to reverse pre-existing calcification. Whether this goal is achievable is not currently known. This review examines the potential of various therapeutic interventions in reducing the CVC burden in patients with CKD. Moreover, the review is intended to stimulate more research in this area because the efficacy of these interventions has not been examined in controlled clinical trials.

“…Several studies in cholesterol-fed animal models (Ginsburg et al, 1983;Blumlein et al, 1984;Watanabe et al, 1987) have indicated that calcium antagonists can reduce the extent of lesion formation and the number of new lesions in patients (Lichtlen et al, 1990). In addition, it has been demonstrated that some antioxidant phenol derivates (probucol, khellin, di-BHA, etc.…”

Section: Introductionmentioning

confidence: 99%

Action of probucol in arteries from normal and hypercholesterolaemic rabbits

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²

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³

et al. 1996

British J Pharmacology

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1 The effect of probucol on the vascular reactivity of different arteries isolated from rabbits was studied as well as its effects on the development of atherosclerosis in a cholesterol-fed rabbit model. 2 Probucol 1O6-5 x 10-4 M produced a concentration-dependent inhibition of the contractile responses induced by KCl (80 mM), the sequence for the IC50 was: mesenteric artery (5th branch, 4.8+2.6 x 10-5 M) >aorta (8.2+2.3 x l0-M) >femoral artery (>5 x 0-4 M). The response to noradrenaline was: mesenteric artery (5th branch, 4.2+ 1.3 x 10-5 M) >aorta (3.2+ 3.0 x 10-4 M) >femoral (> 5 X 10-4 M). 3 In the aorta, probucol (10-_-10-4 M) shifted the concentration-response curves to Ca2+ downward and to the right. 4 Probucol at 5 x 10' M and 5 x 10-4 M showed a reduction in the 45Ca2+ uptake in resting, nonstimulated aortic rings as well as the uptake induced by both noradrenaline 10-6 M and KC1 80 mM. 5 In experiments in vivo, probucol did not affect lipid profiles; however, drug-treatment significantly decreased the cholesterol content of aortic tissue and the extent of intimal surface covered with atherosclerotic lesions. 6 The vascular reactivity was recovered in femoral arteries from rabbits on the atherogenic diet plus probucol. 7 It is concluded that the effect of probucol in vascular smooth muscle can be attributed to an inhibition of Ca2+ entry through both potential-and receptor-operated pathways. Moreover our findings suggest that the effects of probucol on movement of calcium in vascular smooth muscle may play an important role in the mechanism of antiatherogenic properties of this drug.

“…No mortality data are available for treatment with calcium channel blockers in diabetic nephropathy. However, these agents have been repeatedly shown to increase mortality in patients with coronary heart disease in randomised controlled trials [28][29][30]. Because coronary heart disease is a particularly frequent finding in patients with diabetic nephropathy [27], calcium channel blockers should be used restrictively in such patients before their safety has been convincingly demonstrated.…”

Section: Patients With Iddmmentioning

confidence: 99%

Antihypertensive treatment and mortality in diabetic patients What is the evidence?

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1997

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In follow-up studies patients with hypertension and non-insulin-dependent diabetes mellitus (NIDDM) have a four to sevenfold increase in total mortality when compared to non-diabetic normotensive subjects. Recently, the risk of mortality associated with hypertension in diabetes was assessed in 3648 newly diagnosed NIDDM patients [1], hypertension was present in 35 % of women and 46 % of men. When compared to normotensive diabetic patients the mortality risk associated with hypertension was doubled over a median follow-up period of 4.6 years. Cardiac events including sudden death accounted for 58 % and stroke for 13 % of all causes of death.Patients with insulin-dependent diabetes mellitus (IDDM) exhibit a dramatically reduced life expectancy when they develop diabetic nephropathy which is nearly always associated with hypertension [2]. Without antihypertensive treatment the 10-year mortality approaches 80 % in these patients and the main causes of death are myocardial infarction, cardiac failure, sudden death and stroke [3,4].Hence, there is no doubt that hypertension adds considerably to the already increased morbidity and mortality risk in NIDDM patients and is the major determinant of the prognosis in nephropathic IDDM patients. Evidence from intervention studies Patients with NIDDMTo date no prospective randomised intervention trials aiming at the relevant end points of cardiovascular morbidity and mortality have been published for hypertensive NIDDM patients. At least in Germany, the majority of these patients at diagnosis of diabetes are already above 65 years of age; until recently, there has been controversy over whether elderly patients would benefit from antihypertensive treatment. At the beginning of this decade intervention trials in older patients with essential hypertension were published including about 10 % NIDDM patients [5][6][7]. These trials have impressively shown that antihypertensive treatment with thiazide diuretics and beta blocking agents reduces morbidity and mortality both in patients with systolic and/or diastolic hypertension and gave no indication that these beneficial effects would be different in diabetic patients.The evidence from intervention trials in essential hypertension indicates that the overall benefit of antihypertensive treatment in the intervention group rises with an increase of the mortality risk in the control group. In a recent overview-evaluation of intervention trials in essential hypertension the mortality risk in the intervention group was correlated with the mortality risk in the control group and an equation for this linear correlation was proposed [8]. According to this equation it should be possible to estimate the benefit of antihypertensive treatment when the baseline risk of an untreated hypertensive population is known: y = 0.47x -2.9 (y = reduction of mortality due to antihypertensive treatment; x = mortality risk without antihypertensive treatment). Applying this equation to the increased mortality risk in newly diagnosed hypertensive NIDDM patients ...

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