Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary artery disease (CAD) results from atherosclerosis, a systemic vascular disorder that is the leading cause of death and disability throughout much of the developed world. Because cellular changes associated with vulnerable atherosclerotic plaque are characterized by a loss of normal calcium regulation, there is strong interest in a potential antiatherosclerotic role for calcium channel blockers. This hypothesis has been supported by investigational studies conducted in well-defined cellular and animal models of atherosclerosis. In addition, several clinical studies have tested the benefit of calcium channel blockers among patients with mild-to-moderate CAD. More recent trials have shown reductions in cardiovascular events after treatment with amlodipine, a long-acting, dihydropyridine-type calcium channel blocker. The Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial (PREVENT) demonstrated that patients with documented CAD treated with amlodipine experienced marked reductions in cardiovascular events compared with patients receiving placebo. Amlodipine also was associated with significant slowing of carotid atherosclerosis, an important surrogate marker for CAD, independent of blood pressure modification. These results have renewed interest in potential plaque stabilization properties of third-generation calcium channel blockers and their possible therapeutic role in CAD.
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PMID:Mechanisms of plaque stabilization for a charged calcium channel blocker in coronary artery disease. 1156 Jan 91

Coronary artery disease (CAD) is the result of atherosclerosis, a vascular disorder characterized by abnormalities in vasoconstriction and endothelial function, ultimately leading to partial or complete vessel occlusion. Because the atherosclerotic plaque is marked by changes in calcium regulation, there has been interest in a potential antiatherosclerotic role for calcium antagonists. In support of this hypothesis, a recent clinical study demonstrated in patients with CAD that treatment with the lipophilic dihydropyridine-type calcium antagonist amlodipine resulted in significantly fewer cardiovascular procedures and events. The Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial (PREVENT) evaluated the effects of amlodipine on the development and progression of atherosclerotic lesions in coronary and carotid arteries in 825 patients with documented CAD. The results of PREVENT showed that patients receiving amlodipine had marked reductions in hospitalization for revascularization and unstable angina compared with placebo in a population consisting of either normotensive or controlled hypertensive patients. Ultrasound approaches determined that amlodipine therapy was also associated with significant slowing in carotid atherosclerosis-an important surrogate marker for CAD-over the 3-year period. This vascular-wall benefit associated with amlodipine treatment was not related to changes in blood pressure. The findings from PREVENT were consistent with a second reported study known as the Coronary Angioplasty Amlodipine Restenosis Study (CAPARES). These clinical results have led to an interest in potential plaque-stabilization properties of this lipophilic calcium antagonist. In this article, cellular and molecular mechanisms of action that may contribute to a beneficial role for a calcium antagonist in the treatment of atherosclerosis will be reviewed.
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PMID:Mechanisms of atherosclerotic plaque stabilization for a lipophilic calcium antagonist amlodipine. 1170 16

Coronary artery disease (CAD) is the consequence of atherosclerosis, a vascular disorder that is the leading cause of death and disability throughout much of the developed world. Certain cellular changes in the vulnerable atherosclerotic plaque are characterized by a loss of normal calcium regulation. This observation has led to interest in a potential antiatherogenic role for calcium channel blockers (CCBs), independent of their effects on vasodilation. The Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial (PREVENT) demonstrated that treatment with amlodipine, a third-generation CCB, in patients with documented CAD produced marked reductions in cardiovascular events as compared with placebo, without a reduction in coronary luminal loss. Amlodipine therapy was also associated with significant slowing in carotid atherosclerosis, an important surrogate marker for CAD, independent of blood pressure changes. The findings from PREVENT were remarkably consistent with another study known as the Coronary Angioplasty Amlodipine Restenosis Study (CAPARES). A reduction in the progression of carotid atherosclerosis has also been recently reported for lacidipine, another third-generation dihydropyridine CCB. These clinical findings have led to a renewed interest in potential plaque stabilization properties of certain CCBs, as will be systematically reviewed in this article. It is also probable that vascular protective agents, such as amlodipine may work in a synergistic fashion with other established treatments, including HMG-CoA reductase inhibitors, to effectively improve outcomes in patients who are at risk for or have established CAD.
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PMID:Mechanisms of plaque stabilization for the dihydropyridine calcium channel blocker amlodipine: review of the evidence. 1241 68