Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent multicentre studies evaluating the therapeutic value of calcium antagonists in reducing the incidence of cardiovascular complications after myocardial infarction (secondary prevention) and in retarding the development of atherosclerosis in coronary artery disease (tertiary protection) are reviewed. The prognosis of patients after acute myocardial infarction can be improved not only by interventional measures such as aortocoronary bypass surgery or percutaneous transluminal catheter angioplasty, but also by various drugs. Numerous studies have shown that beta-blockers and platelet aggregation inhibitors can reduce mortality and reinfarction rates. Calcium antagonists in secondary prevention trials after acute myocardial infarction, however, have produced variable results. Whereas the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT) [Israeli SPRINT Study Group 1988] with nifedipine showed no beneficial effect of the drug, studies with verapamil in the Danish Verapamil Infarction Trial II (DAVIT II) [Danish Study Group on Verapamil in Myocardial Infarction 1990] and diltiazem in the Multicentre Diltiazem Postinfarction Trial (MDPIT) [Multicenter Diltiazem Postinfarction Trial Research Group 1988] as secondary prevention have demonstrated improvements in survival and cardiovascular complications, but these improvements were restricted to patients without heart failure. In view of the ability of calcium antagonists to reduce atheroma progression in coronary artery disease in animal models, the antiatherosclerotic effects of these agents in clinical studies have generally been disappointing. In the International Nifedipine Trial on Antiatherosclerotic Therapy (INTACT) [Lichtlen et al. 1990], however, nifedipine treatment was associated with a 28% reduction in new lesion development, but did not affect the development of severe lesions. Similar results have been obtained with nicardipine.
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PMID:Secondary and tertiary prevention with calcium antagonists in coronary artery disease. 137 87

Postinfarction cardiac rupture is the result of thrombotic occlusion of a functional end artery with no previous myocardial damage in the perfusion area of the occluded artery. The pre-existing atherosclerotic stenosis at the site of thrombosis is thus"non-critical" in relation to development of collateral vessels and/or irreversible myocardial damage. Eleven cases of postinfarction cardiac rupture were studied by microscopy of cross-sections of the thrombosed segments. At the site of the thrombosis, pre-existing atherosclerosis had narrowed the lumen to 11% or less of its normal cross-sectional area. Maximal pre-existing narrowing of the proximal left anterior descending artery was found in a case with 97% stenosis (histologically measured cross-sectional area reduction) and an estimated residual lumen of 0.71 mm2. The prestenotic luminal area which is usually considered angiographically as "normal" was in all cases shown histologically to be severely narrowed by a diffuse intimal thickening. It is concluded that organic coronary stenosis must be far greater than 75% to be responsible for the development of collateral vessels and/or irreversible myocardial damage.
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PMID:Coronary artery narrowing without irreversible myocardial damage or development of collaterals. Assessment of "critical" stenosis in a human model. 710 20

Postinfarction remodeling of the heart (PIRH) has unfavorable prognostic value because is associated with elevated risk of fatal arrhythmias, emergence and progression of heart failure. Reversibility of PIRH in early period after myocardial infarction causes interest. We followed dynamics of echocardiographical parameters in a patient who had undergone myocardial infarction with subsequent aorto-coronary bypass operation. Values of left ventricular end diastolic and end-systolic volumes were as follows: baseline - 147 and 70, in the process of infarction - 281 and 141, in 1 month after infarction - 298 and 194, in 10 days after surgery - 194 and 88, in 1 year after surgery - 194 and 83 ml, respectively. Thus PIRH is substantially reversible in the early period after myocardial infarction followed by adequate cardiac muscle revascularization. In can be supposed that at the moment of infarction an abrupt progression of stenotic atherosclerosis of the coronary arteries occurs due to complete or subtotal occlusion of vessels, what aggravates myocardial ischemia and predominantly determines course of subsequent PIRH.
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PMID:[Possibilities of early surgical correction of postinfarction remodeling of the heart]. 1826 Aug 49