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)

Stable angina is the most common form of presentation of ischemic heart disease, being more common in women (65%) than men (37%), while the reverse is true for the prevalence, being present in about 3.5% of men over 55 as opposed to 1.5% of women. The overall 10 year survival for individuals with stable angina at a mean age of 60 years is 58% for men and 68% for women. Prognosis is related to several factors: age, sex, the number of coronary vessels involved, collateral flow, ventricular function, and the extent of myocardium at risk. It is estimated that stable angina of recent onset is associated with single-vessel disease in about 40% of cases. Angina is a clinical diagnosis but, if doubt exists, one should exclude coronary atherosclerosis or spasm by cardiac catheterization and not rely on noninvasive techniques. Therapy for unstable angina or acute infarction receives considerable attention and is reasonably well defined, but such is not the case for stable angina. Conventionally, it consists of secondary prevention and prescription of nitrates, calcium blockers, or beta-blockers. There are several problems: No studies have been performed to assess efficacy in reducing the development of unstable angina. The group of drugs most appropriate for first-line therapy has not been identified. It has not been determined if nitrate tolerance is a major problem. The effect of beta-blockers on prognosis in patients with unstable angina has not been defined. A noninvasive means of identifying high and low risk patients with unstable angina has not been developed.
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PMID:Stable angina as a manifestation of ischemic heart disease: medical management. 286 48

Unstable angina pectoris is a high-risk ischemic syndrome with complex, interacting pathophysiologic mechanisms that include coronary atherosclerosis, coronary vasoconstriction, and thrombosis. The roles of various medical strategies, including nitrates, beta blockers, calcium antagonists, and antiplatelet, anticoagulant, and thrombolytic agents, are discussed in conjunction with revascularization procedures such as coronary angioplasty and bypass surgery.
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PMID:Therapeutic choices in unstable angina. 287 56

Percutaneous transluminal coronary angioplasty (PTCA) is indicated for many patients with symptomatic coronary atherosclerosis. It can be safely used in patients with unstable angina pectoris, multivessel coronary disease (in selected instances), multiple stenoses in single vessels, stenoses in coronary artery bypass grafts, and recent total coronary occlusion. PTCA may be useful in reestablishing coronary flow after acute myocardial infarction with coronary occlusion and in association with thrombolytic therapy for acute myocardial infarction. The primary success rate of PTCA in experienced hands should be approximately 90%. If restenosis occurs after successful PTCA, a second procedure can be used to dilate the segment with restenosis and the success rate is high. Acute coronary events are the major complications of PTCA. Less than 5% of patients need emergency coronary surgery. Mortality for PTCA is less than 1%. Complications of PTCA diminish with increasing operator experience. PTCA is not indicated for patients with long-standing complete coronary occlusions, diffuse atherosclerotic coronary stenoses without discrete stenotic segments, multiple sites of total occlusions, or "skip" areas in vessels served by bridging collaterals. Patients with main left coronary stenoses and stenoses involving both sides of large-vessel bifurcations are not considered for PTCA in most centers. The choice for or against PTCA should be made after careful assessment of the risk/benefit ratio of PTCA vs coronary bypass surgery.
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PMID:Percutaneous transluminal coronary angioplasty: role in the treatment of coronary artery disease. 293 84

There is now considerable evidence to suggest that some aspects of early lesion formation and later lesion growth are a reaction to injury. Hemodynamic factors are important in determining the site of injury and may produce injury directly. Injury can lead to atherogenesis in animal models as well as in humans. Superficial injury exposes the subendothelium, allowing platelet adhesion, which at high shear rates is dependent on vWF. Platelet adhesion and degranulation release PDGF, which stimulates smooth muscle cell proliferation, synthetic functions, and vasoconstriction. LDL stimulates smooth muscle cell growth as well as damages endothelium in some experimental systems. Thus, a link is provided between platelet and lipid involvement in atherosclerosis. Direct evidence for a role of platelets in atherogenesis comes from studies in which animals were treated to reduce platelet number or function or in which platelet function is genetically impaired (pigs with von Willebrand's disease). In these models, reduced platelet function is associated with less atherosclerosis. Deeper injury exposes collagen, with subsequent platelet aggregation, thrombin and fibrin generation. The role of reduced production of PGI2 and fibrinolytic agents following severe damage is unknown. Deep injury to the vessel occurs during plaque fissuring, the pathologic process underlying most cases of myocardial infarction, unstable angina, and some cases of sudden death. Angioplasty produces amelioration of many patients' symptoms and is safe. However, acute occlusion occurs occasionally, and restenosis in the first year occurs in some 30 percent of patients treated. Angioplasty damages the arterial wall, with endothelial denudation and intimal and medial splitting. Why does this, and plaque injury, by stimulating platelet deposition, not produce more restenosis? Changes in arterial anatomy are likely to be important: the increase in vessel diameter and in blood flow produce conditions less favorable for thrombotic or arteriosclerotic restenosis.
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PMID:Role of platelets in atherogenesis: relevance to coronary arterial restenosis after angioplasty. 295 94

A method of apheresis of plasma euglobulin fraction, cryoglobulins and Willebrand factor was developed. In one session of plasmapheresis 1500-1700 ml of patient's plasma were removed, fractionated and returned. The method was used in 2 patients with immune complex vasculitides. In one of them the disease developed against a background of chronic active hepatitis, in the other patient it manifested itself in cryoglobulin- and cryofibrinogenemia. Clinical improvement was noted in both cases: the absence of myalgia, arthralgia, hemorrhagic eruption, and ulcerative-necrotic skin changes. The normalization of increased ristomycin-cofactor activity of Willebrand factor and CIC levels was noted in one case. A decrease in the content of plasma cryoglobulins, cryofibrinogen, and urine protein concentration (from 1.5 up to 0.03%) was noted in the other case. A possibility of the use of the method in other pathological conditions (DIC-syndrome, unstable angina, atherosclerotic angiopathy) accompanied by endothelial damage, was discussed. Willebrand factor multimers form complexes with low density lipoproteins therefore the removal of these complexes may be useful in the treatment of hypercholesteremia and atherosclerosis.
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PMID:[Apheresis of euglobulins, cryoglobulins and the von Willebrand factor in vasculitis]. 295 14

Decreased oxygen supply rather than increased demand may be the primary pathogenic mechanism of myocardial ischemia in patients with unstable angina. Coronary artery spasm and in vivo platelet aggregation may play an important role in the mechanism by which the magnitude of fixed obstruction secondary to coronary atherosclerosis is transiently exacerbated. In this case report, we describe a patient who developed chest pain accompanied by ischemic ECG changes during coronary arteriography, due to a transient thrombotic aggravation of a fixed, significant coronary stenosis. Percutaneous transluminal coronary angioplasty was performed with relief of the coronary stenosis and of the symptoms.
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PMID:Transient platelet aggregation as a mechanism of unstable angina. Aggressive treatment with coronary angioplasty. 297 56

The use and type of antithrombotic therapy for patients with cardiac disease are described based on an understanding of the pathophysiologic mechanisms involved, the risk of thromboembolism, and the evidence from prospective and, if necessary, retrospective clinical trials. The indications and intensity of anticoagulant therapy in patients with valvular heart disease and prosthetic valves are first discussed. We recommend that the prothrombin time be reported as a ratio and standardized using the International Normalized Ratio. The pivotal role of platelets and the clotting system in the initiation and progression of atherosclerosis and the acute coronary syndromes is described. There is no evidence to date that antiplatelet therapy is of value in primary prevention or in patients with stable angina, but the value of aspirin in patients with unstable angina was clearly shown in two well-designed studies. Adequate prophylactic therapy to prevent the thrombotic complications of acute myocardial infarction (i.e., venous thrombosis and intracardiac thrombosis) is described, and the available data on the prevention of coronary reocclusion after thrombolysis reviewed. There is now convincing evidence from studies in animals and in patients that vascular injury during aortocoronary vein bypass graft surgery requires antitihrombotic therapy starting before the procedure to minimize acute platelet thrombus deposition and prevent occlusion. Restenosis after arterial angioplasty appears to be related to acute platelet thrombus deposition on the site of deep arterial injury. Therapeutic interventions should probably involve both anticoagulants and platelet inhibitor therapy. Implications derived from recent animal studies are discussed.
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PMID:Antithrombotic therapy for patients with cardiac disease. 307 28

Increased levels of an endogenous inhibitor of tissue-plasminogen activator (t-PA) have been thought to relate to the genesis of acute myocardial ischemia. To examine the role of the rapid inhibitor of t-PA, plasma samples were analyzed from 75 patients with chest pain syndrome undergoing coronary angiography (mean age 57 years), 24 patients with clinically documented coronary artery disease (unstable angina, positive exercise stress test or previous history of myocardial infarction; mean age 58 years) and 15 young normal subjects (mean age 26 years). Plasma t-PA inhibitor levels were similar in age-matched patients regardless of the absence or presence (and degree) of coronary artery disease. Plasma t-PA inhibitor levels correlated significantly with age (r - 0.46, p less than 0.005), suggesting an age-dependent decrease in fibrinolytic activity. Plasma t-PA inhibitor levels also correlated significantly with serum triglyceride levels (r - 0.60, p less than 0.001), but not with coronary risk factors such as serum cholesterol, diabetes, hypertension, serum uric acid levels or body weight. Association of high levels of inhibitor of t-PA with hypertriglyceridemia may be of importance in the development of coronary thrombosis, especially in elderly patients. Nonetheless, this study does not suggest a pathogenic role of t-PA inhibitor in coronary atherosclerosis.
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PMID:Plasma tissue plasminogen activator inhibitor levels in coronary artery disease: correlation with age and serum triglyceride concentrations. 310 May 98

Ninety one patients with unstable angina were evaluated by clinical and angiographic study. Of 91 patients, 42 (46%) responded poorly to the intensive medical treatment. Emergency coronary arteriography was then performed on these patients. The important pathoanatomical mechanisms contributing to instability of angina pectoris and/or refractoriness to the intensive medical treatment were observed in 19 of 42 patients (45%). These include: 1) More severe disease with left main lesion; 2) Refractory coronary spasm; 3) Coronary dissection; 4) Rapid progression of atherosclerosis; 5) Ulcerating plaque and 6) Coronary thrombus. Our results presented here suggest that an appropriate knowledge regarding pathophysiology might improve the approach to treatment.
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PMID:Exact mechanisms contributing to instability and refractoriness to therapy in patients with unstable angina: coronary arteriographic evaluation. 312 86

Recent clinical, angiographic, and pathologic evidence has prompted reexamination of the natural history of coronary atherosclerosis. Abrupt anatomic complications of atherosclerotic plaques or thrombosis on a plaque may precipitate the "malignant" syndromes of sudden death, acute myocardial infarction, or unstable angina before the plaque itself is large enough to limit coronary flow. This concept of a bimodal pattern of presentation has important clinical and therapeutic implications.
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PMID:Bimodal presentation of the clinical syndromes of coronary atherosclerosis: a review. 315 31


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