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)

Coronary artery spasm is the most frequent cause of ischemic heart disease without coronary atherosclerosis once other causes such as cardiomyopathy, arteritis, coronary ectasia, valvular heart disease or hypertensive heart disease are eliminated. We report 23 patients, 15 males and 8 females, whose ages ranged from 34 to 63 years, with a mean age of 47 years, with demonstrated angina pectoris and myocardial ischemia, whose cardiac cineangiography showed no signs of atherosclerosis. Nevertheless, a significant retardation in the progression speed of the contrast medium was observed, as indirect evidence of the increment in coronary resistance at the arteriole level. Coronary spasm was ruled out by administration of intracoronary ergonovine, and other causes of myocardial ischemia, such as muscular bridges, were also discarded. The clinical presentation of the ischemic heart disease was unstable angina (UA) in 21 patients and myocardial infarction (MI) in 2. In the UA group, 14 patients showed ischemic changes in the ECG while the pain lasted, and in 8 patients the changes were present during the stress test. In all of them, the stress test perfusion scan with thallium 201 showed myocardial ischemia. In the IM group, the diagnosis was based on the clinical findings, the ECG, the enzyme curve, and the technetium 99 cardiac scintigram. In the two-year follow-up the prognosis has been favorable with treatment based on calcium antagonists. Nowadays 18 patients are asymptomatic, four have stable angina and only one has unstable angina.
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PMID:[X syndrome. Angiographic findings]. 278 88

The diagnosis of coronary artery spasm is confirmed by angiography, for example, change in caliber of the coronary arteries plus evidence of ischemia. The prevalence and contribution of coronary artery spasm in the individual patient with symptoms of ischemic heart disease is not known and depends on how the condition is defined. The prognosis of patients with coronary artery spasm appears to depend on the presence or absence of severe coronary atherosclerosis, that is, those with severe disease have a worse prognosis. Nitrates should be used to initiate therapy in all patients with this problem. Intravenous nitrates have proven useful in patients whose symptoms are difficult to control and who require hospitalization. beta blockers used alone may be detrimental in patients with coronary artery spasm, but studies supporting the detrimental effects are few. The combination of nitrates, beta blockers and nifedipine has proved effective therapy for many patients with recurrent angina at rest, possibly related to coronary artery spasm. Several open-label and double-blind placebo control trials have shown that all of the calcium antagonists are effective short-term agents for patients with proven coronary artery spasm. When nifedipine was compared with isosorbide dinitrate in a randomized crossover, double-blind trial in patients with coronary artery spasm, both drugs were shown to be efficacious and neither was superior. The traditional alpha-blocking agents have not been shown to be an effective therapy, but a recent study of prazosin, a selective alpha blocker, revealed excellent results in patients whose conditions were resistant to therapy with traditional calcium blockers, beta blockers and, in 1 case, phenoxybenzamine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Large vessel coronary vasospasm: diagnosis, natural history and treatment. 285 17

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 death rate due to myocardial infarction appears to vary with dietary consumption of Mg. This could be due to effects on atherosclerosis, coronary artery spasm, altered pathogenesis of myocardial infarction, increased vulnerability to arrhythmia, or some combination of these. Mg deficiency (MD) has been found to increase the severity of a coronary occlusive event in terms of the amount of necrosis produced by a given occlusion. MD is also associated with increased likelihood of arrhythmia development. In addition, reduced extracellular magnesium concentration (Mgo) is associated with contraction of vascular smooth muscle that may be the equivalent of arterial spasm. In hamsters, MD leads to fibrinoid necrosis thought to be secondary to Ca overload. These 3 effects: coronary artery spasm, cardiac arrhythmia, and increased vulnerability to myocardial necrosis following coronary occlusion, may all be dependent on changes in myocardial and vascular smooth muscle electrolyte metabolism that follow from the reduced Mgo that is associated with MD.
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PMID:Effects of magnesium deficiency on the pathogenesis of myocardial infarction. 301 33

Injury to the endothelial lining of arteries is an important mechanism in both the early and late stages of the development of atherosclerosis. Platelets can contribute to the early lesions by releasing factors that cause smooth muscle cell migration and proliferation. In the later stages, the formation of large platelet-fibrin thrombi that become organized into the vessel wall contributes to the development of focal atherosclerotic narrowing of arteries. Injury to the vessel wall can also be a factor in causing spasm of coronary arteries, particularly at sites of stenosis. The spasm may cause ischemia, anginal pain, and, in some individuals, ventricular fibrillation and death. In other individuals, the spasm may not cause death but may persist long enough for an occlusive thrombus to form and cause myocardial infarction. The events leading to thrombosis involve not only the release of arachidonic acid and the formation of TXA2, but other pathways that are independent of the arachidonate pathway. In some circumstances thrombin (which causes platelet aggregation and release that are largely independent of the arachidonate pathway and TXA2 formation) is the primary stimulus causing the initiation and growth of the thrombus. The role of products of the arachidonate pathway in causing spasm is not understood. PGI2 produced by the vessel wall could be important in preventing or minimizing coronary artery spasm. The best way to prevent the development of atherosclerosis and its clinical complications is to prevent or minimize injury of the endothelium.
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PMID:Platelets, endothelium, and vessel injury. 315 7

Clinical, angiographic, and pathologic data support the contention that atherosclerosis, platelet aggregation, and coronary vasomotility work in unison to cause coronary thrombosis, which in turn leads to myocardial infarction. A patient is described in whom, 2 months after an acute myocardial infarction, inducible coronary artery spasm and a nonocclusive thrombus were angiographically demonstrated at the site of a minimal atherosclerotic narrowing in the infarction-related vessel. This report, to the best of our knowledge, is the first time that these three pathophysiologic mechanisms have been shown, in vivo, to be occurring concomitantly in an infarct-related vessel. Documentation of the unified occurrence of these phenomena support the current concept of the pathophysiology of myocardial infarction.
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PMID:Angiographic demonstration of atherosclerotic stenosis, arterial spasm, and thrombus formation in an infarct-related coronary artery. 319 7

Coronary artery spasm is reported to occur with exercise. In patients without severe coronary atherosclerosis, the evidence for exercise-induced coronary artery spasm is limited. Three patients with positive exercise tests but no severe coronary atherosclerosis are presented. Coronary artery spasm was provoked and verified by angiography in all three, but coronary angiography during exercise failed to demonstrate spasm. The literature is reviewed and the value of a routine protocol for evaluation is discussed.
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PMID:Coronary artery spasm and its relationship to exercise in patients without severe coronary obstructive disease. 341 14

Myocardial infarction is increasingly recognized as a complication of cocaine abuse. A significant number of persons suffering from myocardial infarction associated with cocaine abuse do not have significant coronary atherosclerosis, and the mechanism for infarction in these patients has remained obscure. This report describes a young man with angiographically normal coronary arteries in whom cocaine abuse produced coronary artery spasm leading to coronary thrombosis and infarction.
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PMID:Recurrent myocardial infarction associated with cocaine abuse in a young man with normal coronary arteries: evidence for coronary artery spasm culminating in thrombosis. 349 49

Sudden death, a major cause of mortality in the Western world, usually results from electrophysiologic phenomena in chronically damaged hearts with advanced coronary atherosclerosis. The exact pathophysiologic mechanisms are not known, but there is reasonable circumstantial evidence to implicate myocardial ischemia--clinically manifest or silent--as one of probably multiple factors of pathogenetic significance. This may be on the basis of coronary artery spasm, platelet aggregation, left ventricular dysfunction perpetuating a vicious circle of hypoperfusion and ventricular vulnerability to electrical instability. The increasing use and quality of continuous ambulatory electrocardiographic (Holter) monitoring have allowed improved detection of ST-segment changes and arrhythmias. The majority of sudden deaths result from ventricular tachyarrhythmias degenerating into ventricular fibrillation, and a more significant proportion of these than had been previously thought may be ischemically mediated. Importantly, as many as 20 to 25 per cent of the approximately 450,000 yearly terminal events represent bradyarrhythmias that may be preceded or accompanied by silent myocardial ischemia. Research is still required to determine the incidence, role, and mechanisms of silent myocardial ischemia in sudden death, with the hope that this common catastrophic event can be better prevented.
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PMID:Silent myocardial ischemia as a mechanism of sudden cardiac death. 377 20

A 34-year-old man with allergic asthma died an (instantaneous) sudden cardiac death as a result of multiple myocardial infarcts. These occurred in the absence of coronary atherosclerosis. The major mechanism by which the infarcts occurred was recurrent coronary artery spasm. The latter can occur spontaneously, asthma patients being particularly prone to it. However, various medications prescribed by different physicians may also have played a role.
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PMID:Fatal nonatherosclerotic myocardial infarction in a young man with allergic bronchial asthma. 379 70


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