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)

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

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

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

Angiographically irregular coronary stenoses usually represent plaque rupture with or without superimposed thrombi. Long-segment coronary stenoses with diffuse irregularities (type IIB morphology) have been shown to be more prevalent than focal irregular lesions (type IIA morphology) in survivors of cardiac arrest without acute myocardial infarction. To further understand the pathogenetic importance of type IIB morphology, the clinical and angiographic characteristics in 59 such patients were analyzed. Type IIB lesions accounted for 63% of all type II lesions. Type IIB patients were older than type IIA patients (p less than 0.05). There was a tendency for type IIB morphology to be associated with more extensive disease than other types of lesion morphology (p less than 0.10). Type IIB morphology probably reflects more advanced atherosclerosis. Platelet microemboli may precipitate spasm and/or acute ischemic ventricular tachyarrhythmias. It is possible that long-segment coronary ulcerations are associated with a higher risk for local coronary thromboembolism, and hence with sudden death, than focal lesions.
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PMID:Long-segment coronary ulcerations in survivors of sudden cardiac death. 319 27

Atherosclerosis may be important in the modulation of arterial vasoreactivity and coronary artery flow. Since the endothelium is reduced or absent in atherosclerosis, drug effects are enhanced or modulated. To examine this hypothesis, vasoreactivity induced by serotonin (5-HT) was studied in isolated, perfused, and pharmacologically responsive normal and atherosclerotic human coronary arteries obtained within five hours post mortem. In this model, flow was maintained through the vessels and the effects of vasospasm and vasorelaxation on decreasing and increasing flow respectively were measured. Vessels 3 cm long and approximately 1.5 mm in internal diameter were dissected free and perfused at constant pressure (30 mm Hg) with oxygenated Krebs bicarbonate solution. 5-HT was introduced in the perfusate at 10(-5) M final concentration as a pulse of 100 ml followed by a 1-l washout with drug-free solution. Flow rate and total flow were measured. Normal and atherosclerotic coronary arteries showed peak reductions in flow rate of 22% and 92% respectively, while the times to peak reduction of flow averaged 6 and 4 min and the times to 50% relaxation averaged 13 and 24 min. Ultrasound imaging showed that heavily atherosclerotic regions with extensive focal plaque maintained the induced spasm for a longer period than regions with less disease within the same vessel. Silver nitrate staining showed that these heavily atherosclerotic regions were devoid of endothelium. Thus, atherosclerotic human coronary arteries show a larger magnitude of spasm which persists for a longer period of time as compared to normal coronaries.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasoreactivity in isolated perfused atherosclerotic human coronary arteries. 322 33

Fluid shear stress in arteries and arterioles partially obstructed by atherosclerosis or spasm may exceed the normal time-average level of 20 dyne/cm2. In vitro, at fluid shear stresses of 30 to 60 dyne/cm2 applied for 30 seconds, platelet aggregation occurs. At these shear stresses, either large or unusually large von Willebrand factor (vWF) multimers in the suspending fluid exogenous to the platelets mediates aggregation. Adenosine diphosphate (ADP) is also required and, in these experiments, was released from the platelets subjected to shear stress. At 120 dyne/cm2, the release of endogenous platelet vWF multimers can substitute for exogenous large or unusually large vWF forms in mediating aggregation. Endogenous released platelet vWF forms, as well as exogenous large or unusually large vWF multimers, must bind to both glycoproteins Ib and the IIb/IIIa complex to produce aggregation. Shear-induced aggregation is the result of shear stress alteration of platelet surfaces, rather than of shear effects on vWF multimers. It is mediated by either large plasma-type vWF multimers, endogenous released platelet vWF forms, or unusually large vWF multimers derived from endothelial cells, requires ADP, and is not inhibited significantly by aspirin. This type of aggregation may be important in platelet thrombus formation within narrowed arterial vessels, and may explain the limited therapeutic utility of aspirin in arterial thrombosis.
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PMID:Shear-induced platelet aggregation can be mediated by vWF released from platelets, as well as by exogenous large or unusually large vWF multimers, requires adenosine diphosphate, and is resistant to aspirin. 325 70

From January 1970 to June 1985, transient electrocardiographic changes at rest were documented in 652 patients admitted to our coronary care unit. Patients were stratified according to the type of electrocardiographic alteration at rest: 295 had ST-segment elevation (group 1), 106 T-wave changes (group 2) and 251 ST-segment depression (group 3). Patients in group 3, compared with groups 1 and 2, were more likely to have symptoms of coronary artery disease dating back many years (p less than 0.01 and p less than 0.01, respectively), a previous myocardial infarction (p less than 0.05 and difference not significant), a positive exercise test (p less than 0.01 and p less than 0.01), transient ST-T changes occurring in a higher number of electrocardiographic leads (p less than 0.01 and p less than 0.01), multivessel disease (p less than 0.001 and p less than 0.01) and poor ventricular function (p less than 0.01 and p less than 0.05). Despite these differences, the occurrence of acute myocardial infarction and cardiac death during hospitalization was much more frequent in group 1 compared with groups 2 (p less than 0.02) and 3 (p less than 0.05). However, death occurred in those patients who had poor ventricular function and severe atherosclerosis. A greater susceptibility of group 1 patients to severe vasoconstriction documented by the ergonovine test and by the occurrence of spontaneous spasm seems to account for different in-hospital outcome.
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PMID:Electrocardiographic manifestations and in-hospital prognosis of transient acute myocardial ischemia at rest. 333 14

Acute myocardial infarction was precipitated by hyperventilation in a 65 year old man. His coronary arteriogram in the chronic phase showed almost normal coronary arteries. Injection of acetylcholine (50 micrograms) into the left coronary artery induced spasm of the circumflex artery with chest pain in association with ST-segment elevation in the inferior leads and ST-segment depression in the precordial leads. In this patient there may have been atherosclerosis of the coronary arteries with absent or dysfunctional endothelium, despite an almost normal angiographic appearance. In the absence of endothelium the response of the smooth muscle to acetylcholine is constriction.
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PMID:Possible role of coronary spasm in acute myocardial infarction precipitated by hyperventilation. 334 64

Acute myocardial infarction without obstructive atherosclerosis is a well known entity characterized by the young age of the patients, the low incidence of risk factors and the absence of pre- and post infarction angina. The myocardial necrosis is probably caused by a thrombotic phenomenon perhaps initiated and/or exacerbated by a coronary spasm. It is generally thought that recurrence is rare and long term prognosis relatively benign but this may be a misconception. Three cases are reported of patients who had a second myocardial infarction, transmural infarction in each case, 17 to 36 months after the initial event. Prophylactic treatment after the second accident seems undoubtedly indicated. Until large randomized trials have established the best treatment, it appears logical to prescribe antithrombotic drugs (antiplatelet or anticoagulant drugs) with, perhaps, coronary spasmolytic drugs like calcium antagonists.
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PMID:[Recurrent infarction without coronary atheromatosis]. 340 6

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


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