Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Percutaneous transluminal laser angioplasty of the peripheral arteries was performed in 16 patients with pain at rest, objective evidence of severe peripheral ischemia, conditions requiring amputation, and/or medical contraindications to surgery. In 14 patients the ipsilateral femoral artery was entered in an antegrade direction using the Seldinger technique, base-line angiograms taken, and laser angioplasty performed using argon ions transported to the target site by a 400-mu quartz fiber. Patency was established in 50% of cases and correlated directly with both total energy delivered and time and power per exposure: the lower the energy, the higher the patency rate. Complications included spasm, pain, and mechanical or laser perforation. The authors conclude that while percutaneous transluminal laser angioplasty of peripheral arteries using argon radiation is possible in man, its clinical value has not been established.
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PMID:Percutaneous transluminal laser angioplasty for treatment of peripheral vascular disease. Clinical experience with 16 patients. 316 Nov 18

Pain in arterial pathology is classified according to pathogeny: true arterial pain (embolism, spasm); vasomotor pain, in particular the fact of reactional vasodilation during Raynaud's syndrome, inflammation in the region surrounding zones of ischemic necrosis, and infection of ulcers; ischemia of sense receptors, pain of short duration in the case of acute ischemia, giving way to anesthesia, the intermittent pain of compensated chronic ischemia (Fontaine's stage II), and the constant pain of uncompensated chronic ischemia (stage III); pain due to arterial compression, trapped arteries, muscular contractions; cortical pain, so-called 'phantom pain', sensation-memory of the pain fixed in the cortex or more often irritation of the nerves in the stump.
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PMID:[Pain in arterial pathology]. 322 13

To assess the significance and accuracy of noninvasive tests in detecting significant coronary artery disease (CAD; greater than 50% stenosis), the Master's exercise test, treadmill exercise test and dipyridamole-loading myocardial perfusion scintigraphy were performed and their results were compared with coronary angiographic findings in 60 patients with angina but without myocardial infarction. Among these, 27 patients had significant CAD. The Master's test performed in outpatient clinics had an 85% sensitivity and a 76% specificity in detecting significant CAD, when the degree of ST depression was equal to or exceeded 1 mm. The sensitivity further improved to 96% by adding chest pain to the criteria; then all patients with multivessel disease or critical ischemia were identified by the Master's test. Treadmill tests performed after admission had a 78% sensitivity and a 67% specificity. When the severity of ischemia was judged either by exercise capacity or the degree of ST depression or the coronary T wave, the treadmill test was superior to the Master's test. Although patients without significant CAD had longer exercise capacity and the higher maximum heart rate in the treadmill test than did those in the Master's test, these trends were similar but less marked in patients with significant CAD. Dipyridamole-loading myocardial perfusion scintigraphy showed an excellent sensitivity and specificity; 96% and 94%, respectively, in detecting significant CAD. It was particularly useful in distinguishing false positive exercise results due to left ventricular hypertrophy and coronary spasm and that in women, from true positive results. In conclusion, the Master's test is a simple and useful method for screening CAD in community hospitals and in outpatient clinics.
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PMID:[Accuracy of the Master's exercise test in detecting significant coronary artery disease]. 326 34

Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease of unknown cause that is characterized by a hypertrophied, nondilated, hypercontractile left ventricle. Its etiology and pathogenesis remain undefined but the three principal factors implicated are a genetic predisposition, a hypersensitivity to catecholamines, and an abnormal calcium metabolism. The hypertrophy typically involves the intraventricular septum to varying degrees, but may also involve the apex or free wall and even be concentric. The disease occurs in either an obstructive or a nonobstructive form depending on whether an intraventricular pressure gradient can be demonstrated at rest or on provocation. The gradient and obstruction to outflow is usually seen in patients with asymmetric septal hypertrophy (ASH) and anterior motion of the mitral valve during systole (SAM). Abnormal left ventricular diastolic function characterized by inadequate filling and impaired relaxation has been shown to be very important in both the obstructive and nonobstructive forms of the disease. In addition, inadequate coronary vasodilator reserve as a result of small vessel disease, microvascular spasm, and/or low capillary density per unit myocardial mass has been implicated as an important cause of ischemia in patients without coronary artery disease. HCM is a disease of young adulthood with relatively slow progression; young patients are often asymptomatic, whereas older patients are more limited by dyspnea, angina, dizziness, or syncope. Supraventricular tachyarrhythmias occur in 30% of patients, and high-grade ventricular arrhythmias occur in over 75%. The annual mortality is 3-5%. The common mode of demise is sudden cardiac death. Therefore, the primary objectives of treatment are the amelioration of symptoms, the control of arrhythmias, and the prevention of sudden death. Beta-adrenoreceptor blocking agents decrease myocardial contractility and oxygen demands and increase ventricular volume; therefore, they are most useful in patients with the obstructive form of HCM. Calcium channel antagonists enhance left ventricular relaxation, relieve microvascular spasm, and improve coronary filling and therefore are the agents of choice in patients with diastolic dysfunction. The ability of the calcium channel antagonists to decrease contractility makes them valuable in patients with obstructive HCM. Arterial vasodilators, diuretics, nitrates, and inotropic agents should be avoided because they can increase the intraventricular gradient. Myomyectomy is reserved for those patients with the obstructive form of HCM whose symptoms are refractory to medical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypertrophic cardiomyopathy: current views on etiology, pathophysiology, and management. 331 Jun 37

Multivessel coronary spasm has been described but its incidence in patients with variant angina still remains unclear. Thirty-three patients with variant angina were studied during coronary angiographic examination with selective intracoronary injection of acetylcholine (ACh). In all but three patients, the location of ischemia during attack was determined by the electrocardiographic findings, by exercise 201Tl myocardial scintigraphy, and by two-dimensional echocardiography during a hyperventilation test, and the coronary artery (or arteries) responsible for the attack was predicted before the study. ACh induced spasm of at least one coronary artery in all but one patient. ACh induced spasm of both the left and right coronary arteries (i.e., multivessel coronary spasm) in 24 patients: in two of the four patients who were predicted to have spasm of the left coronary artery, in six of the 11 predicted to have spasm of the right coronary artery, in 13 of the 15 predicted to have spasm of both the left and right coronary arteries, and in three of the three in whom coronary artery responsible for attack had not been predicted. This ACh-induced spasm of the left and right coronary arteries occurred separately and no patients showed hemodynamic instability during attack. In one patient in whom multivessel coronary spasm had been predicted and ACh failed to induice coronary spasm, ergonovine maleate (0.2 mg) induced spasm of both the left and right coronary arteries simultaneously, resulting in severe prolonged hypotension. Nineteen of the 25 patients in whom multivessel coronary spasm was documented showed angiographically normal or nearly normal coronary arteries after administration of nitroglycerin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Multivessel coronary spasm in patients with variant angina: a study with intracoronary injection of acetylcholine. 334 84

A patient with primary angina showed intermittent ST elevation (with and without chest pain), during two exercise tests performed on consecutive days; the same ST changes were also seen during the recovery phase. The electrocardiographic changes recorded in this patient may be considered an example of myocardial response to spasm-related ischemia.
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PMID:Exercise-induced intermittent angina and ST-segment elevation in Prinzmetal's angina. 334 65

We describe a patient who experienced focal cerebral and brainstem ischemia in the setting of postpartum eclampsia. Cerebral angiography showed spasm of large- and medium-caliber arteries. This case provides rare documentation that vasospasm may account for cerebral ischemia in eclamptic women with focal signs. This observation suggests that in such patients cerebral angiography may be informative and useful.
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PMID:Cerebral vasospasm and eclampsia. 335 16

In the absence of fixed coronary artery disease, thyrotoxicosis is rarely associated with acute myocardial infarction and/or ischemia. There are no known reports on the association of acute myocardial infarction with iatrogenic or factitious thyrotoxicosis in the absence of fixed coronary artery stenosis or coronary artery spasm. A 68-year-old woman, clinically in a state of thyrotoxicosis as a result of taking 0.3 g/d of exogenous thyroid replacement, sustained a severe, reversible myocardial ischemic event. Echocardiographic and scintigraphic evaluations demonstrated a large apical dyskinetic region. Subsequently, after the original dose of levothyroxine sodium was reduced to 0.15 mg and the patient became euthyroid, two-dimensional echocardiography and scintigraphic and cardiac catheterization studies demonstrated normal left ventricular contractility and normal coronary anatomy. Coronary artery spasm was not induced by ergonovine maleate therapy. Exogenous thyroid administration may directly influence myocardial oxygen supply and demand, exclusive of coronary artery disease and coronary spasm. A critical imbalance may then result in acute myocardial ischemia and reversible left ventricular segmental wall motion abnormalities.
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PMID:Myocardial infarction, severe reversible ischemia, and shock following excess thyroid administration in a woman with normal coronary arteries. 337 27

Five patients, all women in their 50s and all with a documented history of migraine headaches, had ischemic chest pains investigated. Four patients had angina primarily occurring at rest, with documented ischemic electrocardiographic changes during pain in all five. Three subjects sustained myocardial infarction, one shortly after taking ergotamine tartrate for an acute attack of migraine. Subsequent coronary angiography in all five subjects revealed no evidence of atherosclerotic coronary artery disease, suggestive of spasm as the cause of ischemia. In subjects with known migraine, the occurrence of chest pain may represent coronary artery spasm, and should be investigated with concurrent electrocardiographs, as these two clinical entities may be related as part of a generalised vasospastic disorder. The use of ergot preparations should be contraindicated in such patients, as exacerbation of chest pain and frank myocardial infarction may result. These chest pains responded favourably to calcium channel blockers.
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PMID:A possible relationship between migraine and coronary artery spasm. 346 72


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