Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The beneficial effects on nitrates are related to a combination of coronary and non-coronary effects of the drugs. Patients with different forms of ischaemic heart disease may respond differently. For instance, in a patient with rest angina due to coronary artery spasm, nitrates will reverse or prevent coronary artery spasm. In contrast, the patient with severe coronary artery stenosis and reproducible angina during exercise, may obtain relief because nitrates decrease venous return, left ventricular size and left ventricular pressure, thus decreasing myocardial oxygen demands. Nitrates can be used to treat patients with chronic angina, unstable angina and myocardial infarction. In patients with chronic angina, oral nitrate preparations with sustained-release action have been shown to decrease the indices of myocardial oxygen demand for up to 12 h. In patients with unstable angina, intravenous nitrates usually relieve symptoms in patients refractory to oral therapy. In patients with acute myocardial infarction, early administration with intravenous nitrates may benefit patients as suggested by randomized prospective trials. Nitrate tolerance and nitrate dependence does not seem to be an important clinical problem. Perhaps this is related to the way the drug is given, i.e. intermittently. In some instances, however, when high doses are used or the drug is administered intravenously or by the transdermal route, constant levels of nitroglycerine may be attained and the patients may develop tolerance. Although nitrates are effective drugs, it is native to think that they will be used alone to manage the complex problems associated with ischaemic heart disease. Other than hypotension and adverse effects of the drug, there seems to be no contraindication to the combination of nitrates with calcium antagonists or beta blockers.
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PMID:Nitrate therapy for ischaemic heart disease. 399 35

Although arrhythmias caused by myocardial ischemia are a well recognized cause of sudden death, the potential influence of cardiogenic reflexes originating in areas of ischemia has received less attention. In this study, 12 patients with well documented single vessel coronary artery spasm, with a total of 2,240 episodes of transient transmural ischemia, are described. Continuous electrocardiographic and hemodynamic recordings were analyzed to determine possible relations between the anatomic area of ischemia and patterns of change in blood pressure and heart rate. Of seven patients with ischemia of the posterior or inferior left ventricular wall, six had associated bradycardia and hypotension, an apparent Bezold-Jarisch response. Only one of five patients with anterior ischemia had a similar response. A hypertensive, tachycardiac response resembling the James reflex was seen in two of the patients with anterior ischemia, with an increase in blood pressure of 36/22 +/- 12/6 mm Hg and an increase in heart rate of 8 +/- 3 beats/min. This increase began before the onset of chest pain and was seen even in asymptomatic episodes. These reflexly mediated hemodynamic responses may modulate the direct effects of myocardial ischemia and could play a role in sudden cardiac death.
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PMID:Reflexes unique to myocardial ischemia and infarction. 399 36

Coronary collateral vessels appear transiently during vasospasm. To examine the functional role of such collaterals in acute myocardial ischemia, regional coronary flow was determined in patients who showed isolated total spasm in the proximal left anterior descending coronary artery associated with (n = 7, group I) and without (n = 9, group II) collaterals, which were donated by the nonspastic right coronary artery during ergonovine provocative test. Aortic pressure and heart rate were not significantly different in the 2 groups before and during spasm. During vasospasm, the levels of pulmonary artery end-diastolic pressure were significantly higher in group II (19 +/- 2 mm Hg, mean +/- standard error) than in group I (15 +/- 1 mm Hg, p less than 0.05). Under these conditions, great cardiac vein flow (GCVF) measured by thermodilution was markedly reduced in group II (from 60 +/- 4 ml/min to 37 +/- 4 ml/min, p less than 0.01), whereas GCVF was slightly reduced in group I (from 56 +/- 4 ml/min to 51 +/- 4 ml/min), indicating that residual GCVF was greater in patients with than in those without collaterals (p less than 0.05). The calculated coronary collateral resistance index during vasospasm was significantly lower in group I (2.06 +/- 0.18 mm Hg min/ml) than in group II (2.91 +/- 0.30 mm Hg min/ml, p less than 0.05). Total left anterior descending coronary artery spasm with collaterals was less frequently associated with ST elevation in the precordial electrocardiogram recorded during spasm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional significance of transient collaterals during coronary artery spasm. 403 20

Dietary Mg deficiency is thought to promote coronary artery spasm, probably through Ca overloading of vascular smooth muscle (VSM) cells. We now report the demonstration of a coronary arteriopathy in hamsters fed a Mg-deficient diet for 10 days or more. Affected arteries showed endothelial and VSM cell hyperplasia and pleomorphism, chronic inflammation of the media and adventitia, and fibrinoid necrosis. Lesions of myocardial ischemia, distinct from the well-known lesions of myocardial necrosis and calcification common in Mg deficient animals, were also present. Von Kossa positive granules were found in the VSM of Mg-deficient, but not control, hamsters. This vasculopathy is a new factor to be considered in the pathophysiology of Mg deficiency. It is consistent with the view that Ca loading of VSM plays an important role in this condition and could be related to the occurrence of coronary artery spasm.
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PMID:Coronary arterial lesions in Mg-deficient hamsters. 404 48

Coronary artery spasm can now be well documented in the cardiac catheterization laboratory. At present, reliable criteria are available for the diagnosis of severe episodes that are characteristic of patients with Prinzmetal's variant angina. Newer criteria for the diagnosis of milder episodes of spasm are gradually being developed. Optimal criteria may become available with further progress of quantitative angiography. Provocation techniques for the induction of an attack of spasm in the cardiac catheterization laboratory are widely available. Of these, ergonovine testing is the most popular. The tests can usually be performed by experienced angiographers with impressive safety and provide a high degree of sensitivity and specificity when used in patients with the clinical diagnosis of variant angina. Although the research applications of such techniques are extremely broad, their practical clinical indications are somewhat limited to the work-up of patients with infrequent chest pains and normal or near-normal coronary arteriograms. There are other indirect methods for the diagnosis of coronary spasm, but the ideal technique is not available yet. Further expansion of newer modalities for the diagnosis of coronary artery spasm will certainly enhance our understanding of myocardial ischemia and will improve our ability to manage patients with ischemic heart disease.
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PMID:The diagnosis of coronary artery spasm in the cardiac catheterization laboratory. 408 22

Although beta-adrenergic blocking agents reduce myocardial oxygen consumption and symptoms of myocardial ischemia in patients with coronary artery disease (CAD), propranolol has been reported to exacerbate coronary artery spasm in some patients with variant angina. To determine whether increased coronary vasomotor tone can be induced by beta-adrenergic blockade, we measured the changes in coronary vascular resistance (CVR) during cold pressor testing (CPT) in 15 patients, nine with severe CAD and six with normal left coronary anatomy, before and after i.v. propranolol (0.1 mg/kg). Coronary blood flow was measured by coronary sinus thermodilution. CVR was calculated as mean arterial pressure divided by coronary sinus blood flow. Heart rate was maintained constant at a paced subanginal rate of 95 +/- 5 beats/min. Before propranolol, CPT induced significant increases in coronary vascular resistance in patients with CAD (15.0 +/- 2.2%, p less than 0.02), but no increase in CVR in the normal patients. After propranolol, the CVR change during CPT was augmented for patients with CAD (29 +/- 6%, p less than 0.01) and for the normal population (9 +/- 5%, NS). The potentiated increase in CVR occurred without significant changes in resting CVR or in the magnitude of the hypertensive response to CPT. We conclude that beta-adrenergic blockade with propranolol can potentiate coronary artery vasoconstriction in some patients with CAD, possibly mediated by unopposed alpha-adrenergic vasomotor tone. These changes may be important in patients in whom intense adrenergic stimulation may increase coronary artery tone and adversely influence the balance between myocardial oxygen supply and demand.
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PMID:Potentiation of coronary vasoconstriction by beta-adrenergic blockade in patients with coronary artery disease. 613 36

The calcium channel blocking drugs--nifedipine, verapamil, and diltiazem--are an important adjunct to treatment of typical exertional angina and are the treatment of choice for angina due to coronary artery spasm. These drugs are as effective as nitrates and beta-adrenergic blocking agents in treatment of patients with ischemic heart disease. With certain precautions, they may also be used in combination with nitrates and beta blockers. The three calcium blockers are not completely interchangeable because each has distinctive therapeutic applications and side effects. Detailed knowledge of each drug is important for its intelligent application in treatment of angina pectoris.
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PMID:Calcium blockers in angina. How they work, when to prescribe. 614 93

Platelets are thought to be involved in the initiation and propagation of arterial and venous thrombi. A new formation of platelet thrombus in a coronary artery has been implicated in the genesis and extension of myocardial infarction. Experimental evidence suggests that platelet aggregates may be responsible for occlusion of small coronary arteries and subsequent ischemia. Whether the thrombotic component of myocardial infarction is primary or secondary in a given patient, platelet function alterations can influence many mechanisms - operating at the microenvironment level from which depends if the thrombotic lesion grows or sends platelet emboli to the smaller myocardial vessels. Although myocardial infarction is usually associated with arteriographic evidence of atherosclerotic coronary obstruction, examples of infarction in the absence of coronary artery disease have been reported. ARterial thrombosis, small vessel coronary disease and arterial spasm are several possibilities that have been described. Recently in some cases of myocardial infarction, coronary artery spasm has been demonstrated angiographically; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets during myocardial ischemia as an increase of prostaglandin synthesis, like prostacyclin, is stimulated by ischemia and hypoxia. The local release of these substance may modify the myocardial cell viability and regional blood flow. The aim of the present study was to investigate some changes in platelet function in relation to the time stimulated with thrombin. The tests showed, in the first three days, an augmented release of BTG levels with a platelet "exhaustion", demonstrated by a reduced formation of MDA by platelets changing to a state of hyperactivity, with a maximal production of MDA in 10th-15th day.
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PMID:[MDA formation by platelets and plasmatic BTG levels in patients suffering from acute myocardial infarction (author's transl)]. 617 83

Although coronary artery spasm has been implicated as an important cause of myocardial ischemia in humans, an animal model of reversible segmental coronary constriction has not been described. To provoke coronary spasm in open-chest dogs, selected vasoconstricting agents adsorbed to viscous ion exchange gels were applied topically to the surface of epicardial coronary arteries. The procedure provided a sustained localized release of drug, and minimized effects on contiguous myocardium or on the systemic circulation. Segmental arterial constrictor responses were evaluated by sonomicrometry, arteriography, and electromagnetic flow measurements. Potassium evoked sustained constrictions or spasms, and concomitantly reduced flow by -42 +/- 4% (SE; n = 34). Serotonin likewise produced sustained decreases in flow of -22 +/- 6% (SE; n = 5). Other constrictors, including norepinephrine and angiotensin, failed to evoke sustained constrictions. Spasms nearly abolished reactive hyperemic responses elicited by temporary complete occlusion of the artery. Intravenous nitroglycerin and dihydropyridine calcium antagonists promptly relieved the spasms. Scanning electronmicroscopic examination of the intimal surface of arteries undergoing sustained spasm revealed no platelet thrombi. Thus, nonthrombotic, vasodilator-sensitive segmental coronary spasms were elicited by endogenous constrictors which may play a role in regulating flow to ischemic myocardium.
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PMID:Coronary artery spasm in intact dogs induced by potassium and serotonin. 629 10

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of coronary artery spasm in ischemic heart disease. Therapeutic implications. 633 45


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