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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

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

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.
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PMID:[Are calcium inhibitors useful in the treatment of effort angina pectoris]. 640 53

The in-vivo effects of the new antithrombotic compound nafazatrom on experimental thrombosis of the left circumflex coronary artery, on hemodynamics and on ultimate infarct size were studied in pentobarbital-anesthetized, open-chest dogs. Coronary artery thrombosis was induced by low amperage stimulation (150 microA, DC for 6 hr) of the circumflex artery intimal lining. The effects of oral pretreatment of 1%-Tylose suspension as drug diluent and 5 mg/kg nafazatrom plus vehicle were determined. Both agents were administered twice a day before onset of current stimulation. In the drug vehicle group, coronary thrombosis caused severe hemodynamic alterations, e.g. blood pressure and left ventricular pressure decrease, as well as reduction in the LV dP/dtmax associated with increases in end-diastolic filling pressure and heart rate. Time to coronary artery occlusion was delayed by nafazatrom (5.2 +/- 1.1 vs 3.1 +/- 0.4 hr, p less than 0.05). Smaller blood pressure and LV dP/dtmax reductions and minor heart rate and filling pressure increases around the time of thrombus formation suggested cardioprotection with the drug. Smaller R wave changes and S-T segment elevation indicated minor ischemia at the time of occlusive coronary artery occlusion in nafazatrom-treated hearts (24 +/- 0.5 vs 72 +/- 7% ST segment elevation, p less than 0.01). Thrombus wet weight was 18.4 +/- 2.6 mg in the nafazatrom group, but 63.7 +/- 3.1 mg in controls (p less than 0.01). Thus, ultimate infarct size was smaller in nafazatrom-treated hearts as related to left ventricular mass (8.4 +/- 1.4 vs 32.3 +/- 3.1%, p less than 0.02) or to the occluded artery perfusion area at risk for infarction (16 +/- 3.4 vs 53 +/- 6.2%, p less than 0.05). No ex-vivo effect of nafazatrom on collagen-induced platelet aggregation was observed. These results may indicate efficacy of the drug in prevention of acute coronary artery disease as one cause of ischemic jeopardy of the myocardium and/or therapeutic value in coronary artery spasm.
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PMID:The effects of oral nafazatrom (= BAY g 6575) on canine coronary artery thrombosis and myocardial ischemia. 661 99

To examine the angiographic features of vasospastic angina associated with ST segment depression, we attempted to analyze the coronary arteriograms of 12 patients who exhibited ST segment depression during the ergonovine provocative test. Right and left coronary arteriograms were obtained successively within a short period when the ergonovine administration revealed ST segment depression. Eight out of 12 patients showed non-total spastic obstructions in one of the major coronary arteries. Among them, a collateral augmentation was found only in one patient. Two cases exhibited the well-developed collateral channels during non-anginal periods and in one case a collateral blood supply was reduced by the spasm occurred in the donating artery. In another one, the collateral circulation did not change during anginal period. Three out of 4 patients who showed total spastic obstructions demonstrated transiently augmented collateral circulation which was supplied by the non-spastic artery. These findings may indicate that ST segment depression during coronary artery spasm could attribute to a subendocardial ischemia caused by an incomplete occlusion of large coronary artery and transient reduction or augmentation of collateral blood flow.
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PMID:Arteriographic features of angina pectoris associated with ST segment depression during coronary arterial spasm. 665 93

Twenty-four-hour ambulatory ECG recording was performed in 26 patients with variant angina to evaluate the diurnal distribution of ST-segment elevation in relation to chest pain and the incidence of arrhythmias during the episodes. During a recording period of 52 days, 364 ST-segment elevations of 1 mm or greater were observed and 79% were asymptomatic. ST-segment elevation frequently occurred between 0:00 and 9:00 hours (72%) and most frequently between 5:00 and 6:00 hours (13%). Only a few episodes occurred between 10:00 and 18:00 hours. Premature atrial contractions, premature ventricular contractions (PVCs), ventricular tachycardia (VT) and complete atrioventricular block occurred during 12% of the episodes and were more common during painful episodes (32%) than during painless ones (6%). However, VT and severe forms of PVCs (couplets and bigeminy) appeared eight times during painless episodes and nine times during painful ones. Arrhythmias occurred more frequently when the elevated ST segment started to return or was returning to the control level (n = 38) than when the ST segment was rising (n = 8). The incidence of arrhythmias was lower when the daily frequency of ischemic episodes was high. This study shows that episodes of asymptomatic coronary artery spasm predominantly occur early in the morning as symptomatic episodes; complex dysrhythmias appear during the asymptomatic episodes; arrhythmias occur predominantly during a "reperfusion period;" and more arrhythmias accompany infrequent daily episodes of ischemia than frequent ones.
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PMID:Diurnal distribution of ST-segment elevation and related arrhythmias in patients with variant angina: a study by ambulatory ECG monitoring. 668 20

Nineteen patients survived a cardiac arrest not associated with an acute myocardial infarction, and had a normal electrophysiologic study with no inducible ventricular tachycardia despite programmed stimulation with one to three extrastimuli at two or more ventricular sites. Among 14 patients who had obstructive coronary artery disease, cardiac arrest occurred during exertion or an episode of angina pectoris in 11; 24 hour ambulatory electrocardiographic recordings demonstrated infrequent or no premature ventricular complexes in 10 and an ischemic response occurred during stage I or II (Bruce protocol) in 6 of 9 patients who underwent exercise testing. Treatment of these patients consisted of myocardial revascularization (eight patients) or antianginal medications (six patients). Only three patients were also treated with an antiarrhythmic drug. Over a follow-up period of 26 +/- 15 months (mean +/- standard deviation), only one patient died suddenly. Two patients who had coronary artery spasm were treated with coronary vasodilator medications and had no recurrence of cardiac arrest over 7 and 36 months of follow-up, respectively. Three patients who had cardiomyopathy or no identifiable structural heart disease were treated with nadolol or amiodarone and had no recurrence of cardiac arrest over 3 to 27 months of follow-up. Among patients who survive a cardiac arrest and have a normal electrophysiologic study, those with obstructive coronary artery disease or coronary artery spasm generally have an excellent prognosis with treatment directed primarily at the underlying heart disease. The clinical features of these patients suggest that cardiac arrest was related to ischemia rather than a primary arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical features and prognosis of patients with out of hospital cardiac arrest and a normal electrophysiologic study. 673 52

Diltiazem, a calcium channel blocking agent, has potent cardiovascular effects that are directly related to its influence on vascular smooth muscle, ventricular myocardium, and specialized conducting tissue. It causes coronary and peripheral vasodilation, has a negative chronotropic and dromotropic effect, and little to no negative inotropic effect in patients with normal ventricular function. Diltiazem has potential use in a wide variety of cardiovascular disorders. It has been shown extremely effective in relieving the coronary artery spasm associated with variant angina. When compared with nitrates in patients with exertional angina, diltiazem has similar efficacy. Preliminary work indicates it will have a therapeutic role in the treatment of unstable angina. Because of its ability to improve the balance between myocardial oxygen supply and demand and reduce cellular injury secondary to ischemia, it is likely that diltiazem will be of benefit in the treatment of acutely ischemic myocardium during cardiopulmonary bypass and possibly acute myocardial infarction. It has proven efficacy in treating re-entrant supraventricular tachycardia. Adverse effects are seen in less than 5% of patients, indicating that it is well tolerated.
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PMID:The use of diltiazem hydrochloride in cardiovascular disorders. 676 99

Coronary artery spasm usually responds to sublingual nitroglycerin. This report describes four patients with variant angina and one patient with rest angina who had coronary spasm that was refractory to sublingual or i.v. nitroglycerin. In four patients, spasm occurred spontaneous and in one patient after 0.05 mg of ergonovine. In each case, 25-100 micrograms of intracoronary nitroglycerin promptly (30-45 seconds) resulted in reopacification of the vessel involved in spasm and resolution of evidence for ischemia. Thus, intracoronary nitroglycerin can reverse coronary artery spasm that does not respond to systemic nitroglycerin administration.
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PMID:Action of intracoronary nitroglycerin in refractory coronary artery spasm. 679 53


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