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)

M-mode echocardiograms were recorded in 12 patients with Prinzmetal's angina during 29 episodes of transient myocardial ischemia at rest (18 spontaneous and 11 ergonovine-induced). At peak ST segment elevation a regional mechanical impairment was observed in the interventricular septum during 23 episodes of angina and in the posterior wall during six episodes. In the 18 spontaneous episodes the left ventricular ischemic wall, when compared to the basal state, was found to have a significant reduction in motion (-76.3 +/- 9.1%) (mean +/- SEM), in diastolic thickness (-11.7 +/- 2.5%), and in percent systolic thickening (-88.0 +/- 5.6%). Increase in left ventricular end-diastolic diameter (+13.1 +/- 2.1%) and decrease in percent fractional shortening (-38.1 +/- 3.7%) were also observed. When ST segment was back to the isoelectric line, a transient overshoot in regional left ventricular function was observed. In induced episodes statistically significant changes could be detected by M-mode echocardiography even before appearance of ST segment elevation and anginal pain. No significant difference was found in type or degree of mechanical impairment between induced and spontaneous episodes. Therefore, in patients with Prinzmetal's angina: (1) M-mode echocardiography allows detection of mechanical changes due to transient myocardial ischemia; and (2) mechanical impairment occurs earlier than clinical (pain) and electrocardiographic (ST segment elevation) signs of transmural ischemia.
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PMID:Transient changes in left ventricular mechanics during attacks of Prinzmetal's angina: an M-mode echocardiographic study. 669 89

This study was designed to test the hypothesis of a possible role of serotonin in the pathogenesis of myocardial ischemia in patients with pure vasospastic angina, since serotonin is known to cause contraction in isolated coronary arteries. This effect, as well as serotonin-induced platelet aggregation, is reversed by ketanserin, a specific S2-receptor blocker. Five male patients (49 to 68 years old) with more than six episodes/day of myocardial ischemia at rest as characterized by ST segment elevation on the electrocardiogram (ECG) were selected for the study after a 2 day run-in period of continuous ECG Holter monitoring in the absence of any therapy except that with sublingual nitrates. In a double-blind crossover protocol they received consecutive infusions of 6 hr each of ketanserin (2 mg/hr iv, preceded by a 10 mg bolus in three patients) and placebo in the following sequence: ketanserin-placebo-ketanserin-placebo in the first and placebo-ketanserin-placebo-ketanserin in the second 24 hr period. The efficacy of the infused drug was tested by exposing platelet-rich plasma, obtained from the study patients at a fixed morning time before and during ketanserin infusions, to a series of serotonin concentrations from 10(-5) to 10(-8)M in a conventional aggregometer. A complete suppression of aggregation curves in the range of serotonin concentrations tested resulted during administration of ketanserin. The efficacy of the drug in preventing ischemic episodes was assessed by computing the ischemic episodes (recorded by Holter monitoring) and nitroglycerin consumption in each 6 hr ketanserin period and in the corresponding placebo period. A total of 171 ischemic episodes were recorded, 33 of which (19%) were symptomatic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A double-blind, placebo-controlled study of ketanserin in patients with Prinzmetal's angina. Evidence against a role for serotonin in the genesis of coronary vasospasm. 670 64

A mental arithmetic stress test was performed by 122 consecutive patients undergoing diagnostic coronary arteriography. Twenty-two patients showed significant ST segment abnormalities during the test (group 1). Of these patients, 20 performed a bicycle exercise test, which was positive in all of them. Seventy patients had a negative mental stress but a positive exercise test (group 2), whereas in 30 patients both tests were negative (group 3). There were no patients with a positive mental stress test and a negative exercise test. Mental stress induced a significant increase in heart rate and systolic blood pressure in the three groups of patients. Group 1 patients, however, achieved higher values of double product during mental stress and had a shorter exercise duration than group 2 and group 3 patients. The extent of coronary artery disease (CAD) was similar in groups 1 and 2, while group 3 patients had a significantly lower prevalence of two or more vessel disease. To investigate the pathogenetic mechanism of mental stress-induced myocardial ischemia, great cardiac vein flow was measured by means of the thermodilution technique in four patients with isolated left anterior descending artery disease, who showed ST segment depression in anterior leads in response to mental stress. In three patients without vasospastic angina the calculated coronary resistance decreased during mental stress, as a result of a normal vasodilatory response to the increased myocardial oxygen consumption induced by the test. By contrast, in one patient with variant angina, coronary resistance increased suggesting coronary vasoconstriction. Our findings demonstrate that mental arithmetic stress testing may induce significant ST segment abnormalities in patients with CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mental arithmetic stress testing in patients with coronary artery disease. 673 Dec 83

To examine the possible existence of collateral circulation during coronary artery spasm, we attempted to visualize the transient appearance of collateral vessels that could serve to salvage otherwise jeopardized ischemic areas. In three patients with vasospastic angina, total spastic obstruction of a major coronary artery was associated with transient collateral augmentation, which was supplied by the nonspastic artery during anginal period associated with ST-segment depression. These collateral vessels disappeared when the angina and ST changes resolved after nitroglycerin administration. These findings suggest that the collateral blood supply could transiently occur through preexisting vessels to perfuse the ischemic area during coronary artery spasm and that such collateral flow could have a role in preventing transmural myocardial ischemia, resulting in a lesser degree of ischemia associated with ST-segment depression.
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PMID:Transient collateral augmentation during coronary arterial spasm associated with ST-segment depression. 682 15

Thirty-five of 70 patients with vasospastic angina at rest complained of chest pain during exercise or during usual daily activity. In 22, the angina threshold was described as variable during exercise: that is, the amount of exertion that induced angina was not always the same. In 12 patients with variable threshold exertional angina, 3 exercise tests performed in the morning on different days yielded different results, because chest pain and ischemic electrocardiographic changes occurred at different work loads with a wide range in heart rate-systolic pressure product. Two patients, in whom great cardiac vein flow was measured during exercise before and after taking nifedipine, tolerated heavier work loads after receiving the drug, with a more marked increase in flow during exercise. It is concluded that variable threshold exertional angina can be objectively demonstrated by repeat exercise tests in patients with vasospastic angina. Variability of the angina threshold may be due to a functional mechanism that causes myocardial ischemia in addition to the increased myocardial metabolic requirements provoked by exercise. Because in such patients fluctuations in coronary arterial tone play an important role in determining the response to exercise, calcium antagonistic drugs, which lower coronary tone and prevent the occurrence of coronary spasm, are effective in increasing exercise capacity.
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PMID:Variable threshold exertional angina in patients with transient vasospastic myocardial ischemia. Repeat exercise test results and therapeutic implications. 682 54

A total of 60 patients with coronary heart disease were examined and divided into 2 groups: (I)53 patients with classical angina pectoris at rest and of effort; (II)7 patients with variant angina pectoris. The results of 24-hour ECG monitoring, bicycle exercise test and coronary angiography were studied. By giving an objective ECG pattern during myocardial ischemia attack. 24-hour ECG monitoring enabled one to differentiate various clinical forms of angina pectoris, establish their connection with heart rhythm disturbances, thus forming the basis for the differential approach to the treatment.
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PMID:[24-hour ECG monitoring of patients with different clinical forms of stenocardia]. 686 Apr 84

With the arteriographic demonstration of coronary arterial spasm, fundamental questions have been raised concerning the role of spasm in myocardial ischemia and infarction. It is now clear that coronary arterial spasm is the cause of Prinzmetal's variant angina pectoris in patients with and without coronary atherosclerosis. In most patients with coronary heart disease, major ischemic events frequently result from increased myocardial oxygen demand or coronary thrombosis. However, recent evidence suggests that coronary arterial spasm may initiate or contribute to the development of unstable angina pectoris, acute myocardial infarction, and sudden death in these patients. Thus, episodes of myocardial ischemia and infarction are induced by factors, acting singly or in combination, that augment myocardial oxygen demand or diminish myocardial oxygen supply, and the latter alteration can result from thrombotic coronary occlusion or a dynamic increase in coronary arterial tone (that is, coronary arterial spasm).
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PMID:The role of coronary arterial spasm in ischemic heart disease. 689 63

In order to evaluate the usefulness of a stress T1-201 myocardial scintigraphy in semiquantifying the myocardial perfusion, 10 normal subjects and 71 patients with coronary artery diseases were studied with sequential imaging over 3 hours. Myocardial to background ration (M/B) in the exercise phase was significantly higher in the normal subject group than in the coronary artery disease groups. Three hours after exercise (redistribution phase), M/B decreased significantly in the normal subject group but remained unchanged in the coronary artery disease groups. Percent change of M/B with exercise was lower in the effort angina pectoris group (97 +/- 11.2%), and the old myocardial infarction group (101 +/- 14.5%) than in the normal subject group (127 +/- 12%). Sensitivity and specificity of this method were 93% and 47%, respectively. Out of 11 patients with variant angina pectoris, 9 patients showed positive scintigram. Of the 9, however, 6 cases were without organic coronary stenosis in the coronary angiography. There was a significant correlation between M/B on redistribution images (RD.M/B) and ejection fraction determined by left ventriculograms (r = 0.61, p less than 0.001), indicating a close relation between the amount of the residual viable myocardium and the left ventricular function. M/B and its percent change with stress T1-201 myocardial scintigraphy reflect the myocardial perfusion and myocardial perfusion reserve and their semiquantitative analysis provides a useful means for detection of ischemic heart disease.
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PMID:Clinical evaluation of stress myocardial scintigraphy with thallium-201 in patients with ischemic heart disease. Semiquantitative analysis of single dose myocardial imaging. 706 55

In 10 cases of Prinzmetal's angina in which episodes of myocardial ischemia were easily and reproducibly induced by hyperventilation, this test was performed 111 times, 41 times under control conditions and 70 times during treatment with one or more of the following drugs: phentolamine, isosorbide dinitrate, propranolol, verapamil, nifedipine and amiodarone. Seventeen of 18 negative tests performed under the influence of a long-acting drug coincided with total remission of the patient's anginal episodes when this drug was administered on a short- or long-term basis. No patient died or sustained infarction during a follow-up period of 10.9 months. A negative test was thus a good indication that the clinical response to the corresponding drug would be favorable. The electrocardiographic changes and chest pain provoked by hyperventilation occurred not when alkalosis was greatest (hydrogen ion [pH] change from 7.42 to 7.58, p less than 0.001), but when pH was approaching normal or control values. The onset of electrocardiographic changes occurred an average of 175 seconds after the end of hyperventilation and, in two cases, the time lag was as much as 480 and 705 seconds, respectively. This raises several questions regarding the true mechanism triggering coronary spasm under such conditions. The hyperventilation test appears to be a useful and safe procedure for selecting the best possible drug for long-term treatment of Prinzmetal's angina as well as for comparing the relative efficacy of different drugs.
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PMID:The hyperventilation test as a method for developing successful therapy in Prinzmetal's angina. 706 32

Coronary arterial spasms are thought to be responsible for acute myocardial infarction in some patients with normal coronary arteries. A report is presented on a patient with a history of Prinzmetal angina pectoris involving ST-segment elevations in the electrocardiogram and recurrent ventricular fibrillation. Selective coronary arteriography revealed normal coronary arteries. Administration of nifedipin and isosorbide dinitrate brought about prompt relief of pain. One year after cardiac catheterization the patient developed recurrent ventricular arrhythmias when administration of nifedipin was discontinued. It is concluded that coronary arterial spasms may occur in patients with normal coronaries and may cause transient myocardial ischemia with severe ventricular arrhythmias. A history of Prinzmetal angina pectoris is usually present and medical treatment consists in administration of nifedipin and isosorbide dinitrate.
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PMID:[Coronary artery spasms with normal coronary arteries as the cause of recurrent ventricular fibrillations]. 725 31


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