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)

The calcium antagonists provide a unique tool to reduce myocardial oxygen demand and prevent increases in coronary vasomotor tone. For patients with Prinzmetal's variant angina, diltiazem, nifedipine and verapamil are extremely effective in preventing episodes of coronary vasospasm and symptoms of ischemia. Unstable angina pectoris is a more complex pathophysiologic syndrome with episodes of ischemia due to increases in coronary vasomotor tone, intermittent platelet aggregation or alterations in the underlying atherosclerotic plaque. Each of the calcium antagonists is effective as monotherapy in decreasing the frequency of angina at rest. Nifedipine is the only calcium antagonist that has been studied in a combination regimen with beta blockers and nitrates for patients with unstable angina, and control of angina is better with the combination regimen than with either form of therapy alone. Although symptoms of myocardial ischemia in unstable angina are reduced by calcium antagonists, these agents do not seem to decrease the incidence of adverse outcomes. Antiplatelet therapy appears to improve morbidity and mortality in patients with unstable angina, suggesting that thrombus formation may play a central role in that disorder. Episodes of silent or asymptomatic myocardial ischemia, identified by ST-segment monitoring, occur in a variety of disorders of coronary disease. Among patients with Prinzmetal's variant angina and unstable angina, episodes of silent ischemia appear to be as frequent as episodes of angina and the calcium antagonists are effective in decreasing episodes of ischemia regardless of the presence or absence of symptoms. Persisting episodes of silent ischemia among patients with unstable angina despite maximal medical therapy identify patients at high risk for an early unfavorable outcome. Among patients with stable exertional angina, episodes of silent ischemia may be up to 5 times as frequent as episodes of angina, and may be due to increases in coronary vasomotor tone, transient platelet aggregation or increases in myocardial oxygen demand. Preliminary experience suggests that calcium antagonists and beta blockers are effective in decreasing episodes of silent ischemia in patients with stable exertional angina and that a combination regimen may be more effective than either form of therapy alone.
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PMID:Calcium antagonists for Prinzmetal's variant angina, unstable angina and silent myocardial ischemia: therapeutic tool and probe for identification of pathophysiologic mechanisms. 354 88

The second Pisa Conference nine years ago established the frequency of transient reduction of coronary flow, as a cause of angina. Understanding of mechanisms remains very incomplete and there is great overlap between different clinical syndromes. The following facts appear established: Episodes of spontaneous ischemia are frequently asymptomatic and may occur even in patients with classic stable angina of effort: Large coronary arteries exhibit tone; they do not take part in autoregulation: In the presence of advanced organic obstruction, large coronary artery tone may be sufficiently increased by physiological alpha-adrenergic stimulation to provoke ischemia. The following deductions seem justifiable: Clinically, increased large coronary tone can be suspected as a cause of ischemia when there is a background of severe organic coronary narrowing with effort angina, when rest attacks occur in association with stimuli such as cold or isometric stress and when their frequency can be reduced by alpha blockade: Spasm, as distinct from physiological increase in tone, can be suspected when there is minimal organic disease, an absence of effort angina and when attacks are unrelated to stress: The mechanism of spasm is unknown; it may be associated with intimal trauma and probably is more frequent in the presence of early atherosclerotic change: Spasm may be simulated by pseudo-spasm where a physiological increase in tone may cause marked luminal narrowing at a site of still pliable quite mild intimal proliferation; it may be suspected when apparent localised spasm is associated with diffuse acute narrowing of all coronary arteries. Apart from the smooth muscle, acute luminal narrowing with rest angina can result from coronary thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of transient myocardial ischemia. 375 98

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 +/- 18 vs 117 +/- 18 beats/min, p less than 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, myocardial ischemia frequently develops during daily life; silent ischemia is an important component of this syndrome; and increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.
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PMID:Transient myocardial ischemia during daily life in patients with syndrome X. 378 14

The diagnostic value of 24-hour ECG monitoring was assessed in 81 patients with stable angina of effort (functional classes II-IV) and 8 spontaneously-anginal patients. The pattern and frequency of transitory ST displacements, and their distribution by the hours of the day are reviewed. The results of 24-hour ECG monitoring are compared with clinical, bicycle-ergometric and coronaroangiographic findings. Spontaneously anginal patients showed peculiar episodes of transitory ischemia, with typically elevated ST, shorter duration and the occurrence mostly during the night and morning hours; 2/3 of such episodes were painless. High diagnostic value of the method for the assessment of the efficacy of anti-anginal drugs is demonstrated.
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PMID:[Role of many hours of ECG monitoring (Holter method) in the diagnosis of ischemic heart disease and the selection and evaluation of antianginal therapy]. 390 80

Adaptation to exercise or the "warm up phenomenon" has been observed in some patients with angina pectoris. To investigate adaptation, eleven patients with exertional angina pectoris and angiographic evidence of coronary artery disease underwent two identical bouts of sequential tachycardia stress separated by a brief recovery period. Manifestations of ischemia were less during the second stress, as evidenced by a reduction in the severity of angina pectoris, less ST segment depression, and improved lactate extraction. Peak coronary blood flow during the second stress (81 +/- 20 ml/min) was not significantly different from that during the first (95 +/- 32 ml/min). Regional myocardial oxygen consumption, however, was significantly (p = .03) lower during the second stress (8.8 +/- 2.4 ml O2/min) when compared with the first (11.4 +/- 3.0 ml O2/min). Thus, patients with coronary artery disease can develop anginal tolerance to the stress of tachycardia similar to that observed after repeated bouts of exercise. A relative reduction in myocardial oxygen consumption, rather than an increase in coronary blood flow, appears to account for this phenomenon.
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PMID:Adaptation to the stress of tachycardia in patients with coronary artery disease: insight into the mechanism of the warm-up phenomenon. 397 38

The aim of the present study was to assess the incidence of myocardial ischemia during cold pressor test in patients with stable exertional angina pectoris. Thirty-seven patients with proven coronary artery disease were submitted to cold pressor and exercise stress testing; computer assisted electrocardiographic recordings were obtained throughout the examinations. Cold stimulation provoked electrocardiographic signs of subendocardial ischemia only in 3 patients. They had suffered of a previous myocardial infarction and showed low exercise tolerance and severe coronary lesions (one with triple vessel and 2 with left main disease). Interestingly, only one of these patients gave an history of angina during cold exposure. Thus these data indicate that chest pain and electrocardiographic signs of ischemia are an uncommon event during cold pressor stimulation which occurs more likely in patients with fairly severe coronary narrowings. More sensitive markers of ischemia and/or different modalities of cold application are required for studies concerning the relationship between cold exposure and angina pectoris.
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PMID:[Myocardial ischemia induced by the cold pressor test in patients with exertion angina. Case contribution]. 406 72

The effect of 10 mg intravenous isoptin on myocardial hemodynamics, contractility and metabolism during an anginal attack provoked by the atrial stimulation test was examined in 15 coronary patients with angina of effort. Isoptin administration increased anginal threshold, reduced the values indicative of cardiac activity and myocardial oxygen requirement and had no basic effect on coronary flow, while metabolic manifestations of ischemia were neutralized. Isoptin is recommended as an effective means of treatment for angina of effort in patients with atherosclerotic lesions of coronary arteries.
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PMID:[Effect of isoptin on myocardial hemodynamics and contractility during an anginal attack induced by the atrial stimulation test]. 406 54

It is widely accepted that the occurrence of chest pain and/or ST segment elevation during ergonovine testing is a hallmark of abnormal coronary constriction. However, the negativity of this test cannot be considered as an incontrovertible proof of the absence of coronary sensitivity to vasoconstriction. Indeed, it could only indicate that the resulting effect is inadequate to critically reduce coronary blood flow. To test this hypothesis we studied 12 patients with proven coronary artery disease and negative ergonovine test who had complained of chronic exertional angina pectoris and referred variable threshold for the occurrence of pain. They were submitted to atrial pacing (starting from 90 bpm, with 10 bpm increments every 2 min) before (control) and after ergonovine administration (total dose = 0.675 mg). Time, heart rate and rate pressure product were evaluated at the onset of angina and significant ischemia (0.1 mV ST segment depression). After ergonovine, angina was achieved earlier (405 +/- 173 vs 526 +/- 180 sec, p less than 0.005) than during control and at a lower heart rate (116 +/- 15 vs 131 +/- 15 bpm, p less than 0.001) and rate pressure product (15.8 +/- 2.0 vs 18.8 +/- 2.3 X 10(3) U, p less than 0.001). Changes in anginal threshold were widely variable among cases being that the time to onset of pain was dramatically reduced in certain patients but unchanged in one. Similar results were obtained when substituting the ischemic to the anginal threshold. Thus, negativity to ergonovine testing does not imply the absence of coronary constriction which may be revealed when increasing myocardial oxygen demand by atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in angina threshold induced by administration of ergonovine maleate during pacing in patients with chronic exertional angina]. 409 10

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 reproducibility of the direction of R wave amplitude response to exercise was analyzed in patients with coronary artery disease. Forty-three serial exercise tests were performed by 10 patients with exertional angina pectoris and documented coronary artery disease (CAD). Seventeen tests (37%) resulted in no change or an increase in R wave amplitude (abnormal response). Twenty-six tests (63%) resulted in a decrease in R wave amplitude. The direction of the R wave amplitude response was variable in at least one exercise test in 7 of 10 patients with CAD, all of whom had reproducible ischemic ST segment responses during serial testing. The inconsistent R wave response in these patients was unrelated to heart rate, workload, or duration of exercise. Because of the variability in the directional R wave response during serial exercise testing in CAD patients, we conclude that the R wave response during exercise is unreliable for the detection of CAD or ischemia-related myocardial dysfunction.
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PMID:Directional variability in the R wave response during serial exercise testing in patients with coronary artery disease. 648 11


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