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 purpose of this study was to evaluate jogging in place as an electrocardiographic exercise test. Jogging in place continuously recorded via an ordinary single-channel electrocardiograph was compared with the Bruce treadmill protocol with a three-channel monitor and recorder in 141 cases with a wide spectrum of chest complaints. Agreement for the presence or absence of electrocardiographic ischemia (ST-segment displacement greater than or equal to 1 mm at 80 ms from the J point, or U-wave inversion) for the two tests was observed in 91 percent of the cases (95 percent confidence intervals: 86 percent to 95.5 percent). One hundred of the previous cases with paired electrocardiographic exercise tests were compared with the presence of reversible defects on exercise myocardial thallium-201 scintigraphy. The electrocardiographic ischemia had a similar correct classification rate in both methods (83 percent with jogging in place and 85 percent with Bruce treadmill protocol; not significant) against the finding of scintigraphic ischemia. This was also true for 52 cases having selective coronary arteriography. The correct classification rate was 54 percent (28/52) with jogging in place and 48 percent (25/52) with Bruce treadmill protocol (not significant). Given the safety and the easy applicability, even in older persons, this simplified test can be recommended as a valid alternative to the established multistage exercise tests.
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PMID:Jogging in place. Evaluation of a simplified exercise test. 279 82

It has been demonstrated in animal experiments that heparin accelerates the coronary collateral development induced by repeated coronary occlusion. We used this effect of heparin for the treatment of patients with stable effort angina. In 10 patients, treadmill exercise was performed according to standard Bruce protocol twice a day for 10 days. A single intravenous dose of heparin (5000 IU) was given 10 to 20 min before each exercise period. Exercise with heparin pretreatment increased the total exercise duration from 6.3 +/- 1.9 (SD) to 9.1 +/- 2.2 min (p less than .001) and the maximal double product (DP) from 18,900 +/- 5100 to 25,500 +/- 6800 mm Hg.beats/min (p less than .001). The DP at the onset of angina was also increased by 35% (p less than .01) and the DP at which ST depression (0.1 mV) first appeared was 19% (p less than .05) greater after treatment. Repeat coronary cineangiography revealed an increase in the extent of opacification of collaterals to the jeopardized myocardium. In an additional six patients, treadmill exercise was performed with no medication twice a day for 10 days. All of the above-mentioned variables of treadmill capacity remained unchanged, despite 20 exercise periods without heparin pretreatment. Thus, heparin accelerates exercise-induced coronary collateral development by promoting angiogenesis. The development of such a therapeutic modality will open a new field for the treatment of patients with ischemia.
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PMID:Improvement of treadmill capacity and collateral circulation as a result of exercise with heparin pretreatment in patients with effort angina. 283 15

Calcium channel blockers and beta-receptor blockers improve symptoms of myocardial ischemia by potentially different mechanisms. Accordingly, combination therapy may entail additive benefits. Twenty-four patients with symptomatic stable effort angina despite full beta-blockade were randomized to a double-blind Latin square protocol in which they received propranolol in a dose producing full beta-receptor blockade, diltiazem, 240 mg/day, in divided doses and a combination of propranolol and diltiazem, 240 or 360 mg/day. Treadmill testing (Bruce protocol) was utilized to assess exercise tolerance, radionuclide ventriculography to assess left ventricular function and clinical follow-up to assess adverse effects and overall clinical response. Comparable treadmill exercise times were observed with monotherapy (344 +/- 83 seconds with propranolol and 341 +/- 87 seconds with diltiazem) and the lower dose combination (361 +/- 87 seconds). With propranolol and diltiazem, 360 mg/day, however, there was a significant increase in treadmill time (393 +/- 106 seconds; p less than 0.05). In five patients whose treadmill exercise was limited by angina on all therapies, there was a significant improvement in the time to onset of chest pain with both low dose and high dose combinations (311 +/- 71 seconds, p less than 0.05 and 336 +/- 76 seconds, p less than 0.01, respectively). Improved treadmill performance was supported by the clinical response, while an increase in adverse effects was not observed. Thirteen of 24 patients blindly selected the higher dose diltiazem combination as their optimal therapy. Left ventricular dilation was observed (by radionuclide ventriculography) in response to exercise in each phase of therapy; this was related to stress-induced ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effort angina with adequate beta-receptor blockade: comparison with diltiazem alone and in combination. 286 30

Nicorandil therapy was compared with placebo therapy in 11 patients with chronic stable angina pectoris. A computer-assisted treadmill exercise test was performed after administration of either 10 or 30 mg of nicorandil. Analysis of variance showed a significant difference among placebo and nicorandil treatments (p less than 0.01). Ten milligrams of nicorandil prolonged time to onset of ischemia 36% (p less than 0.05) but increased the exercise duration only 15%. Thirty milligrams of nicorandil prolonged time to onset of ischemia 82% (p less than 0.01) and exercise duration 45% (p less than 0.01). Both time to onset of ischemia and exercise duration increased progressively from the 10-mg to the 30-mg dose (p less than 0.05). Heart rate at rest was significantly higher and systolic pressure at rest significantly lower with 30 mg of nicorandil than with placebo. After administration of 30 mg of nicorandil there was a significant reduction in ST depression associated with a slight decrease in the double product at the end of Bruce stage 2 exercise. The peak double product was greater after administration of 30 mg of nicorandil than after placebo, indicating an increased myocardial oxygen supply to the ischemic area. The plasma concentration of nicorandil averaged 78 +/- 83 ng/ml with the 10 mg and 313 +/- 142 ng/ml with 30 mg. There was an increase in exercise duration of more than 1 minute in 8 of 9 patients who had plasma nicorandil concentrations greater than 100 ng/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative efficacy of high-dose versus low-dose nicorandil therapy for chronic stable angina pectoris. 294 20

The elevation of cardiac filling pressure induces the release of atrial natriuretic peptide into the circulation. Ischemia during exercise in patients with coronary artery disease may manifest itself with elevation of cardiac filling pressure before the onset of electrocardiographic changes or chest pain. Thus, patients with ischemic heart disease might have an elevated circulating atrial natriuretic peptide after exercise. The present study investigated the effect of exercise on circulating atrial natriuretic peptide in patients with and without ischemic heart diseases. Group 1 was composed of five patients who had ischemic heart disease by clinical history, previous myocardial infarction, angina or angiographically proven coronary artery disease and positive electrocardiogram during exercise. Group 2 was composed of five patients without ischemic heart disease and negative electrocardiogram response. Heart rate, blood pressure, and atrial natriuretic peptide were measured during routine treadmill exercise testing using the Bruce protocol. Our results indicate that the rate of rise of heart rate (12.3 +/- 1.8 vs. 8.5 +/- 0.7 beats/min/min), blood pressure (7.1 +/- 1 vs. 4.2 +/- 0.8 mm Hg/minute), and atrial natriuretic peptide (4.1 +/- 1 vs. 1.4 +/- 0.3 pg/ml/min) was significantly elevated in patients with ischemic heart disease compared to the group 2 patients. These findings suggest that the disproportionate elevation of atrial natriuretic peptide after exercise in ischemia may be caused by elevation of cardiac filling pressure, which may provide a noninvasive method for the diagnosis of ischemic heart disease.
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PMID:The differential response in atrial natriuretic peptide release during exercise in patients with and without ischemic heart disease. 296 77

Although silent myocardial ischemia is a well recognized phenomenon, the reasons for the lack of symptoms in patients with coronary artery disease (CAD) is unclear. Because the endogenous opioid beta-endorphin has been related to pain modulation, plasma beta-endorphin levels were studied before, during and after exercise-induced ischemia in symptomatic and asymptomatic men. Because beta-endorphin responses have been closely linked to adrenocorticotropic hormone (ACTH) and cortisol responses, these hormones also were measured. Nine symptomatic and 12 asymptomatic patients with a high probability (at least 95%) of CAD and 8 apparently healthy men completed a Bruce protocol treadmill test. Blood samples were drawn before, during and 10 minutes after exercise. During exercise the measured hormones showed no significant increases from basal levels. However, plasma beta-endorphin, ACTH and cortisol levels were significantly elevated (p less than or equal to 0.01) 10 minutes after exercise in all 3 groups. There was no significant difference in plasma beta-endorphin levels during or after exercise between the symptomatic and asymptomatic patients with CAD. Thus, differences in circulating levels of beta-endorphin, ACTH and cortisol are not associated with the presence or absence of pain during exercise-induced myocardial ischemia.
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PMID:Plasma beta-endorphin levels in silent myocardial ischemia induced by exercise. 303 88

A 26-year old white male with Prader-Willi syndrome (PWS) and non-insulin-dependent diabetes mellitus presented with asymptomatic bilateral lower limb swelling. An electrocardiogram was consistent with an inferior wall myocardial infarction of unknown age and a graded exercise test using the Bruce protocol was consistent with inferolateral ischemia. Subsequent cardiac catheterization showed severe, inoperable, three-vessel coronary artery disease. Atherosclerotic coronary artery disease in PWS has been documented only once in the literature, and then only postmortem. This case provides further (and for the first time, premortem) documentation that premature atherosclerotic coronary artery disease may play an important but presently unrecognized role in the morbidity and mortality in PWS.
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PMID:Premature coronary artery atherosclerosis in a patient with Prader-Willi syndrome. 368 25

To better understand the relationship between the transient myocardial ischemia seen during an exercise test and ischemic activity out of hospital, 39 patients with well-documented coronary artery disease underwent standard treadmill exercise testing (Bruce protocol) and 24 to 48 hr of continuous ambulatory electrocardiographic monitoring during normal daily activities. A total of 245 episodes of transient ischemia were recorded in 21 of 32 patients with positive exercise electrocardiograms (group I), whereas seven patients with negative test results (group II) had no episodes of transient ischemia, during monitoring out of hospital (p less than .01). Certain measures in the exercise test were related to the severity of ischemia out of hospital: there were more episodes and a greater total duration of transient ischemia per 24 hr of ambulatory monitoring in patients who developed ischemic electrocardiographic changes before 6 min of exercise (p less than or equal to .021) or at a heart rate of less than 150 beats/min (p = .005) and in those in whom these ST segment changes persisted for more than 5 min after exercise (p less than or equal to .016). In contrast, there was no relationship between transient ischemia out of hospital and the commonly quoted exercise variables: chest pain, total exercise duration, and the maximum levels of heart rate, systolic blood pressure, and double product. Thus, patients with coronary artery disease and negative exercise electrocardiograms are most unlikely to experience active ischemia during normal daily life.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Features of the exercise test that reflect the activity of ischemic heart disease out of hospital. 370 81

The sensitivity of dipyridamole--2-dimensional (2-D) echocardiography was assessed for detection and localization of ischemia in 21 patients with severe chronic stable angina pectoris, a clearly positive exercise stress test response and multivessel coronary atherosclerosis. Regional wall motion during dipyridamole infusion (0.6 mg/kg intravenously over 4 minutes) was compared with control and recovery by 2 blinded observers in consensus. Transient regional wall motion abnormalities were observed in 11 patients. Angina and ST-segment changes occurred in 9 of these 11 patients with positive responses, but in none of those who showed no transient abnormality of regional wall motion. Localization of regional wall motion abnormalities correlated well with angiographic severity of coronary lesions. Endocardial area contraction, evaluated by a computerized system, was reduced significantly after dipyridamole administration in patients with a positive response (from 51 +/- 10% to 35 +/- 11%, p less than 0.001), whereas it did not change significantly in the others (from 43 +/- 6% to 42 +/- 8%). In the 11 patients with a positive response, coronary reserve assessed by exercise testing (modified Bruce protocol) was more impaired than in those with a negative response (time to 1 mm of ST depression 177 +/- 148 seconds and 472 +/- 179 seconds, respectively, p less than 0.01). In patients with severe angina and multivessel coronary artery disease, dipyridamole--2-D echocardiography appears to identify the vessel in which flow reserve is most limited. Although this information may be valuable, indications for the test are restricted to patients with severely limited exercise capacity.
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PMID:Limitations of dipyridamole-echocardiography in effort angina pectoris. 381 69

Abnormalities of the 12 lead electrocardiogram (ECG) are often used to localize the anatomic site of myocardial ischemia and vessel involvement in patients (pts) with coronary artery disease. This study is to determine if ischemia of specific vascular segments can be identified by exercise induced ST segment depression (STD) on 12-lead ECG. One hundred and forty three pts with a positive treadmill stress testing (TST) who had coronary arteriography within one month of TST were reviewed. There were 114 men and 29 women, aged 34-74 years (mean 55 years). The Bruce protocol was used for TST. Significant coronary stenosis was defined as obstruction of 70% or greater of the luminal diameter. The pattern of STD on 12 lead ECG during exercise was similar in pts with single vessel disease involving the left anterior descending artery (LAD), right coronary artery (RCA) or circumflex artery (Cx). This pattern of STD in single vessel disease was also comparable to 2-vessel, 3-vessel or left main stem disease. Twenty-two percent of pts with LAD disease had isolated STD in inferior leads. Twenty-five and 29% of pts with RCA and Cx disease respectively had STD in the anterior leads alone during exercise testing. It is concluded that exercise induced STD in 12 lead ECG can not predict ischemia of specific vascular segments or specific vessel involvement.
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PMID:Localization of coronary artery disease with exercise induced ST segment depression: coronary angiographic correlation. 385 Jul 71


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