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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of doxazosin (alpha-1-inhibitor) and enalapril (ACE-inhibitor) on blood pressure and exercise stress test were assessed in 10 hypertensive patients (8 M, 2 F, age 58 +/- 9 years) with coronary artery disease and exertional myocardial ischemia. A single blind, cross-over, placebo controlled trial was performed. Placebo was administered for 2 periods of 2 weeks, doxazosin and enalapril for at least 3 weeks. The sequence of the active drugs was randomized and the single daily dose, obtained by titration, was 7 +/- 5 mg for doxazosin and 18 +/- 13 mg for enalapril. Blood pressure measurements and treadmill tests (Bruce protocol) were performed at the end of each period. Rest systolic and diastolic pressures after placebo were respectively 173 +/- 15 and 106 +/- 9 mmHg and were reduced to 153 +/- 11 and 93 +/- 12 mmHg (p less than 0.05) after doxazosin and to 150 +/- 24 and 93 +/- 12 mmHg (p less than 0.05) after enalapril. Total exercise time was 473 +/- 91 s after placebo and increased to 545 +/- 84 s (p less than 0.05) after doxazosin and 529 +/- 100 s (p less than 0.05) after enalapril. Time to 1 mm ST depression (ST1) was 297 +/- 102 s after placebo and increased to 414 +/- 96 s (p less than 0.05) after doxazosin and to 396 +/- 133 s (p less than 0.05) after enalapril. Double product at peak exercise and at ST1 were respectively 26.3 +/- 2.8 and 22.1 +/- 2.8 x 10(3) and remained unchanged after enalapril and doxazosin. Peak exercise diastolic blood pressure was 107 +/- 5 mmHg after placebo, was reduced to 94 +/- 15 mmHg (p less than 0.05) after doxazosin and was unchanged after enalapril (101 +/- 10 mmHg, NS). Thus, doxazosin and enalapril induced a comparable decrease of rest blood pressure and a similar increase of exercise time in hypertensive patients with exertional myocardial ischemia. Doxazosin but not enalapril reduced exercise diastolic blood pressure.
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PMID:[Comparative effects of doxazosin and enalapril in patients with arterial hypertension and exercise-induced acute myocardial ischemia]. 168 51

The prognostic value of exercise thallium-201 myocardial perfusion imaging has not been studied in an elderly (aged greater than or equal to 70 years) population. Retrospective analysis of 120 consecutive elderly patients undergoing Bruce protocol exercise stress with quantitative planar thallium-201 scintigraphy, followed clinically for a mean of 36 +/- 12 months after testing, revealed a 10% cardiac event rate (6 cardiac deaths from arrhythmia or congestive heart failure, and 5 fatal and 1 nonfatal myocardial infarction). There were no exercise stress-related complications. Survival without cardiac events was associated with greater exercise duration (5.6 +/- 2.4 vs 3.1 +/- 2.4 minutes; p less than 0.0007) and peak exercise heart rate (131 +/- 18 vs 120 +/- 19 beats/min; p less than 0.05). Univariate variables associated with higher cardiac event rates included: (1) peak exercise less than or equal to stage I (18 vs 6%; p = 0.04); (2) maximal ST-segment depression greater than or equal to 2 mm (27 vs 6%; p = 0.003); and (3) presence of a fixed or reversible thallium-201 perfusion defect (18 vs 2%; p = 0.004). Multivariate stepwise logistic regression analysis identified the combination of peak exercise less than or equal to stage I and any thallium-201 perfusion defect as the most powerful predictor of subsequent cardiac events (relative risk = 5.3 at 1 year). Thus, exercise thallium-201 scintigraphy in elderly patients is safe and provides important prognostic information.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic significance of exercise thallium-201 testing in patients aged greater than or equal to 70 years with known or suspected coronary artery disease. 172 66

The importance of low-level (warm-up) exercise for reducing exercise-induced myocardial ischemic symptoms in patients with coronary artery disease is well-recognized by clinicians. Whether altering the abruptness of exercise, such as that which occurs during different frequently used testing protocols, affects myocardial ischemic variables and maximal exercise capacity has not been resolved. This study seeks to determine the effects of altering the increment of work-rate change per exercise stage on both the ischemic threshold and maximal exercise capacity using 2 frequently used exercise testing protocols. Thirty-two patients with documented coronary artery disease and previously positive exercise tests (ischemic ST depression greater than or equal to 1.0 mm) performed symptom-limited exercise tests using both the standard and modified Bruce protocols in random order, 1 hour apart. Exercise electrocardiograms were analyzed to determine the ischemic threshold, defined as heart rate at onset of greater than or equal to 1.0 mm ischemic ST depression. Patients achieved a higher peak heart rate (124 +/- 19 vs 117 +/- 21 beats/min; p less than 0.0001), rate-pressure product (21.4 +/- 3.9 vs 19.8 +/- 4.1 beats/min x mm Hg x 10(3); p less than or equal to 0.0001) and oxygen consumption (VO2) (18.5 +/- 3.7 vs 16.5 +/- 4.4 ml/kg/min; p less than or equal to 0.001) with the standard than with the modified Bruce protocol. At matched submaximal exercise stages there were no differences in VO2, heart rate or oxygen pulse between protocols. Time to ischemic threshold was significantly reduced with the standard compared with the modified Bruce protocol (312 +/- 107 vs 607 +/- 221 seconds; p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of ischemic and physiologic responses during exercise tests in men using the standard and modified Bruce protocols. 172 72

It has recently been demonstrated that treadmill capacity and collateral circulation improve as a result of exercise with heparin pretreatment in patients with effort angina. In the present study, we assessed whether heparin alone is effective in increasing treadmill capacity in 14 patients with effort angina. Patients were randomly assigned to one of two treatment arms: (1) group A--20 treadmill exercise periods with standard Bruce protocol twice a day for 10 days with heparin (5000 IU intravenously) pretreatment (seven patients) or (2) group B--10 injections of heparin calcium (10,000 IU subcutaneously) once a day for 10 days (seven patients). In group A, total exercise time was increased from 6.9 +/- 1.2 (SD) to 9.9 +/- 1.9 minutes (p less than 0.0005), as was the maximal double product, from 21,700 +/- 3,500 to 27,000 +/- 4,800 mm Hg/min (p less than 0.05). The double product at the onset of angina was also increased by 34% (p less than 0.05), and the double product at which ST depression (0.1 mV) first appeared was 22% (p less than 0.05) greater after treatment. In contrast, in group B, all of the above-mentioned parameters of treadmill capacity remained unchanged. These data indicate that heparin does not serve as an angiogenic factor by itself, but that it potentiates the ischemia-derived angiogenic factor.
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PMID:Comparative effect of heparin treatment with and without strenuous exercise on treadmill capacity in patients with stable effort angina. 185 25

This study was performed to evaluate the presence of angina pectoris, electrocardiographic changes and reversible thallium-201 defects resulting from 2 different levels of exercise in 19 patients with known coronary artery disease and evidence of exercise-induced ischemia. The exercise protocols consisted of a symptom-limited incremental exercise test (Bruce protocol) followed within 3 to 14 days by a submaximal, steady-state exercise test performed at 70% of the maximal heart rate achieved during the Bruce protocol. The presence and time of onset of angina and electrocardiographic changes (greater than or equal to 0.1 mV ST-segment depression) as well as oxygen uptake, exercise duration and pressure-rate product were recorded. Thallium-201 (2.5 to 3.0 mCi) was injected during the last minute of exercise during both protocols, and the images were analyzed using both computer-assisted quantitation and visual interpretations. Incremental exercise resulted in anginal symptoms in 84% of patients, and electrocardiographic changes and reversible thallium-201 defects in all patients. In contrast, submaximal exercise produced anginal symptoms in only 26% (p less than 0.01) and electrocardiographic changes in only 47% (p less than 0.05), but resulted in thallium-201 defects in 89% of patients (p = not significant). The locations of the thallium-201 defects, when present, were not different between the 2 exercise protocols. These findings confirm the sequence of the ischemic cascade using 2 levels of exercise and demonstrate that the cascade theory is applicable during varying ischemic intensities in the same patient.
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PMID:Comparison of chest pain, electrocardiographic changes and thallium-201 scintigraphy during varying exercise intensities in men with stable angina pectoris. 187 74

The purpose of this study was to elucidate the mechanism that induces an improvement in exercise capacity by nitrates in patients with stable effort angina pectoris. The study population was composed of 19 patients: group A, 10 patients with chronic stable effort angina who had a well-developed coronary collateral circulation to the potentially ischemic region; group B, 9 patients with chronic stable effort angina who had no collateral circulation to the jeopardized myocardium. Treadmill exercise was performed according to the standard Bruce protocol with and without pretreatment with orally administered 10 mg isosorbide dinitrate. Percent increases (mean +/- SE) in exercise duration were not significantly different between groups A and B (25 +/- 6 vs. 14 +/- 6%). Percent increases in the maximal rate-pressure product tended to be greater in group A than in group B (27 +/- 6 vs. 10 +/- 6%). Percent increases in the rate-pressure product at the onset of angina pectoris were significantly greater in group A than in group B (37 +/- 7 vs. 7 +/- 6%; p less than 0.01). Percent increases in the rate-pressure product at 0.1 mV S-T segment depression were also significantly greater in group A than in group B (26 +/- 6 vs. 1 +/- 5%; p less than 0.01). These results suggest that isosorbide dinitrate dilates epicardial collateral vessels with smooth muscle layers, but fails to dilate the coronary arteries with significant organic stenoses.
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PMID:Importance of coronary collateral circulation for increased treadmill exercise capacity by nitrates in patients with stable effort angina pectoris. 188 50

A moose (Alces alces gigas) was inoculated with Brucella suis biovar 4 to better understand the effects of brucellosis in this species. Serum antibody titers increased rapidly and peaked within 21 to 56 days. Fever, leukocytosis, recumbency, anorexia and depression were observed starting 42 days post inoculation. Brucella suis biovar 4 was isolated from blood, lymph nodes, liver and spleen.
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PMID:Experimental Brucella suis biovar 4 infection in a moose. 192 Jun 68

The accuracy of exercise electrocardiography in detecting a physiologically significant coronary artery stenosis has been assessed previously by comparing the exercise test with a coronary arteriogram. The inherent inaccuracy of visually determined percent diameter stenosis measurements might have lead to the conclusion that the exercise electrocardiogram was less accurate than it truly was. To determine the accuracy of the exercise electrocardiography in detecting a physiologically significant coronary stenosis, we studied 40 patients with one-vessel, one-lesion coronary artery disease, a normal resting electrocardiogram, and no hypertrophy or prior infarction. Each patient underwent exercise electrocardiography (Bruce protocol) that was interpreted as abnormal if the ST segment developed 0.1-mV or greater depression 80 msec after the J point. The physiological significance of each coronary stenosis was assessed by measuring of coronary flow reserve (peak divided by resting blood flow velocity) in the stenotic artery using a Doppler catheter and intracoronary papaverine (normal, 3.5 or greater peak/resting velocity). The percent diameter and percent area stenosis produced by each lesion were determined using quantitative angiography (Brown/Dodge method). Of the 17 patients with reduced coronary flow reserve (3.5 or greater peak/resting blood flow velocity) in the stenotic artery, 14 had an abnormal exercise electrocardiogram (sensitivity, 0.82; 95% confidence interval, 0.70-0.94). Conversely, 20 of 23 patients with normal coronary flow reserves had normal exercise tests (specificity, 0.87; 95% confidence interval, 0.77-0.97). The exercise electrocardiogram was abnormal in each of 11 patients with markedly reduced coronary flow reserve (less than 2.5 peak/resting velocity) and in three of six patients with moderately reduced reserve (2.5-3.4 peak/resting velocity). The products of systolic blood pressure and heart rate at peak exercise were significantly correlated with coronary reserve in patients with truly abnormal exercise tests. In comparison, the sensitivity (0.61; 95% confidence interval, 0.46-0.76) and specificity (0.73; 95% confidence interval, 0.60-0.86) of exercise electrocardiography in detecting a 60% or greater diameter stenosis may be significantly lower (p less than 0.05). Exercise electrocardiography, therefore, was a good predictor of the physiological significance (assessed by coronary flow reserve) of a coronary stenosis in patients with a normal resting electrocardiogram and no hypertrophy or prior infarction. Its value in a broader and larger patient population will require further study. These results, however, underscore the importance of a physiological gold standard in assessing the accuracy of noninvasive studies for detecting coronary artery disease.
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PMID:Accuracy of exercise electrocardiography in detecting physiologically significant coronary arterial lesions. 199 65

The relation between ambulatory myocardial ischemia and the results of exercise testing in patients with ischemic heart disease remains undefined, because of the dissimilar results of previous reports. To further investigate this issue and, in particular, to ascertain the importance of the exercise protocol in determining that relation, 70 patients with stable coronary artery disease underwent 48 h ambulatory electrocardiographic (ECG) monitoring and treadmill exercise tests after withdrawal of medications. Patients exercised using two different protocols with slow (National Institutes of Health [NIH] combined protocol) and brisk (Bruce protocol) work load increments. Exercise duration was longer with the NIH combined protocol (14.1 +/- 5 versus 6.8 +/- 2 min; p less than 0.0001), but the maximal work load and peak heart rate achieved were greater with the Bruce protocol (9.8 +/- 2 versus 6.5 +/- 2 METs, and 142 +/- 19 versus 133 +/- 22 beats/min, respectively; p less than 0.0001). A close inverse correlation between exercise testing and the results of ambulatory ECG monitoring was observed using the NIH combined protocol; the strongest correlation was observed between time of exercise at 1 mm of ST segment depression and number of ischemic episodes (r = -0.86; p less than 0.0001). With the Bruce protocol a significantly weaker inverse correlation was found (r = -0.35). The mean heart rate at the onset of ST segment depression was similar during monitoring and during exercise testing with the NIH combined protocol (97.2 +/- 13 versus 101.0 +/- 17 beats/min, respectively) but it was significantly higher (110.4 +/- 13) when using the Bruce protocol (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prediction of the frequency and duration of ambulatory myocardial ischemia in patients with stable coronary artery disease by determination of the ischemic threshold from exercise testing: importance of the exercise protocol. 199 85

We studied the effect of propranolol administration on risk assessment based on submaximal exercise testing performed early after myocardial infarction. A total of 70 patients with recent infarction underwent modified Bruce treadmill testing with simultaneous measurement of expired gases in the absence of antianginal agents including beta-antagonists. Among these, 31 patients who had at least one of the following abnormalities--ST depression greater than or equal to 1 mm (22 patients), chest pain (four patients), or treadmill time less than 360 seconds (12 patients)--were studied in a randomized double-blind fashion and received either placebo or 240 mg of propranolol/day. A total of 28 patients completed the randomized phase and were able to undergo repeat exercise testing an average of 3.4 +/- 1.8 days later. Randomized groups were equivalent at baseline except for a higher peak oxygen consumption and carbon dioxide production (p less than 0.05) in the propranolol compared with the placebo group; these differences were taken into account in statistical analyses of the study data. Resting heart rate (59 +/- 1.2 versus 82 +/- 4.2 beats/min) and peak heart rate x systolic blood pressure (14,208 +/- 496 versus 20,075 +/- 1,062) were both significantly less (p less than 0.01) after propranolol than after placebo. Eight of nine patients treated with placebo maintained ST depression greater than or equal to 1 mm from the initial to the randomized exercise test, compared with only 4 of 13 receiving propranolol (p less than 0.01). In those with continued ST depression, time to positivity was significantly longer in those receiving propranolol compared with those taking placebo (538 +/- 73 versus 318 +/- 44 seconds, p less than 0.05). In contrast, the peak ratio between carbon dioxide production and oxygen consumption was higher in those receiving propranolol compared with those receiving placebo (0.93 +/- 0.04 versus 0.81 +/- 0.03, p less than 0.05). We conclude that propranolol therapy reduces evidence of ischemia and changes traditional estimates of potential cardiac risk derived from submaximal postinfarction exercise testing.
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PMID:Propranolol therapy alters estimation of potential cardiovascular risk derived from submaximal postinfarction exercise testing. 203 80


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