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

STUDY OBJECTIVE - The aim of the study was to verify the reproducibility of a canine model of treadmill exercise induced regional myocardial dysfunction designed to mimic exertional angina pectoris in man. DESIGN - Dogs trained to run on a treadmill were chronically instrumented with a microtip manometer in the left ventricle, a hydraulic occluder around the circumflex branch of the left coronary artery, two pairs of crystals for sonomicrometry, and arterial and venous catheters. Experiments were started 10 d after surgery, when the animals were submitted to seven treadmill exercise cycles, each of 3 min, with a 7 min recovery period. Ischaemia was adjusted so as not to impair regional function at rest but to produce progressive dysfunction with increasing work load. Flestolol (1 microgram.kg-1.min-1) was infused intravenously during the third and fourth exercise cycle. SUBJECTS - Six mongrel dogs, 13.5-29.5 kg, were used. MEASUREMENTS and RESULTS - Flestolol caused a marked reduction in the exercise induced increase in left ventricular positive dP/dtmax, and minor reductions in heart rate and systolic blood pressure, resulting in a decrease in myocardial oxygen demand and an improvement in regional function in the circumflex area of the left coronary artery. The functional improvement was transient and disappeared entirely after termination of flestolol infusion. CONCLUSIONS - The results show that flestolol is beneficial in conditions of limited coronary reserve and exercise induced myocardial dysfunction. The fact that the extent of regional myocardial dysfunction was comparable before and after flestolol infusion confirms the stability and usefulness of this experimental model in the evaluation of antianginal drugs.
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PMID:Verification of a canine model of transient exercise induced myocardial dysfunction: antianginal effects of flestolol, an ultra short acting beta adrenoceptor antagonist. 197 Feb 78

The anti-ischemic effects of atenolol and nifedipine were compared in a randomized double-blind crossover manner in 24 patients with stable exertional angina and transient silent ischemia during ambulatory electrocardiographic (ECG) monitoring. Both atenolol and nifedipine were effective (p less than 0.005) in reducing the average number and duration of transient ischemic events, but therapy with atenolol was associated with a significantly greater reduction in the mean number (p less than 0.05) and duration (p less than 0.01) of silent ischemic events. Analyses of the silent ischemic activity during the morning hours revealed that only therapy with atenolol produced a significant reduction in the average duration per patient (139 +/- 54 vs. 1,609 +/- 468 s, p less than 0.01) and in the average duration of silent ischemia per event between 6 AM and 12 noon (62 +/- 21 vs. 208 +/- 24 s, p less than 0.005). There were fewer adverse experiences during therapy with atenolol. These results show that although both atenolol and nifedipine are effective in reducing silent ischemic events, treatment with atenolol is associated with significantly greater efficacy, particularly on the morning surge of silent myocardial ischemia.
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PMID:Anti-ischemic effects of atenolol versus nifedipine in patients with coronary artery disease and ambulatory silent ischemia. 199 34

Silent ischemia is common in diabetic patients with coronary heart disease. These patients may also have more subtle alteration in the perception of angina as reflected by prolongation of anginal perceptual threshold--the time from onset of 0.1 mV ST segment depression to the onset of chest pain during treadmill exercise. Silent ischemia may be associated with a generalized hyposensitivity to pain, although the pathophysiologic mechanism is obscure. The purpose of the present study was to determine whether diabetic patients with prolonged anginal perceptual thresholds are also hyposensitive to painful stimuli and to investigate whether this is associated with autonomic neuropathy. Nineteen diabetic and 25 nondiabetic patients with exertional angina were exercised on a treadmill to measure anginal perceptual threshold. Somatic pain threshold was measured by calf sphygmomanometry. The cuff was inflated rapidly until pain occurred, and six repeat inflations were done to test reproducibility. Because there was no significant difference between measurements (coefficient of variation = 0.156) the mean value for each patient provided a measure of somatic pain threshold. The diabetic group had a longer anginal perceptual threshold (138 +/- 64 seconds vs 34 +/- 51 seconds, p less than 0.001), which correlated positively with the somatic pain threshold (r = 0.5, p = 0.03); patients with more prolonged anginal perceptual thresholds tended to have higher somatic pain thresholds. In the diabetic group anginal perceptual (r = -0.3, p = NS) and somatic pain (r = -0.4, p = 0.05) thresholds tended to increase as the ratio of peak to minimal heart rate during the Valsalva maneuver fell below 1.21, but these variables were unrelated in the nondiabetic group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The perception of angina in diabetes: relation to somatic pain threshold and autonomic function. 159 62

The purpose of this study was to determine whether low doses of carbon monoxide (CO) exacerbate myocardial ischemia during a progressive exercise test. The effect of CO exposure was evaluated using the objective measure of time to development of electrocardiographic changes indicative of ischemia and the subjective measure of time to onset of angina. Sixty-three male subjects (41-75 years) with well-documented coronary artery disease, who had exertional angina pectoris and ischemic ST-segment changes in their electrocardiograms, were studied. Results from three randomized, double-blind test visits (room air, low and high CO) were compared. The effect of CO exposure was determined from the percent difference in the end points obtained on exercise tests performed before and after a 1-hr exposure to room air or CO. The exposures resulted in postexercise carboxyhemoglobin (COHb) levels of 0.6% +/- 0.3%, 2.0% +/- 0.1%, and 3.9% +/- 0.1%. The results obtained on the 2%-COHb day and 3.9%-COHb day were compared to those on the room air day. There were 5.1% (p = 0.01) and 12.1% (p less than or equal to 0.0001) decreases in the time to development of ischemic ST-segment changes after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. In addition, there were 4.2% (p = 0.027) and 7.1% (p = 0.002) decreases in time to the onset of angina after exposures producing 2.0 and 3.9% COHb, respectively, compared to the control day. A significant dose-response relationship was found for the individual differences in the time to ST end point and angina for the pre- versus postexposure exercise tests at the three carboxyhemoglobin levels. These findings demonstrate that low doses of CO produce significant effects on cardiac function during exercise in subjects with coronary artery disease.
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PMID:Effects of carbon monoxide on myocardial ischemia. 204 Feb 54

To examine whether acute myocardial ischemia activates the coagulation system and platelet activation in the coronary circulation, we measured plasma levels of fibrinopeptide A and beta-thromboglobulin in the coronary sinus and the aortic root simultaneously in 15 patients with coronary spastic angina before and after the left coronary spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Fifteen patients with chest pain but normal coronary arteries and no coronary spasm served as controls. The coronary sinus-arterial difference of fibrinopeptide A increased markedly (p less than 0.001) from 0.1 +/- 0.2 to 4.3 +/- 0.7 ng/ml after the anginal attacks in the coronary spastic angina group. However, fibrinopeptide A levels remained unchanged after the attacks in the stable exertional angina group and after intracoronary injection of acetylcholine in the control group. Plasma beta-thromboglobulin levels remained unchanged after the attacks in both patient groups and after acetylcholine in the control group. Our data indicate that coronary spasm induces thrombin generation and may lead to thrombus formation in the coronary artery involved, but pacing-induced ischemia does not activate the coagulation system.
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PMID:Fibrinopeptide A is released into the coronary circulation after coronary spasm. 214 92

Patients with diabetes are prone to silent myocardial infarction and silent exertional ischemia. Although the mechanism is not clear, it may reflect a specific impairment of the sensory innervation of the heart. To test this hypothesis, anginal perceptual threshold was measured in 32 diabetic patients and 36 nondiabetic control patients, all of whom had typical exertional angina. Anginal perceptual threshold was defined as the time from onset of 0.1 mV ST depression to the onset of chest pain during treadmill stress electrocardiography. Although ST depression occurred earlier in the diabetic than in the nondiabetic group (111 +/- 82 versus 216 +/- 162 s, p less than 0.005), the anginal perceptual threshold in the diabetic group was delayed by a mean of 86 s (149 +/- 76 versus 63 +/- 59 s, p less than 0.001), with 95% confidence intervals of 53 to 119 s. Autonomic function tests were abnormal in the diabetic group, and in both groups regression analyses (using a third order polynomial) showed marked prolongations of anginal perceptual threshold as the heart rate responses to the Valsalva maneuver decreased to below the normal range (r = 0.5, p less than 0.001). There was a similar though less pronounced relation between anginal perceptual threshold and the heart rate responses to deep breathing (r = 0.3, p less than 0.02). These data suggest that prolongation of the anginal perceptual threshold may be caused by autonomic neuropathy involving the sensory innervation of the heart. To test sensory function, median nerve conduction studies were performed in 19 patients (10 diabetic and 9 nondiabetic).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exertional myocardial ischemia in diabetes: a quantitative analysis of anginal perceptual threshold and the influence of autonomic function. 229 45

Great cardiac vein blood flow by thermodilution and great cardiac vein oxygen saturation were measured in 14 patients with stable exertional angina and an angiographic pattern of complete occlusion of the proximal left anterior descending artery retrogradely filled by collateral vessels supplying still viable myocardium. Measurements were obtained under control conditions, at peak atrial pacing and after dipyridamole administration (0.56 mg/kg intravenously over 4 minutes). Both stress tests induced ischemic electrocardiographic changes in all patients, but dipyridamole administration resulted in greater ST-segment depression in 11 patients (1.6 +/- 0.5 vs 2.4 +/- 1.6 mm, p less than 0.05) and transient ST-segment elevation in 3 patients. Dipyridamole provoked ischemia at a lower value of rate-pressure product (145.3 +/- 30.6 vs 202.9 +/- 36.6 beats/min . mm Hg . 10(-2), p less than 0.0005) and anterior region myocardial oxygen consumption (9.32 +/- 4.76 vs 11.39 +/- 3.91 ml/min, p less than 0.05), despite a greater increase in great cardiac vein flow (139.4 +/- 45 vs 93 +/- 27.4 ml/min, p less than 0.0025) and a greater decrease in the calculated index of anterior region coronary resistance (0.87 +/- 0.27 vs 1.46 +/- 0.43 mm Hg/ml/min, p less than 0.0005). Moreover, great cardiac vein oxygen saturation increased more significantly during dipyridamole-induced ischemia than at peak pacing (63 +/- 12 vs 35 +/- 8%, p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of atrial pacing and dipyridamole administration on coronary hemodynamics of collateralized myocardial regions in stable angina pectoris. 231 50

The purpose of this study was to determine, using more objective evidence than that reported in previous studies, whether or not exposures to carbon monoxide that produce approximately 2% or 4% blood carboxyhemoglobin levels cause an exacerbation of myocardial ischemia during a progressive exercise test. The objective measurements were based on the development of electrocardiographic evidence of ischemia. In addition, time to onset of angina pectoris was studied. Male subjects, ages 35 to 75, with stable exertional angina pectoris and positive exercise treadmill tests with reproducible ischemic ST-segment changes in their electrocardiograms, were studied. In addition, each subject fulfilled at least one of the following criteria of coronary artery disease: angiographic evidence of at least a 70% occlusion of one or more major coronary artery; prior documented myocardial infarction; or a positive exercise thallium test. Each subject was evaluated on four separate occasions, a qualifying visit and three blinded test visits, which involved exposure (in random order) to air without added carbon monoxide and to air that contained carbon monoxide concentrations calculated to produce approximately 2.2% or 4.4% carboxyhemoglobin, measured by gas chromatography, at the end of the exposure period. These immediate postexposure target levels were set 10% higher than the desired postexercise carboxyhemoglobin levels of 2.0% and 4.0% because exercise while breathing room air results in loss of carbon monoxide. The actual one-minute postexercise levels reached were 2.0% +/- 0.1% (mean +/- standard error of the mean) and 3.9% +/- 0.1%. On each test day, the subject performed a symptom-limited exercise test on a treadmill, was exposed for approximately one hour to air or to one of two levels of carbon monoxide in air, and then performed a second exercise test. Time to the onset of ischemic ST-segment changes and time to the onset of angina were determined for each exercise test. The percent difference for these endpoints on the pre- and postexposure exercise tests was determined, and then the results on the 2%-COHb-target day and the results on the 4%-COHb-target day were compared to those on the control day. Data from the 63 subjects who completed the three test visits and met all protocol criteria were analyzed. There were 5.1% (p = 0.01) and 12.1% (p less than or equal to 0.0001) (trimmed mean) decreases in the time to development of ischemic ST-segment changes after the 2%- and 4%-COHb-target exposures, respectively, compared to the control day.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute effects of carbon monoxide exposure on individuals with coronary artery disease. 260 18

Prevalence of silent myocardial ischemia in exercise test was retrospectively reviewed from 749 tests performed for 513 patients with definite evidence of ischemic heart disease. The clinical significance was studied and absence of transient ischemia, occurrence of transient ischemia with and without pain were observed in 48%, 30% and 22% of the tests, respectively. Anginal pain was frequently observed in exercise tests for patients with severe coronary artery disease and low exercise tolerance. A large number of tests showing ischemic response were discontinued due to symptoms other than anginal pain and hence silent myocardial ischemia could be thought to be a result of ischemic state which does not reach the angina threshold. Silent myocardial ischemia was frequently observed during usual daily life. However, a definite correlation between severity of transient ischemia and presence or absence of chest pain in the same individuals was not obtained from the study. A day to day variation in the angina threshold might be responsible. In general, silent myocardial ischemia was not rare. However, the consistent condition was very unusual. In angina of effort (EA) and old myocardial infarction (OMI), 3.7% and 12.3% were silent, respectively. A higher incidence was obtained in OMI than in EA. This is important for the management of these patients. The mechanism of silent myocardial ischemia and the cause of the different incidence of this state between EA and OMI were not defined and remained to be further studied.
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PMID:Prevalence and clinical significance of silent myocardial ischemia in exercise test. 262 68

The purpose of the present study was to clarify the characteristics of myocardial ischemic attacks in patients with exertional angina (EA, 56 cases), exertional and rest angina (ERA, 28 cases), rest angina (RA, 4 cases), and variant angina (VA, 39 cases). The Holter electrocardiographic findings were compared among the four types of angina pectoris. The frequency of symptomatic ischemic attacks in descending order was 46.0% in EA, 29.0% in ERA, 28.1% in RA, and 21.6% in VA, while the frequency of asymptomatic ischemic attacks was in the reverse order. The maximal heart rates during symptomatic ischemic attacks were in descending order, EA, ERA, RA, and VA. The maximal heart rate during ischemic attacks was significantly lower in patients with spontaneous angina than in those with exercise-induced ischemia for all types of angina (p less than 0.05, respectively). Further, the difference in maximal heart rate during ischemic attacks between the ambulatory electrocardiogram and exercise test was greater in patients with RA and VA than in those with EA. Therefore, this suggests that increased coronary vascular tone is a cause of spontaneous ischemic attacks in each type of angina pectoris.
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PMID:Characteristics of symptomatic and asymptomatic myocardial ischemia during ambulatory electrocardiographic monitoring in patients with angina pectoris. 272 37


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