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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A randomized, double-blind, placebo-controlled study was performed to investigate the effect of dipyridamole at a usual oral dose of 150 mg/day on 18 patients with angina pectoris and positive treadmill exercise electrocardiography. After their angina pectoris was stabilized in phase 1, the patients were randomly assigned to sequence group A or B. Group A received a placebo 3 times daily in phase 2 and then 50 mg of dipyridamole 3 times daily in phase 3. Group B received the treatment in the reverse order. The degree of ST depression and the threshold for angina pectoris in treadmill exercise electrocardiography, which was performed on the last days of phases 2 and 3, were compared. The mean duration of exercise was 5 minutes and 23 seconds during dipyridamole and 5 minutes and 13 seconds during placebo administration, with no significant difference. Dipyridamole caused an aggravating effect on the ST change (earlier appearance of ST depression and/or deeper total sum of ST depression at the end of the exercise) in 3 patients, a salutary effect in 5 and no effect in 10. Dipyridamole decreased the threshold for angina pectoris in 5 patients, increased it in 6 and did not change it in 7. To summarize, dipyridamole showed adverse effects (aggravative effects on the ST change and/or on the threshold for angina pectoris) in 6 patients, beneficial effects in 8 and no effect in 4. A usual oral dose of dipyridamole induced myocardial ischemia during exercise in some patients while it improved it in a similar number of patients.
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PMID:Effect of dipyridamole at the usual oral dose on exercise-induced myocardial ischemia in stable angina pectoris. 219 63

Anginal perceptual threshold (the time from onset of 0.1 mV of ST segment depression to onset of angina during treadmill exercise) is prolonged in diabetic patients with coronary artery disease. In the present study, the functional significance of this perceptual abnormality was evaluated by analysis of its effect on exercise capacity and the severity of myocardial ischemia. Treadmill exercise in 32 diabetic patients and 36 nondiabetic control patients showed a close linear correlation between the time to onset of electrical ischemia (ST segment depression) and exercise capacity in both groups (r = 0.8 and 0.9, respectively; p less than 0.001). However, the slope of the relation was flatter in the diabetic group because prolongation of the anginal perceptual threshold permitted continued exercise as ischemia intensified. The anginal perceptual threshold itself showed a close linear correlation with exercise capacity in the diabetic group (r = 0.8, p less than 0.001), although in the nondiabetic group these variables were unrelated. The permissive effect of a prolonged anginal perceptual threshold on exercise capacity is undesirable as reflected by its correlation with ischemia at peak exercise (r = 0.6, p less than 0.001): the longer the threshold, the greater the exercise capacity and the more severe the ischemia. Indeed, the inverse relation between the severity of ischemia at peak exercise and exercise capacity in the nondiabetic group (r = 0.4, p less than 0.02) was completely lost in the diabetic group. Thus, in diabetic patients with coronary artery disease, anginal perceptual threshold is a major determinant of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prolonged anginal perceptual threshold in diabetes: effects on exercise capacity and myocardial ischemia. 222 58

We studied the values of oral dipyridamole needed to detect coronary arterial disease using 12-lead electrocardiography. The relationship between dipyridamole-induced ST segment depression and coronary arterial lesions, coronary collaterals and myocardial infarction was investigated. 375 mg oral dipyridamole was given to 31 patients (22 with coronary arterial disease, 9 controls). 12-lead electrocardiogram was recorded before and 45 minutes after the test. The control group and the patients, who had no ST segment depression after dipyridamole, performed isometric contraction (handgrip) for 5 minutes and then the 12-lead electrocardiogram was recorded. All patients had coronary angiography. We also performed treadmill stress testing in 28 patients. Dipyridamole testing was positive (greater than or equal to 1 mm ST depression on electrocardiogram) in 7 of 22 patients with coronary arterial disease, of whom 6 had positive treadmill stress testing. Only 2 patients had previous myocardial infarction in the group with positive dipyridamole tests. Of the 15 in whom dipyridamole testing was negative, 5 had positive treadmill stress testing, while 13 of them had had previous myocardial infarction. All patients in the control group had negative dipyridamole stress testing and normal coronary angiograms. No additional ST segment changes were observed in the group who had performed isometric contraction test (both dipyridamole test negative and control groups). Sensitivity and specificity of the test were 32 and 100%, respectively. Comparison of collateral vessels between the groups positive and negative for dipyridamole revealed no difference. But the number of patients with old myocardial infarction was higher in those testing negative than in those who proved positive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of coronary arterial disease by oral dipyridamole stress testing using 12-lead electrocardiography. 228 88

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

Effects of nicardipine, a dihydropyridine calcium antagonist, on regional myocardial blood flow (RMBF), myocardial oxygen tension (PO2), and excitation and conduction abnormalities during the occlusion of the left anterior descending coronary artery (LAD) were examined in anesthetized dogs, and compared with those of nifedipine and dipyridamole. RMBF was calculated from the H2 gas clearance curves, and PO2 was measured using a membrane-coated Pt wire. Excitation and conduction abnormalities during the LAD occlusion were represented in terms of the degree of ST-T alternans (STTA), TQ depression, and conduction delay, which appeared in epicardial electrograms. Nicardipine and nifedipine in a dose of 10 micrograms/kg increased RMBF and PO2 levels in nonischemic and mildly ischemic tissues, but not in severely ischemic tissues. Nicardipine in a dose of 100 micrograms/kg and nifedipine in a dose of 10 micrograms/kg attenuated the degree of STTA, TQ depression, and conduction delay observed in severely ischemic tissues. In mildly ischemic tissues where only TQ depression was observed without STTA, nicardipine in a dose of 30 micrograms/kg attenuated TQ depression. Dipyridamole in a dose of 1 mg/kg produced only a slight attenuation of STTA and conduction delay. These results suggest that the beneficial effects of nicardipine as well as of nifedipine on myocardial ischemia are due to the increase in the myocardial PO2 levels caused by the increased RMBF and also to direct protecting effects on ischemic myocardial cells. In the severely ischemic tissues, the latter is a main effect of the drugs. In increasing the PO2 level, nicardipine was similarly potent as nifedipine, but in the direct effect, nicardipine was less potent, and dipyridamole was almost ineffective.
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PMID:Effects of nicardipine, a dihydropyridine calcium antagonist, on regional myocardial blood flow, myocardial oxygen tension, and electrical abnormalities during acute coronary artery occlusion in dogs. 241 Jun 98

We investigated the effect of diltiazem on dipyridamole-induced myocardial ischemia in eight patients with coronary artery disease. Dipyridamole was infused at a rate of 0.142 mg/kg/min for 4 min, and 87-lead mapping was performed to determine the number of leads with ischemic ST-segment depression greater than or equal to 0.05 mV (nST). The range of nST was 8-24 (mean, 13.8) in the control study. Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5). It was concluded that diltiazem could suppress the myocardial ischemia following dipyridamole infusion.
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PMID:Inhibition of dipyridamole-induced myocardial ischemia by diltiazem in patients with coronary artery disease. 243 3

To assess the indication for percutaneous transluminal coronary angioplasty (PTCA) and coronary artery bypass grafting (CABG), we studied 93 patients with angina pectoris but without myocardial infarction. All patients had significant stenosis (greater than 50%) in at least one coronary artery, including the left anterior descending artery. Fifty-eight patients received medical treatment (Group I), 12 had PTCA (Group II) and 23 had CABG (Group III). Findings of coronary angiography, treadmill exercise tests and dipyridamole perfusion scintigraphy as well as the frequency of cardiac events during follow-up were assessed in each group. 1. Coronary angiography revealed 1 vessel disease in 38% of the patients in Group I, 58% in Group II, and 13% in Group III; 2 vessel disease in 33%, 25% and 61%; and 3 vessel disease in 29%, 17% and 26%, respectively. 2. Exercise duration with the treadmill test was 4.7 min in Group I, 4.0 min in Group II and 3.7 min in Group III. ST depression (greater than or equal to 1 mm) was induced in 75%, 83% and 95%, respectively. Exercise duration improved from 4.0 to 6.0 min after PTCA and from 3.7 to 4.5 min after CABG. Exercise-induced ST depression also became less frequent; from 83% to 25% after PTCA and from 95% to 32% after CABG. Dipyridamole perfusion scintigraphy showed reversible defects in 86% of the patients in Group I and in all patients in Groups II and III. Reversible defects were observed in 17% of the patients after PTCA and in 21% after CABG. 3. During a mean follow-up period of 26 months, cardiac deaths occurred in one patient (2%) in Group I and 2 (7%) in Group III. Nonfatal cardiac events (myocardial infarction and unstable angina or those necessitating revascularization--late PTCA or CABG) were observed in 12 patients (21%) in Group I, 4 (24%) in Group II and 10 (36%) in Group III. Anginal attacks at least once weekly remained in 12% of the patients in Group I, 19% in Group II and 14% in Group III at the last follow-up. In conclusion, PTCA and CABG appear to be effective methods for improving ischemia and exercise tolerance. However, preventive PTCA and CABG may not be indicated in patients with mild angina, because the prognosis is also excellent in medically-treated patients with angina but without myocardial infarction or left main coronary artery disease.
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PMID:[Indication for coronary revascularization for angina pectoris: correlation with prognosis of medically-treated patients]. 248 27

Peripheral perfusion abnormalities are considered a possible reason for myocardial ischemia in the absence of visible coronary artery stenoses. In 85 women (age: 41-58 years, mean age: 46 +/- 8) with pathological exercise ECG (precordial mapping: 50 leads), hemodynamic studies were performed without medication, after sublingual nitroglycerin (NTG, 0.8 mg), sublingual Nifedipin (N, 30 mg), and intravenous Dipyridamol (D, 0.5 mg/kg). Eighteen women showed normal coronary arteries and a normal myocardial perfusion (group I), 21 an impaired perfusion due to coronary stenoses (Group II), and 46 women a reduced perfusion without visible changes (Group III). Reference methods were measurement of pulmonary artery pressure, 201-TI-scintigraphy, and coronary angiography. In group II, enddiastolic and endsystolic left ventricular volume (EDV, ESV) as well as enddiastolic pulmonary artery pressure (pAd) were increased, the ejection fraction (EF) was reduced, and cardiac output (CO) was normal. In group III, ESV, EDV, EF, and CO were significantly reduced, while pAd increased. In group II, N led to a normalization of ESV, EDV, EF, and pAd. In group III, NTG led to a reduction of pAd and EDV, and concomitantly to a further reduction of the already low CO. In both groups the reduction of ST-segment depressions after NTG was significant. N led to a moderate reduction of pAd and ST-segment depression, but to an increase of CO in both groups. D exhibited a comparable effect in group III. In group II an increase of ST-segment changes and of pAd with unchanged CO was observed. With regard to longterm treatment of women in group III, N and D seemed to be more efficacious than nitrates due to a beneficial effect on cardiac output.
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PMID:[Differential therapy of myocardial ischemia in females]. 251 81

Microvascular angina - chest pain syndrome in the presence of angiographically normal epicardial coronary arteries and reduced flow reserve - has been also described in patients with essential hypertension and it has been linked to the development of left ventricular hypertrophy. Dipyridamole-Echocardiography Test (DET: 2D-echo and 12 lead ECG monitoring with dipyridamole infusion, up to 0.84 mg/kg over 10') was performed in 28 essential hypertensives meeting the following inclusion criteria; 1) history of chest pain; 2) angiographically normal coronary arteries; 3) normal resting regional and global left ventricular function. A group of 12 (age and sex matched) normotensives with the same inclusion criteria, as well as with negative exercise stress test, was also evaluated. During DET, none, either in essential hypertensives or in control group, developed a regional dyssynergy of contraction; 15 in essential hypertensives, and 2 in control group had a diagnostic (greater than 0.1 mVolt from baseline) ST segment depression on ECG tracing (54 vs 17% p less than 0.01); 16 in essential hypertensives and 2 in control group had chest pain (57 vs 17%, p less than 0.01). None of the control group and 9 of the essential hypertensives had echocardiographically assessed left ventricular hypertrophy. In the essential hypertensives group, ventricular hypertrophy was present in 7/20 patients with and in 2/8 patients without dipyridamole induced chest pain and/or ST segment depression (35 vs 25%, p = ns). In conclusion, essential hypertensives patients with chest pain and angiographically normal coronary arteries frequently show "echocardiographically silent" angina and/or ST segment depression during DET. The presence of ventricular hypertrophy does not appear to be a prerequisite for the induction of angina in these patients.
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PMID:[The dipyridamole-echo-ECG test in hypertensives with microvascular angina]. 253 Apr 14


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