Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was designed to assess the influences of antiarrhythmic therapy on exercise tolerance in patients with coronary artery disease and ventricular arrhythmias. Subjects for this study were subdivided into 3 groups: group I - 46 patients treated with amiodarone 1,200 mg daily during 10 days and 200-600 mg daily within next days, group II - 79 patients receiving disopyramide 300-600 mg daily, group III - 129 patients with combined administration of disopyramide 300-600 mg daily and propranolol 30-240 mg daily. propranolol 30-240 mg daily. Submaximal exercise stress testing was performed in each patient before treatment and after the medication for 4 weeks (group I) and for 2 weeks (groups II, III). The following parameters have been evaluated: maximal archived workload, maximal heart rate blood pressure response, double product (maximal heart rate x maximal systolic blood pressure), reasons for ending the test (target heart rate, typical angina, exhaustion, ST-segment depression greater than or equal to 2 mm, occurrence of ventricular arrhythmia, blood pressure greater than 250/120 mm Hg, significant drop in systolic pressure). Positive result of exercise ECG was defined: horizontal or down-sloping ST-segment depression greater than or equal to 1 mm and/or typical chest pain. The data from the first and second tests were estimated for significance of differences between the mean values with following results: 1) maximal achieved workload, 86 +/- 46 and 103 +/- 49 W (p less than 0.02) in group I; 101 +/- 64 and 106 +/- 50 W (NS) in group II; 107 +/- 55 and 119 +/- 54 W, W (p less than 0.01) in group III.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of amiodarone and disopyramide on the results of electrocardiographic exercise stress testing in patients with coronary disease]. 208 70

In order to study the association between vital exhaustion and different manifestations of coronary heart disease, a prospective study was conducted among 3877 males, aged 39-65. This group was studied during a mean period of 4.2 years. Vital exhaustion, a mental state characterized by unusual fatigue, a feeling of being dejected or defeated, and increased irritability, were assessed by means of the Maastricht Questionnaire. Subjects who scored in the upper third were labelled as exhausted and were compared with those who scored in the lower or middle third. The age-adjusted relative risk of angina pectoris at screening that was associated with vital exhaustion was 4.17 (p less than 0.01); that of unstable angina pectoris at screening was 17.21 (p less than 0.001). No association was observed between vital exhaustion and past myocardial infarction, except in the youngest age group (OR = 3.76; p = 0.05). Among the subjects free from coronary heart disease at screening, 54 cases of angina pectoris, 38 cases of non-fatal myocardial infarction, and 21 cases of fatal myocardial infarction were observed during follow-up. The age-adjusted relative risk of angina pectoris at follow-up was found to be 1.86 (p less than 0.03) and that of non-fatal myocardial infarction was found to be 2.28 (p less than 0.001). No association was found between vital exhaustion and fatal events.
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PMID:Fatigue and heart disease. The association between 'vital exhaustion' and past, present and future coronary heart disease. 262 76

We have previously shown that plasma vasoactive intestinal polypeptide (VIP) is increased in normal subjects by low-frequency transcutaneous nerve stimulation. The latter may also increase short-term physical performance in athletes (running, swimming and ergometer cycling). The present study examines whether the plasma VIP level is similarly increased in short-term ergometer exercise in seven healthy volunteers. A group of four patients with angina pectoris were included, since a lowered concentration of VIP is found in diseased heart tissue. In the group of healthy subjects, ergometer exercises with progressive increases in workload until exhaustion, lasting from 16 to 32 min (mean 26 min) and with a corresponding maximum energy output of 1500 to 5100 W (mean 3560 W), resulted in an increase in plasma VIP concentration from a pre-stimulatory level of 3.3 pmol . l-1 to 5.3, 5.2 and 5.6 pmol . l-1, measured 3, 10 and 20 min respectively, following termination of the exercise, i.e. a maximal 70% increase. In the patients with angina pectoris there was no significant VIP increase (cycling time 7-15 min, work performed 400-1350 W). Possible triggering mechanisms for VIP release and its source are discussed.
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PMID:Increase in plasma vasoactive intestinal polypeptide (VIP) in muscular exercise in humans. 372 Nov 87

In patients with cerebral transient ischemic attacks or stroke myocardial infarction is the leading long-term cause of death. Despite the importance of coronary artery disease, patients with cerebrovascular insufficiency are seldom evaluated for the detection of ischemic heart disease and usually the cardiological evaluation is limited to the patients with angina or previous myocardial infarction. In order to identify asymptomatic coronary artery disease 74 consecutive patients with cerebral ischemia, and without symptoms or electrocardiographic signs of ischemic heart disease, underwent a maximal exercise treadmill test according to the Bruce protocol. An exercise Thallium myocardial scintigraphy was performed in patients with positive exercise test. A control group of 74 asymptomatic subjects underwent the same study protocol. The study population (Group I) included 57 men and 17 women; the age ranged from 22 to 72 years (mean age 54 years). An adequate exercise test was obtained in 67 patients. Exercise test was positive (ST-segment depression greater than or equal to 1.5 mm) in 19 cases (28%). The end points were exhaustion in 15 patients, ST-segment depression greater than 3 mm in 2 and systolic blood pressure greater than 240 mmHg in 2. The exercise Thallium myocardial scintigraphy was normal in 2 and abnormal in 17: reversible perfusion defects were detected in 12 cases and fixed defects in 5. In the control group (Group II), comparable for age and sex, exercise test was positive in 4 cases (5%; p less than 0.01 percentage of positive exercise tests in Group I vs Group II); the exercise myocardial scintigraphy was normal in 1 and abnormal in 3 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Early identification of ischemic cardiopathy in patients with cerebrovascular insufficiency.A prospective study with exertion test and perfusion myocardial scintigraphy]. 373 22

During exercise, patients with chronic obstructive pulmonary disease (COPD) increase their pulmonary arterial wedge (Ppaw) and left ventricular (LV) end-diastolic pressures more than normal control subjects. The increase in pressure is commonly attributed to an increase in intrathoracic pressure (Pit). However, mean esophageal pressure (Pes) does not increase with supine exercise in patients with COPD. Because changes in Pes may not represent changes in Pit when recorded in the supine position, we measured Ppaw and Pes during upright exercise in 8 patients with severe air-flow limitation (mean +/- SD) FEV1, 0.88 +/- 0.27 L secondary to COPD and no history or electrocardiographic abnormalities suggesting a previous myocardial infarct, history of angina, evidence of systemic hypertension, or use of cardiac medications. In addition, all patients completed a progressive exercise test to exhaustion without angina or ST segment changes, and all had normal LV function at rest assessed by equilibrium radionuclide ventriculography. The Ppaw increased a mean of 7.2 +/- 4.3 mmHg, whereas Pes increased a mean of only 1.3 +/- 1.6 mmHg. By multiple linear regression analysis, Ppaw was significantly associated with the work level performed (p less than 0.01), but had no significant association with Pes (p greater than 0.1). The change in Ppaw could not be attributed to changes in Pes. If changes in Pes during upright exercise are representative of changes in Pit or juxtacardiac pressure, a rise in Pit does not explain the exercise-induced increase in Ppaw and LV end-diastolic pressure that occurs in patients with COPD.
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PMID:Increases in intrathoracic pressure do not explain the rise in left ventricular end-diastolic pressure that occurs during exercise in patients with chronic obstructive pulmonary disease. 403 36

Forty-five patients with intermittent claudication were first treated with placebo tablets for 3 months and then randomly allocated to double-blind therapy with either suloctidil or placebo for 6 months. Walking distance improved significantly in both groups during the 3 months of placebo treatment. During the 6 months of double-blind treatment with a further significant improvement occurred only in the placebo group when all patients were analyzed. However, when patients who stopped for reasons unrelated to claudication such as angina and exhaustion during repeated walking tests were eliminated, only suloctidil-treated patients improved significantly. The evolution of leg flow and distal pressure was similar in the two treatment groups whether all legs or only legs with abnormal flow and pressure values were considered. By contrast, when the analysis was limited to legs with claudication pain, a significant improvement occurred only in the suloctidil-treated group. These findings suggest that suloctidil may improve the claudication symptoms of patients with chronic arterial obstructive disease and in particular the perfusion of legs experiencing claudication pain. However, the clinical significance of this improvement appears limited.
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PMID:Controlled trial of suloctidil in intermittent claudication. 616 99

Twenty-one patients with intermittent claudication underwent a physical exercise program lasting 8 weeks. The patients were classified on the basis of maximal walking tolerance (MWT) and diagnosis at the initial examination. Seven of the patients had a MWT less than 1,000 m and no symptoms of chronic obstructive airways disease (COAD) or angina (group A), seven had a MWT less than 1,000 m plus angina and/or COAD (group B) and seven had an unlimited (greater than 1,250 m) MWT (group C). At the completion of the training program all three groups showed a significant improvement in walking distance to pain and stress test capacity. During the post-training walking tolerance test, the venous lactate concentrations in group A were lower after 2 min and 4 min of exercise, and at exhaustion (P less than 0.05). Group A patients showed a significant correlation between an increase in MWT after training and a decrease in maximum lactate concentration measured during walking. Although the patients in group B had a significant increase in MWT, blood lactate concentrations in this group were not always decreased by physical training. Group C lactate concentrations were lower after 8 min, 15 min, and 30 min of walking (P less than 0.05). It is concluded that a physical training program increases walking tolerance in different categories of claudicants, and possible mechanisms for the improvement are discussed.
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PMID:Intermittent claudication. The effect of physical training on walking tolerance and venous lactate concentration. 654 Jun 70

200 exercise tests in 106 patients with hypertrophic obstructive cardiomyopathy (HOCM) and 45 exercise tests in 30 patients with hypertrophic non-obstructive cardiomyopathy (HNCM), primarily performed to assess the hemodynamic impairment during stepwise increased maximal exercise, were analysed with respect to incidence and severeness of ventricular arrhythmias by evaluating the continuously recorded ECG. The exercise tests were subdivided in 4 phases: 1. introduction of a Swan-Ganz pulmonary wedge catheter; 2. resting phase until constant hemodynamic basal values were reached; duration 5 to 51, mean 18 +/- 8 min; 3. exercise phase; bicycle ergometer exercise in supine position; increase in work load by steps of 25 Watts to the maximum which was defined by onset of angina pectoris, dyspnea or exhaustion; total duration 6 to 41, mean 18 +/- 6 min; 4. resting phase after exercise, duration 1 to 30, mean 5 +/- 3 min. Ventricular arrhythmias were classified in a modified Lown classification: 1. no ventricular ectopic beats (VEB); 2. single VEB, less than 0.5/min; 3. single VEB, more than 0.5/min; 4. ventricular pairs; 5. ventricular salvos or tachycardias (3 or more QRS complexes). In the total series of 200 exercise tests in patients with HOCM, the highest incidence of ventricular arrhythmias was found during insertion of the pulmonary wedge catheter, i.e., in 75% of the cases. In nearly 20% of the cases, ventricular pairs or tachycardias were observed. The longest tachycardia consisted of 17 QRS complexes. All tachycardias terminated spontaneously. During the following resting phase, ventricular arrhythmias were documented in 52% of the cases, with ventricular pairs, however, in only 11 (5.5%) and ventricular tachycardias in only 5 (2.5%) tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Risk of stress-induced ventricular arrhythmias in hypertrophic cardiomyopathy]. 654 5

To examine the antianginal effects of felodipine, a new calcium antagonist, 8 patients with coronary artery disease and exertional angina pectoris were studied. Hemodynamic measurements were made at rest, during submaximal exercise and during angina-limited exercise before and 30 minutes after oral administration of 0.1 mg/kg of felodipine. Angina pectoris was always prevented after the drug was given and the exercise intensity was increased until recurrence of angina (5 patients) or exhaustion (3 patients). Hemodynamic data were also recorded at this higher exercise capacity. At rest and during submaximal exercise, felodipine increased heart rate and decreased arterial blood pressure and systemic vascular resistance. The prevention of angina pectoris was accompanied by lower mean pulmonary capillary wedge pressure, systemic vascular resistance and ST-segment depression; the pressure-rate product was unchanged. The 20% greater exercise capacity after felodipine was attended by a 20% increase in maximal cardiac output, a 17% increase in maximal heart rate and a 13% increase in maximal pressure-rate product; the maximal arterial blood pressure and ST-segment abnormalities were unchanged and the systemic vascular resistance was lower. The relation between ST-segment depression and the pressure-rate product during exercise was favorably influenced by felodipine. Thus, felodipine is an active antianginal drug; its major mechanism of action is to lower the systemic vascular resistance. The data also suggest that it improves coronary blood flow during exercise.
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PMID:Hemodynamic effects of felodipine at rest and during exercise in exertional angina pectoris. 661 67

To analyze the mechanisms of action of molsidomine, a new antianginal drug, 10 patients with coronary artery disease and exertional angina pectoris were studied. Hemodynamic measurements were made at rest, during submaximal exercise and during angina-limited exercise before and 1 hour after intravenous administration of 2 mg of molsidomine. When angina pectoris was prevented after the drug was given (6 of 10 patients), the exercise intensity was increased until the recurrence of angina (3 patients) or until exhaustion (3 patients), and hemodynamic data were recorded at this higher exercise capacity. At rest and during submaximal exercise, molsidomine increased heart rate and decreased cardiac output and mean systemic and pulmonary arterial pressures. The prevention of angina pectoris was attended by lower mean systemic and pulmonary arterial pressures and pressure-rate product; cardiac output and heart rate were unchanged. The greater exercise capacity (+26 percent) after molsidomine was attended by increases in maximal cardiac output (+19 percent) and in arteriovenous oxygen difference (+6 percent); the maximal pressure-rate product was unchanged and systemic vascular resistance was lower. The mechanisms of action of molsidomine are very similar to those of nitrates and imply a decrease in venous and arterial tone. Molsidomine deserves further study in patients with angina or congestive heart failure.
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PMID:Hemodynamic effects of molsidomine at rest and during submaximal and maximal exercise in patients with coronary artery disease limited by exertional angina pectoris. 689 96


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