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Eighteen patients with neurobrucellosis are described. Eleven patients had meningitis alone or with papilledema, optic neuropathy, or radiculopathy. Four patients had meningovascular complications manifested by stroke or intracerebral hemorrhage from a presumed mycotic aneurysm. Two patients had parenchymatous dysfunction, including a child who had a cerebellar syndrome without evidence of direct infection of the central nervous system. One patient presented with polyradiculopathy. Twelve of 16 patients had pleocytosis; none had cell counts greater than 419 x 10(6)/L. Most patients had hypoglycorrhachia and elevated levels of protein in the cerebrospinal fluid (CSF). Results of an agglutination test for Brucella in serum were positive for all patients. Six of 16 patients had positive blood cultures, and four of 14 had positive CSF cultures. Antimicrobial treatment included concurrent administration of two or more of the following drugs: streptomycin, tetracycline (or doxycycline), rifampin, and trimethoprim-sulfamethoxazole. Eleven patients fully recovered. Five patients were left with residual neurological deficits. Four of these patients suffered permanent hearing loss, one of whom also had significant loss of vision in one eye. One elderly senile patient with meningovascular brucellosis remained in a vegetative state despite receiving antimicrobial therapy for 6 months. One patient died due to rupture of a mycotic aneurysm within 7 days of initiation of therapy. One other patient was treated after sustaining an intracerebral hemorrhage, but this patient's condition was diagnosed only after discharge.
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PMID:Neurobrucellosis: clinical and therapeutic features. 142 Jun 70

A randomized, double-blind, crossover, placebo-controlled study was carried out to evaluate the effects of a single oral 4-mg dose of lacidipine vs. placebo on cardiopulmonary circulation at rest and during exercise. Twelve healthy volunteers were randomized to receive either placebo or 4 mg of lacidipine once daily for 2 days, followed by a 3-day washout period, after which they received alternate treatment. Patients were assessed before and at 60, 90, and 180 min after dosing. At 120 min, a maximum exercise test with a treadmill was performed according to the Bruce protocol. No relevant changes with placebo or lacidipine were observed in the respiratory function tests whereas 4 mg of lacidipine increased pulmonary effective blood flow (Qp. eff.) and stroke volume index (SVI) at 60 min, reaching a peak at 90 min; at 180 min, these effects, although diminished, were still present. The arteriovenous oxygen difference [C(a-v)O2] decreased, but reverted to normal values by 180 min. No differences in maximum attained Qp. eff. and oxygen consumption (VO2) during exercise were observed. Only the heart rate was higher both before and after treatment with lacidipine. Lacidipine increased Qp. eff. in these normal subjects without relevant effects on respiratory function. Performance on exercise testing after dosing was normal, although drug-induced vasodilation was present.
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PMID:Effects of oral lacidipine on cardiopulmonary function at rest and during exercise in normal subjects. 172 9

We studied 14 patients to determine whether sustained-release diltiazem is a satisfactory long-term substitute for the combination of propranolol plus hydrochlorothiazide (HCTZ), control phase, in the treatment of systemic hypertension with coexisting chronic stable angina pectoris. All patients had either one- or two-vessel coronary disease and normal left ventricular systolic function. Measurements were made during the control phase and 4 and 8 weeks after substitution of sustained-release diltiazem. Only the sitting blood pressure was available before the control phase (pretreatment). Blood pressure and heart rate were measured with patients supine, sitting, and 5 minutes after standing. Cardiac output was measured in the supine position using a computerized Doppler system, and stroke volume, mean arterial pressure, and total systemic resistance were calculated. Symptom-limited modified Bruce protocol treadmill tests were performed to determine time to onset of 1 mm ST segment depression, time to termination of exercise, reason for cessation of exercise, and maximum rate-pressure product. The patients were initially receiving 160-240 mg/day of propranolol (40-60 mg q.i.d.) plus 25-50 mg/day of HCTZ and, subsequently, 12 of 14 had substitution with 240 mg/day (120 mg b.i.d.) of sustained-release diltiazem, and two received 360 mg/day with one of these patients also receiving 50 mg/day of HCTZ. These patients are a subset of a larger group of patients in whom the response of blood pressure alone has been previously reported. Diltiazem resulted in reduction of blood pressure equivalent to that with the propranolol plus HCTZ combination.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Response of blood pressure, cardiac output, peripheral resistance, and exercise performance to substitution of calcium blocker for beta-blocker plus thiazide diuretic therapy in patients with both systemic hypertension and mild stable angina. 257 40

The optimal atrioventricular delay at rest and during exercise was investigated in nine patients with heart block and implanted dual chamber pacemakers. All patients studied had normal left ventricular function and a normal sinus node rate response to exercise. Cardiac output was measured by continuous wave Doppler and was calculated as the product of stroke distance measured by Doppler at the left ventricular outflow, aortic root area measured by M mode echocardiography, and heart rate. Pacemakers were programmed in the DDD mode. Cardiac output was measured with the patient at rest while supine and while erect and at the peak of submaximal exercise (the end of stage 1 of the Bruce protocol) with the pacemakers programmed to the following atrioventricular intervals: 75-80 ms, 100-110 ms, 140-150 ms, and 200 ms. During exercise the basic pacing rate was programmed to 70 beats/min. Cardiac output at rest while supine and erect was greatest with an atrioventricular delay of 140-150 ms and it was significantly higher than that with an atrioventricular delay of 75-80 ms. On average there was a 31% decrease in cardiac output when patients stood up. During treadmill exercise, however, cardiac output was greatest when the atrioventricular delay was 75-80 ms, and this was significantly higher than the cardiac output with atrioventricular delays of 150 and 200 ms. During exercise 1:1 atrioventricular relations were maintained in patients at all atrioventricular intervals. In patients with atrioventricular sequential pacemakers cardiac output at rest is greatest with an atrioventricular delay of 140-150 ms but during exercise the optimal atrioventricular delay is shorter. Rate modulation of the atrioventricular interval may improve the haemodynamic response and possibly exercise tolerance in patients with dual chamber pacemakers.
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PMID:Optimal atrioventricular delay at rest and during exercise in patients with dual chamber pacemakers: a non-invasive assessment by continuous wave Doppler. 292 53

This paper describes a rebreathing method for the simultaneous measurement of oxygen consumption (VO2) and effective pulmonary blood flow (QP. eff) at rest and during exercise. Subjects rebreathed a test gas consisting of 35% oxygen, 3.5% chlorodifluoromethane (freon-22), and 10% argon in nitrogen for 30 seconds or until the respired oxygen tension fell to below 13.3 kPa. Sixty normal subjects were studied on a motorized treadmill, the Bruce protocol being used. The rebreathing manoeuvre was performed at three minute intervals, and was initially practised sitting down. Measurements were then made with the subjects standing at rest, and subsequently during the last minute of each stage of the Bruce exercise protocol until the subjects were exhausted. Heart rate was recorded from the electrocardiogram. Oxygen uptake plotted against calculated power (watts) showed a discontinuity between resting and exercise values, probably because power output during treadmill exercise is underestimated. The arbitrary addition of 30 watts to the exercise power output abolished this discontinuity. There was good agreement between rebreathing estimates of oxygen consumption and values measured during a second exercise test by the conventional open circuit argon dilution method. Coefficients of variation of oxygen consumption and effective pulmonary blood flow measured by rebreathing were usually less than 10% even during maximal exertion. At rest mean (SD) effective pulmonary blood flow corrected for body surface area was 2.2 (0.46) l/min/m2. Effective pulmonary blood flow rose linearly with oxygen consumption. At rest the arteriovenous oxygen content difference for pulmonary blood (VO2/QP eff) was 9.1 (1.6) ml/dl, rising to a maximum of 16.4 (1.8) ml/dl. The stroke volume index was 27.5 (6.8) ml/m2, rising to a maximum of 46.5 (7.1) ml/m2 during exertion.
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PMID:Rebreathing method for the simultaneous measurement of oxygen consumption and effective pulmonary blood flow during exercise. 340 13

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

Several investigations have suggested that orthostatic tolerance may be inversely related to aerobic fitness (VO2max). To test this hypothesis, 18 males (age 29 to 51 yr) underwent both treadmill VO2max determination and graded lower body negative pressures (LBNP) exposure to tolerance. VO2max was measured during the last minute of a Bruce treadmill protocol. LBNP was terminated based on pre-syncopal symptoms, and LBNP tolerance (peak LBNP) was expressed as the cumulative product of LBNP and time (torr-min). Changes in heart rate, stroke volume, cardiac output, blood pressure, and impedance rheographic indices of mid-thigh-leg fluid accumulation were measured at rest and during the final minute of LBNP. For all 18 subjects, mean (+/- SE) fluid accumulation index and leg venous compliance index at peak LBNP were 139 +/- 22 ml and 3.9 +/- 0.4 ml . 100 ml . torr-min-2 x 10(3), respectively. Pearson product-moment correlations and step-wise linear regression were used to investigate relationships with peak LBNP. Variables associated with endurance training, such as VO2max and percent body fat, were not found to correlate significantly (P less than 0.05) with peak LBNP and did not add sufficiently to the prediction of peak LBNP to be included in the step-wise regression model. The step-wise regression model included only fluid accumulation index, leg venous compliance index, and blood volume, and resulted in a squared multiple correlation coefficient of 0.978. These data do not support the hypothesis that orthostatic tolerance as measured by LBNP is lower in individuals with high aerobic fitness.
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PMID:Aerobic fitness does not contribute to prediction of orthostatic intolerance. 377 72

The relationship of regional and global left ventricular function to aortic flow dynamics during exercise was determined in 14 normal subjects and 14 patients with coronary artery disease. Doppler and two-dimensional echocardiographic studies were performed before, during, and immediately after an exercise test by the Bruce protocol. Two-dimensional echocardiography was used to determine the ejection fraction and new wall motion abnormalities. The peak ejection velocity, stroke index, and cardiac index were calculated from the pulsed Doppler tracing. In normal subjects the ejection fraction increased significantly (p less than .001) from rest (0.51 +/- 0.07) to peak exercise (0.61 +/- 0.07), while the response in coronary patients was blunted (0.49 +/- 0.11 vs 0.48 +/- 0.16). Similarly, the change in peak ejection velocity throughout exercise in normal subjects (from 0.71 +/- 0.12 to 1.50 +/- 0.35 m/sec) was significantly (p less than .01) greater than that in patients with coronary artery disease (from 0.61 +/- 0.13 to 0.90 +/- 0.29 m/sec). There was a good correlation between the percent change in peak ejection velocity and the percent change in ejection fraction from rest to peak exercise in the entire study group (rs = .64) and in the patients with coronary artery disease (rs = .84). These preliminary data suggest that exercise-induced changes in Doppler echocardiographic variables may offer a potential adjunct in the evaluation of patients with ischemic heart disease.
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PMID:Evaluation of left ventricular function during upright exercise: correlation of exercise Doppler with postexercise two-dimensional echocardiographic results. 380 46

In order to elucidate fundamental relationship between exercise and cardiac reserve, we investigated the parameters of regression equation (VO2 = A X HR + B) between oxygen consumption (VO2 ml/kg/min) and heart rate (HR) during exercise test (Bruce). 62 male children were divided into 3 groups based on history and clinical evaluation. HR related linearly with VO2 (average r = 0.967, range 0.90-0.993). Both of the parameters A and [B] were significantly high in Athlete (A = 0.465 +/- 0.043, [B] = 36 +/- 6.07), low in Failed (0.297 +/- 0.055, 17.4 +/- 6.1) and middle in Ordinary group (0.366 +/- 0.078, 23.5 +/- 8.6) (p less than 0.005). Based on our result of linear VO2-HR relation, and on the previously reported studies that cardiac output linearly and consistently relates with VO2, we considered the meaning of the parameters as follows; A determines the possible maximum stroke volume (SV), and B determines the HR where SV reaches plateau. In conclusion, since the SV is considered as a measure of cardiac function, measuring the parameters of VO2-HR relation allows us to isolate cardiac functional reserve through the exercise tolerance test.
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PMID:Direct estimation of cardiac reserve through analysis of relation between oxygen consumption and heart rate during exercise testing. 383

The effect of propranolol on cardiac patients undergoing exercise training is reported to increase exercise tolerance and maximum oxygen uptake (VO2 max) but its effect on anaerobic threshold (AT) is unknown. It was the purpose of this study to determine the role of exercise training with propranolol on AT in patients with coronary artery disease (CAD). Eight men and one woman with significant (CAD) were selected for this study. Each patient completed a maximum treadmill stress test (MTST) following the Bruce protocol on propranolol 40-160 mg/day as a control study. Cardiorespiratory variables were measured at rest and at each stage of the treadmill test. These patients underwent an exercise training programme for 12-16 weeks on the same dose of propranolol. Training sessions were for a minimum of 30-40 minutes, 3 times a week, with training heart rate of 75%-85% of the pretraining peak heart rate. Training heart rate ranged from 98 to 128 beats/min. They were retested with a MTST after the training programme, on the same dose of propranolol. AT was calculated noninvasively by measuring respiratory variables every 30 seconds in relation to work increment. AT was identified by measuring the time course of VE, VCO2, VE/VO2, etc. in relation to incremental work. The mean values of VO2, O2P and % VO2 max at AT before and after training on propanolol were as follows: VO2 = 1.43 L/min +/- .25 and 1.86 L/min +/- .44, O2P = 14.35 +/- 2.40 and 18.73 +/- 4.00 ml/beat, % of VO2 max = 68.20 +/- 6.31 and 73.59 +/- 5.84. The mean changes of VO2 O2P, and % of VO2 max were + 0.43 L/min +/- 0.20 (P < .003), + 4.38 +/- 2.55 (P < .003) and +/- 5.07% +/- 4.84 (P < .001). After exercise training on propanolol, the mean peak exercise tolerance time and absolute VO2 max increased by 2.8 min (from 9.0 to 11.8 min) (P < .001) and 22.7% (P < .007), respectively. We conclude that the increase in anaerobic threshold in patients with coronary artery disease may be due to improvement in VO2 max, increased stroke volume, and peripheral O2 extraction.
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PMID:Does exercise alter anaerobic threshold in coronary artery disease during beta blockade? 402 93


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