THE CIRCULATORY EFFECTS OF ANGIOTENSIN IN RHEUMATIC HEART DISEASE.
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The hemodynamic effects of nifedipine and propranolol administered intravenously were studied in 17 patients with angina pectoris. Nine patients received nifedipine and eight received propranolol. The hemodynamic parameters were compared at rest and during supine bicycle exercise at work loads known to produce angina. Exercise-induced angina improved in four out of nine patients following nifedipine and in one out of eight patients following propranolol. Nifedipine significantly reduced the increment of left ventricular end-diastolic pressure and Vmax during exercise. Intravenous propranolol significantly suppressed the increment of heart rate, max dp/dt, tension time index, and Vmax during exercise. Although the exact mode of action of nifedipine remains uncertain, it is suggested that it decreases myocardial oxygen requirements primarily through a reduction of left ventricular volume, whereas propranolol suppresses the positive chronotropic and inotropic responses of the heart muscle to exercise.
AIMS: We studied the capability of heart rate (HR) adjusted change in multichannel magnetocardiogram (MCG) to detect exercise-induced ischemia. METHODS AND RESULTS: The MCG and 12-lead ECG were recorded simultaneously during supine exercise testing in 17 healthy controls and 24 patients with single vessel coronary artery disease (CAD). In the MCG analysis, we plotted the orientation of the magnetic field map (MFM) against the HR in each cardiac cycle during recovery. A regression line was fitted to the data and the line slope (degrees/bpm) was determined. In the ECG, the ST-segment depression vs HR (ST/HR) slope was evaluated. The HR adjusted MFM rotation was more extensive in the pooled CAD group, and in all subgroups with different stenosed vessel, than in the control group at the ST-segment (1.5 +/- 2.1 degrees/bpm vs 0.29 +/- 0.25 degrees/bpm, p < 0.0005) and at the T-wave apex (0.95 +/- 0.81 degrees/bpm vs 0.24 +/- 0.25 degrees/bpm, p < 0.0005). Areas under the receiver operating characteristic curves of the HR adjusted MFM rotation at the ST-segment (88.5%) and the T-wave (86.0%) were higher than the ones without HR adjustment (75.5% and 68.1%, respectively), and higher than the area of ST/HR slope in the ECG (80.2%). CONCLUSION: HR adjusted MFM rotation detects transient ischemia independent of the stenosed vessel. HR adjustment improves the performance of the MCG in ischemia detection by the analysis of the ST-segment and the T-wave. The MCG was superior to the 12-lead ECG.
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The rate of depression of the ST segment with increasing heart rate (HR) during exercise has been claimed to predict the extent of coronary artery disease (CAD). To determine whether the maximal ST/HR slope is better than the Bruce treadmill exercise test for predicting the presence of CAD, the maximal ST segment/HR slope was calculated in 81 patients and compared with the results of a standard 12-lead exercise test. In 21 patients (26%), the ST/HR slope could not be calculated. In 60 patients with ST/HR slope values, the extent of CAD was predicted in 24 patients (40%). The sensitivity and specificity of the ST/HR slope in predicting the presence of CAD in the 60 patients with slope values were 91% and 27%, respectively. The sensitivity and specificity of the modified Bruce treadmill exercise test in the 81 patients were 81% and 64%, respectively. Thus, the use of the ST/HR slope does not provide additional information that cannot be obtained using the standard Bruce exercise test.
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AIMS: The Modelflow method can estimate cardiac output from arterial blood pressure waveforms using a three-element model of aortic input impedance (aortic characteristic impedance, arterial compliance, and systemic vascular resistance). We tested the reliability of a non-invasive cardiac output estimation during submaximal exercise using the Modelflow method from finger arterial pressure waveforms collected by Portapres in healthy young humans. METHODS: The Doppler echocardiography method was used as a reference method. Sixteen healthy young subjects (nine males and seven females) performed a multi-stage cycle ergometer exercise at an intensity corresponding to 70, 90, 110 and 130% of their individual ventilatory threshold for 2 min each. The simultaneous estimation of cardiac output (15 s averaged data) using the Modelflow and Doppler echocardiography methods was performed at rest and during exercise. RESULTS AND CONCLUSION: The Modelflow-estimated cardiac output correlated significantly with the simultaneous estimates by the Doppler method in all subjects (r = 0.87, P < 0.0001) and the SE of estimation was 1.93 L min-1. Correlation coefficients in each subject ranged from 0.91 to 0.98. Although the Modelflow method overestimated cardiac output, the errors between two estimates were not significantly different among the exercise levels. These results suggest that the Modelflow method using Portapres could provide a reliable estimation of the relative change in cardiac output non-invasively and continuously during submaximal exercise in healthy young humans, at least in terms of the relative changes in cardiac output.
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BACKGROUND: Although some patients report favorable activity levels late after partial left ventriculectomy (PLV), their exercise physiology has not been well described. METHODS AND RESULTS: We performed upright bicycle hemodynamics in 10 patients (9 men) aged 56+/-12 years at 1.7 years after PLV. Ejection fraction was 25+/-4%. Patients biked 10+/-7 minutes. With exercise, the mean pulmonary arterial pressure rose from 36+/-12 to 52+/-10 mm Hg (P:=0.0003). The mean pulmonary capillary wedge pressure rose from 25+/-14 to 36+/-9 mm Hg (P:=0.0566), and the cardiac index rose from 2.2+/-0.5 to 3.8+/-1.6 L. min(-1). m(-2) (P:=0.0077). The mixed venous oxygenation with exercise declined from 44+/-9% to 24+/-17% (P:=0. 0220), and the pulmonary vascular resistance increased from 2.0+/-0. 9 to 2.3+/-1.1 Wood units (P:=0.5566). CONCLUSIONS: In late follow-up after PLV with exercise, the cardiac index is significantly augmented. However, there are further rises in pulmonary artery and pulmonary capillary wedge pressures, suggesting abnormal compliance, with marked decline in mixed venous oxygenation. Elucidating late physiology after PLV may help pave the way for future innovative heart failure surgeries.
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It has been unclear whether exercise training of patients with coronary artery disease increases the level of myocardial oxygen consumption, as indicated by heart rate and double product of heart rate and systolic blood pressure, at which electrocardiographic evidence of myocardial ischemia develops. To assess this question we evaluated the experience of 10 patients with coronary artery disease who underwent a modest-level exercise training program for 6 months. All of these subjects had achieved a training effect, had developed electrocardiographic evidence of ischemia during initial exercise testing, had not increased the amount of cardiac medication taken, and had not been taking digoxin. After completion of the training period, the mean heart rate at which electrocardiographic evidence of ischemia developed increased from 107 +/- 19 to 119 +/- 23 beats/min (p less than .05) and the mean double product increased from 166 +/- 18 to 209 +/- 51 X 10(2) mm Hg X beats/min (p less than .05). Eight of the 10 patients demonstrated an increase in heart rate at onset of ischemia (p less than .02), and seven of the eight in whom double product could be assessed manifested an increase in this parameter at onset of ischemia (p less than .05). Thus the rate of myocardial oxygen consumption at which myocardial ischemia develops, as indirectly assessed by heart rate and double product, can be favorably altered by 6 months of moderate-level exercise training.