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Biomedical subjects

M B Higginbotham

Publications and source records attributed to M B Higginbotham.

At least 37 records · Page 2Linked to original sources
PubMed1989

A brief self-administered questionnaire to determine functional capacity (the Duke Activity Status Index).

To develop a brief, self-administered questionnaire that accurately measures functional capacity and assesses aspects of quality of life, 50 subjects undergoing exercise testing with measurement of peak oxygen uptake were studied. All subjects were questioned about their ability to perform a variety of common activities by an interviewer blinded to exercise test findings. A 12-item scale (the Duke Activity Status Index) was then developed that correlated well with peak oxygen uptake (Spearman correlation coefficient 0.80). To test this new index, an independent group of 50 subjects completed a self-administered questionnaire to determine functional capacity and underwent exercise testing with measurement of peak oxygen uptake. The Duke Activity Status Index correlated significantly (p less than 0.0001) with peak oxygen uptake (Spearman correlation coefficient 0.58) in this independent sample. The Duke Activity Status Index is a valid measure of functional capacity that can be obtained by self-administered questionnaire.

Activities of Daily Living↗
PubMed1989

Doppler left ventricular diastolic filling abnormalities in aortic stenosis and their relation to hemodynamic parameters.

Doppler mitral flow indexes and their relation to invasively measured hemodynamic diastolic indexes were assessed in 13 patients with isolated aortic stenosis (AS), and compared to Doppler indexes in 10 normal subjects matched for age, heart rate, left ventricular (LV) ejection fraction and LV load. Patients with AS showed no difference in Doppler early filling (E) indexes, but demonstrated greater Doppler atrial filling (A) indexes in comparison to normal subjects: atrial velocity (89 +/- 31 vs 56 +/- 7 cm/s), atrial integral (11.4 +/- 4.8 vs 5.7 +/- 1.6 cm), A/E velocity (1.69 +/- 0.89 vs 1.06 +/- 0.26) and A/E integral (3.53 +/- 6.64 vs 0.81 +/- 0.27) (all p less than 0.05). Doppler indexes in patients with AS did not correlate with hemodynamic indexes of LV relaxation or chamber stiffness. Significant correlations were observed between Doppler and angiographic peak filling rates (r = 0.70) and between Doppler atrial filling velocity and LV end-diastolic volume (r = -0.66), LV end-diastolic pressure (r = -0.48) and LV ejection fraction (r = 0.53) (all p less than 0.05). These data indicate that, compared to matched normal subjects, most patients with AS have an increased atrial contribution to LV filling. However, in patients with decreased LV function, atrial function may also be depressed, as indicated by a decreased atrial contribution to LV filling, resulting in "normalization" of the Doppler mitral flow pattern.

Aged↗
PubMed1989

Chronic stable angina monotherapy. Nifedipine versus propranolol.

A placebo-controlled, double-blind, crossover study was conducted to determine the effects of nifedipine (60 to 90 mg per day) monotherapy and propranolol (240 mg per day) monotherapy on symptoms, angina threshold, and cardiac function in patients with chronic stable angina. Following a two-week placebo period, patients were randomly assigned to receive either nifedipine or propranolol for a five-week treatment period, after which they crossed over to the alternative regimen. All 21 patients were men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. New York Heart Association functional class improved in patients taking either nifedipine or propranolol, and nitroglycerin consumption decreased with both treatments compared with placebo. Nifedipine significantly delayed the onset of chest pain and 1 mm of ST-segment depression during bicycle exercise; increases with propranolol were smaller and not statistically significant. Nine patients had a preferential clinical response to nifedipine compared with six patients to propranolol; this was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvement in radionuclide ejection fraction at identical work loads. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14 percent (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output. Thus, nifedipine is more effective on several measurements than propranolol when administered as single drug therapy in stable angina and has the advantage of preserving cardiac output during exercise.

Adult↗
PubMed1989

Exercise training in patients with chronic heart failure delays ventilatory anaerobic threshold and improves submaximal exercise performance.

We have recently demonstrated that exercise training can induce important hemodynamic and metabolic adaptations in patients with chronic heart failure due to severe left ventricular dysfunction. This study examines the accompanying changes in submaximal exercise performance and the ventilatory response to exercise in these patients. Before and after 16-24 weeks of exercise training, subjects underwent two symptom-limited bicycle exercise tests, one with an incremental graded workload, and one with a constant workload that represented 79 +/- 11% of the pretraining peak oxygen consumption. Breath-by-breath expired gas analysis was performed continuously during each test, and central hemodynamic, leg blood flow, and blood lactate measurements were obtained during the incremental protocol. The ventilatory anaerobic threshold was determined during the incremental exercise study from coplotted breath-by-breath ventilatory data with standard criteria by observers who were unaware of patient identity or training status. As previously reported, exercise training increased peak oxygen consumption by 23% from 16.8 +/- 3.8 to 20.6 +/- 4.7 ml/kg/min and reduced blood lactate levels during submaximal exercise. The training-induced decrease in lactate accumulation was accompanied by a decrease in carbon dioxide production, respiratory exchange ratio, and ventilation during submaximal exercise. The ventilatory anaerobic threshold was delayed from 284 +/- 43 to 352 +/- 91 seconds of exercise (p = 0.02), and it occurred at an increased oxygen consumption (10.1 +/- 1.2 vs. 12.1 +/- 2.6 ml/kg/min, p = 0.01). Exercise duration during the constant workload protocol increased from 938 +/- 410 to 1,429 +/- 691 seconds (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Relation between central and peripheral hemodynamics during exercise in patients with chronic heart failure. Muscle blood flow is reduced with maintenance of arterial perfusion pressure.

We studied the central hemodynamic, leg blood flow, and metabolic responses to maximal upright bicycle exercise in 30 patients with chronic heart failure attributable to severe left ventricular dysfunction (ejection fraction, 24 +/- 8%) and in 12 normal subjects. At peak exercise, patients demonstrated reduced oxygen consumption (15.1 +/- 4.8 vs. 32.1 +/- 9.9 ml/kg/min, p less than 0.001), cardiac output (8.7 +/- 3.2 vs. 18.6 +/- 4.4 l/min, p less than 0.001), and mean systemic arterial blood pressure (116 +/- 15 vs. 135 +/- 13 mm Hg, p less than 0.01) compared with normal subjects. Leg blood flow was decreased in patients versus normal subjects at rest and matched submaximal work rates and maximal exercise (2.1 +/- 1.9 vs. 6.4 +/- 1.4 l/min, all p less than 0.01). Mean systemic arterial blood pressure was no different in the two groups at rest or at matched submaximal work rates, whereas leg vascular resistance was higher in patients compared with normal subjects at rest, submaximal, and maximal exercise (all p less than 0.01). Although nonleg blood flow was decreased at rest in patients, it did not decrease significantly during exercise in either group. Peak exercise leg blood flow was related to peak exercise cardiac output in patients (r = 0.66, p less than 0.01) and normal subjects (r = 0.67, p less than 0.01). In patients, leg vascular resistance was not related to mean arterial blood pressure, pulmonary capillary wedge pressure, arterial catecholamines, arterial lactate, or femoral venous pH at rest or during exercise. Compared with normal subjects during submaximal exercise, patients demonstrated increased leg oxygen extraction and lactate production accompanied by decreased leg oxygen consumption. Thus, in patients with chronic heart failure compared with normal subjects, skeletal muscle perfusion is decreased at rest and during submaximal and maximal exercise, and local vascular resistance is increased. Our data indicate that nonleg blood flow and arterial blood pressure were preferentially maintained during exercise at the expense of leg hypoperfusion in our patients. This was associated with decreased leg oxygen utilization and increased leg oxygen extraction when compared to normal subjects, providing further evidence that reduced perfusion of skeletal muscle is important in causing early anaerobic skeletal muscle metabolism during exercise in subjects with this disorder.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1988

The ventilatory threshold: quantitative analysis of reproducibility and relation to arterial lactate concentration in normal subjects and in patients with chronic congestive heart failure.

The present study evaluates optimal ventilatory criteria and exercise protocols for determining the ventilatory threshold, and assesses the day-to-day reproducibility of the ventilatory threshold and its relation to peak oxygen uptake VO2 and blood lactate concentration in normal subjects and patients with stable chronic congestive heart failure (CHF). Eighteen normal subjects and 18 patients underwent rapid (1-minute stage) and gradual (3-minute stage) bicycle exercise tests on consecutive days. The ventilatory threshold was determined from computer-generated printouts of expired gas variables measured breath by breath. Interobserver variability of ventilatory threshold was small in both normal (0.66 +/- 0.85 ml/min/kg) and CHF patients (0.50 +/- 0.46 ml/min/kg). Variability in the normal subjects was lower for the rapid exercise protocol (0.66 +/- 0.85 ml/min/kg) than the gradual protocol (1.72 +/- 1.63 ml/min/kg) (p less than 0.05), but both protocols produced similar results in the CHF group. Day-to-day reproducibility of ventilatory threshold was high (r = 0.91, standard error of the estimate 1.74 ml/min/kg) and was similar to that of peak VO2 (r = 0.95, standard error of the estimate 3.31 ml/min/kg). The use of co-plotted ventilatory equivalents for oxygen and carbon dioxide yielded ventilatory threshold values comparable to values obtained by using multiple parameters (r = 0.94, p less than 0.0001). Although the ventilatory threshold did not predict a precise lactate level for individual subjects, the lactate increment at the ventilatory threshold occurred within a narrow range in both normal subjects and patients with CHF; the increase was 7.5 +/- 4.5 mg/dl and 7.7 +/- 4.1 mg/dl, respectively, indicating a relation to initial increases in blood lactate.

Aged↗
PubMed1988

Increased exercise ventilation in patients with chronic heart failure: intact ventilatory control despite hemodynamic and pulmonary abnormalities.

This study was designed to determine the pathophysiologic basis of increased exercise ventilation in the presence of chronic heart failure. Sixty-four ambulatory patients with chronic heart failure and 38 age-matched normal control subjects performed exercise according to identical staged, symptom-limited bicycle exercise protocols with measurement of hemodynamic, ventilatory, and metabolic responses. Compared with normal subjects, ventilation and the ratio of ventilation to CO2 production (Ve/VCO2), and pulmonary capillary wedge pressure were elevated in patients at rest and during exercise. The ratio of pulmonary dead space to tidal volume (Vd/Vt) also was elevated in the heart failure group at rest and during exercise and was closely related to Ve/VCO2 (all r greater than .72, p less than .001). Rest and exercise arterial PCO2 regulation was normal in patients. Peak exercise Ve/VCO2 did not correlate with pulmonary vascular pressures, but was inversely related to cardiac output (r = -.49, p less than .001). Thus, neurohumoral ventilatory control mechanisms are intact in patients with chronic heart failure and act to maintain normal PaCO2 levels in the face of increased pulmonary dead space. Activation of abnormal reflexes due to hemodynamic derangements during exercise are not important in determining ventilation in the presence of chronic heart failure. The demonstration of a correlation between decreased cardiac output and increased ventilation in the patient group suggests that attenuated pulmonary perfusion may play a role in causing exercise hyperpnea in the presence of chronic heart failure by producing ventilation perfusion abnormalities and thereby increasing physiologic pulmonary dead space.

Exercise Test↗
PubMed1988

Exercise training in patients with severe left ventricular dysfunction. Hemodynamic and metabolic effects.

We studied the effects of exercise training in patients with chronic heart failure attributed to left ventricular dysfunction (ejection fraction, 24 +/- 10%). Twelve ambulatory patients with stable symptoms underwent 4-6 months of conditioning by exercising 4.1 +/- 0.6 hr/wk at a heart rate corresponding to 75% of peak oxygen consumption. Before and after training, patients underwent maximal bicycle exercise testing with direct measurement of central hemodynamic, leg blood flow, and metabolic responses. Exercise training resulted in a decrease in heart rate at rest and submaximal exercise and a 23% increase in peak oxygen consumption from 16.8 +/- 3.8 to 20.6 +/- 4.7 ml/kg/min (p less than 0.01). Heart rate, arterial lactate, and respiratory exchange ratio were unchanged at peak exercise after training. Maximal cardiac output tended to increase from 8.9 +/- 2.7 to 9.9 +/- 3.2 1/min and contributed to improved peak oxygen consumption in some patients, although this change did not reach statistical significance (p = 0.13). Rest and exercise measurements of left ventricular ejection fraction, left ventricular end-diastolic volume, and left ventricular end-systolic volume were unchanged. Right atrial, pulmonary arterial, pulmonary capillary wedge, and systemic arterial pressures were not different after training. Training induced several important peripheral adaptations that contributed to improved exercise performance. At peak exercise, systemic arteriovenous oxygen difference increased from 13.1 +/- 1.4 to 14.6 +/- 2.3 ml/dl (p less than 0.05). This increase was associated with an increase in peak-exercise leg blood flow from 2.5 +/- 0.7 to 3.0 +/- 0.8 l/min (p less than 0.01) and an increase in leg arteriovenous oxygen difference from 14.5 +/- 1.3 to 16.1 +/- 1.9 ml/dl (p = 0.07). Arterial and femoral venous lactate levels were markedly reduced during submaximal exercise after training, even though cardiac output and leg blood flow were unchanged at these workloads. Thus, ambulatory patients with chronic heart failure can achieve a significant training effect from long-term exercise. Peripheral adaptations, including an increase in peak blood flow to the exercising leg, played an important role in improving exercise tolerance.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1986

Physiologic basis for the age-related decline in aerobic work capacity.

To determine the physiologic mechanisms of the decline in aerobic work performance with age, a cross-sectional study was performed. Twenty-four sedentary male volunteers, aged 20 to 50 years, underwent right-sided cardiac catheterization, arterial cannulation, radionuclide angiography and expired gas analysis for detailed evaluation of central and peripheral cardiovascular function during submaximal and maximal exercise. Habitual physical activity level varied but was well matched across the age range. Over the 3-decade age range studied, there was no detectable change in cardiovascular function at rest. When peak exercise variables were examined, an age-related 25% decrease in O2 consumption was noted (r = -0.43, p = 0.04); this was associated with a 25% decrease in peak cardiac index (r = -0.54, p = 0.01) and a 20% decrease in peak heart rate (r = -0.63, p = 0.002). In addition, there was an age-related increase in calculated systemic and pulmonary vascular resistances and an increase in left ventricular ejection time. No age relation was seen for exercise stroke volume index, end-diastolic volume index, end-systolic volume index, pulmonary artery wedge pressure, ejection fraction or arteriovenous O2 difference. These results indicate that the age-related decline in aerobic work performance among men aged 20 to 50 years results primarily from a reduced exercise heart rate in older subjects rather than from a reduction in stroke volume or peripheral O2 utilization.

Adult↗
PubMed1986

Comparison of nifedipine alone with propranolol alone for stable angina pectoris including hemodynamics at rest and during exercise.

The effects of nifedipine (60 to 90 mg/day) and propranolol (240 mg/day) on symptoms, angina threshold and cardiac function were compared in a placebo-controlled, double-blind, crossover study. Five-week treatment periods with nifedipine and propranolol were compared with 2 weeks of placebo treatment in 21 men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. Compared with placebo, New York Heart Association functional class improved in patients equally with nifedipine (p = 0.001) and propranolol (p = 0.006). Frequency of chest pain decreased with nifedipine (p = 0.001) and propranolol (p = 0.01), and nitroglycerin consumption similarly decreased with both treatments. Nifedipine significantly delayed the onset of chest pain (p = 0.01) and 1 mm of ST-segment depression (p = 0.002) during bicycle exercise; smaller increases with propranolol were not statistically significant. A preferential clinical response to nifedipine (9 patients) or propranolol (6 patients) was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvements in ejection fraction at identical workloads, from 0.48 +/- 0.11 to 0.58 +/- 0.12 (p less than 0.001) and 0.56 +/- 0.14 (p less than 0.001), respectively. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14% (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Value and limitation of biplane rest and exercise radionuclide angiography for assessing individual bypass grafts: a prospective study.

This prospective study evaluated the ability of serial biplane rest and exercise radionuclide angiography to predict the status of individual coronary bypass grafts in 20 patients 2 to 6 months after surgery. The preoperative coronary angiogram was used to assign vessels to 10 regions of distribution on the radionuclide angiogram. Predictions of graft adequacy for individual vessels were based on a detailed assessment of rest and exercise wall motion in their regions of supply. Of 59 grafts, 38 were judged adequate (patent with less than 75% stenosis) and 21 inadequate by postoperative catheterization. Radionuclide prediction of graft status was possible for 32 of the 59 grafts, including 19 of 24 left anterior descending, 7 of 19 circumflex and 6 of 16 right coronary artery grafts. The status of the remaining 27 grafts could not be assessed because of normal wall motion in their region of supply both pre- and postoperatively (22 vessels) or because a region of supply was not represented on the biplane radionuclide angiogram (5 vessels). Of the 32 predictions made, 25 (78%) were correct, including 13 (93%) of 14 predictions of graft adequacy and 12 (67%) of 18 predictions of graft inadequacy. The single incorrect prediction of graft adequacy resulted from improved exercise wall motion in a region supplied by a graft judged as having a 75% anastomotic stenosis. Most incorrect predictions of graft inadequacy were due to new septal or other rest wall motion abnormalities postoperatively. The comparison of pre- and postoperative studies was essential to maintain the predictive ability of the test. Thus, a detailed analysis of regional wall motion by rest and exercise radionuclide angiography can be used to predict the status of individual coronary artery bypass grafts. Reliable predictions can be made for most successful anterior descending grafts, and may permit cardiac catheterization to be deferred in certain cases. However, the method is limited by the need to perform preoperative exercise studies, by the low number of right and circumflex coronary artery grafts that can be evaluated and by the poor specificity of predictions of graft failure.

Adult↗
PubMed1986

Regulation of stroke volume during submaximal and maximal upright exercise in normal man.

To characterize the hemodynamic factors that regulate stroke volume during upright exercise in normal man, 24 asymptomatic male volunteers were evaluated by simultaneous right heart catheterization, radionuclide angiography, and expired gas analysis during staged upright bicycle exercise to exhaustion. From rest to peak exercise, oxygen consumption increased from 0.33 to 2.55 liters/min (7.7-fold), cardiac index increased from 3.0 to 9.7 liters/min per m2 (3.2-fold), and arteriovenous oxygen difference increased from 5.8 to 14.1 vol% (2.5-fold). The increase in cardiac index resulted from an increase in heart rate from 73 to 167 beats/min (2.5-fold), and an increase in left ventricular stroke volume index from 41 to 58 ml/m2 (1.4-fold). During low levels of exercise, there was a linear increase in cardiac index due to an increase in both heart rate and stroke volume index; stroke volume index increased as a result of an increase in left ventricular filling pressure and end-diastolic volume index and, to a much smaller extent, a decrease in end-systolic volume index. During high levels of exercise, further increases in cardiac index resulted entirely from an increase in heart rate, since stroke volume index increased no further. Left ventricular end-diastolic volume index decreased despite a linear increase in pulmonary artery wedge pressure; stroke volume index was maintained by a further decrease in end-systolic volume index. The degree to which stroke volume index increased during exercise in individuals correlated with the change in end-diastolic volume index (r = 0.66) but not with the change in end-systolic volume index (r = 0.07). Thus, the mechanism by which left ventricular stroke volume increases during upright exercise in man is dependent upon the changing relationship between heart rate, left ventricular filling, and left ventricular contractility. At low levels of exertion, an increase in left ventricular filling pressure and end-diastolic volume are important determinants of the stroke volume response through the Starling mechanism. At high levels of exertion, the exercise tachycardia is accompanied by a decrease in end-diastolic volume despite a progressive increase in filling pressure, so that stroke volume must be maintained by a decrease in end-systolic volume.

Adult↗
PubMed1985

Value of radionuclide angiography for predicting specific cardiac events after acute myocardial infarction.

The value of rest and exercise radionuclide angiography (RNA) for predicting specific events including death, recurrent acute myocardial infarction (AMI), coronary care unit readmission for unstable chest pain, and medically refractory angina after AMI was studied in 106 consecutive survivors of AMI. Analysis of the RNA variables using the Cox proportional hazards regression model yielded significant associations of the time to death with ejection fraction at rest and during exercise (X2 = 11.1 and 14.0, respectively). Both variables added significant prognostic information to the clinical assessment (X2 = 4.3 and 5.7, respectively). The change in ejection fraction from rest to exercise predicted the time to coronary artery bypass grafting for medically refractory angina before (X2 = 21.0) and after (X2 = 13.2) adjustment for the clinical descriptors, but did not predict death or other non-fatal events. Significant correlations were found between RNA variables and a variety of clinical descriptors previously reported to have prognostic significance. Clinical and RNA variables that are measures of left ventricular function were predictive of subsequent mortality, whereas those that reflect residual potentially ischemic myocardium were predictive of subsequent nonfatal ischemic events. Rest and exercise RNA after AMI provides significant prognostic information regarding specific events during follow-up independent of that provided by clinical assessment.

Adult↗
PubMed1984

Mechanism and significance of a decrease in ejection fraction during exercise in patients with coronary artery disease and left ventricular dysfunction at rest.

The purpose of this study was to determine whether an exercise-induced decrease in ejection fraction in patients with coronary artery disease and left ventricular dysfunction at rest represents ischemia or the nonspecific response of a compromised left ventricle to exercise stress. Accordingly, radionuclide ejection fraction responses of 246 patients with coronary artery disease and an ejection fraction at rest of less than 0.50 were compared with those of a "nonischemic" control group of 48 patients with idiopathic dilated cardiomyopathy and a similar degree of ventricular dysfunction. The significance of the ejection fraction response in the group with coronary artery disease was further examined by relating it to the angiographic extent of coronary artery disease, severity of angina, incidence of chest pain and electrocardiographic ST segment depression during exercise and long-term prognosis. The ejection fraction decreased by greater than or equal to 0.01 and greater than or equal to 0.05 during exercise in 48 and 28%, respectively, of the patients with coronary artery disease compared with only 8 and 2%, respectively, of the patients with cardiomyopathy. When exercise was limited by fatigue at a submaximal heart rate, the ejection fraction decreased in 25% of the patients with coronary artery disease but in none of the patients with cardiomyopathy. Patients with coronary artery disease whose ejection fraction decreased during exercise had a significantly higher incidence of three vessel disease, exercise-induced chest pain or ST depression and late mortality than did patients whose ejection fraction did not decrease. These relations were confirmed equally in subgroups of patients with moderate (ejection fraction 0.30 to 0.49) and severe (ejection fraction less than 0.30) left ventricular dysfunction. Thus, in patients with coronary artery disease and left ventricular dysfunction at rest, a decrease in ejection fraction during exercise is more likely to indicate ischemia than a nonspecific left ventricular response to exercise stress. In the individual patient, a decrease of 0.05 or greater, or a decrease during submaximal exercise, appears to be highly specific for ischemia. A decrease in ejection fraction identifies a subgroup of patients with a high prevalence of multivessel coronary artery disease and a high risk of death during long-term follow-up on medical therapy.

Adult↗
PubMed1984

Effects of physical conditioning on left ventricular ejection fraction in patients with coronary artery disease.

To address the hypothesis that physical conditioning may improve left ventricular function in patients with coronary artery disease, we performed first-pass radionuclide ventriculography in 53 patients at rest and during upright bicycle exercise before and after 6 to 12 months of exercise training. The peak bicycle workload achieved before the onset of fatigue, dyspnea, or angina increased by an average of 22% (p = .0001) after training, and mean heart rate at a workload equal to the pretraining maximum workload was decreased by 10 beats/min after training (p = .0002). Of 21 subjects with angina or exertional ST segment depression before training, 15 (71%) were able to exercise to the same workload without these manifestations of ischemia after training. Whereas neither mean resting left ventricular ejection fraction (LVEF) nor LVEF at peak exertion was significantly altered, mean LVEF at the pretraining maximum workload was increased from 0.50 to 0.54 (p = .002) after training. There was a significant correlation between the magnitude of training bradycardia and the increment in LVEF at the pretraining maximum workload (p = .009). We conclude that the relative bradycardia at comparable exercise workloads produced by exercise conditioning is associated with improvements in left ventricular performance as assessed by the LVEF. This observation is compatible with the hypothesis that training bradycardia in conditioned subjects with ischemic heart disease is associated with lower myocardial oxygen demand and lesser degrees of ischemia at comparable workloads. However, training effects on ventricular afterload or on ischemia contractile performance of the heart cannot be excluded.

Adult↗
PubMed1984

Sex-related differences in the normal cardiac response to upright exercise.

In previous studies from this laboratory, we found that approximately 30% of women with chest pain and normal coronary arteries demonstrated either a decrease in or a failure to increase radionuclide ejection fraction during exercise. To examine the hypothesis that this apparent abnormality in left ventricular function represents a physiologic difference between men and women, we prospectively studied central and peripheral cardiovascular responses to exercise in 31 age-matched healthy volunteers (16 women and 15 men). A combination of quantitative radionuclide angiography and expired-gas analysis was used to measure ejection fraction and relative changes in end-diastolic counts, stroke counts, count output, and arteriovenous oxygen difference during symptom-limited upright bicycle exercise. Normal male and female volunteers demonstrated comparable baseline left ventricular function and similar aerobic capacity, as determined by weight-adjusted peak oxygen consumption (22.1 +/- 5.1 and 22.6 +/- 4.3 ml/kg/min, respectively). However, their cardiac responses to exercise were significantly different. Ejection fraction increased from 0.62 +/- 0.09 at rest to 0.77 +/- 0.07 during exercise in men (p less than .001), but was unchanged from 0.63 +/- 0.09 at rest to 0.64 +/- 0.10 during exercise in women. The ejection fraction increased by 5 points or more in 14 of 15 men, but in only seven of the 16 women. End-diastolic counts increased by 30% in women (p less than .001), but was unchanged in men. Because decreases in ejection fraction were matched by increases in end-diastolic counts, relative increases in stroke counts and count output were the same for men and women. These data demonstrate a basic difference between men and women with respect to the mechanism by which they achieve a normal response of stroke volume to exercise; these differences must be taken into account when measurements of cardiac function during exercise stress are used for diagnostic purposes.

Adult↗
PubMed1983

Determinants of variable exercise performance among patients with severe left ventricular dysfunction.

The relation between bicycle exercise performance and determinants of central and peripheral cardiovascular function was assessed in 17 patients with class II to III heart failure and in 9 normal subjects. Proportional changes in oxygen consumption (VO2) from rest (R) to maximal exercise (Ex), or Mets, were used as an objective measure of the exercise capacity or functional reserve of the cardiovascular system. Left ventricular ejection fraction (EF) and proportional changes in end-diastolic volume, stroke volume, and cardiac output were determined from appropriate count data by equilibrium radionuclide angiography. Proportional changes in arteriovenous oxygen difference (A-VO2) were derived from the equation Ex/R A-VO2 = Ex/R VO2 divided by Ex/R CO, where CO = count output. Each subject exercised to an anaerobic endpoint. Maximal VO2 was significantly lower in patients than in normal subjects. Because Ex/R A-VO2 was comparable in normal subjects and patients, the lower exercise performance in patients resulted from a reduced count output response. The reduced CO response in patients resulted from failure of the ejection fraction to increase or from an attenuated heart rate response, or both. Exercise performance was variable in both groups. Multivariable analysis in the patient group identified changes in heart rate, count output, and A-VO2 with exercise as important predictors of Mets, but found no relation between Mets and changes in ejection fraction or stroke counts during exercise. Similarly, multiple regression analyses between Mets and determinants of cardiovascular function demonstrated significant correlations with Ex/R heart rate, Ex/R count output, and Ex/R A-VO2 in both groups. In patients, EF at rest ranged from 0.09 to 0.36, but it did not correlate with Mets, nor did changes in ejection fraction, stroke counts, or end-diastolic counts during exercise. The variable exercise performance among patients with severe left ventricular dysfunction was determined predominantly by a variable heart rate and A-VO2 response and not by rest or exercise indexes of left ventricular function.

Adult↗