Relationship between systolic blood pressure, ventricular volume and ischemic pain perception in patients with angina pectoris: a potential role for baroreceptors.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D S Sheps.
Explore the source record for details and available documents.
Limited data are available on the relation between physical fitness and mortality from cardiovascular disease. We examined this question in a study of 4276 men, 30 to 69 years of age, whom we followed for an average of 8.5 years. Examinations at base line included assessment of conventional coronary risk factors and treadmill exercise testing. The heart rate during submaximal exercise (stage 2 of the exercise test) and the duration of exercise were used as measures of physical fitness. Men with incomplete data (n = 308) or who were using cardiovascular drugs (n = 213) were excluded from the analysis. Men who had clinical evidence of cardiovascular disease at base line (n = 649) were analyzed separately. Forty-five deaths from cardiovascular causes occurred among the remaining 3106 men. A lower level of physical fitness was associated with a higher risk of death from cardiovascular and coronary heart disease, after adjustment for age and cardiovascular risk factors. The relative risk of death from cardiovascular causes was 2.7 (95 percent confidence interval, 1.4 to 5.1; P = 0.003) for healthy men with an increment of 35 beats per minute in the heart rate during stage 2, and 3.0 (95 percent confidence interval, 1.6 to 5.5; P = 0.0004) for those with a decrement of 4.4 minutes in the exercise time spent on the treadmill. The corresponding values for death from coronary heart disease were 3.2 (95 percent confidence interval, 1.5 to 6.7; P = 0.003) and 2.8 (95 percent confidence interval, 1.3 to 6.1; P = 0.007), respectively. We conclude that a lower level of physical fitness is associated with a higher risk of death from coronary heart disease and cardiovascular disease in clinically healthy men, independent of conventional coronary risk factors.
Evidence suggests that endogenous opioids, particularly the beta-endorphins and met-enkephalins, are closely involved in stress-induced analgesia and nociceptive pain control. Numerous investigations have been conducted to evaluate the role of opioids in silent vs symptomatic myocardial disease. There is good evidence to suggest that patients with asymptomatic ischemia have defective pain perception compared with those with angina; however, the precise role of the endorphin and enkephalin systems in this phenomenon remains to be elucidated. Possible sources for disparate study results include variation in patient populations, insensitive or improperly timed assay techniques, and differences in amount of ischemia.
This investigation examined the reproducibility of resting and post exercise plasma beta-endorphin levels. Twenty subjects (10 men and 10 women) had their resting endorphin levels measured under controlled conditions on four separate occasions. Concomitantly, the endorphin response of eight trained runners completing three similar ten mile runs was also determined. For the resting data, there was no significant overall variation among trials, but the intra-subject variability was substantial; the within subject variance was 6.16, and it corresponded to an intra-class reliability coefficient of r = 0.239. No gender effect was noted for the average beta-endorphin values for the four occasions (men = 4.6 +/- 1.7; women = 4.4 +/- 2.1 pM/l); however, the males' within-subject variance of 8.548 (r = 0.080) was significantly larger than that of 3.719 (r = 0.485) for females. Of the runners, one outlier subject had a uniquely high average beta endorphin level of 85.67. Analysis including and excluding the outlier subject yielded within-subject variances of 29.61 (r = 0.960) and 34.47 (r = 0.176), respectively; variances for differences in confidence limits for random variation, they must exceed 7 pM/l at rest, 17 pM/l post exercise, and 20 pM/L difference from rest to post exercise.
Acute exposure to carbon monoxide has the potential to impair exercise capacity in patients with ischemic heart disease. The effect of sufficient inhalation of this compound to gradually produce a level of 6% carboxyhemoglobin was studied in 30 nonsmoking patients with obstructive coronary artery disease and evidence of exercise-induced ischemia. After an initial training session, subjects were exposed to air or carbon monoxide on successive days in a randomized double-blind crossover fashion. Cardiac function and exercise capacity were assessed during symptom-limited supine radionuclide ventriculography. On the carbon monoxide day, mean postexposure carboxyhemoglobin was 5.9 +/- 0.1% compared with 1.6 +/- 0.1% (p less than 0.01) after air exposure. The mean duration of exercise was significantly longer after air compared with carbon monoxide exposure (626 +/- 50 s for air versus 585 +/- 49 s for carbon monoxide, p less than 0.05). Actuarial methods suggested that subjects were likely to experience angina earlier during exercise on the day of carbon monoxide exposure (p less than 0.05). Both the level (62 +/- 2.4 versus 60 +/- 2.4%, p = 0.05) and change in left ventricular ejection fraction at submaximal exercise (1.6 +/- 1.6 versus -1.2 +/- 1.6%, p = 0.05) were greater on the air exposure day compared with the carbon monoxide day. The peak exercise left ventricular ejection fraction was not different for the two exposures (57 +/- 2.5% for both). These results demonstrate earlier onset of ventricular dysfunction, angina and poorer exercise performance in patients with ischemic heart disease after acute carbon monoxide exposure sufficient to increase blood carboxyhemoglobin to 6%.
Plasma beta-endorphin levels were measured by radioimmunoassay before and after exercise in 25 patients with coronary artery disease. Eighteen patients were men and 7 were women; age range was 36 to 75 years (mean 60). All patients had angina pectoris, a positive treadmill test response or positive exercise radionuclide findings. The mean preexercise plasma endorphin level was 4.9 +/- 3.0 pmol/liter (range 0.7 to 13.5). The mean postexercise plasma endorphin level of 6.6 +/- 4.6 mol/liter (range 0 to 19.5) was significantly higher (p less than 0.05). A significant positive correlation was seen between postexercise endorphin levels and time to onset of angina (r = 0.4, p = 0.03). There were negative correlations between postexercise endorphin levels and occurrence (r = -0.4, p = 0.04) and duration of angina (r = -0.4, p = 0.05). No association was found for maximal heart rate-blood pressure product, workload, time to ST-segment depression or stress ejection fraction. A positive correlation was found between rest left ventricular ejection fraction and postexercise endorphin levels (r = 0.5, p = 0.02). In conclusion, in patients with exercise-induced myocardial ischemia, plasma beta-endorphin levels are increased after exercise; postexercise endorphin levels are related to timing and occurrence (presence or absence) of angina; and endorphins may alter the perception of pain caused by myocardial ischemia.
The performance of normal subjects during radionuclide ventriculography has been related to age, but the combined effects of age and sex on exercise ventricular function are not well described. We studied 55 normal volunteers, 27 men (age = 30 +/- 10 years) and 28 women (age = 33 +/- 14 years), free of chest pain syndromes, during supine rest/exercise radionuclide ventriculography performed to fatigue. Resting left ventricular ejection fraction did not differ between male and female subjects (64 +/- 5.4 vs 64 +/- 6.1; p = NS). Both the peak left ventricular ejection fraction (78 +/- 4.4 vs 72 +/- 9.2; p less than 0.001) and the change in ejection fraction with exercise (14 +/- 4.0 vs 7.9 +/- 7.0; p less than 0.001) were significantly greater in men compared to respective values in women. Regression analysis showed that sex (r = 0.51; p less than 0.001) but not age (r = -0.18; p = 0.19) was a significant predictor of change in ejection fraction with exercise. Data on left ventricular volume response to exercise, available in 43 subjects, revealed that men had a greater percentage of decline in end-systolic volume with exercise than women (-47 +/- 15 vs -24 +/- 26; p less than 0.001). It is concluded that sex exerts a significant influence on normal left ventricular response to fatigue-limited supine exercise and that the gender difference is mediated, in part, by left ventricular end-systolic volume response to exercise.
To investigate the possibility that patients with single-vessel coronary artery disease (CAD) and recent myocardial infarction (MI) can have ST segment depression on post infarction treadmill testing due to ischemia, we studied 16 such patients who underwent cardiac catheterization and exercise testing after MI. Of the 11 patients with ST segment depression on treadmill testing, 10 failed to increase their ejection fraction and nine had a focal worsening of wall motion during exercise radionuclide ventriculography. Seven of these 11 patients had hypokinesis or normokinesis in the suspected area of infarction. In contrast, four of the five patients without ST segment depression on treadmill stress testing had an increase in ejection fraction with stress which was significantly greater than that seen in patients with ST depression (7.2% vs 0%, p less than 0.05). Short-term follow-up (1.1 years) revealed continued post infarction angina in 10 of the 11 patients with positive treadmill stress tests. Four of these patients underwent either percutaneous transluminal angioplasty or surgery. We conclude that positive post infarction treadmill tests due to exercise-induced ischemia may occur in patients with single-vessel CAD and may be associated with continued angina that requires surgical intervention.
Elective cardioversion of supraventricular arrhythmias has been demonstrated to be an effective procedure which can be performed with minimal risk. The risks of cardioversion are increased in the presence of digoxin intoxication, failure of synchronization, conversion in the presence of high energies, long standing atrial fibrillation, atrial fibrillation with slow ventricular rates, and dysrhythmias in association with ischemic heart disease or cardiomyopathy. However, the risk of cardioversion of supraventricular arrhythmias in the presence of conduction disturbances, although thought to be increased, has never been carefully studied. This study was designed to examine the effects of conduction disturbances (CD) on the success and risk of elective cardioversion of supraventricular arrhythmias (atrial fibrillation and atrial flutter) and to define the role of temporary pacemakers prior to cardioversion in these patients.
To examine the effect of naloxone (an opiate antagonist) on exercise performance, six normal females (20-28 yr) walked on a treadmill (93.8 m/min) with the grade increasing 2.5% every 4 min until exhaustion. Each subject completed three trials: naloxone infusion (0.4 mg/ml saline), saline infusion (1 ml), and an infusion control. The order of trials was randomized and double blind. Each subject responded similarly at each submaximal stage for all three trials. The results during maximal exertion were different. Time to exhaustion was similar for all conditions, averaging 32.6 +/- 3.0 min with a maximal O2 uptake of 38.8 +/- 2.8 ml X kg-1 X min-1 and a lactate of 9.1 +/- 1.1 mmol/l. Maximal ventilation (BTPS) was 7.9 l/min less during the naloxone treatment when compared with either control or placebo trials (P less than 0.05). This difference was attributed to a 4-breath/min reduction in respiratory frequency (P less than 0.05). End-tidal CO2 partial pressure was approximately 4 Torr higher at maximum after naloxone injection. Maximal heart rates averaged 190.8 +/- 3.8 beats/min for both control and placebo trials. This was significantly greater (P less than 0.05) than the 185 +/- 2.4 beats/min recorded for the naloxone trials. Ratings of perceived exertion were 17.0 +/- 1.3 units at maximum, similar for all three trials. Despite these statistically significant cardiorespiratory differences, naloxone produced no effect on maximum O2 uptake or exercise duration.
A 32 year old woman who complained of exercise-induced chest pain was found to have widespread elevation of the ST segment of the electrocardiogram during exercise testing. Coronary angiography demonstrated no obstructive lesions and no evidence of coronary artery spasm despite ergonovine administration, bicycle ergometry and rapid atrial pacing. Exercise thallium-201 scintigraphy demonstrated no perfusion defects despite ST segment elevation. Radionuclide blood pool imaging revealed a slight decrease in ejection fraction with exercise. The available evidence raises the possibility of small vessel coronary artery disease, either structural or vasotonic, as a cause of this patient's symptoms.
Systolic time intervals (STI) obtained during exercise are useful as a method of estimating global left ventricular function. The conventional method, however, which requires a carotid pulse tracing as well as a phonocardiogram of high quality, is technically difficult under conditions of exercise. We have validated a new method of obtaining STI which employs the first derivative of thoracic electrical impedance (DZ/DT). The DZ/DT was recorded using surface electrodes and a microcomputer for automated signal processing. The new method was studied in 20 male normal subjects (aged 18 to 53 years) at rest and during increasing levels of upright exercise. Heart rate ranged from 61 to 173 beats/min. Results obtained simultaneously by both techniques showed no significant difference. Thus impedance cardiography allows continuous monitoring of STI during exercise and may prove to be a valuable addition to multistage stress testing.
A patient with multiple myeloma had systemic amyloidosis exclusively confined to the vascular system. These vascular deposits had the typical tinctorial and ultrastructural characteristics of amyloid. At first, the patient clinically had ischemic heart disease, and at postmortem examination was seen to have had acute and chronic ischemic injury of the heart and kidneys due to vascular narrowing by massive amyloid deposits. Exclusively vascular systemic amyloidosis represents a morphologically and clinically distinctive, but uncommon, variant of amyloidosis.
The effect of the addition of radiographic contrast material (Renografin) to blood on the oxyhemoglobin dissociation curve and P50 was measured by a metabolic deoxygenation technique in a strongly buffered red cell suspension. With incubation time constant, increasing doses produced progressive decreases in P50. With incubation time varied at a constant dose, a decrease in P50 was seen after only one minute. In addition, in vivo studies were performed on 11 patients undergoing cardiac catheterization. Simultaneous proximal coronary sinus and aortic samples were drawn as controls, and then at one minute and five minutes after injection of the left coronary artery. In eight patients studies were performed after, and in three prior to left ventriculography. At one minute after left coronary injection there was a significant decrease of coronary sinus as compared to aortic P50 (p less than .10) (only when left ventriculography was performed prior to coronary arteriography). The magnitude of these effects in vivo is unknown, but they would be expected to be more severe in areas distal to a critical coronary lesion due to stasis of blood flow and ischemic metabolic changes.
Explore the source record for details and available documents.
As recently described by Moe et al., parasystolic modulation implies that the ectopic cycle length of a parasystolic focus can be increased or decreased by electrical influences transmitted across the zone of protection. A search for this phenomenon was made in nine patients with intermittent ventricular parasystole resulting from protection only during specific portions of the cycle. All nine patients had a period of relatively early protection affecting the initial 55-67% of the cycle preceding a period of resetting during which the parasystolic focus was discharged and fully recycled. In addition, two patients had a period of relatively late parasystolic protection. Pseudo-resetting (apparent resetting in the surface leads without interruption of activity within the parasystolic focus itself), seen throughout the entire period of late protection in these two patients, and during the relatively refractory period in one patient, was identified because the R waves causing apparent resetting were encompassed by parasystolic-to-parasystolic intervals equalling twice the ectopic cycle length. Our findings indicate that parasystolic modulation did not occur in the type of intermittent ventricular parasystole included in this study. That is, the parasystolic focus was either not affected (not modulated) during specific (early or late) portions of the cycle, or normally reset (discharged and fully recycled, but neither depressed, nor enhanced) in other portions of the cycle. This study does not exclude the occurrence of modulation in other types of parasystole, nor in some automatic nonparasystolic rhythms.
Explore the source record for details and available documents.
Explore the source record for details and available documents.