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Biomedical subjects

D S Sheps

Publications and source records attributed to D S Sheps.

At least 37 records · Page 2Linked to original sources
PubMed1996

Beta-endorphin but not metenkephalin counteracts adenosine-provoked angina pectoris-like pain.

Whether i.v. infusion of beta-endorphin or metenkephalin can modify adenosine-provoked angina pectoris-like pain was investigated in healthy volunteers with a double-blind controlled design. All seven volunteers experienced dose-related adenosine-provoked chest pain. Metenkephalin did not modulate the dose-effect curve for adenosine while beta-endorphin counteracted (p < 0.01) the development of pain. The results suggest that peripheral p.subtype opioid receptors are involved in the modulation and may play a role in the genesis of silent and painful myocardial ischaemia.

Adult↗
PubMed1996

Association between angina pectoris and ischemic indexes during exercise testing and ambulatory monitoring.

We examined the relation between anginal symptoms and ischemic indexes during ischemia on exercise testing and daily activities in 76 patients (59 men and 17 women, mean age 61.5 years) with documented coronary artery disease and exercise-induced ischemia. All patients underwent upright bicycle exercise testing and 48-hour ambulatory electrocardiographic monitoring (AECG). Angina was reported in 28 patients (37%) during exercise-induced ischemia. A total of 287 ischemic episodes were detected from 44 patients (58%) during AECG. There was a mean number of 7.4 episodes and a mean total duration of 75 min/48 hours. There were no differences in the prevalence and the magnitude of ambulatory ischemia between patients with and without angina during exercise testing. Among the 44 patients who had ischemia during both tests, 50% of patients with angina during exercise testing had symptomatic ischemia during AECG compared to 14% in patients with silent ischemia during exercise testing (p = 0.01). Ninety-two percent of ischemic episodes were preceded by an increase in heart rate (HR) of > 10 beats/min. There was a strong positive correlation (r = 0.70, p < 0.01) between HR at onset of 1 mm ST depression (ischemic threshold) during exercise testing and during AECG. We conclude that (1) patients with exercise-induced angina have significantly more symptoms during ambulatory ischemia, (2) ischemic threshold during exercise testing and daily life are positively correlated, and (3) our findings emphasize the role of increased myocardial oxygen demand in the development of ambulatory ischemia.

Aged↗
PubMed1996

Relationship among depression scores, beta-endorphin, and angina pectoris during exercise in patients with coronary artery disease.

OBJECTIVES: To determine the relationship between depression scores and (1) anginal indices during exercise including time to onset of angina, duration of angina, and severity of angina and (2) beta-endorphin at rest and in response to exercise. DESIGN: Prospective clinical trial. SETTING: Tertiary-care university hospital. PATIENTS: Fifty-eight patients with documented coronary artery disease and exercise-induced ischemia. OUTCOME MEASURES: Anginal indices during exercise (time to onset of angina, duration of angina, severity of angina); hemodynamic measures (systolic blood pressure, heart rate, rate pressure product) at rest, at onset of angina and at peak exercise; and plasma beta-endorphin levels at rest and immediately after exercise. RESULTS: Twenty-two of 58 patients had typical angina and electrocardiographic change indicating myocardial ischemia during exercise. There was a positive correlation between depression scores and duration of angina and a negative correlation between depression scores and time to onset of angina. Among patients with angina during exercise, systolic blood pressure increased to a greater extent in patients with high depression scores. Patients with high depression scores had higher resting beta-endorphin levels. CONCLUSIONS: Patients with depressed mood had greater perception of anginal pain than nondepressed patients, which cannot be explained by differences in the severity of ischemia. Possible mechanisms include an alteration in beta-endorphin regulation or differences in baroreceptor stimulation.

Adult↗
PubMed1995

Increased heart rate response to laboratory-induced mental stress predicts frequency and duration of daily life ambulatory myocardial ischemia in patients with coronary artery disease.

This study assessed the relation between hemodynamic data during a standardized mental stressor and ambulatory ischemia to determine if laboratory-induced responses could predict the magnitude of daily life ischemia. Forty-two men and 11 women, aged 46 to 79 years (mean 61), with coronary artery disease and exercise-induced ischemia were studied. All patients underwent 24- to 48-hour ambulatory electrocardiographic (ECG) monitoring (mean 43 +/- 0.8 hours) and laboratory-induced mental stress using a public speaking task. Hemodynamic data were obtained at rest and every minute during mental stress. Thirty-three of 53 patients (62%) had at least 1 ischemic episode during ECG monitoring. In patients who had ambulatory ischemia, there was a mean number of 7.9 +/- 1.8 episodes (mean total duration 79.2 +/- 24.1 minutes/48 hours). Significant positive correlations were found for peak heart rate and changes in heart rate during mental stress and ambulatory ischemia (r = 0.353 to 0.462, p < 0.05) in patients who had ambulatory ischemia. There was no correlation between systolic blood pressure during mental stress and ambulatory ischemia. Results of this study demonstrate that heart rate response during laboratory-induced mental stress correlates with magnitude of ischemia on ambulatory ECG monitoring in patients with coronary artery disease.

Activities of Daily Living↗
PubMed1995

Psychophysical responses to a speech stressor: correlation of plasma beta-endorphin levels at rest and after psychological stress with thermally measured pain threshold in patients with coronary artery disease.

OBJECTIVES: We tested the hypothesis that psychological stress alters plasma levels of opioid peptides and that these plasma levels are related to pain perception in patients with coronary artery disease. BACKGROUND: Public speaking psychological stress has previously been shown to be associated with silent ischemia. METHODS: After instrumentation and a 30-min rest period, venous blood samples for beta-endorphin were obtained before and immediately after psychological stress in 20 patients with coronary artery disease. Pain threshold was then assessed using a thermal probe technique at baseline and immediately after stress. Patients gave three brief speeches lasting a total of 15 min about real-life hassle situations. RESULTS: Psychological stress significantly increases plasma beta-endorphin levels (4.3 +/- 0.9 pmol/liter [mean +/- SE] at rest to 8.3 +/- 2 pmol/liter after stress, p < 0.05). There was a significant positive correlation between pain threshold and beta-endorphin levels after stress (r = 0.577, p = 0.008). This significant positive correlation was still present while rest blood pressure and change in blood pressure during stress were controlled for by analysis of covariance techniques. CONCLUSIONS: In patients with coronary artery disease and exercise-induced ischemia, public speaking produces psychological stress manifested by increased cardiovascular reactivity and causes an increase in plasma beta-endorphin levels that is significantly correlated with pain thresholds. These findings may explain the predominance of silent ischemia during psychological stress in patients with coronary artery disease.

Blood Pressure↗
PubMed1993

Beta-endorphin response to exercise and mental stress in patients with ischemic heart disease.

UNLABELLED: We compared symptomatic, hemodynamic and opioid responses of heart disease patients to exercise testing and a stressful public speaking task. Plasma beta-endorphins were measured at rest and immediately post stress. Nineteen of 50 patients had angina during exercise; 31 had asymptomatic ischemia. No patient had angina during the speech, but two had ECG changes and 39% had radionuclide changes indicating ischemia. Patients with asymptomatic ischemia on exercise had a significantly greater beta-endorphin response than those with angina. Public speaking elicited a significantly larger beta-endorphin increase relative to change in double product (an index of stress) than did exercise. CONCLUSIONS: (1) Patients with silent vs painful ischemia experience a greater beta-endorphin response to exercise. (2) beta-endorphin response to a speech stressor is greater than to exercise when controlled for an index of stress. (3) Increased beta-endorphin response to a speech stressor may partially explain the predominance of silent ischemia during psychological stress.

Aged↗
PubMed1992

Relation between systemic hypertension and pain perception.

To test the hypothesis that hypertension diminishes pain perception, a study was made that evaluated the relation between arterial blood pressure and thermal pain perception in human subjects. The average mean arterial pressure in all 20 men studied (10 hypertensive, 10 normotensive) proved to be significantly related to both thermal pain threshold (p = 0.05) and tolerance (p = 0.003). The difference between normotensive and hypertensive groups in baseline and posttest plasma levels of beta endorphin was also significant (p = 0.02) and indicated an interaction between endogenous opioids and blood pressure. Other recent studies of hypertension in relation to hypalgesia were also reviewed. An increased pain threshold was found in hypertensive versus normotensive rats. In cats, electrical stimulation of vagal afferent nerves (cardiopulmonary baroreceptors) suppresses nociceptive responses, and both pharmacologic elevation of blood pressure and vascular volume expansion produce antinociception. Together with preliminary findings in human studies, these results indicate an interaction between pain-controlling and cardiovascular regulatory functions that is probably mediated by the baroreceptor system.

Adult↗
PubMed1992

The relationship between plasma beta-endorphin, opioid receptor activity, and silent myocardial ischemia.

OBJECTIVE: To investigate the role of the opioid system in the pathophysiology of silent ischemia through opiate antagonism with naloxone, and to determine the reproducibility of resting and postexercise beta-endorphin levels in predominantly asymptomatic patients with coronary artery disease. DESIGN: Randomized, double-blind, placebo-controlled crossover trial. SETTING: A University hospital referral center. PATIENTS: Ten patients with prior evidence of silent exercise-induced ischemia were studied. INTERVENTION: An infusion of saline placebo or naloxone at two dose regimens of 0.015 mg/kg or 0.15 mg/kg before supine exercise testing during three separate occasions for each patient. OUTCOME MEASURES: Plasma beta-endorphin was measured at rest, immediately after exercise, and 5 min poststress. Timing and severity of angina and exercise hemodynamics were also determined. RESULTS: Seven of 10 patients reported no angina, whereas the other three experienced angina with placebo and after administration of naloxone at both doses. The severity and duration of angina was consistently noted to decrease in these patients after naloxone administration, especially after low-dose naloxone relative to placebo. There were no apparent correlations between beta-endorphin levels and the characteristics of angina in these three patients, nor between beta-endorphin and hemodynamic responses in all patients in the study. CONCLUSIONS: (a) naloxone failed to precipitate angina in this population of patients with silent ischemia; (b) naloxone appears to exert an analgesic effect at low doses; and (c) a variability of 5 pM at rest and 13 pM after exercise might be expected in predominantly asymptomatic patients due to random variation, which is comparable with results found in normal subjects.

Aged↗
PubMed1992

Interrelationships between left ventricular volume and output during exercise in healthy subjects.

To better characterize the relationship between left ventricular volume response and improved ventricular ejection and output during supine exercise in normal subjects, 36 healthy asymptomatic volunteers (age 39 +/- 17 yr) were studied with radionuclide ventriculography during recumbent bicycle ergometry. Relative changes in left ventricular end-diastolic and end-systolic volume were measured at rest and during exercise by a modification of the radionuclide counts-based method that accounted for variability in stress blood pool counts. A biphasic response was noted in left ventricular end-diastolic volume with an initial increase in early exercise (8.5 +/- 11% at 200 kpm/min and 11 +/- 12% at 300 kpm/min) followed by a progressive and significant decline at peak exercise (-3.3 +/- 18% at 547 +/- 140 kpm/min; P < 0.05). There was substantial variation in end-diastolic volume response at peak exercise in the group as a whole, which could be more closely related to changes in end-systolic volume (r = 0.84, P < 0.0001) than in heart rate (r = -0.57, P < 0.01) or age (r = 0.36, P < 0.05) of the study subjects. Despite the decline in ventricular filling, systolic function appeared to improve dramatically at peak exercise (change in left ventricular ejection fraction 15.5 +/- 6.4, P < 0.0001). Although not directly related to increasing systolic ejection, end-diastolic volume was directly related to the percent change in stroke volume at peak exercise among the study subjects (r = 0.88, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Effects of 4 percent and 6 percent carboxyhemoglobin on arrhythmia production in patients with coronary artery disease.

In this study, we assessed the effects of exposure to 4 percent and 6 percent carboxyhemoglobin on ventricular arrhythmias in 41 subjects (nonsmokers) with documented coronary artery disease. We used a randomized, double-blind, crossover design. On day 1, a training session with no exposure, the baseline carboxyhemoglobin level was measured, and a supine bicycle exercise test was done. On days 2 through 4, subjects were exposed to room air, 100 parts per million (ppm)2 carbon monoxide (target, 4 percent blood carboxyhemoglobin), or 200 ppm carbon monoxide (target, 6 percent blood carboxyhemoglobin), and they then did a supine bicycle exercise test. Radionuclide ventriculography was performed at rest and during exercise. Ambulatory electrocardiogram recordings were made during the four consecutive days to determine the frequency of premature ventricular contractions at various intervals. The frequency of single premature ventricular contractions per hour during exercise was significantly greater on the 6 percent carboxyhemoglobin day than on the room air day (167.72 +/- 37.99 for 6 percent carboxyhemoglobin compared with 127.32 +/- 28.22 for room air, p = 0.03). The frequency of multiple premature ventricular contractions per hour was also significantly greater during exercise on the 6 percent carboxyhemoglobin day compared with the room air day (9.59 +/- 3.70 for the 6 percent carboxyhemoglobin day compared with 3.18 +/- 1.67 for the room air day, p = 0.02). Patients who developed increased arrhythmias during exercise on the 6 percent carboxyhemoglobin day were significantly older than those who had no increased arrhythmia, and, in addition, exercised longer and had a higher peak workload during exercise. No effect of carbon monoxide exposure was seen on the 4 percent carboxyhemoglobin day.

Aged↗
PubMed1990

Production of arrhythmias by elevated carboxyhemoglobin in patients with coronary artery disease.

OBJECTIVE: To assess the effects of exposure to 4% and 6% carboxyhemoglobin on ventricular arrhythmias in patients with coronary artery disease. DESIGN: Randomized, double-blind, crossover design. SETTING: Exercise laboratory with an environmentally controlled exposure. PATIENTS: Forty-one nonsmokers with documented coronary artery disease. INTERVENTION: On day 1, a training session with no exposure, the baseline carboxyhemoglobin level was measured, and a supine bicycle exercise test was done. On days 2 to 4, patients were exposed to room air, 100 ppm carbon monoxide (target, 4% carboxyhemoglobin) or 200 ppm carbon monoxide (target, 6% carboxyhemoglobin), and they then did supine bicycle exercise with radionuclide ventriculography. Ambulatory electrocardiogram recordings were made during the 4 consecutive days to determine the frequency of ventricular premature depolarization (VPD) at various intervals. MEASUREMENTS AND MAIN RESULTS: The frequency of single VPD/h was significantly greater on the 6% carboxyhemoglobin day than on the room air day during the exercise period (167.72 +/- 37.99 for 6% carboxyhemoglobin compared with 127.32 +/- 28.22 for room air, P = 0.03). During exercise, the frequency of multiple VPD/h was greater on the 6% carboxyhemoglobin day compared with room air (9.59 +/- 3.70 on the 6% carboxyhemoglobin compared with 3.18 +/- 1.67 on room air, P = 0.02). Patients who developed increased single VPD during exercise on the 6% carboxyhemoglobin day were significantly older than those who had no increased arrhythmia, whereas patients who developed complex arrhythmias were also older and, in addition, exercised longer and had a higher peak workload during exercise. CONCLUSION: The number and complexity of ventricular arrhythmias increases significantly during exercise after carbon monoxide exposure producing 6% carboxyhemoglobin compared with room air but not after exposure producing 4% carboxyhemoglobin.

Age Factors↗
PubMed1990

Aging and pain perception in ischemic heart disease.

Age is a recognized risk factor for coronary artery disease, but the relationship between age and silent ischemia is not well understood. We analyzed the data from 35 rest/stress radionuclide ventriculography examinations in patients with documented ischemic coronary artery disease who had experienced 1 mm ST segment depression accompanied by angina during exercise testing. An index of ischemic cardiac pain perception (PPI) was calculated by subtracting the time of onset of 1 mm ST segment depression from the time of onset of angina. The mean value of PPI was -97 +/- 311 seconds. PPI was significantly correlated with age (r = 0.37, p = 0.03). This suggests that as age increases, perception of pain during myocardial ischemic episodes becomes muted. This relationship remained significant when we controlled for the presence of medication and severity of disease (change in ejection fraction from rest to peak exercise). These findings suggest that age is an independent risk factor for a decreased perception of ischemic cardiac pain, and thus for silent myocardial ischemia.

Adult↗
PubMed1989

Prevalence of silent myocardial ischemia in survivors of cardiac arrest.

The prevalence and type of ischemia (silent vs painful) in survivors of cardiac arrest not associated with acute myocardial infarction were studied to test the hypothesis that survivors may have an increased prevalence of silent ischemia. Of 48 survivors of cardiac arrest over a 4-year period who had undergone exercise testing, 24 met inclusion criteria. These 24 subjects had documented ventricular fibrillation and coronary artery disease proven by cardiac catheterization or a previous electrocardiographic pattern of myocardial infarction. Thirteen of 24 (54%) had a positive treadmill stress test (greater than or equal to 1.0 mm flat or downsloping ST depression). The mean resting left ventricular ejection fraction was 43%. Nine of 11 patients (82%) who had exercise radionuclide studies performed had ischemic abnormalities (less than 5% increase in left ventricular ejection fraction with new or worsened wall motion abnormalities). Thus, 16 of 24 (67%) had a positive treadmill stress test or radionuclide ventriculogram. Only 1 of 16 (6%) had painful ischemia (p less than 0.001 relative to an even distribution of painful vs painless ischemia). Thus, survivors of cardiac arrest have a high prevalence of exercise-induced ischemia, and in most the ischemia is silent.

Coronary Disease↗
PubMed1989

A comparison of amplitude-modulated and frequency-modulated ambulatory monitoring systems.

To compare the results of monitoring for ischemia with amplitude-modulated (AM) and frequency-modulated (FM) ambulatory recorders, 22 patients with coronary artery disease were monitored during exercise and during 24 to 48 hours of daily activities. Simultaneous recordings were obtained with Oxford Medilog 4000-II and Medilog MR-35 systems from the same 2 bipolar leads. Each potential ischemic episode was interpreted blindly by 2 investigators. Significant ST depression was strictly defined as greater than or equal to 1 mm of horizontal or down-sloping ST depression persisting for 0.06 second beyond the J point and lasting greater than or equal to 1 minute. Of 82 episodes reviewed, 63 (77%) were either positive (37) or negative (26) for ischemia by both systems. However, 17 episodes were interpreted as positive on AM tracings but negative on FM tracings; the converse was true for only 2 episodes (p less than 0.01). For episodes read as positive with both systems, there were close correlations between recorders for duration (r = 0.80) and magnitude (r = 0.90) of ST depression. Because of the greater number of positive AM events, however, the mean total duration of ST depression for patients with ischemia during daily activities was greater on AM than on FM recordings (74 +/- 77 vs 39 +/- 42 minutes, p less than 0.10). Discrepancies between AM and FM tracings were invariably due to small differences in ST-segment morphology or in the magnitude of ST-segment depression. In summary, AM monitors generate complexes similar in appearance to those produced by FM devices in most instances.(ABSTRACT TRUNCATED AT 250 WORDS)

Activities of Daily Living↗
PubMed1989

Sudden death and silent myocardial ischemia.

Recent research indicates that silent myocardial ischemia may play a role in sudden cardiac death. To what extent treatment can reduce occurrence of silent ischemia remains to be assessed. Three classes of silent ischemia patients are identified: type 1--totally asymptomatic; type 2--post myocardial infarction; and type 3--noninfarcted with both silent ischemia and angina. An index of prognostic risk (PR), showing the percent of adverse events attributable to silent ischemia, is calculated to measure the potential impact of successful treatment of silent ischemia on population mortality. Type 1 individuals' PR is estimated at a low 3.8%, suggesting that screening the general asymptomatic population would be unproductive. Type 2 patients exhibit an 80% PR. We lack the empirical information to estimate type 3 patients' PR, but silent ischemia is a recognized adverse prognostic factor in the subgroup exhibiting unstable angina. These results suggest that successful treatment of silent ischemia might favorably influence coronary artery disease patient outcomes.

Coronary Disease↗