beta-endorphin and Myocardial-Ischemia

Topics: beta-Endorphin; Bradykinin; Humans; Myocardial Ischemia; Pain Threshold

Essential hypertension is characterised by reduced pain sensitivity. Hypertensive hypoalgesia has been attributed to elevated endogenous opioids and/or increased activation of descending pain modulation systems. A double-blind placebo-controlled design compared the effects of naltrexone and placebo on cold and ischemic pain in unmedicated newly-diagnosed patients with essential hypertension. Patients performed a cold pressor task while resting and while performing a distracting secondary task. They also performed a forearm ischemia task while resting. Although the cold pressor and ischemia tasks elicited significant increases in pain and blood pressure, pain ratings and pressor responses did not differ between naltrexone and placebo. Cold pain was reduced by distraction compared to rest. The finding that opioid blockade with naltrexone did not moderate the pain and pressor responses to cold and ischemia suggests that pain and associated blood pressure responses are not modulated by opioids in hypertension. The finding that the distracting secondary task successfully reduced pain ratings suggests normal supraspinal pain modulation in essential hypertension.

Topics: Adult; Attention; beta-Endorphin; Cold Temperature; Double-Blind Method; Female; Heart Rate; Humans; Hypertension; Male; Myocardial Ischemia; Naltrexone; Narcotic Antagonists; Pain; Pain Measurement; Touch

The purpose of this study was to test whether cutaneous thermal pain thresholds are related to anginal pain perception.. Few ischemic episodes are associated with angina; symptoms have been related to pain perception thresholds.. A total of 196 patients with documented coronary artery disease underwent bicycle exercise testing and thermal pain testing. The Marstock test of cutaneous sensory perception was administered at baseline after 30 min of rest on two days and after exercise and mental stress. Resting hot pain thresholds (HPTs) were averaged for the two baseline visits and divided into two groups: 1) average HPT <41 degrees C, and 2) average HPT > or =41 degrees C, to be clearly indicative of abnormal hypersensitivity to noxious heat.. Patients with HPT <41 degrees C had significantly shorter time to angina onset on exercise testing than patients with HPT > or =41 degrees C (p < 0.04, log-rank test). Heart rates, systolic blood pressure and rate-pressure product at peak exercise were not different for the two groups. Resting plasma beta-endorphin levels were significantly higher in the HPT <41 degrees C group (5.9+/-3.7 pmol/liter vs. 4.7+/-2.8 pmol/liter, p = 0.02). Using a Cox proportional hazards model, patients with HPT <41 degrees C had an increased risk of angina (p = 0.03, rate ratio = 2.0). These differences persisted after adjustment for age, gender, depression, anxiety and history of diabetes or hypertension (p < 0.01).. Occurrence of angina and timing of angina onset on an exercise test are related to overall hot pain sensory perception. The mechanism of this relationship requires further study.

Topics: Adult; Angina Pectoris; beta-Endorphin; Catecholamines; Electrocardiography; Exercise Test; Female; Hot Temperature; Humans; Male; Middle Aged; Myocardial Ischemia; Pain Measurement; Pain Threshold; Predictive Value of Tests; Psychological Tests; Stress, Psychological

To investigate the effects of carteolol, which is a nonselective beta-adrenergic agent with intrinsic sympathomimetic activity, on silent myocardial ischemia, exercise-induced myocardial ischemia, indexes of heart rate variability, and pain-modulating system, 20 patients (mean 60 +/- 9 years) with chronic stable angina underwent exercise treadmill testing and 24-hour ambulatory electrocardiographic monitoring during 2 weeks of carteolol administration (15 mg/day) in a double-blind, placebo-controlled design. Plasma levels of beta-endorphin and bradykinin and electrical pain stimulation to the skin were measured at rest and peak exercise. Indexes of heart rate variability of both time-domain and frequency-domain analysis were derived from 24-hour ambulatory electrocardiographic monitoring. Carteolol decreased maximal heart rate responses to daily activities during ambulatory monitoring and significantly reduced the median frequency and duration of silent myocardial ischemic episodes (from 1.0 to 0.0 events/24 hr and from 16 to 0 min/24 hr, respectively). Carteolol significantly decreased the rate-pressure product at rest and during exercise with improving maximal ST segment depression, suggesting amelioration of exercise-induced myocardial ischemia. Carteolol did not significantly affect plasma levels of beta-endorphin and bradykinin or pain threshold. It significantly decreased some indexes (standard deviation of all normal sinus R-R intervals in the entire 24-hour recording and standard deviation of the mean of all 5-minute segments of normal R-R intervals of a 24-hour recording) of heart rate variability. These results suggest that carteolol may reduce total myocardial ischemic burden by the reduction of cardiac oxygen demand during daily activities and exercise stress, while not affecting plasma levels of beta-endorphin, bradykinin, and pain threshold. Because carteolol tended to decrease indexes of heart rate variability, significant caution might be necessary in prescribing the beta-blocking agents with intrinsic sympathomimetic activity like carteolol to patients with potential serious arrhythmia.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Aged, 80 and over; beta-Endorphin; Bradykinin; Carteolol; Electrocardiography, Ambulatory; Exercise Test; Female; Heart Rate; Humans; Male; Middle Aged; Myocardial Ischemia; Pain Measurement; Sympatholytics

This study was designed to examine the role of beta-endorphin and met-enkephalin in the pathophysiology of silent myocardial ischemia, with emphasis on their role in the physiologic response to stress.. Silent myocardial ischemia is more common in patients whose perception of pain is reduced. Whether endogenous opiates can contribute to this process remains uncertain largely because of the conflicting findings of previous studies.. Forty-three patients with coronary artery disease and ischemia on treadmill stress testing underwent electrical pain tests and exercise treadmill tests during naloxone and placebo infusion in a randomized, double-blind crossover study. Thirty-one patients developed angina during both treadmill tests (group A), and 12 had silent ischemia (group B). Plasma beta-endorphin, metenkephalin, epinephrine, norepinephrine and cortisol were measured before and after exercise in a subgroup of 17 patients.. Naloxone reduced electrical pain tolerance (1.40 +/- 0.10 [mean +/- SEM] vs. 1.72 +/- 0.19 mA, p = 0.04) but did not affect the time to angina in group A (260 +/- 20 vs. 248 +/- 20 s, p = 0.72) or induce angina in group B patients. Beta-endorphin and met-enkephalin levels during placebo infusion were not significantly different in groups A and B at baseline and after exercise, although beta-endorphin levels were significantly increased during naloxone infusion, confirming effective opiate receptor blockade. Norepinephrine and cortisol increased with exercise, but catecholamines and cortisol were similar in both groups and were unaffected by naloxone.. Beta-endorphin and met-enkephalin were similar in patients with painful and silent ischemia, and naloxone infusion did not influence anginal symptoms despite effective opiate receptor blockade and a reduction in somatic pain tolerance. These findings suggest that endogenous opiates do not play an important role in modulating symptoms in myocardial ischemia. The increase in beta-endorphin with exercise that coincided with an increase in plasma cortisol is most likely due to its release from the anterior pituitary gland as part of the physiologic stress response.

Topics: beta-Endorphin; Double-Blind Method; Electrocardiography, Ambulatory; Enkephalin, Methionine; Epinephrine; Exercise Test; Female; Humans; Hydrocortisone; Male; Middle Aged; Myocardial Ischemia; Naloxone; Norepinephrine; Pain Threshold; Stress, Physiological

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.. Randomized, double-blind, placebo-controlled crossover trial.. A University hospital referral center.. Ten patients with prior evidence of silent exercise-induced ischemia were studied.. 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.. 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.. 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.. (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.

Topics: Aged; Angina Pectoris; beta-Endorphin; Electrocardiography; Exercise Test; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Ischemia; Naloxone; Pain; Receptors, Opioid; Reproducibility of Results

The objective of this study was to examine the involvement of endogenous opioid peptides and opioid receptor (OR) subtypes in the cardioprotective effect of adaptation to chronic hypoxia in rats.. Rats were exposed to continuous normobaric hypoxia (CNH; 12% oxygen) for 3 weeks. Myocardial ischemia was induced by 20-min coronary artery occlusion followed by 3-h reperfusion in anesthetized open-chest animals. Various OR antagonists were administered to rats prior to ischemia. The size of myocardial infarction and the incidence of ischemic ventricular arrhythmias were assessed. Myocardial and plasma concentrations of opioid peptides (met-enkephalin, β-endorphin, and endomorphins) were determined.. Adaptation to CNH significantly increased myocardial and plasma concentrations of opioids, potentiated their further elevation by ischemia/reperfusion, and reduced myocardial infarct size, but it did not affect the incidence of ischemic arrhythmias. The infarct size-limiting effect of CNH was abolished by OR antagonists naltrexone (non-selective), naloxone methiodide (non-selective peripherally acting), TIPP[ψ] (δ-OR), naltriben (δ2-OR), or CTAP (μ-OR), while BNTX (δ1-OR) and nor-binaltorphimine (κ-OR) had no effect.. The results suggest that the infarct size-limiting effect afforded by adaptation to CNH is mediated by activation of peripheral δ2- and μ-ORs by elevated levels of endogenous opioid peptides.

Topics: Adaptation, Physiological; Animals; Arrhythmias, Cardiac; beta-Endorphin; Enkephalin, Methionine; Hypoxia; Male; Myocardial Infarction; Myocardial Ischemia; Myocardial Reperfusion Injury; Narcotic Antagonists; Oligopeptides; Rats; Rats, Wistar; Receptors, Opioid, delta; Receptors, Opioid, mu

There is substantial evidence indicating that endogenous opioid peptides are involved in the pathophysiology of myocardial ischemia and reperfusion. We measured the myocardial and peripheral concentrations of beta-endorphin before and following myocardial ischemia and reperfusion during coronary angioplasty. The results indicate that in patients with coronary artery disease, there was an augmented myocardial concentration of beta-endorphin. Moreover, there was an increased peripheral concentration of beta-endorphin following myocardial ischemia and reperfusion. The data support the previous notion that endogenous opioid peptides are involved in the pathophysiology of ischemic heart disease.

Topics: Aged; Aged, 80 and over; Angioplasty, Balloon, Coronary; beta-Endorphin; Blood Pressure; Coronary Disease; Creatine Kinase; Creatine Kinase, MB Form; Female; Heart Rate; Humans; Isoenzymes; Lactic Acid; Male; Middle Aged; Myocardial Ischemia; Myocardial Reperfusion; Myocardium; Pulmonary Wedge Pressure; Stroke Volume

In rats and rabbits, endogenous opioid peptides participate in ischemic preconditioning. However, it is not known which endogenous opioid(s) can trigger cardioprotection. We examined preconditioning-induced and opioid-induced limitation of cell death in isolated, calcium-tolerant, adult rabbit cardiomyocytes. Cells were subjected to simulated ischemia by pelleting and normothermic hypoxic incubation. Preconditioning was elicited with 15 min of simulated ischemia followed by 15 min of resuspension and reoxygenation. All cells underwent 180 min of simulated ischemia. Cell death was assessed by trypan blue permeability. Morphine protected cells, as did preconditioning; naloxone blocked the preconditioning-induced protection. Exogenous Met5-enkephalin (ME) induced protection, but exogenous beta-endorphin did not. ME-induced protection was blocked by the delta-selective antagonist naltrindole. Additionally, two other proenkephalin products, Leu5-enkephalin and Met5-enkephalin-Arg-Phe, provided protection equipotent to ME. These data suggest that one or more proenkephalin products interact with delta-opioid receptors to endogenously trigger opioid-mediated protection.

Topics: Animals; beta-Endorphin; Cell Hypoxia; Cells, Cultured; Enkephalin, Leucine; Enkephalin, Methionine; Heart; Ischemic Preconditioning; Male; Models, Cardiovascular; Morphine; Myocardial Ischemia; Myocardium; Naloxone; Rabbits; Rats; Receptors, Opioid, delta

Earlier studies have shown that spinal cord stimulation (SCS) has antianginal and anti-ischemic effects in severe coronary artery disease. In the present study, 14 patients were subjected to right-sided atrial catheterization and atrial pacing. The patients were paced to angina during a control session and during spinal cord stimulation. Myocardial extraction of beta-endorphin (BE) during control pacing (8 +/- 22%) changed to release at the maximum pacing rate during treatment (-21 +/- 47%, a negative value representing release). Furthermore, the results indicate local myocardial turnover of leuenkephalin, BE and calcitonin-gene-related peptide. In addition, it is implied that SCS may induce myocardial release of BE which could explain the beneficial effects in myocardial ischemia.

Topics: Aged; Angina Pectoris; beta-Endorphin; Calcitonin Gene-Related Peptide; Cardiac Catheterization; Cardiac Pacing, Artificial; Electric Stimulation Therapy; Electrodes, Implanted; Enkephalin, Leucine; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Myocardium; Radioimmunoassay; Spinal Cord

Beta-endorphin has been reported to play a role in the mechanism of silent myocardial ischemia.. Plasma beta-endorphin levels during coronary angioplasty-induced silent and symptomatic myocardial ischemia were compared with those during exercise-induced silent ischemia.. The study population consisted of 40 nondiabetic patients with angioplasty-indicated coronary artery disease. All patients underwent exercise treadmill testing 2 to 4 days before angioplasty. Patients were divided into three groups: group 1, 10 patients with silent ischemia during exercise and angioplasty; group 2, 15 patients with silent ischemia during exercise and symptomatic ischemia during angioplasty; and group 3, 15 patients with symptomatic ischemia during both exercise and angioplasty. In group 1, plasma beta-endorphin levels during balloon inflation were significantly higher than in groups 2 and 3 and also significantly higher than during exercise. In group 2, plasma beta-endorphin levels were significantly elevated at exercise-induced silent myocardial ischemia and balloon-induced symptomatic myocardial ischemia, but the levels between exercise and balloon inflation were not significantly different.. For "silent" myocardial ischemia, it may be necessary for beta-endorphin levels to increase to sufficiently high levels to suppress anginal symptoms in response to the degree of ischemic stimuli.

Topics: Aged; Angioplasty, Balloon, Coronary; beta-Endorphin; Coronary Disease; Exercise Test; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Prognosis

Topics: Afferent Pathways; Animals; Atrial Fibrillation; beta-Endorphin; Cats; Female; Heart; Male; Myocardial Ischemia; Nodose Ganglion; Vagus Nerve

Topics: Animals; Arrhythmias, Cardiac; Autonomic Nervous System; beta-Endorphin; Cats; Female; Heart; Male; Myocardial Ischemia

Topics: Animals; Anti-Arrhythmia Agents; beta-Endorphin; Cats; Enkephalin, Leucine-2-Alanine; Female; Male; Motor Cortex; Myocardial Ischemia; Somatosensory Cortex; Tachycardia, Ventricular; Ventricular Fibrillation

This study was undertaken to investigate the effect of nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin.. Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG).. Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and nipradilol phases of the study. However, during the nipradilol phase, bradykinin did not change significantly at rest and at peak exercise.. Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.

Topics: Adrenergic alpha-Antagonists; Aged; beta-Endorphin; Bradykinin; Chronic Disease; Electrocardiography, Ambulatory; Exercise Test; Heart Rate; Humans; Male; Middle Aged; Myocardial Ischemia; Propanolamines; Radioimmunoassay

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.. Public speaking psychological stress has previously been shown to be associated with silent ischemia.. 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.. 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.. 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.

Topics: beta-Endorphin; Blood Pressure; Coronary Disease; Electrocardiography; Heart Rate; Humans; Middle Aged; Myocardial Ischemia; Pain Measurement; Pain Threshold; Stress, Psychological

Topics: beta-Endorphin; Blood Pressure; Electrocardiography; Heart Rate; Humans; Myocardial Ischemia; Pain Threshold; Risk Factors; Stress, Psychological

Plasma beta-endorphin levels were estimated in patients with painless myocardial ischaemia. The survey was made in 90 patients with coronary artery disease: 55 of them after myocardial infarction and 35 with chronic stable angina pectoris. The control group comprised 22 healthy persons. Plasma beta-endorphin level was determined in all examined patients immediately before the exercise test, just after finishing exercise test, and 6 minutes after the termination of the exercise test. Beta-endorphin plasma levels has been determined with a radioimmunologic method by the means of "beta-endorphins [125J]RIA Kit" manufactured in NEN Research Products. Study showed that in the patients with silent myocardial ischaemia plasma beta-endorphin level was higher than in patients with painful myocardial ischaemia both at rest during exercise test. Increase of plasma beta-endorphin in examined patients can be one of etiopathogenetic factors of silent myocardial ischaemia.

Topics: Adult; Aged; Angina Pectoris; beta-Endorphin; Exercise Test; Humans; Middle Aged; Myocardial Ischemia

The aims of this study were to correlate beta-endorphin plasma levels and anginal pain in patients with ischemia induced by percutaneous transluminal coronary angioplasty and to detect eventual endorphin variations during balloon occlusion.. The opioid system appears involved in the absence of pain occurring in silent myocardial ischemia.. Beta-endorphin plasma levels were measured 24 h before, just before, during and after coronary angioplasty (performed on the left anterior descending artery) in 53 men with documented coronary artery disease and exercise-induced myocardial ischemia.. Group 1 (33 patients) reported symptoms; group 2 (20 patients) was asymptomatic during angioplasty. In these patients, the prevalence of exercise-induced silent ischemia was 57%. The occurrence of angina during exercise or angioplasty was related to the frequency of angina during daily life when patients were subgrouped. The severity and distribution of coronary artery disease did not differ between the two groups. During angioplasty, the number of balloon inflations and the inflation time and pressure were similar in symptomatic and asymptomatic patients. In each group, no short-term variability of baseline beta-endorphin plasma levels was observed during 2 consecutive days. Corresponding beta-endorphin plasma levels (at baseline and during and after angioplasty) were significantly higher in Group 2. During balloon occlusion, the levels decreased significantly in the symptomatic group at the onset of angina but remained stable in the asymptomatic group.. Methodologic variables and the severity of coronary artery disease did not influence the presence of symptoms during angioplasty-induced ischemia. Beta-endorphin plasma levels were higher and more stable in patients with silent ischemia during angioplasty, suggesting that opiate levels and their variation during ischemia are associated with individual attitude toward anginal pain.

Topics: Adult; Aged; Analysis of Variance; Angina Pectoris; Angioplasty, Balloon, Coronary; beta-Endorphin; Exercise Test; Humans; Male; Middle Aged; Myocardial Ischemia; Prevalence; Time Factors

The differences between diabetic and nondiabetic patients with silent myocardial ischemia were investigated. Based on the results of previous exercise testing, a total of 110 patients (15 diabetic and 95 nondiabetic) with exercise-induced myocardial ischemia were divided into the following 3 groups: 15 diabetics with silent myocardial ischemia, 49 nondiabetics with silent myocardial ischemia, and 46 nondiabetics with anginal symptoms. All patients underwent treadmill exercise testing and 24-hour ambulatory electrocardiographic recording. Before and during exercise, blood samples from the antecubital vein were obtained to determine the plasma beta-endorphin levels, and the pain threshold of each patient was measured with the electrical skin stimulation test. Furthermore, with regard to the ambulatory electrocardiographic recording, the mean of the SDs of all normal sinus RR intervals during successive 5-minute recording periods over 24 hours was analyzed and considered as an index of the autonomic function. The plasma beta-endorphin level during exercise was significantly greater in nondiabetic patients with silent ischemia than in diabetic ones. The SD mean was significantly less in the diabetic group than in the 2 nondiabetic ones. The findings suggest that the role of beta endorphin in diabetic patients with silent myocardial ischemia may be less significant than in nondiabetic ones; therefore, a diabetic neuropathy that affects the autonomic pain fibers that innervate the heart may be involved in the mechanism of silent myocardial ischemia in diabetics.

Topics: Aged; Analysis of Variance; Autonomic Nervous System; beta-Endorphin; Chi-Square Distribution; Diabetes Complications; Diabetes Mellitus; Electric Stimulation; Electrocardiography, Ambulatory; Exercise Test; Female; Humans; Male; Middle Aged; Myocardial Ischemia; Pain Threshold; Skin

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.. (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.

Topics: Aged; Aged, 80 and over; Angina Pectoris; Arousal; beta-Endorphin; Coronary Disease; Exercise Test; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Myocardial Ischemia; Stress, Psychological

Topics: beta-Endorphin; Humans; Myocardial Infarction; Myocardial Ischemia

Topics: beta-Endorphin; Humans; Myocardial Ischemia

Thirteen patients with totally silent myocardial ischemia (group 1) and 15 patients with effort angina (group 2) were studied. The coronary angiography of both groups indicated coronary artery stenosis > or = 50%. In group 1, the beta-endorphin plasma level (beta-EPL) during rest was significantly higher than those in group 2 (15.639 +/- 1.258 pg/ml and 8.920 +/- 1.478 pg/ml, respectively, P < 0.01). There were significant increases in beta-EPL in both groups after exercise as compared with that before exercise (beta-EPL is 33.801 +/- 6.243 pg ml/in group 1, P < 0.01; 18.169 +/- 3.540 pg/ml in group 2, P < 0.01). The difference between two groups after exercise was also significant (P < 0.05). The plasma level of noradrenaline (NE) during rest was 0.267 +/- 0.035 ng/ml, adrenaline (E) was 0.112 +/- 0.018 ng/ml in group 1, and NE was 0.218 +/- 0.032 ng/ml and E was 0.110 +/- 0.015 ng/ml in group 2. After exercise, NE was 1.017 +/- 0.160 ng/ml (P < 0.001), E 0.276 +/- 0.076 ng/ml (P < 0.001), E 0.260 +/- 0.043 ng/ml (P < 0.01) in group 2. There was no difference between two groups both in rest and after exercise (P > 0.05). This study indicates that the high plasma beta-endorphin level might play a major role in the occurrence of totally silent myocardial ischemia.

Topics: Aged; Angina Pectoris; beta-Endorphin; Electrocardiography; Epinephrine; Exercise Test; Humans; Male; Middle Aged; Myocardial Ischemia; Norepinephrine