Assessment of plasma catecholamine and beta-endorphin contents in patients with silent myocardial ischemia and angina pectoris]

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.     

Correlation between beta-endorphin plasma levels and anginal symptoms in patients with coronary artery disease

To verify whether beta-endorphin plasma levels influence the presence of anginal symptoms, 74 consecutive male patients were studied. All patients had previously documented coronary artery disease and reproducible exercise-induced myocardial ischemia. Thirty-five patients (Group I) had a history of angina and reported anginal symptoms during exercise stress testing; 39 patients (Group II) were asymptomatic and had documented silent myocardial ischemia during exercise. Baseline beta-endorphin plasma levels were measured in blood samples taken before exercise stress testing and analyzed by beta-endorphin-I125-RIA Kit-NEN (a radioimmunoassay method). The mean baseline beta-endorphin plasma level was 22.5 +/- 19 pg/ml in patients with anginal symptoms compared with 43.7 +/- 28 pg/ml in asymptomatic patients (p less than 0.001). Baseline blood pressure and heart rate-systolic pressure (rate-pressure) product at baseline and at ischemia threshold (1 mm ST segment depression) were similar in the two groups. Group II patients had a longer exercise duration (p less than 0.01), more pronounced ST segment depression (p less than 0.001) and a higher peak rate-pressure product (p less than 0.01). The extent of coronary artery disease, ejection fraction and left ventricular end-diastolic pressure were similar in the two groups. These data suggest that higher baseline beta-endorphin plasma levels may play a role in the decreased sensitivity to pain in patients with silent myocardial ischemia. In addition, different beta-endorphin levels can be associated with a different sensitivity to pain.     

Regional ejection fraction during exercise: a quantitative measurement to localize coronary artery stenoses in patients with symptomatic or silent myocardial ischemia

To determine the ability of quantitative radionuclide ventriculography to localize coronary artery stenoses in patients with angina and silent myocardial ischemia, the authors studied changes in regional ejection fractions produced by supine bicycle exercise in 49 patients, 16 of whom had silent myocardial ischemia. For example, in 35 patients with 70 per cent or greater stenoses of the left anterior descending and/or left main coronary artery, anteroseptal regional ejection fraction fell from 55 +/- 3 per cent at rest to 50 +/- 4 per cent with exercise (p less than 0.05). In 14 patients with lesser or no stenoses of the left anterior descending and/or left main coronary artery, anteroseptal regional ejection fraction increased from 62 +/- 4 per cent at rest to 67 +/- 5 per cent during exercise (p less than 0.05). Similar findings were obtained in patients with 70 per cent or greater stenoses of the left circumflex and/or right coronary artery in whom inferoposterior regional ejection fraction was measured and compared with that in patients with lesser or no stenoses in these vessels. Thus, evaluation of regional ejection fraction allowed the localization of coronary artery stenoses in coronary patients whether or not their ischemia was accompanied by pain.     

Plasma beta-endorphin levels in silent myocardial ischemia induced by exercise

Although silent myocardial ischemia is a well recognized phenomenon, the reasons for the lack of symptoms in patients with coronary artery disease (CAD) is unclear. Because the endogenous opioid beta-endorphin has been related to pain modulation, plasma beta-endorphin levels were studied before, during and after exercise-induced ischemia in symptomatic and asymptomatic men. Because beta-endorphin responses have been closely linked to adrenocorticotropic hormone (ACTH) and cortisol responses, these hormones also were measured. Nine symptomatic and 12 asymptomatic patients with a high probability (at least 95%) of CAD and 8 apparently healthy men completed a Bruce protocol treadmill test. Blood samples were drawn before, during and 10 minutes after exercise. During exercise the measured hormones showed no significant increases from basal levels. However, plasma beta-endorphin, ACTH and cortisol levels were significantly elevated (p less than or equal to 0.01) 10 minutes after exercise in all 3 groups. There was no significant difference in plasma beta-endorphin levels during or after exercise between the symptomatic and asymptomatic patients with CAD. Thus, differences in circulating levels of beta-endorphin, ACTH and cortisol are not associated with the presence or absence of pain during exercise-induced myocardial ischemia.     

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.     

Myocardial perfusion in silent myocardial ischemia: investigation by exercise stress myocardial tomography with thallium-201

To investigate myocardial perfusion in silent myocardial ischemia, we performed exercise stress myocardial tomography with thallium-201 (T1) in 85 patients with coronary artery disease (CAD). Exercise stress myocardial tomography was obtained both immediately after exercise and three hours later. Patients were classified into two groups according to the presence (Symptomatic Group, n = 36) or absence (Silent Group, n = 49) of chest pain during exercise stress. Clinical features (age, gender and history of myocardial infarction) and arteriographically determined severity of CAD were the same in both groups. The extent of myocardial ischemia (% Ischemia) estimated by exercise stress myocardial tomography was the same in each group (30 +/- 10% in Silent Group, 28 +/- 12% in Symptomatic Group, NS). The severity of exercise-induced myocardial ischemia was expressed as a minimal value of myocardial T1 washout rate (minimal WOR) of each patient. Although exercise heart rate was identical in both groups, minimal WOR in Silent Group was significantly higher than that of Symptomatic Group (4 +/- 10% vs -16 +/- 14%, p less than 0.001). The study in patients who exhibited both silent and symptomatic ischemia showed same results. These findings suggest that the severity of ischemia is a fundamental factor in determining the presence or absence of pain during exercise induced ischemia.     

Silent ischemia: evaluation by exercise and redistribution tomographic thallium-201 myocardial imaging

To compare the amount of myocardium jeopardized during silent ischemia and painful ischemia, 112 consecutive patients undergoing coronary arteriography with ischemia demonstrated by exercise and redistribution tomographic thallium-201 myocardial imaging (SPECT) were divided into two groups: 84 patients without anginal pain (silent ischemia) and 28 with pain (painful ischemia). The SPECT apical, mid and basal ventricular levels of the short-axis view and the apical portion of the long-axis view were divided into 20 segments. The results were 1) 7.4 +/- 4.7 ischemic segments in silent ischemia and 7.6 +/- 3.7 in painful ischemia (p = NS) with 4.7 +/- 3.6 segments in silent ischemia undergoing total redistribution compared with 5.4 +/- 3.4 in painful ischemia (p = NS); 2) no difference in the incidence of single, double or triple vessel disease between silent and painful ischemic groups; 3) similar anatomic distribution of ischemic segments between the two groups; 4) more positive exercise electrocardiographic (ECG) changes in painful ischemia (70%) than in silent ischemia (32%) (p less than 0.001) with equal amounts of ischemia associated with positive and negative exercise ECG findings. Conclusions: 1) Patients with silent and painful ischemia during exercise have similar amounts of ischemic myocardium demonstrated by tomographic thallium-201 imaging and similar extent of angiographically documented coronary artery disease despite the absence of pain and the lower incidence of positive exercise ECG findings in silent ischemia. 2) Positive and negative exercise ECG findings were associated with similar amounts of ischemic myocardium.     

Elevated plasma beta-endorphin levels in patients with congestive heart failure

Recent experimental studies show that the opioid system is important to the pathophysiology of cardiovascular impairment in congestive heart failure. Plasma beta-endorphin levels were measured in 37 patients with congestive heart failure and compared with those of 21 age- and gender-matched normal subjects. The relation of plasma beta-endorphin levels and cardiac function at rest and exercise capacity was assessed in 17 of the patients with dilated cardiomyopathy. Exercise capacity was determined by symptom-limited maximal treadmill exercise with expired gas analysis. Plasma beta-endorphin levels were elevated and correlated with the patients' New York Heart Association functional cardiac status (control: 14.0 +/- 4.4 pg/ml; class II: 17.9 +/- 3.6 pg/ml; class III: 28.3 +/- 8.8 pg/ml; class IV: 46.7 +/- 14.6 pg/ml, mean +/- SD). No relation was found between plasma beta-endorphin levels and left ventricular systolic performance as assessed by M-mode and Doppler echocardiography. Plasma beta-endorphin levels were negatively correlated with cardiac output determined by Doppler echocardiography and positively correlated with systemic vascular resistance (r = -0.733, r = 0.747, respectively, both p less than 0.001), but not correlated with calf blood flow as measured by a plethysmography. A good correlation was found between plasma beta-endorphin levels at rest and exercise capacity. The correlations with peak oxygen consumption, anaerobic threshold, and peak rate-pressure product were r = -0.721, -0.672, and -0.674, respectively (p less than 0.01). The data show that plasma beta-endorphin levels are elevated in patients with congestive heart failure and reflect, to some degree, the severity of the disease.     

Painless myocardial ischemia. Comparison of 2 groups of patients with a positive exercise test after myocardial infarction

Myocardial ischemia usually presents with chest pain, the characteristics of which are well known. However, anginal pain may be absent during true ischemia, an entity known as painless or silent myocardial ischemia. Does this type of ischemia have special clinical, angiographic or ergometric characteristics after posterior myocardial infarction (MI)? In order to answer this question 183 consecutive patients with recent posterior MI who had undergone coronary angiography and who had positive exercise stress tests on bicycle ergometers were separated into two groups depending on whether they had experienced at least one episode of pain after the acute phase of myocardial infarction or during the exercise stress test (Group S: 83 patients, average age 54 +/- 10 years) or not (Group A: 100 patients, average 54 +/- 8 years). The following parameters were commoner in Group A: cigarette smoking, heart rate and load developed during exercise stress testing provoking electrical signs of ischemia, single vessel disease on coronary angiography, long-term medical treatment. On the other hand, the following parameters were statistically more frequent in Group S: hypercholesterolemia, preinfarction angina, degree of ST depression during exercise testing, reperfusion of the distal vessels of the occluded artery responsible for the infarct by a collateral circulation, triple vessel disease and surgical treatment. However long-term follow-up (average 3 years) shows that mortality and recurrence of MI are similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Silent myocardial ischemia in middle-aged asymptomatic patients with type 2 diabetes in Turkish population

The authors investigated silent myocardial ischemia in unselected consecutive middle-aged asymptomatic patients with type 2 diabetes without any evidence of coronary heart disease documented by treadmill exercise test. Ninety asymptomatic patients with type 2 diabetes (48 men; mean age: 49 +/-6 years) were included in the study. Mean duration of diabetes in the study group was 4 +/-4.2 years (range 1 to 21 years); 38% of the study population, diabetes duration was only 1 year). All patients were subjected to treadmill exercise test with Bruce protocol. A positive test was noted in 4 of 90 (4%) study patients. Two male patients (4%) and 2 (4%) women patients developed exercise-induced ST-segment depression, but none had concomitant chest pain. Diabetics with silent myocardial ischemia were older (55 +/-3 years vs 49 +/-6 years, p = 0.04) than those without silent myocardial ischemia. Also, diabetics with silent myocardial ischemia had higher fibrinogen level (372 +/-51 vs 307 +/-71 mg/dL, p = 0.04) than diabetics without silent myocardial ischemia. In treadmill exercise test, diabetics with silent myocardial ischemia had lower total exercise time and peak workload (375 +/-30 vs 474 +/-115 seconds, p = 0.04; 7.3 +/-0.5 vs 8.9 +/-1.9, p = 0.04, respectively) than without silent myocardial ischemia. Insulin resistance is associated with a variety of atherosclerosis risk factors. Exercise test findings show increased cardiac sympathetic activity and parasympathetic withdrawal in increased insulin resistance.     

Excretion of thromboxane A2 and prostacyclin metabolites before and after exercise testing in patients with and without signs of ischemic heart disease

We addressed the hypothesis that platelets are not activated in association with effort-induced myocardial ischemia in stable coronary disease. Seventy-two patients undergoing a diagnostic bicycle exercise test were stratified according to the development of chest pain (yes/no, 33/39) and of exercise-induced ST-segment depression of at least 200 microV in the electrocardiogram (yes/no, 12/60). Noninvasive indexes of platelet activation and of platelet/vessel wall interaction (urinary excretion of the 2,3-dinor-metabolites of thromboxane A2 [Tx-M] and prostacyclin [PGI-M], respectively) were analyzed in samples collected in the basal state and after the test. Basal Tx-M and PGI-M did not differ in patients with (236 +/- 35 and 131 +/- 22 pg/mg creatinine, respectively) and without (185 +/- 16 and 101 +/- 13 pg/mg creatinine, respectively) chest pain, or in those with (178 +/- 45 and 162 +/- 41 pg/mg, respectively) and without (216 +/- 22 and 104 +/- 11 pg/mg, respectively) ST-segment depression during the test. Patients without chest pain or without ST-segment depression moderately increased (p less than 0.05) their urinary Tx-M (by 21% and 13%, respectively) and PGI-M (by 28% and 23%, respectively) after exercise. No significant increases were observed in those developing chest pain or ST depression during exercise. These data indicate that effort-induced myocardial ischemia is not associated with an increase in platelet activation or platelet/vessel wall interaction in patients with stable coronary disease.     

Increased plasma level of atrial natriuretic peptide in patients with stress-induced coronary insufficiency: stretch-independent release of atrial natriuretic peptide?

Plasma levels of atrial natriuretic peptide (ANP) were determined in 34 male patients undergoing diagnostic right heart catheterization. Patients with effort angina exhibited significant higher ANP levels at rest (259 +/- 42 pg/ml; n = 7) than patients without signs of coronary heart disease (78 +/- 30 pg/ml; n = 8). Patients with effort angina also had higher ANP levels at rest than patients exhibiting impaired cardiac function on exertion without signs of ischemia (105 +/- 15 pg/ml; n = 4), patients with only minimal functional alterations due to infarction residues (95 +/- 27 pg/ml; n = 7), or patients with only borderline changes of ST-segments during exertion (61 +/- 19 pg/ml; n = 8). In contrast, mean pulmonary capillary or right atrial pressures were not significantly different between the various groups of patients. The patients with effort angina also exhibited the highest ANP levels during bicycle exercise (846 +/- 238 pg/ml). There was only a weak to moderate linear correlation between ANP levels and pulmonary or right atrial pressures in the whole group of patients (r = 0.1-0.6). The plasma levels of epinephrine and norepinephrine and of ANP were not significantly correlated, with the exception of norepinephrine levels during exercise (r = 0.54). Our observations suggest that in patients with effort angina there may exist additional stretch-independent factors stimulating the release of ANP, possibly associated with repetitive myocardial ischemia.     

Effect of spinal cord stimulation on regional myocardial perfusion assessed by positron emission tomography.

Spinal cord stimulation (SCS) can relieve symptoms in patients with severe angina pectoris refractory to conventional medical or surgical therapy. This symptomatic improvement may result from decreased myocardial ischemia. To test this hypothesis, positron emission tomography (PET) and potassium-38 as a flow tracer were used in 8 patients for the quantitative evaluation of regional myocardial perfusion at rest and after exercise, before and during SCS. Potassium uptake was evaluated as myocardial clearance (flow times net extraction) in ml/min/100 g. Tomographic segments were categorized as nonaffected and affected on the basis of the absence or presence of arterial stenosis on coronary angiography and on the basis of thallium scintigraphic data. In nonaffected segments, before SCS, regional myocardial clearance significantly increased from rest (28 +/- 4) to exercise (47 +/- 13 clearance units; p less than 0.004). A similar increase occurred after SCS. In affected segments, before SCS, regional myocardial clearance barely increased (p = 0.065) from rest (26 +/- 6) to exercise (33 less than or equal to 12). In comparison, after SCS, the resting regional myocardial clearance was slightly elevated (29 +/- 8) reflecting an increased double product, but did not increase (p = 0.192) with exercise (34 +/- 12). However, the magnitude and duration of ST-segment depression decreased during treatment with SCS. Anginal pain occurred in all patients during control exercise, but was attenuated in all but one with SCS. These results indicate that SCS improves exercise-induced angina and electrocardiographic signs of ischemia but this influence does not appear to be mediated by changes in regional myocardial perfusion.     

Endorphins are related to pain perception in coronary artery disease

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.     

Effect of exercise on circulating atrial natriuretic peptide and left ventricular ejection fraction in healthy persons and patients with coronary artery disease

Radionuclide angiographic measurements of left ventricular ejection fraction were performed at rest and during exercise in 10 normal persons and 11 patients with coronary artery disease. Exercise was continued on a supine bicycle exercise table up to a symptom-limited maximum. Plasma levels of atrial natriuretic peptide (ANP) were also determined at rest and during exercise. Ejection fraction in the normal volunteers was 59 +/- 3% (mean +/- SEM) at rest and increased significantly (p less than 0.01) to 69 +/- 3% during exercise. Ejection fraction in the patients was 47 +/- 5% at rest and did not change significantly during exercise (51 +/- 7%). Plasma ANP in the normals rose significantly (p less than 0.01) from 62 +/- 16 pg/ml at rest to 454 +/- 94 pg/ml during exercise. Plasma ANP in the patients also rose significantly (p less than 0.01) from 231 +/- 102 pg/ml to 794 +/- 170 pg/ml. The response of plasma ANP to exercise was enhanced significantly (p less than 0.05) in the patients as compared with the normals in relation to ejection fraction by analysis of covariance. In both the normals and the patients, plasma ANP was inversely and significantly correlated with ejection fraction during exercise (r = -0.46, p less than 0.05, n = 21), however, not at rest. Because it has been reported that plasma ANP is correlated positively with pulmonary artery wedge pressure, the estimation of plasma ANP during an exercise stress test might be used for the evaluation of cardiac reserve in coronary artery disease.     

Increased plasma brain natriuretic peptide level as a guide for silent myocardial ischemia in patients with non-obstructive hypertrophic cardiomyopathy

OBJECTIVES: We measured plasma atrial/brain natriuretic peptide (ANP/BNP) levels at rest and during exercise and correlated the results with various clinical findings, particularly with myocardial ischemia, in asymptomatic hypertrophic cardiomyopathy (HCM). BACKGROUND: In patients with HCM, ANP and BNP levels are elevated and exercise-induced myocardial ischemia is common. However, it has not yet been elucidated how these levels at rest and their change with dynamic exercise are related to ischemia. METHODS: Levels of ANP and BNP were measured at rest and at peak exercise during (99m)Tc-tetrofosmin scintigraphy in 31 asymptomatic patients with non-obstructive HCM and in 10 control subjects. RESULTS: Levels of ANP and BNP at rest and the change of ANP and BNP levels (PG/ML) from rest to exercise were significantly greater in HCM than in control subjects (ANP: rest, 53.2 +/- 31.8 vs. 11.6 +/- 6.1; exercise, 114.5 +/- 74.8 vs. 28.3 +/- 23.4. BNP: rest, 156.7 +/- 104.1 vs. 9.8 +/- 9.6; exercise, 201.6 +/- 131.5 vs. 13.2 +/- 14.5). Septal perforator compression (SPC) and exercise-induced ischemia were observed, respectively, in 20 (64.5%) and in 19 (61.3%) patients with HCM. The increment of ANP during exercise was similar between HCM subgroups with or without inducible ischemia. However, BNP levels at rest and BNP increments during exercise were significantly greater in the HCM subgroup with inducible ischemia than in the subgroup without (rest, 190.5 +/- 116.2 vs. 103.1 +/- 48.3; exercise, 250.5 +/- 142.2 vs. 124.2 +/- 58.6). Multiple logistic regression analysis revealed that SPC and BNP levels at rest were independently associated with exercise-induced ischemia. CONCLUSIONS: Measurement of plasma BNP levels at rest may be useful in predicting silent myocardial ischemia in HCM.     

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 baselin 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.     

Plasma beta-endorphin level in "silent" myocardial ischemia during Holter ECG monitoring]

The results from recent studies suggest that the endogenous opioid beta-endorphin (beta-E) is related to pain modulation. Therefore, plasma beta-E levels were studied in 23 patients with essential hypertension (EH) and in 7 patients with coronary artery disease (CAD) during asymptomatic ischemic events and in 5 patients with CAD during symptomatic ischemic events. Blood samples for beta-E were taken at the moment of silent ST depression, pointed with alarm by the real time ECG monitor "Q Med Monitor" (USA). Control blood samples were taken under the same conditions without ischemic events. Control plasma beta-E levels were significantly higher (p less than 0.01) in patients with EH as compared to that in both groups of patients with CAD (22.9 +/- 4.0 vs 7.0 +/- 1.9 and 4.5 +/- 1.6 pmol/l). At the time of silent ischemia, beta-E showed a significant increase in patients with EH (+10.1 +/- 2.1 pmol/l, p less than 0.01) and in patients with CAD (+10.7 +/- 1.3 pmol/l, p less than 0.05) as compared to the control levels. However, plasma beta-E showed no increase (+1.0 +/- 0.6 pmol/l, p greater than 0.1) during symptomatic ischemia as compared to the control levels. Thus, differences in the circulating levels of beta-E may be associated with the presence or absence of pain during myocardial ischemia.     

Demonstration of exercise-induced painless myocardial ischemia in survivors of out-of-hospital ventricular fibrillation

To ascertain if myocardial ischemia is the mechanism of out-of-hospital ventricular fibrillation (VF), left ventricular (LV) function was assessed at rest and during submaximal exercise in 15 patients who survived out-of-hospital VF. They were separated into asymptomatic (9 patients, group A) and symptomatic (6 patients, group S) groups for a history of angina or myocardial infarction. Both groups had significant (at least 70% diameter stenosis) coronary artery disease. At catheterization no patient had angina during exercise, but 12 of 15 had ST depression or increased ST depression (group A, 1.9 +/- 1.4 mm; group S, 1.1 +/- 1.2 mm) and 11 had abnormal wall motion. From rest to exercise, patients in group S had increased LV end-diastolic pressure (from 21 +/- 9 to 37 +/- 11 mm Hg, p = 0.009) and volume (from 100 +/- 25 to 107 +/- 26 ml/m2, p = 0.006), with no significant change in LV ejection fraction (from 40 +/- 13 to 42 +/- 12%). In group A LV end-diastolic pressure increased from 19 +/- 4 to 31 +/- 8 mm Hg (p = 0.001), but neither end-diastolic volume nor ejection fraction changed significantly (from 83 +/- 13 to 92 +/- 23 ml/m2 and from 55 +/- 13% to 46 +/- 13%, respectively). Thus, patients with coronary artery disease who survive out-of-hospital VF may have evidence of myocardial ischemia during exercise without pain. Painless ischemia may have a role in out-of-hospital VF.     

Silent myocardial ischemia as a potential link between lack of premonitoring symptoms and increased risk of cardiac arrest during physical stress

The risk of cardiac arrest is increased during strenuous physical exercise in patients with stable coronary artery disease (CAD). Because premonitoring symptoms are rarely observed, silent myocardial ischemia may represent the pathophysiological basis for the induction of malignant ventricular arrhythmias. Holter monitoring was, therefore, performed in 40 consecutive patients entering a randomized intervention trial on progression of CAD. In 20 of 21 participants (95%) in the intervention program greater than or equal to 1 episode of silent myocardial ischemia was observed during the initial training session. The mean duration of silent myocardial ischemia per patient was 25 +/- 13 min/hr of training session. During normal daily activity only 5 patients (24%) experienced greater than or equal to 1 episode of silent myocardial ischemia (p less than 0.001) yielding a mean duration of 0.6 +/- 1.3 minutes of silent myocardial ischemia/hr of ordinary activity per patient (p less than 0.001 vs training session). During a control period of 24 hours without exercise training the incidence (33%) and mean duration of silent myocardial ischemia (0.8 +/- 2.1 min/hr/patient) were similar to those during normal daily activity on the day of the training session. During the training session the occurrence of frequent or repetitive ventricular arrhythmias was related to 10 silent myocardial ischemia episodes detected in 5 patients. During normal daily activity in 1 patient only was the onset of malignant ventricular arrhythmias associated with silent myocardial ischemia (p less than 0.05). Conditions and results of the Holter studies in the control group patients were comparable to those of the patients in the intervention group on the day without physical exercise.(ABSTRACT TRUNCATED AT 250 WORDS)