Sauna-induced myocardial ischemia in patients with coronary artery disease.

PURPOSE: Sauna bathing is a popular recreational activity that is generally considered to be safe. However, there have been case reports of adverse cardiac events. We sought to determine whether sauna use caused myocardial ischemia in patients with coronary artery disease. METHODS: Sixteen patients with proven coronary artery disease were submitted to three conditions (rest, exercise, and sauna bathing) with continuous electrocardiographic (ECG) monitoring and regular blood pressure measurements. During each condition, patients were injected with Tc-99 sestamibi followed by nuclear scintigraphic imaging. Perfusion defect scores were calculated in 15 patients. RESULTS: Sauna bathing was well tolerated. There was a mean (+/- SD) increase in heart rate of 32% +/- 20% in the sauna (resting mean heart rate = 60 +/- 9 beats per minute vs sauna mean heart rate = 79 +/- 11 beats per minute, P <0.001) and a 13% +/- 6% drop in systolic blood pressure (resting mean systolic blood pressure = 142 +/- 14 mm Hg vs sauna mean systolic blood pressure = 123 +/- 15 mm Hg, P <0.001). There were no arrhythmias or ECG changes in the sauna. Compared with rest, there was significant ischemia during sauna bathing (average perfusion defect score at rest = -0.44 vs average sauna score = -0.93, P <0.001). The perfusion defect score in the sauna was worse than the resting score in 14 of the 15 patients. Sauna-associated perfusion defect scores were highly correlated with exercise-induced scores (R2 = 0.65, P <0.001). CONCLUSION: In patients with stable coronary artery disease, sauna use is clinically well tolerated but is associated with scintigraphically demonstrated myocardial ischemia.     

Safety and efficacy of repeated sauna bathing in patients with chronic systolic heart failure: a preliminary report

BACKGROUND: We sought to determine the safety and efficacy of repeated 60 degrees C sauna bathing in patients with chronic systolic congestive heart failure (CHF). METHODS AND RESULTS: This study included 15 hospitalized CHF patients (New York Heart Association class = 2.8 +/- 0.4) in stable clinical condition on conventional treatments. Sauna bathing was performed once per day for 4 weeks. Repeated sauna bathing was safely completed without any adverse effects in all patients. Symptoms improved in 13 of 15 patients after 4 weeks. Sauna bathing decreased systolic blood pressure without affecting heart rate, resulting in significant decrease in the rate-pressure product (6811 +/- 1323 to 6292 +/- 1093). Echocardiographic left ventricular ejection fraction was significantly increased from 30 +/- 11 to 34 +/- 11%. Sauna bathing significantly improved exercise tolerance manifested by prolonged 6-minute walking distance (388 +/- 110 to 448 +/- 118 m), increased peak respiratory oxygen uptake (13.3 +/- 1.8 to 16.3 +/- 2.1 mL/kg/min), and enhanced anaerobic threshold (9.4 +/- 1.2 to 11.5 +/- 1.9 mL/kg/min). Four-week bathing significantly reduced plasma epinephrine (40 +/- 42 to 21 +/- 23 pg/mL) and norepinephrine (633 +/- 285 to 443 +/- 292 pg/mL). Sauna bathing reduced the number of hospital admission for CHF (2.5 +/- 1.3 to 0.6 +/- 0.8 per year). CONCLUSION: Repeated 60 degrees C sauna bathing was safe and improved symptoms and exercise tolerance in chronic CHF patients. Sauna bathing may be an effective adjunctive therapy for chronic systolic CHF.     

Hormonal (ACTH, Cortisol, β-Endorphin, and Met-Enkephalin) and Cardiovascular Responses to Hyperthermic Stress in Chronic Alcoholics

Chronic alcohol drinking causes profound alterations in hypothalamic-pituitary function. In the present study, endocrine [corticotropin (ACTH), β-endorphin, cortisol, and met-enkephalin] and cardiovascular (blood pressure) changes in response to hyperthermic stress (sauna at 90°C for 30 min) were evaluated in 25 normal men (25 to 50 years old) and in 48 male alcoholic subjects (34 to 56 years old) after 5 weeks of abstinence. Significantly lower increments in systolic blood pressure were observed in alcoholics than in control subjects. Furthermore, alcoholics showed lower ACTH, β-endorphin, and cortisol increments in response to sauna than normal controls. In contrast, sauna-induced hyperthermia did not change significantly the circulating met-enkephalin levels in either normal controls or chronic alcoholics. These data suggest that an impairment in the adaptive response to stress affects alcoholic men even after a few weeks of abstinence from alcohol.     

Benefits and risks of sauna bathing

Although sauna bathing causes various acute, transient cardiovascular and hormonal changes, it is well tolerated by most healthy adults and children. Sauna bathing does not influence fertility and is safe during the uncomplicated pregnancies of healthy women. Some studies have suggested that long-term sauna bathing may help lower blood pressure in patients with hypertension and improve the left ventricular ejection fraction in patients with chronic congestive heart failure, but additional data are needed to confirm these findings. The transient improvements in pulmonary function that occur in the sauna may provide some relief to patients with asthma and chronic bronchitis. Sauna bathing may also alleviate pain and improve joint mobility in patients with rheumatic disease. Although sauna bathing does not cause drying of the skin-and may even benefit patients with psoriasis-sweating may increase itching in patients with atopic dermatitis. Contraindications to sauna bathing include unstable angina pectoris, recent myocardial infarction, and severe aortic stenosis. Sauna bathing is safe, however, for most people with coronary heart disease with stable angina pectoris or old myocardial infarction. Very few acute myocardial infarctions and sudden deaths occur in saunas, but alcohol consumption during sauna bathing increases the risk of hypotension, arrhythmia, and sudden death, and should be avoided.     

Plasma calcium and cortisol as predisposing factors to alcohol related blood pressure elevation

Mechanisms by which alcohol consumption might cause hypertension were examined in 30 pairs of healthy drinking (greater than 275 g ethanol per week) and teetotal men closely matched for age and obesity. Both systolic and diastolic blood pressures were significantly higher in the drinkers. Plasma calcium levels correlated with diastolic blood pressures (r = 0.51, P = 0.004) in drinkers only. After adjusting for plasma albumin, diastolic pressures increased by 6.9 mmHg for each 0.1 mM increment of plasma calcium. It is proposed that regular alcohol consumption predisposes to hypertension by facilitating calcium accumulation in cells involved in blood pressure regulation. In the combined population of drinkers and teetotallers plasma cortisol correlated positively with diastolic pressure (r = 0.35, P = 0.012) and negatively with plasma potassium (r = -0.38, P = 0.006); this suggests a role for the pituitary/adrenal axis as a significant determinant of blood pressure differences between healthy subjects.     

Alcohol Consumption,Blood Pressure,and the Risk of Stroke

A synergistic effect of alcohol and hypertension has been suggested to increase the risk for stroke. However, the contribution of alcohol-induced hypertension to stroke morbidity and mortality may be greater than observed, because the effects of different drinking patterns have not been separately investigated. Alcohol-induced transient peaks in systolic blood pressure may predispose to stroke. Recent studies have measured time trends of blood pressure elevations in relation to alcohol consumption. They found a significant morning surge in blood pressure, which was related to alcohol intake in a dose-dependent manner and was independent of smoking. Men with a severe form of hypertension showed a 12-fold increased risk for cardiovascular disease mortality associated with heavy binge drinking. Binge drinking is a significant risk factor for stroke. Hypertensive patients should be warned about the risks of alcohol and urged to avoid binge drinking because of an increased risk for all subtypes of stroke.     

Is sauna bathing protective of sudden cardiac death? A review of the evidence

Sudden cardiac death (SCD) is a global public health burden accounting for 15–20% of all deaths. Though established atherosclerotic risk factors explain a large proportion of the risk of SCD, these factors are often absent in a large proportion of SCD victims and the pathogenesis of SCD is still not fully established. It therefore appears that additional factors may be involved. Sauna bathing is a traditional Finnish activity that is mainly used for the purposes of relaxation and pleasure. Beyond its use for these purposes, sauna bathing has been linked with several health benefits. Emerging evidence suggests that sauna bathing is associated with reduced risk of adverse cardiovascular (CV) disease (CVD) and non-CVD outcomes as well as mortality. A number of reports have linked sauna bathing with reduced or increased risk of SCD, but the evidence is uncertain. This review summarizes available studies linking sauna bathing with SCD, the postulated mechanistic pathways underlying these associations, outlines areas of outstanding uncertainty, and the implications for prevention. We employed a comprehensive search for observational studies, randomized controlled trials (RCTs), and non-RCTs from MEDLINE and Embase since their inception until March 2019. Observational data suggest that regular sauna bathing is associated with a substantial risk reduction in SCD. Furthermore, the data suggest that a combination of regular physical activity and sauna baths confers substantial risk reduction for SCD compared with either modality alone. Few reports have linked sauna baths with SCDs, but these single case incidents have been attributed to the effects of dehydration, hypotension, and cardiac arrhythmias due to a combination of sauna exposure and alcohol consumption. Sauna bathing is generally safe for most healthy people and even among patients with stable CVD, if used sensibly and with caution. Plausible pathways underlying the protective effect of sauna bathing on SCD may be linked to the impact on CV function via reduced arterial stiffness, decreases in inflammation and oxidative stress, stabilization of the autonomic nervous system, beneficial changes in circulating lipid profiles and other CVD risk markers, and lowering of systemic blood pressure. Sauna is a potential novel tool to promote SCD prevention in addition to other known means, being an enjoyable way to take care of general health and well-being.     

Haemodynamic role of vasopressin released during Finnish sauna

The effect of vasopressin released during Finnish sauna on blood pressure, heart rate and skin blood flow was investigated in 12 healthy volunteers. Exposure to the hot air decrease body weight by 0.6 to 1.25 kg (mean = 0.8 kg, P less than 0.001). One hour after the end of the sauna sessions, plasma vasopressin was higher (1.7 +/- 0.2 pg/ml, P less than 0.01 mean +/- SEM) than before the sauna (1.0 +/- 0.1 pg/ml). No simultaneous change in plasma osmolality, plasma renin activity, plasma norepinephrine, epinephrine, cortisol, aldosterone, beta-endorphin and metenkephalin levels was observed. Despite the slight sauna-induced elevation in circulating vasopressin, intravenous injection of the specific vascular vasopressin antagonist d(CH2)5Tyr(Me)AVP (5 micrograms/kg) 1 h after the sauna had no effect on blood pressure, heart rate or skin blood flow. These data suggest that vasopressin released into the circulation during a sauna session reaches concentrations which are not high enough to interfere directly with vascular tone.     

Modification of the association of alcohol drinking with blood pressure by cigarette smoking

The purpose of this study was to investigate whether the association of alcohol drinking with blood pressure was modified by cigarette smoking. The subjects were healthy male workers aged 40-59 years and were divided into three different groups by average daily consumption of alcohol (non-drinkers; light drinkers, less than 30 g ethanol per day; heavy drinkers, 30 g or more ethanol per day) and cigarettes (non-smokers; light smokers, less than 20 cigarettes per day; heavy smokers, 20 cigarettes or more per day). The mean levels of both systolic and diastolic blood pressures were significantly lower in the light and heavy smoker groups than in the non-smoker group. In the light and heavy smoker groups, systolic blood pressure was higher in the light drinker subgroup than in the non-drinker subgroup, while there was no significant difference between systolic blood pressures in the non- and light drinker subgroups of non-smokers. In the non-, light and heavy smoker groups, systolic and diastolic blood pressures were significantly higher in the heavy drinker subgroup than in the non-drinker subgroup, and these differences tended to be greater in light and heavy smokers than in non-smokers. The above differences in the relationships of alcohol drinking with blood pressure in non-, light and heavy smokers were also observed when age and body mass index were adjusted and when alcohol intake-matched groups were used. These results suggest that the association of alcohol drinking with blood pressure is stronger in smokers than in non-smokers, independently of age, body mass index and alcohol intake.     

Influence of profuse sweating on systolic time intervals

The influence of profuse sweating on systolic time intervals was investigated. Systolic time intervals were recorded in 21 healthy men before and after sauna bathing. After sauna bathing the ejection time was significantly shortened and the pre-ejection time and ratio of pre-ejection time to ejection time (PEP:ET) were significantly increased. The upper limit of the PEP:ET ratio is generally believed to be 0.42 and this ratio increases when left ventricular performance is impaired. Before sauna bathing the PEP:ET ratio was less than 0.42 in all 21 men, but after sauna bathing it was greater than 0.43 in six (28.5%) of them. Systolic time intervals measured after profuse sweating can give a false impression of cardiac function.     

Influence of profuse sweating on systolic time intervals.

The influence of profuse sweating on systolic time intervals was investigated. Systolic time intervals were recorded in 21 healthy men before and after sauna bathing. After sauna bathing the ejection time was significantly shortened and the pre-ejection time and ratio of pre-ejection time to ejection time (PEP:ET) were significantly increased. The upper limit of the PEP:ET ratio is generally believed to be 0.42 and this ratio increases when left ventricular performance is impaired. Before sauna bathing the PEP:ET ratio was less than 0.42 in all 21 men, but after sauna bathing it was greater than 0.43 in six (28.5%) of them. Systolic time intervals measured after profuse sweating can give a false impression of cardiac function.     

Effect of sauna bathing and beer ingestion on plasma concentrations of purine bases

To determine whether sauna bathing alone or in combination with beer ingestion increases the plasma concentration of uric acid, 5 healthy subjects were tested. Urine and plasma measurements were performed before and after each took a sauna bath, ingested beer, and ingested beer just after taking a sauna bath, with a 2-week interval between each activity. Sauna bathing alone increased the plasma concentrations of uric acid and oxypurines (hypoxanthine and xanthine), and decreased the urinary and fractional excretion of uric acid, while beer ingestion alone increased the plasma concentrations and urinary excretion of uric acid and oxypurines. A combination of both increased the plasma concentration of uric acid and oxypurines, and decreased the urinary and fractional excretion of uric acid, with an increase in the urinary excretion of oxypurines. The increase in plasma concentration of uric acid with the combination protocol was not synergistic as compared to the sum of the increases by each alone. Body weight, urine volume, and the urinary excretion of sodium and chloride via dehydration were decreased following sauna bathing alone. These results suggest that sauna bathing had a relationship with enhanced purine degradation and a decrease in the urinary excretion of uric acid, leading to an increase in the plasma concentration of uric acid. Further, we concluded that extracellular volume loss may affect the common renal transport pathway of uric acid and xanthine. Therefore, it is recommended that patients with gout refrain from drinking alcoholic beverages, including beer, after taking a sauna bath, since the increase in plasma concentration of uric acid following the combination of sauna bathing and beer ingestion was additive.     

Left ventricular size, mass and function in relation to the duration and quantity of heavy drinking in alcoholics.

Left ventricular (LV) hypertrophy and mild dysfunction are frequently observed in alcoholics but little is known about how they relate to the duration and severity of alcohol abuse. LV size, mass and function were studied using echocardiography and systolic time intervals in 78 middle-aged male alcoholics who also gave detailed accounts of the duration of heavy drinking, the quantity of recent ethanol consumption and the duration of abstinence. Compared with 34 healthy nonalcoholics, alcoholics had a higher LV mass index (85 +/- 2 [mean +/- standard error] vs 77 +/- 2 g/m2, p = 0.001), a thicker posterior wall (11 +/- 0.2 vs 10 +/- 0.2 mm, p = 0.02), a longer end-systolic diameter index (18 +/- 0.3 vs 17 +/- 0.3 mm/m2, p = 0.02), and a higher preejection period/ejection time ratio (0.36 +/- 0.01 vs 0.33 +/- 0.01, p = 0.002). In multivariate linear regression models, these abnormalities proved independent of the drinking history, except that posterior wall thickness was weakly related to the duration of heavy drinking (standardized correlation coefficient 0.36, p = 0.01). Univariate analyses suggested that the LV mass index and systolic time interval ratio had, if anything, a curvilinear relation to the total duration of heavy alcohol consumption. It is concluded that the LV hypertrophy and dysfunction found in alcoholics are poorly related to the duration and severity of self-reported alcohol abuse. Together with other data, this suggests that there is no simple linear dose-injury relation in the long-term cardiotoxicity of ethanol. Factors modifying the myocardial effects of ethanol need to be studies more in the future.     

PR and OTc interval prolongation on the electrocardiogram after binge drinking in healthy individuals

BACKGROUND: Acute, excessive alcohol intake has been associated with an increased cardiovascular mortality in otherwise healthy individuals. It predisposes to accelerated atherosclerosis resulting in acute coronary events but also arrhythmias have been described, such as atrial fibrillation and life-threatening re-entrant ventricular arrhythmias. QTc prolongation is associated with an increased risk of ventricular tachyarrhythmias and an independent risk factor for sudden cardiac death. The aim of the study is to investigate the effect of binge drinking on the conduction intervals in healthy individuals. METHODS: Ten of the volunteers drank red wine while the other ten volunteers drank a sweet designer drink. A follow-up of blood pressure, heart rate, ECG and laboratory findings was performed at an ethanol level of 0, 0.4 and 0.8%, respectively. RESULTS: Fifteen volunteers showed a prolongation of the PR interval, 13 of the QRS complex, 9 of the QT interval and 13 of the QTc interval. PR interval increased from 149 +/- 16 ms to 163 +/- 11 ms (p < 0.05). The heart rate-adjusted QT interval increased from 400 +/- 24 ms to 426 +/- 52 ms (p < 0.05). Heart rate and systolic blood pressure did not significantly change due to the ingestion. CONCLUSION: Acute ingestion of alcohol in a healthy population can induce prolongation of PR and QTc interval.     

Left ventricular performance in alcoholic patients without chronic liver disease.

Left ventricular performance was studied non-invasively in 24 chronic alcoholics without liver disease. Twelve patients who had abstained from drinking for at least one month (group A) and 12 sex and age matched patients who had ceased drinking during the preceding 24 hours (group B) were studied at rest and during 50% submaximal exercise. Cardiac output and stroke volume were measured by first passage and left ventricular ejection fraction by multigated radionuclide cardiography. Twelve healthy sex and age matched controls were also studied. Haemodynamic variables were similar in group A and the controls, except that in group A left ventricular end systolic volume index did not decrease during exercise. In group B the heart rate was increased both at rest and during exercise and plasma noradrenaline concentrations were increased. The stroke volume index did not increase significantly during exercise in group B. In addition, the increase in left ventricular ejection fraction was smaller in group B than in controls. End systolic contraction was reduced in group B patients and diastolic blood pressure was increased. These results suggest that cardiac abnormalities in chronic alcoholics may be reversed after cessation of drinking if no chronic liver disease is present. Recent alcohol consumption increases sympathetic nervous activity, impairs cardiac contractility, and increases afterload during physical stress.     

Left ventricular performance in alcoholic patients without chronic liver disease

Left ventricular performance was studied non-invasively in 24 chronic alcoholics without liver disease. Twelve patients who had abstained from drinking for at least one month (group A) and 12 sex and age matched patients who had ceased drinking during the preceding 24 hours (group B) were studied at rest and during 50% submaximal exercise. Cardiac output and stroke volume were measured by first passage and left ventricular ejection fraction by multigated radionuclide cardiography. Twelve healthy sex and age matched controls were also studied. Haemodynamic variables were similar in group A and the controls, except that in group A left ventricular end systolic volume index did not decrease during exercise. In group B the heart rate was increased both at rest and during exercise and plasma noradrenaline concentrations were increased. The stroke volume index did not increase significantly during exercise in group B. In addition, the increase in left ventricular ejection fraction was smaller in group B than in controls. End systolic contraction was reduced in group B patients and diastolic blood pressure was increased. These results suggest that cardiac abnormalities in chronic alcoholics may be reversed after cessation of drinking if no chronic liver disease is present. Recent alcohol consumption increases sympathetic nervous activity, impairs cardiac contractility, and increases afterload during physical stress.     

Effects of endothelin-1 and endothelin-1 receptor blockade on cardiac output,aortic pressure,and pulse wave velocity in humans

Endothelin-1 (ET-1) is a potent vasoconstrictor. Its effect on arterial wave reflections and central pressure augmentation is unknown. We studied whether ET-1, in plasma concentrations present in disease, increases pulse wave velocity (PWV) and augmentation index (AIx) and therefore compromises cardiac output, and whether the ET-1 receptor blocker VML-588 (previously AXV-034343 and Ro 61-1790) prevents such effects. Nine healthy men received a 2-hour infusion with ET-1 (2.5 ng x kg(-1) x min(-1)) superimposed on vehicle or VML-588 (0.05, 0.20, or 0.40 mg x kg(-1) x h(-1)) (randomized order). Arterial tonometry and pulse wave contour analysis were used to assess aortic PWV and central aortic pressures and impedance cardiography for cardiac output. ET-1 slightly increased mean arterial pressure and peripheral resistance but had no significant effect on systolic blood pressure and pulse pressure. PWV increased from 5.4+/-0.2 to 5.7+/-0.3 m/s (P<0.05), AIx from 9.9+/-3.3 to 17.2+/-3.8 (P<0.05), central systolic blood pressure by 8.7+/-1.7 mm Hg (P<0.05), and central pulse pressure by 5.1+/-1.9 mm Hg (P<0.05). This was associated with a fall in cardiac output by approximately 18% (P<0.05). VML-588 caused a slight decrease in brachial mean arterial pressure, PWV, and AIx, and prevented the effects of ET-1 on central hemodynamics without a clear dose-response effect. In summary, ET-1 in plasma concentrations as found in renal failure and heart failure accelerates PWV, causes a disproportionate increase in central aortic systolic blood pressure and pulse pressure, and decreases cardiac output. These effects can be prevented with an ET-1 receptor blocker such as VML-588. This makes it worthwhile to focus on endothelin as a target to prevent ventricular hypertrophy and to maintain cardiac function in diseases associated with high ET-1.     

Alcohol Consumption and Stroke: Benefits and Risks

The complex relationship between alcohol consumption and stroke includes both benefits and risks. Regular light-to-moderate consumption of alcohol seems to decrease the risk for ischemic stroke by reducing atherothrombotic events, but the undertying mechanism is still unclear. Recent and current (but not previous) heavy drinking increases the risk for both hemorrhagic and ischemic strokes. Young and middle-aged men are stricken more often than women or elderly persons, probably because they are more often current heavy drinkers. Alcoholic cardiomyopathy is a cause of cardioembolic brain infarction. Cardiac arrhythmias caused by regular heavy drinking or binge drinking can precipitate thrombus formation and propagate already existing thrombi from the heart. The maintenance of high blood pressure by heavy drinking may promote cerebral arterial degeneration, but the effect of drinking habits on aneurysm formation is not known. Acute increases in systolic blood pressure and/or alterations in cerebral arterial tone could serve as mechanisms triggering hemorrhagic strokes during alcoholic intoxication. We lack studies to show that prevention of heavy drinking can efficiently influence the occurrence of strokes.     

The pressor and metabolic effects of alcohol in normotensive subjects

Changes in blood pressure, pulse rate, and plasma catecholamines, renin activity, cortisol, and calcium were studied in 16 normotensive subjects (eight with a family history of hypertension) for 5 hours following ingestion of alcohol-free and alcohol-loaded beer. Both systolic and diastolic blood pressure rose after alcohol consumption; maximum responses occurred at peak blood alcohol concentrations and were significantly higher than those seen after placebo. Pulse rate was also significantly higher after alcohol ingestion and continued to rise throughout the study. There was no difference in the pressor response to alcohol between the groups with and without a family history of hypertension. No difference was found in plasma norepinephrine or epinephrine levels between alcohol and placebo phases. However, subjects with no family history of hypertension had significantly higher plasma norepinephrine levels (p less than 0.01) than did those with a family history during both the alcohol and placebo phases, although baseline blood pressures were not significantly different. Plasma epinephrine level was similar in both groups. Plasma renin activity was unchanged throughout, but plasma cortisol fell during both phases. Plasma calcium showed a small but significant fall with alcohol consumption in both groups (p less than 0.001). These results indicate that in normotensive subjects alcohol ingestion causes a rise in systolic and diastolic blood pressure that is not influenced by a family history of hypertension. This effect does not appear to be sympathetically mediated but may be due to a direct vasoconstrictor effect of alcohol, possibly with an alcohol-induced shift in intracellular calcium.     

Acute effects of alcohol on left ventricular dynamics during isometric exercise in normal subjects

The aim of this study was to assess whether drinking social amounts of alcohol impairs myocardial contractility in normal humans. To that end, 17 healthy volunteers performed isometric handgrip exercise before and 60 minutes after an intake of 1 g/kg body weight of ethanol within 60 minutes. Left ventricular M-mode echocardiogram, systolic time intervals, and sphygmomanometric arterial blood pressure were recorded before and at the end of 4-min handgrip at 30% of maximum voluntary contraction. The blood ethanol concentration (mean +/- SD) was 24.4 +/- 2.0 mmol/liter. At rest, ethanol increased heart rate (p less than 0.05), and decreased left ventricular end-diastolic diameter (p less than 0.05), end-systolic diameter (p less than 0.01), and circumferential systolic wall stress (p less than 0.05). The indices of left ventricular performance were unchanged except for the maximum circumferential fiber shortening velocity which was increased after ethanol (p less than 0.001). The cardiac response to isometric exercise was similar before and after ethanol except that the handgrip-induced rise in systolic wall stress was smaller postingestion (p less than 0.05). This study does not support the view that drinking small to moderate amounts of alcohol brings about myocardial depression in normal humans. Although preload, afterload, and heart rate were altered by ethanol at rest, myocardial contractility was not impaired even during the afterload stress imposed by isometric exercise.