[Treatment of chronic heart failure].
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Cardiovascular Agents↗
Biomedical subjects
M Kupari
Publications and source records attributed to M Kupari.
Does alcohol intensify the hemodynamic effects of nitroglycerin?
To evaluate the combined effects of alcohol and nitroglycerin on cardiovascular hemodynamics, M-mode echocardiography and sphygmomanometric blood pressure measurements were performed on two groups of normal subjects, before and after the administration of nitroglycerin, both in the sober state and during alcohol intoxication. In the first part of the study, 0.5 mg of nitroglycerin was given sublingually to 10 healthy volunteers 5-10 minutes after they had ingested 1 g/kg body weight of ethanol within a 30-minute period. Control experiments substituted juice for ethanol. The combined effects of ethanol and nitroglycerin on left ventricular diameters, systolic blood pressure, and wall stress were not significantly different from those of juice and nitroglycerin; heart rate and diastolic blood pressure were increased more (p less than 0.01) by ethanol and nitroglycerin. In the second part of the study, 1.0 mg of nitroglycerin was administered to a second group of 10 healthy volunteers, first in the control state and again 60 minutes after the subjects had ingested 1 g/kg body weight of ethanol within a 60-minute period. Systolic blood pressure and wall stress were significantly lower (p less than 0.01) after ethanol and nitroglycerin than after nitroglycerin before ethanol intake. We conclude that the nitroglycerin-induced reductions in left ventricular preload and afterload are not increased by alcohol during the very early phase of intoxication. However, 1 hour or more after alcohol ingestion nitroglycerin may decrease left ventricular afterload to a level significantly lower than that seen after nitroglycerin in the sober state.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Asymmetric septal hypertrophy in Kearns-Sayre syndrome.
Kearns-Sayre syndrome was diagnosed in a 40-year-old female patient admitted for evaluation of symptomatic bradycardia. In addition to the classic triad--external ophthalmoplegia, pigmentary retinopathy, and heart block--she also had secondary amenorrhea, hearing loss, diabetes, and increased concentrations of blood lactate and pyruvate as manifestations of this multisystem disease. The echocardiographic examination disclosed asymmetric septal hypertrophy with a septal diastolic thickness of 17 mm and a septum to free wall ratio of 1.5. The left ventricular size and function were normal. Thus, asymmetric septal hypertrophy may represent subclinical heart muscle involvement in Kearns-Sayre syndrome.
Adult↗
Reproducibility of M-mode echocardiographic assessment of left ventricular function. Significance of the temporal range of measurements.
The aim of this study was to evaluate the reproducibility of M-mode echocardiography in sequential studies on left ventricular (LV) function. To that end, 3 to 8 serial recordings were performed on 4 groups of healthy subjects (total number, 49) within dissimilar time periods: (1) within 3 h, (2) within 24 h, (3) within 1 to 2 weeks and (4) within 14 to 18 months. The examination technique was carefully standardized and the recordings were analysed by digitization and computer assistance; the data were averaged from 5 beats on each recording. The random variation of LV transverse dimensions and performance was roughly equal in the first 3 of these studies; the mean coefficients of variation ranged from 1.2 to 1.8% for end-diastolic dimension, from 1.7 to 2.3% for end-systolic dimension, and from 2.5 to 3.6% for ejection fraction. In the long-term study the respective mean coefficients were larger: 3.2%, 3.7% and 5.5%. The coefficients of variation for estimates of stroke volume, cardiac output, and peripheral vascular resistance ranged from 4.1 to 8.4% in studies completed within 1 day or inside 1 or 2 weeks but increased to 10-15.5% in the long-term study. The beat-to-beat variability of LV dimensions and performance, as assessed in a subgroup of 11 subjects, was roughly equal in quantity to the variability observed in the long-term study.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Reversibility of alcoholic cardiomyopathy.
A patient with alcoholic cardiomyopathy is described in whom cardiovascular function capacity and radiological heart size fluctuated widely with periods of heavy drinking and abstinence. On two occasions, cessation of drinking resulted in clinical recovery from severe degrees of congestive failure and in complete reversal of cardiac enlargement. Echocardiographic follow-up showed, however, that the true rapidity of myocardial recovery was much slower than estimated clinically and radiologically and than suggested by the previous reports.
Adult↗
[Abdominal pain, impotence and unilateral testicular enlargement in a 51-year-old man].
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Abdomen↗
[Cancer embolization into the lungs].
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Adult↗
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.
Adult↗
Aortic valve closure and cardiac vibrations in the genesis of the second heart sound.
Simultaneous M-mode echocardiograms and external phonocardiograms were recorded in 15 healthy subjects to evaluate the genesis of the second heart sound. The onset of the second sound was found synchronous with the coaptation of the aortic valve cusps and a sharp vibration on the aortic wall. The closed valve was oscillating for 30 to 45 ms after the coaptation of the cusps. Magnified echocardiographic studies of the interventricular septum revealed a consistent, momentary quiver across the septal myocardium a mean of 4 ms after the onset of the second sound. In most subjects, a transient myocardial vibration was observed in temporal association with the first heart sound as well. The present observations suggest that the aortic valve closure initiates the production of the second heart sound, the main audible component resulting, however, from vibrations in the cardiac structures after the valve closure.
Adult↗
Reproducibility of the systolic time intervals: effect of the temporal range of measurements.
The aim of this study was to evaluate the reproducibility of conventionally measured systolic time intervals. To that end, three to eight serial measurements were performed on four different groups of healthy subjects (total number, 49) within dissimilar time periods: 1) within 3 h; 2) within 24 h; 3) within 1 to 2 weeks; and 4) within 14 to 18 months. Judged as the mean coefficients of variation, the variability of the systolic time intervals tended to be smallest in the 3 h measurements and largest in the 24 h measurements. The pooled variances of the serial measurements made within 24 h were in general significantly larger than the respective variances in the measurements made within 3 h. This was due to statistically significant diurnal decreases in left ventricular ejection time and total electromechanic systole in the 24 h study. Otherwise the reproducibility of the method was high. For instance, the mean coefficients of variation for ejection time and total electromechanic systole corrected for heart rate were only 1% and 1.2%, respectively, in serial measurements made at identical diurnal time points within 14 to 18 months. The pooled variances of the measurements made within the shortest and longest temporal ranges were not statistically different. It is concluded that measurement of the systolic time intervals is very applicable to intervention and follow-up studies provided the normal circadian rhythmicity of the phases of systole is adequately taken into account in the design of the study.
Adult↗
Acute effects of alcohol, beta blockade, and their combination on left ventricular function and hemodynamics in normal man.
Twenty-three healthy males, aged 23 to 62 years, were examined by M-mode echocardiography and systolic time intervals for 3 h after (1) ethanol 1 g/kg by mouth taken over 60 minutes; (2) atenolol 100 mg by mouth; (3) ethanol (1 g/kg) + atenolol (100 mg). The peak mean blood ethanol (+/- s.e.) was 112 +/- 4 mg/100 ml in test 1 and 104 +/- 7 mg/100 ml in test 3. During increasing blood ethanol, heart rate (HR), systolic blood pressure (BP), cardiac output (CO) and echocardiographic indices of left ventricular (LV) function were significantly augmented, while total peripheral resistance (TPR) decreased. During declining blood ethanol, systolic BP, LV end-diastolic and end-systolic diameters, stroke volume (SV) and circumferential wall stress were significantly reduced; echocardiographic indices of LV function were unaltered, but the pre-ejection period/LV ejection time ratio was increased. Atenolol decreased HR, systolic BP, SV, CO, and all estimates of LV function, but increased TPR. Ethanol + atenolol tended to cause smaller depressions in the indices of LV function than did atenolol alone, in spite of similar plasma atenolol concentrations (n = 6). It is concluded that ingestion of modest doses of ethanol evokes vasodilation and enhances LV function during increasing blood ethanol, and reduces LV preload and afterload during decreasing blood ethanol without impairing contractility. Social drinking and beta blockade seem not to have any harmful acute combined effects on the heart and circulation, at least in normal subjects.
Adult↗
Drunkenness, hangover, and the heart.
Cardiac effects of ethanol ingestion (1.75 g/kg within 3 hours) were examined in 8 healthy males by echocardiography and systolic time intervals in a controlled study. Heart rate (HR) was increased by 15% (p less than 0.05) during intoxication when blood ethanol (mean +/- SD) was 33.7 +/- 4.1 mmol/l. Left ventricular (LV) end-diastolic dimension was simultaneously shortened by 4% (p less than 0.01) and LV end-systolic dimension by 3% (p less than 0.05). Stroke volume was reduced by 12% (p less than 0.05). Most subjects experienced hangover symptoms 12 hours after the beginning of ethanol intake; blood ethanol was 8.8 +/- 4.0 mmol/l. At this time, HR was raised by 17% (p less than 0.05), ejection fraction by 7% (p less than 0.05), and circumferential fiber shortening velocity by 19% (p less than 0.01); total peripheral resistance was decreased by 17% (p less than 0.001). The resultant increase in cardiac output amounted to 22% (p less than 0.01). In short, the main effect of ethanol at modest blood concentrations was to reduce LV preload without detectably impairing myocardial performance. Hangover was characterized by vasodilation as well as intensified LV myocardial and pump performances.
Adult↗
Cardiovascular effects of acetaldehyde accumulation after ethanol ingestion: their modification by beta-adrenergic blockade and alcohol dehydrogenase inhibition.
Left ventricular function was examined by echocardiography and systolic time intervals in nine healthy male volunteers, who ingested ethanol 0.35 g/kg 4 hr after a 50-mg peroral dose of calcium cyanamide, an aldehyde dehydrogenase inhibitor. Accumulation of acetaldehyde in blood was accompanied by marked increases in heart rate (53%) and cardiac output (78%) as well as by decreases in diastolic arterial blood pressure (19%) and peripheral vascular resistance (46%). Ejection fraction and maximum circumferential fibre shortening velocity increased by 25 and 47%, respectively; the preejection period/ejection time ratio decreased by 31%. 4-Methylpyrazole, an alcohol dehydrogenase inhibitor, efficiently reduced blood acetaldehyde levels when injected intravenously (7 mg/kg) at the height of the reaction. It was as effective as intravenous propranolol (0.1 mg/kg) in attenuating the hyperdynamic circulation and stabilized arterial blood pressure better than propranolol. We conclude that even a very mild alcohol intoxication (30-50 mg/100 ml) causes a marked enhancement of cardiac function, in addition to vasodilation, in subjects with impaired acetaldehyde oxidation. These changes are reversed by preventing acetaldehyde formation through alcohol dehydrogenase inhibition.
Acetaldehyde↗
Acute cardiovascular effects of ethanol A controlled non-invasive study.
The acute cardiac effects of ethanol (1 g/kg orally within 60 minutes) were examined in 22 healthy volunteers (11 men and 11 women) by M-mode echocardiography and systolic time intervals for three hours after beginning ingestion. Each subject also took part in a control study, in which the same volume of juice was substituted for ethanol. Heart rate increased by 15% and cardiac output by 17% during ethanol intake, while total peripheral resistance decreased by 15%. Left ventricular end-diastolic diameter was shortened by 2% during the declining phase of blood ethanol concentration; stroke volume and circumferential wall stress were simultaneously decreased by 7% and 5%, respectively. No ethanol-related changes were noted in echocardiographic indices of left ventricular function, neither were any sex differences observed in the cardiovascular changes after ethanol ingestion. Each of the systolic time intervals was significantly altered even during the control experiment. The responses of each of these intervals to ethanol differed significantly from those in the control test as well. Notably, the pre-ejection period/ejection time ratio rose after ethanol, this change, according to simultaneous echocardiographic data, resulting from reduced preload instead of impaired contractility, as maintained in previous investigations. It is concluded that alcohol in modest doses is capable of altering each of the extramyocardial influences on left ventricular function--heart rate, preload, and afterload--but does not impair myocardial performance, at least in normal subjects.
Adult↗
Alcohol and the heart. Intense hemodynamic changes associated with alcohol flush in orientals.
To evaluate the hemodynamic changes related to alcohol flush, the effects of ethanol intake (0.5 g/kg) were studied by echocardiography and systolic time intervals in 10 Finnish and 9 Japanese healthy volunteers. In 5 Japanese subjects, post-drink facial flush was associated with elevated blood acetaldehyde (peak levels 20-83 mumol/l) and marked cardiocirculatory stimulation. Heart rate was increased directly post ingestion by 65% (p less than 0.01), stroke index by 23% (p less than 0.05), and cardiac index by 106% (p less than 0.05). Diastolic blood pressure was simultaneously decreased by 23% (p less than 0.05), peripheral vascular resistance by 54% (p less than 0.01), and circumferential wall stress by 22% (p less than 0.05); ejection fraction was raised by 26% (p less than 0.01). The other Japanese and the Finnish subjects had no detectable acetaldehyde in blood after ethanol ingestion. The average hemodynamic alterations in them were similar in direction to the changes presented above, but quantitatively 6-10 times smaller (p less than 0.005 for each of these variables). Thus, in Orientals with genetically defective acetaldehyde oxidation, ingestion of even small amounts of alcohol evokes intense enhancement of left ventricular function, probably because of acetaldehyde-induced catecholamine release and peripheral vasodilation.
Acetaldehyde↗
Peripheral hypotensive and central hypertensive effects of cimetidine.
Rapid intravenous (i.v.) injections of high doses (16-128 mumol/kg) of cimetidine induced a short-lasting (5-15 min) hypotension in anaesthetized rats. Diastolic pressure was reduced more than systolic pressure, suggesting vasodilatation. Heart rate was not affected. Diphenhydramine pretreatment (100 mumol/kg i.v.) did not antagonize the hypotensive effect of cimetidine. However, in the presence of diphenhydramine, cimetidine induced bradycardia. Intracerebroventricular administration of cimetidine or metiamide (2 mumol/rat) increased the blood pressure and heart rate. It is concluded that the hypotension after i.v. cimetidine is mediated by peripheral mechanisms. Since diphenhydramine pretreatment had no antagonistic effect cimetidine-induced hypotension could not be due to indirect H1-receptor stimulation caused by histamine liberation.
Animals↗
Possible cardiovascular hazards of the alcohol-calcium carbimide interaction.
Healthy volunteers taking ethanol after pretreatment with calcium carbimide, a drug commonly used in treatment of alcoholism, were studied by echocardiography. Marked facial flushing and accumulation of acetaldehyde after ethanol were accompanied by circulatory acceleration corresponding in magnitude to at least moderate physical exercise. The heart rate (+/- SD) rose from 58 +/- 6 to 107 +/- 11 beats/min (p less than .001) the cardiac output from 4.1 +/- 0.6 to 9.4 +/- 1.1 L/min (p less than .001), and the ejection fraction from 70 +/- 3 to 89 +/- 2% (p less than .001). The systolic blood pressure rose initially from 121 +/- 6 to 143 +/- 5 mmHg (p less than .001). The diastolic blood pressure declined from 80 +/- 0 to 51 +/- 13 mmHg (p less than .01), and the estimated peripheral resistance to one-third of its preethanol level (p less than .001). These marked cardiovascular changes suggest that the ethanol-calcium carbimide interaction can be hazardous to alcoholics with ischaemic or other forms of myocardial diseases.
Acetaldehyde↗
Plasma exchanges in the treatment of rapidly progressive glomerulonephritis associated with chronic dental infection.
A patient is described in whom rapidly progressive, crescentic (in 80% of the glomeruli) glomerulonephritis was associated with chronic dental infection. Eradication of the infection as the sole form of therapy failed to arrest the rapidly advancing renal failure. Institution of plasma exchanges and immunosuppression was accompanied by an abrupt reversal of the renal function and a remission, which until now has lasted for two years.
Aged↗