[Show abstract][Hide abstract] ABSTRACT: Alcohol consumption may have advantageous epidemiologic effects but ethanol also increases the risk of sudden coronary death. Prolongation of QT interval has been reported in chronic alcoholics. Long QT period predisposes to serious arrhythmias, and therefore we studied whether acute alcohol intoxication prolongs repolarization in patients with stable coronary artery disease (CAD).
The effects of acute ethanol steady-state intravenous infusion (0.72 g/kg body weight within 60 min) on QT interval and QT dispersion, assessed by 12-lead electrocardiograms (ECG), were studied in 22 men with stable CAD and in 10 controls. Heart rate variability was measured by Holter recordings.
Mean blood alcohol rose to 26.1 +/- 4.3 mmol/l(1.2 +/- 0.2/1000), and was maintained for 2 h. Heart rate was 56 +/- 7 beats/min before and 54 +/- 8 beats/min during ethanol infusion (NS). The heart rate-adjusted QT interval increased on the average 13-23 ms over the 12-lead ECG (p < 0.005). The QT dispersion remained unaltered. The was no difference in the repolarization response in the patients with CAD compared with the controls. The high- and low-frequency components of heart rate variability remained unaltered.
In middle aged men, regardless of the presence of CAD, moderate amounts of alcohol cause prolongation of ventricular repolarization. Changes in the activity of the autonomic nervous system do not seem to explain the observed phenomenon.
[Show abstract][Hide abstract] ABSTRACT: Inhaled beta-2 agonists raise heart rate, systolic blood pressure and contractility, all of which cause an increase in oxygen consumption of the heart. We performed a study on the influence of inhaled salbutamol on myocardial ischaemia, rhythm, and heart rate variability as assessed by Holter monitoring of 24 patients with coronary artery disease (CAD) and clinically stable asthma or chronic obstructive pulmonary disease (COPD).
In hospital the patients received 0.2 mg (hour 1), 0.4 mg (hour 6), 0.8 mg (hour 13) of salbutamol with a metered-dose inhaler and a spacer, and 5 mg (hour 25) with a nebulizer; symptoms, peak expiratory flow (PEF), 30-h Holter monitoring, and blood pressure (BP) were recorded. The study parameters were compared for the hour preceding and following each dose of salbutamol.
No cardiac symptoms were associated with salbutamol inhalation. PEF increased after all doses (P < 0.005). A dose of 0.2 mg salbutamol induced no changes in heart rate, whereas dose of 0.4 mg increased heart rate from a mean of 75 +/- 13 to 79 +/- 14 beats min-1 (P < 0.005), and a dose of 0.8 mg from 76 +/- 14 to 78 +/- 15 beats min-1 (P < 0.05). No changes in systolic BP appeared after any dose of salbutamol. The diastolic BP was lowered after 0.8 mg of salbutamol from 86 +/- 12 to 82 +/- 10 mmHg (P < 0.05). The 5 mg of nebulized drug provoked no significant changes in heart rate or BP. Myocardial ischaemia, heart rate variability and ventricular arrhythmias remained unaltered with all doses.
The commonly used doses of inhaled or nebulized salbutamol induced no acute myocardial ischaemia, arrhythmias or changes in heart rate variability in patients with CAD and clinically stable asthma or COPD.
Journal of Internal Medicine 05/1998; 243(5):361-6. · 5.79 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: In order to assess additional anti-ischaemic effects of amlodipine (AML) on coronary artery disease (CAD) treated with beta-blockers, 32 patients with CAD, verified on angiograms, and stable angina were randomized to receive 5 mg/day of AML or placebo, increasing to 10 mg/day after 2 weeks. Baseline recording of 24-h ambulatory ECG and blood pressure, echocardiography and bicycle exercise test was repeated after treatment for 2 weeks and for 6 weeks. Reduction of ambulatory ischaemia was not significantly greater with AML than with placebo. In exercise tests the time to 0.1 mV ST segment depression and the total exercise time remained unaltered. Blood pressure was reduced by 10 mg AML. The total variability and the very low frequency component of heart rate were reduced after both doses. The clinical significance of the possible unfavourable change in autonomic modulation of the heart in CAD patients is not known.
[Show abstract][Hide abstract] ABSTRACT: The effects of acute alcohol intake (ethanol blood concentration 1.3 +/- 0.4%) on heart rate variability were evaluated with 24-hour Holter recordings in 20 patients with stable coronary artery disease in a juice-controlled experiment. In the frequency domain analysis, the high-, low-, and very low frequency components were significantly decreased after alcohol: these changes last longer than the elimination of alcohol.
The American Journal of Cardiology 03/1997; 79(4):487-91. · 3.43 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: To evaluate the effect of acute alcohol ingestion on myocardial ischaemia in patients with coronary heart disease and stable angina.
Randomised crossover study using fruit juice with and without ethanol.
Division of cardiology in a university hospital.
20 patients with stable exertional angina and > or = 50% luminal diameter narrowing of at least one major coronary artery.
Each patient was studied on two separate days, once after administration of 1.25 g of ethanol per kilogram of body weight diluted to 15% in juice, and once after an equivalent volume of juice; both tests were in the evening and lasted 90 minutes. The patients were scheduled to have 8 periods of walking for 10 min according to a time table. An ambulatory electrocardiogram and the occurrence of anginal attacks were recorded and blood pressure and blood ethanol concentration were measured until the next morning.
The blood ethanol concentration (mean (SD)) rose to 28.8 mmol/l (1.3 (0.4)/1000). Alcohol raised the systolic blood pressure from 132 (16) to 141 (14) mm Hg (P < 0.05 compared with juice). The mean heart rate increased from 57 (7) to 64 (8) beats/min (P < 0.05) for 13 hours after ethanol ingestion compared with juice. The total duration of ischaemia during the ethanol test was 3.5 (median, range 0-80) min, compared with 0 (range 0-67) min for the juice test (P < 0.05). The difference resulted mainly from more silent ischaemia after ethanol ingestion (2.3 (0-80) v 0 (0-67) min; P < 0.05). The ST segment depression time integral increased during the ethanol test (4.4 (0-170) mm x min) relative to that during the juice test (0 (0-103) mm x min; P < 0.01) and especially during the following 13 hours after alcohol (3.5 (0-123) mm x min) compared with juice (0 (0-67) mm x min; P < 0.005). There were no changes in the number, duration, or ST segment depression time integral of the episodes of symptomatic angina, indicating that ethanol augmented the appearance of silent ischaemia.
Acute heavy ethanol drinking aggravates myocardial ischaemia in patients with stable angina pectoris.
[Show abstract][Hide abstract] ABSTRACT: Profuse spontaneous haemorrhage occurred in association with mediastinitis after median sternotomy for coronary bypass surgery in three men aged 54, 47 and 59 years. The bleeding sites were aorta, right ventricle and saphenous bypass graft. The aortic rupture occurred during closed lavage, the right ventricle ruptured during open saline mediastinal packing and the saphenous vein graft was eroded by a mediastinal drainage tube after discontinuation of closed lavage. This third patient survived and recovered, but the two others died. Previously published reports of 56 patients with 65 bleedings from this rare complication are reviewed. The outcome was fatal in 34% of cases.
Scandinavian journal of thoracic and cardiovascular surgery 02/1996; 30(3-4):167-73.
[Show abstract][Hide abstract] ABSTRACT: We report intermittent mitral valve regurgitation with 17 acute pulmonary edemas over a 16-month period after aortic valve replacement due to combined aortic valve disease in a 51-year-old man. The mechanism of mitral regurgitation was explained by the relatively large size of the prosthetic valve which had had to be sutured partly below the aortic annulus. It was suspected to interfere with the closure of the mildly diseased mitral valve when under pressure or subjected to volume loadings of the left ventricle which provoked free mitral regurgitation. There was no recurrence of pulmonary edema in the 50 months following mitral valve replacement.
International Journal of Cardiology 05/1995; 49(2):131-4. · 6.18 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Although beta-blockers have held their own as the cornerstones of cardiological treatment for almost twenty years, the beneficial effects of these classic agents are not always appreciated in clinical work. Simplified hypertensive treatment or other factors may sometimes argue for the use of newer medicines, but many pathophysiological manifestations of high blood pressure are still best controlled with beta-blockers. The range of available preparations has increased and new compounds are continually appearing on the market.
[Show abstract][Hide abstract] ABSTRACT: A 47-year-old man with apical hypertrophic cardiomyopathy and an apical left ventricular aneurysm with palpitation as the initial manifestation is described. There was no intraventricular pressure gradient. The aneurysm is suggested to be a part of the myocardial disease or to be caused by myocardial bridging of the left anterior descending coronary artery demonstrated by angiography. The 24-hour ambulatory ECG recording showed only isolated ventricular ectopic beats and the clinical course has been favorable during 20 months without therapy.
[Show abstract][Hide abstract] ABSTRACT: Cytomegalovirus infections are common disorders after heart transplantations. Manifestation of the virus without a clinical disease is still more prevalent. Differentiation of clinical infections from cytomegalovirus activations without major pathogenetic importance issues a challenge in the follow-up of patients with cardiac transplants. The case describes a 56-year-old female patient with a multiple organ lethal infection and myocarditis due to cytomegalovirus diagnosed during life with endomyocardial biopsy.
[Show abstract][Hide abstract] ABSTRACT: 1. Eight healthy subjects were studied before digoxin and after successive therapy periods of 1 week 0.125, 0.25 and 0.50 mg of digoxin. The mean serum concentrations (+/- s. d.) were 0.4 +/- 0.2, 0.6 +/- 0.3 and 1.4 +/- 0.5 nmol l-1, respectively. The effects of digitalis were studied by echocardiography and systolic time intervals at rest and after 3 min handgrip exercise. Effects of simultaneous autonomic blockade induced by atropine and propranolol were also examined. 2. Digoxin in increasing doses slowed the heart rate at rest; with the daily dose of 0.50 mg from 63 +/- 10 to 53 +/- 6 beats min-1, and fractional shortening rose from 28 +/- 6 to 33 +/- 3% (P less than 0.05 for both). Preload, afterload and cardiac output did not change. The electromechanic systolic time index (QS2I) decreased (P less than 0.001) and the observed alteration of QS2I was dose-related. 3. The influence of digoxin was similar during isometric exercise, except for unchanged fractional shortening. 4. During autonomic blockade digoxin slowed the intrinsic heart rate from 93 +/- 6 to 86 +/- 6 beats min-1 (0.25 mg) and to 83 +/- 6 beats min-1 (0.50 mg) (P less than 0.01 for both). QS2I was shortened (P less than 0.01). Echocardiographically determined ejection phase indices remained unchanged. 5. When handgrip stress was induced during autonomic blockade, digoxin evoked a clearcut increase in contractile function, resembling the effects of digoxin alone at rest. Thus, fractional shortening increased by 14% and QS2I decreased by 16 ms (P less than 0.01 for both). 6. We conclude that digoxin increases the contractility in normal heart without changes in loading conditions. The rise in inotropy at rest is obvious from both fractional shortening by echo and systolic time intervals. The same takes place during handgrip with autonomic blockade, when the heart lacks sympathetic support. The influence of long-term digoxin on heart rate is partly direct without autonomic mediation. The effect of digoxin is dose-dependent.
British Journal of Clinical Pharmacology 04/1988; 25(3):331-40. · 3.69 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Eleven patients suffering from heart failure were treated with oral ibopamine, a di-isobutyric ester of N-methyldopamine, 100 mg three times a day for 1 week and 200 mg three times a day for 3 weeks. Therapy was discontinued by one patient because of tachycardia. Left ventricular performance was evaluated with echocardiography and systolic time intervals at rest and after 3 minutes of isometric exercise using a handgrip. Six of 10 patients completing the study were in New York Heart Association (NYHA) functional class III, 2 in class IV, and 2 in class II. All patients, except one who remained stable in class II, improved their subjective condition by one functional class during 4 weeks of therapy (p less than 0.01). There were no changes in heart rate, blood pressure, rate-pressure product, cardiac index, or total peripheral vascular resistance. The left ventricular end-systolic diameter decreased after four weeks from 71.2 +/- 12.7 (SD) to 65.9 +/- 13.0 mm (p less than 0.001); the left ventricular end-diastolic diameter did not change. The ejection fraction increased from 26 +/- 8 to 32 +/- 9% (p less than 0.01). Afterload, that is, left ventricular circumferential systolic wall stress, declined as a result of decreased systolic diameter. Systolic time intervals did not vary. There were no changes due to ibopamine during isometric exercise probably owing to increased beta-adrenergic stimulation induced by the handgrip. Neither urine volume nor body weight changed. Side effects were mild except for tachycardia of one patient.(ABSTRACT TRUNCATED AT 250 WORDS)
[Show abstract][Hide abstract] ABSTRACT: The etiology and clinical course of acute nontraumatic rhabdomyolysis and ensuing renal failure was surveyed in a series of 40 consecutive patients. In 28 cases the muscle damage occurred after excessive consumption of ethyl alcohol and/or other intoxications. Prolonged lying immobilized was the reason or contributing factor for rhabdomyolysis in 22 cases. The other evident etiologies were convulsions, vigorous physical exercise, arterial occlusion and hypothermia. Typical local signs of rhabdomyolysis--pain, swelling and weakness of the affected muscles--were absent in one fourth of the patients. In these cases the diagnosis was based on transient elevation of serum creatine kinase enzyme activity. Dialyses were required to manage acute renal failure in 24 subjects. All 36 survivors recovered normal renal function. Neurological defects in the extremities still persisted in 16 patients at three months' follow-up.
Scandinavian Journal of Urology and Nephrology 02/1988; 22(4):305-8. · 1.06 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Sixteen healthy young volunteers were studied with echocardiography and systolic time intervals at rest and after three minutes' isometric exercise before and during autonomic blockade with atropine and propranolol. Isometric exercise increased cardiac output by raising the heart rate from 64 +/- 3 to 72 +/- 4 bpm (SEM) (p less than 0.01). Mean blood pressure increased from 86 +/- 2 to 104 +/- 3 mmHg (p less than 0.001) without any changes in the calculated total peripheral vascular resistance. Afterload (left ventricular systolic wall stress) rose but preload (left ventricular end-diastolic diameter, LVEDD) did not change. There was no variation in fractional shortening, maximal velocity of circumfertial fibre shortening (VCFmax) or pre-ejection period (PEP) despite increased afterload. This indicates stimulated intropy during isometric exercise. Autonomic blockade enhanced cardiac output by increasing heart rate from 64 +/- 3 to 97 +/- 2 bpm (p less than 0.001). Mean blood pressure rose from 86 +/- 2 to 93 +/- 2 mmHg (p less than 0.01) while vascular resistance fell. Afterload did not change but LVEDD shortened form 45.5 +/- 0.9 to 43.5 +/- 0.9 mm (p less than 0.001). Preload-independent VCFmax did not increase despite raised heart rate. PEP rose from 99 +/- 4 to 107 +/- 3 ms (p less than 0.01) and fractional shortening fell from 29 +/- 1 to 25 +/- 1% (p less than 0.001); these changes were greater than expected from the reduced preload. Consequently autonomic blockade seems to impair myocardial contractility despite vagal dominance at rest. Heart rate and cardiac output were not influenced by isometric exercise during autonomic blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
Annals of clinical research 02/1988; 20(3):169-76.
[Show abstract][Hide abstract] ABSTRACT: Nine healthy volunteers were studied with echocardiography and systolic time intervals at rest and after 3 minutes' isometric exercise by hand grip. The recordings were repeated after intravenous administration of 1 mg digoxin before and after autonomic blockade induced with atropine and propranolol. During hand grip the heart rate rose from 61 +/- 3 (mean +/- SEM) to 73 +/- 5 bpm (p less than 0.05). Afterload, i.e. left ventricular systolic wall stress, increased by 21% from 260 +/- 19 x 10(3) dyn/cm2 (p less than 0.05). Preload, i.e. left ventricular end-diastolic diameter (LVEDD), fractional shortening and the ratio of the pre-ejection period to the left ventricular ejection time (PEP/LVET) did not change, indicating increased contractility. After digoxin heart rate rose during handgrip from 50 +/- 2 to 65 +/- 5 bpm, and wall stress increased by 19% from 274 +/- 21 x 10(3) dyn/cm2 (p less than 0.01 for both). Even though LVEDD rose from 44.8 +/- 1.4 to 46.6 +/- 1.3 mm (p less than 0.05), fractional shortening decreased from 33 +/- 2 to 30 +/- 2% (p less than 0.05) and PEP/LVET increased from 0.292 +/- 0.014 to 0.327 +/- 0.014 (p less than 0.01). This suggests that autonomic reflexes due to digoxin obscured the increase in inotropy during static exercise. Autonomic blockade raised heart rate under digoxin from 50 +/- 2 to 90 +/- 4 bpm and mean blood pressure from 87 +/- 2 to 99 +/- 3 mmHg (p less than 0.001 for both) without changes in loading conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
Annals of clinical research 02/1987; 19(6):383-90.