PubMed Health⌕ Search

Biomedical subjects

H Just

Publications and source records attributed to H Just.

At least 19 recordsLinked to original sources
PubMed1992

Patent foramen ovale in patients with haemodynamically significant pulmonary embolism.

The prevalence of a patent foramen ovale is about 1 in 4. In cases with venous thromboembolism and raised right heart pressures, a patent foramen ovale may permit paradoxical emboli, which could complicate the course of patients with pulmonary embolism. Echocardiography enables detection of a patent foramen ovale in life. We have studied 85 patients who presented with haemodynamically significant pulmonary embolism as judged by clinical, echocardiographic, or haemodynamic indices and who had an echocardiographic evaluation for patent foramen ovale. 33 patients (39%) had a patent foramen ovale. Clinical symptoms suggestive of paradoxical embolism were more likely in patients with than in those without a patent foramen ovale (39% vs 6%, p = 0.00034), with new neurological deficits occurring in 11 patients (9 vs 2, p = 0.005) and a vascular occlusion in 8 (7 vs 1, p = 0.0096). Arterial oxygen tension was lower in patients with a patent foramen ovale (mean 55 [SD 14] vs 62 [16] mm Hg, p = 0.038). Mortality was not different between the two groups (27% vs 19%). Cardiopulmonary complications in terms of resuscitation, intubation, or the use of catecholamines were more frequently observed in patients with a patent foramen ovale (48% vs 23%, p = 0.028). Patients with a patent foramen ovale and haemodynamically significant pulmonary embolism are more likely to have arterial hypoxaemia and vascular occlusions, possibly due to paradoxical emboli.

Adult↗
PubMed1992

Endothelial function in chronic congestive heart failure.

There is evidence that the endothelium plays an important role in the control of human vascular tone by releasing endothelium-derived nitric oxide. The hypothesis that an impairment of this mechanism is involved in the increased peripheral vasoconstriction of patients with chronic congestive heart failure (CHF) was tested. Acetylcholine and N-monomethyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthesis from L-arginine, were infused in the brachial artery of healthy volunteer subjects (controls) and patients with severe CHF. The radial artery diameter was determined by a high-precision A-mode ultrasound device, using a 10 MHz probe. Forearm blood flow was calculated from vessel diameter and blood flow velocity measured simultaneously by Doppler. The blood flow response to acetylcholine was blunted in patients with CHF compared with that in control subjects. In contrast, the decrease in blood flow induced by L-NMMA was exaggerated in CHF, and the blood flow response to nitroglycerin was preserved. The changes in radial artery diameter induced by acetylcholine and L-NMMA were not significant in control subjects and CHF patients, but dilation of the radial artery by nitroglycerin was significantly reduced in CHF. The results demonstrate an impaired endothelium-dependent dilation of forearm resistance vessels in CHF, suggesting a reduced release of nitric oxide on stimulation. In contrast, the basal release of nitric oxide from endothelium of forearm resistance vessels is preserved or may even be enhanced, and may play an important compensatory role in chronic CHF by antagonizing neurohumoral vasoconstrictor forces in CHF.

Acetylcholine↗
PubMed1992

Alterations of the force-frequency relationship in the failing human heart depend on the underlying cardiac disease.

We investigated the force-frequency relationship (0.5-3 Hz) in non-failing human myocardium and in end-stage failing human myocardium due to dilated cardiomyopathy or subacute myocarditis. In non-failing myocardium, force of contraction increased with increasing stimulation frequency. In end-stage heart failure, the force-frequency relationship was inverse in myocardium from dilated cardiomyopathy, but was similar to control in myocardium from subacute myocarditis. After increasing extracellular Ca(2+)-concentration from 2.5 to 7.2 mM, the shape of the force-frequency relationship was not changed in nonfailing myocardium. In dilated cardiomyopathy, the decline in force with increasing frequencies was even more pronounced at 7.2 mM compared to 2.5 mM extracellular Ca2+. In subacute myocarditis, at Ca2+ 7.2 mM, increasing frequencies increased force in the lower frequency range (less than 1.75 Hz) only, whereas at higher stimulation rates force declined again. These results indicate that (1.) alterations of the force-frequency relationship in the failing human heart depend on the underlying cardiac disease and/or the time-course of the disease, and (2.) an increase in the extracellular Ca(2+)-concentration aggravates changes in the force-frequency relationship in the failing myocardium.

Calcium↗
PubMed1992

Contractile protein function in failing and nonfailing human myocardium.

Isometric heat and force measurements were used to relate mechanical performance to function of contractile proteins in muscle strips from failing and nonfailing human hearts (37 degrees C, 60 beats per minute). Compared to control myocardium, crossbridge behavior was altered in myocardium from hearts with end-stage failing dilated and ischemic cardiomyopathy, resulting in increased crossbridge force-time integral by 33% and 36%, respectively. Peak isometric twitch tension was reduced significantly by 46% in muscle strips from hearts with dilated cardiomyopathy. In myocardium from hearts with ischemic cardiomyopathy peak isometric twitch tension was comparable to values from nonfailing hearts. Including all three types of myocardium, there was a close correlation between the number of crossbridge interactions during the isometric twitch (tension-dependent heat) and peak twitch tension (r = 0.88; p less than 0.001). Compared to control, in failing myocardium from dilated cardiomyopathic hearts, tension-independent heat (calcium cycling) was significantly reduced. This indicates that in dilated cardiomyopathy reduced peak twitch tension results from decreased calcium activation of contractile proteins with reduced number of crossbridge interactions during the isometric twitch. In ischemic cardiomyopathy mechanisms different from those observed in dilated cardiomyopathy seem to be involved in the development of heart failure.

Actomyosin↗
PubMed1992

Modulation of myocardial sarcoplasmic reticulum Ca(++)-ATPase in cardiac hypertrophy by angiotensin converting enzyme?

Myocardial hypertrophy in response to hemodynamic overload is an established risk factor for cardiovascular morbidity and mortality. Partially, this may be due to alterations in cardiac gene expression, resulting in a more fetal-like myocyte phenotype with a fragile Ca(++)-homeostasis. Depressed expression of the sarcoplasmic reticulum Ca(++)-ATPase is the hallmark of this overload phenotype, contributing to prolonged cytosolic Ca(++)-transients, disturbed diastolic relaxation, altered force-frequency relation, and probably, electrophysiologic instability with susceptibility to malignant arrhythmias. Since angiotensin II is a growth-promoting factor in several cellular systems, the local formation of angiotensin II within the myocardium might contribute to the trophic response and the phenotype shift of overloaded myocardium. Several observations are consistent with this hypothesis: the cardiac expression of ACE and angiotensinogen is enhanced in experimental myocardial overload and in human endstage congestive heart failure; prolonged observations of experimental cardiac overload with hypertrophy-induced putative normalisation of myocardial systolic wall stress demonstrated a renormalization of ventricular tissue ACE activity and of ventricular sarcoplasmic Ca(++)-ATPase expression and activity; normalizing ventricular tissue ACE activity in experimental cardiac overload by chronic nonhypotensive ACE inhibitor therapy caused a parallel partial normalization of hypertrophy and underexpression of sarcoplasmic CA(++)-ATPase. This partial normalization of myocyte Ca(++)-homeostasis in overload hypertrophy by non-hypotensive chronic ACE-inhibition is attenuated by concomitant chronic application of bradykinin-2 receptor blockade, indicating an involvement of altered bradykinin metabolism in the phenotype modulation due to chronic ACE inhibition. While these observations are consistent with a direct influence of local ACE activity on the sarcoplasmic reticulum, the cell type contributing to the enhanced ACE expression in overload and the specific mechanism of this influence are unknown.

Animals↗
PubMed1992

Energetics of calcium cycling in nonfailing and failing human myocardium.

Using sensitive antimony-bismuth thermopiles, isometric force and heat output were measured in muscle strips from nonfailing human hearts and from failing dilated cardiomyopathic hearts at a stimulation rate of 60 beats per minute (37 degrees C). This frequency was chosen because analysis of the force-frequency relation showed significant differences in isometric force between failing and nonfailing human myocardium at 60 beats per minute and at higher frequencies, whereas at lower rates of stimulation (30 beats per minute) force of contraction was similar in failing and nonfailing myocardium. The liberated initial heat was partitioned into its two components, tension-dependent heat and tension-independent heat from high-energy phosphate hydrolysis by contractile proteins and excitation-contraction coupling processes, respectively. Tension-dependent heat reflects the total number of crossbridge interactions, and tension-independent heat is an index of the amount of calcium cycling during the contraction-relaxation cycle. In failing compared to nonfailing human myocardium, peak twitch tension, maximum rate of tension rise and maximum rate of tension fall were reduced significantly. Reduced mechanical performance was associated with reduced liberation of both tension-dependent and tension-independent heat in the failing heart. The reduction of tension-dependent heat by 61% and of tension-independent heat by 69% indicate considerable decreases in the number of crossbridge interactions activated and calcium ions cycled during the isometric twitch. In addition, the rate of calcium removal was reduced in the failing human heart as is indicated by a 71% reduction in tension-independent heat rate. The efficiency of excitation-contraction coupling with respect to crossbridge activation was similar in failing and nonfailing myocardium. These data indicate that impaired myocardial performance in dilated cardiomyopathy may result from disturbed excitation-contraction coupling with reduced amount of calcium cycling and reduced rate of calcium removal.

Calcium↗
PubMed1992

Percutaneous mitral balloon valvuloplasty--a comparative evaluation of two transatrial techniques.

The efficacy and safety of two different percutaneous transfemoral mitral balloon valvuloplasty procedures were evaluated in 45 patients. A double-balloon technique with Mansfield balloons was applied in the first 22 patients (group A), and an Inoue single-balloon technique was used in the subsequent 23 patients (group B). Mean diastolic gradient decreased from 17 +/- 7 mm Hg to 8 +/- 3 mm Hg (p < 0.001) in group A and from 13 +/- 4 mm Hg to 8 +/- 3 mm Hg (p < 0.001) in group B. The mitral orifice area increased from 1.1 +/- 0.3 cm2 to 2.2 +/- 0.8 cm2 (p < 0.001) in group A and from 1.2 +/- 0.4 cm2 to 1.7 +/- 0.7 cm2 (p < 0.001) in group B. The length of the total procedure and the total fluoroscopy time were considerably shorter in group B (86 +/- 24 minutes and 18 +/- 7 minutes) compared with group A (128 +/- 38 minutes and 35 +/- 14 minutes; p < 0.001). Mitral regurgitation (grade 3/4) was observed after the procedure in two patients in group A but in nine patients in group B. Cardiac tamponade occurred in two patients in group A, but no major complications were seen in group B. The Inoue single-balloon technique seemed to be safe, easier to perform, and equally effective.

Adult↗
PubMed1992

Arrhythmias during the acute phase of reperfusion therapy for acute myocardial infarction: effects of beta-adrenergic blockade.

In 107 patients with acute myocardial infarction, the incidence of ventricular arrhythmias during the acute phase of thrombolysis was examined by means of Holter monitoring. In patients with a patient infarct-related artery as assessed angiographically at 90 minutes, the occurrence of accelerated idioventricular rhythms was noted significantly more frequently than in patients with a permanent occluded vessel. This arrhythmia peaked in the first 180 minutes after the start of thrombolysis. In addition, single ventricular premature beats and runs of ventricular tachycardia were also more common in patients with successful reperfusion. The effects of acute intravenous administration of beta-blockers were examined in 66 patients without contraindications to this therapeutic approach. There were no differences in the occurrence of any type of rhythm disorders in patients with (n = 43) or without beta-blockade (n = 23). Thus ventricular arrhythmias particularly accelerated idioventricular rhythms, and single ventricular premature beats occur more frequently in patients with a patent infarct artery within the first 24 hours after thrombolysis. Acute intravenous beta-blockade does not appear to exert significant antiarrhythmic effects during this period.

Adrenergic beta-Antagonists↗
PubMed1992

Efficacy and safety of sotalol in patients with complex ventricular arrhythmias.

Sotalol is a unique beta-blocker that prolongs repolarization. Its use in 626 patients with complex ventricular ectopic activity, as reported in the literature, resulted in suppression of arrhythmia in 50 to 60% of treatment attempts. Detailed analysis of data on arrhythmias in 356 patients that were entered prospectively into a database revealed a median reduction in ventricular premature beats of 76%, compared to a median suppression of repetitive ventricular ectopic activity of 91% and of episodes of nonsustained ventricular tachycardia of 97% (p = 0.002 vs reduction of ventricular premature beats). This marked antiarrhythmic potency of sotalol in repetitive ventricular arrhythmias is thought to be due to its class III activity. Drug efficacy was independent of age, sex, the presence or absence of organic heart disease and the degree of sotalol-induced prolongation of corrected QT interval. Evaluation of left ventricular function in 215 patients treated with the drug demonstrated that depression of left ventricular ejection fraction occurred far less frequently than expected with conventional beta-blockers. Even patients with severely depressed pump function tolerated sotalol surprisingly well. There is a propensity of the drug to aggravate arrhythmia, which resulted in serious proarrhythmic events in 30 (3.5%) of 853 patients. These often consisted of torsades de pointes (9 of 30 patients). Proarrhythmia occurred primarily within the first 3 days of dosing, and exhibited a dose-dependence. In conclusion, sotalol is an effective and well-tolerated antiarrhythmic drug in patients with complex ventricular ectopic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effects of amiodarone versus quinidine and verapamil in patients with chronic atrial fibrillation: results of a comparative study and a 2-year follow-up.

Rapid, reliable and safe reestablishment of sinus rhythm is the major aim of pharmacologic treatment in patients with chronic atrial fibrillation. The mainstay of therapy in this arrhythmia has been quinidine. More recently, amiodarone was shown in non-comparative studies to be superior to class IA agents under certain conditions. In 40 patients with atrial fibrillation persisting for 4 weeks up to 2 years, the efficacy and safety of either quinidine and verapamil (days 1 to 3, quinidine 1,500 mg/day; days 4 to 6, quinidine 1,500 mg + verapamil 240 mg/day) or amiodarone therapy (days 1 to 3, amiodarone 1,200 mg/day intravenously; days 4 to 14, amiodarone 800 mg/day orally) were randomly examined. Responders continued on their effective medication for 3 months. Thereafter, all patients were treated with a fixed regimen of quinidine (480 mg/day) plus verapamil (240 mg/day) for up to 2 years. During atrial fibrillation, quinidine reduced mean ventricular cycle length by 40 ms (-5%), quinidine and verapamil increased mean cycle length by 57 ms (8%) and amiodarone by 192 ms (28%, p less than 0.01). In addition, quinidine and verapamil had a characteristic "rate-smoothing" effect on atrioventricular conduction during atrial fibrillation. The rhythm was converted to sinus rhythm after quinidine in 5 (25%) of 20 patients and after the combination of quinidine and verapamil in 11 (55%) of 20 patients. Amiodarone restored sinus rhythm in 12 (60%) of 20 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗
PubMed1992

Short- and long-term antiarrhythmic and hemodynamic effects of d,l-sotalol in patients with symptomatic ventricular arrhythmias.

The antiarrhythmic and hemodynamic effects of sotalol (160 to 480 mg/day), a beta-blocking agent that prolongs ventricular repolarization, were examined in 38 patients with complex symptomatic ventricular ectopic activity. During ambulatory monitoring, 24 patients (63%) exhibited a reduction of greater than 75% in single ventricular premature beats (VPBs) and greater than 90% reduction in repetitive arrhythmia. In contrast to the effects of other agents, left ventricular ejection fraction as determined by radionuclide angiography was not impaired, increasing slightly from 45 +/- 14% to 47 +/- 14% during therapy (p less than 0.05). Antiarrhythmic drug efficacy did not correlate with baseline ejection fraction or sotalol-induced changes in ventricular function. Late follow-up studies disclosed that antiarrhythmic efficacy and tolerance were maintained in the majority of patients. Repeat radionuclide angiography at 6 months revealed no late drug-induced depression of left ventricular function. Sotalol appears to be an effective and well tolerated agent for treatment of complex ventricular ectopic activity, even in the setting of compromised cardiac function.

Adult↗
PubMed1992

ST segment analysis for assessment of coronary artery patency: comparison of surface ECG and Holter recordings.

In a prospective trial in 124 patients with acute myocardial infarction, Holter and surface ECG recordings were obtained simultaneously and compared for their ability to assess thrombolysis-induced ST segment changes. Accuracy in predicting patency of the infarct-related artery was evaluated in both methods. Success or failure of thrombolysis was determined angiographically 90 min after the start of therapy. For both methods, sensitivity, specificity, and positive predictive value for correct prediction of the perfusion status ranged between 64% and 92%. However, the negative predictive value was considerably lower (40-53%). There were no significant differences in any parameter evaluated for either method. Thus, two surface ECG recordings before and 2 h after the start of therapy yield the same predictive value as continuous Holter monitoring with respect to thrombolysis-induced coronary artery reperfusion. However, for triage of patients to early coronary interventions, more sophisticated methods are needed for non-invasive prediction of coronary artery patency due to the low negative predictive value of ST segment analysis.

Adult↗
PubMed1992

Intraindividual reproducibility of heart rate variability.

Heart rate variability was determined from three consecutive Holter recordings performed on days 1, 7, and 28 in 17 normal subjects, in 13 patients with angiographically normal coronary arteries, and in 9 patients with remote myocardial infarctions. Group data of several time and frequency domain measures of heart rate variability were highly reproducible (correlation coefficients 0.629-0.894). However, some individuals exhibited considerably larger day-to-day variations in heart rate variability. Single heart rate indices differed by up to 50% between two Holter recordings. Such potential differences must be considered when repeated heart rate variability determinations are used to assess changes in neurocardiac reflex regulation or effects of therapeutic interventions.

Chest Pain↗
PubMed1992

Short-term and long-term treatment with propafenone: determinants of arrhythmia suppression, persistence of efficacy, arrhythmogenesis, and side effects in patients with symptoms.

OBJECTIVE: To assess the clinical criteria predicting the short and long-term efficacy of propafenone, an agent with class IC antiarrhythmic activity and a broad pharmacological profile. DESIGNS: Prospective study of propafenone at doses of 450 to 900 mg/day during a six week dose titration period (including a placebo phase with two separate 24 Holter recordings). Responders to treatment were followed for one year. PATIENTS: One hundred patients with frequent ventricular arrhythmias (greater than 30 extrasystoles/h) of Lown class III and IVA/B and without evidence of myocardial infarction within the past six months. ANALYSIS: Multivariate regression analysis of spontaneous arrhythmia variability and of different clinical variables to determine the short and long-term efficacy and safety of propafenone. MEASUREMENTS AND MAIN RESULTS: Propafenone 450 mg/day was effective in 30/100 patients (30%), and at 600 mg/day another 14 responded. The efficacy of propafenone correlated with a low spontaneous arrhythmia variability and, as shown by multivariate analysis, with a lower patient age (p less than 0.05). When the dose was increased to 900 mg/day a further six (12%) patients responded. However, with increasing doses of propafenone, the one year probability of effective treatment decreased from 86% (450 mg/day) to 67% (600 mg/day) and to 44% (900 mg/day). After restudying the patients at three, six, and 12 months and after dose adjustment in 11/44 patients (25%), 31 patients (70%) remained responders. Loss of permanent antiarrhythmic efficacy was best predicted by the initial dose that achieved a response. No patient died suddenly or had arrhythmogenic effects during Holter monitoring. Side effects occurred in 36% of patients but these rarely limited long-term treatment. CONCLUSIONS: A younger age, low spontaneous arrhythmia variability, and particularly a low titration dose were the best predictors of the short and long term efficacy of propafenone. All other responders should have repeated Holter recordings during the first year of treatment.

Adult↗
PubMed1992

Prevalence, circumstances, mechanisms, and risk stratification of sudden cardiac death in unipolar single-chamber ventricular pacing.

BACKGROUND: Permanent cardiac pacing is well established for the improvement of prognosis and quality of life in patients with severe bradycardia. However, sudden cardiac death still remains an unresolved problem, as it occurs in approximately 20-30% of paced patients. This 2-year follow-up study was directed at prospectively assessing prevalence, circumstances, and mechanisms of sudden death in 2,021 permanently paced patients. METHODS AND RESULTS: During the observation period, 220 patients (11%) died (mean pacing interval, 50.5 +/- 7 months). Lethal cerebrovascular events in 66 of 220 patients (30%) and sudden death in 49 of 220 patients (23%) were the two most frequently reported modes of death. Nonsudden (first year, 20%; subsequent years, 6.9%; p less than 0.01) and sudden death mortality rate (4% versus 1.8%, p less than 0.05) were highest during the first year. Mortality was unrelated to the patient's activity status at the time of death. Sudden cardiac death occurred more often in male patients (increased risk, 1.7 versus female patients; p less than 0.001) and patients younger than 60 years of age (5.2 versus patients older than 60 years, p less than 0.001). Patients with severe bradycardia (sudden death rate, 28%), severe atrioventricular block (25%), or atrial fibrillation with low ventricular rate (25%) before pacemaker implantation were more likely to suffer from sudden cardiac death than patients with previous syncopal attacks (sudden death rate, 15%) or sick sinus syndrome (17%). The highest incidence of sudden death was observed in patients with bifascicular and trifascicular bundle branch block. In this group, 35% of patients died suddenly during the follow-up period compared with 18% of patients without bundle branch block. In a subsequent study in 90 consecutive patients with various types of bundle branch block, undersensing of up to 13% of ectopic ventricular beats occurred in patients with bifascicular block. Pacing-induced tachyarrhythmias and ventricular fibrillation were documented in 10% of undersensed ectopic ventricular beats as well as in the setting of atrial fibrillation associated with ventricular arrhythmias. CONCLUSIONS: Young age, male sex, and a severely diseased heart indicated by the presence of bifascicular and trifascicular bundle branch block are the strongest predictive clinical parameters for sudden cardiac death, especially in the first year after pacemaker implantation.

Aged↗