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Biomedical subjects

H Just

Publications and source records attributed to H Just.

At least 253 records · Page 14Linked to original sources
PubMed1989

[Status of the technic of angiography procedures].

Angiocardiography continues to expand inspite of competitive non-invasive imaging techniques (echocardiography, CT, nuclear magnetic resonance). Only angiography yields images of sufficient spatial and temporal resolution as they are needed for coronary diagnostic work and interventional catheter therapy. Angiographic systems are mono- or biplane with high degree of mobility and flexibility for oblique and angulated projections. Currently available systems do not fulfill the requirements. Image resolution and contrast are today satisfactory, however, still not sufficient for interventional techniques. Only digital image processing will allow further improvement, thereby enhancing contrast and detail while reducing radiation dose (pulsed, high-contrast fluoroscopy, on-line image processing). Cine-filming seems not needed in all cases. In the future, angiocardiography will hardly be needed for study of cardiac chambers, valves or great vessels. Instead, specialized systems of extreme mobility and flexibility with high resolution and digital image processing for image improvement and documentation, radiation reduction for coronary and general arterial diagnostic and therapeutic interventions will be developed.

Angiocardiography↗
PubMed1989

[Ventricular arrhythmia in silent myocardial ischemia--diagnosis and clinical relevance].

Silent myocardial ischemia and ventricular arrhythmias were known to be independent risk factors in patients with coronary artery disease. This has become more important since the technique of Holter monitoring has been improved and has demonstrated a high incidence of silent myocardial ischemia in the majority of patients with coronary artery disease, as well as a close relation to the occurrence of sudden cardiac death. Unfortunately, prospective data on the interaction of both risk factors are missing. We therefore studied patients undergoing exercise-testing, percutaneous transluminal angioplasty and 24-h-Holter-monitoring to assess such an interaction. During exercise testing the total incidence of ventricular arryhthmias in patients with asymptomatic ST segment depression was 42%; 6% of patients had frequent ventricular arrhythmias, 6% had ventricular pairs, and 1% had ventricular tachycardia. The incidence was similar to patients with symptomatic ST depression, but was 3.2-times higher as compared to patients without ST segment depression. During 103 attempts of percutaneous transluminal angioplasty, in 26 patients ventricular arrhythmias occurred, the incidence of ventricular tachycardia was 1-3%. No difference was observed for symptomatic and asymptomatic attempts. In 36 patients with severe coronary stenosis (greater than 90%) 24-h-Holter-monitoring showed 145 episodes of myocardial ischemia with a total duration of 967 min; two-thirds of episodes were asymptomatic. The incidence was similar in patients with symptomatic and asymptomatic episodes of myocardial ischemia, but 30 to 50-times higher as compared to the interval with ischemia. In summary, episodes of myocardial ischemia have a higher risk of ventricular arrhythmias, however, there is no difference between symptomatic and asymptomatic myocardial ischemia.

Arrhythmias, Cardiac↗
PubMed1988

Regional blood flow in congestive heart failure: concept of compensatory mechanisms with short and long time constants.

With physiologic stress to the cardiovascular system, some circulatory compensatory mechanisms are designed to restore homeostasis quickly (e.g., sympathetic nervous system activation and the Frank-Starling mechanism). These compensatory mechanisms are not nearly as effective when there is a chronic pathologic stress such as congestive heart failure (CHF). In this circumstance, other mechanisms that operate with longer time constants come into play (e.g., activation of the renin-angiotensin-aldosterone system, myocardial hypertrophy and deconditioning). The most successful chronic drug therapies of CHF are those that are designed to reverse the latter group of compensatory mechanisms, a process that is slow. It takes especially long to reverse those CHF-induced changes in blood vessels and skeletal muscle metabolism that are activated to cope with inadequate delivery of oxygenated blood to working muscles. The concept that compensatory mechanisms have either short or long time constants for activation, effectiveness and reversal may help explain why the improvement in exercise tolerance with effective heart failure therapy lags behind hemodynamic improvement.

Adaptation, Physiological↗
PubMed1988

Skeletal muscle blood flow, metabolism and morphology in chronic congestive heart failure and effects of short- and long-term angiotensin-converting enzyme inhibition.

Blood flow to skeletal muscle during exercise is limited in patients with chronic congestive heart failure compared with normal persons. This may, in part, be attributed to the inability of the vessels to dilate adequately. In addition, an abnormal skeletal muscle metabolism with oxidative capacity can be demonstrated in patients with chronic congestive heart failure. The latter may partially explain why vasodilators and inotropes that improve central hemodynamics, global leg perfusion or skeletal muscle blood flow during exercise do not increase oxygen uptake by working muscle after acute drug administration. Furthermore, increases in blood flow to skeletal muscle may be redistributed to inactive or less oxygen-dependent muscle fibers. Although acute angiotensin-converting enzyme inhibition usually neither exerts substantial improvement in exercise hemodynamics nor interferes with leg perfusion during exercise, skeletal muscle blood flow and oxygen uptake gradually increases with long-term angiotensin-converting enzyme therapy, leading to improved systemic oxygen consumption and exercise tolerance. Several factors, such as reduction in plasma and vascular angiotensin II and sympathetic nervous activity, increased prostaglandin levels and renal function may contribute to this beneficial long-term effect.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1988

Influence of enoximone and UDCG-115 on coronary hemodynamics in idiopathic dilated cardiomyopathy.

Coronary hemodynamics were studied in 24 patients with idiopathic dilated cardiomyopathy and in 17 patients without any significant heart disease under resting conditions using the argon method. Neither myocardial blood flow normalized for 100 g muscle tissue nor myocardial oxygen consumption per minute (MVO2) or oxygen supply-demand ratio were different between these 2 groups of patients. When enoximone (1 to 2 mg/kg body weight) was given intravenously in patients with idiopathic dilated cardiomyopathy, myocardial oxygen consumption decreased by only 8% (difference not significant), whereas a significant (p less than 0.05) 26% decrease of myocardial oxygen consumption was observed after UDCG-115 (1.25 mg/hour intravenously). However, with both substances the oxygen supply-demand ratio significantly increased from 1.46 +/- 0.10 to 1.57 +/- 0.20 (p less than 0.025; enoximone) and from 1.40 +/- 0.08 to 1.56 +/- 0.19 (p less than 0.05; UDCG-115), respectively. It is concluded from these data that (1) resting coronary hemodynamics related to a unit of myocardium are not different between normal and idiopathic dilated cardiomyopathy, and (2) phosphodiesterase inhibitors exert beneficial effects on coronary hemodynamics by improving the oxygen supply-demand ratio.

Cardiomyopathy, Dilated↗
PubMed1988

The German multicenter trial of anisoylated plasminogen streptokinase activator complex versus heparin for acute myocardial infarction.

A multicenter randomized trial of anisoylated plasminogen streptokinase activator complex (APSAC) versus heparin in patients with acute myocardial infarction of less than 4 hours' duration was undertaken in 19 hospitals. Of the 313 patients, 151 received heparin and 162 APSAC (30 U as intravenous injection). Within 28 days of hospital stay, 19 deaths (12.6%) occurred in the heparin group and 9 deaths (5.6%) in the APSAC group (p = 0.032). After 24 hours, patients in the APSAC group had a significantly lower incidence of cardiogenic shock (3.2 vs 9.5%, p = 0.031), asystole (3.8 vs 10.8%, p = 0.015) and need for resuscitation (5.1 vs 11.5%, p = 0.039). There was no difference in global and infarct-related ejection fraction between the 2 groups. Thus, APSAC favorably influences prognosis and clinical course in hospital.

Anistreplase↗
PubMed1988

Mode of death in idiopathic dilated cardiomyopathy: a multivariate analysis of prognostic determinants.

A total of 110 patients with idiopathic dilated cardiomyopathy were followed prospectively for 53 +/- 8 (range 41 to 69) months to determine prognostic factors identifying patients at risk for sudden death or death from congestive heart failure. During the follow-up period 39 patients died, 14 of congestive heart failure and 25 suddenly. The incidence of cardiac death after 1 year was 18%, after 2 years 35%, and after 4 years 39%. Multivariate logistic regression analysis identified four independent prognostic factors: left ventricular ejection fraction, cardiac index, number of ventricular pairs/24 hours, and atrial rhythm (sinus rhythm or atrial fibrillation). With the final model of logistic regression 77 of 88 patients (88%) could be classified correctly as being at risk for death from chronic heart failure or sudden cardiac death. Patients who were likely to die of congestive heart failure were characterized by a markedly impaired left ventricular function (measured in terms of left ventricular ejection fraction, cardiac index, or both) and a low number of pairs/24 hours. The association between frequent complex ventricular arrhythmias and depressed left ventricular function identifies patients who are at risk for sudden death. The presence of atrial fibrillation significantly increases the risk of sudden death and death from congestive heart failure.

Adult↗
PubMed1988

Influence of disposable ('Conchapak') and reusable humidifying systems on the incidence of ventilation pneumonia.

The contamination of disposable ('Conchapak') and reusable humidifying systems and their influence on the incidence of pneumonia was studied in 116 patients requiring continuous mechanical ventilation therapy. The water reservoirs of 11 (15.9%) of the 69 disposable systems became colonized, but all reusable systems were found to be sterile. In four of the 11 samples, the organisms isolated corresponded with those cultured from tracheal secretions several days before. Ventilator-associated pneumonia occurred in 36 (31.0%) of the patients, but there was no statistically significant difference in the incidence of pneumonia between the patients treated with the disposable or the reusable humidifying systems. Gram-negative bacteria were the predominant organisms isolated from tracheal aspirates of patients who developed ventilator-associated pneumonia. These results suggest that disposable humidifying systems do not influence the rate of ventilator-associated pneumonia in mechanically ventilated patients.

Adult↗
PubMed1988

Prediction of efficacy and tolerance of oral mexiletine by intravenous lidocaine application.

In a controlled crossover trial, 15 patients with frequent ventricular arrhythmias were treated with lidocaine to predict efficacy and safety of oral mexiletine. After an initial control period, patients received intravenous lidocaine (bolus infusion of 200 mg/20 min followed by 3.6 gm/24 hr and for 7 days oral mexiletine (200 mg four times a day). Efficacy was controlled by 24-hour Holter monitoring (responders = suppression of single premature ventricular beats [PVB] greater than 84% and of complex PVB greater than 90%). After lidocaine, 10 of 15 patients (67%) were responders (mean PVB reduction: 97%). After mexiletine, five of 15 patients (33%) were responders (mean PVB reduction: 81%); efficacy was closely related to the plasma concentration. When efficacy of both agents was compared, lidocaine infusion had a positive predictive value of only 50%; however, the negative predictive value was 100%. Thus in nonresponders to lidocaine, mexiletine is very likely to fail in the suppression of ventricular ectopy.

Administration, Oral↗
PubMed1988

[Diprafenone--comparative study of anti-arrhythmia therapy with propafenone].

Diprafenone is a new antiarrhythmic agent with a dominant local anesthetic action and additional beta-sympathicolytic activity. In a randomized study, we analyzed the antiarrhythmic efficacy and tolerance of diprafenone (450-600 mg/day) in comparison to that of propafenone (450-500 mg/day) in ten patients with frequent and complex ventricular premature beats. After an initial control period, all patients received either diprafenone 450 mg/day or propafenone 450 mg/day for 5 days. In the case of a drug response (VPB suppression greater than 84%, suppression of ventricular pairs greater than 90%, suppression of ventricular tachycardia greater than 100%), after a wash-out period of 7 days patients were treated with the second antiarrhythmic medication for 5 days. In the case of nonresponsiveness, the dose of diprafenone and propafenone was increased to 600 mg/day and treatment continued for a second 5-day period. During the control period and at every drug administration, 24-h-Holter monitoring and ECG were performed, and plasma concentration and side effects were checked. After individual dose titration, 7/10 cases were effectively treated with diprafenone (mean dose: 471 mg; mean VPB suppression: 92%) and 5/10 cases with propafenone (mean dose: 540 mg; mean VPB suppression: 80%). Altogether four patients reported side effects, mainly gastrointestinal, which limited therapy in one patient in each group. Compared to propafenone, diprafenone had a strong effect on AV-nodal and ventricular conduction intervals; however, in no patient was therapy limited by these changes. Thus, also in comparison to propafenone, diprafenone is effective in the treatment of ventricular arrhythmias.

Aged↗
PubMed1988

[Significance of atrial natriuretic peptide in heart failure: experimental findings].

We investigated the role of atrial natriuretic peptide (ANP) in a rat model of chronic heart failure (CHF) (coronary ligation) by four different studies: (1) stimulation of secretion of ANP by volume loading, (2) infusion of 1 micrograms/min of rat ANP (99-126), (3) correlations of pressure measurements of right atrium (RAP) and LVEDP versus plasma ANP levels and ANP mRNS versus infarct size, (4) blocking endogenous plasma levels of ANP with monoclonal ANP antibody. In severe CHF, volume loading did not exert a significant increase in plasma ANP, in contrast to moderate CHF or to normal animals. Infusion of ANP reduced RAP and LVEDP without significant increase in renal blood flow (radioactive microspheres) in rats with severe cardiac failure, in contrast to normal animals. A close relationship was found between LVEDP and atrial plasma levels. After injection of ANP antibody, filling pressures and systemic vascular resistance increased, indicating that removal of ANP may enhance arterial vasoconstriction or elevated endogenous ANP to exert a vasodilatory action in severe heart failure. Nevertheless, the cardiocirculatory effects, primarily on renal blood flow, appear to be limited.

Animals↗