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Biomedical subjects

J Thormann

Publications and source records attributed to J Thormann.

At least 145 records · Page 8Linked to original sources
PubMed1976

Long-term observation of cardiac arrhythmias during and after cardiac surgery. II. Congenital heart disease.

Twelve arrhythmias that occurred in conjunction with surgery for congenital heart disease were studied in a group of 38 randomly selected patients. Halothane was used for anaesthesia and procaine-magnesium-aspartate solution for cardiac arrest. Registration and analysis of rhythm disturbances were carried out at 10 different time points, spaced narrowly in the intra- and early postoperative phases, then more widely up to the 96th hour of observation. Arrhythmic incidence per case and occurrence per case and phase are given, thereby also allowing an account of transient arrhythmias. The peak occurrence of intra-operative rhythm disturbances was found at about the time of aortic cross-clamping and release (ischaemia and halothane effect). A decline in arrhythmic incidence in the 1st-6th post-bypass hours was followed by a 2nd peak in the 6th-23rd postoperative hours (electrolyte and acid-base disturbances and/or a digitalis effect). All 12 arrhythmia types of the cardiopulmonary bypass group, as well as the separately considered ventricular arrhythmias of the first "arrhythmia peak", did not reveal any significant relation to: patients' age, total anaesthesia time, total surgery time and total bypass time. It is recognized that any comparative evaluation of operative arrhythmias, and especially a study of the causes and development of "surgically induced" A-V block, is problematic.

Adolescent↗
PubMed1976

[Function and reserve of the hypertrophic left ventricle in aortic valve disease].

Left ventricular function was analyzed by angiography in 31 patients with aortic valve disease and in 12 patients without heart disease (control group). Ejection fraction, percentage shortening of minor equator, mean velocity of fiber shortening and men left atrial pressure were considered as parameters of left ventricular function. Contractile reserve was tested by a single postextrasystolic beat. Patients with pure aortic stenosis and an increase of left ventricular muscle mass to 220% of the normal value showed no impairment of left ventricular function. Patients with pure aortic regurgitation and a left ventricular muscle mass of 260% of normal showed no significantly impaired function. Both groups increased ejection fraction and percentage shortening of the minor equator after premature beat comparable to the control group. Patients with combined lesions of the aortic valve had a left ventricular muscle mass of 360% of normal. This group showed decreased ejection fraction, percentage shortening of minor equator and mean velocity of fiber shortening as compared to the control group while mean left atrial pressure was significantly elevated. After premature beat all parameters remained depressed as compared to control group. We conclude that the degree of hypertrophy determinates cardiac function in aortic valve disease. Moderate hypertrophy shows normal function at rest, while severe hypertrophy shows impaired function.

Adult↗
PubMed1975

[Intra-atrial cardioversion in supraventricular tachycardial arrhythmia].

Cardioversion by rapid atrial stimulation has been carried out in 29 patients with supraventricular tachycarida and 12 patients with "coarse" atrial fibrillation. Atrial stimulation rates of 60-1200/min and electrical impulses of 6-25 mA were used. Intracardial conversion was successful in 86% of the cases presenting supraventricular tachycardia. Cardioversion was not achieved with atrial fibrillation but atrial flutter and atrial tachycardia were both found to be easily converted. Transformation of an arrhythmia into sinus rhythm or into stable atrial fibrillation with a slowed ventricular rate was the criterion for a successful conversion. Transient arrhythmias prior to an eventual stable rhythm was observed in 28% of the cases. Two mechanisms to explain the induced change in supraventricular tachycardias are discussed: (1) interruption of atrial or junctional foci (overdrive suppression) and (2) interruption of a re-entry circle by single premature beats. Cardioversion using atrial stimulation is indicated in atrial flutter, atrial tachycardias and junctional tachycardias. The method is of advantage in that it does not require anesthesia or interruption of digitalis therapy and its use involves no complications. Cardioversion using DC-shock is to be preferred in all cases of atrial fibrillation.

Adult↗
PubMed1975

[Labile repolarization changes in the ECG of patients without heart disease (author's transl)].

Nine patients with suspicious repolarization (ST-T segment) changes in the ECG were further investigated. Each had ten different additional ECG tests (after various degrees of exercise, and orciprenaline, amylnitrite, glucose, potassium chloride, and propranolol injections). The ECG changes became normal in all patients, orciprenaline and propranolol injection providing optimal results. Clinical investigation, left-heart angiocardiography and coronary angiography were normal in all. The questionably abnormal repolarization distrubances were, therefore, judged to be benign. As both beta-stimulation and beta-blockade normalized the ECG it can be safely assumed that the ECG changes were induced by autonomic nervous system factors. Cardiac catheterization appears, therefore, not indicated in each case and a potential iatrogenic heart disease can be avoided by relatively simple means.

Adolescent↗
PubMed1975

[Vagal effect on sino-atrial node frequency and A-V overdrive in hypersensitive carotid sinus reflex and sick sinus syndrome].

Two syndromes, hypersensitive carotid sinus reflex (HCSR) and "sick sinus syndrome" (SSS) were studied in 28 patients, 6 of whom served as controls. Carotid sinus pressure was performed during sinus rhythm (CSP 1) and atrial stimulation just above the sinus rate (CSP 2). Overdrive suppression was also tested. Vagal stimulation provoked different effects in HCSR and in SSS. The vagal reaction to CSP 1 was more manifest in HCSR than in both SSS and the controls. After CSP 2 A-V conduction was delayed longer in HCSR than in SSS and the controls. Following atropine, the vagal effect on HCSR was more pronounced than on SSS and the controls. With HCSR, the duration of vagal influence on R-R intervals (A-V conduction) was significantly shorter than on P-P intervals (sinus rate). After atropine, there was less vagal effect on A-V conduction than on the sinus rate in HCSR, meaning that A-V conduction was shorter and less affected than the sinus rate by carotid sinus pressure. Prolonged suppression following overdrive established the diagnosis of SSS. This suppression was found not to be affected by atropine. A dependency of suppression on the rate and duration of overdrive could not be ascertained for SSS. The newly formulated "postdrive P-P interval recovery time" subdivided SSS in such a way that two different degrees of severity could be illustrated. The conclusion was that HCSR was caused by an excessive reaction to vagal stimulation rather than by a dysfunction of the sinus node or A-V conduction system. SSS might be based on tissue damage in the sinus nodal region but it did not show increased sensitivity to vagal influence.

Adult↗
PubMed1975

[Contraction disorders of the left ventricle in ischemic heart disease. Studies using atrial stimulation].

Sixty-one patients with suspected ischemic heart disease (IHD) have been investigated by atrial stimulation (AST). Group A patients had normal coronarograms and served as controls. Group B patients had pathological conronarograms (at least 50% stenosis in one of the 3 vessels) and normal ventriculograms. Group C patients had pathological coronarograms and ventricular aneurysms. During AST, group C patients exhibited lower dp/dt max and dp/dt min as well as higher left ventricular end-diastolic pressure (LVEDP) and/or mean pulmonary artery pressure (MPAP) than groups A and B. Group B differed from group A only by increased MPAP during AST. When compared to controls, contractility in group C was reduced even at rest. AST offers an excellent means of diagnosing IHD if heart rates of 140/min and above are used. An abnormal increase in MPAP serves as the simplest parameter for IHD. Elevated MPAP at rest prompts suspicion of ventricular aneurysm. It is possible to deduce a quanitative estimate of contracitility by correlating dp/dt max to LVEDP. A hyperbolic relation results.

Adult↗
PubMed1975

Recalcitrant pustular eruptions of the extremities.

Forty-seven biopsies of pustules from patients with recalcitrant pustular eruptions of the palms and soles were examined blind and the results were subsequently compared among three clinical sub-groups: acrodermatitis continua, pustular psoriasis and pustulosis palmaris et plantaris. With the exception of three cases, it was not possible to make a diagnosis of psoriasis on the basis of histology alone. Histological findings were otherwise uniform and typical: intra-epidermal, unilocular, well-delineated pustules. No significant differences were found among the three subgroups. In view of the uniform histology, the unknown etiology and the uncertain clinical classification, the authors prefer the clearly descriptive term pustulosis palmaris et plantaris.

Acrodermatitis↗
PubMed1975

Frequency potentiation and postextrasystolic potentiation in patients with and without coronary arterial disease.

Frequency potentiation and postextrasystolic potentiation of myocardial contractility were induced in 17 patients found not to have cardiac disease (group 1) and in 10 patients with coronary arterial disease (group 2). Atrial stimulation was performed starting at a rate of 110/min and going up to 200/min (frequency potentiation). Single, premature ventricular beats with decreasing coupling intervals were induced every fifteenth beat during basal atrial stimulation at 125/min, after which compensatory pauses were provided (posts used an an index of contractility. With increasing heart rate dp/dt max was augmented equally, in both groups of patients, by frequency increases and premature beats (the coupling interval of the extrasystole being expressed as heart rate). dp/dt min and left ventricular systolic pressure remained unchanged while left ventricular end-diastolic pressure decreased in both groups of patients with the two forms of potentiation It was concluded that both these forms of potentiation have the same augmenting effect on myocardial contractility. Shortening the coupling intervals of premature beats caused a decreased in left ventricular end-diastolic pressure, suggesting that the Frank-Starling mechanism was not involved in postextrasystolic potentiation. Patients with coronary arterial disease had lower values of dp/dt max, dp/dt min, and higher values of left ventricular end-diastolic pressure during rest and stimulation procedures, while the systolic pressures equalled those in the control group. Though individual case values from the healthy and diseased hearts might be similar, it was only under the stress of potentiation that the true state of contractility was made apparent. Impairment of dp/dt min was not found without an impairment of dp/dt max in the presence of myocardial ischaemia.

Adolescent↗
PubMed1975

Analysis of re-entry mechanisms in the three patients with concealed Wolff-Parkinson-White syndrome.

Three patients with recurring attacks of supraventricular tachycardia and no electrocardiographic evidence of the Wolff-Parkinson-White syndrome (WPW syndrome) were studied using intracardiac recordings and atrial stimulation. The findings are interpreted as evidence of a concealed WPW syndrome. In all patients there was antegrade block of the anomalous atrioventricular (A-V) pathway while retrograde conduction was unimpaired and allowed the initiation of the observed reciprocating tachycardias. The diagnosis was based on the assumption that the ventricular myocardium was an essential link in the re-entry circuit. The three most important findings to support this assumption are: 1) retrograde conduction time, measured by the Q-A' interval (Q in ECG to atrial echo), and the rate of tachycardia were dependent on the mode of intraventricular conduction: 2) the first Q-A' interval of the tachycardia was independent of the A-H interval (initiation of atrial impulse to first activation of the His bundle) of the initiating premature atrial depolarization (PAD); 3) there was retrograde conduction following a ventricular premature beat during tachycardia at a time when the A-V node and/or the bundle of His would be refractory.

Adolescent↗
PubMed1975

Mechanical and electrical causes for lack of frequency potentiation in normal patients, in coronary artery disease and in left bundle branch block.

Nine atrial pacing (SP) runs and 8 ventricular pacing (VP) runs were carried out in patients without heart disease, and 10 AP runs in patients with coronary artery disease (CAD). For evaluation of myocardial contractility, the time derivative of left ventricular pressure (dpdt) was used. Comparing rest and AP at 155/min, AP in normal patients revealed a significant increase in dP/dtmax and a significant decrease in left ventricular end-diastolic pressure (LVEDP). This represents frequency potentiation. When comparing rest and VP values at 155/min in normal patients, no changes in dP/dtmax and LVEDP were seen. AP in patients with CAD demonstrated no change in dP/dtmax, but a decrease in LVEDP when compared to the rest values. dP/dtmin and left ventricular systolic pressure did not change in the 3 groups. VP, and even AP, in 2 additional patients with isolated left bundle branch block (LBBB) AND WITHOUt associated heart disease, revealed the same constellation of parameters as VP in normal patients. Our results show a lack of frequency potentiation in normal patients during VP and in patients with isolated LBBB during both AP and VP. It is concluded that the lack of frequency potentiation during AP in CAD is produced primarily by mechanical asynchrony of contraction, angiographically demonstrated as akinesia and dyskinesia. The lack of frequency potentiation in normal patients during VP and in patients with isolated LBBB due to asynchrony of activation resulting in asynchrony of contraction.

Action Potentials↗
PubMed1975

Vagal role and pacemaker indication in hypersensitive carotid sinus reflex.

The effect of carotid sinus pressure (CSP) on sinus rate was studied in 24 patients with sinoatrial pauses below 3 sec (control) and 23 patients with sinoatrial pauses above 3 sec (hypersensitive carotid sinus reflex equal to (HCSR). For registration of P waves, intraatrial electrograms were used. CSP was applied several times before and after atropine. Patients with HCSR showed inconstant response to CSP. The maximal result was considered diagnostic. No difference in the lengths of sinoatrial pauses was found between patients without dizziness or syncopes in the presence of HCSR and patients with dizziness that proved clinically to be based on the existence of HCSR. It was concluded that CSP-induced asystole can serve neither as a differential diagnostic criterion nor as an indication for pacemaker application. Sick sinus syndrome, and thereby dysfunction of the sinus node, were excluded by rapid atrial stimulation. Patients with HCSR showed overall higher age, slower resting heart rate before and after atropine and less atropine response during CSP compared to control. Hypersensitivity of the carotid sinus reflex was interpreted as a part of the physiological augmentation of vagal tone in elderly people.

Adult↗
PubMed1975

The pharmacodynamics of orally taken verapamil and verapamil retard as judged by their negative dromotropic effects.

The widely recognized, negative dromotropic effects of alpha-isopropyl-alpha-[N-methyl-N-homaveratryl)-gamma-aminopropyl]-3-4-dimethoxyphenylacetonitrile (verapamil, Isoptin) on arterio-venous (A-V) nodal conductions were studied using long-term atrial stimulation (AS) in 7 healthy volunteers whose mean age was 30 years. A control group consisting of three of the volunteers who underwent long-term atrial stimulation without medication was established. Since an isolated, well-known drug effect was studied over a long period of time, it was felt that this was an acceptable method for reaching valid pharmacodynamic conclusions. Atrial stimulation was carried out at hourly intervals up to 14-16 h and continued to the highest possible rate without the occurrence of 2nd degree A-V block before and following oral application of verapamil, 240 mg. The stimulus-Q (S-Q) prolongation at increased pace rates was compared to the control. Verapamil retard was tested in a similar course of investigation the following day. The results clearly demonstrated that both forms of verapamil are effective when taken orally. Verapamil acts 2 h after oral application. The peak effectiveness of the drug is found at 5 h and at this point A-V block can occur at low atrial stimulated rates. The effect of verapamil retard is obvious only after 6 h but is still apparent after 14 h and it remains constant with no peak in effectiveness. Characteristics of the resulting regressions allow to distinguish the effect of verapamil on A-V conduction from influences that might be mediated by the diurnal changes in tone of the autonomic nervous system only. The effect of verapamil after oral application is more pronounced with higher heart rates. The pharmacodnaymics of verapamil evaluated with regard to a single well-known pharmacological effect, have not necessarily to be identical with the pharmacokinetics and the bioavailability of the drug.

Adult↗