Abolished compensation of cardiac performance after nitroglycerin in patients with ventricular asynergy.
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Biomedical subjects
Publications and source records attributed to M Schlepper.
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In 10 patients with hypertrophic obstructive cardiomyopathy (HOCM) and in 10 patients without heart disease (normals) left ventricular function and myocardial reserve under isoproterenol (Iso) infusion (0.3 microgram/kg B.W./min) were measured. From the monoplane cineangiography of the left ventricle diastolic wall thickness as well as ejection phase contractile indices, ejection fraction (EF) mean velocity of fiber shortening (VCF) and mean normalized systolic ejection rate (MNSER), were calculated. Maximum total load (TL) served as measure for afterload. Wall thickness in HOCM was higher by 73% as compared to normals (p less than 0.001). Hemodynamic values for normals at rest were as follows: EF 68.9 +/- 8.0%, VCF 1.22 +/- 0.19 circ/sec, MNSER 2.25 +/- 0.25 vol/sec and TL 228.6 +/- 37.4 dynes . 10(5). Values for HOCM at rest were as follows: EF 77.4 +/- 7.71% (p less than 0.05), VCF 1.53 +/- 0.3 circ/sec (p less than 0.05); MNSER 2.66 +/- 0.35 vol/sec (p less than 0.01) and TL 288.5 +/- 55.5 dynes . 10(5) (p less than 0.01) as compared to normals. The values under Iso in normals resulted in a significant fall of the TL (p less than 0.05), the enddiastolic volume (EDV, p less than 0.05) and of the enddiastolic pressure (EDP, p less than 0.05), VCF rose by 89% (p less than 0.001), MNSER by 66% (p less than 0.001) and EF by 23% (p less than 0.001). In HOCM under Iso TL rose by 45% (p less than 0.05), EDV and EDP did not change (p less than 0.05), VCF and MNSER rose by 23% (p less than 0.05 respectively p less than 0.01). VCF and MNSER in HOCM with Iso were reduced by 17% respectively by 13% (p less than 0.01) as compared to normals, the EDP was increased by factor 4, while EDV showed no significant difference (p less than 0.05). Our results indicate that the left ventricle in HOCM in spite of its marked hypertrophy is unable to adequately compensate for an acute gain of afterload as induced by the effect of catecholamines. Therefore, we assume stress-related congestive symptoms in HOCM to be caused--aside from other mechanisms--by diminished ejection reserve.
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In 20 patients with WPW-syndrome, the effective refractory periods of accessory A-V conduction were measured by programmed atrial stimulation during His-bundle electrography. The effects of basic heart rate on this parameter were evaluated. Three groups of patients were distinguished: A) The effective refractory periods of accessory A-V conduction were clearly longer than the effective refractory periods of the right atrium in 12 patients. In these patients, acceleration of heart rate shortened the effective refractory period of accessory A-V conduction. Refractoriness of accessory A-V conduction was a linear function of cycle length. B) Block of accessory A-V conduction occured at a rather long basic cycle length in three patients. No rate dependency of refractoriness could be evaluated. Methodical problems regarding the determination of effective refractory period of accessory A-V conduction were discussed. The significance of the parameter in question in respect to the trigger mechanism of paroxysmal supraventricular tachycardias (echozone) and the ventricular rate during atrial tachycardias were demonstrated.
The first clinical results of 100 patients, operated since November 1973 using ECC and acupuncture anesthesia are reported. The method of combined chinese and european procedures of analgesia is described. Advantages and problems of the new method are discussed.
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Alterations of hemodynamics and contractility were studied in 6 patients in whom two consecutive runs of supraventricular tachycardias (SVT) were electrically induced. Following initiation there was an abrupt decrease of arterial blood pressure, left ventricular systolic pressure, dp/dtmax, cardiac index and stroke work index (SWI). These parameters -- with the exception of SWI -- increased in the course of the SVT, however, control values were not reached. Mean pulmonary artery pressure steadily increased and remained on an elevated level until the tachycardia was stopped. When the SVT was electrically terminated, there was a transient overshoot of mean arterial and left ventricular systolic pressure, while mean pulmonary artery pressure slowly returned to control values. When the tachycardia was stopped by i.v. infusion of N-)diethylamino-3-propyl)-N-phenyl-indanamine-2 (aprindin, Amidonal) -- started at the 7th minute -- there was no statistically significant difference, neither during the SVT nor after cessation as compared to the values of the first run. Only mean pulmonary artery pressure remained at a higher level after SVT was stopped. It may, therefore, be concluded that in patients with otherwise normal hearts aprindin applied in a dosage sufficient to stop the SVT, does not exhibit noteworthy inotropic side effects.
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From October 1973 to May 1975 cardiae surgery with extracorporal circulation using Acupuncture as Analgesia was performed in 131 patients in the surgical clinic of the University of Giessen. Acupuncture is performed by electric-stimulation of 8 points at the lower legs, the neck and ears with 90 V and 5--6 Htz. All patients are intubated; controlled respiration is maintained with 50% O2 and 50% N2o. During the whole operation, 20 min after intubation the patients are responsible. The main advantage of the new method we see in a good postoperative cooperation of the patients, which are generally extubated in the operation-room.
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In patients with evidence of dual AV conduction, a premature atrial depolarization is normally conducted via a fast conducting pathway with a long refractory period. At a critically timed coupling interval, the effective refractory period is reached and now the impulse is conducted over a pathway with a slow conduction velocity and a short effective refractory period. At this moment in the His bundle electrocardiogram, a sudden increase in the AH interval occurs which is called the 'break' phenomenon. This phenomenon was studied in 14 patients, with a history of supraventricular paroxysmal tachycardia, at the patient's own heart rate, at different paced heart rates, and after the administration of atropine. In 11 patients the 'break' phenomenon could be elicited during sinus rhythm,; in 3 when the heart rate was accelerated. The effective refractory period of the fast conducting pathway was prolonged in 9 patients, remained unchanged in 3, and was shortened in 2 when the heart rate was increased. The effective refractory period of the slow conduting pathway was reached when block occurred proximal to the His bundle. This parameter was increased in 8 patients, remained unchanged in 3, and was decreased in 1 patient with augmentation of the heart rate. This effective refractory period was not measured in 2 patients. Atropine led to a shortening of the refractory period of both pathways in 8 patients studied. Atrial echo phenomena indicating the beginning of a re-entry circuit occurred at an AH prolongation that was not always identical to that measured at the point of 'break'. Widening, as well as narrowing, of the echo zone was found, indicating that the re-entry circuit was in a state of labile equilibrium. In cases where shortening of the pathways involved in the re-entry circuit was found, structures other than nodal may exist; therefore paranodal bypass must be considered.
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.
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.
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