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Biomedical subjects

G Breithardt

Publications and source records attributed to G Breithardt.

At least 487 records · Page 27Linked to original sources
PubMed1980

[The electrophysiological effects of the Ca-antagonists gallopamil (D 600), dimeditiapramine (Ro 11-1781) and verapamil in man (author's transl)].

The electrophysiological effects of D 600 (D) (0.03 mg/kg i.v., 10 pts) and Ro 11-1781 (Ro) (1.0 mg kg i.v., 10 pts) were compared with those of verapamil (V) (0.1 mg/kg i.v., 20 pts). All three Ca-antagonists caused a slight shortening of the cycle length which was only significant after verapamil. There was practically no change in SNRT. As a consequence, the SNRT corrected for heart rate (CNSRT) increased insignificantly in all three groups (control C): 359.7 +/- 174.8 ms, V: 397.1 +/- 204.6 ms; C: 362.5 +/- 125.2 ms, Ro: 420.8 +/- 179.0 ms; C: 339.5 +/- 93.6 ms, D: 407.7 +/- 272.0 ms). In addition, the calculated "sinoatrial conduction time" increased insignificantly (C: 84.3 +/- 23.0 ms, V: 101.3 +/- 39.4 ms; C: 105.2 +/- 35.1 ms, Ro: 114.8 +/- 31.9 ms) or did not change (C: 105.9 +/- +/- 20.6 ms, D: 101.6 +/- 32.2 ms). The conduction time from high-to-low right atrium (HRA-A) as well as the His-ventricle time (HV) and the conduction interval from the septum to the right ventricular apex (V RVA) did not change. In contrast, the conduction time through the AV node (A-H) was significantly prolonged by all three drugs (C: 78.1 +/- 16.0 ms, V: 88,4 +/- 19.5 ms; C: 92.9 +/- 16.2 ms, Ro: 104.3 +/- 19.1 ms; C: 88.5 +/- 20.0 ms, D: 102.5 +/- 22.6 ms). The effective refractory period of the AV node (ERP AVN) was significantly prolonged by verapamil (C: 290.0 +/- 77.6 ms, V: 360.5 +/- 93.3 ms) and by D 600 (C: 266.7 +/- 72.6ms, D: 380.0 +/- 112.7 ms). Ro 11-1781 did not show any effect on this parameter. As a consequence, the Wenckebach point during high rate atrial pacing was significantly lowered by Verapamil and D 600, but only insignificantly by Ro 11-1781. The refractoriness of the right atrium and ventricle was not altered by any of the drugs. The results show that all three Ca-antagonists have similar electrophysiological effects in man after acute i.v. application. In the dose given, D 600 and verapamil are equipotent, whereas Ro 11-1781 is less effective.

Blood Pressure↗
PubMed1980

[Paradoxic response to disopyramide and quinidine (author's transl)].

Until recently, severe paradoxic responses to disopyramide have been believed to occur only, if at all, at extremely high doses. This credo has been shaken by some recent reports on severe ventricular tachyarrhythmias occurring in some patients on disopyramide. A further case (62 years, female, mitral commissurotomy in 1966, combined mitral valve lesion) is presented in whom a normal oral regimen (100 mg disopyramide four times daily) induced syncope due to ventricular tachycardia and flutter. The patient exhibited a long QT time before medication without deafness. Indication for treatment was the preservation of sinus rhythm as intermittent atrial fibrillation or flutter has been documented before. The serum potassium level was in the range of normal. Similar side-effects occurred some days later when the patient received quinidine sulfate. A survey of the most recent literature reveals a total of 20 patients with proven or suspected paradoxic responses to disopyramide. Factors that might favour the occurrence of paradoxic effects were preexisting QT prolongation, hypokaliemia, or massive overdosage. Though the total incidence of these side-effects seems to be relatively low, disopyramide should be given to special subgroups of patients only under careful monitoring.

Adult↗
PubMed1979

Intraoperative electrophysiologic mapping during cardiac surgery.

Intraoperative mapping is a method to document the surgical anatomy of cardiac tissues with electrophysiologic importance cartographically at time of surgery. The presented communication gives a survey of the present status of the technique of electrophysiologic mapping and its essential clinical applications. Special attention in this regard is directed to the intraoperative identification of the specialized AV conduction system in congenital cardiac malformations with unpredictable location of His bundle, to the detection of accessory AV bundles in patients with the Wolff-Parkinson-White syndrome and to the intraoperative morphological study of ventricular reentry tachycardias. Suitable technical equipment for "clinical" intraoperative electrophysiologic mapping is described in detail.

Cardiac Surgical Procedures↗
PubMed1979

[Electrophysiological mapping during open-heart surgery (author's transl)].

Intraoperative electrophysiological mapping provides a method to identify the specialized atrioventricular conduction system and to localize the morphological origin of different tachycardiac rhythm disorders at time of surgery. The basic technical aspects and methodical implications are presented with respect to its clinical applications.

Atrioventricular Node↗
PubMed1978

Prognosis and possible presymptomatic manifestations of congestive cardiomyopathy (COCM).

In order to find evidence of prognosis and of presymptomatic manifestation of congestive cardiomyopathy (COCM) in fifty-eight patients, the extent of morphological changes of endomyocardial catheter biopsy (EMCB), clinical and haemodynamic data were correlated to the clinical course. In addition, clinical, haemodynamic, angiographic, morphological and His-bundle electrographic studies were performed in patients with left bundle branch block (LBBB), normal left ventricular end-diastolic volume, and normal coronary arteries (n = 43). Related to a 10-year mortality rate of 70% from the onset of symptoms, COCM is one of the most severe heart diseases. Endomyocardial catheter biopsy (EMCB) allowed clear prognostic separation in patients with COCM and seems to be of diagnostic value in patients with only slightly enlarged hearts and in patients with a short history of symptoms. The studies also revealed much evidence that at least some patients with LBBB, normal left ventricular end-diastolic volume (LVEDV) and normal coronary arteries exhibit an early stage of COCM. In these patients especially EMCB with severe changes of heart muscle cells and/or impaired left ventricular function may indicate subsequent COCM. So that there is now a new indication for performing EMCB.

Adult↗
PubMed1978

[The effect of some antiarrhythmic drugs on systolic time intervals in normal subjects (author's transl)].

Eleven healthy volunteers (mean age 30.1 +/- 4.3 yrs.) were repeatedly studied by measurement of systolic time intervals (QS2c, PEPc, LVETc, PEP/LVET) and arterial blood pressure (cuff method) before and after 24-hour oral application of four antiarrhythmic drugs (quinidine, disopyramide, prajmaliumbitartrate, propafenone) and two beta-blocking agents (propranolol, atenolol). The studies were repeated in the same group of volunteers with a different drug after an interval of one week. PEPc significantly increased after all antiarrhythmic agents at therapeutic doses by 6.1 to 9.4 ms (p less than 0.05 and p less than 0.01 resp.), whereas LVETc did not change significantly. PEP/LVET increased on an average by 0.033 +/- 0.006 (p less than 0.01). QS2c increased by 7.5 and 7.6 ms resp. (p less than 0.05) after prajmaliumbitartrate and propafenone. Heart rate remained unchanged after disopyramide and propafenone whereas it increased significantly (p less than 0.05) after quinidine and prajmaliumbitartrate. Blood pressure did not change significantly after any of these antiarrhythmic drugs. After application of the two beta-blocking agents propranolol and atenolol, no significant changes in STI could be observed. Mean arterial blood pressure significantly dropped after both, propranolol (minus 2.8 mm Hg) and atenolol (minus 9.7 mm Hg; p less than 0.05 and p less than 0.01, resp.). Heart rate decreased by minus 8.1 b.p.m. after propranolol (p less than 0.01) and minus 11.5 b.p.m. after atenolol (p less than 0.01). The results clearly indicate that at the dosage used, the four antiarrhythmic agents (quinidine, disopyramide, prajmaliumbitartrate, propafenone) exert a negative inotropic effect on left ventricular function as far as it can be judged from the measurement of STI. The lack of a significant negative inotropic effect of an oral treatment with beta-blocking agents on the STI can be explained by opposing effects of a decrease in blood pressure and a negative inotropic action.

Adult↗