Search PubMed⌕ Search

Biomedical subjects

S Laniado

Publications and source records attributed to S Laniado.

At least 145 records · Page 8Linked to original sources
PubMed1983

Non-invasive recording of late ventricular activity using an advanced method in patients with a damaged mass of ventricular tissue.

Late potentials occurring after the QRS complex were detected on the body surface using an advanced signal averaging technique. ECG waveforms were recorded from patients with and without recurrent ventricular tachycardia who had a damaged mass of ventricular tissue (left ventricular aneurysm or right ventricular dysplasia). The recorded analog data were digitized by a 10 bit A/D converter with a sampling rate of 1280 Hz onto digital magnetic tape. The digitized waveforms were averaged with a CDC-6600 computer using an advanced algorithm which employs a cross correlation function to extract fiducial synchronizing marks for the signal averaging. Waveforms were filtered with a digital bandpass filter with 30 Hz and 250 Hz low and high cut-off frequencies, respectively. Late potentials were detected in seven out of ten patients with left ventricular aneurysm (or right ventricular dysplasia) and recurrent ventricular tachycardia and in four out of five patients with left ventricular aneurysm (or right ventricular dysplasia) but without recurrent ventricular tachycardia. The delayed depolarizations, which were recorded, had an amplitude of 3.0-27.0 microV and extended a mean of 90 msec beyond the termination of the QRS complex. In three patients with left ventricular aneurysm the delayed waveforms were abolished by aneurysmectomy. In nine control subjects no late potentials were detected. We conclude that late potentials which represent late depolarization of a damaged mass of ventricular tissue can be detected in patients with and without recurrent ventricular tachycardia.

Adolescent↗
PubMed1983

An advanced non-invasive technique for the recording of His bundle potential in man.

A new method for external recording of the His bundle electrical activity is described. Four hundred standard ECG waveforms were recorded and digitized at 1.28 kHz (8 bit resolution) and averaged with the aid of a CDC 6600 computer to reduce the random noise. A cross correlation function, which operates in the frequency domain using the Fast Fourier Transform algorithm, was employed to extract fiducial synchronizing marks for the waveforms alignment (triggering). Waveforms were filtered with a digital bandpass filter (30 Hz and 250 Hz low and high cut off frequencies respectively). The activity of the His bundle which was thus obtained was present on an isoelectric line, with signal amplitude of 4 to 7 microV. A strong correlation (r = 0.95, n = 10) was found between the HV intervals and the HQ intervals obtained from intracardiac electrograms and the new technique. It was concluded that the new method is convenient, reliable and can be successfully applied for the management of patients with various problems in their cardiac conducting system.

Adolescent↗
PubMed1983

Determination of the left bundle branch refractoriness by distal His bundle pacing in patients with left bundle branch block.

Electrophysiological studies were carried out in two patients with an idiopathic left bundle branch block. Consistent distal His bundle pacing resulted in the normalization of the QRS complex in both patients. Extrastimulation during basic distal His pacing at several cycle lengths was carried out successfully. Using this technique, the refractory periods of the left bundle branches were measured and found to be within the normal range. In addition, they decreased with the shortening of the basic cycle length. These results demonstrated the possibility of determining the refractoriness of the left bundle branch by His bundle pacing in patients with left bundle branch block. Hypotheses are postulated about the presumed location of the lesion responsible for the left bundle branch block.

Adult↗
PubMed1983

[Unusual supraventricular tachycardias in Wolff-Parkinson-White syndrome].

Two unusual types of narrow-QRS tachycardias were initiated during electrophysiological investigation of a patient with the Wolff-Parkinson-White syndrome. In the first type, the QRS complexes were preceded by atrial activation, the chronological sequence of depolarisation of which was similar to the sinus rhythm, suggesting the mechanism of sino-atrial reentry. The narrow QRS complex during tachycardia was related to the fact that the refractory period of the accessory pathway was longer than the tachycardia cycle. The second type of tachycardia was associated with I/I retrograde atrial activation within the QRS complex, suggesting the mechanism of intranodal reentry. The main point of interest of this case is that the accessory pathway, which only conducted in the anterograde direction, did not participate in the mechanism of either of these tachycardias.

Adult↗
PubMed1982

Initiation of ventricular tachycardia by supraventricular beats.

9 patients (6 males and 3 females, age 5-69 years) with ventricular tachycardia induced by supraventricular beats are reported. 3 patients had had previous myocardial infarction, 1 patient had mitral valve prolapse and in 5 patients no organic heart disease could be demonstrated. Ventricular tachycardia was initiated by a single atrial premature beat in 4 patients, double atrial premature beats in 3 patients (in 1 of them following exercise), by nonsustained AV nodal tachycardia in 1 patient, by rapid atrial pacing in 3 patients and exercise-related ectopic atrial tachycardia in 1 patient. Programmed ventricular stimulation induced ventricular tachycardia in all patients in whom the tachycardia was induced by atrial stimulation. Verapamil abolished sustained ventricular tachycardia in 1 of the 3 patients in whom this drug was administered. Hypotheses are made on the electrophysiological mechanisms of the arrhythmias and clinical implications are listed.

Adult↗
PubMed1982

Effects of tiapamil on myocardial performance in coronary artery disease.

Tiapamil has been extensively investigated for treatment of cardiac arrhythmias. Concern persists, however, that, as a calcium antagonist, it may seriously depress myocardial function. To investigate this possibility, 20 patients were given tiapamil intravenously and studied by radionuclide ventriculography. Tiapamil markedly lowered arterial pressure. Left ventricular ejection fraction increased from 54 +/- 3.3 to 57 +/- 3.3%. No significant change in heart rate was noted. Tiapamil did not increase the extent of left ventricular asynergy. The potent vasodilator properties of tiapamil compensate for any intrinsic decrease in left ventricular contractibility, and therefore overall cardiac function is not worsened by the drug in patients with normal or moderately reduced resting ventricular ejection fractions.

Blood Pressure↗
PubMed1982

Physiologic mechanisms in aortic insufficiency. I. The effect of changing heart rate on flow dynamics. II. Determinants of Austin Flint murmur.

We studied the dynamic changes in mitral flow patterns and in mitral valve motion before and after producing acute, reversible aortic insufficiency (AI) in nine open-chest dogs. Phasic mitral flow, the mitral valve echocardiogram, and intracardiac phonocardiogram and other hemodynamic variables were measured. During moderate AI (mean regurgitant fraction 52 +/- 5%) (+/- SD), the antegrade filling volume decreased from 31 +/- 7 to 24 +/- 6 ml (p less than 0.01), but the peak protodiastolic mitral flow rate increased from 139 +/- 37 to 157 +/- 42 ml/sec (p less than 0.01), reflecting the shift of a larger fraction of total mitral filling volume to early diastole. In six dogs, atrial pacing was used to examine the hemodynamic effects of tachycardia. Increasing the heart rate from 90 to 120 beats/min increased cardiac output from 2.64 +/- 0.56 to 3.3 +/- 0.831/min (p less than 0.05) and decreased left atrial pressure from 24 +/- 8 to 17 +/- 7 mm Hg (p less than 0.05). Increasing heart rate to 150 beats/min compromised mitral filling, reduced cardiac output and increased left atrial pressure. Moderate tachycardia improves cardiac performance in AI by reducing regurgitant volume, without significantly reducing transmitral filling volume. The mitral valve echocardiogram showed only a small decrease in cusp opening amplitude during AI. A low-pitched left ventricular inflow tract murmur was recorded in protodiastole and corresponded in time to the rapidly increasing mitral flow. We conclude that the major determinant of the turbulence responsible for the creation of the austin flint murmur is the antegrade mitral flow stream and its mixing with the retrograde aortic flow.

Animals↗
PubMed1982

Intrauterine and postnatal atrial fibrillation in the Wolff-Parkinson-White syndrome.

A fetal tachyarrhythmia was discovered at the thirty-second week of gestation of a 22-year old woman. Fetal echocardiography revealed atrial fibrillation with rapid ventricular rate, without any other demonstrable cardiac abnormality. In spite of therapeutic maternal blood levels of digoxin, the fetal ventricular rate and cardiac size increased, which prompted us to perform cesarean section at the thirty-fourth week of gestation. A baby with a Wolff-Parkinson-White syndrome but no other cardiac anomaly was delivered. Recurrent episodes of nonsustained atrial fibrillation with conduction over the accessory pathway occurred in the first hours of life. The Wolff-Parkinson-White pattern was not present on subsequent ECG recordings. The use of echocardiography in the diagnosis and management of this rare fetal tachyarrhythmia is emphasized.

Adult↗
PubMed1982

Mechanisms of immune haemolysis: cell-dependent destruction of autologous red blood cells in penicillin-induced haemolytic anaemia.

The mechanisms of red blood cell destruction in 2 patients with penicillin-induced immune haemolytic anaemia were investigated. Anti-penicillin antibodies of the IgG subclass were found in the patients' sera and in the eluates of their direct antiglobulin positive red blood cells. Using a rapid 51Cr in vitro assay it was shown that fresh peripheral blood mononuclear phagocytes and granulocytes but not lymphocytes from both patients lysed and phagocytosed autologous red blood cells previously treated in vivo or in vitro by penicillin and autologous anti-penicillin antibody. Antibody-dependent cell-mediated cytotoxicity (ADCC) as well as antibody-dependent phagocytosis (ADPh) were proportional to serum concentration and to the number of attacking cells. Anti-penicillin antibody from 1 patient activated the complement system in vitro but failed to induce lysis of penicillin-treated red blood cells in the presence of complement. These results suggest that ADCC as well as ADPh participate in the destruction of red blood cells in penicillin-induced haemolysis in vivo.

Adult↗