Search PubMed⌕ Search

Biomedical subjects

L N Horowitz

Publications and source records attributed to L N Horowitz.

At least 127 records · Page 7Linked to original sources
PubMed1980

Electrophysiologic characteristics of sustained ventricular tachycardia occurring after repair of tetralogy of fallot.

The electrophysiologic characteristics of sustained ventricular tachycardia occurring after total repair of tetralogy of Fallot are reported. Four patients, 8 to 31 years of age, who had spontaneous episodes of sustained ventricular tachycardia underwent electrophysiologic study to determine the mechanism and site of origin of the tachycardia. In each patient, the tachycardia could be reproducibly initiated and terminated by programmed electrical stimulation. In two patients, initiation and maintenance of the tachycardia depended on the development and perpetuation of continuous electrical activity in the right ventricular outflow tract. These observations suggested a reentrant mechanism. In each patient, catheter endocardial mapping demonstrated the site of origin to be the right ventricular outflow tract. In two patients intraoperative mapping showed the reentrant circuit originating at the site of healed right ventriculotomy site. We conclude that sustained ventricular tachycardia after repair of tetralogy of Fallot in our patients was caused by reentry at the site of the previous operation in the right ventricular outflow tract.

Adolescent↗
PubMed1980

Strength-interval relation in the human ventricle: effect of procainamide.

The effects of procainamide on strength-interval relations were evaluated in 18 patients. At plasma concentrations of 4.3 to 13.6 micrograms/ml procainamide had minimal effects on threshold current in late diastole, but in early diastole it shifted the strength-interval curve to the right. The basic strength-interval relation (that is, decreasing refractory period as current is increased) was not altered. The control refractory period decreased by a mean of 44 ms as the current was increased from threshold to 10 mA, whereas a mean decrease of 42 ms was observed after procainamide. However, the steep portion of the strength-interval curve(absolute refractory period) was shifted to longer coupling intervals by a mean value of 24 ms. These findings suggest that procainamide may primarily affect active membrane properties, but exert little net effect on passive membrane properties late in diastole.

Action Potentials↗
PubMed1980

The surgical treatment of ventricular tachycardia.

Recurrent ventricular tachycardia is a well-recognized complication of ischemic heart disease. Coronary bypass operation with or without aneurysmectomy has been disappointing as therapy for these arrhythmias. With the advent of programmed electrical stimulation, it has become possible to distinguish automatic and reentrant ventricular tachyarrhythmias. The latter have recently proved amenable to operative intervention. This review examines the pathophysiology and diagnosis of ventricular tachycardia using programmed electrical stimulation. Surgical therapy with resection, revascularization, autonomic modulation, thermal ablation, cardiac pacing, reentrant circuit interruption, and endocardial excision is explored. Operation for cardiac arrhythmias is on a firm electrophysiological foundation. Surgical treatment of refractory ventricular tachyarrhythmias is now rational, recommended, and rewarding.

Cardiac Pacing, Artificial↗
PubMed1980

Recurrent ventricular tachycardia: an electrophysiologic approach.

Programmed stimulation of the heart can reproducibly initiate and terminate a sustained tachycardia mimicking clinical disease. This and localization of the site of origin of the tachycardia with endocardial mapping make it possible to directly select the most effective antiarrhythmic agent and to determine whether surgical ablation of the arrhythmogenic locus may be feasible if drug therapy should fail.

Anti-Arrhythmia Agents↗
PubMed1980

Comparison of endocardial catheter mapping with intraoperative mapping of ventricular tachycardia.

To validate the accuracy of catheter endocardial mapping to localize the origin of ventricular tachycardia (VT), we compared cathether endocardial mapping with intraoperative epicardial and endocardial mapping of 24 morphologically distinct VTs in 18 patients undergoing surgery. Twelve had VT with left bundle branch block morphology and 12 had VT with right bundle branch block morphology. Catheter endocardial mapping localized 23 VT morphologies to the border of a left ventricular aneurysm or myocardial infarction and one VT to a right ventriculotomy scar. Intraoperative epicardial mapping showed epicardial breakthrough on the right ventricle in 10 VTs with left bundle branch block morphology and on the left ventricle in two. In 12 VTs with right bundle branch block morphology, intraoperative epicardial mapping revealed the earliest site of VT with left bundle branch block morphology (11 patients) and VT with right bundle branch block morphology (12 patients) at the border of a left ventricular aneurysm, and one VT with left bundle branch block morphology in the right ventricle. Catheter endocardial mapping predicted the origin of VT within 4--8 cm2 of that determined by intraoperative endocardial mapping, which always identified the earliest site. These data validate the accuracy of catheter endocardial mapping in localizing the origin of VT.

Adult↗
PubMed1980

Epicardial and endocardial activation during sustained ventricular tachycardia in man.

Ventricular activation during ventricular tachycardia was studied by intraoperative epicardial and endocardial mapping in 21 patients with coronary artery disease and previous myocardial infarction who underwent operation for recurrent ventricular tachycardia. Twenty-nine morphologically distinct tachycardias were mapped; 18 tachycardias had a right bundle branch block morphology and 11 had a left bundle branch block morphology. After cannulation for bypass, the tachycardias were induced and electrograms were recorded at 55-75 epicardial sites. After starting cardiopulmonary bypass, the infarction was incised and electrograms were recorded at 28-55 left ventricular endocardial sites during ventricular tachycardia. All mapping data were analyzed with three simultaneously recorded ECG lead and two reference electrograms. Earliest activation in all tachycardias occured on the endocardial surface of the infarction. In each tachycardia, endocardial electrical activity was recorded before the onset of the QRS complex. Earliest epicardial activation in the 29 tachycardias occurred 10 msec after the onset of QRS complex. Epicardial breakthrough occurred on the right (19 tachycardias) as well as the left ventricle (10 tachycardias). We conclude that ventricular tachycardia associated with ischemic heart disease originates near the endocardial surface of the left ventricle along the border of the infarction and that epicardial mapping alone is insufficient to identify the site of origin of these tachycardias.

Aged↗
PubMed1980

Electrophysiologic management of recurrent ventricular tachycardia in acute and chronic ischemic heart disease.

The refinement of the techniques of programmed stimulation and intracardiac recording has provided an understanding of the mechanism of ventricular tachycardia which can be applied clinically to the development of therapeutic regimens. The efficacy of drug therapy can be assessed by sequential studies evaluating the ability of drugs to prevent the initiation of the arrhythmia. The efficacy of pacemaker therapy can be evaluated by the effects of stimulation during the tachycardia. The recent development of endocardial mapping provides the surgeon with a tool to guide therapeutic surgical ablation. We believe that such an electrophysiologic approach to recurrent ventricular tachycardia can lead to the rapid development of successful therapy under controlled conditions.

Arrhythmias, Cardiac↗
PubMed1980

Comparison of standard aneurysmectomy and aneurysmectomy with directed endocardial resection for the treatment of recurrent sustained ventricular tachycardia.

Nineteen patients undergoing a standard aneurysmectomy for recurrent ventricular tachycardia are compared with 30 patients unergoing electrophysiologically directed endocardial excision and aneurysmectomy. The electrophysiologically nondirected and electrophysiologically directed groups were aneurysmectomy. The electrophysiologically nondirected and electrophysiologically directed groups were similar for age (56.8 versus 57.5 years), interval after myocardial infarction (26.2 versus 28.3 months), preoperative episodes of ventricular tachycardia (13.2 versus 19.7), cardiac index (2.95 versus 2.79 L/min/m2), left ventricular end-diastolic pressure (15.5 versus 18.2 torr), and ejection fraction (34 versus 28%). Operative mortality rate in the nondirected group was 42%, with all but one of the deaths resulting from uncontrolled postoperative ventricular tachycardia. In the nondirected group 78.9% (15/19) of patients had recurrent ventricular tachycardia postoperatively. The operative mortality rate in the electrophysiologically directed group was 6.7% (2/30), and both patients died of left ventricular failure. Three patients (10%) have ventricular tachycardia inducible with programmed stimulation. We conclude that standard left ventricular aneurysmectomy is not an effective operation for recurrent sustained ventricular tachycardia. Conversely, electrophysiologically directed endocardial excision characteristically controls the arrhythmia at an acceptable surgical risk.

Adult↗
PubMed1980

Surgical correction of recurrent sustained ventricular tachycardia following complete repair of tetralogy of Fallot.

Ventricular arrhythmias occur in 0.3% to 3% of patients following complete repair of tetralogy of Fallot. These life-threatening arrhythmias do not appear related to the hemodynamic success of the repair. This report presents the case histories of two patients who experienced from 30 to 150 documented episodes of sustained ventricular tachycardia (VT) following complete repair of tetralogy of Fallot. Pharmacologic and pacing regimens failed to prevent recurrence in both patients. The source of the arrhythmia was localized to the right ventriculotomy scar by electrophysiological mapping. This scar was surgically excised. VT was not inducible following operation and has not recurred in the 6 months and 18 months following discharge of the patients from the hospital. If medical therapy fails, operation combined with extensive preoperative and intraoperative electrophysiological study may be a realistic option in the treatment of selected patients with VT following complete repair of tetralogy of Fallot.

Adult↗
PubMed1979

Diagnosis of acute myocardial infarction in the emergency room: a prospective assessment of clinical decision making and the usefulness of immediate cardiac enzyme determination.

This study evaluates (a) the ability of house staff physicians to diagnose acute myocardial infarction (AMI) in patients with chest pain and (b) the usefulness of immediate ("stat") creatine kinase determinations in aiding the decision to hospitalize patients with chest pain. Of 80 emergency room patients with chest pain, 34 were admitted to an intensive care unit and 46 were either discharged or admitted to a general medical unit. Of the 34 patients admitted to intensive care, 11 fulfilled criteria for AMI. Of the 46 who were not admitted, two met criteria for AMI: one had abnormal initial enzyme values; the other had normal initial values but diagnostic 48-hour values. Both had abnormal electrocardiograms. On the other hand, 11 patients who were not admitted had elevated initial enzyme values but did not have myocardial infarctions and might have been admitted inappropriately on the basis of their initial enzyme values. Five patients who were admitted had normal initial values but did develop infarctions and might have been sent home inappropriately on the basis of initial enzymes values. We conclude that: (a) physicians discharged 2 of 13 patients with AMI drawn from a population of 80 with chest pain and (b) the availability of stat cardiac enzymes could have prevented the discharge of only 1 patient and may have caused the inappropriate admission of 11 and discharge of 5 patients.

Adult↗
PubMed1979

Ethmozin: a new antiarrhythmic agent developed in the USSR. Efficacy and tolerance.

Ethmozin, a phenothiazine derivative, was developed in the Soviet Union as a new antiarrhythmic agent. We evaluated ethmozin using a controlled single-blinded in-hospital protocol in 14 ambulatory patients with ventricular ectopy ranging from an average of 48 to 1,801 depolarizations per hour and in eight patients with atrial ectopy ranging from 63 to 693 depolarizations per hour. Placebo was administered for the first 3 days, followed by ethmozin from 2.4 to 11.2 mg./Kg./day administered orally every 8 hours for 7 days and concluding with placebo for the final 3 days. Continuous 24-hour long-term electrocardiographic monitoring for 13 days was employed to measure drug efficacy accurately. Six of eight (75 per cent) patients with atrial ectopy and 10 of 14 (71 per cent) patients with ventricular ectopy had statistically significant reductions in ectopy during ethmozin therapy. Atrial ectopy was reduced at a lower dose and plasma level of ethmozin than was ventricular ectopy. With the exception of mild nausea in one patient, no side effects of ethmozin therapy were noted. Ethmozin appears to be a well-tolerated, effective antiarrhythmic agent with a dosage regimen that can promote patient compliance for long-term use.

Adult↗
PubMed1979

Relationship of atrial fibrillatory wave amplitude to left atrial size and etiology of heart disease. An old generalization re-examined.

It is commonly stated that coarse f waves in atrial fibrillation suggest the presence of rheumatic heart disease and large left atrial size, whereas fine f waves indicate non-rheumatic disease and small left atrial size. Using echocardiography as a more reliable indicator of left atrial size, 37 consecutive patients with chronic atrial fibrillation were evaluated. The correlation coefficients between left atrial size and maximum f wave amplitude was -0.12 and -0.07, using average f wave amplitude. Only 53 per cent (9 of 17) of patients with rheumatic heart disease had f wave greater than 1 mm. and 56 per cent (10 of 18) of patients with f wave size less than or equal to 1 mm. had non-rheumatic disease. This study refutes the contention that the f wave amplitude in atrial fibrillation is correlated with either left atrial size or etiology of heart disease. It is possible that an intra-atrial conduction defect is responsible for coarse f wave morphology.

Atrial Fibrillation↗
PubMed1979

Electrophysiologic approach to therapy of recurrent sustained ventricular tachycardia.

The refinement of the techniques of programmed stimulation and intracardiac recording has led to understanding of the mechanism of ventricular tachycardia and these techniques can be applied clinically to the development of therapeutic regimens. The efficacy of drug therapy can be assessed in sequential studies evaluating the ability of drugs to prevent initiation of the arrhythmia by electrical stimulation. The efficacy of pacemaker therapy can be evaluated by assessing the effects of stimulation during the tachycardia. The recent development of endocardial mapping provides the surgeon with a tool to guide therapeutic surgical ablation of the site of origin of the tachycardia. Such an electrophysiologic approach to recurrent ventricular tachycardia can lead to the rapid development of successful therapy under controlled conditions.

Adolescent↗