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Biomedical subjects

L N Horowitz

Publications and source records attributed to L N Horowitz.

At least 19 recordsLinked to original sources
PubMed1992

The contraction of stunned myocardium: isovolumetric bulging and wasted ejection shortening in dog heart.

OBJECTIVE: The aim of the study was to assess the contraction of myocardium stunned by repetitive brief coronary occlusions by examining the response to alterations in loading and inotropy of systolic contraction on isovolumetric and ejection phase shortening. METHODS: Fourteen open chest anaesthetised dogs were used for the studies. After destruction of the sinus node, the heart was atrially paced and atrial extrasystoles were introduced followed by a short (400 ms) or long (700 ms) postextrasystole. The left anterior descending coronary artery was occluded for 5 min and reperfused for 10 min a total of eight times to produce stunned myocardium, followed by a final 60 min of reflow. Regional function was assessed with segment length sonomicrometers. RESULTS: With successive periods of occlusion there was an increase in the end diastolic segment length and a progressive decrease in total percent systolic shortening (baseline 22.3%, 1st reflow 14.5%, 8th reflow 7.9%) with some recovery after 60 min of reflow (12.0%). This was predominantly due to the development of bulging during isovolumetric systole (4.5%, -4.9%, and -8.3%, respectively) which diminished during 60 min recovery to -3.1%. Ejection shortening was relatively constant (17.8%, 19.4%, 16.3%, and 15.1%, respectively). Postextrasystolic potentiation resulted in an increased in total percent systolic shortening, but not to the baseline value, as slight isovolumetric bulging persisted. Similar changes were seen with the short and long postextrasystoles although the latter had a greater increase in ejection shortening. CONCLUSIONS: The decrease in function after repetitive occlusion and reflow is predominantly due to bulging during isovolumetric systole which persists after postextrasystolic potentiation in our model of stunned myocardium.

Animals↗
PubMed1991

Clinical electrophysiological effects of intravenous recainam: an antiarrhythmic drug under investigation for the treatment of ventricular and supraventricular arrhythmias.

This open-label, multicenter study was designed to assess the electrophysiological properties of intravenous recainam, an investigational Class I antiarrhythmic agent. In 25 patients undergoing electrophysiological studies for the evaluation of arrhythmias, recainam was administered intravenously in a loading infusion (0.1 mg/kg/min) for 40 minutes, followed by a maintenance infusion (0.02 mg/kg/min) until the completion of the study. Electrophysiological measurements were obtained at baseline, 30 minutes after initiation of the loading infusion, and 30 minutes after termination of the infusion during washout. Conduction intervals, refractory periods, and sinus node recovery times were measured during sinus rhythm and during atrial or ventricular pacing. Vital signs were obtained and recorded before, during, and after recainam infusion. The results showed no change in mean arterial pressure, but heart rate increased slightly by 4 beats/min following recainam infusion. Recainam produced a generalized slowing of intracardiac conduction. The mean intraatrial conduction time, measured at an atrial paced cycle length of 600 msec, increased during recainam loading infusion by 44%, from 38.8% +/- 2.8 to 53.0 +/- 5.4 msec; intranodal conduction time increased by 10%, from 102.0 +/- 5.5 to 112.1 +/- 5.2 msec; and infranodal conduction time increased by 31% from 53.1 +/- 3.0 to 70.7 +/- 3.8 msec. Slowed conduction persisted during washout. The mean right atrial effective refractory period was significantly prolonged (+7% at 600 msec cycle length and +8% at 450 msec cycle length, P less than 0.05 and P less than 0.01, respectively) during recainam loading and remained so during washout.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Device interaction--antitachycardia pacemakers and defibrillators for sustained ventricular tachycardia.

We evaluated the combined use of permanent automatic antitachycardia pacemakers and implanted defibrillators in ten patients with recurrent monomorphic sustained ventricular tachycardia (VT). Pacemaker programming was VVI-T automatic burst in eight patients, VVI-T magnet mode in one patient, and VVI in one patient. Device interactions occurred in four patients, requiring changes in pacemaker programming. These included defibrillator multiple counting during pacing, inappropriate pacemaker bursts initiating VT, inappropriate reset of the pacemaker antitachycardia mode by defibrillation, defibrillator discharge after pacemaker VT termination, and defibrillator VT reinitiation. Two patients required pacemaker programming out of the antitachycardia mode, and two required a change in antitachycardia pacing parameters. Seven patients remain in automatic VVI-T and three in VVI modes. Mean follow-up is 13 months and all patients are alive. Thus, although pacemaker/defibrillator combinations function well for patients with more than one VT rate, device interactions occur frequently and may require pacemaker reprogramming or elimination of the overdrive mode. Combined use of these devices should be cautiously considered when single device therapy is unsatisfactory. Devices that combine both pacing and defibrillation features may reduce adverse interaction.

Algorithms↗
PubMed1991

Managing geriatric arrhythmias, I: General considerations.

Cardiac arrhythmias become increasingly common as people age, but they are not always clinically significant. Sinus node dysfunction, AV conduction disturbances, and ventricular and supraventricular arrhythmias will be found but are not always symptomatic. Treatment of asymptomatic arrhythmias is controversial and probably not indicated, but in symptomatic elderly, therapy is indicated, since even the very elderly have been found to benefit from it as much as younger patients. There are specific guidelines, however, that apply to this age group based on its susceptibility to side effects.

Aged↗
PubMed1991

Managing geriatric arrhythmias, II: Drug selection and use.

Age-related impairments in antiarrhythmic drug distribution, metabolism, and excretion may result in accumulation of these potent drugs, increasing the risk of adverse drug reactions and drug interactions in the elderly. These risks are minimized by using modest initial dosage with slow dosage titration. Therapeutic drug monitoring is a method which employs antiarrhythmic concentration data and a determination of drug clearance in order to develop an optimal dosing regimen. The pharmacology, indications for use, and adverse effects of currently available antiarrhythmics are reviewed. Dosing guidelines for the geriatric population are provided.

Aged↗
PubMed1990

Efficacy of moricizine in malignant ventricular arrhythmias.

Moricizine hydrochloride has been shown to be effective in the treatment of a variety of ventricular arrhythmias. It has been evaluated for the treatment of malignant ventricular arrhythmias in several hundred patients. When assessed by noninvasive techniques, moricizine effectively suppresses spontaneous unsustained ventricular tachycardia (VT) in approximately 60% of patients. Efficacy is sustained during long-term therapy. Evaluation of moricizine therapy for sustained VT using programmed stimulation has been carefully performed in more than 100 patients. The initiation of sustained VT is suppressed in 20 to 25% of patients. Moricizine is generally well tolerated. Because of its minimal effects on left ventricular function, a common clinical problem in patients with malignant ventricular arrhythmias and relatively low potential for proarrhythmia, moricizine has a role in the treatment of malignant ventricular arrhythmias in selected patients.

Anti-Arrhythmia Agents↗
PubMed1990

Angiographic and electrophysiologic substrates of ventricular tachycardia in chronic Chagasic myocarditis.

Forty-three consecutive symptomatic patients with chronic Chagasic myocarditis and ventricular tachycardia (VT) underwent clinical evaluation, 24-hour Holter monitoring, left ventricular angiography and electrophysiologic testing including programmed ventricular stimulation at 3 drive cycle lengths at 2 sites in the right ventricle. The mean ejection fraction was 42 +/- 10%. Sixteen patients had clinical sustained VT and 27 nonsustained VT. VT was reproducibly initiated in 13 of 16 (81%) patients with sustained VT and in 14 of 27 (52%) patients with nonsustained VT. Electrocardiographic conduction disturbances were seen in 15 of 16 (94%) patients with sustained VT and in 17 of 27 (63%) patients with nonsustained VT (p less than 0.05). Five of 16 (31%) sustained VT and none of nonsustained VT patients had left ventricular aneurysms (p less than 0.05). These data indicate that VT is frequently inducible in patients with sustained VT and nonsustained VT and chronic Chagasic myocarditis. An association appears to be present between conduction disturbances on the electrocardiogram, left ventricular aneurysms and development of sustained ventricular arrhythmias.

Adult↗
PubMed1989

Ventricular arrhythmias: control of therapy by Holter monitoring.

Ventricular arrhythmias can be classified into categories based on the risk of sudden death associated with them. Patients with benign ventricular arrhythmias are those with minimal or no heart disease and normal ventricular function. Arrhythmias encountered in this group include ventricular premature complexes and unsustained ventricular tachycardia. In patients with prognostically significant ventricular arrhythmia, the arrhythmias are the same, namely, ventricular premature complexes and/or unsustained ventricular tachycardia. This group differs, however, in that the patients have organic heart disease and the risk of the arrhythmia increases as left ventricular function decreases. Patients with malignant ventricular arrhythmia, sustained ventricular tachycardia and ventricular fibrillation have the highest risk of sudden death. While no conclusive studies are available, some studies do suggest that the suppression of ambient ventricular arrhythmia as documented by Holter monitoring (and possibly exercise testing) identifies antiarrhythmic regimens which are effective in preventing sudden death. Variability in the frequency of ambient ventricular ectopy must be considered in assessing both efficacy and toxicity of antiarrhythmic regimens. Holter monitoring may also be useful in assessing the substrate of malignant ventricular arrhythmias and autonomic tone.

Arrhythmias, Cardiac↗