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Biomedical subjects

T J Cohen

Publications and source records attributed to T J Cohen.

At least 73 records · Page 4Linked to original sources
PubMed1991

Mixed venous oxygen saturation for differentiating stable from unstable tachycardias.

Current antitachycardia systems are incapable of adequately distinguishing stable from unstable tachycardias. Previously, integration of a pressure sensor or an impedance sensor, together with electrogram analysis, has been investigated as an improved method of identifying unstable arrhythmias. A mixed venous oxygen saturation sensor was investigated for differentiating stable from unstable paced and induced tachycardias in 10 patients. During rapid pacing at 600, 500, 400, 350, 300, and 250 msec cycle lengths, mixed venous oxygen saturation decreased as cycle length decreased. For any given cycle length, rapid ventricular pacing tended to result in greater mixed venous oxygen desaturation compared with atrial pacing. Mixed venous oxygen saturation decreased similarly during induced ventricular tachycardias at cycle lengths greater than 230 msec. However, ventricular tachycardias at cycle lengths less than or equal to 230 msec and ventricular fibrillation had no effect on mixed venous oxygen saturation until after termination. Subsequently, a mixed venous oxygen saturation-tiered therapy algorithm (cycle length less than or equal to 230 msec = unstable; cycle length greater than 230 msec and MVO2 greater than or equal to 6% over 30 seconds = unstable) was developed and was tested retrospectively in 113 paced and induced tachyarrhythmias in these 10 patients for detecting unstable tachycardias (defined as a decrease from baseline systolic arterial pressure of greater than or equal to 50 mm Hg at 15 seconds). The mixed venous oxygen algorithm had 93% sensitivity and 96% specificity compared with rate-only (rate greater than or equal to 170 beats/min) detection with 93% sensitivity and 71% specificity.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗
PubMed1991

Patients with supraventricular tachycardia presenting with aborted sudden death: incidence, mechanism and long-term follow-up.

A total of 13 (4.5%) of 290 patients with aborted sudden death had either documented (7; 54%) or strong presumptive evidence of supraventricular tachycardia that deteriorated into ventricular fibrillation. Six (46%) of the 13 had an accessory conduction pathway and either atrial fibrillation (5 patients) or paroxysmal atrioventricular (AV) reentrant tachycardia (1 patient) that deteriorated into ventricular fibrillation. Three patients with AV node reentrant tachycardia and four with atrial fibrillation and enhanced AV node conduction presented with supraventricular arrhythmias that deteriorated into ventricular fibrillation. Patients were treated with medical, surgical or catheter ablative procedures designed to prevent recurrences of supraventricular arrhythmias. Four patients received an implanted automatic defibrillator, but none had an appropriate device discharge. Over a follow-up period of 41.6 +/- 33.6 months, 12 patients are alive without symptomatic arrhythmias. One patient died because of severe chronic lung disease and heart failure. Supraventricular tachycardia was the cause of aborted sudden death in approximately 5% of patients referred for evaluation of sudden cardiac death. Treatment directed at prevention of supraventricular tachycardia was associated with an excellent prognosis. Current treatment techniques appear to obviate the need for automatic defibrillator therapy in these patients.

Adult↗
PubMed1991

Radiofrequency catheter ablation for treatment of bundle branch reentrant ventricular tachycardia: results and long-term follow-up.

Seven of 120 consecutive patients with inducible sustained ventricular tachycardia (from September 1, 1988 to January 1, 1991) had bundle branch reentrant tachycardia and underwent percutaneous radiofrequency ablation of the right bundle branch. The seven patients had been unsuccessfully treated with a mean of 3 +/- 1 drugs. Four patients presented with syncope and three with aborted sudden death. The baseline electrocardiogram revealed a left bundle branch block pattern in three patients and an intraventricular conduction defect in four. The baseline HV interval was prolonged in each case (79 +/- 2 ms). With use of programmed ventricular extrastimuli, sustained bundle branch reentrant tachycardia was inducible in all patients at a mean cycle length of 283 +/- 17 ms (range 230 to 350). Bundle branch reentrant tachycardia characteristics included atrioventricular dissociation, a His deflection that preceded each QRS complex and spontaneous His to His variation that preceded changes in ventricular tachycardia cycle length. A quadripolar catheter was positioned across the tricuspid valve with the distal electrode tip of the catheter near the right bundle branch. One to three applications of continuous unmodulated radiofrequency current at 300 kHz between the distal electrode and a large posterior skin patch resulted in complete right bundle branch block in all patients, after which none had inducible bundle branch reentrant tachycardia on restudy. On restudy, three of the seven patients had ventricular tachycardia of myocardial origin (not bundle branch reentry). One patient required no therapy; drug or defibrillator therapy was used in the others.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Implantable cardioverter defibrillator proarrhythmia: case report and review of the literature.

A 31-year-old man who received an automatic cardioverter defibrillator subsequently underwent exercise testing. During exercise, a sinus tachycardia resulted above his device detect rate prompting two shocks, the second of which produced an unstable polymorphous ventricular tachycardia. In this article, we review the literature on automatic cardioverter defibrillator-induced ventricular tachyarrhythmias as well as the management of exercise testing in patients with these devices.

Adult↗
PubMed1991

Candida albicans pacemaker site infection.

A 69-year-old man with a history of diabetes and episodic lymphocytopenia underwent pacemaker implantation for complete heart block. Despite prophylactic antibiotics, pocket irrigation, and strict sterile technique, a fungal (Candida albicans) pacemaker site infection developed that required pacemaker explanation and systemic amphotericin B therapy. After 3 days of temporary pacing, a second pulse generator was implanted on the opposite side. At 2-year follow-up, he has had no recurrence of pacemaker infection. This report underscores the predilection of diabetics for infections, and in particular, their susceptibility to Candida albicans.

Aged↗
PubMed1991

Biosensor applications to antitachycardia devices.

Current arrhythmia detection algorithms are unable to adequately distinguish stable from unstable tachycardias; therefore application of a biosensor to antitachycardia devices has been proposed to improve their performance. Right heart pressures and impedance have been investigated for incorporation into these systems. Integration of other parameters (oxygen saturation, preejection period, pH, cardiac output, flow, and temperature) into these devices might also prove useful. The status of these biosensor arrhythmia detection algorithms and their application to antitachycardia devices are described below.

Algorithms↗
PubMed1990

A hemodynamically responsive antitachycardia system. Development and basis for design in humans.

Current automatic implantable cardioverter-defibrillators detect tachyarrhythmias primarily by rate-only algorithms and cannot adequately distinguish hemodynamically stable from unstable tachyarrhythmias. The responses of right atrial (mean) and right ventricular pressures (mean, systolic, diastolic, and pulse) to 64 induced and paced supraventricular and ventricular tachyarrhythmias were studied in 10 patients (left ventricular ejection fraction of 32 +/- 6%) to develop an algorithm capable of differentiating stable from unstable rhythms. Tachyarrhythmias were defined as hemodynamically unstable when mean arterial pressure decreased by 25 mm Hg or more during 15 seconds. Mean right atrial, right ventricular systolic, and right ventricular pulse pressures were found to be useful in distinguishing the hemodynamic significance of a tachyarrhythmia. A combined detection algorithm was developed that identified a hemodynamically unstable rhythm when the heart rate was 150 beats/min or more and mean right atrial pressure increased by 4 mm Hg or more and right ventricular systolic pressure decreased by 5 mm Hg or more during 15 seconds. This algorithm was then applied to the next 20 consecutive patients (left ventricular ejection fraction of 34 +/- 4%) and compared with the current rate-only algorithm (heart rate of 150 beats/min or more) in 143 tachyarrhythmias, and the sensitivity and specificity for detection of hemodynamically unstable tachyarrhythmias were determined. The rate-only detection algorithm had 100% sensitivity but only 68% specificity for detection of unstable tachyarrhythmias, whereas the combined rate-mean right atrial pressure-right ventricular systolic pressure detection algorithm had sensitivity and specificity of 100%. Therefore, the performance of an antitachycardia system may be significantly improved by detection algorithms that integrate hemodynamic and rate criteria.

Blood Pressure↗
PubMed1988

Hemodynamic responses to rapid pacing: a model for tachycardia differentiation.

The hemodynamic responses to rapid atrial and ventricular pacing were examined in 10 closed-chest anesthetized dogs in an attempt to distinguish hemodynamically stable from unstable tachycardias. Pressure monitoring catheters were placed in the femoral artery, right atrium, and right ventricle to measure mean arterial pressure, mean right atrial pressure, and mean right ventricular pressure at baseline heart rate and after rapid high right atrial and right ventricular apex pacing. Pressures recorded during rapid pacing (average of the pressures at 30 and 60 seconds of pacing) at pacing rates of 180, 250, and 280/minute were compared to those recorded initially at baseline heart rates. Rapid right ventricular apex pacing resulted in significant increases in mean right atrial pressure (from 6 +/- 1 mmHg (mean +/- standard error) to 12 +/- 1 mmHg, a 100% increase, P less than 0.001) and mean right ventricular pressure (from 11 +/- 1 mmHg to 16 +/- 1 mmHg, a 45% increase, p less than 0.02) with marked hemodynamic compromise (mean arterial pressure decreased from 85 +/- 6 mmHg to 50 +/- 6 mmHg, a 41% decrease, P less than 0.01). These parameters remained stable (no statistically significant difference from baseline) during high right atrial pacing. In half of the dogs high right atrial pacing at rates greater than or equal to 250 resulted in atrioventricular Wenckebach. Thus, it is concluded that mean right atrial pressure and mean right ventricular pressure may be useful in distinguishing hemodynamically significant tachycardias, and in the future design of antitachycardia devices.

Animals↗
PubMed1984

A theoretical right atrial pressure feedback heart rate control system to restore physiologic control to the rate-limited heart.

Physiologic control of heart rate may be limited by sinus node injury or congenital conduction defects. Control theory may be applied to restore physiologic rate control. Mean right atrial pressure is a likely candidate for incorporation into an artificial control system because of its: (1) stability at rest; (2) tendency to increase during exertion in the rate-limited heart; (3) ability to decrease with increasing heart rate in the rate-limited heart; and (4) accessibility for measurement via the transvenous route. A theoretical right atrial pressure feedback heart rate control system is presented; applications to physiologic pacing of patients with sick sinus syndrome, rate control of the transplanted heart, and pump frequency control of the total artificial heart are discussed.

Arrhythmias, Cardiac↗
PubMed1978

The levels of cyclic GMP and glucose 1,6-diphosphate, and the activity of phosphofructokinase, in muscle from normal and dystrophic mice.

A striking reduction in the levels of glucose 1,6-diphosphate and an increase in cyclic GMP were found in muscle from dystrophic mice. Concomitant to these changes, the allosteric activity of phosphofructokinase was found to be markedly reduced. These findings could offer an explanation for the observed reduction in glycolysis in the dystrophic muscle.

Allosteric Regulation↗