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Biomedical subjects

R Waksman

Publications and source records attributed to R Waksman.

4 recordsLinked to original sources
PubMed1992

Autodecremental pacing for the interruption of ventricular tachycardia and atrial flutter.

The efficacy and safety of autodecremental pacing (ADP) to interrupt ventricular tachycardia (VT) and atrial flutter was examined. Once tachycardia was recognized, ADP was initiated using a short train of stimuli with gradual shortening (3%) of the interstimulus interval. ADP was applied to 13 consecutive patients during 75 episodes of VT (mostly following induction by ventricular stimulation). Successful interruption of VT occurred in 88% of the episodes. In 6 episodes (8%), ADP resulted in ventricular fibrillation and in 3 episodes VT was unaffected by ADP. The only significant discriminator between the failure or success of ADP was the rate of VT. ADP was also applied to 17 consecutive patients with an atrial flutter that was resistant to conventional antiarrhythmic agents. Successful conversion of atrial flutter to sinus was seen in only 8 patients (47%). A temporary acceleration to atrial fibrillation appeared in 3 patients (18%), and in 6 patients atrial flutter was unaffected by ADP. ADP was successful in 70% (7/10) of patients with type 1 (< 300 beats/min) atrial flutter. The authors conclude that ADP is beneficial in the interruption of VT and atrial flutter in a selected group of patients, especially with a slower rate of tachyarrhythmia (atrial rate during atrial flutter < 300 beats/min and ventricular tachycardia < 180 beats/min).

Adult↗
PubMed1990

Systemic embolization following thrombolytic therapy for acute myocardial infarction.

We describe a patient with acute inferior myocardial infarction who developed a "saddle" aortic embolus during streptokinase infusion. Three months previously, this patient had sustained an anterior infarction, and an apical aneurysm was found. This patient's embolus had most probably originated from a left ventricular mural thrombus that had been dislodged by streptokinase. As fibrinolytic treatment is gaining wide acceptance, physicians should be aware of this rare, but possible, complication.

Aged↗
PubMed1988

Nitrendipine prevents the development of cardiac hypertrophy in DOCA-salt-treated hypertension-prone (SBH) and -resistant (SBN) rats through nonhemodynamic mechanisms.

Recent studies indicate that cardiac and renal hypertrophy develop during desoxycorticosterone acetate (DOCA)-salt (DOC) treatment in hypertension-prone (SBH) and -resistant (SBN) rats, irrespective of systemic hemodynamic changes. The effect of nitrendipine on the development of left and right ventricular hypertrophy (LVH and RVH, respectively) was evaluated in 16-week-old rats. Members of each strain were divided into six groups (n = 10): 1--control; 2--nitrendipine treated for 3 weeks; 3, 4, and 5--DOC for 10 days, 3 weeks, and 6 weeks, respectively; 6--DOC for 6 weeks and nitrendipine for the last 3 weeks. Cannulae were inserted into the left ventricle and abdominal aorta. The radioactive reference sample microsphere technique was used to measure cardiac index. Mean arterial pressure (MAP) and total peripheral resistance index (TPRI) were unchanged in all six groups of SBN rats, whereas MAP and TPRI increased progressively in the DOC-treated SBH groups. Concomitant administration of nitrendipine in Group 6 was associated with a reduction of MAP and TPRI to control levels. Cardiac index and heart rate did not change in any group. Despite the different hemodynamic changes, both SBH and SBN rats developed LVH and RVH. The concomitant administration of nitrendipine prevented the progression of LVH and allowed regression of RVH in both strains. It is concluded that nitrendipine can affect the pathogenesis of LVH through nonhemodynamic mechanisms.

Animals↗