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Biomedical subjects

V Santinelli

Publications and source records attributed to V Santinelli.

At least 37 records · Page 2Linked to original sources
PubMed1987

Ventricular parasystole and ventricular couplets: a re-entry within the parasystolic focus?

We report a 62-year-old man with a persistent ventricular rhythm originating in a parasystolic focus associated with frequent ventricular couplets with fixed coupling. Both intravenous (IV) procainamide (1 g) and propafenone (70 mg IV) promptly suppressed only the second component of ventricular couplets, suggesting that re-entry rather than enhanced automaticity was the mechanism of ventricular couplets. On the contrary, the nonresponse of ventricular rhythm and ventricular couplets to verapamil (10 mg IV) suggested that triggered activity should not play a role in the genesis of this ventricular rhythm. The mechanisms of the ventricular couplets (rapidly discharging parasystolic focus vs. re-entry) are discussed.

Arrhythmias, Cardiac↗
PubMed1984

Sick sinus syndrome: the role of hypervagotonia.

A 58-year-old man with persistent symptomatic sinus bradycardia (52 beats/min) showed a markedly prolonged postpacing pause (3240 msec) after atrial pacing at a cycle of 840 msec. In addition, Wenckebach block occurred following atrial pacing at a cycle length of 700 msec. After atropine (2 mg) postpacing pauses returned to normal value and type 1 second-degree AV block completely reversed to 1:1 AV conduction until paced rates greater than 140/min. It may be that in some patients marked and persistent vagal overactivity may predispose to "intrinsic" sinus node dysfunction; in later stages, sinus node function may paradoxically result unaffected by changes in autonomic tone.

Heart Block↗
PubMed1984

Nonparoxysmal atrioventricular junctional rhythm. A clinical and electrophysiologic study.

The patient, a 74-year-old man, developed a persistent nonparoxysmal junctional accelerated rhythm at rate of 60-75 beats min-1 because of chronic depressed sinus node function. Intravenous atropine resulted in no change of junctional pacemaker rate but i.v. isoproterenol significantly accelerated it suggesting that autonomic neural imbalance might underlie the mechanism of nonparoxysmal junctional rhythm. Intravenous verapamil (10 mg) induced no change in the junctional pacemaker rate and postpacing pauses suggesting that the slow inward current did not play an important role in the nonparoxysmal junctional rhythm.

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