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Cocaine use is associated with adverse events in nearly every organ system. Cardiovascular complications include hemorrhagic and ischemic stroke, aortic dissection, cardiomyopathy, accelerated coronary artery disease, myocardial infarction, and sudden cardiac death. Syncope may be the presenting symptom in these conditions. However, cocaine-induced bradyarrhythmias have been scarcely mentioned. As this case exemplifies, clinicians should be aware of this association when they evaluate syncope, especially in young patients.

A man with ventricular extrasystoles is described. To our knowledge, this is the first report of bradycardia dependent appearance of manifest extrasystoles in concealed trigeminy. The mechanism was satisfactorily explained, using the concepts of longitudinal dissociation and concealed 3:2 Wenckebach periodicity in the reentrant pathway of extrasystoles.

A patient with obstructive sleep apnea was monitored five times during three years while his weight fluctuated within a range of 26 kg. The number of apneas per hour of sleep varied from 59.6 at 111 kg of weight to 3.1 at 85 kg. The relation between apneas per hour of sleep and body weight was a logarithmic function. A modest decrease in weight was thus associated with a disproportionally larger decrease in the rate of apneas. Typical SaO2 levels during the apneic episodes also had a logarithmic relation with body weight. Apnea-related sinus bradycardia and sinus tachycardia were only present at the highest weight. The results suggested that dieting and weight loss lead to an improvement in sleep apnea and related sequelae.

A recurrent tachyarrhythmia complicated the course of a patient with a permanent atrioventricular sequential (bifocal) demand pacemaker. Investigation by intracardiac electrocardiographic studies revealed that the arrhythmia was associated with normally functioning bifocal pacemaker, whose atrioventricular sequential interval approximated the patient's conduction time from atrium to ventricle. The mechanism of initiation and conversion of the arrhythmia was elucidated. Appreciation of this arrhythmia is necessary for appropriate clinical use of a bifocal demand pacemaker.

This report describes the clinical course of a patient with bradycardia and tachycardia-dependent atrioventricular block. Bradycardia dependent A-V block (phase 4 block) was transient and precipitated by spontaneous slowing of the sinus rate, atrial and ventricular extrasystoles; The degree of slowing (critical RP interval) required to induce A-V block increased progressively over a three-day period. Bradycardia-dependent A-V block was terminated mostly by critically times spontaneous or paced ventricular escape beats, but normally conducted atrial impulses also appeared to restore A-V conduction on several occasions. The tachycardia-dependent component was manifested by an unusual fatigue phenomenon in the His-Purkinje system seen only at an atrial pacing rate of 150 per minute. These observations document the presence of both bradycardia and tachycardia-dependent A-V block in the presence of a normal H-V time and also illustrate the dynamic nature of both phase 4 block and the period of "supernormal" intraventricular conduction.

Drugs interfering with sympathetic tone may result in depression of the function of the sinus node, especially in patients with disease of the sinus node. In 11 patients presenting with palpitations, vertigo, or syncope, the heart rate, the recovery time of the sinus node, the carotid sinus pressure slowing, and the atrioventricular conduction capacity were assessed before and every five minutes up to 30 minutes after intravenous administration of 0.15 mg of clonidine. The following significant maximal mean effects were noted at about 15 minutes after the administration of clonidine: the heart rate decreased 12 percent (59 vs 52 beats per minute); and the atrioventricular conduction capacity (ie, paced heart rate at second-degree atrioventricular block) decreased by 9 percent (132 vs 121 beats per minute), while the maximal recovery time of the sinus node increased by a factor of two (1,704 vs 3,562 msec) when atrial overdrives of 120, 150, and 200 beats per minute were used for each five minute period. In analyzing maximal carotid sinus pressure slowing after administration of clonidine, three of 11 patients developed hypersensitive carotid sinus reflex de novo, and two patients showed a decrease and three patients an increase of carotid sinus pressure slowing, while three patients had no carotid sinus pressure slowing both before and after administration of clonidine. We conclude that caution should be taken in administering clonidine to patients with signs indicative of dysfunction of the sinus node.

The management of symptomatic bradyarrhythmias can be challenging in patients in whom cardiac pacing is not indicated, such as in the terminally ill or severely demented. We applied a transdermal scopolamine patch on one such patient with resultant substantial improvement in his supraventricular bradyarrhythmia.