Charles Kanakis

Arrhythmias documented by 24-hour continuous ambulatory electrocardiographic monitoring in young women without apparent heart disease

Results are reported of 24-hour ambulatory ECG recordings in 50 young women without apparent heart disease. During waking periods, maximum (sinus) rates ranged from 122 to 189 beats/min (bpm) (153 +/- 14 mean +/- SD) and minimum rates from 40 to 73 bpm (56 +/- 7). During sleeping periods, maximum and minimum rates ranged from 71 to 128 bpm (105 +/- 13) and from 37 to 59 bpm (48 +/- 6), respectively. Thirty-two subjects (64%) had atrial premature beats, with only one subject (2%) having greater than 100 beats/24 hrs. Twenty-seven subjects (54%) had ventricular premature beats, with only three subjects (6%) having greater than 50 beats/24 hrs. One subject (2%) had one three-beat episode of ventricular tachycardia. Two subjects (4%) had transient type I second-degree atrioventricular block.

The effects of delta-9-tetrahydrocannabinol (cannabis) on cardiac performance with and without beta blockade.

Systolic time intervals (STI) were measured in ten healthy male volunteers before and after intravenous (i.v.) administration of 25 μg/kg delta-9-tetrahydrocannabinol (A-9-THC). Mean ± SEM heart rate increased 32 ± 7 beats/min, while systolic and diastolic blood pressures were unchanged after lv-9-THC. Total electromechanical systole lengthened 17 ± 4.2 msec, left ventricular ejection time (LVETC) prolonged 24 ± 4.0 msec and pre-ejection period (PEP) shortened 17 ± 5.1 msec after A-9-THC. All these changes were significant (P < 0.01). In nine other subjects who underwent prior beta adrenergic blockade, similar but less marked changes were noted in heart rate, blood pressure, and STI after A-9-THC. The shortening of PEP after A-9-THC was only 9 msec (NS) in beta blocked subjects. Thus, A-9-THC significantly increased heart rate, shortened PEP and prolonged LVETC without any change in afterload. Beta adrenergic blockade prevented significant shortening of PEP and blunted other responses. These findings suggest that A-9-THC enhanced cardiac performance. Partial inhibition of this effect was achieved with prior beta adrenergic blockade.

The electrophysiological effects of delta-9- tetrahydrocannabinol (cannabis) on cardiac conduction in man

Summary Electrophysiologic studies were performed in six patients before and after administration of 25 mcg./Kg. of intravenous delta-9-tetrahydrocannabinol (Δ-9-THC). The mean±SEM sinus length was 785±76 msec. prior to and 563±42 msec. after THC (p In conclusion, Δ-9-THC produces a potent effect on the heart, probably centrally mediated through the autonomic nervous system, with markedly enhanced sinus automaticity and facilitation of sinoatrial and A-V nodal conduction. The clinical significance (therapeutic or deleterious) of these pharmacological effects needs further evaluation.

Significance of site of origin of premature ventricular contractions

Abstract One hundred and sixty-five inpatients with premature ventricular contractions (PVCs) were clinically evaluated in regard to the presence (130 patients) or absence (35 patients) of organic heart disease. PVCs were classified based on QRS morphology (bundle branch block pattern) in Lead V 1 as being either left ventricular (66 patients), right ventricular (71 patients), or of both ventricles (28 patients). The incidence of organic heart disease was significantly greater in patients with left ventricualr PVCs 60 of 66 (91 per cent) and biventricular PVCs 25 of 28 (89 per cent) than in patients with right ventricular PVCs 45 of 71 (63 per cent) (p These data suggest the following conclusions regarding inpatients with PVCs: (1) Organic heart disease is frequent in patients with right ventricular PVCs and almost universally present in patients with left ventricular and biventricular PVCs. (2) Patients without organic heart disease primarily have PVCs of right ventricular origin. The mechanism of the latter association is unknown.

Return of normal conduction after paroxysmal heart block. Report of a case with major discordance of electrophysiological and pathological findings.

This report describes a 52-year-old male with paroxysmal heart block as well as left and right bundle branch block, resulting in Stokes-Adams attacks. The patient experienced a return to 1:1 atrioventricular (A-V) conduction with narrow QRS within 48 hours of the attacks and heart block never recurred. Electrophysiological studies three weeks later revealed a narrow QRS, a normal H-V interval (36 msec), 1:1 A-V conduction up to an atrial paced rate of 210 beats/min, and normal refractory periods with atrial extrastimulus techniques (His-Purkinje system refractory periods less than 370 msec). The patient died from a cerebral embolus incurred during diagnostic left heart catheterization two days after electrophysiological studies. Postmortem examination revealed calcific aortic stenosis with calcific impingement upon the pars membranacea resulting in compression of the distal His bundle and marked disruption of the proximal portions of both bundle branches. This report documents a major limitation of electrophysiological studies, this limitation being that these studies may be totally normal on one occasion in a patient with pathologically significant chronic conduction disease, which may become clinically manifest on another occasion.

Lack of Cardiovascular Effects of Delta-9-Tetrahydrocannabinol in Chemically Denervated Men

We have previously reported that 25 micrograms/kg of intravenous (i.v.) delta-9-tetrahydrocannabinol (delta-9-THC) produces marked increases in heart rate, prolongation of left ventricular ejection time corrected for heart rate (LVETc), and a shortening of the pre-ejection period in normal volunteers. Beta-adrenergic blockade partially attenuates these responses. To elucidate further the mechanism of action of delta-9-THC, we gave 10 normal volunteers 0.1 mg/kg of i.v. propranolol and 2 mg of i.v. atropine before they received 25 micrograms/kg of i.v. delta-9-THC. Systolic time intervals were compared in the denervated subjects before and after delta-9-THC. Post delta-9-THC responses were measured at a time approximating peak psychologic high. Mean +/- SEM heart rate before and after delta-9-THC was 89 +/- 4 and 87 +/- 3 beats/min (NS); mean +/- SEM pre-ejection period before and after delta-9-TCH was 107 +/- 5 and 109 +/- 4 ms (NS); and mean +/- SEM LVETc before and after delta-9-THC was 433 +/- 6 and 429 +/- 6 ms (NS). Since previous denervation of our subjects with atropine and propranolol totally abolished changes in heart rate and systolic time intervals, the cardiac effects of delta-9-THC appear to be mediated totally via the autonomic nervous system, probably reflecting direct central nervous system stimulation.