Abstract

Marijuana is the most commonly abused recreational substance. With the increasing legalization of marijuana, its use is expected to rise. Delta-9-tetrahydrocannabinol (THC) is the psychotropic component of marijuana, acting via CB1 and CB2 G-protein coupled cannabinoid receptors. Marijuana has serious cardiovascular effects including tachycardia, orthostatic hypotension, angina and myocardial infarction to name a few. Previous reports by our group and others documented various arrhythmias other than atrioventricular nodal reentrant tachycardia (AVNRT) that are associated with marijuana use. In this report, we present a case of AVNRT associated with marijuana use. Marijuana in high doses stimulates parasympathetic nerves. While parasympathetic stimulation can increase the refractory period of the fast conduction pathway, it has no effect on the slow and retrograde pathways, therefore its use creates an ideal milieu for AVNRT initiation and maintenance. Our case report highlights the importance of including marijuana use in the differential diagnosis, as a possible trigger, for patients presenting with AVNRT that is otherwise unexplainable.

1. Introduction

Marijuana is the most common drug of abuse in the United States, with use expected to rise due to legalization for medical and recreational purposes ¹. Delta-9-tetrahydrocannabinol (THC) is the psychotropic component of marijuana, acting via CB1 and CB2 G-protein coupled cannabinoid receptors, which are also present in the heart ^{2, 3}. Marijuana with increased potency has become available in recent years ⁴. Tachycardia, hypotension, myocardial infarction and decreased time to angina are among the cardiovascular effects reported with marijuana use ⁵. To our knowledge, we present the first reported case of atrioventricular nodal reentrant tachycardia (AVNRT) associated with marijuana use, and discuss the possible mechanism of marijuana initiated AVNRT.

2. Case Report

A 40 year-old male with no known past medical history presented with palpitations that started within one hour after smoking marijuana. The palpitations were associated with substernal chest pain, which was non-radiating, not pleuritic, and not related to change in position. The patient denied dizziness or syncope. Exercise tolerance at baseline was more than 1 mile. At time of presentation, his heart rate was 190 beats per minute, blood pressure was 117/57 mmHg, respiratory rate was 18 per minute, and he was afebrile. Electrocardiography revealed the rhythm to be AVNRT (Figure 1). The patient spontaneously converted to normal sinus rhythm with premature ventricular complexes (Figure 2). Bloodwork revealed no electrolyte abnormalities and the patient was euthyroid. Urine toxicology was positive for marijuana use and negative for other illicit drugs. Mild troponin elevation was noted, with values of 0.018, 0.213, and 0.138 ng/mL (normal value < 0.010 ng/mL). The levels were attributed to demand ischemia. The patient underwent AVNRT ablation without complications.

3. Discussion

Two distinct atrial impulses approach the atrioventricular node (AV) node—one from the fast pathway located in the anterior portion of the triangle of Koch, and the other via the posterior pathway located in the posterior portion of the triangle of Koch. As the name suggests, the anterior pathway has faster conduction but a longer refractory period; and the posterior pathway conducts more slowly but has a shorter refractory period. This difference in the refractoriness of the two pathways is key in the pathophysiology of AVNRT. In normal sinus rhythm the conduction occurs via the fast pathway. In susceptible individuals, a premature atrial beat may find the fast pathway refractory; however, the slow pathway may be available for conduction. If the impulse reaches the common end when the fast pathway has repolarized there may be retrograde conduction via the fast pathway back to the atrium. Thus, a re-entrant pathway of the “slow to fast” variety of AVNRT may be established. This type of AVNRT is referred to as typical AVNRT ^{5, 6}. In typical AVNRT the P-waves may be buried in QRS complex or appear at the end of the QRS complex ⁷. Nicotine, alcohol, exercise, stimulants, and a surge in vagal tone are reported triggers of AVNRT ⁸.

The effect of marijuana on the conduction system of the heart are not fully understood. Various arrhythmias reported to date are summarized in Table 1. A change is P-wave morphology may be noted following marijuana use suggesting an effect on the atrium ³³. Decreased sinoatrial (SA) conduction, delayed atrium to bundle of His (A to H interval) conduction, and a decreased AV node refractory period are reported effects of THC ³⁴. Autonomic nervous system mediated increases in SA and AV node conduction have been reported ³⁵. There are differences in the regional sympathetic and parasympathetic neuronal distributions in the heart. Vagal influence is predominant in the SA node and sympathetic nerves predominate in the atrium ³⁶. Marijuana’s effect on sympathetic and parasympathetic nerves appear to be dose dependent, with sympathetic nerves stimulated at lower doses and parasympathetic at higher doses ³⁷. Vagal tone has different effects on the fast and slow pathways. Vagal tone increases the refractory period of the fast pathway but does not have this effect on the slow pathway and retrograde fast pathway ³⁸. This may explain the occurrence of AVNRT during periods of heightened parasympathetic tone ³⁸. Marijuana induced parasympathetic stimulation may cause inhibition of the fast pathway, and a premature atrial complex generated at this time may be conducted antegrade via the slow pathway with subsequent retrograde conduction, thus initiating AVNRT.

In conclusion, marijuana may be a trigger for AVNRT. Health care providers should be aware of this and consider marijuana use as a potential trigger of AVNRT. A focused history and urine toxicology screen may aid in the diagnosis.

Acknowledgements

This work is supported, in part, by the efforts of Dr. Moro O. Salifu M.D., M.P.H., M.B.A., M.A.C.P., Professor and Chairman of Medicine through NIH Grant number S21MD012474.

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