Cannabis and coronary thrombosis: What is the role of platelets?

To the editor

It has been established that cannabis has pathophysiological effects on the cardiovascular system. The relation between cannabis consumption and myocardial infarction is limited and existing data are controversial. We present a case of a young man, cannabis consumer, who was presented for refractory cardiac arrest secondary to an anterior myocardial infarction with left main coronary and left ventricle thrombus.

We report the case of a 20-year-old man, tobacco and cannabis smoker, with no cardiovascular past medical history who presented for a sudden cardiac arrest. He lost consciousness after a class course. He received cardiopulmonary resuscitation and was transferred to a coronary catheterization laboratory center. On arrival, after a transfer period of nearly 2 h, he had electrical signs of an anterior myocardial infarction. The echocardiography showed a harsh myocardial dysfunction (LVEF estimated at 10%) with a left ventricular apical thrombus (Figure 1). The coronary angiography highlighted a huge thrombus of the distal left main coronary artery (Figure 2A) that occlude the ostium of the left anterior descending (LAD) artery and embolize distally to the Circumflex artery (Cx) (Figure 2B). The right coronary artery (RCA; Figure 2C) was normal and supplied by retrograde course the occluded LAD (Figure 2D). The disseminated coronary emboli led us not to treat the left main thrombus. Facing the recurrence of cardiac arrests and the hemodynamic instability despite the full inotropic support with continuous infusion of vasoactive drugs, he was immediately assisted by a veno-arterial extra-corporeal membrane oxygenation to discharge the right side of the heart, and a left-to-right shunt was created by a blade and balloon atrioseptostomy to discharge the left side (Figure 3A and B). Later, he was transferred to the intensive care unit (ICU) and treated with UFH in order to obtain an activated clotting time of 170–200 s. Antithrombin III, prothrombin time, partial thromboplastin time, fibrinogen, homocystein, protein S, protein C, and plasminogen activator inhibitor-1 were in the normal range. Lupus anticoagulant, factor V Leiden, and prothrombin G20210A tests were negative. His stay in the ICU was marked by a multiple organ failure that regressed progressively. Later, he underwent heart transplantation and presented positive neurological signs but a severe septic shock of unknown entry point probably favored by immunosuppressive therapy led to a dramatic deterioration of his clinical status and death.

Figure 1. Cardiac ultrasound showing apical thrombus (arrow).

Figure 2. Coronary angiography showing thrombus of the left main coronary artery at its distal part (arrow) with zooming (A), abrupt obstruction (arrow) of the distal Circumflex artery (Cx) by emboli (B), normal RCA (C) which supply by retrograde course the occluded LAD artery (D).

Figure 3. Marshal balloon inflation in the atrial septum at its early phase with balloon imprints (arrows) (A) and its late phase (B) and the created atrial septum defect (ASD) on color Doppler cardiac ultrasound (C).

The cannabis smoke has been evoked as a trigger for cardiovascular events. The data concerning the effects of acute cannabis on thrombosis formation are controversial.

Platelet membrane preparations were positive to cannabinoid receptor CB1 and CB2 suggesting that platelets are potential target cells for cannabinoids (CBD) [1]. At high concentrations of cannabinoids, the platelets aggregate non-reversibly, independently of an added inducer, apparently due to lysis and release of endogenous inducers [2]. The platelets synthesize endogenous cannabinoid, the D9-tetrahydrocannabiol (THC). Some authors reported that large concentrations of THC inhibit the platelets aggregation by direct inhibition effect of an agonist-induced platelet aggregation [3], whereas others documented an increased platelets’ aggregation in the presence of THC [2]. Collagen- and thrombin-induced aggregations of washed platelets are hardly affected by the cannabinoids. THC and CBD also curtail ADP-induced reversible aggregation in platelet-rich plasma, while serotonin release and irreversible aggregation, caused by either ADP, collagen or thrombin, are not affected by the cannabinoids in platelet-rich plasma [2]. Moreover, this active metabolite, the THC, stimulates the sympathic system, inhibits the parasympathic system and induces the inflammatory response at the level of the arterial wall (oxidative stress, platelets activation, deformation of oxidize LDL and hyper-reactivation of factor VII) which leads to an endothelial erosion and thrombus formation in case of normal coronary arteries [4–10]. The reduced availability of nitric oxide secondary to the cannabinoids led to the disturbance of the endothelium function and resulted to activation, adhesion and aggregatrion of platelets [7]. Another explanation is that the glycoprotein IIb-IIIa and P selectin were expressed on the platelets surface subsequently to an enhancement by THC in a concentration-dependent manner [1] what led to platelets aggregation.

In our case, the cannabis in association with tobacco smoke were the only risk factors for thrombus formation in the left main coronary artery in this young patient with smooth normal coronary artery. In conclusion, numerous cases of acute myocardial infarction after using cannabis were reported. We wanted to emphasize that the risk of acute myocardial infarction is elevated after cannabis usage and the cannabis smoking could be a trigger to coronary thrombus formation. Therefore, we must worry about a chest pain in very young people especially when occurring in cannabis smokers.

Conflict of interest: None