In this EP-EDGE podcast episode, Dr. Niraj Sharma, cardiac electrophysiologist, breaks down the latest evidence linking modern high-THC cannabis to cardiovascular and electrophysiologic risk. Drawing from large real-world datasets, mechanistic studies, and global meta-analyses, this episode explains how today’s cannabis products—vapes, edibles, dabs, and synthetic cannabinoids—are very different from the low-potency marijuana of the past.

We explore the science behind CB1 receptor activation, autonomic imbalance, endothelial dysfunction, platelet activation, and how these mechanisms translate into real-world clinical outcomes—including:

• Atrial fibrillation and supraventricular tachycardia
• Premature atrial and ventricular beats
• Ventricular tachycardia and ventricular fibrillation
• Myocardial infarction and stroke in young adults
• Endothelial dysfunction as an early vascular warning sign
• Why high-potency THC and route of use (vaping, edibles, dabs) matter

This episode reviews landmark studies from JACC Advances, Heart, JAMA Cardiology, European Heart Journal, and Heart Rhythm, including massive EHR-based cohorts involving millions of patients. We also address common misconceptions, including why some older studies show neutral risk—and why those findings do not apply to modern high-potency cannabis use.

Whether you are a cardiologist, electrophysiologist, primary care clinician, or an informed patient, this episode provides a clear, evidence-based framework to understand why modern cannabis is not cardiovascularly benign and how it should be discussed in clinical practice—especially in patients with atrial fibrillation, ventricular arrhythmias, or unexplained cardiac events.

References, infographics, and detailed study breakdowns are available in the EP-EDGE LinkedIn Newsletter (December 2025 issue).

In this issue, we trace the fascinating evolution of atrial fibrillation (AF) therapy — from the Cox Maze procedure to Haïssaguerre’s discovery of pulmonary vein ectopy, through Pappone’s wide antral isolation, and onward to the era of pulse field ablation (PFA).

We explore how ablation technologies have transformed — radiofrequency, cryo, and PFA — yet the success rates remain stubbornly static. Why do some ablations fail? Are we reaching the limits of substrate modification, or simply targeting the wrong mechanisms?

Join Dr. Sharma as he dissects the mechanistic layers of ablation failure — from pulmonary vein reconnection and atrial substrate remodeling to inflammation, fibrosis, and autonomic imbalance. The discussion looks ahead to next-generation strategies that may redefine success in AF therapy.

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For questions, suggestions, or collaboration ideas, reach out at EPEdgeCast@gmail.com

What if stroke prevention in atrial fibrillation no longer meant trading protection for bleeding risk?

Factor XI inhibition—led by trials like AZALEA–TIMI 71, LILAC–TIMI 76, and LIBREXIA–AF—is poised to rewrite the anticoagulation playbook. By targeting the intrinsic pathway, these agents may decouple thromboembolic protection from major bleeding, potentially reshaping the role of left atrial appendage occlusion (LAAO) in stroke prevention strategies.

In this episode of EP Edge, Dr. Niraj Sharma breaks down the evolving data, drug classes, mechanistic rationale, and implications for future guidelines—while also looking at where structural interventions may still fit in this shifting landscape.

For: Source data/infographics see EPEDGE Newsletter on LinkedIn
For feedback, collaborations, or questions, email Dr. Niraj Sharma at epedgecast@gmail.com or connect on LinkedIn