Further, we show that disruption of caveolae nanodomains in a cardiac-specific Cav-3 conditional knock-out (Cav-3KO) mouse model and in an 8-week post-myocardial infarction mouse HF model impairs the synchronization of the pacemaker components and leads to LCR-to-AP failure, sinus pauses, increased heart rate lability, tachycardia-bradycardia paroxysms, and enhanced atrial ectopy. Here, CAV3 is linked to myocardial infarction.