Casq2 deletion causes sarcoplasmic reticulum volume increase, premature Ca²⁺ release, and catecholaminergic polymorphic ventricular tachycardia
J. Clin. Invest. Björn C. Knollmann, et al. 116:2510 doi:10.1172/JCI29128 [Go to this article.]

Figure 3
Casq2^–/– mice display catecholaminergic ventricular ectopy and exercise-induced polymorphic VT. (A and B) Continuous heart rate plot and examples of surface ECG (lead 1) recordings from an anesthetized Casq2^+/+ (A) and Casq2^–/– mouse (B) injected with the β-adrenergic receptor agonist isoproterenol (1.5 mg/kg i.p.; arrowhead). Note the multifocal PVCs (*) at the peak of the heart rate response in the Casq2^–/– mouse. (C) Example of a telemetric ECG recording from a conscious Casq2^–/– mouse obtained shortly after a treadmill exercise tolerance test. PVCs, couplets (#), and runs of polymorphic VT were frequently observed in Casq2^–/– mice. All episodes of polymorphic VT reverted spontaneously back to sinus rhythm (b, sinus beat; lower record). (D) Example of bidirectional VT recorded in another Casq2^–/– mouse. Bidirectional VT was initiated after several bigemini and couplets and terminated into stable bigemini. (E) Average rate of PVCs and VT episodes during a 10-minute period of post-exercise telemetric ECG recordings. n = 5 mice per genotype; ^†P < 0.05, **P < 0.01.