Mechanism and onset
The mechanism of VA in patients with MVS can include increased automaticity, BBR VT, and scar-related reentry. In our analysis, scar-related reentry was the major mechanism of arrhythmia. Increased automaticity and BBR were documented mostly with early-onset VT. The proximity of the His bundle to the mitral valve annulus makes it vulnerable to any pathological process or surgery involving the valve.24,25 Furthermore, hemorrhagic trauma to the His bundle and proximal bundle branches has been documented after MVS.25 These factors could facilitate BBR VT in the setting of elevated catecholamines and autonomic imbalance postoperatively. While VT has been well delineated in this patient cohort, less is known about non-BBR VT in these patients.10,12-16 Unlike BBR VT, scar-related reentry tends to be implicated in late-onset VA. A study of 29 patients with VT after valve surgery found that the BBR VT was responsible for VT in 8 (73%) of the 11 patients who presented within 30 days after surgery.11 Conversely, of 18 patients presenting with VT more than 30 days after their valve surgery, 17 had “myocardial” VT with only 1 having BBR VT. Though the mechanism of VT was not determined in these 17 patients, it is assumed that scar-related reentry is most likely given that 75% of these patients had CAD and reduced EF.
Another study has evaluated the VT characteristics and ablation outcomes in 20 patients with prior valve surgery including 6 patients with lone MVS and 2 patients with mitral and aortic valve surgery.10 Four patients had VT within 30 days of surgery, 2 of them were non-inducible, 1 was BBR VT and 1 was scar-related reentry. On the other hand, 81% of patients with late-onset VT (1 to 16 years after surgery) had scar-related reentry VT. Out of the 8 patients with MVS, 6 patients had inducible VT at EP study where scar-related reentry was the mechanism of VT in 5 patients and automatic VT was found in one patient. In 3 out of the 6 MVS patients with inducible VT, the origin of arrhythmia involved the mitral valve annulus with RBB morphology. This is consistent with our findings where RBB was the dominant morphology. However, the origin of VA did not involve the mitral annulus in the majority of our cohort.
Although electrophysiological scar was a universal finding in our patients, it is difficult to identify whether perimitral scar is related to MVS or the primary valve pathology that led to MVS. However, the absence of mitral annulus disjunction in our cohort may suggest that the scar was related to MVS though was often not critical to the observed arrhythmias. 26,27