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