Comment
CLVD often represent novel territory with regards to management and, at
times, diagnosis for most heart teams. Not only is the prevalence fairly
low, ubiquitously lower than 1% as previously described, but
additionally the natural history of the disease is not well delineated.
There are two distinct pathologies that are clearly described in the
literature, with CLVD representing an outpouching from the ventricle,
with synchronous contraction, and histologically similar to that of the
ventricular wall from which it protrudes. Congenital left ventricular
aneurysm (CLVA) represents the other end of the spectrum, whereby the
outpouching is dyskinetic or altogether akinetic, and histologically
composed of fibrous tissue, dissimilar to that of the ventricular wall
[5]. Despite the dearth of epidemiological data, CLVD are not
clinically silent, with reports of important cardiac complications such
as thromboembolism, ventricular arrhythmias, and myocardial ischemia.
Additionally, catastrophic CLVD rupture has been described, leading to
sudden death [6].
Due to the rarity of CLVD, there is little guidance for the clinician
regarding appropriate treatment paradigms, be it a surgical or
conservative approach. In a review of 809 patients published since 1816
with either CLVD or CLVA, 4.5% of patients with CLVD were found to have
an episode of rupture, and a 5.0% reported rate of cardiac death. Other
significant complications included ventricular tachycardia/fibrillation
in 13.1%, embolic events 3.6%, and syncope 5.1% [7].
Despite the existence of a concise review of the cases reported to date,
there is little in the way of a detailed surgical approach. Some authors
have reported closure of the diverticulum neck with a patch, with
surgical glue closure and plication with aneurysmorrhaphy [8]. Other
authors have described their technique as suture reapproximation in a
double layered fashion with the use of felt [9], while some describe
removal of the outpouching cavity and closure with an in-situ patch
[10].
Due to the catastrophic events associated with CLVD, our institution
prefers surgical management for patients with symptomatic CLVD. The
first patch of our two patch technique helps retain the native geometry
of the left ventricle. Meanwhile, linear closure of the CLVD may cause a
reduction of the ventricular diameter and distortion of contractile
force vectors. The addition of a second patch to the ventricular
epicardial surface in our approach decreases early postoperative
bleeding and should minimize long term aneurysm formation and rupture.
Further study is necessary to determine the benefits of this technique.