Letter:
To the Editor:
The article ”Septal myectomy in the era of genetic testing” by Vincent
Chauvette et al. has been read with a great deal of passion and
curiosity. 1 This manuscript, which is brief and enlightening for
readers, is the result of the writers’ extraordinary efforts. Positive
genetic tests are associated with different features than negative ones.
Four distinct echocardiographic characteristics are exhibited by
patients. Only patients with a positive genetic test exhibit the type 3
phenotype. Importantly, regardless of the outcome of the genetic test,
the midterm outcomes of septal myectomy appear to be favorable.
Nonetheless, we feel compelled to highlight certain issues that would
have considerably improved the quality of this post and influenced its
outcomes.
First, we anticipate that the matching of samples would have raised
several doubts regarding the reliability of the results. The authors
recruited 21% females in the negative testing group and 45% females in
the positive testing group, with no gender parity. For illustration,a
2021 research by Roy Huurman et al.2 included 94 percent females and 95
percent males, recognizing the significance of a proper proportions of
both sexes, and concluded that women undergo septal myectomy in older
age and appear to have more aggressive disease based on
echocardiographic findings. However, the lag to myectomy was not longer,
indicating that the generational gap is not primarily due to a delay in
care. The clinical results of myectomy are satisfactory for both men and
women. Furthermore, authors should have emphasized on the midterm and
long-term survival outcomes after septal myectomy and its consequences.
Iatrogenic ventricular septal rupture is a well-known consequence of the
treatment, and electrocardiographic alterations such as left and right
bundle branch block, atrial fibrillation, and ventricular arrhythmias
are serious complications after septal myectomy.3 As mitral valve
leaflets and subvalvular apparatus anomalies play a significant role in
the pathophysiology of HOCM, the surgical care of the mitral valve has
been regarded as a crucial component of myectomy. Mitral regurgitation
is caused by the lack of coaptation of mitral leaflets caused by SAM.
Although medical therapy remains the firstline treatment, septal
myectomy is intended to improve symptoms and reduce sudden cardiac
deaths when the peak instantaneous left ventricular outflow tract
gradient is 50 mmHg at rest or with incitement and there are distressing
symptoms resistant to medical care.3
Fourth, more than 11 mutations of the sarcomere genes are known to be
responsible for HOCM. Two mutations in sarcomere-encoding genes, -myosin
heavy chain-(MYH7) and myosinbinding protein C, account for 70% of HOCM
cases in individuals for whom genetic testing was possible (MYBPC3).
Asymptomatic patients with MYH7 and MYBPC mutations exhibited an
increased left ventricular ejection fraction (LVEF) as well as diastolic
dysfunction.4 Surgical septal myectomy (modified Morrow technique) and
alcohol septal ablation are intended to decrease the LV bulk (ASA).
Surgical treatment is regarded as the gold standard, with an American
Guidelines class IIa recommended.