The clinical diagnosis of HOCM is conventionally
made most commonly with two-dimensional
echocardiography. In HOCM, the flow against the
abnormally positioned mitral valve apparatus results
in drag force on a portion of the mitral valve leaflets
during ventricular systole which pushes the leaflets
into the outflow tract. The outflow obstruction causes
an increase in the LV systolic pressure, leading
to prolongation of ventricular relaxation and, thus,
elevation of LV diastolic pressure, mitral regurgitation,
myocardial ischemia, and decrease in cardiac output
eventually.[
10,
11]
Although there are no randomized trials
comparing SM and SAA in the literature, several
meta-analyses have shown that both procedures
improve functional status with a comparable
procedural mortality rate.[12] In the present study,
we compared the systolic gradient of the LVOT in
the patients who underwent SM versus SAA using
two-dimensional transthoracic echocardiography.
According to our study, although the differences at
the mean gradient of LVOT between the SM and
SAA increased from early after procedures to one
year later, these differences were not statistically
significant.
However, it is important to show that each
technique does not give as much harm, as it is useful or
induce new problems due to the procedure. Magnetic
resonance imaging studies have demonstrated that
SAA infarct may be both transmural and extensive.[13]
In SM, unlike SAA, distribution of septal perforator
coronary arteries for which precise targeting of the
septum that contribute to mechanical LV outflow
obstruction can be visualized by the surgeon. However,
it has been suggested that the alcohol-induced scar
does not represent a true infarction due to its chemical
origin, rather than ischemic, and controlled size.[6]
While deciding the most optimal treatment choice
of the HOCM, SM, rather than SAA, is recommended
in patients with an indication for septal reduction
therapy and other indications requiring surgical
intervention (e.g., mitral valve repair/replacement, papillary muscle intervention) as a Class I indication
by the European Society of Cardiology (ESC)
guidelines.[8] Mitral regurgitation is usually present
caused by the apposition of the anterior leaflet of the
mitral valve through the bulging of the thickened
septum of the LVOT during systole, namely systolic
anterior motion. In this study, the presence of systolic
anterior motion and mitral regurgitation were found
to be associated with the higher gradient of LVOT
in each procedure. Not surprisingly, in this group
patients, the LA volume index was also higher.
The appropriate selection of patients for treatment
procedure is an important predictor of outcome and
should be individualized. The American College of
Cardiology/American Heart Association (ACC/AHA)
guidelines recommend the decision to proceed with
SAA in advanced age, in the presence of a significant
comorbidity which selectively increases the surgical
risk, (e.g., significant concerns about lung or airway
management), and in case of the patient’s strong desire
to avoid open heart surgery after a thorough discussion
of both options.[14] Due to the absence of a surgical
incision and general anesthesia, SAA has the potential
for greater patient satisfaction. Besides less overall
discomfort, SAA recovery time is also shorter. Due to
the variable septal artery anatomy in each case, which
may not supply the targeted area of the septum in up
to 20 to 25% of patients, SAA may have hemodynamic
and symptomatic improvement compared to SM, if
the area of the systolic anterior motion-septal contact
can be accessed by the first septal perforator and
ablated.[15] After the procedure, a decrease in resting
and provocable gradients usually occurs immediately;
however, due to stunning, remodeling can result in
continued gradient reduction over the first three
months following the procedure. In our study, we
showed the gradient reduction early after surgery and
at the first year of the procedure. At the end of the first
year, there was no statistically significant difference
in the maximal gradient of the LVOT of the patients
between the procedures.
It has been suggested that at least 50 successful
procedures are required to overcome the SAA learning
curve. If the patient who is either a good candidate
for SM or SAA, a shared decision-making approach
should be used to provide the patient all available data
on the advantages and disadvantages of both strategies.
In patients with a septal thickness of <15 to
18 mm, SM poses a risk for ventricular septal defect. Also, atrioventricular block is a common complication
of SAA. In our study, we included the patients
with successfully treated by SM or SAA without
any complication. We also believe that systematic
long-term follow-up studies are necessary to evaluate
whether alcohol-induced myocardial infarction or SM
poses an increased risk for ventricular arrhythmias of
sudden death.
In conclusion, although the surgical SM is
considered the preferred treatment in patients with
HOCM, SAA may be an alternative approach to SM
in the LVOT gradient reduction in experienced centers
for high-risk surgical patients.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect
to the authorship and/or publication of this article.
Funding
The authors received no financial support for the research
and/or authorship of this article.
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