Discussion
The key issue issues in this case are that urgent PTSMA was applied to
treat heart failure due to exacerbated LVOT obstruction after surgical
AVR, which is an under‑recognized cause of postoperative hemodynamic
compromise(2).
The impact of a prosthesis–patient mismatch on LVOT thickening cannot
be overlooked. Peak prosthetic aortic jet velocity in this patient was
<3 m/s.
A prospective study has shown that flow velocity is abnormal in 14% of
patients at rest after AVR for aortic stenosis and that it can be
provoked or worsened by ventricular unloading or inotropic stimulation.
The mechanism of a dynamic intraventricular pressure gradient in the
setting of a hypertrophic left ventricle might include systolic cavity
obliteration or outflow tract obstruction caused by SAM. The role of
cavity squeezing rather than SAM is the fundamental mechanism of
abnormal flow velocity after AVR for aortic stenosis.
Afterload is increased in patients with aortic stenosis, and the
ventricle is often small and hypertrophic. Valve replacement induces a
dramatic decrease in afterload that might further decrease left
ventricular volume and increase fiber shortening. A combination of these
factors might lead to cavity squeezing, which in turn will increase
systolic flow velocity(3).
Percutaneous transluminal septal myocardial ablation was initially
reported in 1995 as a novel technique for the nonsurgical reduction of
septal hypertrophy in patients with hypertrophic cardiomyopathy
(HCM)(4). Surgical myectomy remains the gold standard of treatment for
symptomatic patients who have LVOT obstruction that is refractory to
medical therapy, as it is safe and effective over the long-term.
However, PTSMA in expert hands can effectively reduce the gradient in
selected patients with low procedural complication rates(5).
Both myectomy and PTSMA reduce LVOT obstruction and significantly
improve New York Heart Association functional class in patients with
HCM. However, each type of therapy has advantages and disadvantages that
must be counterbalanced when deciding how to treat LVOT obstruction.
One case report has described successful PTSMA for heart failure due to
significant LVOT obstruction that manifested after AVR(6). Although
PTSMA relieved LVOT obstruction and symptoms during the acute phase,
modest recurrence was confirmed six months later. In contrast LVOT
obstruction and symptoms have not recurred in our patient during 3 years
of follow-up after PTSMA.
Both case reports underline the need for PTSMA options with low
procedural morbidity to treat LVOT obstruction, particularly for highly
symptomatic patients who are contraindicated for surgery.
Conclusion: Urgent PTSMA might be a safe option for treating heart
failure due to exacerbated LVOT obstruction after surgical AVR.