Age-related hemodynamic and morphologic differences in patients undergoing alcohol septal ablation for hypertrophic

Josef Veselka1, Radka Duchonová, Jana Pálenícková

  • 1Department of Cardiology, University Hospital Motol, Prague, Czech Republic. veselka.josef@seznam.cz

Insights

Alcohol septal ablation (ASA) effectively treats hypertrophic obstructive cardiomyopathy (HOCM) in all age groups. Younger patients with HOCM may have thicker septums and slower initial hemodynamic improvement after ASA.

Area of Science:

  • Cardiology
  • Interventional Cardiology
  • Cardiac Imaging

Background:

  • Alcohol septal ablation (ASA) is a treatment for highly symptomatic hypertrophic obstructive cardiomyopathy (HOCM).
  • The procedure aims to decrease the left ventricular (LV) outflow gradient and alleviate symptoms.
  • This study investigates early changes in younger versus elderly HOCM patients undergoing ASA.

Purpose of the Study:

  • To evaluate early hemodynamic, morphologic, and clinical changes after ASA in HOCM patients.
  • To compare these changes between younger and elderly patient cohorts.
  • To identify factors influencing outcomes post-ASA.

Main Methods:

  • Forty-four HOCM patients (age 24-81) underwent ASA.
  • Clinical and echocardiographic data were collected at baseline and up to 12 months post-procedure.
  • Statistical analysis, including multivariate adjustment, was used to assess correlations and influences.

Main Results:

  • A significant correlation was found between basal septum thickness and age at baseline and post-procedure.
  • Septal thickness changes over follow-up were significantly influenced by age.
  • A decrease in LV outflow gradient was observed in all age groups, influenced by age and peak creatine kinase-MB levels.

Conclusions:

  • ASA is an effective HOCM treatment regardless of patient age.
  • Younger patients present with thicker basal septums and experience slower early hemodynamic improvement post-ASA.
  • Age and peak creatine kinase-MB are significant factors in the hemodynamic response to ASA.
Abstract

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