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Sustained cavity obliteration and apical aneurysm formation in apical hypertrophic cardiomyopathy

Kinya Matsubara1, Takashi Nakamura, Toshiro Kuribayashi

  • 1Department of Medicine, Kyoto Municipal Hospital, Kyoto, Japan. mtbrkydy@hera.eonet.ne.jp

Journal of the American College of Cardiology
|July 24, 2003
PubMed

Insights

In apical hypertrophic cardiomyopathy, severe cavity obliteration (CO) is linked to apical aneurysms and cardiac issues. This study clarifies the relationship between CO severity and clinical findings in ApHCM patients.

Area of Science:

  • Cardiology
  • Cardiovascular Imaging
  • Pathophysiology

Background:

  • Apical hypertrophic cardiomyopathy (ApHCM) can lead to apical aneurysm.
  • Apical cavity obliteration (CO) is common in ApHCM, often alongside hypertrophy and ischemia.
  • The relationship between CO, hypertrophy, ischemia, and aneurysm development in ApHCM requires further elucidation.

Purpose of the Study:

  • To estimate the severity of left ventricular apical cavity obliteration (CO) in ApHCM patients.
  • To correlate CO severity with clinical findings, including apical aneurysm.
  • To investigate the pathophysiological mechanisms underlying aneurysm formation in ApHCM.

Main Methods:

  • 46 ApHCM patients underwent M-mode echocardiography to measure CO time, corrected by R-R interval (cCOT).
  • Patients were categorized into no/mild CO (cCOT ≤200 ms), moderate CO (200 < cCOT ≤350 ms), and severe CO (cCOT >350 ms) groups.
  • Comparisons of apical aneurysm, hypertrophy, ischemia, and QT interval were made across the groups.

Main Results:

  • Severe CO was exclusively observed in 11 patients with apical aneurysm and paradoxic jet flow.
  • 10/11 severe CO patients showed irreversible defects on thallium-201 SPECT; moderate CO patients had reversible defects; no defects were seen in mild CO.
  • Left ventricular hypertrophy and corrected QT interval (QTc) were highest in the severe CO group, with strong correlations between cCOT, hypertrophy, ischemia, and QTc.

Conclusions:

  • Sustained CO is a critical pathophysiological factor in ApHCM, alongside hypertrophy, ischemia, and prolonged QTc.
  • These factors interact to promote the development of apical aneurysms in ApHCM.
  • Understanding these relationships is crucial for managing ApHCM and preventing complications like ventricular tachycardia and thrombus formation.
Abstract

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