[Left ventricular ejection dynamics in apical hypertrophy, a form of hypertrophic nonobstructive cardiomyopathy]
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Insights
Apical hypertrophy (AH) in hypertrophic nonobstructive cardiomyopathy (HNCM) shows a distinct ejection pattern, completed early in systole. Segmental analysis is key for diagnosing AH, distinguishing it from secondary hypertension-induced hypertrophy.
Area of Science:
- Cardiology
- Cardiovascular Imaging
- Biomedical Engineering
Context:
- Apical hypertrophy (AH) is a form of hypertrophic nonobstructive cardiomyopathy (HNCM).
- Understanding LV ejection dynamics is crucial for diagnosing cardiac conditions.
- Comparison between AH, secondary myocardial hypertrophy, and normal subjects provides diagnostic insights.
Purpose:
- To analyze and compare left ventricular (LV) ejection dynamics in patients with AH (group I), secondary myocardial hypertrophy (group II), and normal subjects (group III).
- To identify the characteristic ejection pattern of HNCM and its diagnostic value.
- To investigate the role of segmental wall motion and LV mass in AH.
Summary:
- LV cineangiograms revealed significantly lower end-diastolic, end-systolic, and stroke volumes in AH patients.
- A distinct LV ejection pattern, completed within two-thirds of systole, was observed in AH, characteristic of HNCM.
- Systolic function in AH is maintained by compensatory hyperkinesis of basal and midzonal segments, despite impaired apical contraction.
Impact:
- The identified ejection pattern in AH is diagnostically valuable, differentiating it from hypertensive hypertrophy.
- Segmental analysis of LV ejection phase proved most sensitive for diagnosing AH.
- Global LV performance parameters may appear supernormal, masking underlying systolic dysfunction in AH.
Abstract:
The left ventricular (LV) cineangiograms of ten patients with apical hypertrophy (AH, group I) as a form of hypertrophic nonobstructive cardiomyopathy (HNCM) were analyzed. The left ventricular ejection dynamics, the extent and pattern of left ventricular contraction were compared with eight patients with secondary myocardial hypertrophy due to arterial hypertension (group II) and eight normal subjects (group III). End-diastolic, end-systolic and stroke volumes were significantly lower in group I. The analysis of left ventricular ejection dynamics with frame-by-frame-analysis revealed the typical ejection pattern of hypertrophic nonobstructive cardiomyopathy: Left ventricular ejection was completed within two thirds of the systolic ejection period. This ejection pattern is of diagnostic value when compared with the dynamics in group II. Although the apical segment in group I shows a good fiber shortening, the overall contribution to systolic performance is low; systolic function in apical hypertrophy is maintained by a compensatory increase in regional wall motion of the basal and midzonal part of the left ventricular free wall. There is no striking difference between apical hypertrophy with and without giant negative T waves with respect to the ejection pattern. Within these subgroups, the only difference was the greater left ventricular mass in patients with giant T wave inversion. Thus, the ejection dynamics in apical hypertrophy is typical of hypertrophic nonobstructive cardiomyopathy. Global parameters of systolic left ventricular performance revealed supernormal values even though systolic function is impaired. Segmental analysis of ejection phase was most sensitive in establishing the diagnosis.