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Published on: October 28, 2020
Clinicopathological characteristics of left ventricular myocardium with transient asynergy: report of three cases
K Chida1, T Taniguchi, S Maeda
1Division of Cardiology, Tokyo Metropolitan Geriatric Hospital, Japan.
Insights
Transient left ventricular asynergy following acute ischemic events often involves normal heart muscle or minor subendocardial damage. This finding suggests the heart muscle can recover significantly after such insults.
Area of Science:
- Cardiology
- Pathology
Background:
- Acute ischemic insults can cause transient left ventricular asynergy.
- Understanding the underlying histopathologic substrates is crucial for patient management.
Purpose of the Study:
- To investigate the histopathologic basis of transient left ventricular asynergy in patients experiencing acute ischemic events.
- To correlate clinical and echocardiographic findings with myocardial pathology.
Main Methods:
- Retrospective analysis of three patients with prolonged chest pain, new Q waves, and ST segment elevation.
- Echocardiography to assess left ventricular function and structure.
- Histopathologic examination of myocardial tissue.
Main Results:
- Echocardiograms revealed severe hypokinesis/akinesis and thinning in the anteroseptal and apical regions.
- Clinical and echocardiographic abnormalities resolved within weeks.
- Histopathology showed either normal myocardium, small subendocardial scars, or scattered necrotic myocytes in the jeopardized regions.
Conclusions:
- Transient left ventricular asynergy post-ischemia is often associated with normal myocardium or minimal subendocardial lesions.
- The myocardium in these cases demonstrates significant recovery potential.
Abstract:
The aim of the present retrospective study was to clarify the histopathologic substrates of left ventricular myocardium with transient asynergy due to acute ischemic insult in man. Three patients who had had prolonged chest pain, new abnormal Q waves and new ST segment elevation were studied. There was no significant elevation of serum creatine phosphokinase activity in two of the three patients. Echocardiograms on admission or the next day showed severe hypokinetic or akinetic motion and thinning of the anteroseptal and apical portions of the left ventricle and regional dilatation of the same portions. Disappearance of the abnormal Q waves, ST segment elevation resolution, and early T wave inversion were observed later. Complete improvement of the echocardiographic abnormalities was confirmed after a few weeks in all patients. Manifest ischemic lesions of subendocardial scars of the anteroseptal region of the left ventricle were detected in only one of the three cases by gross examination. However, on microscopic examination, islands of necrotic myocytes were interspersed with islands of viable cells throughout the jeopardized region in one case, although the scattered necrotic foci were restricted to the subendocardium and the trabeculae. Normal myocardium and subendocardial scars were observed in the other two cases. In conclusion, left ventricular myocardium with transient asynergy. detected clinically during acute ischemic attack, consists of normal myocardium or small ischemic lesions primarily in the subendocardium.
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