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Local characteristics of the normal and asynergic left ventricle in man
Insights
This study links ventricular asynergy severity in coronary artery disease patients to muscle loss and epicardial Q waves. Even severely asynergic areas can contain normal heart muscle tissue.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
- Cardiac Pathology
Background:
- Ventricular asynergy is crucial for prognosis and surgical risk in coronary artery disease.
- Ventriculography is used to delineate asynergy, but underlying histopathologic and electrographic features require further investigation.
Purpose of the Study:
- To determine the histopathologic and electrographic features of left ventricular asynergy.
- To correlate ventricular asynergy severity with myocardial damage and electrical abnormalities.
Main Methods:
- Studied 39 patients undergoing open heart surgery.
- Obtained 36 histopathologic specimens (biopsies and resections).
- Recorded epicardial electrograms from 35 areas in 29 patients.
Main Results:
- Significant muscle loss (>50%) and fibrosis (>75%) were found in akinetic and dyskinetic areas.
- Progressive asynergy severity correlated with increased frequency of abnormal Q waves.
- Epicardial Q waves were present in most akinetic and dyskinetic areas, while R waves were associated with normal or minimally damaged myocardium.
Conclusions:
- A strong correlation exists between ventriculographic asynergy severity, degree of muscle loss, and presence of epicardial Q waves.
- Histologically and electrographically normal myocardium can be present even in severely asynergic regions.
Abstract:
The significance of ventricular asynergy in determining medical prognosis and surgical risk in patients with coronary artery disease and its delineation by ventriculography have been of increasing interest. To determine the underlying histopathologic and electrographic features of left ventricular asynergy, 39 patients undergoing open heart surgery were studied. Thirty-six histopathologic specimens were obtained in 31 patients (26 as transmural needle biopsies and 10 as aneurysm resections). In four normally contracting areas and 12 hypokinetic areas, neither fibrosis nor early changes of myocardial damage was evident. In contrast, of eight akinetic areas there was more than 50 per cent muscle loss in four and from 30 to 35 per cent muscle loss in three, in only one area was there less than 10 per cent muscle loss. Of 12 dyskinetic zones there was more than 75 per cent muscle loss in 10 zones, 35 per cent in one and no pathologic abnormalities in one. Epicardial electrograms were obtained from 35 areas in 29 patients. Of 10 normally contracting ventricles, in one, pathologic Q waves were demonstrated only over the inferior area. Progressive increases in the severity of asynergy were associated with a progressive increase in frequency of initial abnormal Q waves. In only one of nine hypokinetic areas were epicardial Q waves exhibited, but they were present in six of 10 akinetic and five of six dyskinetic areas. Both histopathologic and electrographic data were available from 20 asynergic areas in 16 patients. Initial epicardial R waves were associated with normal biopsy specimens in seven of eight hypokinetic areas. Of seven akinetic areas, initial R waves were associated with 30 to 35 per cent muscle loss in three; of four areas with initial Q waves, there was a 35 per cent muscle loss in one and more than 50 per cent muscle loss in three. Similarly, of five dyskinetic segments, a QS pattern was associated with more than 75 per cent fibrosis in four. In one dyskinetic area there was an intial R wave in association with a normal appearing biopsy specimen. In summary, a good correlation exists between the severity of asynergy by ventriculography, the degree of muscle loss and the presence of epicardial Q waves. However, a significant amount of histologically and electrographically normal myocardium may be present even in severely asynergic areas.