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Myocardial ischaemia in constrictive pericarditis--a morphometric and electron microscopical study
Insights
Constrictive pericarditis (CP) causes myocardial dysfunction. This study found that myocardial ischemia, not disuse atrophy, is the primary cause of this dysfunction in CP patients.
Area of Science:
- Cardiology
- Pathology
- Cardiac Surgery
Background:
- Constrictive pericarditis (CP) is a condition characterized by impaired cardiac filling due to pericardial thickening.
- The underlying myocardial pathology in CP has been attributed to disuse atrophy from prolonged cardiac compression.
Purpose of the Study:
- To investigate the myocardial pathology in constrictive pericarditis (CP).
- To compare the myocardial structure in CP with normal controls.
- To determine the primary etiological factor in myocardial dysfunction in CP.
Main Methods:
- Morphometric and morphological examination of left ventricular biopsies from CP patients and atrial septal defect (ASD) controls.
- Ultrastructural analysis of myocardial fibers.
Main Results:
- Myocardial fiber diameters in CP were within normal limits morphometrically, but the range was extended.
- Ultrastructural analysis revealed two types of myofibers in CP: normal and large, oedematous fibers.
- Oedematous fibers showed abnormal nuclei, organelles, and myofibrillar dissolution, indicative of ischemia.
Conclusions:
- Myocardial ischemia, characterized by specific ultrastructural changes, is a significant factor in CP.
- Myocardial ischemia appears to be a more critical factor in the etiology of myocardial dysfunction in CP than disuse atrophy.
Abstract:
Left ventricular biopsies, taken during pericardiectomy, were morphometrically and morphologically examined to determine the pathology of the myocardium in constrictive pericarditis (CP). To serve as a normal control a similar appraisal was made of tissue from the left ventricle of a patient undergoing atrial septal repair. Morphometrically, mean cross-fibre diameters at the position of the nucleus in atrial septal defect (ASD) and CP hearts were within a range previously reported as normal. In hearts from patients with CP, the range of individual myocardial fibre diameters was extended. Ultrastructurally the myocardium in ASD appeared normal. In CP, myofibres could be divided into two groups: (a) small and morphologically normal; and (b) large and oedematous. Oedematous fibres contained abnormal nuclei and sarcoplasmic organelles and myofibrillar dissolution was a prominent feature in many cells. These pathological features are among those previously used to characterize myofibre ischaemia. In CP, prolonged cardiac compression is thought to predispose the heart to atrophy due to its inability to function properly (disuse atrophy). The results of this study suggest that in CP, myocardial ischaemia is a more important factor in the aetiology of myocardial dysfunction than is atrophy which arises from enforced cardiac disuse.