Myocardial structure in volume-overloaded hearts before and after valve replacement
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Volume overload from heart valve disease causes left ventricular muscle changes. Surgery improves dimensions and fibrosis, but some changes persist, impacting postoperative ventricular size.
Area of Science:
- Cardiovascular Pathology
- Cardiac Surgery
- Histology
Background:
- Volume overload in hearts, often due to valvular regurgitation, leads to significant left ventricular remodeling.
- Understanding the histological changes in myocardial tissue is crucial for assessing cardiac function and surgical outcomes.
Purpose of the Study:
- To evaluate the histological characteristics of left ventricular muscle in patients with volume-overloaded hearts.
- To correlate preoperative and postoperative histological findings with echocardiographic and angiographic data.
Main Methods:
- Preoperative myocardial biopsies were obtained from 31 patients with mitral and/or aortic regurgitation.
- Histological findings were correlated with echocardiographic and angiographic data.
- Postoperative tissue samples from 15 patients were analyzed one year after valve replacement surgery.
Main Results:
- Myocardial cell diameter correlated positively with left ventricular dimensions and negatively with wall thickness-to-radius ratio.
- Increased interstitial fibrosis was proportional to myocardial cell diameter.
- Valve replacement significantly reduced left ventricular dimensions and volumes, myocardial cell diameter, and interstitial fibrosis, though some remained above normal.
Conclusions:
- Left ventricular remodeling in volume overload involves myocyte hypertrophy and interstitial fibrosis.
- Valve replacement surgery leads to significant histological improvements but does not fully normalize myocardial structure.
- Persistent myocardial hypertrophy and fibrosis influence postoperative left ventricular dilatation.
Abstract:
The purpose of this study was to evaluate the histological characteristics of left ventricular muscle in volume-overloaded hearts. A preoperative biopsy was obtained in 31 patients: 14 with mitral regurgitation, 14 with aortic regurgitation and 3 with mitral regurgitation and aortic regurgitation. Postoperative tissue samples were available in 15 patients. Histological findings were correlated with echocardiographic and angiographic data before (preop) and one year after (postop) operation. Myocardial cell diameter was correlated with both the end-diastolic (r = 0.77, p less than 0.01) and end-systolic (r = 0.78, p less than 0.01) dimensions of the left ventricle, but was inversely correlated with the end-diastolic wall thickness-to-radius (h/R) ratio (r = -0.71, p less than 0.01). Percent fibrosis increased proportionally to the diameter (r = 0.42, p less than 0.05). For one year after operation, echocardiographic left ventricular dimensions and angiographic left ventricular volumes were significantly reduced (p less than 0.05), but in some patients postoperative values remained greater than normal. With regard to left ventricular morphology, myocardial cell diameter and interstitial fibrosis decreased significantly after valve replacement (p less than 0.05). However, the myocardial fiber remained hypertrophied and interstitial fibrosis remained above normal after surgery. Thus, postoperative ventricular dilatation was dependent upon the degree of myocardial fiber hypertrophy and interstitial fibrosis.