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High prevalence of atrial fibrosis in patients with dilated cardiomyopathy
Insights
Cardiomyopathy significantly increases left atrial fibrosis, particularly in hypertrophic cardiomyopathy. This atrial fibrosis may stem from unknown mechanisms, not solely mechanical overload from left ventricular dysfunction.
Area of Science:
- Cardiovascular Pathology
- Cardiac Fibrosis Research
- Myocardial Disease Mechanisms
Background:
- Left atrial dysfunction is implicated in heart failure progression.
- Atrial fibrosis is less studied than ventricular fibrosis in cardiomyopathies.
Purpose of the Study:
- To quantify left atrial fibrosis in human cardiomyopathic hearts.
- To explore the link between left ventricular dysfunction and left atrial fibrosis.
Main Methods:
- Analysis of 38 autopsied hearts (controls, dilated cardiomyopathy, hypertrophic cardiomyopathy, myocardial infarction).
- Quantification of left atrial and left ventricular fibrosis using an automatic image analyzer.
- Histological sections from specific atrial and ventricular regions.
Main Results:
- Significantly higher left atrial fibrosis in dilated cardiomyopathy (13.1%) and hypertrophic cardiomyopathy (26.5%) compared to controls (3.8%).
- Left ventricular fibrosis was lower in dilated cardiomyopathy (12.9%) than in hypertrophic cardiomyopathy (35.8%) or myocardial infarction (38.4%).
- Atrial fibrosis correlated with left ventricular ejection fraction only in the myocardial infarction group.
Conclusions:
- High prevalence of left atrial fibrosis in dilated and hypertrophic cardiomyopathy.
- Atrial fibrosis in these conditions likely arises from mechanisms other than mechanical overload.
Objectives:
We examined the extent of fibrotic changes in the left atrium of cardiomyopathic human hearts and investigated the relation of mechanical overload caused by left ventricular dysfunction to fibrosis of the left atrium.
Background:
Left atrial dysfunction in dilated cardiomyopathy may contribute to progression of heart failure. In contrast to fibrosis of the left ventricle, atrial fibrosis has not been extensively studied in cardiomyopathic hearts.
Methods:
The extent of fibrosis in the left atrium and left ventricle was determined by an automatic image analyzer in 38 autopsied hearts obtained from 9 patients who died of noncardiac illness (control group), 16 patients with dilated cardiomyopathy, 6 patients with hypertrophic cardiomyopathy with features mimicking dilated cardiomyopathy and 7 patients with a previous myocardial infarction. Transverse sections were obtained at the upper margins of the foramen ovale and left auricle in the left atrium and the median level of the left ventricle.
Results:
There were no significant differences in extent of left atrial dilation, left ventricular dysfunction or duration of illness among the three groups with cardiac disease. Percent area of left atrial fibrosis (mean +/- SD) was significantly greater in the specimens from patients with dilated cardiomyopathy (13.1 +/- 6.1%, p < 0.01) and hypertrophic cardiomyopathy mimicking dilated cardiomyopathy (26.5 +/- 9.5%, p < 0.01) than in those from patients with an old myocardial infarction (3.8 +/- 1.1%). Percent area of left ventricular fibrosis in hearts from patients with dilated cardiomyopathy (12.9 +/- 8.6%) was significantly smaller than that in hearts from patients with hypertrophic cardiomyopathy mimicking dilated cardiomyopathy (35.8 +/- 11.9%, p < 0.01) and a previous myocardial infarction (38.4 +/- 8.0%, p < 0.01). Percent area of atrial fibrosis was significantly correlated with left ventricular ejection fraction in the group with a previous myocardial infarction but not in the other groups.
Conclusions:
There was a high degree of fibrotic change in the left atrium in the groups with dilated cardiomyopathy and hypertrophic cardiomyopathy mimicking dilated cardiomyopathy. Our findings suggest that atrial fibrosis in these patients may not have been related to mechanical overload of the left atrium but to some other, still unknown mechanisms.