Related Experiment Videos
Functional and structural abnormalities in patients with dilated cardiomyopathy
A S Bortone1, O M Hess, A Chiddo
1Division of Cardiology, University of Bari, Italy.
Insights
Dilated cardiomyopathy can present with normal myocardial stiffness despite impaired systolic function. Increased interstitial fibrosis correlates with elevated myocardial stiffness, indicating advanced disease.
Area of Science:
- Cardiology
- Biomedical Engineering
- Pathology
Background:
- Dilated cardiomyopathy (DCM) is characterized by impaired left ventricular systolic function.
- Passive diastolic properties, crucial for cardiac function, are often altered in DCM.
- Understanding myocardial stiffness in DCM is vital for disease staging and management.
Purpose of the Study:
- To assess passive diastolic properties of the left ventricle in patients with DCM.
- To investigate the relationship between myocardial stiffness and structural abnormalities in DCM.
- To determine if myocardial stiffness can differentiate disease severity in DCM.
Main Methods:
- Simultaneous left ventricular angiography and pressure measurements were performed.
- Left ventricular pressure-volume and stress-strain relations were used to calculate chamber and myocardial stiffness constants.
- Morphometry of right ventricular endomyocardial biopsies assessed interstitial fibrosis and fibrous content.
Main Results:
- Patients with DCM had significantly higher left ventricular end-diastolic pressure and lower ejection fraction than controls.
- Myocardial stiffness (beta) was normal in one DCM group but significantly increased in another, correlating with higher interstitial fibrosis (up to 43%).
- An exponential relationship was found between myocardial stiffness and interstitial fibrosis.
Conclusions:
- Myocardial stiffness can be normal in DCM patients with severely depressed systolic function.
- Increased myocardial stiffness in DCM is likely due to structural alterations, specifically increased fibrous tissue.
- The myocardial stiffness constant (beta) can identify patients with severe structural changes, potentially indicating advanced DCM.
Abstract:
Passive diastolic properties of the left ventricle were determined in 10 control subjects and 12 patients with dilated cardiomyopathy. Simultaneous left ventricular angiography and high fidelity pressure measurements were performed in all patients. Left ventricular chamber stiffness was calculated from left ventricular pressure-volume and myocardial stiffness from left ventricular stress-strain relations with use of a viscoelastic model. Patients with dilated cardiomyopathy were classified into two groups according to the diastolic constant of myocardial stiffness (beta). Group 1 consisted of seven patients with a normal constant of myocardial stiffness less than or equal to 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a beta greater than 9.6. Structural abnormalities (percent interstitial fibrosis, fibrous content) in patients with dilated cardiomyopathy were assessed by morphometry from right ventricular endomyocardial biopsies. Heart rate was similar in the three groups. Left ventricular end-diastolic pressure was significantly greater in patients with cardiomyopathy (18 mm Hg in group 1 and 22 mm Hg in group 2) than in the control patients (10 mm Hg). Left ventricular ejection fraction was significantly lower in groups 1 (37%) and 2 (36%) than in the control patients (66%). Left ventricular muscle mass index was significantly increased in both groups with cardiomyopathy. The constant of chamber stiffness (beta*) was slightly although not significantly greater in groups 1 and 2 (0.58 and 0.58, respectively) than in the control group (0.35). The constant of myocardial stiffness beta was normal in group 1 (7.0; control group 6.9, p = NS) but was significantly increased in group 2 (23.5). Interstitial fibrosis was 19% in group 1 and 43% (p less than 0.001) in group 2 (normal less than or equal to 10%). There was an exponential relation between both diastolic constant of myocardial stiffness (beta) and interstitial fibrosis (IF) (r = 0.95; p less than 0.001) and beta and fibrous content divided by end-diastolic volume index (r = 0.93; p less than 0.001). It is concluded that myocardial stiffness can be normal in patients with dilated cardiomyopathy despite severely depressed systolic function. Structural alterations of the myocardium with increased amounts of fibrous tissues are probably responsible for the observed changes in passive elastic properties of the myocardium in patients with dilated cardiomyopathy. The constant of myocardial stiffness (beta) helps to identify patients with severe structural alterations (group 2), representing possibly a more advanced stage of the disease.