Functional and structural abnormalities in patients with dilated cardiomyopathy

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 f...

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Veröffentlicht in:Journal of the American College of Cardiology 1989-09, Vol.14 (3), p.613-623
Hauptverfasser: Bortone, Alessandro S., Hess, Otto M., Chiddo, Adele, Gaglione, Antonio, Locuratolo, Nicola, Caruso, Gilda, Rizzon, Paolo
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container_issue 3
container_start_page 613
container_title Journal of the American College of Cardiology
container_volume 14
creator Bortone, Alessandro S.
Hess, Otto M.
Chiddo, Adele
Gaglione, Antonio
Locuratolo, Nicola
Caruso, Gilda
Rizzon, Paolo
description 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 (β). Group 1 consisted of seven patients with a normal constant of myocardial stiffness ≤ 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a β >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 (β*) 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 β 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 < 0.001) in group 2 (normal ≤ 10%). There was an exponential relation between both diastolic constant of myocardial stiffness (β) and interstitial fibrosis (IF) (r = 0.95; p < 0.001) and β and fibrous content divided by end-diastolic volume index (r = 0.93; p < 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 tissue are probably responsible for the observed changes in passive elastic properties of the myocardium in patients with dilated cardiomyopathy. The constant of myocardial stiffness (β) helps to identify patients with severe structural alterations (group 2), representin
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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 (β). Group 1 consisted of seven patients with a normal constant of myocardial stiffness ≤ 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a β &gt;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 (β*) 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 β 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 &lt; 0.001) in group 2 (normal ≤ 10%). There was an exponential relation between both diastolic constant of myocardial stiffness (β) and interstitial fibrosis (IF) (r = 0.95; p &lt; 0.001) and β and fibrous content divided by end-diastolic volume index (r = 0.93; p &lt; 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 tissue are probably responsible for the observed changes in passive elastic properties of the myocardium in patients with dilated cardiomyopathy. 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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 (β). Group 1 consisted of seven patients with a normal constant of myocardial stiffness ≤ 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a β &gt;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 (β*) 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 β 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 &lt; 0.001) in group 2 (normal ≤ 10%). 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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 (β). Group 1 consisted of seven patients with a normal constant of myocardial stiffness ≤ 9.6 (normal range 2.2 to 9.6) and group 2 of 5 patients with a β &gt;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 (β*) 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 β 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 &lt; 0.001) in group 2 (normal ≤ 10%). There was an exponential relation between both diastolic constant of myocardial stiffness (β) and interstitial fibrosis (IF) (r = 0.95; p &lt; 0.001) and β and fibrous content divided by end-diastolic volume index (r = 0.93; p &lt; 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 tissue are probably responsible for the observed changes in passive elastic properties of the myocardium in patients with dilated cardiomyopathy. The constant of myocardial stiffness (β) helps to identify patients with severe structural alterations (group 2), representing possibly a more advanced stage of the disease.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>2768711</pmid><doi>10.1016/0735-1097(89)90102-2</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Biological and medical sciences
Cardiology. Vascular system
Cardiomyopathy, Dilated - pathology
Cardiomyopathy, Dilated - physiopathology
Diastole
Elasticity
Female
Heart
Heart - physiopathology
Hemodynamics
Humans
Male
Medical sciences
Middle Aged
Myocardial Contraction
Myocarditis. Cardiomyopathies
title Functional and structural abnormalities in patients with dilated cardiomyopathy
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