Increased left ventricular diastolic stiffness in the early phase of hereditary cardiomyopathy.
Isolated hearts from normal and cardiomyopathic hamsters (160 to 180 days of age) were perfused through the aorta and assessed by echocardiographic and 31P-NMR (nuclear magnetic resonance) techniques. A decreased left ventricular systolic pressure in cardiomyopathic hamsters was associated with diminished cardiac size and left ventricular wall thickness. However, the ratio of inner/outer cross-sectional area and estimated left ventricular volume at any given left ventricular weight was significantly higher, indicating relative left ventricular chamber enlargement in cardiomyopathic hamsters. Left ventricular volumes were increased with an intraventricular balloon. Gradual inflation of the balloon resulted in increments of left ventricular systolic and developed stress that rose to the same values in both groups. At this point, the normalized stress-strain relationship was approximately two times steeper for cardiomyopathic hamsters, while at lower strain values the diastolic stress in cardiomyopathic hamsters was less than in controls, possibly due to cardiac dilatation. Almost the same degree of dilatation was induced in control hearts by the acute addition of 1% alcohol, but it was not followed by increased diastolic stiffness. Examination of hearts by 31P-NMR techniques revealed a decreased phosphocreatine/inorganic phosphate (PCr/Pi) ratio in the cardiomyopathic hamsters that progressed further with balloon inflation and was associated with a relative fall in PCr and adenosine triphosphate (ATP) content. Results suggest increased diastolic stiffness in cardiomyopathic hamsters, which was not seen in acute cardiac depression with alcohol. Diastolic volume overload with increased wall stress is probably the major factor contributing to increased diastolic stiffness early in the cardiomyopathy.
Department of Medicine, University of California, San Francisco.
V I
VI
Kapelko
W W
WW
Parmley
S
S
Wu
R D
RD
Stone
G
G
Jasmin
J
J
Wikman-Coffelt
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D001794:Blood Pressure; D009202:Cardiomyopathies / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D006224:Cricetinae; D004195:Disease Models, Animal; D004452:Echocardiography; D000431:Ethanol / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006352:Heart Ventricles / Q000187:drug effects / Q000503:physiopathology; D008647:Mesocricetus; D009206:Myocardium / Q000032:analysis / Q000473:pathology; D010710:Phosphates / Q000032:analysis; D010725:Phosphocreatine / Q000032:analysis
D010710:Phosphates; D010725:Phosphocreatine; D000431:Ethanol; D000255:Adenosine Triphosphate