Nonuniformity is a determinant of diastolic function. In patients with hypertrophic cardiomyopathy, hypertrophy, abnormal calcium handling, and regional ischemia can also play a role. This study was designed to assess regional mechanics, asynchrony, and asynergy in patients with hypertrophic cardiomyopathy.Methods and Results.
Nine control subjects and 22 patients with hypertrophic cardiomyopathy were studied by biplane left ventriculography and high-fidelity pressure tracings for the assessment of diastolic function by computing the time constant of isovolumic relaxation, peak filling rate, and the constant of passive chamber stiffness. Regional mechanics were evaluated by dividing the left ventricle into six sectors in the right and left anterior oblique projections. Systolic and diastolic asynchrony were assessed from the coefficient of variation of the regional time intervals from end diastole to end systole and to peak filling rate, respectively. Asynergy was evaluated from the coefficient of variation of the regional area reduction. Regional passive elastic properties were estimated by computing the regional constant of chamber stiffness. In patients with hypertrophic cardiomyopathy, isovolumic relaxation was prolonged (time constant of isovolumic relaxation 101±41 versus 51±16 milliseconds in control subjects;P<.001) and the constant of chamber stiffness was increased (0.056±0.038 versus 0.025±0.010 mL−1;P<.001). Both systolic and diastolic asynchrony as well as asynergy were found. Regional mechanics showed hyperkinesia in the free wall, whereas the septum exhibited normal wall motion and increased constant of chamber stiffness.Conclusions.
Diastolic function is impaired in hypertrophic cardiomyopathy, and such an impairment is the consequence of nonuniformity and hypertrophy. The regions where the myopathic process is more pronounced show normal wall motion but increased stiffness. The inhomogeneity of regional wall motion with regional hyperkinesia and normokinesia of neighboring regions results in left ventricular asynergy. (Circulation.1993;88[part 1]:2206–2214.)