title: Pacing tachycardia exaggerates left ventricular diastolic dysfunction but not systolic function and regional asynergy or asynchrony in patients with hypertrophic cardiomyopathy.
abstract: OBJECTIVE
  Myocardial ischaemia and angina have been demonstrated in patients with hypertrophic cardiomyopathy (HCM). We hypothesized that left ventricular (LV) systolic or diastolic dysfunction would be provocated by pacing tachycardia in patients with HCM.
  
  
  RESULTS
  We investigated LV global and regional systolic and diastolic function in 17 patients with HCM without LV outflow obstruction and 7 normal subjects by analysing LV angiograms and simultaneously obtained high-fidelity LV pressures before and after rapid cardiac pacing (150 b.p.m.). Biplane LV silhouettes were digitized frame by frame (50 frames/s). To quantify regional dynamics, the ventricular area of the right anterior oblique projection was divided into six sections originating from the midpoint of the long axis at end-diastole. There were no significant changes in LV function after pacing in normal subjects. In HCM, the ejection fractions remained unchanged. However, LV end-diastolic pressures rose (+12 mmHg, P < 0.01), and the time constants of isovolumic pressure decay were significantly increased (T(1/2): +5.2 ms, P < 0.01; T(1/)(e): +6.8 ms, P < 0.01). The LV global diastolic pressure-volume relationships and regional diastolic pressure-area relationships of regional myocardium shifted upward (indicating decreased diastolic distensibility) in all patients. These diastolic abnormalities were not accompanied by regional asynchrony or asynergy.
  
  
  CONCLUSIONS
  Most patients with HCM have a reduced reactive capacity to chronotropic stress, which is haemodynamically characterized by evenly distributed diastolic dysfunction. In contrast with coronary artery disease, these diastolic abnormalities were not accompanied by systolic dysfunction, regional asynchrony, asynergy, or inhomogenous diastolic distensibility.
authors.affiliation: Department of Cardiology, Mie University of Medicine, Tsu, Mie, Japan.
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Tarumi
authors.forename: Shigeto
authors.initials: S
authors.lastname: Takebayashi
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Fujita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nakano
authors.forename: Masaaki
authors.initials: M
authors.lastname: Ito
authors.forename: Tetsu
authors.initials: T
authors.lastname: Yamakado
mesh_terms: D000328:Adult; D000368:Aged; D002304:Cardiac Pacing, Artificial; D002312:Cardiomyopathy, Hypertrophic / Q000503:physiopathology*; D003971:Diastole / Q000502:physiology*; D005260:Female; D006339:Heart Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D013599:Systole / Q000502:physiology*; D018487:Ventricular Dysfunction, Left; D055815:Young Adult