This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Koiwa, Y. Articles by Takishima, T. Search for Related Content PubMed PubMed Citation Articles by Koiwa, Y. Articles by Takishima, T. Pubmed/NCBI databases Medline Plus Health Information Cardiomyopathy Heart Failure

(Circulation. 1997;95:156-162.)
© 1997 American Heart Association, Inc.

Articles

Modification of Human Left Ventricular Relaxation by Small-Amplitude, Phase-Controlled Mechanical Vibration on the Chest Wall

Yoshiro Koiwa, MD; Hideyuki Honda, MD; Takehiko Takagi, MD; Jun-ichi Kikuchi, MD; Nobuo Hoshi, MD; Tamotsu Takishima, MD

the First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.

Correspondence to Yoshiro Koiwa, MD, The First Department of Internal Medicine, Tohoku University School of Medicine, 1-1, Seiryo-machi, Aoba-ku, Sendai 980-77, Japan.

Background Direct clinical manipulation to improve an impairment of left ventricular (LV) relaxation has not been reported. We investigated whether the LV relaxation rate in humans could be modulated by phase-controlled mechanical vibration applied to the patient's anterior chest wall and whether there are some quantitative differences in the responses of normal (N), hypertrophied (H), and failing (F) ventricle.

Methods and Results In 46 patients (N, 10; H, 18 [hypertrophic cardiomyopathy]; F, 18 [heart failure]), the vibrator was attached to the precordium and a 50-Hz, 2-mm sinusoidal mechanical vibration was applied, with the timing restricted from the onset of isovolumic relaxation to end-diastole during cardiac catheterization. Heart rate and peak LV pressure showed no difference with vibration. However, in all patients, precordial vibration caused an acceleration of the LV pressure fall. The magnitude of the induced reduction of the time constant of LV pressure decay (T) was larger (P<.01) in H and F than in N (4.6±2.3, 4.0±1.6, and 0.6±1.5 ms for H, F, and N, respectively). T correlated strongly with the magnitude of impaired relaxation and the magnitude of transmitted vibration to the ventricle.

Conclusions Phase-controlled, small-amplitude vibration on the chest wall can directly modulate LV relaxation rate, especially in those with hypertrophy or failing ventricle.

Key Words: cardiomyopathy • hypertrophy • diastole

This article has been cited by other articles:

				B. S. Cain, D. R. Meldrum, K. S. Joo, J.-F. Wang, X. Meng, J. C. Cleveland Jr., A. Banerjee, and A. H. Harken Human SERCA2a levels correlate inversely with age in senescent human myocardium J. Am. Coll. Cardiol., August 1, 1998; 32(2): 458 - 467. [Abstract] [Full Text] [PDF]