Modification of human left ventricular relaxation by small-amplitude, phase-controlled mechanical vibration on the chest wall

• Published in: Circulation (New York, N.Y.) Vol. 95; no. 1; pp. 156 - 162
• Main Authors: KOIWA, Y, HONDA, H, TAKAGI, T, KIKUCHI, J.-I, HOSHI, N, TAKISHIMA, T
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 07.01.1997; American Heart Association, Inc
• Subjects: Adult; Biological and medical sciences; Cardiology. Vascular system; Cardiomyopathy, Hypertrophic - physiopathology; Cardiomyopathy, Hypertrophic - therapy; Diastole; Heart; Heart Failure - physiopathology; Heart Failure - therapy; Heart Ventricles - physiopathology; Hemodynamics; Humans; Mathematics; Medical sciences; Middle Aged; Myocarditis. Cardiomyopathies; Regression Analysis; Ventricular Dysfunction, Left - physiopathology; Ventricular Dysfunction, Left - therapy; Ventricular Pressure; Vibration - therapeutic use; Human; Relaxation; Vibration; Diastole; Heart disease; Hypertrophic cardiomyopathy; Mechanics; Cardiovascular disease; Exploration; Myocardial disease; Left ventricle
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.cir.95.1.156

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. 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 (delta 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). Delta T correlated strongly with the magnitude of impaired relaxation and the magnitude of transmitted vibration to the ventricle. Phase-controlled, small-amplitude vibration on the chest wall can directly modulate LV relaxation rate, especially in those with hypertrophy or failing ventricle.