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Featured researches published by Damon Smith.


Circulation | 1987

Disparity between ejection and end-systolic indexes of left ventricular contractility in mitral regurgitation.

Barbara Berko; William H. Gaasch; N Tanigawa; Damon Smith; Ernest Craige

To examine left ventricular function in mitral regurgitation (MR), we compared the ejection phase indexes of left ventricular contractility with maximal systolic elastance (Emax) in an experimental preparation of MR. In eight anesthetized open-chest dogs, pressure-volume loops were derived during afterload manipulation with methoxamine and nitroprusside from simultaneous left ventricular pressure and dimensional (sonomicrometry techniques) data before and after creation of MR. From these data maximal systolic elastance (Emax), the end-systolic pressure-volume relationship (ESPVR), and the end-systolic stress-volume relationship (ESSVR) were determined by linear regression analysis. After creation of MR, end-diastolic volume increased significantly (40 +/- 13 to 53 +/- 18 ml, p less than .001); likewise end-systolic volume increased (28 +/- 11 to 33 +/- 15 ml, p less than .05). Ejection fraction increased after MR (35 +/- 6% to 44 +/- 8%, p less than .005), as did the mean velocity of fiber shortening (0.62 +/- 0.20 to 1.02 +/- 0.39 sec-1, p less than .02). In contrast, Emax declined significantly (4.63 +/- 2.5 to 3.54 +/- 1.94 mm Hg/ml, p less than .05); ESPVR and ESSVR showed similar directional changes. An inverse relationship was found between systolic elastance and end-diastolic volume in both control and MR states. When Emax, ESPVR, and ESSVR were normalized to end-diastolic volume, they were unchanged after MR. These results suggest that either there was a decline in left ventricular contractile state after MR, or that contractility was unchanged (if elastance is normalized for increased contractility, but occurred as a consequence of increased preload with no significant change in afterload.


Circulation | 1983

Origin of the third heart sound. II. Studies in human subjects.

Yukio Ozawa; Damon Smith; Ernest Craige

We report noninvasive and invasive studies designed to clarify the mechanism of the third heart sound (S3) in humans. The noninvasive observations were made using a miniature accelerometer attached to the skin surface at the cardiac apex. In subjects with no S3, the tracings were either flat or showed very low undulations throughout diastole. Those with an S3, however, demonstrated a distinct reduction of acceleration, or negative jerk, of the rapid filling movement at the apex at the time of the sound. The invasive studies in the cardiac catheterization laboratory consisted offrame-by-frame measurements of left ventricular dimensions in the transverse and long axes during early diastole in patients with diastolic overload abnormalities to investigate the temporal sequence of filling in these two principal axes. The maximal long-axis filling rate occurred after the short axis, a finding that helps to resolve a discrepancy noted in the time of maximal short-axis filling and S3 production. These studies support the concept that the S3 is due to a sudden intrinsic limitation of longitudinal expansion of the left ventricular wall during early diastolic filling, resulting in a negative jerk that is transmitted to the skin surface.


Circulation | 1983

Origin of the third heart sound. I. Studies in dogs.

Yukio Ozawa; Damon Smith; Ernest Craige

We studied 13 anesthetized dogs in which a third heart sound (S3) was repeatedly induced by hypoxemia plus fluid overload. A miniature accelerometer with a mass of about 1.1 g was applied at three levels intact chest wall over cardiac apex, on the pericardium and on the epicardium to record motion of the structures under observation as well as sound. Intraventricular pressure and sound were monitored using a Millar catheter. Application of two accelerometers simultaneously over the epicardium permitted observation of the chronologic sequence of ventricular wall dynamics in early diastole. The S3 at each level occurred simultaneously with the sudden onset of reduced acceleration, or negative jerk. These dynamic phenomena were maximal at or near the cardiac apex. We conclude that the event that triggers the S3 is a sudden intrinsic limitation of longitudinal expansion of the left ventricular wall.


American Journal of Cardiology | 1985

Influence of the aortic component of the second heart sound on left ventricular maximal negative dP dt in the dog

Damon Smith; Ernest Craige

Maximal negative left ventricular dP/dt is widely used as a measure of isovolumic muscular relaxation of the left ventricle. In the course of canine experiments designed to elucidate the hemodynamic events responsible for the aortic component of the second heart sound, high-fidelity left ventricular pressure and dP/dt signals were recorded and accelerations detected on the root of the aorta and epicardium at the cardiac apex. The second heart sound was coincident with maximal negative dP/dt and affected its magnitude to a variable and unpredictable extent. This may account for some of the unexpected variations in magnitude of maximal negative dP/dt that have been described in various disease states and in laboratory experiments where the effects of physiologic and pharmacologic interventions have been studied.


Journal of the American College of Cardiology | 1984

Mechanical vibration transmission characteristics of the left ventricle: Implications with regard to auscultation and phonocardiography

Damon Smith; Toshiyuki Ishimitsu; Ernest Craige

Systolic-diastolic phasic alteration of left ventricular mechanical vibration transmissibility was studied in an open chest canine preparation. A continuous vibratory tone was applied to the base of the heart, and a miniature heart surface vibration sensor applied to the epicardium near the ventricular apex. This allowed the detection of the percent of the vibration that was transmitted from source to sensor. These data were compared with those from intracardiac phonocardiograms obtained using a micromanometer-tipped catheter. It was found that in systole, the ventricle transmitted a vibratory tone from the cardiac base to the apex so that it was readily detected by the heart surface sensor. In marked contrast, during diastole the relaxed ventricle failed almost completely to transmit the vibration to the apical position. When the dog experienced heart failure during hypoxia, the ventricular diastolic vibration transmissibility was found to equal or exceed that of the systolic phase.


Journal of the American College of Cardiology | 1985

Origin of the third heart sound: comparison of ventricular wall dynamics in hyperdynamic and hypodynamic types.

Toshiyuki Ishimitsu; Damon Smith; Barbara Berko; Ernest Craige

To investigate the left ventricular wall dynamics conducive to the third heart sound (S3) in both hyper- and hypodynamic filling conditions, eight dogs were studied in which an S3 was produced by hypoxemia and in eight others by acute mitral regurgitation. Pulse transit sonomicrometry crystals were used to measure external left ventricular dimension dynamics in the two principal axes. A miniature accelerometer was used to detect the epicardial S3 vibration. The development of the S3 was invariably associated with an increased peak velocity of long-axis external dimensional expansion in early diastole. This enhanced long-axis filling activity was not dependent on increased global chamber or short-axis filling dynamics and sometimes occurred when global filling rate was unchanged. In addition, the short-axis filling rate was sometimes reduced as the S3 developed. It is concluded that the common denominator of S3 generation in this acute dog model is exaggerated long-axis diastolic expansion activity which is present in both hyper- and hypodynamic left ventricular filling.


Circulation | 1983

Chest wall velocity and the second heart sound. An improved sensor of S2 splitting.

Damon Smith; Yukio Ozawa; Ernest Craige

We report a new method of detection of the timing of the aortic and pulmonary valve closure that depends not on the registration of audible vibrations, but rather, on subtle but distinct movements of the chest wall, which are external manifestations of these events. We studied these phenomena in six openchest dogs and in 69 human subjects. The dog studies show that the two distinct inward movements detected by a motion sensor applied to the epicardium in the vicinity of the right ventricular outflow tract correlate with the timing of the incisural notches of the pressure signals from the great vessels. In humans, these movements are transmitted to the skin surface and can be detected noninvasively. In 48 of the 69 human subjects (70%), these spikes provided a significantly better indication of the timing of semilunar valve closure than did the conventional phonocardiogram.


Japanese Circulation Journal-english Edition | 1991

The influence of left ventricular relaxation in determination of the intensity of the aortic component of the second heart sound

Naoshi Tanigawa; Damon Smith; Ernest Craige


American journal of noninvasive cardiology | 1988

Heart Sounds: Toward a Consensus Regarding Their Origin^1

Damon Smith; Ernest Craige


Archive | 1986

Mechanism ofthedicrotic pulse

Damon Smith; Ernest Craige

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Ernest Craige

University of North Carolina at Chapel Hill

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Barbara Berko

Hospital of the University of Pennsylvania

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Toshiyuki Ishimitsu

University of North Carolina at Chapel Hill

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