P. D. Stein

Pressure-diameter relations during early diastole in dogs. Incompatibility with the concept of passive left ventricular filling.

We studied left ventricular (LV) pressure-diameter relations in 13 open-chest mongrel dogs to explore whether ventricular filling is passive, active, or a combination of both. Left ventricular internal diameter along the minor axis and thickness of the LV free wall were measured with ultrasonic dimension gauges. Pressures in the LV, left atrium (LA), and aorta were measured with catheter-tip micromanometers. Pressure in the LV during the rapid filling phase of diastole decreased from 13 ± 1 mm Hg to 3 ± 0.4 nun Hg (mean ± SE). During this period, LV internal diameter increased from 32.6 ± 1.5 to 36.7 ± 1.5 nun, and this represented 49% of the total change of LV diameter that occurred during diastole. The pressure-diameter relation that we observed during the rapid phase of filling suggests that active enlargement rather than passive distension of the left ventricle occurred. Reduction of pressure within the left ventricle during rapid filling, while the ventricular diameter increased, appears to be due to forces within the LV wall that act to restore the LV to its diastolic dimensions. This allows the LV to draw blood from the atrium by creating a pressure in the LV that is lower than in the LA. On the other hand, during the latter part of diastole, following atrial contraction, the pressure-diameter relation suggests that the left ventricle undergoes passive distention. Circ Res 45: 357-365, 1981

Modulating effect of regional myocardial performance on local myocardial perfusion in the dog.

We studied the effect of regional contractile performance on regional coronary blood flow and flow distribution in 10 dogs. The left anterior descending (LAD) coronary artery was cannulated and perfused. Maximal vasodilation was obtained with adenosine. Consequently, variations of LAD flow reflected changes of extravascular resistance, lidocaine injected in the LAD caused a localized reduction of contractile performance as shown by the absence of systolic wall thickening. Global left ventricular performance and pressure were unchanged. Coronary extravascular resistance diminished and LAD flow increased from 4.8 ± 0.5 to 6.2 ± 0.6 ml/min per g (P< 0.02). The endocardia!: epicardial ratio increased from 1.02 ± 0.07 to 1.28 ± 0.07 (P < 0.001). Isoproterenol in the LAD augmented systolic wall thickening. Regional coronary flow diminished from 5.1 ± 0.5 to 3.3 ± 0.4 ml/ min per g (P < 0.001), and the endocardia!:epicardial ratio diminished from 1.08 ± 0.07 to 0.75 ± 0.07 (P < 0.01). These data indicate that myocardial contractility is a major component of extravascular coronary resistance and is a mechanical determinant of coronary blood flow and its transmural distribution. Circ Res 45: 634-841, 1979

Frequency of the first heart sound in the assessment of stiffening of mitral bioprosthetic valves.

SUMMARY The frequency spectrum of the first heart sound (S1) was measured noninvasively in 54 patients with porcine bioprosthetic valves inserted in the mitral position. Phonocardiograms were recorded on magnetic tape on line with a signal processor with which the frequency spectrum and peak frequency of S1 were determined. In 19 patients with normal natural mitral valves, the apparent peak frequency within the range of measured frequencies of S1 was 46 ± 2 Hz (mean ± SEM). In 11 patients with porcine bioprosthetic valves implanted in the mitral position for < 1½ years, the apparent peak frequency of S1 was 43 ± 3 Hz, which was not significantly different from S1 in patients with normal mitral valves. However, in 33 patients with porcine bioprosthetic valves in place 5–7 years, the apparent peak frequency of S1 was higher, 67 ± 2 Hz (p < 0.001). In patients in whom the porcine bioprosthetic valve was implanted 5 years or longer, the frequency spectrum of S1 showed a greater proportion of sound energy at frequencies between 50–200 Hz compared with patients in whom the prosthetic valve was implanted 1½ years or less. Changes of the frequency of S1 in these patients may be a manifestation of stiffening of the valve as a result of early degenerative changes.

Negative diastolic pressure in the intact canine right ventricle. Evidence of diastolic suction

To determine whether the canine right ventricle (RV) can develop a negative diastolic pressure indicative of suction, RV pressure was measured in 15 dogs, with catheter-tip micromanometers. Six dogs were studied only with the chest closed. In these dogs intrapleural pressure was measured medially (near the heart) in four and laterally in two. In nine dogs, RV pressure was evaluated with the chest closed and after the chest had been opened. In all dogs, with the chest closed, minimal RV diastolic pressure during expiration was negative, −4.8 ± 0.3 mm Hg. The lowest diastolic pressures occurred during early diastole. Intrapleural pressure during expiration was never this low. Intrapleural pressure measured medially in four dogs was positive during expiration (1.0 ± 0.6 mm Hg). In the two dogs in which it was measured in the lateral pleura! space, it was somewhat negative during expiration (−2.6 and −1.3 mm Hg, respectively). After the chest had been opened (nine dogs) minimal RV pressure during early diastole was negative in six dogs and positive in three (range: −1.8 to 0.8 mm Hg). These results indicate that the negative RV diastolic pressure during expiration did not result from a negative intrathoracic pressure. It appears that the RV during early diastole can create a sucking effect which may contribute to the filling process.

Comparison of the distribution of intramyocardial pressure across the canine left ventricular wall in the beating heart during diastole and in the arrested heart. Evidence of epicardial muscle tone during diastole.

Computations of compliance of the left ventricle (LV) during diastole assume passive tissue characteristics. To evaluate this assumption, we measured diastolic LV intramyocardial pressure simultaneously in the subepicardium and subendocardium in 18 open-chest dogs, using 1-mm in diameter micromanometers. Subepicardial pressure, 26 ± 1 mm Hg (mean ± SKM) exceeded subendo-cardial pressure, 14 ± 1 mm Hg (P < 0.001), and it exceeded left ventricular end-diastolic pressure (LVEDP) (9 ± 1 mm Hg) (P < 0.001). After an infusion of dextran-40 (10 dogs), subepicardial diastolic pressure increased to 42 ± 4 mm Hg which was higher than diastolic subendocardial pressure, 26 ± 2 mm Hg (P < 0.001) and LVEDP, 24 ± 2 mm Hg (P < 0.001). Following cardiac arrest (12 dogs) with the intramyocardial probes unchanged in position, LV intracavitary pressure, 9 ± 1 mm Hg, and suben-docardial pressure, 13 ± 3 mm Hg, did not differ significantly from the pressures in the beating heart. Subepicardial pressure, 9 ± 1 mm Hg, was lower than in the beating heart (P < 0.001). Following distension of the arrested LV (12 dogs), subepicardial pressure, 31 ± 7 mm Hg, was lower than both subendocardial pressure, 58 ± 12 mm Hg (P < 0.001) and LV intracavitary pressure, 54 ± 11 mm Hg (P < 0.001). These observations indicate that tone is maintained by the subepicardium during diastole. Furthermore, the LV wall does not appear to behave as a passive shell during ventricular filling. Circ Res 47: 258-267, 1980

Patterns of Flow in the Left Coronary Artery

The purpose of this investigation is to describe our preliminary observations of the overall pattern of flow in a mold of the left coronary artery of a pig. Flow in the coronary mold was visualized by the injection of dye into the sinus of Valsalva. Studies were performed during steady flow at rates of 100, 200, 300, 400, and 500 mL/min. Studies were also performed during pulsatile flow, using a pulse duplicator that simulated the magnitude and phasic pattern of coronary flow at rest and during reactive hyperemia. At conditions that simulated rest, mean coronary flow was adjusted to 121 mL/min of which 24 mL/min (20 percent) was systolic. During simulated reactive hyperemia, mean flow was 440 mL/min. Visualization of flow revealed the absence of disturbances of turbulence during both steady and pulsatile flow in the left anterior descending (LAD) and left circumflex (CIRC) coronary arteries throughout the entire range of flow studied. Prominent spiraling of flow occurred during steady and pulsatile flow. Spiraling of flow was not observed in the LAD at rest during pulsatile flow, but developed during simulated reactive hyperemia. Helical flows were observed in the CIRC both during simulated rest and reactive hyperemia. These observations suggest that helical flows may be characteristic features of flow in the left coronary artery; whereas turbulence may not be a feature of this flow field. Whether the spiraling of flow that we observed related to the spiral distribution of early atheroma reported by others, is undetermined.

TURBULENT STRESSES IN THE REGION OF AORTIC AND PULMONARY VALVES.

The specific features of turbulent flow that are likely to be damaging to the blood cells and platelets are the stresses which are intrinsic to turbulence, known as Reynolds stresses. These include normal stresses as well as shear stresses. The purpose of this study is to determine the magnitude of the turbulent stresses that may occur during ejection in the vicinity of normal and diseased aortic valves near normal pulmonary valves. Both Reynolds normal stresses and Reynolds shear stresses were calculated from velocities obtained in vitro with a laser Doppler anemometer in the region of two severely stenotic and regurgitant human aortic valves. Reynolds normal stresses were also calculated from velocities obtained with a hot-film anemometer in 21 patients in the region of normal and diseased aortic valves. In seven of these patients, it was calculated in the region of the normal pulmonary valve. The Reynolds normal stress in patients with combined aortic stenosis and insufficiency was prominently higher than in patients with normal valves. In the former, the Reynolds normal stress during ejection transiently reached 18,000 dynes/cm2. This was in the range of the Reynolds normal stress observed in vitro. The Reynolds shear stress measured in vitro transiently reached 11,900 dynes/cm2 during ejection. Because the Reynolds normal stresses in the presence of the severely stenotic and regurgitant valves were comparable in vitro and in patients, it is likely that the Reynolds shear stress in patients is also comparable to values measured in vitro. These values were well above the stresses which, when sustained, have been shown to have a damaging effect upon blood cells and platelets.

Exploration of the cause of the low intensity aortic component of the second sound in nonhypotensive patients with poor ventricular performance.

SUMMARYThis investigation was undertaken to explore the cause of the diminished second sound (S2) that may occur in normotensive patients with poorly performing ventricles. Intraaortic sound and pressure were measured in 16 patients with angina; eight had normal ventricular performance (ejection fraction .60%) and eight had poor performance (ejection fraction < 50%). The amplitude of S, was lower in patients with poor ventricular performance as was negative dp/dt. Aortic pressure was com- parable in both groups. The ampitude of S2 was linearly related to the rate of change of the pressure gradient that developed across the aortic valve during diastole (r = 0.82). The latter also correlated with negative dp/dt (r = 0.82). These observations indicate that in patients with poor ventricular performance, isovolumic relaxation may be compromised. This would cause a reduction of the rate of development of the diastolic pressure gradient, which would result in a diminished S2.

Surface topography of stenotic aortic valves by scanning electron microscopy.

Surface features of 19 stenotic aortic valves from patients undergoing valve replacement were investigated by scanning electron microscopy. Villi, prominent on five valves, were distributed either singularly or in clusters and differed in shape. Endothelial cells had microvilli and bulbous surface projections. Endothelial disruption with a focal loss of endothelial cells was uniformly observed. Erythrocytes were found scattered over the exposed subendothelial surface or enmeshed within fibrin networks on 11 of the valves. Activated leukocytes were seen on four valves and showed veil-like projections as well as microvilli. Platelets, observed on three valves, displayed pseudopodial formation and hyalomeric spreading, signifying an increased degree of membrane response. Most platelet aggregates were composed entirely of dendritic forms (reversible aggregates), but a few also contained spread forms (irreversible aggregates). Focal deposits of crystalline material, presumably containing calcium, were observed in areas of endocardial disruption.

Flow Visualization in a Mold of an Atherosclerotic Human Abdominal Aorta

Flow in a mold of an atherosclerotic human abdominal aorta and common iliac arteries was studied by flow visualization at a mean Reynolds number of 500 during both pulsatile and steady flow. Flow separation and transient flow reversals were found distal to atherosclerotic plaques during pulsatile flow; whereas flow separation resulting in regions of permanent eddies were observed distal to plaques only during steady flow.