Earl T. Hawkins

Blood velocity in the right coronary artery: Relation to the distribution of atherosclerotic lesions

Vascular endothelial injury by high shear stresses and adverse effects of low shear rates on mass transfer across the arterial wall have been suggested as factors in atherogenesis. This study describes differences in blood velocity, and therefore differences of shear rate, across the lumen of the right coronary artery (RCA) of man. Selective coronary arteriograms of 30 patients without obstructive RCA disease were reviewed. Velocity was assessed qualitatively based on the rate of clearance of contrast material. There was a rapid clearing of contrast material along the outer wall of the RCA as it curved around the border of the heart. A much slower clearing occurred along the inner wall, bordering the myocardium, which persisted 2 to 6 cardiac cycles after the outer wall had cleared. This suggests that velocity, and therefore shear rate, is much lower along the inner wall of the RCA. To determine the relation of the distribution of atherosclerotic plaques in the RCA to local blood velocity, the RCA in 17 randomly selected human subjects who died of noncardiac disease were studied histologically. There was an uneven distribution of atherosclerotic plaques in the RCA with greater involvement of the inner wall. These observations demonstrate an association between the lower shear rate along the inner wall of the RCA and the site of higher concentration of atherosclerosis.

Flow separation in the renal arteries.

To determine the nature of the flow In the proximal portion of the renal arteries, a common site for the development of atherosclerosis, we performed pulsatile flow studies In a clear acrylic mold of a normal human aorta and renal arteries. The mold was developed from a cast of the renal arteries prepared In situ during the autopsy of a 27-year-old woman. Flow in the mold was visualized by the Illumination of bouyant particles (100 to 300 μ). A range of branch (renal) to trunk (aorta) flow ratios of 0.053 to 0.350 was studied. Flow separation during systole was considered present when particles near the wall reversed direction. Flow separation occurred throughout systole at the superior aspect of the origin of both the left and right renal arteries at a branch-to-trunk flow ratio of 0.053. As the branch-to-trunk flow ratio Increased, flow separation occurred during the deceleration phase of right renal flow. At a branch-totrunk flow ratio of 0.350, flow separation was no longer present. This suggests that flow separation may occur near the renal ostla If renal flow falls appreciably while aortic flow remains elevated. Because flow separation Involves low wall shear, mass transfer across the arterial wall may be adversely affected and possibly contribute to the formation of atheroma.

Hepatic and splenic injury in dogs caused by direct impact to the heart.

The purpose of this study was to explore the possibility that nonpenetrating cardiac impact can directly result in hepatic and splenic injury through hemodynamic effects. Impact upon the anterior surface of the heart was produced in 34 open-chest anesthetized dogs. In 15 dogs the velocity of impact was 12 m/sec and in 19 dogs it was 18 m/sec. Pressure in the inferior vena cava transiently reached 194 +/- 25 mm Hg in the dogs impacted at 12 m/sec and 377 +/- 44 mm Hg in dogs impacted in 18 m/sec. Aortic pressure transiently reached 449 +/- 32 mm Hg in dogs impacted at 12 m/sec and 682 +/- 33 mm Hg in dogs impacted at 18 m/sec. Gross capsular lacerations of the liver occurred in six dogs (18%) following cardiac impact. All dogs showed hepatic congestion and most showed microscopic injury of liver cords, central veins, and portal tracts. Dogs that survived cardiac impact for the duration of observation (90 minutes) showed focal acute inflammation of liver triads and hepatic sinusoids, indicating a more subtle degree of injury. The spleens of eight dogs showed areas of grossly visible subcapsular hemorrhage. Subcapsular congestion of the spleen occurred in almost all dogs. This study shows therefore that nonpenetrating cardiac impact may result in hepatic and splenic injury. A likely mechanism may be the extraordinarily high venous pressure that develops at the instant of impact, although transient striking elevations of arterial pressure may also contribute.

Longitudinal evaluation of left ventricular performance in dogs following nonpenetrating cardiac trauma

To investigate the temporal changes of global left ventricular function following nonpenetrating cardiac impact, studies were performed in ten purpose-bred dogs. Under full anesthesia and after hemodynamic and angiographic measurement, a midline thoracotomy was performed and a 12 m/sec blunt impact was delivered to the anterior surface of the heart in eight dogs with an air-pressurized impactor. Two dogs were sham operated and did not undergo trauma. After closing the chest, the hemodynamic measurements were repeated at 3 hours, 3 days, 2 weeks, and 5 weeks after impact. Hemodynamic measurements included left ventricular end-diastolic pressure and peak left ventricular positive and negative rates of change of pressure. Left ventricular ejection fraction was calculated from ventriculograms obtained with the dog positioned on its right side. All indices of left ventricular performance in dogs that underwent trauma were depressed at 3 hours after impact and recovered gradually to near normal levels at 2 to 5 weeks after trauma. Recovery of left ventricular function occurred in spite of residual patchy scarring of the left ventricular myocardium in the region of impact. No variability of left ventricular function indices was observed over the course of the study in the two sham-operated dogs. The results indicate that blunt cardiac impact can cause depression of left ventricular performance in the immediate post-impact period, but near complete recovery of function occurs within 2 to 5 weeks after the injury, in spite of residual scarring.

Extrinsic compression of the coronary arteries following cardiac trauma in dogs

The purpose of this study was to explore the possibility of extrinsic coronary artery compression following nonpenetrating cardiac trauma. Direct impact on the anterior surface of the heart was produced by a blunt air-pressurized impactor in 34 open-chest anesthetized dogs. Sections from the left anterior descending coronary artery and the left circumflex coronary artery were obtained for microscopic examination from each of the 17 dogs that survived the duration of observation (90 minutes). Gross examination of the external surface of the heart showed contusions over the anterior surface and prominent extravascular hemorrhage that followed the course of the left anterior descending coronary artery, showed no contusion or extravascular bleeding. In most instances, light microscopy showed narrowing of the lumen of the left anterior descending coronary artery with concave deformation resulting from compression by blood around the vessel. The cross-sections of the circumflex coronary artery, although sometimes oblong, showed no concave deformation. These observations suggest that extrinsic compression of the coronary artery may cause coronary narrowing following nonpenetrating cardiac trauma.

Construction of Molds of Complex Arterial Segments

Molds of arterial segments would be advantageous for in-vitro assessments of arterial flow dynamics. Previous techniques have been limited because of their technical difficulty or because they were limited to short planar segments. This paper presents a method, based on the lost wax technique, that is readily accomplished, and permits the fabrication of a mold of any arterial bed, irrespective of its complexity.

Right ventricular outflow obstruction secondary to nonpenetrating blunt trauma to the canine myocardium.

The purpose of this study was to investigate the development of a right ventricular (RV) outflow tract obstruction of sufficient severity to produce a systolic murmur following blunt cardiac trauma. A nonpenetrating impact directly on the anterior surface of the heart was produced in 34 open chest anesthetized dogs. Impact velocity was 12 m/sec in 15 dogs and 18 m/sec in 19 dogs. Seventeen dogs died immediately following impact. Pressures in the pulmonary artery and RV were measured during the control period in all dogs, and intermittently for 90 minutes following impact in ten of the 17 surviving dogs. At 90 minutes following impact a systolic pressure gradient of 9 +/- 2 mm Hg (range, 3 to 22 mm Hg) developed across the RV outflow tract and was associated with a prominent ejection murmur. At autopsy, RV wall thickness measured at the midventricular level was 13.5 +/- 1 mm (mean +/- SEM) which was thicker than in dogs that died immediately following impact, 6 +/- 1 mm (p less than 0.001). Microscopy of the RV myocardium of dogs that survived impact showed interstitial bleeding with prominent accumulations of blood between muscle bundles, whereas dogs that died immediately after impact showed no interstitial bleeding. The obstruction seems to have resulted from the increased RV wall thickness due to interstitial bleeding. In the absence, therefore, of other evidence to explain a new systolic murmur in patients following nonpenetrating cardiac trauma, the possibility of RV outflow obstruction might be considered.