Biomedical subjects

K C Dellsperger

Publications and source records attributed to K C Dellsperger.

43 records · Page 3Linked to original sources

PubMed1989

Effect of prosthetic mitral valve geometry and orientation on flow dynamics in a model human left ventricle.

Pulsatile flow dynamics through bileaflet (St Jude and Duromedics), tilting disc (Bjork-Shiley and Omniscience), caged ball (Starr-Edwards), pericardial (Edwards) and porcine (Carpentier-Edwards) mitral valves in a model human left ventricle (LV) were studied. The model human ventricle, obtained from an in situ diastolic casting, was incorporated into a mock circulatory system. Measurements were made at various heart rates and flow rates. These included the transvalvular pressure drop and regurgitation in percent and cm3 beat-1. The effect of valve geometry and the orientation of the valve with respect to the valve annulus was analyzed using a flow visualization technique. Qualitative flow visualization study indicates certain preferred orientations for the tilting disc and bileaflet valve prostheses in order to obtain a smooth washout of flow in the LV chamber.

Heart↗

PubMed1989

Comparison of the effects of increased myocardial oxygen consumption and adenosine on the coronary microvascular resistance.

The purposes of this study were to determine if coronary dilation secondary to an increase in myocardial oxygen consumption (MVO2) affects the microcirculation in a homogeneous or heterogeneous manner and to determine if comparable degrees of coronary dilation produced by increasing MVO2 or exogenous (intravenous adenosine) or endogenous (intravenous dipyridamole) adenosine have similar effects in the coronary microcirculation. The epimyocardial coronary microcirculation was observed through an intravital microscope by stroboscopic epi-illumination in anesthetized open-chest dogs. Aortic pressure and heart rate were controlled by an aortic snare and atrioventricular sequential pacing, respectively, during experimental procedures. In group 1 (n = 15), coronary arterial microvessel diameters were measured under control condition and during rapid pacing at 300 beats/min, which doubled MVO2. Increases in MVO2 caused heterogeneous vasodilation in coronary arterial microvessels (40-380 microns). There was an inverse relation between control diameter and percent increase in diameter. In group 2 (n = 15) or group 3 (n = 10), adenosine or dipyridamole was infused intravenously to increase myocardial perfusion to the same level as that obtained with rapid pacing. Adenosine and dipyridamole did not change MVO2. Adenosine and dipyridamole also caused heterogeneous vasodilation, but the effects of adenosine and dipyridamole were restricted to arterial microvessels smaller than 150 microns. From these results, we conclude that increases in MVO2 produce widespread but heterogeneous vasodilation, that is, greater dilation in smaller arterial microvessels. Comparable increases in coronary flow produced by increasing MVO2 or endogenous and exogenous adenosine do not produce identical changes in the distribution of coronary microvascular resistance.

Adenosine↗

PubMed1988

The effects of pressure-induced cardiac hypertrophy on the functional capacity of the coronary circulation.

Pressure-induced cardiac hypertrophy has many effects on the functional capacity of the coronary circulation. Many studies have been performed in both animal and humans and the major findings are as follows: 1. Most types of myocardial hypertrophy are associated with the decrement in coronary vasodilator reserve; 2. The magnitude of the decrement in coronary reserve in myocardial hypertrophy is usually much more prominent in patients with myocardial hypertrophy than in animal models; 3. Left ventricular hypertrophy secondary to systemic hypertension is associated with altered autoregulation of myocardial perfusion; 4. The perfusion abnormalities associated with hypertension and left ventricular hypertrophy are affected by various factors such as age of onset, ventricular involvement, and the stimulus for hypertrophy; 5. Left ventricular hypertrophy secondary to renal hypertension markedly augments the adverse effects of coronary occlusion. In this setting, coronary occlusion is associated with a three-fold increase in the incidence of lethal ventricular arrhythmias and a 35% increase in infarct size. Thus, pressure-induced hypertrophy profoundly alters the coronary circulation.

Angina Pectoris↗

PubMed1988

Detection, localization, and quantitation of bioprosthetic mitral valve regurgitation. An in vitro two-dimensional color-Doppler flow-mapping study.

The usefulness of two-dimensional color-Doppler flow-imaging (2D Doppler) in the detection, localization, and quantitation of bioprosthetic mitral valve regurgitation is uncertain. Mitral bioprostheses, before and after the creation of transvalvular (n = 33), paravalvular (n = 17), or combined (n = 23) defects, were mounted in a pulsed duplication system (flow rates, 2.5-6.5 l/min; pulse rate, 70 beats/min). An Aloka 880 2D Doppler system (Japan) was used to image the regurgitant jets in the simulated left atrial chamber, analogous to images obtained with transesophageal echocardiography. Jet area was corrected to an estimate of stroke volume: 2D Doppler measurements were divided by [(valve effective orifice area) X (continuous-wave Doppler-determined mean diastolic filling velocity)]/pulse rate. Regurgitant fraction and regurgitant volume were measured by an electromagnetic flow probe. 2D Doppler correctly identified the presence and location of paravalvular regurgitation. In transvalvular and combined transvalvular-paravalvular defects, there were six incorrect interpretations, all having transvalvular regurgitant volumes less than 4 ml/beat. In the presence of transvalvular regurgitation, jet area, length, and width correlated linearly with regurgitant volume (r = 0.82, 0.80, and 0.68, respectively; p less than 0.0001) and regurgitant fraction (r = 0.62, 0.61, and 0.45, respectively; p less than 0.001). Correlations with regurgitant fraction were improved when 2D Doppler measurements were corrected for stroke volume (r = 0.78, 0.79, and 0.67, respectively; p less than 0.0001). Mitral bioprostheses with transvalvular defects were also studied at varying flow rates (3.2-7.5 l/min) and pulse rates (70, 90, and 110 beats/min). The correlation between jet area and regurgitant volume was improved with a second-order polynomial regression (r = 0.93, p less than 0.0001). Our conclusions are that 1) in this in vitro model analogous to transesophageal imaging, 2D Doppler accurately detects and localizes bioprosthetic mitral valve regurgitation; 2) in transvalvular bioprosthetic mitral valve regurgitation, 2D Doppler measurement of jet area has a curvilinear relation with regurgitant volume, and correlation with regurgitant fraction is improved with correction for stroke volume; and 3) in paravalvular bioprosthetic mitral valve regurgitation, correlations between 2D Doppler measurements and regurgitant volumes are weaker, possibly because of jet eccentricity.

Animals↗

PubMed1988

Acceleration of the wavefront of myocardial necrosis by chronic hypertension and left ventricular hypertrophy in dogs.

Previous studies have shown that hypertension and left ventricular hypertrophy (HT-LVH) increase completed infarct size. Myocardial infarction progresses in a wavefront of myocardial necrosis from the subendocardium to the subepicardium. We tested two hypotheses: First, HT-LVH accelerates the wavefront of myocardial necrosis when compared with normotensive animals; and second, lowering of arterial pressure by infusing nitroprusside 1 hour after coronary artery occlusion exerts a salutary effect on infarct size. To test these hypotheses, systemic hypertension (mean aortic pressure = 141 +/- 3 mm Hg) and left ventricular hypertrophy (18% increase in left ventricular mass) were induced in dogs using a single-kidney, single-clip model. Seventeen adult mongrel dogs were used as controls. We measured mean aortic pressure, heart rate, left atrial pressure, and myocardial perfusion (microspheres) in several groups of normal and HT-LVH awake dogs. In two groups (normal and HT-LVH), 1 hour of circumflex coronary artery occlusion was followed by 4 hours of reperfusion. In two additional groups (normal and HT-LVH), 3 hours of circumflex coronary artery occlusion was followed by 90 minutes of reperfusion. In another group with HT-LVH, nitroprusside was infused to reduce mean arterial pressure to 100 mm Hg beginning 1 hour after occlusion and was continued for the duration of reperfusion period (HT-LVH + N). Infarct size was assessed using triphenyltetrazolium chloride stain and risk area was determined using postmortem barium angiography. Fifteen of 17 (88%) control animals survived coronary artery occlusion, whereas only 17 of 42 (40%) dogs with HT-LVH survived coronary occlusion (p less than 0.05). Infarct-to-risk ratios in the various layers of the left ventricular wall were determined for survivors in all groups. After 1 hour of coronary occlusion more than twice as much mid-wall and epicardium was infarcted in the HT-LVH group compared with the control group. After 3 hours of coronary occlusion significantly more endocardium, mid-wall, and epicardium was infarcted in the dogs with HT-LVH. In the nitroprusside-treated HT-LVH dogs, the infarct sizes were similar to control animals. From these data we conclude: 1) the rate of infarction is accelerated in animals with HT-LVH; 2) nitroprusside infused 1 hour after coronary artery occlusion and continued throughout the reperfusion period exerts beneficial effect on infarct size when compared with control animals; and 3) acute coronary artery occlusion in animals with HT-LVH is associated with significantly greater mortality when compared with control animals.

Animals↗

PubMed1983

Regurgitation of prosthetic heart valves: dependence on heart rate and cardiac output.

Prosthetic heart valves exhibit closure and leakage backflow; however, no well-controlled study to evaluate the influence of factors such as cardiac output and heart rate on backflow has been reported to date. Four clinically used prosthetic aortic valves (size 27 mm)--St. Jude Medical, Björk-Shiley Spherical Disc, Björk-Shiley Convexo Concave, and Starr-Edwards model 1260--were studied in the aortic chamber of a pulse duplication system at heart rates of 50, 80, 110, and 140 beats/min, cardiac output of 2, 4, 6, and 8 liters/min, and mean aortic pressure of 100 mm Hg. Regurgitation was calculated in percentage and found to vary directly with heart rate and inversely with cardiac output. The range of values obtained were 5.5% for the Starr-Edwards model 1260 valve at 110 beats/min and 8 liters/min, to 37.5% for the Björk-Shiley Convexo Concave valve at 140 beats/min and 2 liters/min. Regurgitation was also calculated in milliliters/stroke and ranged from 3.4 ml/stroke for the Starr-Edwards model 1260 valve at 140 beats/min and 2 liters/min, to 17.3 ml/stroke for the Björk-Shiley spherical disc valve at 50 beats/min and 2 liters/min. Regurgitation associated with prosthetic heart valves may present a problem clinically, particularly under conditions of low cardiac output and tachycardia.

Cardiac Output↗

PubMedDate not supplied

The QT interval following carotid artery resection.

BACKGROUND: Right radical neck dissection has been shown to prolong the QT interval, reportedly caused by surgical trauma to the cervical autonomic system, which may result in malignant ventricular arrhythmias. Carotid artery resection would be expected to be more likely to cause dangerous arrhythmias. METHODS: We prospectively studied eight patients with electrocardiograms before and after carotid resection. Four patients had left-sided procedures and four patients had right-sided procedures. In addition, 11 patients were studied retrospectively. QT intervals were normal in all patients preoperatively. RESULTS: Preoperative corrected QT intervals (QTc) were in the normal range used by our institution for all eight patients in the prospective group. There were no significant QTc changes after either left-sided or right-sided carotid resection. However, the retrospective group did show significant changes in QTc following right carotid resection (n = 5), but not left resection (n = 6). CONCLUSIONS: EKG changes associated with carotid resection may not be uniform and may depend on surgical technique or specific anatomic factors. Controlled prospective studies are needed to confirm the prevalence of QT interval changes in radical neck surgery.

Adult↗