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Featured researches published by Philip E. Aylward.


Journal of the American College of Cardiology | 1989

Feasibility of identifying amyloid and hypertrophic cardiomyopathy with the use of computerized quantitative texture analysis of clinical echocardiographic data

Krishnaswamy Chandrasekaran; Philip E. Aylward; Steven R. Fleagle; Trudy L. Burns; James B. Seward; A. Jamil Tajik; Steve M. Collins; David J. Skorton

Ultrasound tissue characterization, the evaluation of certain physical properties of a tissue based on its acoustic properties, is an evolving application in echocardiography. The ability to identify acutely and chronically injured tissue has been demonstrated in a number of animal studies, but data in humans are limited. The present study tested the hypothesis that quantitative echocardiographic texture analysis, a method of evaluating the spatial pattern of echoes in echocardiographic images, would differentiate amyloid and hypertrophic cardiomyopathy from normal myocardium. Routine clinical echocardiographic data were obtained on 34 subjects at the Mayo Clinic (10 normal subjects, 10 patients with amyloid heart disease, 8 patients with hypertrophic cardiomyopathy and 6 patients with left ventricular hypertrophy due to hypertension). Standard videotape recordings of these echocardiograms were analyzed at the University of Iowa. Echocardiographic data were digitized with use of a calibrated, 256 gray level digitization system. Quantitative texture analysis was performed on data from the ventricular septum and posterior left ventricular wall in end-diastolic and end-systolic, short-axis and long-axis echocardiographic images. The gray level run length texture variables were able to discriminate hypertrophic cardiomyopathy and amyloid heart disease from normal myocardium and from each other (p less than 0.0083 for comparisons of the quantitative texture features of amyloid versus hypertrophic cardiomyopathy versus normal by multivariate analysis of variance). The texture of the myocardium in hypertensive left ventricular hypertrophy not associated with amyloid or hypertrophic cardiomyopathy was in general not significantly different from that of normal myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)


Hypertension | 1987

Paroxysmal hypertension due to sinoaortic baroreceptor denervation in humans.

Timothy R. Aksamit; John S. Floras; Ronald G. Victor; Philip E. Aylward

A 41-year-old man with a remote history of neck and mediastinal radiation was seen with severe paroxysms of hypertension, headache, and cutaneous flushing after bilateral carotid bypass surgery. Investigation revealed marked parallel fluctuations in blood pressure and heart rate and elevation of plasma norepinephrine to 1164 pg/ml during a paroxysm. We systematically evaluated his arterial and cardiopulmonary baroreceptor reflex function by assessing changes in heart rate, arterial pressure, and efferent muscle sympathetic nerve activity, which was measured directly by the microneurographic technique. Elevating resting arterial pressure from 130/88 to 164/100 mm Hg with phenylephrine or lowering it to 88/56 mm Hg with nitroprusside produced no reflex changes in heart rate or efferent sympathetic nerve activity. In contrast, decreases in cardiac filling pressures with lower body negative pressure produced a marked increase in sympathetic nerve activity. These findings indicate complete loss of the afferent limb of the arterial baroreceptor reflex but preservation of the cardiopulmonary baroreceptor reflex. They suggest that both carotid and aortic baroreceptors were impaired by the previous radiation and surgery. Despite the loss of arterial baroreceptor function, the patient did not have sustained hypertension. The paroxysms of hypertension appear to be due to spontaneous fluctuations in central sympathetic drive not buffered by arterial baroreceptors in a manner similar to that seen in sinoaortic-denervated animals.


Journal of Vascular Research | 1990

Role of Vasopressin in Cardiovascular and Blood Pressure Regulation

Francois M. Abboud; J.S. Floras; Philip E. Aylward; G.B. Guo; B.N. Gupta; P.G. Schmid

At low concentrations and in physiologic states vasopressin is a potent antidiuretic hormone. Its cardiovascular effects have been more complex and their role in circulatory adjustments to hypovolemia and hypotension difficult to define with precision. Although recognized as a powerful vasoconstrictor, its pressor effect in intact animals, even at high concentrations, is minimal. The reasons for this blunted pressor response have been explored. This report is a review of previously published work from our laboratories which highlights the direct and indirect vasodilator actions of this hormone in animals and humans. The indirect vasodilator effect is caused by inhibition of sympathetic efferents, and facilitation of the baroreflex through a central action of the hormone and its sensitization of arterial baroreceptors as well as cardiac afferents.


Ultrasonic Imaging | 1986

Ultrasound characterization of acute myocardial ischemia by quantitative texture analysis

David D. McPherson; Philip E. Aylward; Boyd M. Knosp; Judy A. Bean; Richard E. Kerber; Steve Collins; David J. Skorton

In this study we tested the efficacy of quantitative texture analysis in the identification of acute myocardial ischemia using an ultrasound data acquisition system that digitizes and stores echocardiographic data in polar format. In nine closed-chest dogs, data were acquired before and after coronary occlusion using a 2.4 MHz echocardiographic system. Regions of interest were analyzed at end-diastole and end-systole from the ischemic area and normal area at the same depth of field. Ultrasound data were evaluated using previously reported quantitative gray level texture measures. After occlusion, texture changes indicative of ischemia were found in systolic images. The directional component of the data analysis was important; analysis in the azimuthal direction was more accurate than in the axial direction. Six texture measures exhibited significant changes in the ischemic region from control to occlusion when analyzing data in the azimuthal direction. One false positive result occurred (significant texture change in the normal region from control to occlusion) in the azimuthal direction. Several false positive alterations in the normal regions from control to occlusion were found when the texture was evaluated in the axial direction. For accurate assessment of ischemic changes, preocclusion image data were required. We conclude that quantitative echocardiographic texture analysis using polar format data can identify subtle changes in myocardial texture such as that due to acute ischemia, using data acquired through the chest wall.


Hypertension | 1987

Inhibition of muscle sympathetic nerve activity in humans by arginine vasopressin.

J S Floras; Philip E. Aylward; F. M. Abboud; Allyn L. Mark

Arginine vasopressin, a potent vasoconstrictor, does not raise arterial pressure in normal humans even at pathophysiological plasma levels. To examine whether the pressor effect of vasopressin in humans is buffered by baroreceptor reflex inhibition of sympathetic nerve activity, we recorded postganglionic muscle sympathetic nerve activity directly from the peroneal nerve in 12 normal men before, during, and after a 20-minute intravenous infusion of vasopressin, 4 ng/kg/min, that increased mean plasma concentrations from 6.2 +/- 0.6 to 320 +/- 68 (SE) pg/ml. During the first 5 minutes (n = 8), mean arterial pressure increased from 91 +/- 3 to 97 +/- 4 mm Hg (p less than 0.05) and integrated sympathetic nerve activity decreased from 271 +/- 45 to 156 +/- 33 units (p less than 0.05). At 15 minutes (n = 12), arterial pressure did not differ from control values whereas forearm vascular resistance fell (p less than 0.05) and central venous pressure and heart rate increased (p less than 0.05). Sympathetic nerve activity remained below control levels throughout the infusion (202 +/- 31 vs 254 +/- 40 units before infusion; p less than 0.05). An effect of vasopressin on ganglionic transmission was excluded, since the sympathoexcitatory response to apnea was not attenuated during vasopressin. Thus, pathophysiologic levels of vasopressin in humans cause inhibition of muscle sympathetic nerve activity that is not due to a ganglionic blocking action. The sympathoinhibition may be caused in part by the modest increases in mean arterial and central venous pressures and attendant stimulation of arterial and cardiac baroreceptors. The reflex decrease in sympathetic nerve activity would be expected to buffer the direct vasoconstrictor effects of vasopressin.


Journal of the American College of Cardiology | 1985

Defibrillator Electrode-Chest Wall Coupling Agents: Influence on Transthoracic Impedance and Shock Success

Philip E. Aylward; Robert A. Kieso; Pamela Hite; Francis M Charbonnier; Richard E. Kerber

The purpose of this study was to determine if the difference in transthoracic impedance produced by different coupling agents affects the success of shocks for defibrillation. Three different coupling agents, Harco pads (Hewlett-Packard), Littman pads (3M) and Redux paste (Hewlett-Packard), were assessed in 10 anesthetized dogs in which ventricular fibrillation was induced by electrical stimulation of the right ventricle. Defibrillation was attempted 15 seconds later, using 50, 100 and 150 joules (selected energy). Actual delivered energy, current, impedance and the percent of the shocks that achieved defibrillation were determined for the three coupling agents. Redux paste gave significantly lower impedance and higher current than the two disposable performed coupling pads tested. Despite this, there were no significant differences in shock success among the three coupling agents. Thus, in this experimental model, over a three-fold energy range, disposable coupling pads were as effective as electrode paste for defibrillation despite the slightly higher impedance of the disposable pads.


Ultrasonic Imaging | 1985

Two-Dimensional Echocardiographic Image Texture Analysis: Reduction of Regional Variability Using Polar Coordinates

Philip E. Aylward; Boyd N. Knosp; David D. McPherson; Doug A. Eltoft; Charles E. Yurkonis; Judith A. Bean; David J. Skorton; Steve M. Collins

Factors inherent to the ultrasound imaging system can influence quantitative ultrasound image texture and may produce changes that mask or mimic those due to alterations in tissue structure. In this study, we assessed the effect of the method of image data acquisition and analysis on the variations in quantitative texture measures that occurred solely due to the position of a region of interest (ROI) within the field of view. When ROIs, which varied in range and azimuth within the image of a tissue equivalent phantom (of uniform composition), were assessed by conventional analysis of scan-converted (rectangular coordinate) data, over 50 percent of all texture measures showed significant differences. Pseudo polar analysis reduced the number of texture measures showing regional variation by 80 percent (p less than 0.01) and true polar coordinate data analysis reduced the number by 74 percent (p less than 0.01). True polar analysis completely abolished differences in texture measures between ROIs separated in azimuth. Acquisition and analysis of tissue texture data using polar coordinates should allow a more definitive identification of abnormal tissue.


Hypertension | 1989

Postexercise hypotension and sympathoinhibition in borderline hypertensive men.

J S Floras; Christine A. Sinkey; Philip E. Aylward; D R Seals; P N Thoren; Allyn L. Mark


Echocardiography-a Journal of Cardiovascular Ultrasound and Allied Techniques | 1986

Ultrasound Tissue Characterization in Ischemic Heart Disease

Philip E. Aylward; David D. McPherson; Richard E. Kerber; David J. Skorton; Steve M. Collins


Canadian Journal of Physiology and Pharmacology | 1987

Modulation of cardiovascular reflexes by arginine vasopressin

John S. Floras; Philip E. Aylward; Badri N. Gupta; Allyn L. Mark; Francois M. Abboud

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John S. Floras

University Health Network

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A. Jamil Tajik

University of Wisconsin-Madison

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