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Dive into the research topics where Andrew J. Buda is active.

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Featured researches published by Andrew J. Buda.


The New England Journal of Medicine | 1979

Effect of Intrathoracic Pressure on Left Ventricular Performance

Andrew J. Buda; Michael R. Pinsky; Neil B. Ingels; George T. Daughters; Edward B. Stinson; Edwin L. Alderman

Left ventricular dysfunction is common in respiratory-distress syndrome, asthma and obstructive lung disease. To understand the contribution of intrathoracic pressure to this problem, we studied the effects of Valsalva and Müller maneuvers on left ventricular function in eight patients. Implantation of intramyocardial markers permitted beat-by-beat measurement of the velocity of fiber shortening (VCF) and left ventricular volume. During the Müller maneuver, VCF and ejection fraction decreased despite an increase in left ventricular volume and a decline in arterial pressure. In addition, when arterial pressure was corrected for changes in intrapleural pressure during either maneuver it correlated better with left ventricular end-systolic volumes than did uncorrected arterial pressures. These findings suggest that negative intrathoracic pressure affects left ventricular function by increasing left ventricular transmural pressures and thus afterload. We conclude that large intrathoracic-pressure changes, such as those that occur in acute pulmonary disease, can influence cardiac performance.


Circulation | 1987

The physiologic basis of dobutamine as compared with dipyridamole stress interventions in the assessment of critical coronary stenosis

Anthony Fung; Kim P. Gallagher; Andrew J. Buda

Noninvasive cardiac imaging with echocardiography or thallium-201 scintigraphy utilizing pharmacologic agents as alternatives to exercise is gaining popularity. We investigated the physiologic rationale underlying the optimal choice of pharmacologic stress for functional versus perfusion imaging. With the use of an open-chest dog model, a critical stenosis of the left circumflex coronary artery was produced with total ablation of hyperemic response to a 15 sec period of complete occlusion. Regional left ventricular wall thickening was assessed by quantitative two-dimensional echocardiography. Regional myocardial blood flow was determined by microspheres in both the flow-restricted left circumflex area and the control area supplied by the left anterior descending artery. Eight dogs received 15 micrograms/kg/min dobutamine intravenously for 10 min, and nine dogs received 0.14 mg/kg/min dipyridamole intravenously for 4 min. Dobutamine induced wall thickening abnormalities in all dogs while dipyridamole induced dysfunction in only 55% of the animals studied (p less than .01). Subendocardial blood flow to the left circumflex area was unchanged after both dobutamine and dipyridamole when compared with baseline blood flow. However, subendocardial blood flow increased markedly after dipyridamole in the control area. Regional subendocardial blood flow ratio (left anterior descending/left circumflex) was 3.74 +/- 0.09 (mean +/- SEM) after dipyridamole versus 1.27 +/- 0.09 after dobutamine (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)


Circulation | 1986

Direct measurement of inner and outer wall thickening dynamics with epicardial echocardiography.

J. H. Myers; Mack C. Stirling; M. Choy; Andrew J. Buda; Kim P. Gallagher

Simple geometric models of the left ventricle and indirect experimental measurements suggest that the inner myocardial wall contributes the largest fraction to total wall thickening. We measured transmural differences in regional wall thickening directly, using an epicardial M mode echocardiographic transducer (6 mm diameter, 5 MHz) placed on the anterior free wall of the left ventricle. Wall thickness was partitioned into inner and outer regions by inserting a waxed, 3-0 suture at different depths within the wall. The suture was used as an intramural echo target that was imaged simultaneously with the endocardium to determine inner and outer fractional contribution to total wall thickness. Data were collected in open-chest dogs at rest, during inotropic stimulation with isoproterenol, and during right heart bypass, which was used to vary cardiac output and preload. Results obtained with this method demonstrated that systolic wall thickness was nonuniform at rest and during each intervention. The fractional contributions to total wall thickening of the inner, middle, and outer thirds of the myocardial wall were estimated from the data to be 58%, 25%, and 17%, respectively. The experimental findings corresponded closely to theoretical predictions, supporting the conclusion that a gradient of thickening exists across the myocardial wall, with the inner portion of the wall contributing the largest fraction to total systolic thickening.


Circulation | 1986

Failure of superoxide dismutase and catalase to alter size of infarction in conscious dogs after 3 hours of occlusion followed by reperfusion

Kim P. Gallagher; Andrew J. Buda; D Pace; R. A. Gerren; M. Shlafer

Superoxide dismutase (SOD) and catalase (CAT), enzymes that degrade superoxide anion and hydrogen peroxide, respectively, reduce size of infarction in anesthetized, open-chest dogs subjected to coronary occlusion followed by reperfusion. To evaluate potential protective effects of these enzymes in conscious animals, three groups of dogs were instrumented at sterile surgery with a hydraulic occluder on the left circumflex (LCX) coronary artery, sonomicrometers to measure regional wall thickness, and catheters to monitor arterial and left ventricular pressures. Ten to 14 days after surgery, the animals were sedated with morphine sulfate (0.5 mg/kg). The LCX artery was occluded for 3 hr by inflation of the hydraulic cuff. Infusions of SOD (n = 7), CAT (n = 6), or saline (control group, n = 7) were begun 15 min before reperfusion and lasted for 45 min of reperfusion. The doses of SOD and CAT were 5 mg/kg, dissolved in 60 ml of saline, and infused at a rate of 1 ml/min. Myocardial blood flow was measured with tracer-labeled microspheres (15 micron diameter) before occlusion, after 5 to 10 min of occlusion, after 150 min of occlusion, and 5 to 10 min after reperfusion. Size of infarction was measured 24 hr later by dual-perfusion staining with Evans blue and triphenyl tetrazolium. Size of infarction (expressed as a percentage of area at risk) did not differ significantly among the three groups: control, 32 +/- 17% (mean +/- SD); SOD, 38 +/- 17%; CAT, 27 +/- 17%. Hemodynamic parameters and myocardial blood flows (measured before infusion of any agents) were not significantly different among the three groups. Serum SOD levels in SOD-treated dogs were 19 +/- 2 micrograms/ml at the onset of reperfusion and 29 +/- 3 micrograms/ml at the end of the infusion. Blood assays collected after infusion showed a monoexponential decay of SOD levels with a half-life of 22 +/- 6 min. We conclude that myocardial protection by SOD or CAT is model dependent. In conscious dogs subjected to 3 hr of coronary occlusion followed by reperfusion, SOD and CAT failed to alter size of infarction.


IEEE Transactions on Medical Imaging | 1988

Detecting left ventricular endocardial and epicardial boundaries by digital two-dimensional echocardiography

C.H. Chu; Edward J. Delp; Andrew J. Buda

Cardiac function is evaluated using echocardiographic analysis of shape attributes, such as the heart wall thickness or the shape change of the heart wall boundaries. This requires that the complete boundaries of the heart wall be detected from a sequence of two-dimensional ultrasonic images of the heart. The image segmentation process is made difficult since these images are plagued by poor intensity contrast and dropouts caused by the intrinsic limitations of the image formation process. Current studies often require having trained operators manually trace the heart walls. A review of previous work is presented, along with how this problem can be viewed in the context of the computer vision area. A novel algorithm is presented for detecting the boundaries. This algorithm first detects spatially significant features based on the measurement of image intensity variations. Since the detection step suffers from false alarms and missing boundary points, further processing uses high-level knowledge about the heart wall to label the detected features for noise rejection and to fill in the missing points by interpolation.


American Journal of Cardiology | 1987

Pulsed Doppler assessment of left ventricular diastolic filling in coronary artery disease before and immediately after coronary angioplasty

Barry E. Wind; A. Rebecca Snider; Andrew J. Buda; William W. O'Neill; Eric J. Topol; Lee R. Dilworth

To determine if left ventricular (LV) diastolic filling abnormalities are detectable by Doppler echocardiography in patients with coronary artery disease (CAD), 34 patients with CAD and 24 normal, age-matched control subjects underwent mitral valve pulsed Doppler examination. At catheterization, all CAD patients had typical angina, at least 70% diameter narrowing of 1 major coronary artery, ejection fraction of 50% or more and no valvular heart disease. Seventeen CAD patients underwent coronary angioplasty and had a Doppler examination 1 day before and 1 day after the procedure. Doppler diastolic time intervals, peak velocities at rapid filling (E velocity), atrial contraction (A velocity) and the ratio peak E/peak A velocities were measured. The following areas under the Doppler velocity envelope and their percentage of the total area were calculated: first third of diastole (0.33 area), triangular area under the peak E velocity (E area), and triangular area under the peak A velocity (A area). Patients with CAD and normal subjects were significantly different (p less than 0.01) in peak E velocity (CAD 0.60 +/- 0.12 m/s, normal 0.68 +/- 0.12 m/s), peak A velocity (CAD 0.59 +/- 0.12 m/s, normal 0.48 +/- 0.11 m/s), ratio peak E/peak A velocities (CAD 1.0 +/- 0.27, normal 1.5 +/- 0.32), A area (CAD 0.052 +/- 0.015 m, normal 0.036 +/- 0.010 m), ratio E area/A area (CAD 1.7 +/- 0.53, normal 2.5 +/- 0.69), and all area fractions. In the CAD patients who had undergone coronary angioplasty, no differences were found in any Doppler index before and immediately after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)


American Heart Journal | 1986

Prognostic significance of vegetations detected by two-dimensional echocardiography in infective endocarditis.

Andrew J. Buda; Rainer J. Zotz; Mary Sue Lemire; David S. Bach

Although 2DE is considered the most sensitive method for detecting vegetations in infective endocarditis, the independent clinical significance of these vegetations continues to be debated. To further examine this, we identified 74 patients who were diagnosed as having infective endocarditis over a 54-month period. The 50 patients who underwent 2DE examination form the basis of this report. Definite vegetations were present in 21 (42%) patients and measured 1.2 +/- 0.2 cm2. The vegetation was localized to the aortic valve in 10 patients, the mitral valve in eight, and the tricuspid valve in three. A major complication, defined as death, new-onset congestive heart failure, major arterial embolus, or valve surgery occurred in 86% of the vegetative endocarditis patients compared to 62% of those without vegetations. Among those patients with vegetations, death occurred in 24%, heart failure in 38%, arterial embolus in 48%, and surgery in 43%. This compared to 7%, 21%, 21%, and 24%, respectively, in those patients without vegetations. These data support the concept that 2DE detection of a vegetation defines a high-risk subgroup of patients with infective endocarditis in whom careful monitoring and aggressive management are warranted.


IEEE Transactions on Medical Imaging | 1988

A method for a fully automatic definition of coronary arterial edges from cineangiograms

Paul H. Eichel; Edward J. Delp; Kenneth F. Koral; Andrew J. Buda

The authors describe a novel algorithm, known as sequential edge linking (SEL), for the automatic definition of coronary arterial edges in cineangiograms. This algorithm is based on sequential tree searching of possible coronary artery boundary locations. Using a coronary artery phantom, the authors compared the results obtained using SEL with hand-traced boundaries. Using a magnification of 2x, the results are generally good, with the average error being 1.7% of the diameter. Actual coronary artery images were also processed and a similar comparison indicated that total areas were comparable but the hand-drawn stenoses were, on average, 7% greater than the unobstructed diameter. Based on these data it is concluded that the SEL algorithm is an accurate method for fully automatic definition of coronary artery dimensions.


IEEE Transactions on Biomedical Engineering | 1992

Time-frequency transforms: a new approach to first heart sound frequency dynamics

John C. Wood; Andrew J. Buda; Daniel T. Barry

The binomial joint time-frequency transform is used to test the hypothesis that first heart sound frequency rises during the isovolumic contraction period. Cardiac vibrations were recorded from eight open-chest dogs using an ultralight accelerometer cemented directly to the epicardium of the anterior left ventricle. Three characteristic time-frequency spectral patterns were evident in the animals investigated: (1) a frequency component that rose from approximately 40-140 Hz in a 30-50-ms interval immediately following the ECG R-wave, (2) a slowly varying or static frequency of 60-100 Hz beginning midway through the isovolumic contraction period, and (3) broadband peaks occurring at the time of the Ia and Ib high frequency components. The binomial transform provided much better resolution than the spectrograph or spectrogram. By revealing the onset and dynamics of first heart sound frequencies, time-frequency transforms may allow mechanical assessment of individual cardiac structures.<<ETX>>


International Journal of Cardiology | 1981

Abnormalities of pulmonary artery wedge pressures in sleep-induced apnea

Andrew J. Buda; John S. Schroeder; Christian Guilleminault

Six patients with sleep apnea syndrome were studied with continuous hemodynamic monitoring during sleep. Sleep apnea had been previously documented with an average number of apneas per hour of sleep ranging from 23 to 93 ((mean 63). There was significant decrease in heart rate during sleep (82 +/- 5 to 69 +/- 6, P less than 0.01). There was a significant rise in systemic blood pressure (103 +/- 2 mn Hg to 116 +/- 6 mm Hg, P less than 0.05) and pulmonary artery pressure (20 +/- 1 mm Hg to 32 +/- 5 mm Hg) during sleep. In addition, pulmonary artery wedge pressure increased (12 +/- 2 mm Hg to 20 +/- 3 mm Hg, P less than 0.05) during sleep and 5 of the 6 patients developed an abnormal pulmonary wedge pressure. There was a significant decrease in PO2 during sleep (71 +/- 3 mm Hg to 49 +/- 2 mm Hg, P less than 0.005). These findings suggest that increases in pulmonary wedge pressures may be contributing to increase in pulmonary artery pressures in these patients during sleep.

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Bertram Pitt

Johns Hopkins University

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