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Dive into the research topics where William A. Baxley is active.

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Featured researches published by William A. Baxley.


American Journal of Cardiology | 1966

Usefulness and limitations of radiographic methods for determining left ventricular volume

Harold T. Dodge; Harold Sandler; William A. Baxley; Richard R. Hawley

Abstract The various methods currently being used to determine left ventricular chamber volumes from biplane angiocardiograms are described and discussed. The spatial direction and change of direction and length of the long axis of the left ventricle over the heart cycle is described. The long axis of the left ventricle is in most subjects directed approximately 20 degrees from being parallel with the frontal plane of the body and results in only slight foreshortening of the long axis of the left ventricle on films taken in the anteroposterior projection. A method is described and evaluated for determining left ventricular chamber volume from angiocardiograms taken in a single anteroposterior projection. Values for normal end-diastolic volume and systolic ejection fraction obtained by various investigators using the radiographic methods are given. The application of these radiographic methods to estimate aortic and mitral valve regurgitant flow is reviewed. Pressure-volu ne relations of the diastolic left ventricle have been determined in 176 patients and demonstrate large patient-to-patient differences of ventricular distensibility in patients with different types and durations of heart disease. Measurement of compliance of the diastolic left ventricle from the pressure-volume curves is discussed. By relating pressure and volume curves over the entire heart cycle, left ventricular pressure-volume curves can be constructed and from these the various components of pressure-volume work determined: systolic work, work done in distending the ventricle during diastole, and net work. Values obtained for these various components of ventricular work in patients with heart and valvular disease are discussed. A method for calculating wall tension and stress from measurement of chamber pressure and chamber dimensions is reviewed. Left ventricular mass can be calculated from chamber dimensions and wall thickness determined from angiocardiograms. A value of 92 ± 16 gm. has been obtained by this method in patients without left ventricular disease, and this is similar to values obtained in earlier postmortem studies. Measurement of left ventricular oxygen consumption and mechanical efficiency in patients with heart disease is discussed.


Circulation | 1966

Quantitative Angiocardiography I. The Normal Left Ventricle in Man

J. Ward Kennedy; William A. Baxley; Melvin M. Figley; Harold T. Dodge; John R. Blackmon

Quantitative angiocardiography has been utilized to study the left ventricle of seven women and 15 men who had no evidence of heart disease. The left ventricular enddiastolic volume, end-systolic volume, and stroke volume were calculated in 15 individuals and left ventricular mass was determined in all 22 subjects. The mean end-diastolic volume was 70 cc/m.2 The left ventricular wall thickness during diastole averaged 8.9 mm for women and 11.9 mm for men and the mean left ventricular mass was 76 g/m2 for women and 99 g/m2 for men. The ventricular volumes did not correlate well with age, sex, body surface area, or weight, but correlated in a negative manner with heart rate. There was a significant difference between left ventricular wall thickness and mass in normal men and women. Values for normal left ventricular volumes obtained by other investigators using angiocardiographic and indicator-dilution methods are compared with the results of this study. The values obtained for left ventricular mass by the angiocardiographic method used in this study are similar to those obtained by other investigators in postmortem hearts.


American Journal of Cardiology | 1973

Quantitative evaluation of cineaortography in the assessment of aortic regurgitation

David G. Hunt; William A. Baxley; J. Ward Kennedy; Terrance P. Judge; J.Edmund Williams; Harold T. Dodge

Cineaortography, quantitative biplane left ventricular angiocardiography and Fick cardiac output studies were performed in 69 patients with aortic regurgitation to evaluate the usefulness of the aortogram in quantitating regurgitation. Thirteen patients had coexistent aortic stenosis and 12 had coexistent mitral stenosis. Patients with concomitant mitral regurgitation were excluded because their aortic regurgitant flow cannot be separately quantified with biplane ventriculography. Twenty-eight other patients without valvular regurgitation were also studied to assess further the accuracy of the quantitative ventriculography, and the stroke volumes derived from Fick and angiographic methods were found to correlate well (r = 0.97). Aortic regurgitation in the 69 patients, graded on a 1 to 5 scale from the aortogram, correlated significantly with the percent and volume of regurgitation (r = 0.56 and 0.65, P < 0.01), respectively). However, there was a wide range in amount of regurgitant flow within the aortographic grades, especially in grades 4 and 5, and there was considerable overlap between the grades. The degree of aortic regurgitation was more commonly overestimated than underestimated from the aortogram, but the correlation tended to be better in the patients with a large end-diastolic volume and normal ejection fraction and without aortic or mitral stenosis.


American Journal of Cardiology | 1968

Hemodynamic aspects of heart failure

Harold T. Dodge; William A. Baxley

Abstract Heart failure may occur as a result of failure of the contractile mechanisms of the myocardium, a large pressure-volume load imposed on the heart, or a combination of an increased load and diminished contractility. In patients with chronic heart disease, the consequences of an increased volume load are cardiac dilatation and hypertrophy appropriate for the volume load. Chronic pressure loads are associated with ventricular hypertrophy but essentially normal left ventricular end-diastolic volume and systolic ejection fraction. Myocardial disease in itself, or in association with conditions that place an added mechanical burden on the left ventricle, is characterized by inappropriate dilatation and hypertrophy of the left ventricle. Failure of these mechanisms of dilatation and hypertrophy to compensate for myocardial disease or work load results in the hemodynamic alterations associated with heart failure.


American Journal of Cardiology | 1967

Left ventricular mass: A comparison of angiocardiographic measurements with autopsy weight☆

J. Ward Kennedy; Dennis D. Reichenbach; William A. Baxley; Harold T. Dodge

Abstract A previously described angiocardiographic method has been used to determine left ventricular mass in 28 patients. Weight of the left ventricle at autopsy has been compared with calculated mass. The method has been shown to be reliable in the absence of marked right ventricular hypertrophy, pericardial effusion, or adhesive pericarditis.


Circulation | 1968

A Quantitative Angiocardiographic Study of Left Ventricular Hypertrophy and the Electrocardiogram

William A. Baxley; Harold T. Dodge; Harold Sandler

The QRS amplitude, duration, and mean axis direction of the standard 12-lead electrocardiogram were compared with left ventricular mass, volume, wall thickness, and stroke work in 112 adult patients. These patients had normal left ventricles or various degrees of left ventricular dilatation or hypertrophy. Left ventricular volumes and mass were determined by a quantitative angiocardiographic method. A significant but not a close correlation between left ventricular mass and ECG voltage was found. Enddiastolic volume, stroke volume, stroke work, wall thickness, and “total left ventricular volume” (volume of left ventricular muscle and cavity at end-diastole) had generally lesser degrees of correlation with the QRS amplitude than did the mass alone. Subgrouping of patients into those with pressure overload on the left ventricle, volume overload, aortic valve disease, or anatomic left ventricular hypertrophy did not improve correlations. The left ventricular hypertrophy voltage criteria of Sokolow and of Grant were assessed; respectively, 68% and 67% of 75 patients with anatomic hypertrophy had hypervoltage. The direction of the anatomic long axis of the left ventricle was not significantly related to the mean QRS-vector direction.


Annals of Internal Medicine | 1971

Left Ventricular Anatomical and Functional Abnormalities in Chronic Postinfarction Heart Failure

William A. Baxley; William B. Jones; Harold T. Dodge

Abstract Fifty patients with chronic postmyocardial infarction heart failure had quantitative biplane angiocardiography; 42 also had coronary angiography. Mitral regurgitation, localized ventricula...


Circulation | 1973

Hemodynamics in Ruptured Chordae Tendineae and Chronic Rheumatic Mitral Regurgitation

William A. Baxley; J. Ward Kennedy; Bolling Feild; Harold T. Dodge

Twenty-five patients with proven ruptured mitral chordae tendineae and 25 patients with chronic rheumatic mitral regurgitation were studied with quantitative biplane left-heart angiocardiography. Compared to the rheumatic patients, the ruptured chordae group had strikingly smaller left atrial maximum volume (mean: 119 ± 47 vs 267 ± 131 ml/m2 mean) and less compliant left atrium (mean: 1.61 ± 1.52 vs 5.14 ± 4.31 ml/mm Hg-m2); less impressively but significantly smaller left ventricular end-diastolic volume (mean: 142 ± 43 vs 188 ± 75 ml/m2) and mass (mean: 133 ± 27 vs 166 ± 50 mm/m2), and relatively insignificant tendency toward smaller left ventricular stroke volume and regurgitant flow per stroke. Ejection fractions, ventricular pressures, and forward flow per stroke were not significantly different. Within the ruptured chordae group, the duration of heart failure was not significantly correlated with any hemodynamic variable. These results indicate quantitatively the spectrum of abnormal hemodynamics in these two different etiologic forms of mitral insufficiency. The most striking differences between the two groups are in atrial dynamics. In spite of the usually more acute nature of ruptured chordae, significant compensatory dilatation and hypertrophy of the left ventricle is common in those patients. In both groups, large regurgitant flows with relatively normal ventricular function as expressed by ejection fraction is the usual finding.


Circulation | 1977

Left ventricular mechanical efficiency in man with heart disease.

William A. Baxley; Harold T. Dodge; Charles E. Rackley; Harold Sandler; David G. Pugh

Thirty-eight adults with valvular and/or myocardial disease had heart catheterization with coronary blood flow and myocardial 02 consumption (MVO2) per 100 g measured by the nitrous oxide washout technique. Quantitative biplane angiocardiography was performed to assess left ventricular volume, mass, ejection fraction and work. Left ventricular efficiency was calculated from work, MVO2/100 g and mass. Efficiency ranged from 4 to 40% and was normal in some patients with severe ventricular pressure-volume work overloads. Total left ventricular MVO2 ranged up to 461 ml/min. Neither total MVO2 nor MVO2/100 g was significantly related to ventricular work, ejection fraction, or tension-time index. These data suggest 1) a relationship between left ventricular efficiency and myocardial function in chronic valvular or myocardial disease, 2) that efficiency may be normal in hypertrophied ventricles, and 3) that chronic increases in resting ventricular metabolic requirements are met by hypertrophy rather than by increased MVO2/100 g.


Annals of Internal Medicine | 1968

Hemodynamic Abnormalities of the Postinfarction Left Ventricle.

William A. Baxley; Harold T. Dodge

Excerpt Twenty patients with chronic postinfarction angina or left ventricular failure were studied with cardiac catheterization and either quantitative biplane or cineangiocardiography or both. Te...

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Harold T. Dodge

United States Public Health Service

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Harold Sandler

University of Washington

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Alberto Barcia

University of Alabama at Birmingham

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Augusto D. Pichard

MedStar Washington Hospital Center

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Bolling Feild

University of Washington

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