Search PubMed⌕ Search

Biomedical subjects

B F Waller

Publications and source records attributed to B F Waller.

At least 19 recordsLinked to original sources
PubMed1995

Pathology of pulmonic valve stenosis and pure regurgitation.

Little morphologic information is available on operatively excised pulmonic valves. The causes of pulmonic stenosis are limited to a few conditions: (1) rheumatic and (2) nonrheumatic (congenital, carcinoid, infective endocarditis). Congenital causes of pulmonic stenosis constitute well over 95% of these conditions. Congenital types of pulmonic stenosis include acommissural dome-shaped, dysplastic, and bicuspid. Rare acquired causes of pulmonic stenosis include carcinoid, rheumatic, and infective endocarditis. Of the acquired causes of pulmonic stenosis, carcinoid is the most common condition. In contrast, causes of pure pulmonic regurgitation are multiple. Two major categories of pure pulmonic regurgitation include (1) conditions associated with anatomically abnormal valve cusps (congenital, rheumatic, carcinoid, trauma, and infective endocarditis) and (2) conditions associated with anatomically normal cusps (elevated pulmonary artery systolic pressures, idiopathic dilated pulmonary trunk, and Marfan's syndrome).

Humans↗
PubMed1995

Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part I.

This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis are reviewed. In over 90% of stenotic tricuspid valves, the etiology is rheumatic disease. In isolated tricuspid stenosis, the etiology is either carcinoid or congenital. Rare causes of tricuspid stenosis include active infective endocarditis, metabolic or enzymatic abnormalities (Fabry's, Whipple's disease), and giant blood cysts.

Carcinoid Heart Disease↗
PubMed1995

Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part II.

This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis were reviewed. In Part II, conditions producing pure tricuspid regurgitation are discussed. In contrast to the relatively few causes of tricuspid stenosis, the causes of pure (no element of stenosis) tricuspid regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy tricuspid valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and Ebstein's anomaly.

Carcinoid Heart Disease↗
PubMed1995

Right pulmonary artery occlusion secondary to a dissecting aortic aneurysm.

This report describes a case of right pulmonary artery obstruction caused by a dissecting aneurysm of the thoracic aorta. Initial ventilation-perfusion (V/Q) scan revealed no perfusion to the right lung. Lack of right lung perfusion plus other clinical abnormalities led to an initial diagnosis of massive embolism in the right lung. Bilateral pulmonary arteriography of the thoracic and abdominal aorta revealed extrinsic compression of the right pulmonary artery near its origin and the suggestion of an ascending aortic dissection. Subsequent ascending aortography and computed tomography (CT) confirmed a dissection of the ascending aorta. Aortography in the true lumen of the aorta revealed trivial aortic insufficiency. These diagnostic procedures confirmed the presence of an acute dissecting aneurysm of the ascending aorta that caused compression of the right pulmonary artery. The finding of a massive unilateral segmental defect with normal ventilation upon lung scanning does not always ensure a diagnosis of acute pulmonary embolus. Patient presentation with massive unilateral perfusion defect merits further evaluation with pulmonary arteriography.

Aged↗
PubMed1995

Pathology of tricuspid valve stenosis and pure tricuspid regurgitation--Part III.

This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part III, morphometric analysis of tricuspid valve annular circumference, leaflet area, and the product of annular circumference and leaflet area are shown to be useful in establishing etiology for the purely regurgitant tricuspid valves and in assessing the anatomic basis of pure tricuspid regurgitation in the presence of mitral stenosis.

Blood Pressure↗
PubMed1995

Intracardiac thrombi: frequency, location, etiology, and complications: a morphologic review--Part V.

Intracardiac thrombus may develop as a consequence of multiple underlying cardiac disorders. Other systemic disorders may predispose formation of thrombus within the heart, or the heart may be the site of emboli in transit--thrombus originating elsewhere and traveling through the heart to the pulmonary or arterial circulation. Part V of this five-part series on intracardiac thrombus will focus on "migrating thrombi," miscellaneous systemic conditions associated with intracardiac thrombi, and echocardiographic detection of intracardiac thrombus.

Heart Diseases↗
PubMed1995

Incorporation of screening echocardiography in the preparticipation exam.

We sought to evaluate the economic aspects and benefits of adding a limited screening echocardiogram to our annual athletic preparticipation examinations. It was our belief that this screening echocardiogram would add valuable information beyond the history and physical exam alone and could be included in our station-by-station format with little increase in time or cost. Controversy exists concerning the best method of detecting cardiovascular conditions that may predispose the athlete to sudden death. During our 1992 preparticipation examinations, we included a single-view parasternal long- and short-axis two-dimensional screening echocardiogram. This screening can detect four potentially fatal congenital heart defects. We performed a total of 2,997 echocardiograms at an average cost of $7.34 per examination. Overall 64 echocardiographic abnormalities were found. Mitral valve prolapse and bicuspid aortic valve were the two most common abnormalities. The sensitivity of the history and physical examination in detecting cardiovascular abnormalities was extremely low. Incorporating the echocardiogram into our station-to-station format did not add a significant amount of time to the overall process. We conclude that a screening echocardiogram provides important information and can be used efficiently and economically in the athletic preparticipation examination.

Adolescent↗
PubMed1995

The enigma of sudden cardiac death related to dieting.

The use of liquid protein products for treatment of obesity in the United States in the 1960s and '70s was associated with an increased risk of sudden cardiac death. The latter was related to long QT interval occurring in the absence of structural abnormalities of the heart. In an attempt to increase understanding of this phenomenon, the authors examined the possible role of diet-related circumstances. No evidence of increased incidence of sudden cardiac death or significant lengthening of QT interval in obesity, weight loss, starvation and dieting by methods other than liquid protein intake were found. It was concluded that sudden cardiac death during use of liquid protein products remains an enigma, but that other methods of properly medically supervised dieting appear to be safe.

Death, Sudden, Cardiac↗
PubMed1994

Pathology of aortic valve stenosis and pure aortic regurgitation: a clinical morphologic assessment--Part II.

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant aortic valves. Part I discussed stenotic aortic valves and Part II discusses causes of purely regurgitant aortic valves. In over 95% of stenotic aortic valves, the etiology is one of three types: congenital (primarily bicuspid), degenerative, and rheumatic. Other rare causes included active infective endocarditis, homozygous type II hyperlipoproteinemia, and systemic lupus erythematosis. The causes of pure aortic regurgitation are multiple but can be separated into diseases affecting the valve (normal aorta) (infective endocarditis, congenital bicuspid, rheumatic, floppy), diseases affecting the walls of aorta (normal valve) (syphilis, Marfan's dissection), disease affecting both aorta and valve (abnormal aorta, abnormal valve) (ankylosing spondylitis), and disease affecting neither aorta nor valve (normal aorta, normal valve) (ventricular septal defect, systemic hypertension). Diseases affecting the aortic valve alone are the most common subgroup of conditions producing purely regurgitant aortic valves.

Aortic Diseases↗
PubMed1994

Pathology of mitral valve stenosis and pure mitral regurgitation--Part I.

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. In Part I, conditions producing mitral valve stenosis are reviewed. In over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenital malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. In Part II, conditions producing pure mitral regurgitation will be discussed. In contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendinae.

Calcinosis↗
PubMed1994

Pathology of mitral valve stenosis and pure mitral regurgitation--Part II.

This two-part article examines the histologic and morphologic basis for stenotic and purely regurgitant mitral valves. In Part I, conditions producing mitral valve stenosis were reviewed. In over 99% of stenotic mitral valves, the etiology is rheumatic disease. Other rare causes of mitral stenosis include congenitally malformed valves, active infective endocarditis, massive annular calcium, and metabolic or enzymatic abnormalities. In Part II, conditions producing pure mitral regurgitation are discussed. In contrast to the few causes of mitral stenosis, the causes of pure (no element of stenosis) mitral regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy mitral valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and ruptured chordae tendineae.

Cardiomyopathies↗
PubMed1994

Indications for and applications of the Gianturco-Roubin coronary stent.

The Gianturco-Roubin coronary stent is approved for and effective in the management of acute or threatened closure after unsuccessful coronary intervention. Factors critical to successful stenting include patient and lesion selection, preprocedure identification of patients in potential need of stenting, selection of stent-compatible ancillary equipment, appropriate antiplatelet and anticoagulant therapy, postdeployment stent dilatation, and careful sizing of stents. Further refinements of technique and adjunctive drug therapy should continue to improve results and avoid acute complications. Published clinical experience and potential future applications are discussed.

Angioplasty, Balloon, Coronary↗
PubMed1993

Histologic analysis of directional coronary atherectomy samples. A review of findings and their clinical relevance.

Histologic analysis of atherectomy samples from > 400 patients who received directional coronary atherectomy at 3 separate institutions disclosed 2 major categories of tissue: atherosclerotic plaque (with or without thrombus) and intimal proliferation (hyperplasia, with or without thrombus). The predominant tissue type in atherectomy samples from native, primary, or de novo coronary artery stenoses was atherosclerotic plaque. The predominant tissue type in atherectomy samples from restenosis lesions (prior balloon angioplasty, atherectomy, or both) was intimal proliferation with variable amounts of atherosclerotic plaques (with or without thrombus). Deep vessel wall components (media, adventitia) were identified at varying frequencies. The clinical relevance of atherectomy tissue is reviewed.

Atherectomy, Coronary↗
PubMed1993

Anatomy, histology, and pathology of the cardiac conduction system: Part I.

Normal anatomic and histologic features of the sinus node, atrial myocardium, and interatrial conduction of the cardiac impulse are reviewed. The controversy surrounding atrial conduction via specialized atrial cells versus specific internodal tracts (between sinus and atrioventricular nodes) is discussed.

Age Factors↗
PubMed1993

Anatomy, histology, and pathology of the cardiac conduction system: Part II.

Normal anatomic and histologic features of the atrioventricular junction (transitional cell zone, atrioventricular node, penetrating portion of bundle) and the bifurcation of the penetrating portion into bundle branches are reviewed. Terminal ventricular Purkinje fibers are also discussed.

Atrioventricular Node↗