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C F Wooley

Publications and source records attributed to C F Wooley.

At least 19 recordsLinked to original sources
PubMed1997

The morphologic characteristics of flail mitral leaflets by transesophageal echocardiography.

BACKGROUND AND AIMS OF THE STUDY: Mitral valve prolapse due to floppy mitral valve (MVP/FMV) is a common valvular abnormality with a variable clinical course. Flail mitral valve leaflet resulting in severe mitral regurgitation is a complication of MVP/FMV. METHODS: In order to understand the structural correlates of flail mitral valve leaflet in MVP, we reviewed the morphologic characteristics of the mitral valve by transesophageal echocardiography (TEE) in 72 patients (24 normal; 26 mitral valve prolapse; 22 flail mitral valve leaflet). RESULTS: Compared with the normal group, the mitral valve prolapse group had greater anterior and posterior mitral valve leaflet thickness and anterior mitral valve leaflet length. Patients with flail mitral valve leaflets as a complication of FMV had greater anterior and posterior mitral valve leaflet length and posterior mitral valve leaflet thickness compared with MVP patients without flail mitral valve leaflets. Posterior mitral valve leaflet length was the only echocardiographic independent predictor of flail mitral valve leaflet. Older FMV patients with increased mitral valve leaflet length and thickness are predisposed to flail mitral valve leaflets and severe mitral regurgitation. CONCLUSIONS: TEE may identify patients with MVP/FMV with the greatest structural abnormalities who are at risk for complications such as flail mitral valve leaflet(s).

Adolescent↗
PubMed1996

Spectrum of structural abnormalities in floppy mitral valve echocardiographic evaluation.

Posterior displacement of the mitral valve with billowing into the left atrium has been the major echocardiographic criterion used for the diagnosis of mitral valve prolapse (MVP). However, the current criteria are limited by the influence of hemodynamic factors on the degree of prolapse, whereas complications such as mitral regurgitation, endocarditis, and need for surgery have been associated with redundancy or thickening of the leaflets. Sixty-eight normal subjects (mean age, 40 years; range, 18 to 76 years) were compared with 58 patients with MVP (mean age, 37 years, range, 18 to 83 years). Leaflet displacement across the annular plane in the parasternal long-axis view was mandatory for the diagnosis of MVP. Transthoracic echocardiographic measurements of anterior and posterior leaflet thickness, leaflet length, and chordal length were made from the parasternal long-axis view and the mitral annular diameter, from the apical four-chamber and two-chamber views. The MVP group had greater anterior thickness (4.1 +/- 0.4 mm vs 5.3 +/- 0.7 mm; p = 0.0001), posterior thickness (3.2 +/- 0.4 mm vs 4.7 +/- 0.9 mm; p = 0.0001), anterior length (22.8 +/- 2.0 mm vs 25.7 +/- 1.7 mm; p = 0.0001), posterior length (12.8 +/- 1.0 mm vs 15.7 +/- 2.5 mm; p = 0.0001), chordal length (25.6 +/- 2.7 mm vs 28.0 +/- 2.5 mm; p = 0.0001), and annular diameter (29.1 +/- 1.5 mm vs 31.3 +/- 2.6 mm; p = 0.0001). Of the MVP group, >80% had at least one abnormality identified and >50% had at least two abnormalities. In addition, patients with MVP with significant regurgitation had greater anterior thickness (5.2 +/- 0.7 mm vs 5.8 +/- 0.8 mm; p = 0.015), posterior thickness (4.5 +/- 0.9 mm vs 5.3 +/- 0.7 mm; p = 0.024), posterior length (15.1 +/- 1.6 mm vs 17.9 +/- 4.2 mm; p = 0.004), and annular diameter (36.0 +/- 2.0 mm vs 33.3 +/- 2.1 mm; p = 0.0001). The majority of patients with floppy mitral valves resulting in MVP have structural abnormalities that may be defined by echocardiography. A spectrum of floppy valve structure is demonstrated by echocardiography, with mitral regurgitation occurring more frequently in patients with multiple and more severe anatomic abnormalities. In addition to the presence of prolapse and regurgitation, the assessment of leaflet thickness, leaflet length, annular diameter, and chordal length is fundamental to the definition and stratification of patients with MVP associated with the floppy mitral valve.

Adolescent↗
PubMed1996

Aortic function.

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Aorta, Thoracic↗
PubMed1995

Left atrial volumes and function in orthotopic cardiac transplantation.

Early ventricular filling and therefore passive left atrial emptying may be impaired in patients with cardiac transplantation. As a result, left atrial function may be an important factor in maintaining stroke volume in recipients of orthotopic cardiac transplants. Left atrial volumes maximal (mitral valve opening), minimal (mitral valve closure), and onset of atrial systole (P wave on electrocardiogram) were determined by echocardiography using the biplane area-length method in 12 patients after cardiac transplantation and 12 control subjects. Maximal and minimal left atrial volumes and left atrial volumes at onset of atrial systole were larger in patients who had cardiac transplantation than in control subjects (89.8 vs 41.8 cm3, 48 vs 15.2 cm3, and 70.4 vs 27.0 cm3, respectively; p < 0.01). In patients undergoing cardiac transplantation, good correlations were found between left atrial maximal volume and left ventricular mass (r = 0.56) and between left atrial maximal volume and mean pulmonary capillary wedge pressure (r = 0.81). Left atrial passive emptying volume (maximal minus volume at P wave), was not statistically different between the two groups (19.3 in patients receiving transplants vs 14.7 cm3 in control subjects), but left atrial stroke volume (beginning atrial systole to minimal) was larger in patients receiving transplants than in control subjects (22.4 vs 11.8 cm3, respectively; p < 0.001). Thus left atrial contraction contributed 42% to the left ventricular stroke volume in patients who had cardiac transplantation but only 17% in control subjects (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Function, Left↗
PubMed1995

Left atrial performance indices in chronic mitral valve disease.

Multidimensional left atrial (LA) performance indices have not been extensively studied in chronic mitral valve disease. LA maximal volume, stroke volume (LA volume at atrial systole minus LA minimal volume), LA ejection fraction (stroke volume/volume at atrial systole) and A-wave velocity, were measured in 14 patients with mitral stenosis (mean mitral valve area 1.5 cm2); 14 patients with chronic mitral regurgitation all in sinus rhythm; and were compared to 20 age and sex matched normal control subjects using biplane transthoracic echo and pulsed Doppler. Although LA volumes--maximal and at onset of atrial systole--were greater in mitral regurgitation and mitral stenosis (p < 0.01) compared to normal subjects, LA ejection fraction was not statistically different among the three groups. LA stroke volume was greater in mitral regurgitation and mitral stenosis compared to normal subjects, p < 0.01. LA kinetic energy (LAKE) = 1/2 mv2 (m = LA stroke volume x 1.06, blood's specific gravity, v = A wave velocity) was increased in mitral stenosis and mitral regurgitation compared to normal subjects (p < 0.001). An inverse correlation (r = 0.66, p < 0.01) was present between LAKE and mitral valve area in mitral stenosis. It is concluded that LA function, a complex interplay of multiple factors, requires multidimensional methods of analysis beyond standard measurements of size and volume, which provide additional insight into normal LA function, and better definition of LA function changes involved in the natural history of chronic mitral valve disease.

Adult↗
PubMed1994

Anti-beta-receptor antibodies in familial cardiomyopathy: correlation with HLA-DR and HLA-DQ gene polymorphisms.

The presence of beta-receptor autoantibodies and their relationship to restriction fragment length polymorphisms of the human leukocyte antigen (HLA) class II genes were studied in 42 affected and unaffected members of a family with a heritable disorder of the conduction system and cardiac muscle. Antibodies were detected in 34% of all members (59% of affected and 22% of unaffected; p < 0.01). Significant differences between affected and unaffected individuals and between anti-beta-receptor antibody positive and negative individuals were noted in the prevalence of polymorphisms obtained with Taq I for the HLA-DR beta and HLA-DQ alpha genes. In affected individuals, there was a strong positive correlation between these polymorphisms and the presence of anti-beta-receptor antibodies. These results suggest that autoimmune mechanisms under the control of the class II genes play an important role in the pathogenesis of familial cardiomyopathy.

Arrhythmias, Cardiac↗
PubMed1994

Valvular heart disease: the influence of changing etiology on nosology.

The many changes in classification of cardiovascular disease during the twentieth century reflect changing etiology of diseases, clinical comprehension and technological advances. In particular, the etiology of valvular heart disease has changed dramatically in the last five decades. The significant reduction of acute rheumatic fever and its sequelae, and the recognition of non-rheumatic causes of valvular disease are responsible for the metamorphosis in the etiology of valvular disorders. Valvular heart disease can be classified as follows: 1) Heritable-congenital causes of valvular heart disease e.g., floppy mitral valve with mitral valve prolapse, bicuspid aortic valve, and the Marfan syndrome; 2) Inflammatory-immunologic causes such as rheumatic fever, acquired immune deficiency syndrome, endocardial proliferative disorders, and antiphospolipid syndrome; 3) Myocardial dysfunction-ischemic cardiomyopathy, dilated or hypertrophic cardiomyopathy-resulting in valvular heart disease; 4) Diseases and disorders of other organs as causes of valvular heart disease, e.g., chronic renal failure and carcinoid heart disease; 5) Valvular heart disease related to aging: calcific aortic stenosis and mitral annular calcification; 6) Valvular disease following interventions such as valvuloplasty, valve reconstructive surgery and valve replacement; and 7) Valvular disease related to drugs and physical agents, such as chronic ergotamine use, radiation therapy and trauma. In clinical practice the most common causes of mitral regurgitation are floppy mitral valve with mitral valve prolapse, ischemic heart disease, dilated cardiomyopathy and mitral annular calcification, while the most common cause of mitral stenosis is rheumatic fever. The most common causes of isolated aortic regurgitation are bicuspid aortic valve and floppy aortic valve, while the most common causes of isolated aortic stenosis are related to the bicuspid aortic valve and the development of calcific senile aortic stenosis. The most common causes of tricuspid regurgitation are dilated cardiomyopathy, ischemic cardiomyopathy, floppy tricuspid valve with tricuspid valve prolapse and infectious endocarditis. Combined mitral and tricuspid regurgitation occur with heritable connective tissue disorders, dilated or ischemic cardiomyopathy, while the most common cause of mitral stenosis plus aortic regurgitation is rheumatic fever. Statistics obtained from cardiac surgery and necropsy may underestimate the true incidence of certain valvular diseases by selection bias. This is particularly so with valvular disease associated with significant ventricular dysfunction, or in the elderly who may not be surgical candidates, or in cases where the valvular disease is not severe enough to require surgical intervention. Recent advances in hemodynamic and imaging technology allow clinicians to define valvular structure and function and to accurately classify valvular heart disease in clinical practice.

Heart Valve Diseases↗
PubMed1993

Mitral valve prolapse: left ventricular hemodynamics in patients with chest pain, dyspnea or both.

Patients with mitral valve prolapse may present with chest pain and dyspnea. Left ventricular hemodynamics as a cause for these symptoms have not been completely evaluated in these patients. The present study was undertaken to investigate left ventricular hemodynamics in symptomatic patients with mitral valve prolapse. One hundred and three patients with mitral valve prolapse (female 72, male 31, age 56 +/- 11 years) had diagnostic cardiac catheterization for evaluation of chest pain (n = 44), dyspnea (n = 10) and for chest pain plus dyspnea (n = 49). All patients had diagnostic auscultatory findings and angiographic documentation of mitral valve prolapse. Patients with coronary artery disease and mitral regurgitation greater than mild were excluded from the study. Left ventricular end diastolic pressures before (chest pain 9.3 +/- 3.7 mmHg; dyspnea 8.2 +/- 4.2 mmHg; chest pain plus dyspnea 9.3 +/- 4.1 mmHg) and after left ventriculography (chest pain 11.6 +/- 5.5 mmHg; dyspnea 10.2 +/- 2.3 mmHg; chest pain plus dyspnea 11.7 +/- 5.6 mmHg) were normal in the majority of patients and similar in all three groups. Likewise, the left ventricular end diastolic volume index (chest pain 72.0 +/- 16 cm3, dyspnea 69.1 +/- 20 cm3, chest pain plus dyspnea 70.0 +/- 16 cm3) and ejection fraction (chest pain 64.0 +/- 8.4%, dyspnea 64.1 +/- 6.1%, chest pain plus dyspnea 64.3 +/- 6.1%) were normal in the majority of patients and similar in the three groups. Symptomatic patients with mitral valve prolapse without significant mitral regurgitation had normal left ventricular hemodynamics, and their symptoms cannot be explained on the basis of hemodynamic abnormalities alone.

Adult↗
PubMed1992

T-cell receptor gene polymorphisms in familial cardiomyopathy: correlation with anti-beta-receptor autoantibodies.

Cardiac autoantibodies have been detected in a significant proportion of patients with dilated cardiomyopathy, but their relation to the pathogenesis of the disease remains unknown. This issue was examined in 41 members of an Ohio family with a heritable disorder of the cardiac conduction system and the myocardium. In 41.5% of all members studied, serum anti-beta-receptor antibodies were identified by a combination of techniques: ligand binding inhibition assay, enzyme-linked immunoassay of a beta 1-receptor peptide, and adenylate cyclase inhibition. The prevalence of autoantibodies was significantly higher (p < 0.01) in the affected (64.7%) than in the unaffected (25.0%) members. A 10.0 kb restriction fragment length polymorphism of the C beta region of the T-cell receptor gene was also overrepresented in affected males (60% versus 30% unaffected males, p < 0.01). In males, the presence of anti-beta-receptor antibodies was linked to the 10.0 kb C beta polymorphism. In affected males, a BlgII C alpha 2.14 kb polymorphism was also more frequent (62% versus 32% in unaffected, p < 0.01) and was linked to the presence of anti-beta-receptor antibodies. The distribution of haplotypes defined by V beta 8, C alpha, and C beta probes was significantly different between affected and unaffected (p < 0.04) and between antibody-positive and antibody-negative individuals. Since the major function of the T-cell receptor is the recognition of processed autoantigens, these results provide additional support for the role of autoimmunity in dilated cardiomyopathy.

Adult↗
PubMed1992

The Marfan syndrome: cardiovascular physical findings and diagnostic correlates.

Correlations among cardiac symptoms and auscultatory and phonoechocardiographic findings in Marfan syndrome have not been completely defined. A total of 24 patients with Marfan syndrome (16 men and 8 women; mean age 28.2 +/- 8.6 years) were studied. Mitral valve prolapse was noted in 22, of whom 19 had either nonejection systolic click or mitral regurgitation murmur. Mitral regurgitation was noted in 12 patients by Doppler imaging. Aortic root dilatation was noted in 20 patients and aortic regurgitation in six, five of whom had aortic regurgitation murmur (5 of 20 patients had undergone surgery). Proximal aortic dissection was noted in two. Dyspnea (n = 12) was associated with progressive mitral or aortic regurgitation in four, but in the others dyspnea could not be explained by valvular or ventricular abnormalities. Chest pain was related to pneumothorax in five and aortic dissection in two but was not associated with either in 15 patients. Palpitations (n = 12) and lightheadedness (n = 6) were not associated with specific arrhythmias. In conclusion, mitral valve prolapse and aortic root dilatation were the most common cardiovascular abnormalities in Marfan syndrome. Mitral valve prolapse was frequently associated with typical auscultatory findings and symptoms including dyspnea, chest pain, palpitations, and lightheadedness, whereas aortic root dilatation could be clinically silent unless complicated by aortic regurgitation or aortic dissection.

Adult↗
PubMed1991

The Marfan syndrome: abnormal aortic elastic properties.

Aortic distensibility and aortic stiffness index were measured at the ascending aorta (3 cm above the aortic valve) and the mid-portion of the abdominal aorta from the changes in echocardiographic diameters and pulse pressure in 14 patients with the Marfan syndrome and 15 age- and gender-matched normal control subjects. The following formulas were used: 1) Aortic distensibility = 2(Changes in aortic diameter)/(Diastolic aortic diameter) (Pulse pressure); and 2) Aortic stiffness index = ln(Systolic blood pressure)/(Diastolic blood pressure)(Changes in aortic diameter)/Diastolic aortic diameter. Pulse wave velocity was also measured. Compared with normal subjects, patients with the Marfan syndrome had decreased aortic distensibility in the ascending and the abdominal aorta (2.9 +/- 1.3 vs. 5.6 +/- 1.4 cm2 dynes-1, p less than 0.001 and 4.5 +/- 2.1, vs. 7.7 +/- 2.5, cm2 dynes-1, p less than 0.001, respectively) and had an increased aortic stiffness index in the ascending and the abdominal aorta (10.9 +/- 5.6 vs. 5.9 +/- 2.2, p less than 0.005 and 7.1 +/- 3.1 vs. 3.9 +/- 1.2, p less than 0.005, respectively). Aortic diameters in the ascending aorta were larger in these patients than in normal subjects, but those in the abdominal aorta were similar in the two groups. Linear correlations for both aortic distensibility and stiffness index were found between the ascending and the abdominal aorta (r = 0.85 and 0.71, respectively). Pulse wave velocity was more rapid in the patients than in the normal subjects (11.6 +/- 2.5 vs. 9.5 +/- 1.4 m/s, respectively, p less than 0.01). Thus, aortic elastic properties are abnormal in patients with the Marfan syndrome irrespective of the aortic diameter, which suggests an intrinsic abnormality of the aortic arterial wall.

Adult↗