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Biomedical subjects

C F Wooley

Publications and source records attributed to C F Wooley.

At least 55 records · Page 3Linked to original sources
PubMed1988

Mitral valve prolapse syndrome. Evidence of hyperadrenergic state.

Although mitral valve prolapse (MVP) is a common valvular abnormality, its diagnostic classification has not been well defined. MVP is considered to be an anatomic entity with specific pathologic tissue characteristics and pathophysiologic consequences. The term "MVP syndrome" (MVPS) is used to refer to symptoms due to neuroendocrine or autonomic dysfunction that occur in patients with MVP and that cannot be explained on the basis of valvular abnormality alone. Several studies have shown that patients with MVPS have high urinary epinephrine and norepinephrine excretion, high plasma catecholamine concentrations, abnormal catecholamine response to volume expansion, and hyperresponse to adrenergic stimulation. In patients with MVPS and ventricular arrhythmias, the frequency of premature ventricular contractions parallels the urinary and plasma catecholamine values. The clinical presentation of MVPS may be related in part to high adrenergic tone and/or hyperresponse to adrenergic stimulation. Therefore, certain patients with MVPS and high adrenergic tone may benefit from beta blockade.

Adrenergic beta-Antagonists↗
PubMed1988

Mitral stenosis: mitral dome excursion at M1 and the mitral opening snap--the concept of reciprocal heart sounds.

The dynamics of the delayed accentuated mitral component (M1) of the first heart sound and the MOS were studied in 11 patients with mitral stenosis of varying severity. Echophonocardiographic (M-mode and 2D) studies were performed with analysis of LA dimensions, dynamics, and mitral valve excursion at the time of M1 and MOS. LA area and length, mitral annular diameter, and mitral dome area (from anulus plane to fused valve tip) and length were measured at M1 and MOS. Significant dynamic increases in mitral dome area and length occurred from M1 to MOS, with less striking but consistent increases in LA area, LA length, and mitral annular diameter. Conversely, mitral dome area and length decreased significantly from MOS to M1, with less striking but consistent decreases in LA area, LA length, and mitral annular diameter. Frame-by-frame video tape analysis showed that dome movement was separate from anulus motion. Mitral dome descent into the left ventricle terminated at MOS and reversal of dome motion terminated at M1. The conformational and dimensional changes that terminated abruptly at MOS reversed and terminated abruptly in a reciprocal manner at the time of the delayed, accentuated M1. When considered in light of known hemodynamic, pressure pulse, and imaging correlates in mitral stenosis, these observations strengthen the hypothesis that the mechanisms involved in the production of M1 and MOS in mitral stenosis are paired or reciprocal in nature, and the delayed, accentuated M1 and the MOS of mitral stenosis are reciprocal cardiovascular sounds.

Adult↗
PubMed1988

Postural exercise abnormalities in symptomatic patients with mitral valve prolapse.

The hemodynamics of the supine and upright exercise response in 16 symptomatic women with mitral valve prolapse (Group I) was compared with that in 8 asymptomatic normal control women (Group II). All subjects had supine and upright echocardiography and phonocardiography at rest and none demonstrated mitral regurgitation. All participants then underwent same day graded bicycle exercise, with simultaneous radionuclide angiography in both the upright and the supine posture. Catecholamines were measured, and a variety of volumetric and hemodynamic data were obtained. Group I (patients with mitral valve prolapse) demonstrated a reduced exercise tolerance, especially during upright exercise, as measured by both total exercise duration and maximal work load achieved. Mean total catecholamine measurements were similar between the two study groups at comparable mean heart rate, mean blood pressure and mean rate-pressure (double) product. No difference was observed in the ratio of right to left ventricular stroke counts at rest or during exercise regardless of posture, suggesting that exercise-induced mitral regurgitation did not occur. A difference was noted, however, in left ventricular end-diastolic volume index. At rest, Group I patients exhibited a 42% decrease in this index when sitting upright, and this difference from supine values persisted at submaximal (300 kpm/min) and peak work loads (34 and 29% difference, respectively). This contrasted with the control subjects whose upright end-diastolic volumes at rest, at 300 kpm/min and at peak exercise were reduced 21, 10 and 3%, respectively, compared with supine values. Cardiac index measurements reflected the reduced left ventricular end-diastolic volume observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Floppy mitral valve chordae tendineae: histopathologic alterations.

Pathologic studies of floppy or myxomatous mitral valves have focused primarily on changes in the valve cusps, with little attention given to the chordae tendineae. In a systematic study of the histopathology of floppy mitral valve chordae tendineae, 128 nonruptured chordae from 8 severely regurgitant floppy mitral valves were compared to 152 chordae from 10 normal control mitral valves and to 152 chordae from 8 control mitral valves with severe regurgitation due to ischemic heart disease. Collagen alterations were observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 38% of floppy mitral valve chordae. Moderate or severe acid mucopolysaccharide accumulation was observed in 2% of normal mitral valve chordae and 3% of control regurgitant mitral valve chordae compared to 39% of floppy mitral valve chordae. Nonuniform histopathologic alterations, rare in normal and control regurgitant mitral valve chordae tendineae, were frequent in floppy mitral valve chordae tendineae (p less than 0.001). Histopathologic alterations provide the basis for abnormal physical properties previously demonstrated in floppy mitral valve chordae tendineae and may predispose to chordal elongation and rupture.

Aged↗
PubMed1988

Mitral valve prolapse syndrome: neuro-endocrinological aspects.

Based on analysis of 399 symptomatic patients with mitral valve prolapse (MVP) and the reported experience of others, we developed a clinical classification in order to improve nosology, provide better identification and promote insight into the mechanism of symptoms in patients with MVP. The heading of anatomic MVP designates those in whom symptoms or complications were primarily or directly related to valvular dysfunction and the heading of MVP syndrome designates those patients in whom symptoms cannot be explained on the basis of valvular dysfunction alone. Patients with MVP syndrome present with a symptom complex which results from various forms of neuroendocrine or autonomic dysfunction; the most common symptoms include chest pain, palpitations, cardiac arrhythmias, orthostatic phenomena, syncope, presyncope, fatigue, exercise intolerance, dyspnea and neuropsychiatric symptoms (Table 1). Mechanisms underlying the condition have been shown to include increased adrenergic activity, disturbances of catecholamine regulation, hyperresponsiveness to adrenergic stimulation, anomalous beta-adrenergic receptors, dysfunction of the parasympathetic portion of the autonomic nervous system, disturbances in renin-aldosterone regulation, decreased intravascular volume, diminished left ventricular diastolic volume in the upright position as well as abnormal secretion of atrial natriuretic factor (Table 2). In MVP syndrome, alterations of the heart, kidney, the adrenals and the autonomic nervous system coexist and interact, creating a complex "neuro-endocrine cardiovascular process" which may account for many of the symptoms otherwise unexplained on the basis of the valvular abnormality alone.

Arousal↗
PubMed1988

Aortic distensibility in post-stenotic aortic dilatation: the effect of co-existing coronary artery disease.

Aortic distensibility is decreased in patients with coronary artery disease (CAD) and the angiographically normal aorta. To determine if the same is true in patients with aortic stenosis and post-stenotic dilatation, two groups were studied. Group A consisted of 15 patients with post-stenotic aortic dilatation and normal coronary arteries, and group B, 14 patients with post-stenotic aortic dilatation and CAD. The patients were compared to 18 normal subjects. The area of the first 6 cm of the aorta above the valve obtained by aortography was planimetered and the mean diameters were calculated. Distensibility was calculated using the formula: (formula; see text) Distensibility was greater in group A (2.5 +- .4 cm2.dynes-1) compared to group B (1.0 +- 8 cm2.dynes-1, p less than 0.001). Distensibility in normal subjects reported recently from this laboratory (3.4 +- .4 cm2.dynes-1) was greater compared to both groups A and B (p less than 0.001). Thus, distensibility was decreased in patients with post-stenotic aortic dilatation. The further decrease in distensibility in patients with co-existing coronary artery disease may be partially related to abnormal nutrition of the arterial wall since the vasa vasorum of the ascending aorta are derived from the coronary arteries.

Adult↗
PubMed1987

Aortic distensibility abnormalities in coronary artery disease.

Vasodilatory capacity of nonstenotic arteries in experimental animals with atherosclerosis is decreased. It was postulated that aortic distensibility may be abnormal in patients with coronary artery disease (CAD). Aortic distensibility was determined in 24 normotensive patients with CAD and an angiographically normal aorta and values were compared with those in 18 age-matched normal subjects. Aortic diameters were measured at 3 levels--2, 4 and 6 cm above the aortic valve--by angiographic techniques. The area of the first 6 cm of the aorta above the aortic valve was planimetered and mean aortic diameters were calculated. Distensibility was calculated using the formula: [2 X (changes of the aortic diameter)/(diastolic aortic diameter) X (changes of the aortic pressure)]. CAD patients had similar aortic pressures but markedly lower distensibility than normal subjects: 0.7 +/- 0.2 vs 1.7 +/- 0.3 (p less than 0.02); 1.5 +/- 0.3 vs 4.0 +/- 0.6 (p less than 0.02); and 1.2 +/- 0.2 vs 5.3 +/- 0.6 (p less than 0.001) at 2, 4 and 6 cm above the aortic valve, respectively. Distensibility was also calculated from the mean aortic diameters and was greater in normal subjects than in CAD patients (3.4 +/- 0.4 vs 1.6 +/- 0.1, p less than 0.001). Decreased aortic distensibility in CAD may be related to the common atherosclerotic process or to reduced ascending aorta vasa vasorum flow from coronary arteries.

Adult↗
PubMed1987

The equilibrium position of the mitral valve: an accurate model of mitral valve motion in humans.

A "semiopen" diastolic equilibrium position of the mitral valve that is assumed in the absence of transmitral flow has been demonstrated in instrumented dogs. It has been suggested that the papillary muscles and chordae tendineae play an integral role in returning the valve to this position after initial diastolic opening. To determine whether such a model of mitral valve motion is valid in noninstrumented humans without underlying valvular disease, M-mode and Doppler ultrasound studies were performed in 6 subjects who underwent prolonged periods of ventricular diastole and atrial inactivity. After maximal opening, the mitral valve assumed a stable open position in which mean separation of the anterior and posterior mitral leaflets was 52% of maximal separation. This position was maintained for a mean duration of 585 ms, during which time transmitral flow fell to 0 m/s. Peak mitral valve opening preceded the early transmitral flow peak by an average of 42 ms, suggesting an active closure of the mitral valve as flow continued to accelerate. It is concluded that a semiopen equilibrium position of the mitral valve is assumed during prolonged diastolic periods in the absence of transmitral flow and is an accurate model describing diastolic mitral valve motion in noninstrumented humans. The chordae tendineae and papillary muscles may actively participate in the genesis and maintenance of the equilibrium position.

Adult↗
PubMed1987

Morphologic and functional characteristics of the heart in Friedreich's ataxia.

The purpose of this study was to characterize the heart in patients with Friedreich's ataxia by two-dimensional echocardiography, systolic time intervals, and heart biopsy. Ten patients with Friedreich's ataxia (seven females and three males, age 15 +/- 7 years) were compared with 10 age-matched normal subjects (five males and five females, age 16 +/- 7 years). The mean systolic blood pressure in the patients with Friedreich's ataxia was lower (114 +/- 9 mm Hg) than that in the control subjects (122 +/- 8 mm Hg; p less than 0.05); diastolic blood pressures were the same. The heart rate in the patients with Friedreich's ataxia (102 +/- 17 beats/minute) was greater than that in the control subjects (76 +/- 12 beats/minute; p less than 0.001). The interventricular septal wall thickness was much greater in Friedreich's ataxia (13 +/- 2 versus 8 +/- 1 mm, p less than 0.001) as was the posterior wall thickness (13 +/- 3 versus 8 +/- 1 mm, p less than 0.001). The left ventricular end-diastolic diameter was smaller in Friedreich's ataxia (35 +/- 6 mm versus 47 +/- 6 mm; p less than 0.01), and the fractional change of the left ventricular minor axis with systole was greater in Friedreich's ataxia (40 +/- 9 percent versus 33 +/- 5 percent; p less than 0.05). An 11th patient with Friedreich's ataxia (age 33) had clinical heart failure, but his course was complicated by alcohol abuse. Heart biopsy in three patients with Friedreich's ataxia demonstrated myocyte hypertrophy (21.5 +/- 2.0 microns diameter; normal, 14 to 17 microns) and increased fibrosis (16 +/- 9 percent; normal, less than 5 percent). Thus, heart disease in Friedreich's ataxia is characterized by myocyte hypertrophy, interstitial fibrosis, increased left ventricular wall thickness, decreased left ventricular cavity size, sinus tachycardia, and normal systolic function. Further biochemical analysis of tissues may lead to the link of the neurologic and cardiac diseases and eventually to more effective therapy of this condition.

Adolescent↗
PubMed1987

Cardiovascular disease of connective tissue origin.

Inherited abnormalities of connective tissue elements often cause changes in the structure and function of the cardiovascular system. Well-known heritable disorders of connective tissue in which cardiovascular abnormalities are prominent include the Marfan syndrome and the Ehlers-Danlos syndrome. Connective tissue abnormalities also occur without the associated features of a recognized syndrome. These include isolated valvular prolapse and anuloaortic ectasia. In this review, the cardiovascular features of connective tissue abnormalities--both the recognized syndromes and the isolated abnormalities--are described, important concepts in the diagnosis and treatment of these disorders are reviewed, and the classification of inherited connective tissue abnormalities of the cardiovascular system is discussed.

Cardiovascular Diseases↗
PubMed1987

Atrial septal defect: attenuation of respiratory variation in systolic and diastolic time intervals.

The effects of pathologic states on right and left ventricular function have been studied extensively. However, there have been few studies on the interrelations between right and left ventricular function in normal human subjects and in patients with disease. Respiratory effects on ventricular interrelations reflected by diastolic time, right or left ventricular systolic time and ventricular performance (pre-ejection period/ejection time ratio) were studied in 12 normal subjects and 15 patients with a normal pressure-large shunt atrial septal defect. Simultaneous pulmonary artery (intracardiac manometer recordings) and left ventricular external recordings were performed in both groups. Left ventricular diastolic time increased with inspiration in the normal subjects and decreased in the patients with atrial septal defect (12.6 +/- 2.39 [1 SE] versus -13.4 +/- 3.48 ms, p less than 0.001). Left ventricular systolic time and ejection time decreased with inspiration in the normal group and remained unchanged in the patient group (-7.6 +/- 0.95 versus -0.9 +/- 0.77 ms, p less than 0.001 and -10.4 +/- 1.09 versus -1.7 +/- 0.80 ms, p less than 0.001, respectively). Left ventricular pre-ejection period/ejection time ratio increased with inspiration in the normal subjects and remained unchanged in the patients with atrial septal defect (0.03 +/- 0.008 versus 0 +/- 0.01, p less than 0.01). Right ventricular diastolic time decreased with inspiration in normal and patient groups (-8.8 +/- 1.6 versus -17 +/- 3.87 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

The mitral valve prolapse epidemic: fact or fiction.

In spite of two decades of research, the precise relationship of anatomic mitral valve prolapse (floppy valve) to the neuroendocrine disorder (MVP syndrome) remains unclear. In all likelihood they are two separate genetic disorders which travel together in some fashion. Mitral valve prolapse is a common disorder but progressive mitral regurgitation usually occurs late in life and in only a few patients. Other complications such as bacterial endocarditis, stroke, and sudden death are far less common but can occur at younger ages. The neuroendocrine syndrome in civilian life is mainly seen in young females (interestingly the peak incidence years correspond to peak female sex hormone output) but can be seen in males when subjected to unusual stress such as military service. More recent echocardiographic studies have questioned whether all prolapsing valves are truly abnormal. It has been shown that echographic prolapse can be produced in normal subjects by reducing venous return and impaired venous return may be present in some patients with the MVP syndrome. However, clicks and murmurs are apparently not heard when normal valves prolapse. It is our opinion that the presence of a click or typical murmur requires some anatomic abnormality of the mitral valve. One wonders if minimal valve abnormality (noted and dismissed by Davies) is the valve abnormality present in many young females with MVP syndrome, and that it may remain a mild abnormality throughout life. Recent psychiatric studies suggest that MVP is present in 30% of patients with Panic Disorder. It is not clear that this psychiatric syndrome is the same thing as the MVP syndrome. In Devereux's study, anxiety proneness was no different in the MVP cohort than in relatives without MVP. It is possible that diagnostic mixing of two similar but separate disorders has occurred, as has been the case since World War I. Perhaps the most important question is whether young patients with MVP syndrome and no echocardiographic criteria for "floppiness" will develop progressive mitral regurgitation or other complications in later life. In other words, how often is MVP syndrome in a young individual without echocardiographic evidence of a floppy valve a precourser to eventual progressive mitral regurgitation? Are there two different populations? Because of the long course of the disorder, several more years of observation (and, it is hoped, prospective longitudinal study) will be required to answer this question.

Female↗
PubMed1986

Evidence for progression from mild to severe mitral regurgitation in mitral valve prolapse.

Little information is available concerning the progression of mild to severe mitral regurgitation (MR) in patients with mitral valve prolapse (MVP). This study reports 86 patients, average age 60 years, who presented with cardiac symptoms, precordial systolic murmur, severe MR and a high incidence of MVP on echocardiography (57 of 75 [75%] ) and left ventriculography (61 of 84 [73%] ). Seventy-five surgically excised mitral valves appeared grossly enlarged and floppy. Histologic studies showed extensive myxomatous changes throughout the leaflets and chordae. Eighty patients had had precordial murmurs first described at average age 34 years, but the average age at which symptoms of cardiac dysfunction appeared was 59. However, once symptoms developed, mitral valve surgery was required within 1 year in 67 of 76 patients who had undergone surgery. Atrial fibrillation, present in 48 of 86 patients (56%), or ruptured chordae tendineae, present in 39 of 76 patients (51%), may have contributed to this rapid progression and deterioration. Additionally, 13 patients had a remote history of documented infective endocarditis. Twenty-eight patients had at least 1 type of serial clinical evaluation that indicated progressive MR in all 28 patients on the basis of changing auscultatory findings (24 of 26), progressive radiographic cardiomegaly (24 of 25), echocardiographic left atrial enlargement (4.3 to 5 cm in 11 patients) and angiographically worsening MR (14 of 15). Twenty-four of these patients had evidence of MVP on at least 1 of their initial studies. Thus, mild MR due to MVP and myxomatous mitral valves is a progressive disease in some patients with MVP.

Adult↗