Breast reconstruction. State-of-the-art for the 1990s.
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Biomedical subjects
Publications and source records attributed to B F Byrd.
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Tricuspid regurgitation refers to a systolic leak of blood between the right ventricle and right atrium, across the tricuspid valve. Doppler echocardiographic examination of large numbers of normal individuals has shown that trivial tricuspid regurgitation is extremely common. Measurement of the peak velocity of the regurgitant frequency spectrum on Doppler echocardiography is of considerable clinical importance since it may be used to calculate peak right ventricular and, consequently, peak pulmonary systolic pressure. Doppler recording of the frequency spectrum of a tricuspid regurgitation jet optimally shows a smooth, parabolic, sharply demarcated envelope. In many individuals with trivial tricuspid regurgitation, however, this frequency spectrum is incomplete and its envelope is poorly demarcated. Such inadequate signals do not allow measurement of the spectrum's peak velocity. Like other contrast agents, air-filled microspheres composed of sonicated human serum albumin enhance reflection of Doppler ultrasound and thus have the potential to enhance incomplete tricuspid regurgitation spectra. Furthermore, since sonicated albumin microspheres can cross the pulmonary circulation intact, they have the potential to enhance mitral regurgitation spectra. The purpose of our study was to investigate whether injection of sonicated albumin microspheres enhances incomplete tricuspid and mitral regurgitation frequency spectra to a diagnostic quality. Sonicated albumin microsphere injection enhanced tricuspid regurgitation spectra to optimal quality in 11 of 15 patients (73%). Microsphere injection caused a minor degree of enhancement of the mitral regurgitant spectrum in 1 patient, but did not optimize the spectra in any of 10 patients tested. Saline contrast injection optimally enhanced tricuspid regurgitation spectra in all 8 patients in whom it was used.(ABSTRACT TRUNCATED AT 250 WORDS)
Proximal aortic dissection in a 79-year-old woman was complicated by cardiac tamponade, aortic regurgitation, and pleural leak. Following pericardiocentesis and control of her hypertension, she survived without an operation for more than four years.
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Doppler superior vena cava (SVC) flow patterns were studied in 34 patients with pericardial disease and in 8 normal adults; the pulse transducer on the echocardiographic instrument was used for respiratory monitoring, rather than a separate nasal thermistor-based device. First expiratory SVC diastolic flow velocities (Dfe) did not differ in normal subjects and patients with hemodynamically insignificant pericardial effusions (23 +/- 3 cm/s and 29 +/- 13 cm/s, difference not significant). Dfe were less than 15 cm/s only in the 14 patients with cardiac tamponade (9 +/- 3 cm/s, p less than 0.01). A ratio of systolic to diastolic flow velocity less than or equal to 1.1 in the first expiratory beat distinguished constrictive pericarditis from all other groups (p less than 0.01), although not from restrictive cardiomyopathy. Expiratory ablation of diastolic SVC flow mimicking cardiac tamponade was not observed in constrictive pericarditis. Respiratory variation in SVC flow velocities was slight in normal subjects and patients with constrictive pericarditis, increased in patients with hemodynamically insignificant pericardial effusions (p less than 0.01) and greatest in patients with cardiac tamponade (p less than 0.01). Quantitative analysis of SVC flow velocity patterns is a useful addition to the echocardiographic evaluation of pericardial disease.
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Diastolic Doppler flow signals (greater than or equal to 0.2 m/s) in the left ventricular outflow tract have not been well characterized, and their origin and significance remain controversial. Fifty-nine patients (55 +/- 16 years of age) with technically good Doppler echocardiographic studies were studied prospectively. There were 14 normal subjects, 21 patients with left ventricular hypertrophy, 10 with dilated cardiomyopathy and 14 with other cardiac disease. The rhythm was sinus in 55 and atrial fibrillation in 4. Two distinct Doppler flow signals were detected in the left ventricular outflow tract during diastole. These were termed E' (early) and A' (active) because they occurred 40 to 100 ms after higher velocity mitral inflow E (passive filling) and A (atrial contraction) signals. Among 59 patients, E' signals were present in 48 (81%) and had a mean velocity of 0.41 +/- 0.23 m/s. In 55 patients with normal sinus rhythm, A' signals were present in 52 (95%) and had a mean velocity of 0.52 +/- 0.24 m/s. No A' signals were present in the four patients with atrial fibrillation. The E' and A' velocities by pulsed wave Doppler ultrasound were low at the left ventricular apex and increased along the basal septum in the left ventricular outflow tract. Prominent A' velocities (greater than or equal to 0.45 m/s) were seen in 62% of patients with left ventricular hypertrophy, 50% of normal subjects and 10% of patients with dilated cardiomyopathy. The A' velocity was higher in patients with left ventricular hypertrophy (0.63 +/- 0.26 m/s) than in those with a normal heart (0.45 +/- 0.16 m/s; p less than 0.05) or dilated cardiomyopathy (0.25 +/- 0.13 m/s; p less than 0.01). The major determinants of diastolic outflow tract velocity were the mitral inflow E and A velocities and left end-diastolic dimension, particularly when combined (r = 0.64, p less than 0.0001 for E'; r = 0.72, p less than 0.0001 for A'). Distinctive E' and A' Doppler outflow tract signals result from mitral inflow and may be detected in most patients with normal heart size. These E' and A' velocities increase from apex to base and are more prominent in patients with a small, normally contracting heart or left ventricular hypertrophy.
In conclusion, an understanding of the physiology of cardiac tamponade and pericardial constriction allows accurate interpretation of the changes in SVC and transatrioventricular valve Doppler flow velocities that characterize each abnormality. Meticulous attention to detail in obtaining the studies is essential for accurate diagnosis, because relative changes in flow velocities during respiration may be obscured or misinterpreted if poor-quality data are obtained. In our laboratory, SVC Doppler studies have proved to be the most technically feasible in patients with cardiac tamponade, but transvalvular studies provide important complementary data and are critical in constrictive pericarditis. Hepatic vein Doppler offers an alternative approach to the analysis of systemic venous return, particularly in stable patients with dilated hepatic veins. These studies must always be interpreted with attention to possible confounding variables such as previous pericardiotomy, significant tricuspid regurgitation, severe chronic lung disease, or restrictive cardiomyopathy. As physiologic rather than anatomic indicators, they are a valuable addition to echocardiography in assessing the hemodynamic significance of pericardial abnormalities.
Left ventricular mass (LVM) measurements made by the truncated ellipsoid algorithm from clinical two-dimensional echocardiograms (2DE) were compared to autopsy weights in 37 patients. All six 2DE instruments were calibrated with an ultrasound phantom to standardize LVM measurements. Measurements were made by an experienced echocardiographer (LVME) and by an echocardiographer (LVMN) newly trained in LVM measurement from clinical 2DE tapes of patients with LV weights later confirmed at autopsy. LVME (r = 0.91, SEE +/- 41 gm) were more accurate than LVMN for all 2DE, but LVMN equalled LVME in accuracy for technically good 2DE. Interobserver variability was 36 gm, or 17% of LVM for all 2DE, and fell to 27 gm, or 12% of LVM for technically good 2DE. Segmental wall motion abnormalities and time from 2DE to death did not influence measurement accuracy significantly. LVM measurements by the 2DE truncated ellipsoid formula are accurate and reproducible in patients with normal and abnormal hearts.
Both two-dimensional and M-mode echocardiography provide accurate estimates of left ventricular mass. However, their reproducibility in serial studies has not been compared, although this issue is critical to evaluation of regression of hypertrophy. To determine which technique provides more reproducible estimates of left ventricular mass, three serial studies were performed prospectively in each of eight normal adults over 5 months. Both two-dimensional and M-mode echocardiograms were obtained at each of these 24 studies. Measurements were performed by two independent observers who did not know patient identity. For the two-dimensional method, left ventricular mass was determined with use of a computer light-pen system and the truncated ellipsoid formula. For the M-mode method, mass was calculated from Penn convention measurements with use of the cube formula. At study 1 the group mean left ventricular mass by two-dimensional echocardiography (115 +/- 20 g) did not differ from that by M-mode study (127 +/- 37 g, p = NS). However, serial estimates of left ventricular mass were more reproducible by two-dimensional echocardiography. The mean difference among the three serial two-dimensional studies in each individual was 4.8 +/- 4 g (4.2 +/- 3%) by the two-dimensional method, but was 18.5 +/- 13 g (14.9 +/- 10%) by the M-mode method (p = 0.01). Interobserver results for left ventricular mass by two-dimensional echocardiography correlated closely (r = 0.95, n = 24, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
PURPOSE: To further the understanding of diabetic heart disease, we tested the hypothesis that an asymptomatic group of normotensive diabetic patients between 20 and 50 years old had a restrictive cardiomyopathy independent of clinically significant coronary artery disease. PATIENTS AND METHODS: Quantitative two-dimensional echocardiography and stress myocardial perfusion scintigraphy were performed to detect and characterize the cardiac abnormalities in this study group comprising 88 patients with rigorously classified diabetes and 65 volunteer control subjects. RESULTS: Diabetic patients were shown to have a mildly reduced left ventricular end-diastolic volume index: 50.1 +/- 8.2 and 52.1 +/- 14.7 mL/m2 for patients with type I and type II diabetes, respectively, versus 58.9 +/- 11.7 mL/m2 for control subjects. The left ventricular diastolic filling was also impaired in diabetic patients as reflected by a lower atrial emptying index: 0.73 +/- 0.24 and 0.76 +/- 0.3 for type I and type II diabetics, respectively, compared with 1.14 +/- 0.24 for control subjects. Exercise tolerance was normal in subjects with type I diabetes and slightly reduced in subjects with type II diabetes. Only one patient developed regional ischemia on thallium exercise testing. CONCLUSION: Using a comprehensive, noninvasive approach, we have shown that asymptomatic normotensive patients with type I or type II diabetes who were between 20 and 50 years old had a restrictive cardiomyopathy characterized by mildly reduced left ventricular end-diastolic volume and altered left ventricular compliance independent of critical coronary artery disease.
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The Action and Planning Committee on Breast Cancer Control was formed in 1970 by the American Cancer Society, based on their earlier successful experience with early-detection programs for uterine cancer. The original intention was to support 12 centers for 2 years, but with the passage of the Conquest of Cancer Act in 1971, and the consequent availability of more funds for cancer programs, the American Cancer Society and the National Cancer Institute decided jointly to expand the program to 27 Breast Cancer Detection Demonstration Project Centers, with 280,000 women participating, who would be examined annually for 5 years. Data from the examinations, which included history, physical examination, mammogram, and thermogram, were subjected to a continuing computer analysis. The thermogram was deleted after the second year. Although patients were randomly selected, there was an almost identical number of subjects in two age groups--35-49 years and 50-75 years. The results of the study are presented, and the importance of the program's efforts at breast self-examination education as contained in the program's original protocol, is discussed.
Whether anesthetic technique affected the incidence of myocardial ischemia in 60 patients undergoing carotid endarterectomy was investigated. The patients were randomly assigned to receive halothane or isoflurane (with nitrous oxide) either at a low concentration alone or at a higher concentration with phenylephrine added to support blood pressure. Blood pressure was maintained within 20% of each patient's average ward systolic pressure. Seven leads of electrocardiograms (ECG) and echocardiograms were analyzed for segmental wall motion. The echocardiograms were analyzed using standard formulae for end-systolic meridional wall stress (SWS) and rate-corrected velocity of fiber shortening (Vcfc). Because of the nature of these calculations, only echocardiograms with normal regional wall motion could be accurately analyzed. The patients had postoperative ECG and creatinine phosphokinase (CPK) isoenzyme determinations and regularly scheduled clinical examinations to detect perioperative myocardial infarction and neurologic deficits. Although blood pressures were similar, the patients who received a higher concentration of anesthetic plus phenylephrine had a higher wall stress, regardless of the choice of anesthetic agent. All four techniques allowed provision of the same stump pressures (the marker surgeons used for adequacy of collateral carotid flow). No difference could be found in wall stress or incidence of myocardial ischemia between isoflurane and halothane. The patients who received phenylephrine had a threefold greater incidence of myocardial ischemia than did the patients who had light anesthesia to maintain similar systolic blood pressures and stump pressures. The groups were demographically and hemodynamically similar; in particular, the heart rates were not different.(ABSTRACT TRUNCATED AT 250 WORDS)
This study was performed to measure the effect on cardiovascular functional parameters of remaining in an inverted position for a relatively short period of time. With the aid of radionuclide gated bloodpool scanning techniques, left ventricular ejection fraction (LVEF), heart rate (HR), systolic blood pressure (SBP), systolic average rate of left ventricular emptying (dV/dt), and double product (DP) measurement values were obtained from 16 normal, healthy subjects in four positions: supine, standing, half-inverted, and fully inverted. When comparing full-inversion to supine values, the HR and double product were not significantly different, the SBP was significantly higher, and the LVEF and dV/dt values were significantly lower. There were no significant differences between the partial and fully inverted positions. Comparison of standing to fully inverted positions reveals no significant change in SBP or double product. HR, LVEF, and dV/dt values were significantly lower in inverted subjects. It is suggested that these findings reflect the mechanism by which the cardiovascular system compensates for increased ventricular end-diastolic volume. Suggestions for future investigations include inverted cardiac ultrasound and right ventricular function studies.
We identified eight hypertensive patients who developed severe bradycardia during oral clonidine hydrochloride therapy. Seven patients had sinus bradycardia, four had long sinus pauses, two had junctional bradycardia, and two had high-degree atrioventricular block. Three populations at risk for severe bradycardia during oral clonidine therapy were identified: patients with renal insufficiency, patients with clinical sinus node dysfunction, and patients who had developed bradycardia while taking other sympatholytic agents or who were currently receiving another sympatholytic drug. Clonidine effects were dissociated in two patients who were not hypotensive despite severe bradycardia. Asymptomatic patients required only dose reduction or discontinuation of clonidine therapy. Symptomatic patients responded inconsistently to intravenous atropine sulfate therapy; one responded to isoproterenol therapy, and one required temporary artificial pacing. Awareness of the variable presentation and response of this bradycardia to medical therapy will assist patient management. The incidence of this complication is low (less than 0.3%), but attention to risk factors should make clonidine-induced bradycardia even less frequent.
Although the morphology of mitral valve prolapse (MVP) has been described, abnormalities of chordal arrangement and insertion have not been emphasized. We retrospectively reviewed 23 surgically-excised MVP and 10 control mitral valves removed at necropsy. Two-dimensional echocardiograms (2DE) were available in 10 MVP and in six additional controls. 2DE accurately assessed the length of anterior leaflet (AL) and posterior leaflet (PL) of the mitral valve (3.2 +/- 0.7 cm and 2.2 +/- 0.6 cm, respectively) as compared to morphologic measurements (3.0 +/- 0.4 cm and 2.1 +/- 0.4 cm, respectively). However, annular diameter as assessed by echocardiography was significantly less (4.6 +/- 0.7 cm) than that derived by morphologic measurements of annular circumference (AC) (5.3 +/- 0.7 cm). The AL and PL lengths and the mitral anuli were significantly larger in patients with MVP as compared to controls (p less than 0.01) when assessed both by 2DE and by morphology. The ratio of the maximum distance of chordal separation/AC was 0.11 +/- 0.04 in MVP and 0.13 +/- 0.02 in controls (p less than 0.05). Chordal divisions were increased in MVP (4.2) compared to controls (3.1, p less than 0.01). The most striking morphologic feature of MVP was abnormal chordal insertion and a random, unpredictable pattern of chordal distribution. We postulate that abnormal chordal architecture may be responsible for unequal stress on the valve leaflets and may thus lead to MVP.