Biomedical subjects
Publications and source records attributed to Christine O'Sullivan.
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BACKGROUND: Mustard repair for transposition of the great arteries (TGA) is frequently associated with impaired systemic (right) ventricular function and sometimes exercise intolerance. We hypothesized that a simple quantitative measurement of ventricular function, during rest and pharmacological stress, could identify abnormalities and predict objective exercise capacity. METHODS AND RESULTS: We quantified the performance of systemic and pulmonary (left) ventricles by using echocardiography, at rest and during dobutamine stress, in 27 adults who had undergone Mustard repair for TGA. Systolic and diastolic function of the systemic ventricle were markedly disturbed with respect to pulmonary ventricular function. We also measured exercise capacity by cardiopulmonary exercise testing for peak oxygen uptake. Exercise capacity was significantly predicted by systemic ventricular long-axis excursion both at rest (r=0.66, P<0.001) and at peak dobutamine stress (r=0.53, P=0.006) but not by pulmonary ventricular long-axis excursion at rest (r=0.04) or on stress (r=0.11). Exercise capacity was also predicted by the septal long-axis excursion at rest (r=0.61, P=0.001) but not pulmonary ventricular free wall excursion (P>0.05) or fractional shortening (P>0.05). Peak aortic velocity at maximum dobutamine stress correlated with exercise capacity (r=0.46, P=0.029) but not at rest (r=0.36). Multivariate analysis revealed systemic ventricular long-axis excursion to be the sole significant independent predictor of exercise capacity. CONCLUSIONS: Systemic ventricular function is depressed in most patients with Mustard repair. Quantitative echocardiographic evaluation shows systemic ventricular function to be a key determinant of exercise capacity.
BACKGROUND: Pulsed Wave Tissue Doppler (PWTD) recording of myocardial velocities has been widely used for assessing ventricular function but the output trace has finite thickness that leads to potential ambiguity in determining velocity and timing. OBJECTIVE: To determine optimal method of measurement of PWTD traces by comparing them with those obtained from digitised M-mode recorded from the atrioventricular (AV) valve ring (septal, LV and RV free wall). METHODS: We studied 100 subjects, 49 normal and 51 with coronary artery disease (15 patients with reduced left ventricular wall motion, mean systolic amplitude of LV free wall 0.8+/-0.3 cm), mean age 53+/-15 years. We recorded AV ring motion using PWTD and M-mode echo techniques. PWTD velocity signals were measured separately at: outer, inner and mid-points of the envelope and compared with peak velocities obtained from digitised M-mode long axis. RESULTS: Peak systolic (S), early diastolic (E) and late diastolic (A) PWTD velocities at outer, inner and middle envelope correlated closely with the corresponding M-mode measurements at left, septal and right ventricular free wall. However, only the midpoint S and E wave PWTD signal velocities agreed numerically with those obtained by digitised M-mode velocities; S (left 6.56+/-1.80 vs. 6.54+/-1.91 cm/s N.S.); E (left 8.50+/-3.25 vs. 7.65+/-3.30 cm/s N.S.). Agreement was somewhat less satisfactory for A wave; left 7.40+/-2.13 vs. 6.23+/-2.09 cm/s p<0.05. CONCLUSION: Atrioventricular valve ring echo provides an excellent in vivo calibration model for validating tissue Doppler velocity estimates. Since the mid-point of the envelope of the tissue Doppler signal is the most closely related value to that of the digitised M-mode, it may be recommended as a convention for routine practice.
BACKGROUND: In a small but significant group of elderly patients who present with breathlessness, dynamic left-ventricular outflow tract obstruction (DLVOTO) may be responsible for symptom generation. The aim of our study was to investigate the effect of beta-blockade on ventricular physiology and symptoms in patients with DLVOTO. METHODS: We performed a pilot study in 15 patients (age 76+/-10 years, mean+/-S.D., 14 female) with symptoms of exercise intolerance (New York Heart Association, NYHA, class 2.7+/-0.5). All patients had normal resting left ventricular (LV) systolic function together with DLVOTO based on the presence of basal septal hypertrophy and the development of high outflow tract velocities on stress echocardiography. All were commenced on oral atenolol (mean dose 45+/-19 mg), but this could not be tolerated in four patients due to a deterioration in clinical status. RESULTS: In the remaining 11 patients who could tolerate atenolol therapy, the rate pressure product was significantly lower (23%, P=0.028) and there was a marked reduction in LV outflow tract velocity (23%, P=0.001) following beta-blockade. Patient symptoms improved significantly following atenolol therapy, with a reduction in mean NYHA class from 2.8+/-0.4 to 1.5+/-0.5 (P<0.0001). CONCLUSIONS: Beta-blockade may represent a beneficial therapeutic approach in selected patients with DLVOTO as identified by stress echocardiography.