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Alison Duncan

Publications and source records attributed to Alison Duncan.

7 recordsLinked to original sources
PubMed2006

Lymphoepithelioma-like carcinoma of the skin: a case with lymph node metastases at presentation.

We report a case of a primary lymphoepithelioma-like carcinoma (LELC) of the skin. The patient was a 73-year-old man with a lump on his back for 18 months. A biopsy and subsequent excision was performed. He also had axillary node clearance for metastatic disease. The tumor was composed of islands of pleomorphic cells with a lymphocytic infiltrate. Differential diagnoses included squamous cell carcinoma, adnexal carcinoma, Merkel cell tumors, lymphoepithelial lesions, lymphomas, and skin metastases. The histopathologic and immunohistochemical features were those of a LELC of the skin. It was negative for Epstein-Barr virus. Just over 30 cases of primary LELCs arising in the skin have been reported with only 1 documented fatality. We report a case with extensive vascular involvement and bilateral lymph node metastases.

Aged↗
PubMed2005

Dobutamine stress-induced ischemic right ventricular dysfunction and its relation to cardiac output in patients with three-vessel coronary artery disease with angina-like symptoms.

We investigated markers of ischemic dysfunction and their relation to overall right ventricular (RV) performance during dobutamine stress echocardiography in patients who had coronary artery disease. Thirty-three patients (58 +/- 10 years old) who had 3-vessel coronary artery disease were compared with 17 age-matched controls (58 +/- 11 years old). RV long-axis amplitude (M mode), systolic and diastolic myocardial tissue Doppler velocities, and filling and ejection velocities were measured, and cardiac output (CO) was calculated at rest and during peak stress. There was no difference in RV size (inlet dimension <3.5 cm), RV systolic long-axis amplitude, systolic and diastolic velocities, peak early/late diastolic velocity ratio, and RV CO between patients and controls at rest. During stress, RV systolic long-axis amplitude increased in controls (from 24 +/- 6 to 30 +/- 5 mm) and CO increased significantly (from 4.9 +/- 1.2 to 12.5 +/- 2.1 L/min, p <0.001 for the 2 items). In contrast, RV amplitude did not change with stress in patients (from 24 +/- 5 to 22 +/- 6 mm, p = NS), and the stress-increment in CO was augmented (from 4.2 +/- 1.2 to 8.3 +/- 2.0 L/min, p <0.001 vs control stress increment). Failure to increase RV systolic amplitude >2 mm was 79% sensitive and 88% specific for detecting ischemic RV dysfunction, and there was a close correlation between stress-induced change in RV systolic amplitude and change in CO in patients (r = 0.56, p <0.001). Early diastolic velocity increased in controls (from 10.8 +/- 3.2 to 13.1 +/- 3.6 cm/s, p <0.01) but did not change in patients (from 11.5 +/- 3.7 to 11.3 +/- 4.8 cm/s, p = NS). RV shortening after ejection did not appear in any control subject but did develop in 8 of 33 patients, thus contributing to the decrease in RV peak early/late diastolic velocity ratio in patients (from 1.1 +/- 0.3 to 0.76 +/- 0.4, p <0.001) compared with that in controls (1.3 +/- 0.3 to 1.0 +/- 0.2, p <0.001). In conclusion, markers of RV dysfunction are not related to left ventricular wall motion score index or long-axis changes with stress.

Cardiac Output↗
PubMed2004

Relation of biventricular function quantified by stress echocardiography to cardiopulmonary exercise capacity in adults with Mustard (atrial switch) procedure for transposition of the great arteries.

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.

Adrenergic beta-Agonists↗
PubMed2004

Electromechanical left ventricular resynchronisation by coronary artery bypass surgery.

OBJECTIVE: In patients with coronary artery disease (CAD), the normal electromechanical response to dobutamine stress is deranged: QRS duration lengthens rather than shortens, left ventricular asynchrony develops, post-ejection shortening appears, and total isovolumic time (the time in the cardiac cycle when the ventricle is neither ejecting nor filling) increases rather than falls, all of which blunt the normal rise in cardiac output. We aimed to study the effect of revascularisation on these stress-induced electromechanical abnormalities and their effect on peak cardiac output after coronary artery bypass grafting (CABG). METHOD: 20 unselected patients were studied before and after CABG. Long axis asynchrony was determined by (i) delay in the onset of shortening, (ii) amplitude and (iii) duration of post-ejection shortening. Total isovolumic time (in s/min), calculated as [60-(total ejection time+total filling time)] and cardiac output were measured by Doppler echocardiography. RESULTS: Before CABG: QRS duration broadened with stress (by 7+/-8 ms, P<0.01) and post-ejection shortening increased (amplitude by 1.1+/-0.7 mm, P<0.01, duration by 8+/-9 ms, P<0.01). Total isovolumic time increased (by 3+/-3 s/min, P<0.01) and cardiac output rose (by 2.8+/-1.2 l/min, P<0.01). After CABG: QRS duration shortened with stress (by 5+/-4 ms, P<0.01) post-ejection shortening decreased (amplitude and duration fell by 0.4+/-0.5 mm and 22+/-14 ms, respectively), total isovolumic time shortened (by 3+/-3 s/min) and cardiac output increased (by 5.1+/-1.8 l/min, all P<0.01). Changes in total isovolumic time and duration of post-ejection shortening with stress were independent predictors of the increase in peak cardiac output after revascularisation (total R(2)=0.69). Independent predictors of changes in total isovolumic time with stress were those in QRS duration and the duration of post-ejection shortening (total R(2)=0.75). In turn, changes in the duration of post-ejection shortening were closely associated with alterations in the delay in long axis shortening (r(2)=0.50) which correlated with changes in QRS duration (r(2)=0.59, all P<0.001). CONCLUSIONS: Revascularisation resynchronises left ventricular wall motion by restoring the normal activation response to stress, thereby reducing total isovolumic time and normalising peak cardiac output response to stress.

Aged↗
PubMed2003

The effect of the Q wave infarct on left ventricular electromechanical function.

OBJECTIVE: To assess the nature of left ventricular (LV) electrical and mechanical dysfunction in Q compared to non-Q anterior myocardial infarction (MI). SUBJECTS: We used ECG and echocardiography to study 54 unselected patients, age 57+/-15 years, 32 male, with old (>6 months after) anterior MI (39 Q and 15 non-Q), confirmed by enzyme rise and regional wall motion abnormality, and compared them with 21 normals of similar age. METHODS: Analysis of resting LV minor and long axis function and 12-lead surface electrocardiogram. RESULTS: Only 10% of normals did not have a normal septal Q wave compared with 46% of non-Q wave MI and 84% Q wave MI (P<0.001). All patients with Q wave MI had a scarred anteroseptal wall but none of the non-Q wave MI. LV minor axis dimensions were increased only with Q wave MI: 6.0 +/- 0.9 vs. 4.9 +/- 0.5 cm at end-diastole and 4.5 +/- 1.1 vs. 3.3 +/- 0.5 cm at end-systole and fractional shortening was reduced 27 +/- 8 vs. 33 +/- 3% (P<0.001 for all). Total left ventricular long axis amplitude of motion was reduced at the left, septal and posterior sites only in Q wave MI but was not different from controls in non-Q wave MI. The onset of long axis shortening was delayed by 20 ms at the left and septal sites in non-Q wave MI and by an additional 20 ms at the three sites in Q wave MI. Peak long axis shortening rate was reduced in the two patient groups, with the same distribution as post-ejection shortening (greater than 1 mm), which occurred in 21% of patients with non-Q wave MI and 76% of patients with Q wave MI (P<0.001). In diastole, the onset of long axis lengthening was delayed by 20 ms at the left and septal sites in non-Q wave MI and at the three sites in Q wave MI (P<0.001). Peak long axis lengthening rate was reduced with a similar distribution in the two patient groups. CONCLUSION: Patients with Q wave MI have an increased LV dimension and reduced FS, whereas patients with non-Q wave MI appear to have morphologically normal LV minor axis dimensions and fractional shortening apart from the anterior wall hypokinesis. In the latter, however, long axis function shows significant systolic and diastolic disturbances affecting the anteroseptal and lateral walls. The absence of conduction disturbances in non-Q wave MI suggests intrinsic myocardial dysfunction that may be reversible.

Adult↗
PubMed2002

Beta-blocker therapy for dynamic left-ventricular outflow tract obstruction.

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.

Adrenergic beta-Antagonists↗