Search PubMed⌕ Search

Biomedical subjects

William D Anderson

Publications and source records attributed to William D Anderson.

8 recordsLinked to original sources

Effect of acute increases in pulmonary vascular pressures on exercise pulmonary gas exchange.

The purpose of this study was to determine the effect of acute increases in pulmonary vascular pressures, caused by the application of lower-body positive pressure (LBPP), on exercise alveolar-to-arterial PO2 difference (A-aDO2), anatomical intrapulmonary (IP) shunt recruitment, and ventilation. Eight healthy men performed graded upright cycling to 90% maximal oxygen uptake under normal conditions and with 52 Torr (1 psi) of LBPP. Pulmonary arterial (PAP) and pulmonary artery wedge pressures (PAWP) were measured with a Swan-Ganz catheter. Arterial blood samples were obtained from a radial artery catheter, cardiac output was calculated by the direct Fick method, and anatomical IP shunt was determined by administering agitated saline during continuous two-dimensional echocardiography. LBPP increased both PAP and PAWP while upright at rest, and at all points during exercise (mean increase in PAP and PAWP 3.7 and 4.0 mmHg, respectively, P<0.05). There were no differences in exercise oxygen uptake or cardiac output between control and LBPP. Despite the increased PAP and PAWP with LBPP, A-aDO2 was not affected. In the upright resting position, there was no evidence of shunt in the control condition, whereas LBPP caused shunt in one subject. At the lowest exercise workload (75 W), shunt occurred in three subjects during control and in four subjects with LBPP. LBPP did not affect IP shunt recruitment during subsequent higher workloads. Minute ventilation and arterial PcO2 were not consistently affected by LBPP. Therefore, small acute increases in pulmonary vascular pressures do not widen exercise A-aDO2 or consistently affect IP shunt recruitment or ventilation.

Adult↗

Does fitness level modulate the cardiovascular hemodynamic response to exercise?

Subjects with greater aerobic fitness demonstrate better diastolic compliance at rest, but whether fitness modulates exercise cardiac compliance and cardiac filling pressures remains to be determined. On the basis of maximal oxygen consumption (VO2max), healthy male subjects were categorized into either low (LO: VO2max=43+/-6 ml.kg-1.min-1; n=3) or high (HI: VO2max=60+/-3 ml.kg-1.min-1; n=5) aerobic power. Subjects performed incremental cycle exercise to 90% Vo(2max). Right atrial (RAP) and pulmonary artery wedge (PAWP) pressures were measured, and left ventricular (LV) transmural filling pressure (TMFP=PAWP-RAP) was calculated. Cardiac output (CO) and stroke volume (SV) were determined by direct Fick, and LV end-diastolic volume (EDV) was estimated from echocardiographic fractional area change and Fick SV. There were no between-group differences for any measure at rest. At a submaximal workload of 150 W, PAWP and TMFP were higher (P<0.05) in LO compared with HI (12 vs. 8 mmHg, and 9 vs. 4 mmHg, respectively). At peak exercise, CO, SV, and EDV were lower in LO (P<0.05). RAP was not different at peak exercise, but PAWP (23 vs. 15 mmHg) and TMFP (12 vs. 6 mmHg) were higher in LO (P<0.05). Compared with less fit subjects, subjects with greater aerobic fitness demonstrated lower LV filling pressures during exercise, whereas SV and EDV were either similar (submaximal exercise) or higher (peak exercise), suggesting superior diastolic function and compliance.

Adult↗

Effect of statin therapy prior to elective percutaneous coronary intervention on frequency of periprocedural myocardial injury.

This study evaluated whether pretreatment with statins was associated with a decreased incidence of periprocedural myocardial injury. Periprocedural myocardial injury occurs after percutaneous coronary intervention (PCI) and is associated with adverse outcomes. The pleiotropic properties of statins stabilize plaque and decrease the inflammatory milieu of atherosclerotic lesions. Accordingly, we hypothesized that preprocedural statin therapy would decrease periprocedural myocardial injury. We enrolled 425 patients who underwent successful PCI. The control arm (n = 150) included patients not on statin therapy at the time of PCI, and the statin arm (n = 275) included patients who were taking statin medication before PCI. All patients had serial enzymes measured, including creatine kinase (CK), CK-MB, and troponin I. The incidence of increased levels of CK and CK-MB >3 times normal and the absolute increase in CK and troponin I were compared between groups. The control arm had significantly higher periprocedural levels of CK. In the control group, 6% of patients had CK increases >3 times the upper limit of normal compared with 1.8% in the statin group (p = 0.02). The control arm had a higher frequency of CK-MB increases >3 times the upper limit of normal (7.3% vs 2.2%, p = 0.01). There was a trend toward higher levels of troponin I in the control group (3.21 vs 1.85 ng/ml, p = 0.06). Thus, statin therapy before elective PCI was associated with lower levels of periprocedural CK.

Aged↗

Intra-pulmonary shunt and pulmonary gas exchange during exercise in humans.

In young, healthy people the alveolar-arterial P(O(2)) difference (A-aDO(2)) is small at rest, but frequently increases during exercise. Previously, investigators have focused on ventilation/perfusion mismatch and diffusion abnormalities to explain the impairment in gas exchange, as significant physiological intra-pulmonary shunt has not been found. The aim of this study was to use a non-gas exchange method to determine if anatomical intra-pulmonary (I-P) shunts develop during exercise, and, if so, whether there is a relationship between shunt and increased A-aDO(2). Healthy male participants performed graded upright cycling to 90% while pulmonary arterial (PAP) and pulmonary artery wedge pressures were measured. Blood samples were obtained from the radial artery, cardiac output was calculated by the direct Fick method and I-P shunt was determined by administering agitated saline during continuous 2-D echocardiography. A-aDO(2) progressively increased with exercise and was related to (r = 0.86) and PAP (r = 0.75). No evidence of I-P shunt was found at rest in the upright position; however, 7 of 8 subjects developed I-P shunts during exercise. In these subjects, point bi-serial correlations indicated that I-P shunts were related to the increased A-aDO(2) (r = 0.68), (r = 0.76) and PAP (r = 0.73). During exercise, intra-pulmonary shunt always occurred when A-aDO(2) exceeded 12 mmHg and was greater than 24 l min(-1). These results indicate that anatomical I-P shunts develop during exercise and we suggest that shunt recruitment may contribute to the widened A-aDO(2) during exercise.

Adult↗

Effects of prolonged exercise to exhaustion on left-ventricular function and pulmonary gas exchange.

The purpose of this study was to simultaneously examine left-ventricular (LV) function and pulmonary gas exchange during prolonged constant-rate cycling in an attempt to explain the exercise-induced impairment in gas exchange. Eleven competitive cyclists rode their racing bicycles on a computerized cycle trainer at 25 W below the lactate threshold until exhaustion (exercise time = 2.51 +/- 0.86 h). LV systolic function was evaluated with two-dimensional echocardiography while arterial blood gases were used to assess pulmonary gas exchange. All variables were assessed concurrently before, during, and after exercise. LV function and cardiac output increased at the onset of exercise and were maintained until exhaustion. The alveolar-arterial P(O(2)) difference (A-a D(O(2))) increased within 15 min of the onset of exercise, was unchanged through to exhaustion, and returned to baseline 5 min post-exercise. Gas exchange was not related to cardiovascular function at the onset, or at end exercise. The results indicate that the widening A-aD(O(2)) during exercise is due to a readily reversible change in gas exchange function.

Adult↗

Dermatofibrosarcoma protuberans of breast.

We describe the case of a 57-year-old woman with a tumor of the breast suspected of being a dermatofibrosarcoma protuberans (DFSP). To confirm the diagnosis, molecular studies were performed on fixed tumor and revealed the presence of the fusion product of the COL1A1-PDGFB genes characteristic of DFSP.

Breast Neoplasms↗