Pulmonary transit of agitated contrast is associated with enhanced pulmonary vascular reserve and right ventricular function during exercise.
Pulmonary transit of agitated contrast (PTAC) occurs to variable extents during exercise. We tested the hypothesis that the onset of PTAC signifies flow through larger-caliber vessels, resulting in improved pulmonary vascular reserve during exercise. Forty athletes and fifteen nonathletes performed maximal exercise with continuous echocardiographic Doppler measures [cardiac output (CO), pulmonary artery systolic pressure (PASP), and myocardial velocities] and invasive blood pressure (BP). Arterial gases and B-type natriuretic peptide (BNP) were measured at baseline and peak exercise. Pulmonary vascular resistance (PVR) was determined as the regression of PASP/CO and was compared according to athletic and PTAC status. At peak exercise, athletes had greater CO (16.0 ± 2.9 vs. 12.4 ± 3.2 l/min, P < 0.001) and higher PASP (60.8 ± 12.6 vs. 47.0 ± 6.5 mmHg, P < 0.001), but PVR was similar to nonathletes (P = 0.71). High PTAC (defined by contrast filling of the left ventricle) occurred in a similar proportion of athletes and nonathletes (18/40 vs. 10/15, P = 0.35) and was associated with higher peak-exercise CO (16.1 ± 3.4 vs. 13.9 ± 2.9 l/min, P = 0.010), lower PASP (52.3 ± 9.8 vs. 62.6 ± 13.7 mmHg, P = 0.003), and 37% lower PVR (P < 0.0001) relative to low PTAC. Right ventricular (RV) myocardial velocities increased more and BNP increased less in high vs. low PTAC subjects. On multivariate analysis, maximal oxygen consumption (VO(2max)) (P = 0.009) and maximal exercise output (P = 0.049) were greater in high PTAC subjects. An exercise-induced decrease in arterial oxygen saturation (98.0 ± 0.4 vs. 96.7 ± 1.4%, P < 0.0001) was not influenced by PTAC status (P = 0.96). Increased PTAC during exercise is a marker of pulmonary vascular reserve reflected by greater flow, reduced PVR, and enhanced RV function.
La Gerche
André
A
Department of Medicine, St. Vincent's Hospital, University of Melbourne, Melbourne, Australia. Andre.LaGerche@svhm.org.au
MacIsaac
Andrew I
AI
Burns
Andrew T
AT
Mooney
Don J
DJ
Inder
Warrick J
WJ
Voigt
Jens-Uwe
JU
Heidbüchel
Hein
H
Prior
David L
DL
D000222:Adaptation, Physiological; D000328:Adult; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D002302:Cardiac Output; D003287:Contrast Media / Q000378:metabolism; D015150:Echocardiography, Doppler; D018618:Echocardiography, Doppler, Color; D018619:Echocardiography, Doppler, Pulsed; D015444:Exercise; D005780:Gelatin / Q000097:blood; D006352:Heart Ventricles / Q000000981:diagnostic imaging*; D006439:Hemodynamics; D006801:Humans; D008168:Lung / Q000098:blood supply*; D045423:Microbubbles; D009200:Myocardial Contraction; D020097:Natriuretic Peptide, Brain / Q000097:blood; D010100:Oxygen / Q000097:blood; D010101:Oxygen Consumption; D010313:Partial Pressure; D010807:Physical Endurance; D011237:Predictive Value of Tests; D011652:Pulmonary Circulation; D013386:Succinates / Q000097:blood; D014655:Vascular Resistance; D016278:Ventricular Function, Right
D015415:Biomarkers; D003287:Contrast Media; D013386:Succinates; D020097:Natriuretic Peptide, Brain; C060085:succinylated gelatin; D005780:Gelatin; D010100:Oxygen