Dobutamine Stress Echocardiography for the Assessment of Pressure-Flow Relationships of the Pulmonary Circulation
What is the relationship between dobutamine infusion and pulmonary artery flow and pressure in patients with pulmonary arterial hypertension (PAH) and normal healthy controls?
Dobutamine stress echocardiography (DSE) at doses of 5, 10, 15, and 20 µg/kg/min was performed in 16 patients with PAH and 22 healthy control subjects. Additionally, data from 22 different healthy control subjects who had undergone supine bicycle stress echocardiography were compared for the effect on pulmonary flow and pressure. Mean pulmonary artery pressure (mPpa) was calculated as 0.6 x systolic Ppa +2. Forward flow (Q) was calculated from the time velocity integral of the left ventricular outflow tract and left ventricular outflow diameter. Pulmonary vascular resistance (PVR) was calculated as mPpa/Q. The pulmonary vascular distensibility coefficient (α), defined as percentage change in diameter per mm Hg increase in transmural pressure, was also calculated.
The control subjects undergoing DSE and exercise stress were statically identical in age and other features. For patients with PAH, systolic Ppa at rest was 73 ± 17 mm Hg, mean Ppa 46 ± 11 mm Hg, pulmonary arterial wedge 8 ± 5 mm Hg, and mean right arterial pressure 9 ± 5 mm Hg. All PAH patients were on active therapy directed at PAH at the time of investigation. Etiology of PAH included idiopathic (n = 6), connective tissue disease (n = 0), and portopulmonary hypertension (n = 1). Peak dobutamine dose was similar for controls and PAH patients. mPpa at rest was 50 ± 14 and rose to 67 ± 18 mm Hg in PAH patients, and was 15 ± 3 rising to 20 ± 4 for control subjects (both p < 0.0001). Resting Q was 4.6 ± 1.1 in PAH and 4.9 ± 0.6 for control subjects (p = 0.12), and rose to 8.2 ± 2.0 and 9.7 ± 2.1 mm Hg/L/min, respectively (p < 0.0001). The slope of the mPpa-Q relationship in control subjects was 1.1 ± 0.7 mm Hg/L/min, and was 5.1 ± 2.5 mm Hg/L/min in PAH (p < 0.001). The distensibility coefficient α was reduced in PAH compared with control subjects (0.003 ± 0.001 mm Hg vs. 0.02 ± 0.01 mm Hg, p < 0.001). PAH patients in functional class III or IV had lower mPpa-Q slopes compared to those with functional class I or II (3.7 ± 1.2 mm Hg/L/min vs. 6.5 ± 2.5 mm Hg/L/min, p = 0.1). Within the control subjects, exercise stress resulted in a greater maximum flow than DSE (17.7 ± 3.7 L/min vs. 9.7 ± 2.1 L/min, p < 0.001) and a steeper slope of the mPpa-Q relationship (1.6 ± 0.7 vs 1.1 ± 0.7 mm Hg/L/min, p = 0.03). After limiting the range of maximum flow to values equivalent to those seen with DSE in normal controls, the exercise mPpa-Q slope was 2.2 ± 1.7 mm Hg/L/min (p = 0.06 vs. DSE).
The authors concluded that a noninvasive assessment of mPpa-Q is feasible with DSE, and identifies specific pathophysiologic responses in PAH compared to normal controls.
Exercise-induced elevation in pulmonary pressures is well described in normal controls and in various disease states including PAH. The majority of data have been with exercise and have generally revealed steeper slopes of PA pressures at matched stages of exercise in PAH than in normal individuals. DSE has been less extensively evaluated and presents a number of unique challenges including a direct effect on the pulmonary vascular resistance of dobutamine, which predominately results in vasodilation. It should be noted, however, that the magnitude and nature of the effect of dobutamine on pulmonary vascular resistance may be dependent on the presence or absence of underlying disease and its impact on left ventricular hemodynamics. Limitation on the data presented here is that multiple etiologies of PAH were included in this study. A potential clinical utilization of DSE in pulmonary hypertension may include screening of patients at risk of ‘PAH’ or preclinical ‘PAH.’ Establishing an anticipated range of changes including mPpa-Q slopes will certainly be of clinical value. It should also be emphasized that for appropriate integration of these data, individuals must be free of left-sided heart disease, which under the stress of dobutamine, could alter downstream resistance and provide yet an additional drive for elevated PA pressures independent of a primary pulmonary vasculature problem.
Keywords: Connective Tissue Diseases, Heart Diseases, Pulmonary Circulation, Dobutamine, Vasodilation, Arterial Pressure, Echocardiography, Stress, Hypertension, Pulmonary, Vascular Resistance, Pulmonary Artery, Hemodynamics
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