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Chest. 2014 Oct;146(4):959-966. doi: 10.1378/chest.13-2300.

Dobutamine stress echocardiography for the assessment of pressure-flow relationships of the pulmonary circulation.

Author information

1
Discipline of Medicine, Sydney Medical School, University of Sydney, Sydney, NSW, Australia; Department of Respiratory Medicine, Royal Prince Alfred Hospital, Sydney, NSW, Australia; Department of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, Australia. Electronic address: edmundmtlau@gmail.com.
2
Department of Pathophysiology, Free University of Brussels, Brussels, Belgium.
3
Discipline of Medicine, Sydney Medical School, University of Sydney, Sydney, NSW, Australia; Department of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, Australia.
4
Department of Cardiology, Royal Prince Alfred Hospital, Sydney, NSW, Australia.
5
Discipline of Medicine, Sydney Medical School, University of Sydney, Sydney, NSW, Australia; Department of Respiratory Medicine, Royal Prince Alfred Hospital, Sydney, NSW, Australia.
6
Department of Cardiology, Second University of Naples, Naples, Italy.

Abstract

BACKGROUND:

Stress testing of the pulmonary circulation (via increasing pulmonary blood flow) can reveal abnormal mean pulmonary artery pressure-cardiac output (mPpa-Q) responses, which may facilitate early diagnosis of pulmonary vascular disease. We investigated the application of dobutamine stress echocardiography (DSE) for the noninvasive assessment of mPpa-Q relationships.

METHODS:

DSE using an incremental dose protocol (≤ 20 μg/kg/min) was performed in 38 subjects (16 patients with pulmonary arterial hypertension [PAH] and 22 healthy control subjects). An additional 22 healthy control subjects underwent exercise stress echocardiography as a comparator group. Multipoint mPpa-Q plots were analyzed, and the pulmonary vascular distensibility coefficient α was calculated.

RESULTS:

DSE was feasible and informative in 93% of subjects. The average dobutamine-induced mPpa-Q slope was 1.1 ± 0.7 mm Hg/L/min in healthy control subjects and 5.1 ± 2.5 mm Hg/L/min in patients with PAH (P < .001). The dobutamine-induced α was markedly reduced in patients with PAH (0.003 ± 0.001 mm Hg vs 0.02 ± 0.01 mm Hg in control subjects, P < .001). When exercise and dobutamine stress were compared in healthy control subjects, the exercise-induced mPpa-Q slope was modestly higher (1.6 ± 0.7 mm Hg/L/min, P = .03 vs dobutamine). In patients with PAH, lower functional class status was associated with lower dobutamine-induced mPpa-Q slopes (P = .014), but not with resting total pulmonary vascular resistance.

CONCLUSIONS:

Noninvasive assessment of mPpa-Q relationships is feasible with dobutamine stress. DSE may potentially be a useful noninvasive technique for stress testing of the pulmonary vasculature.

PMID:
24626933
DOI:
10.1378/chest.13-2300
[Indexed for MEDLINE]

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