Introduction: Functional assessment of the pulmonary vasculature is an important tool in the diagnosis of pulmonary hypertension. The effect of adenosine on pulmonary haemodynamics in left heart disease is not well understood
Methods: Right heart catheterisation was performed in eight subjects with mean PA pressure (mPAP) >25 mm Hg. In four subjects this was due to scleroderma (SCL) whilst four patients had heart failure with normal ejection fraction (HFNEF) defined by a pulmonary capillary wedge pressure (PCWP, mm Hg) >18 mm Hg and an ejection fraction >50%. Invasive haemodynamic measures were obtained before and during an adenosine infusion (140 mcg/kg/mins)
Results: Four SCL patients had a mean age of 58 ± 13 years, all were female and none were on pulmonary vasodilator therapy. Four HFNEF patients had a mean age of 62 ± 8 years, all were female and were receiving systemic antihypertensive therapy. The four patients with HFNEF all had LV end diastolic pressure >18 mm Hg (mean 21.5 ± 4.2 mm Hg). The effect of adenosine on pulmonary haemodynamics is summarised in the table: in patients with SCL, adenosine infusion resulted in a significant decrease in PVR in both groups, and an increase in CO in HFNEF patients. Despite the reduction in PVR, there was a trend to increased mPAP in HFNEF patients
Conclusions: Adenosine is an effective pulmonary vasodilator. Further study is required to elucidate whether the effect on pulmonary arterial and wedge pressures may vary with the etiology of pulmonary hypertension.
Tabled
1
| SCL pre | SCL adenosine | HFNEF pre | HFNEF adenosine | |
|---|---|---|---|---|
| mPAP | 47.5 ± 12.9 | 45.3 ± 10.2 | 27.8 ± 5.9 | 30.3 ± 3.7 |
| PCWP | 15.3 ± 6.6 | 16.8 ± 6.6 | 18.2 ± 6.2 | 20.0 ± 5.0 |
| CO | 5.9 ± 1.7 | 8.1 ± 4.4 | 6.2 ± 1.5 | 10.1 ± 2.3 |
| PVR | 5.8 ± 2.3 | 4.2 ± 2.3 | 1.6 ± 0.6 | 1.1 ± 0.4 |
* p < 0.05 for paired t-test comparison with pre adenosine.
† p < 0.01 for paired t-test comparison with pre adenosine.
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© 2011 Published by Elsevier Inc.
