Abstract
Purpose: Pulmonary hypertension (PH) is associated with a poor prognosis regardless of aetiology. Reduced pulmonary vascular capacitance, in addition to increased resistance, may be an important determinant of pulmonary afterload and thus increasing pulmonary pressure. Methods: Subjects referred for diagnostic right heart catheterisation with suspected PH underwent assessment of pulmonary haemodynamics pre- and post-IV adenosine using a pressure and temperature-sensing guidewire (PressureWire) positioned in a second order branch pulmonary artery (PA) providing high fidelity pressure measurement and thermodilution derived mean transit time (Tmn). Capacitance index (CI, mL/mmHg) was defined as 1000/(heart rate × PA pulse pressure × Tmn). Diastolic dysfunction (DD) was defined as LVEDP greater than 18 mmHg and PH as mean PA pressure greater than 25 mmHg. Results: Thirty-one consecutive patients were analysed: 10 with pulmonary arterial hypertension (PAH, either primary or secondary to scleroderma), six had DD with PH, seven had both scleroderma and DD, four had mitral valve disease and four were normal. Adenosine infusion resulted in decreased Tmn (0.47 ± 0.05 vs 0.33 ± 0.03, p < 0.001) and increased CI (1.79 ± 0.28 vs 2.33 ± 0.3, p < 0.005), but no change in heart rate nor mean PA pressure. Higher PA pressure was associated with lower CI, both pre adenosine (r = −0.62, p < 0.003) and post adenosine (r = −0.54, p < 0.003). Conclusion: Capacitance index is reduced with increasing severity of PH and to a greater extent in patients with PAH than those with DD. This novel index may have utility in early diagnosis and tracking subtle changes in haemodynamics in patients with PH.
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