Author + information
- Received July 18, 2011
- Revision received October 3, 2011
- Accepted November 1, 2011
- Published online April 1, 2012.
- Gerin R. Stevens, MD, PhD⁎,⁎ (, )
- Ana Garcia-Alvarez, MD, MSC‡,§∥,
- Sheila Sahni, MD†,
- Mario J. Garcia, MD⁎,
- Valentin Fuster, MD, PhD‡,§ and
- Javier Sanz, MD‡
- ↵⁎Reprint requests and correspondence:
Dr. Gerin R. Stevens, Center for Advanced Cardiac Therapy, Montefiore Medical Center, Greene Medical Arts Pavilion, 3400 Bainbridge Avenue, 7th Floor, Bronx, New York, New York 10467-2490
Objectives This study investigated whether right ventricular (RV) adaptation to chronic pressure overload is associated with pulmonary artery (PA) stiffness beyond the degree of severity of pulmonary hypertension (PH).
Background Increased PA stiffness has been associated with reduced survival in PH. The mechanisms for this association remain unclear.
Methods Right heart catheterization and cardiac magnetic resonance were performed within 1 week in 124 patients with known or suspected chronic PH. Pulmonary vascular resistance index (PVRI) and PA pressures were quantified from right heart catheterization. Cardiac magnetic resonance included standard biventricular cine sequences and main PA flow quantification with phase-contrast imaging. Indexes of PA stiffness (elasticity, distensibility, capacitance, stiffness index beta, and pulse pressure) were quantified combining right heart catheterization and cardiac magnetic resonance data. RV performance and adaptation were measured by RV ejection fraction, right ventricular mass index (RVMI), RV end-systolic volume index, and right ventricular stroke work index (RVSWI).
Results All indexes of PA stiffness were significantly correlated with measures of RV performance (Spearman rho coefficients ranging from −0.20 to 0.61, p < 0.05). Using multivariate regression analysis, PA elasticity, distensibility, and index beta were independently associated with all measures of RV performance after adjusting PVRI (p ≤ 0.024). PA capacitance was independently associated with RV ejection fraction, RVMI, and RVSWI (p < 0.05), whereas PA pulse pressure was associated with RVMI and RVSWI (p ≤ 0.027). Compared with PVRI, PA elasticity, distensibility, capacitance, and index beta explained 15% to 68% of the variability in RV ejection fraction, RVMI, and RV end-systolic volume index. Relative contributions of PA stiffness for RVSWI were 1.2× to 18.0× higher than those of PVRI.
Conclusions PA stiffness is independently associated with the degree of RV dysfunction, dilation, and hypertrophy in PH. RV adaptation to chronic pressure overload is related not only to the levels of vascular resistance (steady afterload), but also to PA stiffness (pulsatile load).
- cardiac magnetic resonance
- pulmonary artery stiffness
- pulmonary hypertension
- right ventricular function
All authors have reported that they have no relationships relevant to the contents of this paper to disclose. Jeroen J. Bax, MD, PhD, served as Guest Editor for this paper.
- Received July 18, 2011.
- Revision received October 3, 2011.
- Accepted November 1, 2011.
- American College of Cardiology Foundation