1791
Association of pulmonary transit time by CMR with diastolic dysfunction and left ventricle deformation in restrictive cardiomyopathy
Yue Gao1, Yuan Li1, and Zhi-Gang Yang1
1west china hospital, chengdu, China
1west china hospital, chengdu, China
Synopsis
Keywords: Myocardium, Cardiovascular
Motivation: Cardiopulmonary circulation usually present hemodynamic congestion in RCM patients. Pulmonary transit time (PTT) and pulmonary blood volume index (PBVi) are physiological parameters reflective of cardiopulmonary hemodynamics statue.
Goal(s): Evaluate the PTT and PBVi in RCM patients, and evaluated the association with LV function and deformation.
Approach: The images of first-pass perfusion were acquired to assess PTT which was normalized to heart rate. PBVi was measured by the product of PTT and RVSV and indexed to BSA.
Results: PTT showed independent association with LVEF and LVMVR, as well as with LV GCPS and GLPS; PBVi was an independent association of LVMI and LV GRPS.
Impact: PTTc and PBVi as the non-invasive marker of cardiopulmonary hemodynamics in patients with RCM, and reflects progression of diastolic dysfunction, and impaired LV global deformation. PTT and PBVI may provide additional information for prognostic management and clinical decision making.
Introduction
RCM patients have a stiff LV with impaired diastolic filling and high filling pressures, which commonly induce pulmonary hypertension and tend to exacerbate heart failure (HF). For RCM patients the cardiopulmonary circulation usually presents hemodynamic congestion. Pulmonary transit time (PTT) and pulmonary blood volume index (PBVi) are physiological parameters reflective of cardiopulmonary hemodynamics status and have been considered to be related to cardiac dysfunction, pulmonary hypertension, and heart failure in previous studies. However, the relationship between PTT and PBVi and diastolic dysfunction in RCM remains unclear. In this study, we aimed to assess the PTT and PBVi in RCM patients, to determine whether PTT and PBVi reflect diastolic dysfunction and evaluated the association with LV function and deformation.
Methods:
One hundred thirty-seven RCM patients and 66 control subjects who underwent echocardiography and contrast-enhanced CMR(Trio Tim, Siemens Medical Solutions, Erlangen, Germany) were included. A comprehensive echocardiographic assessment of LV diastolic function. The dynamic images of first-pass perfusion were acquired to assess peak-to-peak PTT which was subsequently normalized to RR interval duration. PBV was measured by the product of PTT and the anterograde RVSV, and indexed to body surface area. The determinant of reduced LV global peak strain for all RCM patients was assessed using multivariable linear regression analyses.
Results:
PTT and PBVi were significantly higher in patients with RCM than in controls (8.85±2.71 vs. 6.03±1.39 sec, P<0.001; 257.91[179.65,340.94] vs. 218±70.63 mL/m2, P<0.001, respectively). PTT showed positive correlation with E/A ratio (r = 0.271, P = 0.00), PTT showed positive correlation with E/e’ ratio, E/A ratio and diastolic stage (r = 0.214, P = 0.012; r = 0.314, P <0.001; r = 0.195, P = 0.022; respectively). In multivariable analysis, PTTc showed independent association with LVEF and LVMVR (β = 0.472, 0.270, p = 0.001), as well as with LV GCPS (β = 0.299, p=0.001) and LV GLPS (β = 0.328, p < 0.001); PBVi was an independent association of LVMI (β = 0.283, p=0.001) and LV GRPS (β = -0.148, p=0.049).
Conclusion:
For patients with RCM, PTTc and PBVi as the non-invasive quantitative surrogate marker, is associated with diastolic dysfunction degree. The increase of PTTc and PBVi likely reflects impaired LV function and deformation, which may provide additional information for prognostic management and clinical decision-making in patients with RCM.
RCM patients have a stiff LV with impaired diastolic filling and high filling pressures, which commonly induce pulmonary hypertension and tend to exacerbate heart failure (HF). For RCM patients the cardiopulmonary circulation usually presents hemodynamic congestion. Pulmonary transit time (PTT) and pulmonary blood volume index (PBVi) are physiological parameters reflective of cardiopulmonary hemodynamics status and have been considered to be related to cardiac dysfunction, pulmonary hypertension, and heart failure in previous studies. However, the relationship between PTT and PBVi and diastolic dysfunction in RCM remains unclear. In this study, we aimed to assess the PTT and PBVi in RCM patients, to determine whether PTT and PBVi reflect diastolic dysfunction and evaluated the association with LV function and deformation.
Methods:
One hundred thirty-seven RCM patients and 66 control subjects who underwent echocardiography and contrast-enhanced CMR(Trio Tim, Siemens Medical Solutions, Erlangen, Germany) were included. A comprehensive echocardiographic assessment of LV diastolic function. The dynamic images of first-pass perfusion were acquired to assess peak-to-peak PTT which was subsequently normalized to RR interval duration. PBV was measured by the product of PTT and the anterograde RVSV, and indexed to body surface area. The determinant of reduced LV global peak strain for all RCM patients was assessed using multivariable linear regression analyses.
Results:
PTT and PBVi were significantly higher in patients with RCM than in controls (8.85±2.71 vs. 6.03±1.39 sec, P<0.001; 257.91[179.65,340.94] vs. 218±70.63 mL/m2, P<0.001, respectively). PTT showed positive correlation with E/A ratio (r = 0.271, P = 0.00), PTT showed positive correlation with E/e’ ratio, E/A ratio and diastolic stage (r = 0.214, P = 0.012; r = 0.314, P <0.001; r = 0.195, P = 0.022; respectively). In multivariable analysis, PTTc showed independent association with LVEF and LVMVR (β = 0.472, 0.270, p = 0.001), as well as with LV GCPS (β = 0.299, p=0.001) and LV GLPS (β = 0.328, p < 0.001); PBVi was an independent association of LVMI (β = 0.283, p=0.001) and LV GRPS (β = -0.148, p=0.049).
Conclusion:
For patients with RCM, PTTc and PBVi as the non-invasive quantitative surrogate marker, is associated with diastolic dysfunction degree. The increase of PTTc and PBVi likely reflects impaired LV function and deformation, which may provide additional information for prognostic management and clinical decision-making in patients with RCM.
Acknowledgements
Not applicable.References
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Figures
Calculation
of pulmonary transit time.(a1-4)
49-years-old RCM patient with the PTT value of 6.9s, and LV GPLS value of -9.4%;
(bB1-4) 54-years-old RCM patient with the PTT value of 12.2s, and LV GPLS value
of -4.5%.
DOI: https://doi.org/10.58530/2024/1791