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Hemodynamic Evaluation of Severe Tricuspid Regurgitation
Journal of the American College of Cardiology Ó 2013 by the American College of Cardiology Foundation Published by Elsevier Inc.
Vol. 62, No. 20, 2013 ISSN 0735-1097/$36.00 http://dx.doi.org/10.1016/j.jacc.2013.05.100
IMAGES IN CARDIOLOGY
Hemodynamic Evaluation of Severe Tricuspid Regurgitation Jeffrey B. Geske, MD,* Dawn C. Scantlebury, MBBS,* James D. Thomas, MD,y Rick A. Nishimura, MD* Rochester, Minnesota; and Cleveland, Ohio
From the *Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota; and the yDepartment of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio. Manuscript received March 6, 2013; revised manuscript received May 4, 2013, accepted May 14, 2013.
n 83-year-old woman with rheumatic heart disease presented with 1 year of progressive right heart failure following pacemaker implantation. Transthoracic echocardiography demonstrated severe tricuspid regurgitation (TR) with pacemaker lead impingement and incomplete leaflet coaptation (A, Online Videos 1 and 2), further investigated with simultaneous transthoracic echocardiography and high-fidelity micromanometer-tipped right heart catheterization. Simultaneous right atrial (RA, blue) and right ventricular (RV, red) pressures revealed a large V-wave and near equalization of pressures (B). The peak regurgitant velocity (vTR) was 1.6 m/s by continuous-wave Doppler, with conventional echocardiographic estimation of RV systolic pressure (RVSP) of 30 mm Hg. However, the true invasive RVSP was 52 mm Hg. A “V-wave cutoff sign” (C, arrowheads) was present, indicative of a rapid rise of RA pressure. Hepatic vein interrogation using pulse-wave Doppler (D) and color M-mode (E) mirrored RA pressure (blue). Echocardiographic RVSP is the summation of Doppler-derived tricuspid pressure gradient and mean RA pressure from inferior vena cava interrogation. In this case, even with RA pressure estimation of 20 mm Hg, echocardiography underestimated the true RVSP. Comparison of the true RA pressure (B, blue) with a hypothetical RA trace without a large V-wave (green) revealed significantly discrepant pressure differences. With a prominent V-wave, RA pressure is dynamic, invalidating static noninvasive estimates. Additionally, with severe TR and broad, laminar flow, Doppler-derived RVSP via the simplified Bernoulli equation may inaccurately represent true pressures because the inertial component of the Bernoulli equation cannot be neglected (1). Comparison of simultaneous RV-RA pressure difference and 4vTR2 (F) demonstrated a lag in the 4v2-derived pressure curve due to the need to accelerate a large mass of blood across the tricuspid valve. Waveform contour and hepatic vein interrogation remain essential echocardiographic tools in noninvasive hemodynamic evaluation of severe TR.
A
REFERENCE
1. Firstenberg MS, Vandervoort PM, Greenberg NL, et al. Noninvasive estimation of transmitral pressure drop across the normal mitral valve in humans:
importance of convective and inertial forces during left ventricular filling. J Am Coll Cardiol 2000;36: 1942–9.
Vol. 62, No. 20, 2013 ISSN 0735-1097/$36.00 http://dx.doi.org/10.1016/j.jacc.2013.05.100
IMAGES IN CARDIOLOGY
Hemodynamic Evaluation of Severe Tricuspid Regurgitation Jeffrey B. Geske, MD,* Dawn C. Scantlebury, MBBS,* James D. Thomas, MD,y Rick A. Nishimura, MD* Rochester, Minnesota; and Cleveland, Ohio
From the *Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, Rochester, Minnesota; and the yDepartment of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio. Manuscript received March 6, 2013; revised manuscript received May 4, 2013, accepted May 14, 2013.
n 83-year-old woman with rheumatic heart disease presented with 1 year of progressive right heart failure following pacemaker implantation. Transthoracic echocardiography demonstrated severe tricuspid regurgitation (TR) with pacemaker lead impingement and incomplete leaflet coaptation (A, Online Videos 1 and 2), further investigated with simultaneous transthoracic echocardiography and high-fidelity micromanometer-tipped right heart catheterization. Simultaneous right atrial (RA, blue) and right ventricular (RV, red) pressures revealed a large V-wave and near equalization of pressures (B). The peak regurgitant velocity (vTR) was 1.6 m/s by continuous-wave Doppler, with conventional echocardiographic estimation of RV systolic pressure (RVSP) of 30 mm Hg. However, the true invasive RVSP was 52 mm Hg. A “V-wave cutoff sign” (C, arrowheads) was present, indicative of a rapid rise of RA pressure. Hepatic vein interrogation using pulse-wave Doppler (D) and color M-mode (E) mirrored RA pressure (blue). Echocardiographic RVSP is the summation of Doppler-derived tricuspid pressure gradient and mean RA pressure from inferior vena cava interrogation. In this case, even with RA pressure estimation of 20 mm Hg, echocardiography underestimated the true RVSP. Comparison of the true RA pressure (B, blue) with a hypothetical RA trace without a large V-wave (green) revealed significantly discrepant pressure differences. With a prominent V-wave, RA pressure is dynamic, invalidating static noninvasive estimates. Additionally, with severe TR and broad, laminar flow, Doppler-derived RVSP via the simplified Bernoulli equation may inaccurately represent true pressures because the inertial component of the Bernoulli equation cannot be neglected (1). Comparison of simultaneous RV-RA pressure difference and 4vTR2 (F) demonstrated a lag in the 4v2-derived pressure curve due to the need to accelerate a large mass of blood across the tricuspid valve. Waveform contour and hepatic vein interrogation remain essential echocardiographic tools in noninvasive hemodynamic evaluation of severe TR.
A
REFERENCE
1. Firstenberg MS, Vandervoort PM, Greenberg NL, et al. Noninvasive estimation of transmitral pressure drop across the normal mitral valve in humans:
importance of convective and inertial forces during left ventricular filling. J Am Coll Cardiol 2000;36: 1942–9.