Nora Ngai
Stony Brook University
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Featured researches published by Nora Ngai.
Journal of Magnetic Resonance Imaging | 2011
Jie J Cao; Yi Wang; William Schapiro; Jeannette McLaughlin; Joshua Cheng; Michael Passick; Nora Ngai; Philip Marcus; Nathaniel Reichek
To evaluate the performance of lung perfusion imaging using two‐dimensional (2D) first pass perfusion MRI and a quantitation program based on model‐independent deconvolution algorithm.
Circulation-cardiovascular Imaging | 2012
Jie J Cao; Yi Wang; Jeannette McLaughlin; Peter Rhee; Michael Passick; Nora Ngai; Joshua Cheng; Ronald J. Gulotta; Andrew D. Berke; George A. Petrossian; Nathaniel Reichek
Background—Cardiac hemodynamics affect pulmonary vascular pressure and flow, but little is known of the effects of hemodynamics on lung perfusion at the tissue level. We sought to investigate the relationship between hemodynamic abnormalities in patients with left heart failure and global and regional lung perfusion using lung perfusion quantification by magnetic resonance imaging. Methods and Results—Lung perfusion was quantified in 10 normal subjects and 28 patients undergoing clinically indicated left and right heart catheterization and same day research cardiac magnetic resonance imaging. A total of 228 lung slices were evaluated. Global lung perfusion, determined as the average of 6 coronal lung slices through the anterior, mid, and posterior left and right lungs, was significantly lower in patients with reduced cardiac index (<2.5 L/min per m2): 94±30 mL/100 mL per minute versus 132±40 mL/100 mL per minute in those with preserved cardiac index (≥2.5 L/min per m2; P=0.003). The gravitational anterior to posterior perfusion gradient was inversely associated with left ventricular end-diastolic pressure (r=−0.728; P<0.001), resulting in a blunted perfusion gradient in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the perfusion reduction in posterior lung regions. In a multivariate regression analysis adjusting for all hemodynamic variables, altered lung perfusion gradient was most closely associated with increased mean pulmonary arterial pressure (P=0.016). Conclusions—Increased left ventricular filling pressure and the resultant increase in pulmonary arterial pressure are associated with disruption of the normal gravitational lung perfusion gradient. Our findings underscore the complexity of heart-lung interaction in determining pulmonary hemodynamics in left heart failure.Background— Cardiac hemodynamics affect pulmonary vascular pressure and flow, but little is known of the effects of hemodynamics on lung perfusion at the tissue level. We sought to investigate the relationship between hemodynamic abnormalities in patients with left heart failure and global and regional lung perfusion using lung perfusion quantification by magnetic resonance imaging. Methods and Results— Lung perfusion was quantified in 10 normal subjects and 28 patients undergoing clinically indicated left and right heart catheterization and same day research cardiac magnetic resonance imaging. A total of 228 lung slices were evaluated. Global lung perfusion, determined as the average of 6 coronal lung slices through the anterior, mid, and posterior left and right lungs, was significantly lower in patients with reduced cardiac index (<2.5 L/min per m2): 94±30 mL/100 mL per minute versus 132±40 mL/100 mL per minute in those with preserved cardiac index (≥2.5 L/min per m2; P =0.003). The gravitational anterior to posterior perfusion gradient was inversely associated with left ventricular end-diastolic pressure ( r =−0.728; P <0.001), resulting in a blunted perfusion gradient in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the perfusion reduction in posterior lung regions. In a multivariate regression analysis adjusting for all hemodynamic variables, altered lung perfusion gradient was most closely associated with increased mean pulmonary arterial pressure ( P =0.016). Conclusions— Increased left ventricular filling pressure and the resultant increase in pulmonary arterial pressure are associated with disruption of the normal gravitational lung perfusion gradient. Our findings underscore the complexity of heart-lung interaction in determining pulmonary hemodynamics in left heart failure.
Circulation-cardiovascular Imaging | 2012
Jie J Cao; Yi Wang; Jeannette McLaughlin; Peter Rhee; Michael Passick; Nora Ngai; Joshua Cheng; Ronald J. Gulotta; Andrew D. Berke; George A. Petrossian; Nathaniel Reichek
Background—Cardiac hemodynamics affect pulmonary vascular pressure and flow, but little is known of the effects of hemodynamics on lung perfusion at the tissue level. We sought to investigate the relationship between hemodynamic abnormalities in patients with left heart failure and global and regional lung perfusion using lung perfusion quantification by magnetic resonance imaging. Methods and Results—Lung perfusion was quantified in 10 normal subjects and 28 patients undergoing clinically indicated left and right heart catheterization and same day research cardiac magnetic resonance imaging. A total of 228 lung slices were evaluated. Global lung perfusion, determined as the average of 6 coronal lung slices through the anterior, mid, and posterior left and right lungs, was significantly lower in patients with reduced cardiac index (<2.5 L/min per m2): 94±30 mL/100 mL per minute versus 132±40 mL/100 mL per minute in those with preserved cardiac index (≥2.5 L/min per m2; P=0.003). The gravitational anterior to posterior perfusion gradient was inversely associated with left ventricular end-diastolic pressure (r=−0.728; P<0.001), resulting in a blunted perfusion gradient in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the perfusion reduction in posterior lung regions. In a multivariate regression analysis adjusting for all hemodynamic variables, altered lung perfusion gradient was most closely associated with increased mean pulmonary arterial pressure (P=0.016). Conclusions—Increased left ventricular filling pressure and the resultant increase in pulmonary arterial pressure are associated with disruption of the normal gravitational lung perfusion gradient. Our findings underscore the complexity of heart-lung interaction in determining pulmonary hemodynamics in left heart failure.Background— Cardiac hemodynamics affect pulmonary vascular pressure and flow, but little is known of the effects of hemodynamics on lung perfusion at the tissue level. We sought to investigate the relationship between hemodynamic abnormalities in patients with left heart failure and global and regional lung perfusion using lung perfusion quantification by magnetic resonance imaging. Methods and Results— Lung perfusion was quantified in 10 normal subjects and 28 patients undergoing clinically indicated left and right heart catheterization and same day research cardiac magnetic resonance imaging. A total of 228 lung slices were evaluated. Global lung perfusion, determined as the average of 6 coronal lung slices through the anterior, mid, and posterior left and right lungs, was significantly lower in patients with reduced cardiac index (<2.5 L/min per m2): 94±30 mL/100 mL per minute versus 132±40 mL/100 mL per minute in those with preserved cardiac index (≥2.5 L/min per m2; P =0.003). The gravitational anterior to posterior perfusion gradient was inversely associated with left ventricular end-diastolic pressure ( r =−0.728; P <0.001), resulting in a blunted perfusion gradient in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the perfusion reduction in posterior lung regions. In a multivariate regression analysis adjusting for all hemodynamic variables, altered lung perfusion gradient was most closely associated with increased mean pulmonary arterial pressure ( P =0.016). Conclusions— Increased left ventricular filling pressure and the resultant increase in pulmonary arterial pressure are associated with disruption of the normal gravitational lung perfusion gradient. Our findings underscore the complexity of heart-lung interaction in determining pulmonary hemodynamics in left heart failure.
Journal of Cardiovascular Magnetic Resonance | 2008
Mark J Goldman; Dipti Gupta; Suzanne White; William Schapiro; Nora Ngai; Michael Passick; Jing Han; Jie J Cao; Nathaniel Reichek
Methods We studied 218 (99 male, 119 female) normotensive, non-obese (BMI < 28), non-diabetic volunteers aged 20– 90 (mean 54 ± 15) with normal 2-D echocardiograms on a 1.5 T Siemens Sonata scanner. TrueFISP cine imaging was used to obtain contiguous 8 mm short axis slices of the entire RV at end-expiration. Volumetric analysis was performed using Medis MASS. RV volume at end-diastole and end-systole and RV mass were determined and indexed to body surface area (EDVi, ESVi, RVMi) including papillary muscles in the cavity volume.
Circulation-cardiovascular Imaging | 2012
Jie J Cao; Yi Wang; Jeannette McLaughlin; Peter Rhee; Michael Passick; Nora Ngai; Joshua Cheng; Ronald J. Gulotta; Andrew D. Berke; George A. Petrossian; Nathaniel Reichek
Background—Cardiac hemodynamics affect pulmonary vascular pressure and flow, but little is known of the effects of hemodynamics on lung perfusion at the tissue level. We sought to investigate the relationship between hemodynamic abnormalities in patients with left heart failure and global and regional lung perfusion using lung perfusion quantification by magnetic resonance imaging. Methods and Results—Lung perfusion was quantified in 10 normal subjects and 28 patients undergoing clinically indicated left and right heart catheterization and same day research cardiac magnetic resonance imaging. A total of 228 lung slices were evaluated. Global lung perfusion, determined as the average of 6 coronal lung slices through the anterior, mid, and posterior left and right lungs, was significantly lower in patients with reduced cardiac index (<2.5 L/min per m2): 94±30 mL/100 mL per minute versus 132±40 mL/100 mL per minute in those with preserved cardiac index (≥2.5 L/min per m2; P=0.003). The gravitational anterior to posterior perfusion gradient was inversely associated with left ventricular end-diastolic pressure (r=−0.728; P<0.001), resulting in a blunted perfusion gradient in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the perfusion reduction in posterior lung regions. In a multivariate regression analysis adjusting for all hemodynamic variables, altered lung perfusion gradient was most closely associated with increased mean pulmonary arterial pressure (P=0.016). Conclusions—Increased left ventricular filling pressure and the resultant increase in pulmonary arterial pressure are associated with disruption of the normal gravitational lung perfusion gradient. Our findings underscore the complexity of heart-lung interaction in determining pulmonary hemodynamics in left heart failure.Background— Cardiac hemodynamics affect pulmonary vascular pressure and flow, but little is known of the effects of hemodynamics on lung perfusion at the tissue level. We sought to investigate the relationship between hemodynamic abnormalities in patients with left heart failure and global and regional lung perfusion using lung perfusion quantification by magnetic resonance imaging. Methods and Results— Lung perfusion was quantified in 10 normal subjects and 28 patients undergoing clinically indicated left and right heart catheterization and same day research cardiac magnetic resonance imaging. A total of 228 lung slices were evaluated. Global lung perfusion, determined as the average of 6 coronal lung slices through the anterior, mid, and posterior left and right lungs, was significantly lower in patients with reduced cardiac index (<2.5 L/min per m2): 94±30 mL/100 mL per minute versus 132±40 mL/100 mL per minute in those with preserved cardiac index (≥2.5 L/min per m2; P =0.003). The gravitational anterior to posterior perfusion gradient was inversely associated with left ventricular end-diastolic pressure ( r =−0.728; P <0.001), resulting in a blunted perfusion gradient in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the perfusion reduction in posterior lung regions. In a multivariate regression analysis adjusting for all hemodynamic variables, altered lung perfusion gradient was most closely associated with increased mean pulmonary arterial pressure ( P =0.016). Conclusions— Increased left ventricular filling pressure and the resultant increase in pulmonary arterial pressure are associated with disruption of the normal gravitational lung perfusion gradient. Our findings underscore the complexity of heart-lung interaction in determining pulmonary hemodynamics in left heart failure.
Circulation-cardiovascular Imaging | 2012
Jie J Cao; Yi Wang; Jeannette McLaughlin; Peter Rhee; Michael Passick; Nora Ngai; Joshua Cheng; Ronald J. Gulotta; Andrew D. Berke; George A. Petrossian; Nathaniel Reichek
Background—Cardiac hemodynamics affect pulmonary vascular pressure and flow, but little is known of the effects of hemodynamics on lung perfusion at the tissue level. We sought to investigate the relationship between hemodynamic abnormalities in patients with left heart failure and global and regional lung perfusion using lung perfusion quantification by magnetic resonance imaging. Methods and Results—Lung perfusion was quantified in 10 normal subjects and 28 patients undergoing clinically indicated left and right heart catheterization and same day research cardiac magnetic resonance imaging. A total of 228 lung slices were evaluated. Global lung perfusion, determined as the average of 6 coronal lung slices through the anterior, mid, and posterior left and right lungs, was significantly lower in patients with reduced cardiac index (<2.5 L/min per m2): 94±30 mL/100 mL per minute versus 132±40 mL/100 mL per minute in those with preserved cardiac index (≥2.5 L/min per m2; P=0.003). The gravitational anterior to posterior perfusion gradient was inversely associated with left ventricular end-diastolic pressure (r=−0.728; P<0.001), resulting in a blunted perfusion gradient in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the perfusion reduction in posterior lung regions. In a multivariate regression analysis adjusting for all hemodynamic variables, altered lung perfusion gradient was most closely associated with increased mean pulmonary arterial pressure (P=0.016). Conclusions—Increased left ventricular filling pressure and the resultant increase in pulmonary arterial pressure are associated with disruption of the normal gravitational lung perfusion gradient. Our findings underscore the complexity of heart-lung interaction in determining pulmonary hemodynamics in left heart failure.Background— Cardiac hemodynamics affect pulmonary vascular pressure and flow, but little is known of the effects of hemodynamics on lung perfusion at the tissue level. We sought to investigate the relationship between hemodynamic abnormalities in patients with left heart failure and global and regional lung perfusion using lung perfusion quantification by magnetic resonance imaging. Methods and Results— Lung perfusion was quantified in 10 normal subjects and 28 patients undergoing clinically indicated left and right heart catheterization and same day research cardiac magnetic resonance imaging. A total of 228 lung slices were evaluated. Global lung perfusion, determined as the average of 6 coronal lung slices through the anterior, mid, and posterior left and right lungs, was significantly lower in patients with reduced cardiac index (<2.5 L/min per m2): 94±30 mL/100 mL per minute versus 132±40 mL/100 mL per minute in those with preserved cardiac index (≥2.5 L/min per m2; P =0.003). The gravitational anterior to posterior perfusion gradient was inversely associated with left ventricular end-diastolic pressure ( r =−0.728; P <0.001), resulting in a blunted perfusion gradient in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the perfusion reduction in posterior lung regions. In a multivariate regression analysis adjusting for all hemodynamic variables, altered lung perfusion gradient was most closely associated with increased mean pulmonary arterial pressure ( P =0.016). Conclusions— Increased left ventricular filling pressure and the resultant increase in pulmonary arterial pressure are associated with disruption of the normal gravitational lung perfusion gradient. Our findings underscore the complexity of heart-lung interaction in determining pulmonary hemodynamics in left heart failure.
Journal of Cardiovascular Magnetic Resonance | 2010
Danielle Janosevic; Nora Ngai; Marguerite Roth; William Schapiro; Simcha Pollack; Nathaniel Reichek; Jie J Cao
Methods Forty-one normal volunteers were prospectively recruited. Subjects were nonobese, nondiabetic, normotensive and free of cardiovascular history or significant valvular or myocardial disease by screening echocardiography. After volumetric short axis retrospectively gated SSFP cine imaging (1.5 T Siemens Avanto), breath-hold retrospectively gated short axis tagged gradient echo cines were acquired in LV base, midventricular, and apical slices with a nominal FOV 21 × 28 cm, matrix 108 × 144, 6 mm slice thickness, grid tag distance of 8 mm, TE 3.8 ms, TR 58 ms, temporal resolution 35 ms. Tagged images were analyzed using HARP software (Diagnosoft). Results Of 41 individuals, 23 were females. The group was divided by age into tertiles. Twist increased with age>60 years while LV end systolic volume (LVESV) decreased, with associated increases in ejection fraction (LVEF), systolic blood pressure (SBP) and pulse pressure (PP). End diastolic volume (LVEDV), LV mass, systolic circumferential strain and strain rate did not change with age so that LV Mass/ESV ratio increased (Table 1).
Journal of Cardiovascular Magnetic Resonance | 2018
J. Jane Cao; Nora Ngai; Lynette Duncanson; Joshua Cheng; Kathleen Gliganic; Qizhi Chen
Archive | 2018
J. Jane Cao; Nora Ngai; Lynette Duncanson; Joshua Cheng; Kathleen Gliganic; Qizhi Chen
Circulation | 2014
Jie Cao; Kathy Halloran; Joshua Cheng; Michael Passick; Nora Ngai