Jeannette McLaughlin

Left Ventricular Filling Pressure Assessment Using Left Atrial Transit Time by Cardiac Magnetic Resonance Imaging

Background—Left atrial (LA) size and function reflect left ventricular (LV) hemodynamics. In the present study, we developed a novel method to determine LA circulation transit time (LATT) by MRI and demonstrated its close association with LV filling pressure. Methods and Results—All subjects were prospectively recruited and underwent contrast-enhanced MR dynamic imaging. Mean LATT was determined as the time for contrast to transit through the LA during the first pass. In an invasive study group undergoing clinically indicated cardiac catheterization (n=25), LATT normalized by R-R interval (nLATT) was closely associated with LV early diastolic pressure (r=0.850, P=0.001), LV end-diastolic pressure (r=0.910, P<0.001), and mean diastolic pressure (r=0.912, P<0.001). In a larger noninvasive group (n=56), nLATT was prolonged in patients with LV systolic dysfunction (n=47) (10.1±3.0 versus 6.6±0.7 cardiac cycles in normal control subjects, n=9; P<0.001). Using a linear regression equation derived from the invasive group, noninvasive subjects were divided into 3 subgroups by estimated LV end-diastolic pressure: ⩽10 mm Hg, 11 to 14 mm Hg, and ≥15 mm Hg. There were graded increases from low to high LV end-diastolic pressure subgroups in echocardiographic mitral medial E/e′ ratio: 9±5, 11±4, and 13±3 (P=0.023); in B-type natriuretic peptide (interquartile range): 44 (60) pg/mL, 87 (359) pg/mL, and 371 (926) pg/mL (P=0.002); and in N-terminal pro–B-type natriuretic peptide: 57 (163) pg/mL, 208 (990) pg/mL, and 931 (1726) pg/mL (P=0.002), demonstrating the ability of nLATT to assess hemodynamic status. Conclusions—nLATT by cardiac MR is a promising new parameter of LV filling pressure that may provide graded noninvasive hemodynamic assessment.

Effects of respiratory cycle and body position on quantitative pulmonary perfusion by MRI.

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.

Effects of Hemodynamics on Global and Regional Lung Perfusion A Quantitative Lung Perfusion Study by Magnetic Resonance Imaging

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.

Effects of Hemodynamics on Global and Regional Lung Perfusion, A Quantitative Lung Perfusion Study by MRI

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.

Association of global and regional central circulation transit time with left ventricular end diastolic pressure using dynamic magnetic resonance imaging

Background Prolonged central circulation transit time (TT) has long been associated with heart failure and left ventricular (LV) dysfunction. However, it is not known which portion of the central circulation is associated with this prolongation. Moreover, the relation of global and regional TT to LV end diastolic pressure (LVEDP) is not defined. In this study we assessed the global and regional TT in each portion of the central circulation and investigated their relations to LVEDP in patients undergoing cardiac catheterization. Methods All patients were prospectively recruited and underwent cardiac MRI within 5 hours of cardiac catheterization. Dynamic MR images were acquired during the infusion of gadopentetate dimeglumine (0.01 mmol/kg) at 6 ml/s. Areas of interest were drawn and propagated through phases in the right atrium (RA), right ventricle (RV), main pulmonary artery (PA), left and right lung, left atrium (LA), LV and ascending aorta to construct timeintensity curves. TT was defined as the time between the peaks of time-intensity curves. All TTs were normalized to RR intervals. Central circulation TT was defined as TT from RA to aorta, while regional TT was defined as RA to RV, RV to PA, PA to lungs (averaged value of the left and right lung), lungs to LA, LA to LV, and LV to aorta. LVEDP was assessed during cardiac catheterization. Results Of the 48 subjects studied the mean age was 59 years and 32 (67%) were male. Average LV ejection fraction (LVEF) was 48±15% and the LVEDP 15±8 mmHg. Central TT was significantly prolonged in patients with elevated LVEDP (>12 mmHg) 15.7±5.8 cardiac cycles vs. 10.5±2.2 cardiac cycles (p=0.002) in those with normal LVEDP (≤12 mmHg). Regional analysis demonstrated that TT prolongation was present in PA to lungs, lungs to LA, LA to LV and LV to aorta but not in RA to RV and RV to PA. The multivariate regression model which included all regional TTs as covariables showed that TT from lung to LA had the strongest association with LVEDP (beta coefficients 0,424, p<0.001) followed by TT from LA to LV (0,325, p=0.007) and TT from PA to lungs (0,240, p=0.037). TTs from other regions were not significantly associated with LVEDP. Conclusions Central and regional circulation TT can be assessed by dynamic MR imaging. Central TT was significantly prolonged in patients with elevated LVEDP largely due to regional TT prolongation in lungs to LA, LA to LV and PA to lungs circulation. Funding None.

Relationship of left atrial size and function to invasive left ventricular filling pressure: a cardiac MRI study

Background Increased left atrial (LA) size measured at left ventricular (LV) end systole is associated with cardiovascular morbidity and mortality in population based studies. LA function can be divided into 3 components: LA filling during LV systole, a passive emptying phase during early diastole and active atrial systole during LV late diastole. We sought to assess the relationships of LA volume and emptying function to invasive LV end diastolic pressure (LVEDP).

Right ventricular responses to abnormal preload and afterload: a comparison of right ventricular regional displacement by cardiac MRI to elevated right heart pressures by catheterization.

Background Cardiac MRI (CMR) is valuable in assessing right ventricular (RV) structure and function. However, RV mechanical parameters such as regional wall displacement have not been fully explored using CMR. We sought to understand effects of increased RV preload and afterload on RV regional wall displacement. Methods Research subjects included 10 normal volunteers undergoing CMR and 36 patients undergoing clinically indicated right and left heart catheterization and a research CMR within 5 hours. Cine images were acquired to evaluate RV volumes and RVEF. Radial and longitudinal RV segmental displacement during systole were evaluated at the right sided septal endocardium and RV free wall on 4-chamber cine images using Feature Tracking software. Hemodynamics assessed during catheterization included RVSP, RVEDP, PASP, mean PAP and LVEDP. In normal controls, RVSP was estimated by echocardiography. Results Mean age was 60 years in patients and 55 in controls (NS). In the patient group mean RV end diastolic volume was 73±41 ml/m2 and RVEF 50± 15%. Reduced radial displacement of the septum was significantly associated with increased RVSP (r=-0.63, p<0.001), RVEDP (r=-0.55, p=0.001), PASP (r=-0.55, p=0.002), mean PAP (r=-0.51, p=0.003) and LVEDP (r=0.583, p=0.001). Mean septal displacement had the strongest association with hemodynamics compared to the sub-segmental analyses of the basal, mid and apical septum although all were significantly correlated with pressures. In a multivariate regression model with all pressure indices included, RSVP was the only variable that was independently associated with radial displacement of the septum (model R=0.625, p<0.001). While longitudinal displacement of the septum and longitudinal and radial displacement of the RV free wall were all associated with RVEF (r=0.522, p=0.002; r=0.428, p=0.014; r=0.369, p=0038, respectively) they were not sensitive to increased RV preload or afterload. Conclusions

Effects of Hemodynamics on Global and Regional Lung PerfusionClinical Perspective: A Quantitative Lung Perfusion Study by Magnetic Resonance Imaging

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.

Assessment of left ventricular filling pressure using mean left atrial transit time from contrast enhanced dynamic MRI

Left atrial (LA) size and function are often regarded as a reflection of left ventricular (LV) hemodynamics. Purpose:In this study we investigated the hemodynamic correlates of contrast transit time within the left atrium (LA) in patients with LV systolic dysfunction by cardiac magnetic resonance imaging (CMR).

Impaired lung perfusion in patients with congestive heart failure by quantitative MRI perfusion

Methods Study subjects were prospectively enrolled and underwent cardiac MRI at 1.5 T. First-pass perfusion was performed with 0.01 mmol/kg gadopentetate in 3 coronal slices covering anterior, mid and posterior lung fields during inspiration using a saturation recovery SSFP sequence. Mean signal intensity of all pixels in pulmonary parenchyma at each time point was evaluated using a custom modelindependent deconvolution program for perfusion quantitation. Pulmonary transit time was measured as the time interval between peak signal intensity in the main pulmonary artery and peak signal intensity in the left atrium. Cardiac function was assessed using SSFP standard short axis cine imaging. Pulmonary flow was measured by through plane phase contrast imaging in the main pulmonary artery. Results Of the 25 subjects enrolled 7 were normal controls and 15 were patients with systolic CHF in I-III NYHA functional class who completed lung perfusion imaging in inspiration. Average lung perfusion was reduced in CHF patients, 81 ± 32 ml/100 ml/min vs 118 ± 48 ml/100 ml/min in controls (p = 0.046). Similar to normal controls patients with CHF maintained a perfusion gradient in the gravity direction with the highest perfusion in posterior and the lowest in anterior lung field. However, the absolute perfusion was reduced in all lung fields with anterior, mid and posterior perfusion 58 ± 26, 85 ± 38, 106 ± 36 ml/100 ml/min in CHF patients and 73 ± 53, 116 ± 53, 165 ± 45 ml/100 ml/min in controls. Reduced lung perfusion was associated with lower pulmonary flow (indexed by BSA) (r = -0.771, p < 0.001), longer pulmonary transit time (r = -0.729, p < 0.001), a marker of total pulmonary resistance, lower LVEF (r = 0.443, p = 0.039) and lower RVEF (r = 0.474, p = 0.026). In a multivariate regression analysis including all variables associated with lung perfusion and an interaction term for pulmonary flow and pulmonary transit time since they were significantly correlated, the predictors of lung perfusion were pulmonary flow and flow/transit time interaction, suggesting the importance of both forward flow and total pulmonary resistance.