Navin Rajagopalan

Tricuspid Annular Systolic Velocity: A Useful Measurement in Determining Right Ventricular Systolic Function Regardless of Pulmonary Artery Pressures

Assessment of right ventricular (RV) systolic function can be somewhat difficult, particularly in pulmonary hypertension (PH). RV fractional area change (FAC) and tricuspid valve annular motion (TAPSE) although useful in the assessment of RV performance, their use can be sometimes limited and tedious. Thus, a quicker but yet reliable alternative is needed. Accordingly, we compared peak tricuspid annulus systolic (TA Sa) velocities derived from Doppler tissue imaging (DTI) with both RVFAC and TAPSE to estimate RV function in 52 patients (53 ± 16 years) with varying degrees of PH. In this group, mean was RVFAC 49 ± 20, TAPSE was 2.3 ± 0.7 cm, peak TA Sa velocity by DTI was 10.4 ± 3.8 cm/s, left ventricular systolic function was 57 ± 18%, and pulmonary artery systolic pressure was 47 ± 28 mmHg. An excellent correlation was noted between TAPSE and RVFAC (r = 0.91, P < 0.001). Similar correlations were noted between peak TA Sa velocity and RVFAC (r = 0.84, P < 0.001) and between peak TA Sa velocity and TAPSE (r = 0.90, P < 0.001). A TA Sa >10.5 cm/s identified individuals with both a normal RV function and without significant PH. Therefore, we conclude that TA Sa velocity, an easily obtainable DTI measure, that has an excellent correlation with more time‐consuming methods to assess RV systolic function regardless of the degree of PH should be routinely assessed during the initial evaluation and eventual follow‐up of patients either at risk or with documented PH.

Right ventricular dyssynchrony in patients with pulmonary hypertension is associated with disease severity and functional class

BackgroundAbnormalities in right ventricular function are known to occur in patients with pulmonary arterial hypertension.ObjectiveTest the hypothesis that chronic elevation in pulmonary artery systolic pressure delays mechanical activation of the right ventricle, termed dyssynchrony, and is associated with both symptoms and right ventricular dysfunction.MethodsFifty-two patients (mean age 46 ± 15 years, 24 patients with chronic pulmonary hypertension) were prospectively evaluated using several echocardiographic parameters to assess right ventricular size and function. In addition, tissue Doppler imaging was also obtained to assess longitudinal strain of the right ventricular wall, interventricular septum, and lateral wall of the left ventricle and examined with regards to right ventricular size and function as well as clinical variables.ResultsIn this study, patients with chronic pulmonary hypertension had statistically different right ventricular fractional area change (35 ± 13 percent), right ventricular end-systolic area (21 ± 10 cm2), right ventricular Myocardial Performance Index (0.72 ± 0.34), and Eccentricity Index (1.34 ± 0.37) than individuals without pulmonary hypertension (51 ± 5 percent, 9 ± 2 cm2, 0.27 ± 0.09, and 0.97 ± 0.06, p < 0.005, respectively). Furthermore, peak longitudinal right ventricular wall strain in chronic pulmonary hypertension was also different -20.8 ± 9.0 percent versus -28.0 ± 4.1 percent, p < 0.01). Right ventricular dyssynchrony correlated very well with right ventricular end-systolic area (r = 0.79, p < 0.001) and Eccentricity Index (r = 0.83, p < 0.001). Furthermore, right ventricular dyssynchrony correlates with pulmonary hypertension severity index (p < 0.0001), World Health Organization class (p < 0.0001), and number of hospitalizations (p < 0.0001).ConclusionLower peak longitudinal right ventricular wall strain and significantly delayed time-to-peak strain values, consistent with right ventricular dyssynchrony, were found in a small heterogeneous group of patients with chronic pulmonary hypertension when compared to individuals without pulmonary hypertension. Furthermore, right ventricular dyssynchrony was associated with disease severity and compromised functional class.

Noninvasive Estimation of Pulmonary Vascular Resistance in Pulmonary Hypertension

Background: Determination of pulmonary vascular resistance (PVR) in patients with suspected or known pulmonary hypertension (PH) requires right heart catheterization. Our purpose was to use Doppler echocardiography to estimate PVR in patients with PH. Methods: Patient population consisted of 52 patients (53 ± 12 years; 35 females) who underwent Doppler echocardiography and right heart catheterization within 24 hours of each other. The ratio of peak tricuspid regurgitation velocity (TRV) and right ventricular outflow time‐velocity integral (VTIRVOT) was measured via transthoracic echocardiography and correlated to invasively determined PVR. A linear regression equation was generated to determine PVR by echocardiography based upon the TRV/VTIRVOT ratio. PVR by echocardiography was compared to invasive PVR using Bland‐Altman analysis. Results: Significant correlation was demonstrated between TRV/VTIRVOT and PVR by catheterization (r = 0.73; P < 0.001). However, Bland‐Altman analysis showed that agreement between PVR determined by echocardiography and invasive PVR was poor (bias = 0; standard deviation = 4.3 Wood units). In a subset of patients with invasive PVR < 8 Wood units (26 patients), correlation between TRV/VTIRVOT and invasive PVR was strong (r = 0.94; P < 0.001). In these patients, agreement between PVR by echocardiography and invasive PVR was satisfactory (bias = 0; standard deviation = 0.5 Wood units). There was no correlation between TRV/VTIRVOT and invasive PVR in patients with PVR > 8 Wood units (n = 26; r = 0.17). Conclusion: While TRV/VTIRVOT correlates significantly with PVR, using it to estimate PVR in a PH patient population cannot be recommended.

Utility of Right Ventricular Tissue Doppler Imaging: Correlation with Right Heart Catheterization

Objectives: The objective of this study was to correlate tissue Doppler imaging of the right ventricle (RV) with pulmonary hemodynamics in patients referred for right heart catheterization. Methods: Seventy subjects (mean age 54 ± 13; 35 males) prospectively underwent tissue Doppler imaging of the RV and right heart catheterization within 1 day of each other. Peak systolic velocity and strain were measured at the RV free wall and correlated with pulmonary hemodynamics. Results: RV myocardial velocity demonstrated no correlation with any hemodynamic variable. While RV strain demonstrated significant correlation with cardiac index (r =−0.61; P < 0.001), correlations with transpulmonary gradient (r = 0.26; P < 0.05) and pulmonary vascular resistance (r = 0.30; P < 0.05) were weaker. Subgroup analysis revealed that in patients with left ventricular systolic dysfunction (n = 31), RV strain showed no correlation with any hemodynamic variable. In patients with normal left ventricular systolic function (n = 39), correlations were significant between RV strain and mean pulmonary artery pressure (r = 0.59; P < 0.001), pulmonary vascular resistance (r = 0.60; P < 0.001), and cardiac index (r =−0.67; P < 0.001). Conclusions: RV myocardial strain correlates significantly with pulmonary hemodynamics in patients with pulmonary hypertension and normal left ventricular function. However, there is no correlation with RV performance in patients with left ventricular dysfunction.

Abnormal Right Ventricular Myocardial Strain Generation in Mild Pulmonary Hypertension

Background: Although right ventricular (RV) dyssynchrony has been identified in patients with severe pulmonary hypertension due to significant RV enlargement and compromise in systolic function, a more clinically relevant question pertains to RV mechanical properties in patients with mild elevation in pulmonary artery systolic pressures (PASP). Methods: Several echocardiographic parameters and peak longitudinal strain were measured in 40 patients and divided into two groups of 20 patients based on their PASP. Results: Group I included 20 individuals (mean age 48 ± 16 years with a mean PASP of 27 ± 5 mmHg) and Group II included 20 patients (mean age 63 ± 14 years with a mean PASP of 49 ± 7 mmHg.) All time intervals were adjusted for heart rate. RV fractional area change and tricuspid annular plane systolic excursion for Group I (62 ± 12% and 2.74 ± 0.56 cm) and Group II (49 ± 14%; P < 0.02 and 2.09 ± 0.40; P < 0.002) were both normal. However, Group II had lower peak longitudinal RV free wall (RVF) strain (−27.3 ± 7.1 % vs. −31.9 ± 8.7%, P < 0.04), longer time to peak RVF strain (448 ± 57 ms vs. 411 ± 43 ms; P < 0.03) and evidence of significant RV dyssynchrony (−83 ± 55 ms vs. 1 ± 17 ms, P < 0.00001) in contrast to Group I. Conclusion: In conclusion, mild elevations in PASP affect the mechanical properties of the RV and result in RV dyssynchrony despite absence of gross abnormalities in RV size or function.

Comparative echocardiographic analysis of mitral and tricuspid annular motion: differences explained with proposed anatomic-structural correlates.

Background: Annular motion (AM) has been shown to occur during all dynamic phases of the cardiac cycle; but little is known regarding comparisons between mitral and tricuspid AM. We elected to use M‐mode to examine the extent and timing of mitral and tricuspid AM events. Methods: A complete echocardiogram was obtained in 50 patients [mean age 53 ± 16 years, mean left ventricular ejection fraction (LVEF) 57 ± 19%, and mean right ventricular fractional area change (RVFAC) of 49 ± 20%]. Timing of all AM intervals was corrected for heart rate. Results: A strong linear correlation was noted for both LVEF and maximal mitral annular systolic excursion and for RVFAC and maximal tricuspid annular systolic excursion (r = 0.91, P < 0.0001). The amplitude of both maximal mitral annular descent (1.54 ± 0.45 cm) and ascent (0.64 ± 0.23 cm) was significantly smaller than for the tricuspid annulus (2.26 ± 0.73 and 0.98 ± 0.37 cm; P < 0.0001, respectively). Furthermore, while it takes longer for the mitral than for the tricuspid annulus (403 ± 52 ms vs 308 ± 50 ms; P < 0.0001, respectively) to descend to its lowest point; the duration to reach maximal ascent is shorter for the mitral than for tricuspid annulus (90 ± 22 ms vs 115 ± 19 ms; p < 0.0001, respectively). Conclusion: Significant differences exist in both amplitude and timing of AM events between the mitral and tricuspid annuli, likely reflecting intrinsic anatomical and electromechanical differences between both sides of the heart that require further investigation.

Tissue Doppler Imaging of Right Ventricular Decompensation in Pulmonary Hypertension

Right ventricular (RV) function is closely linked to outcomes in pulmonary hypertension (PH). The authors sought to evaluate RV myocardial strain in 3 groups of patients: normal, PH with compensated RV function (PH-C), and PH with decompensated RV function (PH-D). Fifty-six patients (aged 56+/-12 years; 40 women; mean pulmonary artery pressure [MPAP] range, 13-82 mm Hg) underwent right heart catheterization and 2-dimensional echocardiography with tissue Doppler imaging of the RV. Right atrial pressures were 6+/-3, 5+/-2, and 14+/-4 mm Hg; MPAP values were 19+/-3, 44+/-15, and 56+/-13 mm Hg; pulmonary vascular resistances were 1.4+/-0.4, 7.9+/-5.1, and 11.5+/-6.6 Wood units; and cardiac indices were 3.4+/-0.9, 2.8+/-0.8, and 2.2+/-0.7 L/min/m(2) (P<.05 for all for normal, PH-C, and PH-D patients), respectively. RV free wall strain decreased significantly among all 3 groups (-26%+/-6%, -19%+/-7%, and -14%+/-5%; P<.0001). RV free wall strain decreases in PH without hemodynamically decompensated RV function suggesting it may be a preceding step in the development of RV failure. This may be of particular use in following patients sequentially.

Differential strain and velocity generation along the right ventricular free wall in pulmonary hypertension.

BACKGROUND In contrast to the homogeneously distributed deformation properties within the left ventricle, the right ventricular (RV) free wall (RVFW) shows a more inhomogeneous distribution. It has been demonstrated that pulmonary hypertension (PH) results in significant RVFW mechanical delay. OBJECTIVE To assess the effect of the degree of pulmonary arterial systolic pressure on the RVFW strain gradient and on myocardial velocity generation. METHODS Peak longitudinal strain and velocity data were collected from three different segments (basal, mid- and apical) of the RVFW in 17 normal individuals and 31 PH patients. RESULTS A total of 144 RV wall segments were analyzed. RVFW strain values in individuals without PH were higher in the mid and apical segments than in the basal segment. In contrast, RVFW strain in PH patients was higher in basal segments and diminished toward the apex. In terms of RVFW velocities, both groups showed decremental values from basal to apical segments. Basal and mid-RVFW velocities were significantly lower in PH patients than in individuals without PH. CONCLUSIONS PH results in significant alterations of strain and velocity generation that occurs along the RVFW. Of these abnormalities, the reduction in strain from the mid and apical RVFW segments was most predictive of PH. It is important to be aware of these differences in strain generation when studying the effect of PH on the right ventricle. Additional studies are required to determine whether these differences are due to RV remodelling.

Normal Range of Mechanical Variables in Pulmonary Hypertension: A Tissue Doppler Imaging Study

Background: Tissue Doppler imaging (TDI) has been quite useful in determining the mechanical properties of right ventricular (RV) function in patients with pulmonary hypertension (PH). However, to what extent these mechanical properties are expected to identify RV dysfunction in PH patients is less clear. Methods: Our echocardiography database was queried for patients with PH of different etiologies (111 patients, age 55 ± 14 years, mean pulmonary artery pressure 63 ± 24 mmHg) who had undergone TDI analysis and compared to similarly collected data from a group of healthy individuals (35 patients, mean age 45 ± 15 years, mean pulmonary artery pressure 27 ± 5 mmHg). Results: ROC analysis demonstrated that a mechanical delay between the RVFw and IS > 25 ms detects PH while a delay > 37 ms detects abnormal RV performance. Peak RV strain < −20% identifies PH greater than 40 mmHg and a reduced RV systolic function. However, on a stepwise multiple regression analysis model RV dyssynchrony was the most significant predictor of PH (r = 0.515; P = 0.0003) over peak longitudinal RV strain (r = 0.553; P = 0.02) and RVFAC (r =−0.603; P = 0.01). Peak longitudinal strain was the most significant predictor (r =−0.722; P < 0.0001) of an abnormal RVFAC over PH (r =−0.603; P = 0.004) and RV dyssynchrony (r =−0.471; P = 0.01). Conclusion: A normal range of RV mechanical variables in PH patients are provided that can be applied in the assessment of RV performance.

A Delayed Time of the Peak Tricuspid Regurgitation Signal: Marker of Right Ventricular Dysfunction

Background:Worsening degrees of tricuspid regurgitation (TR) have been associated with worse outcomes. We investigated the time it takes for the TR jet to attain its maximum peak (tmpTR) with measures of right ventricular (RV) function. Methods:Several echocardiographic variables of RV size and function and tmpTR corrected for heart rate were collected from 140 patients (mean age 57 ± 20 years). Results:Mean RV end systolic (15 ± 9 cm2) and end diastolic (25 ± 9 cm2) areas, RV fractional area change (44 ± 19%), maximal tricuspid annular motion (1.98 ± 0.71 cm), pulmonary artery systolic pressure (57 ± 33 mm Hg) and tmpTR (248 ± 75 ms). A negative correlation was seen between tmpTR and RV fractional area change (r = −0.74; P < 0.0001) and between tmpTR and maximal tricuspid annular excursion (r = −0.69; P < 0.0001). On a multiple stepwise linear regression analysis tmpTR was better than pulmonary artery systolic pressure in predicting RV dysfunction (P < 0.001). Receiver operating characteristic curve analysis demonstrated that a tmpTR value >240 ms identified RV systolic dysfunction (sensitivity 79% and specificity 94%, areas under the curves 0.923, P = 0.0001). The longest tmpTR values were seen in patients with both RV systolic dysfunction and pulmonary hypertension (310 ± 30 ms, P < 0.0001). Conclusion:A delayed time to peak of the maximum TR jet correlates with RV dysfunction. Patients with normal RV function and no pulmonary hypertension had abnormal tmpTR values (243 ± 57 ms) implying an underlying RV mechanical abnormality that requires further investigation.