Beth Gulyasy

Evidence of robust coupling of atrioventricular mechanical function of the right side of the heart: insights from M-mode analysis of annular motion.

Background: Extensive data exist regarding annular descent and ventricular function. We have already demonstrated significant differences in amplitude and timing of events between maximal mitral (MAPSE) and tricuspid (TAPSE) annular plane systolic excursion as well as described quantitative temporal differences in annular ascent (AA) between the right and left sides of the heart. However, whether any relationship exists between annular ascent and descent components remains uninvestigated. Methods: Left ventricular ejection fraction (LVEF), right ventricular fractional area change (RVFAC), MAPSE, TAPSE, MV, and TV AA as well as pulsed tissue Doppler of the lateral MV and TV annuli were recorded from 53 patients. Results: In this population (age 55 ± 17 years) mean LVEF was 55 ± 19%, mean RVFAC was 47 ± 20%, mean MAPSE was 2.11 ± 0.72 cm, mean TAPSE was 1.48 ± 0.44 cm, mean MV AA was 0.52 ± 0.17 cm, TV AA was 0.96 ± 0.47, MV A‐wave 0.10 ± 0.04 cm/s, and TV A‐wave was 0.13 ± 0.05 cm/s. A more robust correlation was seen between TV AA and RVFAC than between MV AA and LVEF and also between TV AA and pulsed TDI TV A‐wave velocity than between MV AA and pulsed TDI MV A‐wave. Conclusion: Our data reveal that mechanical systolic functions of the atria and the ventricles are more closely coupled on the right than on the left side of the heart. Whether this is a result of anatomic linking or chamber geometry will require further study.

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.

Apical Systolic Eccentricity Index: A Better Marker of Right Ventricular Compromise in Pulmonary Hypertension

Background: Systolic eccentricity index (sEI) has been traditionally measured at the papillary muscle (PM) level. However, this measurement does not take into account the remodeling that occurs in the right ventricle (RV) during chronic pulmonary hypertension (cPH). Methods: Standard echocardiographic data were collected on 50 patients (age 58 ± 14 years) with known cPH (74 ± 22 mmHg; range 45–120 mmHg) who had adequate short‐axis views at the mitral valve (MV), PM, and apical (AP) levels to measure sEI. All had a normal left ventricular ejection fraction (72 ± 10%). Results: In a multivariate analysis, the traditional PM level sEI correlated the best with cPH when pulmonary artery systolic pressures (PASP) ranged between 45 and 60 mmHg (r =−0.569, P < 0.001) while AP level sEI was better when all patients were included in the analysis (r =−0.843, P < 0.0001). Not only was AP level sEI the only echo variable helpful in identifying a dilated end diastolic RV area (r =−0.730, P < 0.0001) but also patients with worse RV systolic performance (r = 0.686, P < 0.0001). MV level sEI was not better than PM level sEI. Conclusions: AP level sEI appears to be superior to traditional PM level sEI measurement as it correlates better with worsening PH severity, RV cavity dilation and RV systolic dysfunction. Further studies are now required to prospectively study how these septal abnormalities in cPH may affect RV as well as LV systolic and diastolic function. (Echocardiography 2010;27:534‐538)

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.

Right ventricular outflow tract spectral signal: a useful marker of right ventricular systolic performance and pulmonary hypertension severity

AIMS Right ventricular outflow tract (RVOT) acceleration shortens with chronic pulmonary hypertension (cPH). However, the overall value of this spectral Doppler signal in the assessment of PH patients is not well understood. METHODS AND RESULTS Markers of RV systolic performance, time to onset, time to peak, and total duration of the RVOT systolic spectral Doppler signal were examined. Group I consisted of 28 patients without PH [50 +/- 15 years and mean pulmonary artery systolic pressure (PASP) of 30 +/- 8 mmHg] and Group II included 52 patients with cPH (56 +/- 14 years and mean PASP of 80 +/- 27 mmHg; P < 0.0001). As expected, Group II patients markers showed worse RV performance. In addition, Group II had a longer time to onset, a shorter time to peak, and a shorter total duration of the RVOT systolic signal than Group I. Both time to onset (r = 0.66 vs. r = -0.53; P < 0.0001) and time to peak (r = 0.65 vs. r = 0.50; P < 0.0001) of the RVOT signal correlated better with PH than RV fractional area change. Conversely, RV fractional area change correlated better with total duration of RVOT ejection (r = 0.66 vs. r = 0.58; P < 0.0001) than with PASP. CONCLUSION Timing of onset and peak of the RVOT systolic spectral signal appears to be useful in characterizing the severity of the PASP, while the total duration of RVOT ejection is a better predictor of the systolic performance of the RV in PH patients. More studies are now required to determine the clinical utility of prospectively measuring RVOT in cPH.

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.

Differences in the Duration of Total Ejection between Right and Left Ventricles in Chronic Pulmonary Hypertension

Background: Chronic pulmonary hypertension (cPH) is known to delay pulmonic valve closure resulting in a closely split second heart sound. We decided to measure total duration of right (RV) and left ventricular (LV) outflow tract (RVOT and LVOT) spectral signals using pulsed Doppler to determine if this approach was useful in identifying this narrowing in auscultation that should then result in a shorter temporal difference between the ejection of both ventricles. Methods: Standard measures of RV and LV performance as well as Doppler data was collected from 85 patients divided into two groups according to their estimated pulmonary artery systolic pressure obtained at the time of their echocardiographic examination. Difference in ejection between the ventricles was defined as the difference in ejection time between RVOT and LVOT, measured in milliseconds. Results: Chronic PH patients had a shorter total duration between RVOT and LVOT ejection time (–15 ± 16 ms vs. 22 ± 14 ms; P < 0.0001) than individuals without PH. This difference in total duration between RVOT and LVOT ejection not only showed a significant negative correlation with both PASP (r =–0.65; P < 0.0001) but also with pulmonary vascular resistance (PVR; r =–0.60; P < 0.0001). Conclusions: Shorter duration between RVOT and LVOT ejection is likely to explain the closely split second heart sound in cPH patients. When accurate echocardiographic assessment of RV function in cPH patients remains problematic due to the unusual geometry of this cardiac chamber; Doppler measures can simplify patient identification and follow up. (Echocardiography 2011;28:509‐515

New Annular Tissue Doppler Markers of Pulmonary Hypertension

Background: Tissue Doppler imaging (TDI) of mitral (MA) and tricuspid annulus (TA) events characterizes systolic and diastolic properties of each respective ventricle. However, the effect of chronic pulmonary hypertension (cPH) on these TDI annular events has not been well described. Methods: Measurements of right ventricular (RV) performance with TDI of the lateral mitral and tricuspid annuli, to measure isovolumic contraction (IVC) and systolic (S) signals were recorded from 50 individuals without PH and from 50 patients with cPH. To avoid confounding variables, all patients had normal left ventricular ejection fraction and were in normal sinus rhythm at the time of the examination. Results: As expected, markers of RV systolic performance were markedly reduced while LV systolic function remained largely unaffected in cPH patients when compared to patients without PH. TDI interrogation of the MA revealed lengthening of the time interval between IVC and systolic signal (70 ± 17 msec) when compared to individuals without PH (43 ± 8 msec; P < 0.0001). In contrast, cPH markedly shortened the time interval between IVC and the TA systolic signal (34 ± 12 msec) when compared to individuals without PH (65 ± 17 msec; P < 0.0001). Conclusions: cPH lengthens time interval between the IVC and the MA systolic signal while shortening this same interval when the TA is interrogated with TDI; reflecting the potential influence that cPH exerts in biventricular performance. Whether measuring these intervals be routinely used in the follow‐up of cPH patients will require further study. (Echocardiography 2010;27:969‐976)