Novel echocardiographic method to assess left ventricular chamber stiffness and elevated end-diastolic pressure based on time-velocity integral measurements of pulmonary venous and transmitral flows.

Aims: The detection of increased left ventricular (LV) chamber stiffness may play an important role in assessing cardiac patients with potential but not overt heart failure. A non-invasive method to estimate it is not established. We investigated whether the echocardiographic backward/forward flow volume ratio from the left atrium (LA) during atrial contraction reflects the LV chamber stiffness. Methods and results: We studied 62 patients who underwent cardiac catheterization and measured their left ventricular end-diastolic pressure (LVEDP) and pressure increase during atrial contraction (ΔPa) from the LV pressure waveform. Using the echocardiographic biplane method of disks, we measured the LV volume change during atrial contraction indexed to the body surface area (ΔVa), and ΔPa/ΔVa was calculated as a standard for the LV operating chamber stiffness. Using pulsed Doppler echocardiography, we measured the time-velocity integral (TVI) of the backward pulmonary venous (PV) flow during atrial contraction (IPVA) and the ratio of IPVA to the PV flow TVI throughout a cardiac cycle (FPVA). We also measured the TVI of the atrial systolic forward transmitral flow (IA) and the ratio of the IA to the transmitral TVI during a cardiac cycle (FA) and calculated IPVA/IA and FPVA/FA. IPVA/IA and FPVA/FA were well correlated with ΔPa/ΔVa (r = 0.79 and r = 0.81) and LVEDP (r = 0.73 and r = 0.77). The areas under the ROC curve to discriminate LVEDP >18 mmHg were 0.90 for IPVA/IA and 0.93 for FPVA/FA. Conclusion: The FPVA/FA, the backward/forward flow volume ratio from the LA during atrial contraction, is useful for non-invasive assessments of LV chamber stiffness and elevated LVEDP.

Relationships of left ventricular strain and strain rate to wall stress and their afterload dependency.

Whether and how left ventricular (LV) strain and strain rate correlate with wall stress is not known. Furthermore, it is not determined whether strain or strain rate is less dependent on the afterload. In 41 healthy young adults, LV global peak strain and systolic peak strain rate in the longitudinal direction (LS and LSR, respectively) and circumferential direction (CS and CSR, respectively) were measured layer-specifically using speckle tracking echocardiography (STE) before and during a handgrip exercise. Among all the points before and during the exercise, all the STE parameters significantly correlated linearly with wall stress (LS: r = -0.53, p < 0.01, LSR: r = -0.28, p < 0.05, CS in the inner layer: r = -0.72, p < 0.01, CSR in the inner layer: r = -0.47, p < 0.01). Strain more strongly correlated with wall stress than strain rate (r = -0.53 for LS vs. r = -0.28 for LSR, p < 0.05; r = -0.72 for CS vs. r = -0.47 for CSR in the inner layer, p < 0.05), whereas the interobserver variability was similar between strain and strain rate (longitudinal 6.2 vs. 5.2 %, inner circumferential 4.8 vs. 4.7 %, mid-circumferential 7.9 vs. 6.9 %, outer circumferential 10.4 vs. 9.7 %), indicating that the differences in correlation coefficients reflect those in afterload dependency. It was thus concluded that LV strain and strain rate linearly and inversely correlated with wall stress in the longitudinal and circumferential directions, and strain more strongly depended on afterload than did strain rate. Myocardial shortening should be evaluated based on the relationships between these parameters and wall stress.

Characteristic systolic waveform of left ventricular longitudinal strain rate in patients with hypertrophic cardiomyopathy.

We analyzed the waveform of systolic strain and strain-rate curves to find a characteristic left ventricular (LV) myocardial contraction pattern in patients with hypertrophic cardiomyopathy (HCM), and evaluated the utility of these parameters for the differentiation of HCM and LV hypertrophy secondary to hypertension (HT). From global strain and strain-rate curves in the longitudinal and circumferential directions, the time from mitral valve closure to the peak strains (T-LS and T-CS, respectively) and the peak systolic strain rates (T-LSSR and T-CSSR, respectively) were measured in 34 patients with HCM, 30 patients with HT, and 25 control subjects. The systolic strain-rate waveform was classified into 3 patterns ("V", "W", and "√" pattern). In the HCM group, T-LS was prolonged, but T-LSSR was shortened; consequently, T-LSSR/T-LS ratio was distinctly lower than in the HT and control groups. The "√" pattern of longitudinal strain-rate waveform was more frequently seen in the HCM group (74 %) than in the control (4 %) and HT (20 %) groups. Similar but less distinct results were obtained in the circumferential direction. To differentiate HCM from HT, the sensitivity and specificity of the T-LSSR/T-LS ratio <0.34 and the "√"-shaped longitudinal strain-rate waveform were 85 and 63 %, and 74 and 80 %, respectively. In conclusion, in patients with HCM, a reduced T-LSSR/T-LS ratio and a characteristic "√"-shaped waveform of LV systolic strain rate was seen, especially in the longitudinal direction. The timing and waveform analyses of systolic strain rate may be useful to distinguish between HCM and HT.

Long-term echocardiographic evaluation of valvular lesions in a patient with nonbacterial thrombotic endocarditis associated with advanced uterine cancer.

Nonbacterial thrombotic endocarditis (NBTE) is characterized by the deposition of thrombi on previously undamaged heart valves in the absence of bacteremia and predominantly affects patients with hypercoagulable state. Although the diagnosis is usually based on transthoracic echocardiography, little is known about the serial changes of the vegetation in response to treatment. We experienced a 42-year-old woman with advanced uterine cancer and asymptomatic cerebral embolization. Plasma d-dimer level was markedly elevated and echocardiography showed highly mobile masses attached to the anterior and posterior mitral leaflets with moderate regurgitation. Based on these findings, she was diagnosed as having NBTE associated with uterine cancer and intravenous administration of heparin and chemotherapy were performed. Follow-up echocardiography revealed the disappearance of the vegetation and reduction of mitral regurgitation. Uterine cancer was successfully treated by surgery and recurrence of the valvular lesion did not occur. .

Myocardial shortening in 3 orthogonal directions and its transmural variation in patients with nonobstructive hypertrophic cardiomyopathy.

BACKGROUND: Although longitudinal strain (LS) is known to be reduced in patients with hypertrophic cardiomyopathy (HCM), it has not been elucidated whether or not circumferential strain (CS) is reduced. We aimed to determine whether multidirectional and layer-specific myocardial strain is reduced in patients with nonobstructive HCM. METHODS AND RESULTS: Speckle-tracking echocardiography was performed in 41 HCM patients and 27 control subjects. Segmental and global LS and CS were measured in the inner, mid, and outer layers. Global LS was significantly lower in the HCM group than in controls in the inner (-10.3±2.9 vs. -14.8±2.0%, P<0.001), mid (-8.7±2.6 vs. -13.8±1.9%, P<0.001), and outer (-7.2±2.6 vs. -11.9±1.9%, P<0.001) layers. Global CS was preserved in the inner layer (-23.8±4.7 vs. -24.3±3.3%, P=0.69) but reduced in the mid (-10.3±3.1 vs. -13.3±2.5%, P<0.001) and outer layers (-6.7±2.3 vs. -8.6±2.3%, P=0.002). Differences in CS between the inner and outer layers correlated with segmental relative wall thickness (r=-0.20, P=0.002). Furthermore, only the absolute value of global CS in the inner layer positively correlated with left ventricular ejection fraction (r=0.32, P<0.01) among these multidirectional and layer-specific strains. CONCLUSIONS: In patients with HCM, not only the LS in all layers but also CS in the mid and outer layers was reduced, presumably reflecting impaired myocardial function. In contrast, CS in the inner layer was preserved, being associated with maintenance of chamber function.

Quantitative and pattern analyses of continuous-wave Doppler-derived pulmonary regurgitant flow velocity for the diagnosis of constrictive pericarditis.

BACKGROUND: Many echocardiographic features of constrictive pericarditis (CP) have been reported, but each alone has a limitation either in sensitivity or in specificity. Continuous-wave Doppler-derived flow velocity of pulmonary regurgitation can reflect the diastolic right ventricular pressure pattern characteristic of CP and be useful for its detection. METHODS: Fifteen patients with CP, 18 patients with restrictive cardiomyopathy, and 20 normal subjects were studied retrospectively. Using continuous-wave Doppler echocardiography, pulmonary regurgitation velocities were measured at the early diastolic peak (VMAx), mid-diastolic inflection point (VIFL), and late diastolic minimal point (VMIN). RESULTS: VIFL, VIFL/VMAx, VMIN, and VMIN/VMAx were significantly lower in the CP group compared with the restrictive cardiomyopathy and normal groups. Prevalence rates of patients with early mid-diastolic inflection, VIFL/VMAx < 0.5, VMIN < 50 cm/sec, and VMIN/VMAx < 0.33 were significantly greater in the CP group compared with the other groups. Sensitivity and specificity for the diagnosis of CP were 93% and 74%, respectively, for the presence of early mid-diastolic inflection, 73% and 100% for VIFL/VMAx < 0.5, 73% and 97% for VMIN < 50 cm/sec, and 93% and 92% for VMIN/VMAx < 0.33. CONCLUSIONS: The quantitative and pattern analyses of continuous-wave Doppler-derived pulmonary regurgitation velocity could enhance the accuracy of echocardiographic detection of CP.

Decreased aorto-septal angle may contribute to left ventricular diastolic dysfunction in healthy subjects.

BACKGROUND: Left ventricular (LV) diastolic dysfunction is often observed in healthy older subjects without structural heart disease, although its exact mechanisms have not been established. A decrease in the aorto-septal angle (ASA), an alteration of LV shape due to aortic elongation, is also frequently seen in elderly subjects. The objective of this study was to evaluate whether it can contribute to LV diastolic dysfunction in healthy subjects. METHODS: Echocardiography was performed in 77 healthy subjects (42 men, mean age 43.2 ± 13.8 years) to measure the ASA, early diastolic transmitral flow velocity (E), isovolumic relaxation time (IRT), and early diastolic mitral annular velocity (e'). The LV peak early diastolic longitudinal strain rate (GSRE ) was measured using a two-dimensional speckle tracking imaging technique. RESULTS: ASA was significantly correlated with E (r = 0.54, p < 0.001), IRT (r = -0.41, p < 0.001), e' (r = 0.57, p < 0.001), and GSRE (r = 0.63, p < 0.001) and shown by stepwise multivariate analysis to be the strongest independent determinant of E, IRT, and GSRE , and one of the independent determinants of e'. CONCLUSIONS: The alteration of LV shape associated with reduced ASA may be one of the causes of LV diastolic dysfunction independently of age in otherwise healthy subjects.

Coexisting cardiac diseases and pressure recovery phenomenon contribute to discrepancy between the echocardiographic severity of aortic stenosis and left ventricular hypertrophy.

BACKGROUND: Assessing left ventricular (LV) hypertrophy (LVH) is an important step in the echocardiographic diagnosis of aortic stenosis (AS). We aimed to investigate the causes of discrepancies between the degrees of AS and LVH. METHODS: The study subjects consisted of 149 consecutive patients with AS having aortic valve area <2.0 cm(2) (mean age 72.5 ± 11.9 years, 67 men and 82 women). Coexisting cardiac diseases were determined based on echocardiographic findings and comprehensive clinical judgment. Echocardiographic measurements included LV mass index (LVMI), aortic valve area index (AVAI), transaortic mean pressure gradient (MPG), valvulo-arterial impedance (Zva), energy loss coefficient (ELCo), and energy loss index (ELI). RESULTS: LVMI was not significantly correlated with AVAI and Zva, and had a weak correlation with MPG (r = 0.305, p = 0.0001). There were 55 patients in group A (non-severe AS without significant LVH), 58 in group B (non-severe AS with significant LVH), 7 in group C (severe AS without significant LVH), and 29 in group D (severe AS with significant LVH). Coexisting cardiac diseases were more frequently observed (p = 0.0003) in group B (50 %) than in group A (18 %). In group C, ELCo and (ELI - AVAI)/ELI were significantly greater than in group D (p = 0.043 and 0.007, respectively). CONCLUSION: Significant LVH seen in less than moderate AS is often due to coexisting cardiac diseases, and there may be an overestimation of AS severity due to pressure recovery among patients with apparently severe AS who do not have significant LVH.

Right ventricular diastolic dysfunction in patients with left ventricular hypertrophy: analysis of right ventricular myocardial relaxation using two-dimensional speckle tracking imaging.

BACKGROUND: Although several previous studies have suggested the presence of right ventricular (RV) diastolic dysfunction in patients with hypertrophic cardiomyopathy (HCM) and those with hypertensive left ventricular hypertrophy (HT-LVH), the mechanisms are still unclear. This study aimed to clarify the relationship between the RV global diastolic dysfunction in these patients and the regional myocardial diastolic function, including synchronicity of the interventricular septum and RV free wall. METHODS: In 20 age-matched patients with HT-LVH, 20 patients with HCM and 22 control subjects without pulmonary hypertension, RV isovolumic relaxation time (IRTR) was measured using continuous-wave Doppler echocardiography. The early diastolic peak strain rate (E SR) and time from QRS to E SR (T-E SR) were measured in the apical, mid-ventricular and basal segments of the interventricular septum and RV free wall using two-dimensional speckle tracking imaging (2DST). RESULTS: IRTR was more prolonged both in HT-LVH and in HCM than in the controls. The averaged septal E SR was reduced both in HT-LVH and in HCM (P < 0.0001, respectively), but the averaged RV free wall E SR was decreased only in HCM (P = 0.0007). E SR averaged for six septal and RV free wall segments was correlated with IRTR (r = -0.46, P = 0.0001). Neither intergroup difference nor correlation with IRTR was observed in a coefficient of variation of T-E SR for the six segments. CONCLUSIONS: RV global diastolic function is impaired in patients with HT-LVH and HCM due to relaxation abnormalities, not an asynchrony, of the myocardium surrounding the RV cavity. The detection of RV free wall relaxation abnormality using 2DST may be useful to differentiate HCM from HT-LVH.