Hitomi Narita

Correlation between Left Ventricular End-diastolic Pressure and Peak Left Atrial Wall Strain during Left Ventricular Systole

OBJECTIVE Left atrial (LA) reservoir function is determined by integration of LA relaxation and left ventricular (LV) systolic function, and LV diastolic dysfunction increases LA volume at end systole. This study investigates the effect of LV end-diastolic pressure on LA wall tension during LV systole. METHODS A total of 101 stable patients with sinus rhythm undergoing cardiac catheterization were studied. LA wall extension during LV systole was evaluated as LA wall strain in the longitudinal direction obtained using two-dimensional ultrasound speckle tracking imaging. LV end-diastolic pressure and LV end-systolic and end-diastolic volumes were obtained in cardiac catheterization, and LV ejection fraction was determined. RESULTS Peak LA wall strain during LV systole had a significant inverse correlation with LV end-diastolic pressure (r = - 0.76, P < .0001). This correlation was also significant in patients with preserved LV systolic function (LV ejection fraction > or =50%) (r = - 0.64, P < .0001). In patients with peak LA wall strain during LV systole of less than 30%, 89% had elevated LV end-diastolic pressure (> or =16 mm Hg). CONCLUSION Elevated LV end-diastolic pressure is associated with a decrease of peak LA wall strain in the longitudinal direction during LV systole. In patients with peak LA wall strain during LV systole of less than 30%, the majority had elevated LV end-diastolic pressure, while most patients with peak LA wall strain during LV systole 45% or higher had normal LV end-diastolic pressures. In patients whose LV ejection fraction is 50% or more, when peak LA wall strain during LV systole is between 30% and 44%, it is not possible to predict LV end-diastolic pressure from peak LA wall strain measures.

Clinical usefulness of carotid arterial wave intensity in assessing left ventricular systolic and early diastolic performance

Wave intensity (WI) is a novel hemodynamic index, which is defined as (dP/dt)·(dU/dt) at any site of the circulation, where dP/dt and dU/dt are the derivatives of blood pressure and velocity with respect to time, respectively. However, the pathophysiological meanings of this index have not been fully elucidated in the clinical setting. Accordingly, we investigated this issue in 64 patients who underwent invasive evaluation of left ventricular (LV) function. WI was obtained at the right carotid artery using a color Doppler system for blood velocity measurement combined with an echo-tracking method for detecting vessel diameter changes. The vessel diameter changes were automatically converted to pressure waveforms by calibrating its peak and minimum values by systolic and diastolic brachial blood pressures. The WI of the patients showed two sharp positive peaks. The first peak was found at the very early phase of LV ejection, while the second peak was observed near end-ejection. The magnitude of the first peak of WI significantly correlated with the maximum rate of LV pressure rise (LV max. dP/dt) (r = 0.74, P ≪ 0.001). The amplitude of the second peak of WI significantly correlated with the time constant of LV relaxation (r = −0.77, P ≪ 0.001). The amplitude of the second peak was significantly greater in patients with the inertia force of late systolic aortic flow than in those without the inertia force (3 080 ± 1 741 vs 1 890 ± 1 291 mmHg m s−3, P ≪ 0.01). These findings demonstrate that the magnitude of the first peak of WI reflects LV contractile performance, and the amplitude of the second peak of WI is determined by LV behavior during the period from late systole to isovolumic relaxation. WI is a noninvasively obtained, clinically useful parameter for the evaluation of LV systolic and early diastolic performance at the same time.

Evaluation of left ventricular early diastolic performance by color tissue Doppler imaging of the mitral annulus

A noninvasive assessment of left ventricular (LV) diastolic performance by tissue Doppler imaging was performed in 56 patients (8 patients with atypical chest pain, 42 with coronary artery disease with a previous myocardial infarction, and 6 without a previous myocardial infarction) who underwent cardiac catheterization. Mitral annular velocity (MAV) during early ventricular diastole was obtained by M-mode color tissue Doppler imaging at the posterior corner of the mitral annulus. In each patient, the negative peak of the first derivative of LV pressure decay (peak -dP/dt) and a time constant of LV relaxation (tau) were calculated from the LV pressure waves obtained by a catheter-tip micromanometer. LV end-systolic volume index was measured from contrast left ventriculography. MAV during early diastole was significantly correlated with tau (r = -0.73, p <0.001), peak -dP/dt (r = 0.58, p <0.001), and LV end-systolic volume index (r = -0.63, p <0.001). On multivariate regression analysis with MAV during early diastole, tau and LV end-systolic volume index were selected as prime determinants (r = 0.80, p <0.001). These findings suggest that MAV during early diastole has a direct relation to LV elastic recoil as well as to LV relaxation. MAV during early diastole gives important information regarding LV behavior in late systole to early diastole where LV early diastolic performance is determined.

Bilirubin as a prognostic marker in patients with pulmonary arterial hypertension

BackgroundLiver dysfunction reflects the status of heart failure, with congestion and low perfusion of the liver serving as causative mechanisms. Previous studies demonstrated relationship between the results of liver function test and the prognosis in patients with heart failure. However, few studies have examined this relationship in patients with pulmonary arterial hypertension (PAH).MethodsThe subjects were 37 patients with PAH (8 men and 29 women; 18 with idiopathic PAH and 19 with connective tissue disease-associated PAH). A blood test was performed after a 3-month period free from hospitalization and without changes in functional class, treatment, heart sounds, body weight, or heart rate.ResultsIn a mean follow-up period of 635 ± 510 days, 12 patients died due to heart failure, 2 died due to pulmonary hemorrhage, and 23 patients survived. Cox proportional hazard analyses identified functional class (p < 0.001), plasma concentration of brain natriuretic peptide (BNP) (p = 0.001), and hyperbilirubinemia (serum total bilirubin > 1.2 mg/dL; p < 0.001; hazard ratio = 13.31) as predictors of mortality. Patients with hyperbilirubinemia had a worse functional class (P = 0.003), a higher right atrial pressure (p < 0.001), a higher plasma concentration of BNP (p = 0.004), and a larger Doppler right ventricular index of the right ventricle (p = 0.041).ConclusionElevated serum bilirubin is a risk factor for death in patients with PAH.

Takayasu's arteritis accompanied with massive pericardial effusion--a case report.

A 40-year-old woman who had been treated for Takayasus arteritis was admitted to the hospital with fever, fatigue, malaise, and severe chest pain. Computed tomography of the chest demonstrated massive pericardial effusion and bilateral pleural effusion. In laboratory data, the C-reactive protein was high at 22.0 mg/dL, and erythrocyte sedi mentation rate was also high at 80 mm/hr. The diagnosis was pericarditis with a recur rence of the systemic inflammatory process of Takayasus arteritis. The patient was treated with methylprednisolone pulse therapy. Her massive pericardial effusion disap peared without pericardiocentesis.

Left ventricular isovolumic relaxation flow and left ventricular systolic performance

We investigated isovolumic relaxation flow in patients with coronary artery disease (CAD) and evaluated the relationship between its velocity and left ventricular performance in 23 patients with atypical chest pain, 30 patients with CAD without prior myocardial infarction (MI), and 57 patients with prior MI, in whom cardiac catheterization was performed. The isovolumic relaxation flow velocity was measured at the basal portion of the left ventricle with pulsed Doppler echocardiography. The isovolumic relaxation flow ( > 15 cm/sec) was detected in 98 of 110 patients. The isovolumic relaxation flow velocity was significantly lower in patients with prior MI than in patients with atypical chest pain (p < 0.001) and in those with CAD without prior MI (P < 0.05). It was significantly lower in patients with CAD without prior MI than in those with atypical chest pain (p < 0.05). The isovolumic relaxation flow velocity showed a significant positive correlation with left ventricular ejection fraction. It also showed a significant negative correlation with left ventricular end-systolic volume index. These findings suggest that the isovolumic relaxation flow velocity is decreased in patients with CAD and is influenced by left ventricular systolic performance. Isovolumic relaxation flow may be a clinical manifestation of elastic recoil of the left ventricle.

Effects of volume loading on pulmonary venous flow pattern in dogs with normal left ventricular function

The effects of altered loading conditions on the pattern of pulmonary venous flow are poorly understood. The authors investigated such effects, therefore, by using volume loading in 6 open-chest dogs. The pulmonary venous flow volume rate curve was obtained with a transit-time ultrasonic flowmeter at a fixed heart rate. Measurements were performed in the control and several states during the intravenous infusion of dextran. The influences of volume loading on hemodynamic and pulmonary venous flow variables were compared between the control state and three interventional states in which mean left atrial pressure was approximately 1, 2, and 3 mm Hg above the control value. The systolic flow volume (SI), which corresponds to left atrial reservoir volume, significantly increased, but the early diastolic flow volume (DI), which corresponds to left atrial conduit volume, did not show significant change with volume loading. The flow volume during left atrial contraction significantly increased with volume loading. The flow volume during one cardiac cycle (PVF) significantly increased with volume loading. Approximately 73% of increased PVF was distributed to the systolic flow. The rest was distributed to the early diastolic flow (14%) and to the flow during left atrial contraction (12%). The change in the ratio of SI/DI significantly and positively correlated with the change in mean left atrial pressure (r=0.87, P < 0.001). These findings indicate that increased pulmonary venous flow induced by volume loading in dogs with normal left ventricular function is mainly distributed to the left atrial reservoir volume.

Comparative effects of volume loading on pulmonary venous flow in dogs with normal heart and with myocardial ischemia

The influences of cardiac loading conditions and left ventricular performance on pulmonary venous flow are poorly understood. The authors studied the effects of volume loading on the pattern of pulmonary venous flow in normal and ischemic hearts. Thirteen anesthetized dogs were equipped with a transit-time ultrasonic flow probe around the left upper pulmonary vein. In 6 of the dogs, the left anterior descending artery was ligated to induce myocardial ischemia. The remaining 7 dogs had normal hearts. Heart rate was fixed at 110 beats/minute by right atrial pacing. Dextran was infused from the femoral vein until mean left atrial pressure increased 3 mm Hg above the baseline value in both groups. In normal heart, systolic pulmonary venous flow volume (SI) increased significantly, but early diastolic flow volume (DI) did not show a significant change during volume loading. The ratio of SI/DI increased significantly (1.12 ±0.34 vs 2.11 ±0.49, P<0.05). After ligation of the left anterior descending artery, the SI and DI decreased significantly. The ratio of SI/DI did not show a significant change (0.88 ±0.32 vs 0.87 ±0.30, ns). In dogs with myocardial ischemia, volume loading caused increases in the SI and DI. However, no significant change was observed in the ratio of SI/DI (0.87 ±0.30 vs 0.97 ±0.36, ns). These findings demonstrate that left ventricular performance influences the alter ation in pulmonary venous flow pattern that is caused by systemic volume loading.

Peak mitral annular velocity during early diastole and propagation velocity of early diastolic filling flow are not interchangeable as the parameters of left ventricular early diastolic function.

The difference between peak mitral annular velocity during early diastole (Ea) and the propagation velocity of left ventricular (LV) early diastolic filling flow (Vp) obtained using Doppler imaging as LV relaxation parameters was not fully elucidated. Thus, this issue was investigated in 117 patients with suspected coronary artery disease. During cardiac catheterization, LV volumes, the LV relaxation time constant Tp, and inertia force of late systolic aortic flow were obtained. Ea significantly and closely correlated with Tp (r = -0.70, p <0.0001) and significantly but weakly correlated with LV ejection fraction (r = 0.37, p <0.0001) and inertia force (r = 0.34, p = 0.0002). Conversely, Vp significantly and closely correlated with both LV ejection fraction (r = 0.66, p <0.0001) and inertia force (r = 0.72, p <0.0001) and significantly but weakly correlated with Tp (r = - 0.35, p = 0.0001). In conclusion, Ea and Vp reflect different aspects of LV behavior from end-systole to early diastole. Ea can be used to index LV relaxation, whereas Vp might not be a proper parameter of LV intrinsic relaxation because it is significantly dependent on LV systolic function and LV chamber size at end-systole. Both parameters are not interchangeable as those of LV early diastolic function. Vp may be a noninvasive parameter of LV elastic recoil.

Is the Blood Flow in the Left Ventricle during the Isovolumic Relaxation Period a Useful Parameter of Left Ventricular Systolic and Early Diastolic Performance

Left ventricular (LV) early diastolic performance is determined by LV behavior in the late systole to early diastole and may relate to the physical potential of patients. Isovolumic relaxation flow (IRF) velocity was obtained by continuous Doppler echocardiography in the left ventricle from the apex in 26 patients with atypical chest pain and 63 patients with coronary artery disease (CAD) with or without prior myocardial infarction (MI) who underwent cardiac catheterization. In each patient, a time constant of LV relaxation (τ) was calculated from the LV pressure waves obtained by a catheter-tipped micromanometer. The LV end-systolic volume index was measured using contrast left ventriculography. IRF velocity in patients having CAD with prior MI (24.8 ± 5.4 cm/s) was significantly less than in those with atypical chest pain (41.2 ± 9.6 cm/s). It was also significantly less than in patients having CAD without prior MI (37.3 ± 6.8 cm/s). IRF velocity significantly correlated with the time constant τ (r = –0.42, p < 0.001) and LV end-systolic volume index (r = –0.84, p < 0.001). This study indicates that IRF velocity obtained by continuous Doppler echocardiography in the left ventricle provides important information regarding LV systolic performance and early diastolic performance.