Early Diastolic Left Ventricular Inflow Research Articles

Relationships between kidney dysfunction and left ventricular diastolic dysfunction: a hospital-based retrospective study.

Preclinical left ventricular diastolic dysfunction (LVDD) is a high-risk state for heart failure. Kidney dysfunction is a known risk factor for heart failure, but its association with asymptomatic LVDD is not well-known. A hospital-based retrospective cohort study was conducted on patients who underwent echocardiogram between 2006 and 2016 to assess the association between baseline kidney function and LVDD on echocardiogram. E/e' ratio was defined as the ratio of peak velocity of early diastolic left ventricular inflow (E) to mitral annular velocity (e'). The primary outcome was time to development of LVDD, which was defined as E/e' ratio > 14. The changes in the E/e' ratio and other echocardiographic parameters were assessed using a mixed effects model. Among 1167 patients, the mean age was 61 years, and the mean baseline E/e' ratio and ejection fraction were 9.6 and 69%, respectively. During a median follow-up of 3.2 years, 231 (19.8%) people developed LVDD. According to eGFR (mL/min/1.73m2), the risk for LVDD based on hazard ratio [95% confidence interval (95% CI)] was 1.20 (0.82, 1.75) for 60 to < 90, 1.42 (0.87, 2.31) for 45 to < 60, and 2.57 (1.61, 4.09) for < 45 (P trend < 0.001). The adjusted risks (95% CI) for annual change in E/e' ratio was 0.09 (0.03, 0.14) overall and 0.28 (0.11, 0.45) in the lowest eGFR group; the trend in changes in annual E/e' ratio by baseline eGFR was significant (P trend = 0.01). Relatively low kidney function was related with the risks for LVDD. Long-term cohort studies are warranted to confirm the association between LVDD and symptomatic heart failure in patients with kidney dysfunction.

A novel color M-mode Doppler echocardiographic index for left ventricular relaxation: depth of the maximal velocity point of left ventricular inflow in early diastole.

Color M-mode Doppler echocardiography (CMD) has been utilized in assessing left ventricular (LV) filling dynamics. We tested a novel CMD index, the depth of the spatiotemporal maximum of early diastolic inflow (D-maxV) in the left ventricle, to clarify its significance in assessing LV diastolic function. In 26 normal subjects and 32 patients with ischemic heart disease, D-maxV was determined with CMD as the distance from the mitral valve opening point to the center of the aliasing area in early diastole. Transmitral flow velocity was measured with pulsed Doppler. During routine catheterization, high-fidelity LV pressure measurements yielded diastolic variables in patients. D-maxV was significantly lower in the patients than the normals (13.0+/-7.0 vs 23.4+/-6.8 mm, P < 0.0001). D-maxV exhibited significant linear correlations with the minimal first derivative of LV pressure (r = 0.72, P < 0.01), the time constant of isovolumic relaxation (r = -0.67, P < 0.01), and LV minimal pressure (r = -0.53, P < 0.02) in the patients with wide ranges of peak early to late inflow velocity ratio (0.43-3.9) and deceleration time of early filling (79-293 ms). D-maxV showed an inverse correlation with LV end-diastolic pressure (r = -0.53, P < 0.02) and no significant correlation with mean pulmonary capillary wedge pressure. Moreover, Kaplan-Meier analysis focusing on the patients with myocardial infarction revealed that the group with D-maxV < 10.4 mm (n = 13) exhibited a lower cumulative cardiac event-free rate than that with D-maxV > or = 10.4mm (n = 14) (49.4% vs 92.9% at 5 years, P < 0.05). The depth of the spatiotemporal maximum of early diastolic LV inflow velocity reflects LV relaxation and is free of pseudonormalization. Evaluation of the LV relaxation separately from preload may have a prognostic value for myocardial infarction.

Preload reduction by a single hemodialysis unmasks abnormal left ventricular inflow jet dynamics and early diastolic incoordinate long axis motion in patients on maintenance hemodialysis

Background. Our objective was to investigate changes in left ventricular inflow jet width and long axis motion in patients on maintenance hemodialysis by preload reduction due to a single hemodialysis. Methods. We evaluated 20 patients on stable maintenance hemodialysis by Doppler echocardiography. Twenty age-matched controls were also examined. Transmitral flow, left ventricular long axis M-mode (LAM) echocardiography, and two-dimensional color Doppler early diastolic left ventricular inflow jet width (JW) were analyzed before and after a single hemodialysis. Results. Before hemodialysis, compared with controls, JW was reduced in patients (2.1 ± 0.4 vs 2.4 ± 0.3 cm; P < 0.01), and early diastolic excursion of LAM (LAM-E) was also reduced. Peak velocity of the Doppler transmitral early diastolic wave (E) and late diastolic wave (A) were both higher, while the E/A ratio was lower. After hemodialysis, compared with the predialysis findings, JW and early diastolic excursion of LAM were unchanged; however, Doppler transmitral flow showed decreased E and E/A. Thus, in hemodialysis patients, inflow jet width was narrow, and unchanged by a single hemodialysis, while the Doppler transmitral flow pattern was changed mainly to dominant A waves and reduced E waves. Conclusions. In patients on maintenance hemodialysis, the abnormal left ventricular inflow jet dynamics and early diastolic incoordinate long axis motion are unmasked by a preload reduction due to single hemodialysis in a different way from a transmitral Doppler flow pattern.

Early diastolic left ventricular inflow pressures in normal subjects and patients with dilated cardiomyopathy. Reconstruction from pulsed Doppler echocardiography.

To estimate early diastolic left ventricular inflow pressures in normal subjects and patients with dilated cardiomyopathy, and thus to assess the potential effect of restoring forces. Early diastolic left ventricular inflow pressures were reconstructed using the ventricular blood as an accelerometer, by measuring velocity at 1 cm intervals within the left ventricle from mitral ring to apex by pulsed Doppler echocardiography, and differentiating the records to obtain the acceleration. Aortic component of second heart sound (A2) was used to fix relative timings. The local pressure gradient was determined from the acceleration at each level, and the total pressure drop during the acceleration (+ peak PD) and deceleration (- peak PD) phases of the filling interval were determined by summing the local increments. The total stroke volume (SV) at the left ventricular outflow tract and the mitral stroke distances (MSD) were also determined, using the time-velocity integral at mitral ring level. Effective flow orifice area was thus SV/MSD. Inflow jet width across the mitral valve was estimated by cross sectional colour Doppler flow mapping. 32 patients with dilated cardiomyopathy with a dominant mitral E or summation wave, and 24 normal subjects of similar ages. Normal + peak PD was 3.9 (SD 0.7) v 7.4 (2.2) mm Hg in dilated cardiomyopathy (P < 0.01). Normal - peak PD was 2.5 (0.9) v 5.6 (2.8) mm Hg in cardiomyopathy (P < 0.01). Normal effective flow orifice area was 5.9 (1.3) v 1.9 (0.8) [range 0.9 approximately 3.7] cm2 in cardiomyopathy (P < 0.01). This corresponded to 71 (18)% of the end systolic cavity cross section in normals v 11 (6)% in dilated cardiomyopathy (P < 0.01). Normal cross sectional colour inflow jet width was 2.7 (0.3) v 1.5 (0.4) cm in cardiomyopathy (P < 0.01). The jet width correlated with flow width calculated from effective flow orifice area (r = 0.82, P < 0.01). (1) Total early diastolic positive and negative peak pressure drop are normally low, so that significant negative left ventricular pressures are not needed to explain normal resting early diastolic mitral flow velocities. (2) These low pressure drops are only possible with a large effective orifice area approaching end systolic left ventricular cavity area. (3) Atrioventricular pressure drops are much greater in dilated cardiomyopathy, where increased inflow accelerations are due to reduced effective flow orifice area. These disturbances will impair filling independently of any abnormality of relaxation or compliance.

Mechanism of physiologic and pathologic S3 gallop sounds.

Although the S3 gallop sound has long been used clinically as an indicator of left ventricular systolic dysfunction, the mechanism responsible for its production remains controversial. The same sound is often found in young healthy individuals, and whether a similar mechanism is responsible is also unknown. The relationship of the S3 gallop sound to the dynamics of left ventricular filling was compared in 18 healthy young triathletes and 15 older subjects with cardiac disease. Twenty healthy normal subjects without an S3 were included as controls. Phonocardiographic, two-dimensional echocardiographic, and Doppler echocardiographic analysis of left ventricular inflow were evaluated. The S3 in both groups always occurred close to peak early filling velocity (E), during early flow deceleration. Mean E deceleration rate was higher in the subjects with S3 (726 +/- 153 cm/sec2 in the triathletes and 819 +/- 274 cm/sec2 in those with cardiac disease) than in control subjects (563 +/- 131 cm/sec2, p less than 0.001 in both cases). Ten triathletes underwent examination both before and immediately after 30 degrees head-up tilt. E deceleration rate dropped significantly with head-up tilt (720 +/- 137 vs 590 +/- 174 cm/sec2, p less than 0.01), while concurrently the S3 disappeared or was diminished in amplitude. Similar changes were seen in subjects with cardiac disease. We conclude that both the "pathologic" and "physiologic" S3 are related to abnormally rapid deceleration of early diastolic left ventricular inflow. Although the presence of the S3 is not dependent on the state of left ventricular systolic function, diastolic filling is characterized by a predominance of early inflow with a rapid flow deceleration rate.

Comparison of Doppler echocardiographic and hemodynamic indexes of left ventricular diastolic properties in coronary artery disease

Transmitral flow velocity was measured by Doppler echocardiography in 15 patients with coronary artery disease simultaneously with high-fidelity recording of left ventricular pressure. Doppler echocardiographic recordings were also performed in 14 age- and heart rate-matched normal subjects. Statistically significant differences (p < 0.05) in acceleration half-time (55.3 ± 8.2 vs 70.4 ± 14.9 ms), deceleration half-time (83.1 ± 17.9 vs 109.5 ± 18.1 ms), deceleration rate (4.9 ± 0.9 vs 3.1 ±0.9 m/s 2), peak velocity of early diastolic left ventricular inflow (E wave) (0.78 ± 0.13 vs 0.61 ± 0.13 m/s) and A E ratio (0.74 ± 0.20 vs 0.98 ±0.31) between normal subjects and patients were noted. There was no significant difference in peak velocity of atrial systolic flow (A wave) between normal subjects and patients. Correlation between transmitral flow indexes and hemodynamic indexes of left ventricular diastolic properties were poor, with r values ranging from 0.02 to 0.65. Significant correlations between deceleration rate versus maximal isovolumic left ventricular pressure decrease (maximum − dP dt ) and A wave versus maximum − dP dt (p < 0.05) were found (0.53 and 0.65, respectively). Deceleration rate was the most sensitive index of isovolumic relaxation assessed by hemodynamic methods, whereas the A E ratio was a poor indicator of hemodynamic measurements of isovolumic relaxation. An abnormal deceleration rate had 100% specificity for detecting abnormal maximum − dP dt , while abnormal acceleration half-time, deceleration half-time and A E ratio had 80% specificity for detecting abnormal time constant. The deceleration rate, acceleration half-time, deceleration half-time and A E ratio had a predictive value of 60 to 100% for the detection of abnormal maximum − dP dt and time constant.