The third heart sound (S(3)) is thought to be caused by the abrupt deceleration of left ventricular (LV) inflow during early diastole, increased LV filling pressures, and decreased LV compliance. We ...sought to determine whether the ratio of early mitral inflow velocity to diastolic velocity of the mitral annulus (E/E') could confirm the proposed mechanism of the S(3).
A total of 90 subjects underwent phonocardiography, echocardiography, tissue Doppler imaging, and left-sided heart catheterization.
Phonocardiography detected an S(3) in 21 patients (23%). Subjects with an S(3) had lower ejection fraction (P = .0006) and increased E deceleration rate (P < .0001), E/E' (P < .0001) and filling pressures (P < .0001). The phonocardiographic S(3) confidence score correlated with E/E' (r = 0.46; P < .0001) and E deceleration rate (r = 0.43, P = .0001). Of the echocardiographic variables, only E/E' was independently associated with the S(3) confidence score (P = .009), independently of invasively determined LV filling pressures (P = .001).
The most important determinants of the pathologic S(3) are an increased deceleration rate of early mitral inflow, elevated LV filling pressures, and abnormal compliance of the myocardium as measured by tissue Doppler imaging.
This report describes a case of heart failure with preserved ejection fraction in a post-menopausal woman with obesity. The case highlights a metabolic phenotype of heart failure with preserved ...ejection fraction that commonly manifests in women, with the discussion focusing on pathophysiology, mechanistic pathways, and potential targeted therapeutic strategies. (Level of Difficulty: Intermediate.)
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This report describes a case of heart failure with preserved ejection fraction in a post-menopausal woman with obesity. The case highlights a metabolic…
Background Recent studies suggest that Doppler echocardiography (DE)-based estimates of pulmonary artery systolic pressure (PASP) may not be as accurate as previously believed. We sought to determine ...the accuracy of PASP measurements using DE compared with right-sided heart catheterization (RHC) in patients with pulmonary hypertension (PH). Methods We compared DE estimates of PASP to invasively measure PASP during RHC in 160 consecutive patients with PH (part one). To account for possible changes in hemodynamics between DE and RHC, we then prospectively determined PASP in an additional 23 consecutive patients undergoing simultaneous RHC and DE (part two). Bland-Altman analyses were performed to evaluate the agreement between RHC and DE measurements of PASP. Accuracy was predefined as 95% limits of agreement within ± 10 mm Hg for PASP estimates. Results In part one, there was moderate correlation between DE and RHC measurements of PASP ( r = 0.68, P < .001). However, using Bland-Altman analysis, the bias for DE estimates of PASP was 2.2 mm Hg with 95% limits of agreement ranging from −34.2 to 38.6 mm Hg. DE estimates of PASP were determined to be inaccurate in 50.6% of patients. In part two, there was moderate correlation between DE and RHC measurements of PASP ( r = 0.71, P < .01). However, despite simultaneous DE and RHC measurements, the bias for DE estimates of PASP was 8.0 mm Hg with 95% limits of agreement ranging from −28.4 to 44.4 mm Hg. Conclusions DE estimates of PASP are inaccurate in patients with PH and should not be relied on to make the diagnosis of PH or to follow the efficacy of therapy.
Abstract Background Although the fourth heart sound (S4 ) is thought to be associated with a stiff left ventricle, this association has never been proven. Recently, single-beat estimation of the ...end-diastolic pressure volume relationship (EDPVR) has been characterized (P = αVβ ), allowing the estimation of EDPVR in larger groups of patients. We hypothesized that the S4 is associated with an upward- and leftward-shifted EDPVR, indicative of elevated end-diastolic stiffness. Methods and Results Ninety study participants underwent acoustic cardiographic analysis, echocardiography, and left heart catheterization. We calculated α and β coefficients to define the nonlinear slope of the EDPVR using the single-beat method for measuring left ventricular end-diastolic elastance. In the P = αVβ EDPVR estimation, α was similar ( P = .31), but β was significantly higher in the S4 group (5.96 versus 6.51, P = .002), signifying a steeper, upward- and leftward-shifted EDPVR curve in subjects with an S4 . The intensity of the S4 was associated with both β ( r = 0.42, P < .0001) and E/E′ ÷ stroke volume index, another index of diastolic stiffness ( r = 0.39, P = .0008). On multivariable analysis, β remained associated with the presence ( P = .008) and intensity ( P < .0001) of S4 after controlling for age, sex, and ejection fraction. Conclusions The S4 is most likely generated from an abnormally stiff left ventricle, supporting the concept that the S4 is a pathologic finding in older patients.
Whether increased severity of heart failure in African Americans is a result of differences in cardiac physiology is uncertain. The end-diastolic pulmonary regurgitation (EDPR) gradient is associated ...with abnormal cardiac physiology. We hypothesized that African American race is associated with an elevated EDPR gradient that may partially predispose African Americans to heart failure.
The Heart and Soul Study prospectively assessed the EDPR gradient in 480 patients with coronary disease. We used multivariable linear regression to investigate the independent association of African American race with EDPR gradient.
Compared with 393 non-African Americans, the 87 African Americans had similar indices of left ventricular systolic and diastolic function, left ventricular mass index, mitral regurgitation, peak tricuspid regurgitation gradient, and pulmonary velocity time integral. However, the EDPR gradient was significantly higher in African Americans (4.2 +/- 3.3 mm Hg) than in Caucasians (3.1 +/- 2.5 mm Hg) or other racial groups (3.5 +/- 2.7 mm Hg) (P = .008). In a multivariable model, African American race was a significant predictor of elevated EDPR gradient (beta coefficient 0.75, P = .03).
African American race is independently associated with an elevated EDPR gradient in patients with coronary artery disease.
Background Istaroxime is a novel intravenous agent with inotropic and lusitropic properties related to inhibition of the Na+ /K+ adenosine triphosphatase and stimulation of sarcoplasmic reticulum ...calcium adenosine triphosphatase activity. We analyzed data from HORIZON-HF, a randomized, controlled trial evaluating the short-term effects of istaroxime in patients hospitalized with heart failure and left ventricular ejection fraction ≤35% to test the hypothesis that istaroxime improves diastolic stiffness in acute heart failure syndrome. Methods One hundred twenty patients were randomized 3:1 (istaroxime/placebo) to a continuous 6-hour infusion of 1 of 3 doses of istaroxime or placebo. All patients underwent pulmonary artery catheterization and comprehensive 2-dimensional/Doppler and tissue Doppler echocardiography at baseline and at the end of the 6-hour infusion. We quantified diastolic stiffness using pressure-volume analysis and tissue Doppler imaging of the lateral mitral annulus (E′). Results Baseline characteristics were similar among all groups, with mean age 55 ± 11 years, 88% men, left ventricular ejection fraction 27% ± 7%, systolic blood pressure (SBP) 116 ± 13 mm Hg, and pulmonary capillary wedge pressure (PCWP) 25 ± 5 mm Hg. Istaroxime administration resulted in an increase in E′ velocities, whereas there was a decrease in E′ in the placebo group ( P = .048 between groups). On pressure-volume analysis, istaroxime decreased end-diastolic elastance ( P = .0001). On multivariate analysis, increasing doses of istaroxime increased E′ velocity ( P = .043) and E-wave deceleration time ( P = .001), and decreased E/E′ ratio ( P = .047), after controlling for age, sex, baseline ejection fraction, change in PCWP, and change in SBP. Conclusions Istaroxime decreases PCWP, increases SBP, and decreases diastolic stiffness in patients with acute heart failure syndrome.
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