Search

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2006.06.020 Byline: Ali Ahmed (a), Gilbert J. Perry (a), Jerome L. Fleg (b), Thomas E. Love (c), David C. Goff (d), Dalane W. Kitzman (d) Abstract: Prior studies demonstrating significant difference in outcomes in systolic and diastolic heart failure (HF) are often limited to hospitalized acute HF patients, and may be confounded by residual bias. In this analysis, we examined long-term mortality and hospitalization in a propensity score matched cohort of ambulatory chronic systolic and diastolic HF patients. Author Affiliation: (a) University of Alabama at Birmingham and VA Medical Center, Birmingham, AL (b) National Heart, Lung, and Blood Institute, Bethesda, MD (c) Case Western Reserve University, Cleveland, OH (d) Wake Forest University, Winston-Salem, NC Article History: Received 4 February 2006; Accepted 6 June 2006 Article Note: (footnote) Dr Ahmed is supported by grants 1-K23-AG19211-04 from the National Institute on Aging, National Institutes of Health, and 1-R01-HL085561-01 from the National Heart, Lung, and Blood Institute, National Institutes of Health., The Digitalis Investigation Group (DIG) study was conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the DIG Investigators. This manuscript has been reviewed by National Heart, Lung, and Blood Institute for scientific content and consistency of data interpretation with previous DIG publications, and significant comments have been incorporated before submission for publication.

We utilized mice with homozygous disruption of angiotensin-converting enzyme (ACE) (-/-), mice with heterozygous deletion of ACE (+/-), and wild-type mice (+/+) to test the hypothesis that genetic variation in ACE modulates tissue and plasma angiotensin (ANG) II concentrations. With the use of ANG I as substrate, kidney, heart, and lung ACE activity was reduced 80% in -/- mice compared with +/+ mice. However, ANG II concentrations and ANG II-to-ANG I ratios in the kidney, heart, and lung did not differ among genotypes. In contrast, plasma ANG II concentrations in -/- mice were angiotensin I; chymase; angiotensin-converting enzyme

Abstract Background Although cardiovascular magnetic resonance (CMR) is frequently performed to measure accurate LV volumes and ejection fractions, LV volume-time curves (VTC) derived ejection and filling rates are not routinely calculated due to lack of robust LV segmentation techniques. VTC derived peak filling rates can be used to accurately assess LV diastolic function, an important clinical parameter. We developed a novel geometry-independent dual-contour propagation technique, making use of LV endocardial contours manually drawn at end systole and end diastole, to compute VTC and measured LV ejection and filling rates in hypertensive patients and normal volunteers. Methods 39 normal volunteers and 49 hypertensive patients underwent CMR. LV contours were manually drawn on all time frames in 18 normal volunteers. The dual-contour propagation algorithm was used to propagate contours throughout the cardiac cycle. The results were compared to those obtained with single-contour propagation (using either end-diastolic or end-systolic contours) and commercially available software. We then used the dual-contour propagation technique to measure peak ejection rate (PER) and peak early diastolic and late diastolic filling rates (ePFR and aPFR) in all normal volunteers and hypertensive patients. Results Compared to single-contour propagation methods and the commercial method, VTC by dual-contour propagation showed significantly better agreement with manually-derived VTC. Ejection and filling rates by dual-contour propagation agreed with manual (dual-contour – manual PER: -0.12 ± 0.08; ePFR: -0.07 ± 0.07; aPFR: 0.06 ± 0.03 EDV/s, all P = NS). However, the time for the manual method was ~4 hours per study versus ~7 minutes for dual-contour propagation. LV systolic function measured by LVEF and PER did not differ between normal volunteers and hypertensive patients. However, ePFR was lower in hypertensive patients vs. normal volunteers, while aPFR was higher, indicative of altered diastolic filling rates in hypertensive patients. Conclusion Dual-propagated contours can accurately measure both systolic and diastolic volumetric indices that can be applied in a routine clinical CMR environment. With dual-contour propagation, the user interaction that is routinely performed to measure LVEF is leveraged to obtain additional clinically relevant parameters.

Background: In 2016, the American Society of Echocardiography (ASE) released guidelines for identifying left ventricular (LV) diastolic dysfunction (DD), but its ability to detect early hemodynamic abnormalities is not well established, especially in the setting of subclinical coronary artery disease (CAD). We hypothesize that the accuracy of ASE categorization of early LVDD is affected by knowledge of whether CAD history is present. Methods: We studied 34 patients (age 62 ± 7 years) with NYHA class I to II symptoms and with transthoracic echocardiography without findings suggesting myocardial disease (all with preserved LV ejection fraction), who underwent cardiac catheterization with high‐fidelity LV pressure measurement. Echocardiographic images were evaluated for LVDD using ASE algorithm without and with knowledge of CAD history and angiography findings. CAD was considered as having DD for the algorithm. Results: CAD was identified in 22 patients at catheterization (65%). Using ASE guidelines without including history of CAD or angiographic results, 29 patients were DD−, 3 were DD+ (all grade II), and 2 were indeterminate. Inclusion of CAD history recategorized 59% (n = 20) patients to DD+ (all grade I) from DD− (P <.0001). Nineteen of the recategorized patients (95%) had increased isovolumetric relaxation time (IVRT). The addition of echocardiographic IVRT improved discrimination between DD− and DD+, when the presence of CAD is unknown. Conclusions: 2016‐ASE algorithm reasonably accurately identifies early LVDD at rest as reflected by LV catheterization when CAD is disclosed, but without knowledge of the presence of CAD, it underdiagnoses DD+ grade I. The addition of IVRT may improve early LVDD diagnostics. [ABSTRACT FROM AUTHOR]