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1.
Am J Cardiovasc Dis ; 11(3): 404-409, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-34322311

RESUMEN

Rheumatoid Arthritis associated valvular heart disease (RA-VHD) may occur in patients in varying degrees of severity. Aortic valve involvement leading to severe symptomatic aortic insufficiency is a rare complication of rheumatoid arthritis. This entity has not been well characterized and its clinical predictors are undefined. The pathology of RA-VHD can extend from benign nodular development to acute valvulitis with late-stage leaflet fibrosis and severe valvular regurgitation. In this report, we describe a rare case of acute heart failure (AHF) resulting from severe aortic valve destruction and insufficiency due to persistent chronic inflammation in a patient with long-standing RA. Persistent systemic inflammation of RA involved the aortic valve causing nodular thickening and leaflet destruction. Our patient had compensated chronic heart failure due to progressive aortic insufficiency resulting from gradual leaflet destruction. However, she suddenly developed AHF requiring valve replacement. Her clinical presentation, gross and histological images suggest an acute/subacute disruption of the friable aortic leaflets that resulted in AHF.

2.
Diagnostics (Basel) ; 9(1)2019 Jan 23.
Artículo en Inglés | MEDLINE | ID: mdl-30678130

RESUMEN

BACKGROUND: While left ventricular ejection fraction (LVEF) has been shown to have prognostic value in ischemic cardiomyopathy (ICMX) patients, right ventricular ejection fraction (RVEF) has not been systematically evaluated in either ICMX or non-ischemic cardiomyopathy (NICMX) patients. Moreover, an accurate estimation of RVEF is problematic due to the geometry of the right ventricle (RV). Over the years, there have been improvements in the resolution, image acquisition and post-processing software for cardiac magnetic resonance imaging (CMR), such that CMR has become the "gold standard" for measuring RV volumetrics and RVEF. We hypothesize that CMR defines RVEF more so than LVEF and might have prognostic capabilities in ischemic and non-ischemic cardiomyopathy patients (ICMX and NICMX). METHODS: Patients that underwent CMR at our institution between January 2005 and October 2012 were retrospectively selected if three-dimensional (3D) LVEF < 35%. Patients were further divided into ICMX and NICMX groups. The electronic medical record (EMR) database inquiry determined all-cause mortality and major adverse cardiovascular events (MACE). Additionally, a Social Security Death Index (SSI) database inquiry was performed to determine all-cause mortality in patients who were lost to follow-up. Patients were further sub-grouped on the basis of 3D RVEF ≥ 20%. Separately, patients were sub-grouped by LVEF ≥ 20% in both ICMX and NICMX cases. A cut-off of ≥20% was chosen for the RVEF based on the results of prior studies showing significance based on Kaplan⁻Meier (KM) survival curves. Cumulative event rates were estimated for each subgroup using the KM analysis and were compared using the log-rank test. The 3D RV/LVEFs were compared to all-cause mortality and MACE. ICMX patients were defined using the World Health Organization (WHO) criteria. RESULTS: From a 7000-patient CMR database, 753 heart failure patients were selected. Eighty-seven patients met WHO definition of ICMX and NICMX (43 ICMX and 44 NICMX). The study patients were followed for a median of 3 years (Interquartile range or IQR 1.5⁻6.5 years). The mean age of patients was 58 ± 13 years; 79% were male. In ICMX, mean 3D LVEF was 21% ± 6% and mean 3D RVEF was 38% ± 14%, while for NICMX, mean 3D LVEF was 16% ± 6% and mean 3D RVEF was 30% ± 14% (p < 0.005 for intra- and inter-group comparison). It should be noted that LVEF < RVEF in both groups and the ejection fraction (EF) in NICMX was less than the corresponding EF in ICMX. Overall mortality was higher in ICMX than NICMX (12/40, 30% vs. 7/43, 16%; p < 0.05). Patients were stratified based on both RVEF and LVEF with a threshold of EF ≥ 20% separately. RVEF but not LVEF was a significant predictor of death for NICMX (χ² = 8; p < 0.005), while LVEF did not predict death in ICMX (χ² = 2, p = not significant). Similarly, time to MACE was predicted by RVEF for NICMX (χ² = 9; p < 0.005) but not by LVEF in ICMX (χ² = 1; p = NS). Importantly, RVEF, while predictive of NICMX MACE, did not emerge as a predictor of survival or MACE in ICMX. CONCLUSIONS: Via 3D CMR in non-ischemic CMX patients, RVEF has important value in predicting death and time to first MACE while 3D LVEF is far less predictive.

3.
PLoS One ; 10(3): e0121810, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-25807234

RESUMEN

BACKGROUND: Healthy middle-aged postmenopausal women have higher endothelium-dependent dilation and lower vasoconstrictor activity of endothelin-1 than men. Whether these sex-specific differences extend to patients with cardiovascular risk factors has not been investigated. The current study aimed to determine whether, in patients with cardiovascular risk factors, sex-specific differences exist in endothelium-dependent dilation and endothelin-1 activity. METHODS: Forearm blood flow responses were measured by strain-gauge plethysmography during the intra-arterial infusion of acetylcholine, sodium nitroprusside, and the selective endothelin type A receptor blocker BQ-123 in 50 women and 64 men with cardiovascular risk factors. RESULTS: Acetylcholine and sodium nitroprusside induced a significant vasodilation in women and men alike (p < 0.01 for both). Also BQ-123 caused a significant vasodilation (p < 0.001) in both groups. The vasodilator response to acetylcholine was greater in women compared to men; however there were no differences in the response to sodium nitroprusside and BQ-123 (p = NS for both) between the two sex groups. CONCLUSIONS: Middle-aged women with cardiovascular risk factors have significantly higher endothelium-dependent dilation than middle-aged men; however, vascular endothelin 1 activity is similar in the two groups. These findings suggest that the presence of cardiovascular risk factors is associated with sex-specific effects on endothelium-dependent dilation but not on endothelin 1 activity. Further study is needed to confirm our findings and to characterize the mechanisms underlying this sex-specific regulation of endothelial function.


Asunto(s)
Enfermedades Cardiovasculares/metabolismo , Enfermedades Cardiovasculares/fisiopatología , Endotelina-1/metabolismo , Endotelio Vascular/metabolismo , Endotelio Vascular/fisiopatología , Vasodilatación/fisiología , Acetilcolina/farmacología , Enfermedades Cardiovasculares/etiología , Antagonistas de los Receptores de Endotelina/farmacología , Endotelio Vascular/efectos de los fármacos , Femenino , Antebrazo/fisiopatología , Humanos , Infusiones Intraarteriales/métodos , Masculino , Persona de Mediana Edad , Nitroprusiato/farmacología , Péptidos Cíclicos/farmacología , Flujo Sanguíneo Regional/efectos de los fármacos , Factores de Riesgo , Caracteres Sexuales , Vasodilatación/efectos de los fármacos , Vasodilatadores/farmacología
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