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Kheradvar A.,University of California at Irvine | Assadi R.,Loma Linda University | Falahatpisheh A.,University of California at Irvine | Sengupta P.P.,Zena And Michael A Wiener Cardiovascular Institute
Journal of the American Society of Echocardiography | Year: 2012

Background: Previous experimental models have related transmitral vortex formation to the longitudinal recoil of left ventricle. However, little is known about the relationships among left ventricular (LV) longitudinal relaxation, transmitral filling patterns, and LV vortex formation in clinical settings. The aim of this study was to compare the vortex formation time index among a heterogeneous group of patients with diastolic dysfunction to understand the relationship between transmitral vortex formation and abnormal diastolic filling patterns. Methods: Echocardiographic data from 107 subjects were retrospectively evaluated. The study population was categorized into four groups on the basis of transmitral early and late diastolic Doppler filling patterns as normal (n = 45), impaired relaxation (n = 14), pseudonormal (n = 26), and restrictive (n = 22). Vortex formation time was computed from the governing equations based on transmitral flow and ejection fraction. Results: Differences in vortex formation time index were found to be significant among all the studied groups (P <.0001). The trend of vortex formation during a cardiac cycle was compared in normal hearts and those with diastolic dysfunction. Mitral annular velocity (e′) was found to decrease significantly (P < .0001) in subjects with abnormal transmitral filling patterns compared with normal subjects. The difference in e′ among all the affected groups was not found to be significant (P =.68). Conclusions: The findings of this study suggest that patients with different patterns of transmitral diastolic filling show significant changes in LV vortex formation time despite the absence of significant differences in mitral annulus recoil during diastole. © 2012 by the American Society of Echocardiography. Source


Feig J.E.,Zena And Michael A Wiener Cardiovascular Institute
Annals of Global Health | Year: 2014

Background: Based on studies that date back to the 1920s, regression and stabilization of atherosclerosis in humans has gone from just a dream to one that is achievable. Review of the literature indicates that the successful attempts at regression generally applied robust measures to improve plasma lipoprotein profiles. Examples include extensive lowering of plasma concentrations of atherogenic apolipoprotein B and enhancement of reverse cholesterol transport from atheromata to the liver. Findings: Possible mechanisms responsible for lesion shrinkage include decreased retention of atherogenic apolipoprotein B within the arterial wall, efflux of cholesterol and other toxic lipids from plaques, emigration of lesional foam cells out of the arterial wall, and influx of healthy phagocytes that remove necrotic debris as well as other components of the plaque. This review will highlight the role key players such as LXR, HDL and CCR7 have in mediating regression. Conclusion: Although much progress has been made, there are many unanswered questions. There is, therefore, a clear need for preclinical and clinical testing of new agents expected to facilitate atherosclerosis regression with the hope that additional mechanistic insights will allow further progress. © 2014 Icahn School of Medicine at Mount Sinai. Source


Feig J.E.,Zena And Michael A Wiener Cardiovascular Institute | Feig J.L.,New York University
Frontiers in Physiology | Year: 2012

Atherosclerosis is the number one cause of death in the Western world. It results from the interaction between modified lipoproteins and cells such as macrophages, dendritic cells (DCs), T cells, and other cellular elements present in the arterial wall. This inflammatory process can ultimately lead to the development of complex lesions, or plaques, that protrude into the arterial lumen. Ultimately, plaque rupture and thrombosis can occur leading to the clinical complications of myocardial infarction or stroke. Although each of the cell types plays roles in the pathogenesis of atherosclerosis, the focus of this review will be primarily on the macrophages and DCs. The role of these two cell types in atherosclerosis is discussed, with a particular emphasis on their involvement in atherosclerosis regression. © 2012 Feig and Feig. Source


Dutt D.P.,Zena And Michael A Wiener Cardiovascular Institute | Pinney S.P.,Mount Sinai School of Medicine
Current Opinion in Cardiology | Year: 2014

PURPOSE OF REVIEW: The Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) I classification encompasses patients with varying clinical presentations and prognoses. The purpose of this review is to discuss four sub-classifications of cardiogenic shock patients (acute myocardial infarction, acute decompensated heart failure, biventricular failure, and myocarditis), and explore management considerations for these groups, with particular emphasis on strategies for device placement. RECENT FINDINGS: In single-center studies, the use of intra-aortic balloon counterpulsation, percutaneous ventricular assist devices, and extra-corporeal membrane oxygenation (ECMO) has allowed approximately half of cardiogenic shock patients to receive an implantable left ventricular assist device (LVAD) or heart transplant, or experience myocardial recovery. Primary implantation of a durable LVAD in well-selected myocardial infarction shock patients was associated with a 1-year survival of 86% in one small case series. Analysis of a multi-institutional database suggests patients older than 65 years have a lower post-implantation survival compared with younger recipients. SUMMARY: Device selection strategies for INTERMACS I patients are predicated on a patients prognosis, hemodynamic stability, end organ, and neurologic status. Percutaneous assist devices may be preferred for patients with favorable prognoses, ECMO for patients with hemodynamic compromise, and durable mechanical support for patients failing to recover sustainable myocardial function after short-term device use. © 2014 Wolters Kluwer Health. Source


Chen-Scarabelli C.,University of Michigan | Scarabelli T.M.,Zena And Michael A Wiener Cardiovascular Institute | Ellenbogen K.A.,Virginia Commonwealth University | Halperin J.L.,Zena And Michael A Wiener Cardiovascular Institute
Journal of the American College of Cardiology | Year: 2015

Atrial fibrillation (AF) is the most common clinically significant arrhythmia and conveys an increased risk of stroke, regardless of whether it is symptomatic. Despite multiple studies supporting an association between subclinical atrial tachyarrhythmias (ATs) detected by cardiac implantable electronic devices and increased risk of thromboembolic events, clinical intervention for device-detected AT remains sluggish, with some clinicians delaying treatment and instead opting for continued surveillance for additional or longer episodes. However, the 2014 updated clinical practice guidelines on AF recommend use of the CHA2DS2-VASc stroke risk score for nonvalvular AF, with oral anticoagulation recommended for scores ≥2, regardless of whether AF is paroxysmal, persistent, or permanent. This paper reviews the epidemiology of AF and mechanisms of stroke in AF, and discusses device-detected AF and its clinical implications. © 2015 American College of Cardiology Foundation. Source

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