Journal of the American College of Cardiology
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J. Am. Coll. Cardiol. · Nov 2014
Clinical impact of atrial fibrillation in patients with the HeartMate II left ventricular assist device.
Atrial fibrillation (AF) is common in patients with the HeartMate II (HMII) left ventricular assist device (LVAD), but the impact of AF on clinical outcomes is uncertain. ⋯ Although PAF is not associated with worse outcomes in patients with the HMII LVAD, PeAF may be associated with increased mortality and HF hospitalization. Patients with AF also may have thromboembolic events at higher INR levels.
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J. Am. Coll. Cardiol. · Oct 2014
Using the CHA2DS2-VASc score for refining stroke risk stratification in 'low-risk' Asian patients with atrial fibrillation.
A new scoring system, the anticoagulation and risk factors in atrial fibrillation (ATRIA) score, was proposed for risk stratification in patients with atrial fibrillation (AF). Whether the ATRIA scheme can adequately identify patients who are at low risk of ischemic stroke remains unknown. ⋯ Patients categorized as low-risk by use of the ATRIA score were not necessarily low-risk, and the annual stroke rates can be as high as 2.95% at 1-year follow-up and 2.84% at 15-year follow-up. In contrast, patients with a CHA2DS2-VASc score of 0 had a truly low risk of ischemic stroke, with an annual stroke rate of approximately 1%.
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J. Am. Coll. Cardiol. · Oct 2014
Multicenter StudyMyocardial atrophy and chronic mechanical unloading of the failing human heart: implications for cardiac assist device-induced myocardial recovery.
In animal models of heterotopic transplantation, mechanical unloading of the normal, nonhypertrophic heart results in atrophy. Primarily on the basis of these animal data, the notion that chronic left ventricular assist device (LVAD)-induced unloading will result in atrophy has dominated the clinical heart failure field, and anti-atrophic drugs have been used to enhance the cardiac recovery potential observed in some LVAD patients. However, whether unloading-induced atrophy in experimental normal heart models applies to failing and hypertrophic myocardium in heart failure patients unloaded by continuous-flow LVADs has not been studied. ⋯ Structural, ultrastructural, microstructural, metabolic, molecular, and clinical functional data indicated that prolonged continuous-flow LVAD unloading does not induce hypertrophy regression to the point of atrophy and degeneration. These findings may be useful in designing future investigations that combine LVAD unloading and pharmaceutical therapies as a bridge to recovery of the failing heart.