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James B. Young

Researcher at Cleveland Clinic

Publications -  538
Citations -  46895

James B. Young is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Heart failure & Transplantation. The author has an hindex of 102, co-authored 517 publications receiving 43826 citations. Previous affiliations of James B. Young include Case Western Reserve University & Baylor University.

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Combined cardiac resynchronization and implantable cardioversion defibrillation in advanced chronic heart failure: the MIRACLE ICD Trial.

TL;DR: Cardiac resynchronization improved quality of life, functional status, and exercise capacity in patients with moderate to severe HF, a wide QRS interval, and life-threatening arrhythmias without proarrhythmia or compromised ICD function.
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Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure

TL;DR: Venous congestion is the most important hemodynamic factor driving WRF in decompensated patients with advanced heart failure.
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Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness

James A. Hill, +56 more
- 05 Oct 2005 - 
TL;DR: Therapy to reduce volume overload during hospitalization for heart failure led to marked improvement in signs and symptoms of elevated filling pressures with or without the PAC, which reached significance for the time trade-off at all time points after randomization.
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Seventh INTERMACS annual report: 15,000 patients and counting

TL;DR: The seventh annual report of the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) summarizes the first 9 years of patient enrollment and a detailed analysis of outcomes after mechanical circulatory support for ambulatory heart failure is presented.
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Proinflammatory cytokine levels in patients with depressed left ventricular ejection fraction: A report from the studies of left ventricular dysfunction (SOLVD)

TL;DR: Circulating levels of proinflammatory cytokines increase in patients as their functional heart failure classification deteriorates, and activation of the neurohumoral axis is unlikely to completely explain the elaboration of pro inflammatory cytokines in heart failure.