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Andrew L. Clark

Researcher at Western Infirmary

Publications -  45
Citations -  6454

Andrew L. Clark is an academic researcher from Western Infirmary. The author has contributed to research in topics: Heart failure & Physical exercise. The author has an hindex of 28, co-authored 45 publications receiving 6169 citations. Previous affiliations of Andrew L. Clark include Imperial College London & Southern General Hospital.

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Wasting as independent risk factor for mortality in chronic heart failure.

TL;DR: The cachectic state was predictive of 18-month mortality independent of age, NYHA class, left-ventricular ejection fraction, and peak oxygen consumption, and a subset of patients at extremely high risk of death was identified.
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Contribution of Muscle Afferents to the Hemodynamic, Autonomic, and Ventilatory Responses to Exercise in Patients With Chronic Heart Failure Effects of Physical Training

TL;DR: In this paper, a neural linkage between peripheral abnormalities and the exaggerated exercise responses in chronic heart failure (CHF) was postulated, and the contribution of the ergoreflex to vagal withdrawal and sympathetic activation was quantified as the percentage responses to exercise maintained by post-handgrip regional circulatory occlusion (PH-RCO).
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Clinical correlates and prognostic significance of the ventilatory response to exercise in chronic heart failure

TL;DR: A high VE-VCO2 slope selects patients with more severe heart failure and is an independent prognostic marker in the assessment of patients with chronic heart failure.
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Exercise limitation in chronic heart failure: Central role of the periphery

TL;DR: The "muscle hypothesis" is put forward as an explanation for many of the pathophysiologic events in CHF, which links the symptoms of breathlessness and fatigue to impaired skeletal muscle function, which causes increased ventilation.
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Insulin Resistance in Chronic Heart Failure: Relation to Severity and Etiology of Heart Failure

TL;DR: CHF is associated with marked insulin resistance, characterized by both fasting and stimulated hyperinsulinemia, but this is not directly mediated through ventricular dysfunction or increased catecholamine levels.