G
George C. Sutton
Researcher at National Institutes of Health
Publications - 79
Citations - 7978
George C. Sutton is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Heart failure & Heart disease. The author has an hindex of 31, co-authored 79 publications receiving 7814 citations. Previous affiliations of George C. Sutton include Hillingdon Hospital & Imperial College London.
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Journal ArticleDOI
The epidemiology of heart failure
Journal ArticleDOI
Value of natriuretic peptides in assessment of patients with possible new heart failure in primary care
Martin R. Cowie,Allan D. Struthers,David R. Wood,Andrew J.S. Coats,Simon G. Thompson,Philip A. Poole-Wilson,George C. Sutton +6 more
TL;DR: In patients with symptoms suspected by a general practitioner to be due to heart failure, plasma BNP concentration seems to be a useful indicator of which patients are likely to have heart failure and require further clinical assessment.
Journal ArticleDOI
Incidence and aetiology of heart failure; a population-based study
Martin R. Cowie,David R. Wood,Andrew J.S. Coats,Simon G. Thompson,P. A. Poole-Wilson,V. Suresh,George C. Sutton +6 more
TL;DR: Within the general population, new cases of heart failure largely occur in the elderly, and the incidence is higher in men than women, and to be relevant to clinical practice, future clinical trials in heart failure should not exclude the elderly.
Journal ArticleDOI
Survival of patients with a new diagnosis of heart failure: a population based study
Martin R. Cowie,David R. Wood,Andrew J.S. Coats,Simon G. Thompson,V. Suresh,P. A. Poole-Wilson,George C. Sutton +6 more
TL;DR: Lower systolic blood pressure, higher serum creatinine concentration, and greater extent of crackles on auscultation of the lungs were independently predictive of cardiovascular mortality.
Journal ArticleDOI
Untreated heart failure: clinical and neuroendocrine effects of introducing diuretics.
TL;DR: Diuretics bring about a considerable clinical improvement in patients with chronic heart failure but they stimulate the renin-angiotensin system, which occurs as a response to diuretic treatment rather than as a result of the disease process itself.