Provocation of hyper- and hypokalemic sudden death during treatment with and withdrawal of converting-enzyme inhibition in severe chronic congestive heart failure

The American Journal of Cardiology

Volume 57, Issue 4, 1 February 1986, Pages 347-348

S.C. Textor et al.
Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril
Am J Med
(1982)
M.H. Weinberger
Influence of an angiotensin converting-enzyme inhibitor on diuretic-induced metabolic effects in hypertension
Hypertension
(1983)
M. Packer et al.
Pathophysiologic factors underlying the development of worsening prerenal azotemia during captopril therapy for severe chronic heart failure (abstr)
Clin Res
(1983)

There are more references available in the full text version of this article.

Management of Volume Overload in Heart Failure
2011, Heart Failure
Management of Volume Overload in Heart Failure
2010, Heart Failure: A Companion to Braunwald's Heart Disease Expert Consult
End-Stage Renal Disease and Sudden Cardiac Death
2009, Cardiac Electrophysiology Clinics
Citation Excerpt :
A significant consequence of alterations in potassium levels is cardiac arrhythmia.18 Both hyper- and hypokalemia have been associated with ventricular arrhythmias and SCD.19–21 A large cohort of more than 81,000 patients receiving hemodialysis was followed over 3 years: in this cohort, potassium levels of less than 4.0 or greater than 5.6 mEq/L were associated with increased mortality.22
Sudden Cardiac Death Syndrome and Pump Dysfunction: The Link
2000, Journal of Heart and Lung Transplantation
The pathophysiology of advanced heart failure
1999, Heart and Lung: Journal of Acute and Critical Care
The pathophysiology of advanced heart failure
1998, American Heart Journal

^∗: Dr. Packer is recipient of Research Career Development Award K04-HL-01229 from the National Heart, Lung and Blood Institute, Bethesda, Maryland.