644-P: QTc Prolongation as a Risk Factor for Increased Mortality in People with Diabetes and Charcot Osteoarthropathy

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 644-P
Author(s):  
JOHAN SCHOUG ◽  
KATARINA FAGHER ◽  
MAGNUS LONDAHL
Keyword(s):  
Risk Factor ◽  
Qtc Prolongation ◽  
Charcot Osteoarthropathy

645-P: QTc Prolongation as a Risk Factor for Five-Year Survival after Above-Ankle Amputation in Patients with Type 2 Diabetes

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 645-P
Author(s):  
SHOBITHA PUVANESWARALINGAM ◽  
KATARINA FAGHER ◽  
MAGNUS LONDAHL
Keyword(s):  
Type 2 Diabetes ◽  
Risk Factor ◽  
Qtc Prolongation

Opioid maintenance patients with QTc prolongation: Congenital long QT syndrome mutation may be a contributing risk factor

2010 ◽  
Vol 112 (3) ◽  
pp. 216-219 ◽  
Author(s):  
Katinka Anchersen ◽  
Viggo Hansteen ◽  
Michael Gossop ◽  
Thomas Clausen ◽  
Helge Waal
Keyword(s):  
Risk Factor ◽  
Long Qt Syndrome ◽  
Qtc Prolongation ◽  
Long Qt ◽  
Qt Syndrome ◽  
Congenital Long Qt Syndrome

QTC Prolongation As A Risk Factor For Mortality in Liver Cirrhosis

2003 ◽  
Vol 73 (2) ◽  
pp. P34-P34 ◽  
Author(s):  
A.Q. Adigun ◽  
N.P. Chalasani ◽  
M.D. Murray ◽  
H. Ho ◽  
S.D. Hall
Keyword(s):  
Liver Cirrhosis ◽  
Risk Factor ◽  
Qtc Prolongation

scholarly journals Effect of Combined Fluoroquinolone and Azole Use on QT Prolongation in Hematology Patients

2012 ◽  
Vol 57 (3) ◽  
pp. 1121-1127 ◽  
Author(s):  
John D. Zeuli ◽  
John W. Wilson ◽  
Lynn L. Estes
Keyword(s):  
Risk Factors ◽  
Risk Factor ◽  
Combination Therapy ◽  
Hematologic Malignancies ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Close Monitoring ◽  
Qtc Interval ◽  
Qtc Prolongation ◽  
Clinically Significant

ABSTRACTQTc prolongation is a risk factor for development of torsades de pointes (TdP). Combination therapy with fluoroquinolones and azoles is used in patients with hematologic malignancies for prophylaxis and treatment of infection. Both drug classes are implicated as risk factors for QTc prolongation. The cumulative effect on and incidence of QTc prolongation for this combination have not been previously described. A retrospective chart review was performed with hospitalized inpatients from 1 September 2008 to 31 January 2010 comparing QTc interval data from electrocardiogram (ECG) assessment at baseline and after the initiation of combination therapy. Ninety-four patients were eligible for inclusion. The majority, 88 patients (93.6%), received quinolone therapy with levofloxacin. Fifty-three patients (56.4%) received voriconazole; 40 (42.6%) received fluconazole. The overall mean QTc change from baseline was 6.1 (95% confidence interval [CI], 0.2 to 11.9) ms. Twenty-one (22.3%) of the studied patients had clinically significant changes in the QTc while receiving combination fluoroquinolone-azole therapy. Statistically significant risk factors for clinically significant changes in QTc were hypokalemia (P= 0.03) and a left-ventricular ejection fraction of <55% (P= 0.02). Low magnesium (P= 0.11), exposure to 2 or more drugs with the potential to prolong the QTc interval (P= 0.17), and female sex (P= 0.21) trended toward significance. Combination therapy with fluoroquinolone and azole antifungals is associated with increased QTc from baseline in hospitalized patients with hematologic malignancies. One in five patients had a clinically significant change in the QTc, warranting close monitoring and risk factor modification to prevent the possibility of further QTc prolongation and risk of TdP.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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