CORRESPONDENCE: LETTER TO THE EDITOR
Diastolic Dysfunction Is an Independent Risk Factor for Death in Patients With Sickle Cell Disease
William O. Ntim, MB, ChB, FACC*,
Bharathi Upadhya, MD and
Julia Cruz, MD
* Section on Cardiology, Department of Internal Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157-1045 (Email: wntim{at}wfubmc.edu).
We read with interest the study by Sachdev et al. (1) that identified diastolic dysfunction as a poor prognostic factor in patients with sickle cell disease.
Absolute serum creatinine in the study cohort may have underestimated the severity of kidney disease. The incidence of renal insufficiency in a cohort of sickle cell patients has been found to be 4% to 7% (2,3). Chronic kidney disease is known to be a prognostic factor for worse cardiovascular outcomes (4). The American Kidney Foundation has proposed creatinine clearance as a better assessment of kidney function (5).
In addition, methadone use for sickle cell-related chronic pain increases the risk of QT prolongation and torsades de pointes-related arrhythmic events (6,7).
Abnormal diastolic function may result from myocardial iron overload (8). Myocardial iron overload has been reported in an autopsy study of sickle cell patients (9). The use of validated cardiovascular T2* magnetic resonance for early diagnosis of myocardial iron overload demonstrated that myocardial iron content cannot be predicted from serum ferritin or liver iron (10).
Creatinine clearance, narcotic use, and myocardial iron overload should therefore be included in studies of mortality among sickle cell patients.
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References
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1. Sachdev V, Machado RF, Shizukuda Y, et al. Diastolic dysfunction is an independent risk factor for death in patients with sickle cell disease J Am Coll Cardiol 2007;49:472-479.[Abstract/Free Full Text]2. Powars DR, Elliott-Mills DD, Chan L, et al. Chronic renal failure in sickle cell disease: risk factors, clinical course, and mortality Ann Intern Med 1991;115:614-620.[Abstract/Free Full Text] 3. Falk RJ, Scheinman J, Phillips G, Orringer E, Johnson A, Jennette JC. Prevalence and pathologic features of sickle cell nephropathy and response to inhibition of angiotensin-converting enzyme N Engl J Med 1992;326:910-915.[Abstract] 4. Sarnak MJ, Levey AS, Schoolwerth AC, Coresh J. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention Circulation 2003;108:2154.[Free Full Text] 5. Eknoyan G, Levin N. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification Am J Kidney Dis 2002;39:S1.[CrossRef][Web of Science][Medline] 6. Krantz MJ, Lewkowiez L, Hays H, Woodroffe MA, Robertson AD, Mehler PS. Torsade de pointes associated with very-high-dose methadone Ann Intern Med 2002;17:137501–4. 7. Porter BO, Coyne PJ, Smith VR. Methadone-related torsade de pointes in a sickle cell patient treated for chronic pain Am J Hematol 2005;78:316-317.[Web of Science][Medline] 8. Palka P, Macdonald G, Lange A, Burstow DJ. The role of Doppler left ventricular filling indexes and Doppler tissue echocardiography in the assessment of cardiac involvement in hereditary hemochromatosis J Am Soc Echocardiogr 2002;15:884-890.[CrossRef][Web of Science][Medline] 9. Darbari DS, Kple-Faget P, Kwagyan J, Rana S, Gordeuk VR, Castro O. Circumstances of death in adult sickle cell disease patients Am J Hematol 2006;81:858-863.[CrossRef][Web of Science][Medline] 10. Anderson LJ, Holden S, Prescott E, et al. Cardiovascular T2* magnetic resonance for the early diagnosis of myocardial iron overload Eur Heart J 2001;22:2171-2179.[Abstract/Free Full Text]
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