key: cord-0701912-zl7fw8p9
authors: Lateef, Aisha; Fisher, Dale Andrew; Tambyah, Paul Ananth
title: Dengue and Relative Bradycardia
date: 2007-04-03
journal: Emerg Infect Dis
DOI: 10.3201/eid1304.061212
sha: 762d9040c711ef9f7ad28c28b7d4b65f9e51296d
doc_id: 701912
cord_uid: zl7fw8p9

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al medical unit from June 1 to October 31, 2005, were reviewed. Patients with a clinical diagnosis of dengue fever and serologic confirmation (IgM or PCR positive) plus a temperature >38°C were included as casepatients. Age-matched controls were selected from the same general medical inpatient units and were admitted during the same period. All had fever, but they had a proven alternative diagnosis, including pneumonia (12 patients), upper respiratory tract infection (9 patients), urinary tract infection (6 patients), tuberculosis, liver abscess, viral fever other than dengue (3 patients each), meningitis, chickenpox, cellulitis, typhoid fever (2 patients each), and appendicitis, psoas abscess, typhus, infective endocarditis, pressure ulcers, and gastroenteritis (1 patient each). Exclusion criteria were the following: no laboratory confirmation, age <18 years or >60 years, preexisting substantial heart or lung disease or concurrent medication affecting heart rate, e.g., β-blockers, β-agonists, calcium channel blockers, or xanthine derivatives.

The peak temperature of all casepatients and controls was recorded within the first 24 hours of admission as well as heart rate and blood pressure at that point. Leukocyte count, hemoglobin concentration, hematocrit, and platelet counts were also noted. Data from 50 case-patients and 50 controls were tabulated and analyzed with Microsoft Excel (Microsoft Corp., Redmond, WA, USA).

The mean age (± standard deviation) for dengue patients was 32.8 (±10.8) years and for controls was 36.5 (±10.2) years (p = 0.08). There were 39 male patients in the dengue group and 31 in the control group. Their mean peak temperatures were comparable: 38.6°C (±0.5) (dengue) and 38.8°C (±0.7) (controls) (p = 0.09). Mean heart rates were significantly lower in the dengue group: 87.6 (±12.5) beats/min (dengue) and 104.6 (±14) beats/min (controls) (p<0.0001).

Electrocardiographs (ECGs) were available for 10 of the dengue group, and all showed normal sinus rhythm. Three patients with bradycardia had an ECG. Results for 2 patients were normal; 1 showed mitral valve prolapse with mild regurgitation. Ten patients in the control group underwent an ECG, and none had any notable abnormality. Four controls had ECGs, results for 2 were normal; 1 had mild mitral regurgitation, and 1 had mild tricuspid regurgitation. The heart rates at peak temperatures for patients with dengue fever were compared with rates for controls at all temperatures. Our findings demonstrate a consistently lower heart rate at all peak temperatures recorded (p<0.0001) (Figure) .

Dengue fever may adversely affect cardiac function. An echocardiographic study by Khongphatthanayothin et al. (7) showed depressed myocardial contractility and suboptimal heart rate response in some patients with dengue hemorrhagic fever. Acute reversible hypokinesia and reduction in left ventricular ejection fraction was also reported by Wali et al. (8) . The underlying mechanisms were postulated to be immune in origin, although myocarditis may be a contributory factor. Fever production in response to exogenous pyrogens is believed to be mediated mostly by cytokine prostaglandin pathways, and neural input is important in the early phases of fever (9) . Concentrations of cytokines, including tumor necrosis factor, interferon-γ, interleukin-8 (IL-8), IL-10, and IL-12, are substantially increased during dengue infection. Their levels likely correlate with specific clinical manifestations and illness severity (10) . The relationship of cytokines to relative bradycardia is unknown. Further studies could consider the relative importance of immune and neural mechanisms and also any direct cardiac pathology in the etiology of dengue-associated relative bradycardia.

Aisha Lateef,* Dale Andrew Fisher,* † and Paul Ananth Tambyah,* † *National University Hospital, Singapore; and †National University of Singapore, Singapore

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To the Editor: West Nile virus (WNV; genus Flavivirus; family Flaviviridae) has been perpetuating in North America since 1999 (1) . However, its status as a self-perpetuating pathogen in South America remains uncertain. Infected horses and birds have been reported in various Caribbean Islands, Mexico, and northern Central America (2, 3) . In South America, isolated reports of infected dead-end hosts (horses) have come from northern Colombia and Argentina, but they lack evidence for infection in avian amplifying hosts (4, 5) . We report serologic evidence of establishment of WNV in South America.Serum samples from birds and horses from 33 locations in Venezuela (Online Appendix Table, available from http://www.cdc.gov/ EID/content/13/4/651-appT.htm) were screened for immunoglobulin G (IgG) antibodies against WNV antigen by ELISA (6) and confirmed by plaque reduction neutralization test (PRNT) as previously described (7)