Chest pain • shortness of breath • fever and nausea • Dx?

,; ,; ,; ,; ,

Case Reports

Chest pain • shortness of breath • fever and nausea • Dx?

J Fam Pract. 2015 May;64(5):282-284

PDF Download

References

1. Nash D, Mostashari F, Fine A, et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med. 2001;344:1807-1814.

2. Orton SL, Stramer SL, Dodd RY. Self-reported symptoms associated with West Nile virus infection in RNA-positive blood donors. Transfusion. 2006;46:272-277.

3. Brown JA, Factor DL, Tkachenko N, et al. West Nile viremic blood donors and risk factors for subsequent West Nile fever. Vector Borne Zoonotic Dis. 2007;7:479-488.

4. Zou S, Foster GA, Dodd RY, et al. West Nile fever characteristics among viremic persons identified through blood donor screening. J Infect Dis. 2010;202:1354-1361.

5. Davis LE, DeBiasi R, Goade DE, et al. West Nile virus neuroinvasive disease. Ann Neurol. 2006;60:286-300.

6. Montgomery SP, Chow CC, Smith SW, et al. Rhabdomyolysis in patients with west nile encephalitis and meningitis. Vector Borne Zoonotic Dis. 2005;5:252-257.

7. Paddock CD, Nicholson WL, Bhatnagar J, et al. Fatal hemorrhagic fever caused by West Nile virus in the United States. Clin Infect Dis. 2006;42:1527-1535.

8. Georges AJ, Lesbordes JL, Georges-Courbot MC, et al. Fatal hepatitis from West Nile virus. Ann Inst Pasteur Virol. 1988;138:237.

9. Perelman A, Stern J. Acute pancreatitis in West Nile Fever. Am J Trop Med Hyg. 1974;23:1150-1152.

10. Sherman-Weber S, Axelrod P. Central diabetes insipidus complicating West Nile encephalitis. Clin Infect Dis. 2004;38:1042-1043.

11. Pergam SA, DeLong CE, Echevarria L, et al. Myocarditis in West Nile virus infection. Am J Trop Med Hyg. 2006;75:1232-1233.

12. van der Meulen KM, Pensaert MB, Nauwynck HJ. West Nile virus in the vertebrate world. Arch Virol. 2005;150:637-657.

13. Kushawaha A, Jadonath S, Mobarakai N. West nile virus myocarditis causing a fatal arrhythmia: a case report. Cases J. 2009;2:7147.

14. Khouzam RN. Significant cardiomyopathy secondary to West Nile virus infection. South Med J. 2009;102:527-528.

15. Kawai C. From myocarditis to cardiomyopathy: mechanisms of inflammation and cell death: learning from the past for the future. Circulation. 1999;99:1091-1100.

16. Caforio AL, Goldman JH, Haven AJ, et al. Circulating cardiac-specific autoantibodies as markers of autoimmunity in clinical and biopsy-proven myocarditis. The Myocarditis Treatment Trial Investigators. Eur Heart J. 1997;18:270-275.

17. Lauer B, Schannwell M, Kühl U, et al. Antimyosin autoantibodies are associated with deterioration of systolic and diastolic left ventricular function in patients with chronic myocarditis. J Am Coll Cardiol. 2000;35:11-18.

Although West Nile virus has been linked to myocarditis in animals, few human cases of WNV myocarditis or cardiomyopathy have been reported.

The patient’s chest pain with syncope, elevated troponin level, and nonspecific EKG changes in the absence of obstructive CAD raised the possibility of Takotsubo cardiomyopathy. The characteristic echocardiogram finding in Takotsubo cardiomyopathy is transient apical ballooning with akinesis or hypokinesis in the apical and/or mid ventricular regions (typical variant) or isolated midventricular hypokinesis (apical sparing variant). Our patient’s echocardiogram did not show any of these focal wall motion abnormalities, but instead showed global hypokinesis. In addition, the persistence of systolic dysfunction during the repeat echocardiogram and the patient’s lack of psychological distress made the diagnosis of Takotsubo cardiomyopathy unlikely.

Dressler’s syndrome, which is also known as post-myocardial infarction (MI) syndrome, typically presents weeks to months after MI as pleuritic chest pain with a pericardial rub, elevated inflammatory markers, typical EKG changes (diffuse ST-segment elevation and PR-segment depression), and pericardial effusion. This did not fit our patient’s presentation.

Supportive care for heart failure is the mainstay of treatment

The standard treatment for WNV myocarditis is supportive care. Diuretics are used as needed for fluid overload, along with angiotensin-converting enzyme inhibitors and beta-blockers for cardiomyopathy with decreased EF.

Our patient’s dyspnea improved with treatment of furosemide 40 mg IV BID, and his blood pressure was controlled with metoprolol 25 mg BID and lisinopril 10 mg BID. His chest pain and fever resolved when his blood pressure improved. He was discharged home after 7 days on the furosemide, metoprolol, and lisinopril, in addition to isosorbide mononitrate 30 mg/d, atorvastatin 40 mg/d, and aspirin 325 mg/d. An echocardiogram performed 6 months later showed persistent systolic dysfunction, with an EF of 35% and global wall motion abnormalities.

THE TAKEAWAY

In addition to acute coronary syndrome, consider alternate etiologies in patients who present with chest pain and elevated cardiac biomarkers, particularly if diagnostic work-up is negative for obstructive coronary artery disease. WNV myocarditis should be considered as a diagnosis when a patient’s symptoms suggest acute coronary syndrome but are accompanied by fever, headache, and other constitutional symptoms, especially during mosquito season or a WNV outbreak.