International Journal of Cardiology 158 (2012) e17–e19
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Letter to the Editor
Acute Q fever myocarditis: Thinking about a life-threatening but potentially curable condition☆ Miguel F. Carrascosa a,⁎, Francisco Pascual Velasco a, Rubén Gómez Izquierdo b, José R. Salcines-Caviedes c, Verónica Gómez Amigo d, Ana M. Canga-Villegas e a
Internal Medicine Department, Hospital of Laredo, Avda Derechos, Humanos s/n, 39770 Laredo, Cantabria, Spain Cardiology Section, Hospital of Laredo, Avda Derechos, Humanos s/n, 39770 Laredo, Cantabria, Spain c Digestive Diseases Section, Hospital of Laredo, Avda Derechos, Humanos s/n, 39770 Laredo, Cantabria, Spain d Emergency Department, Hospital of Laredo, Avda Derechos, Humanos s/n, 39770 Laredo, Cantabria, Spain e Radiology Department, University Hospital Marqués de Valdecilla, Avda Valdecilla s/n, 39008 Santander, Cantabria, Spain b
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Article history: Received 3 October 2011 Accepted 18 October 2011 Available online 9 November 2011 Keywords: Acute Q fever Cardiovascular magnetic resonance imaging Coxiella burnetii Myocarditis
Q fever, a worldwide zoonosis caused by Coxiella burnetii, is a protean disease. Although acute infection is usually mild and selflimiting, people do occasionally die from this disorder [1–3]. Myocarditis is a rare manifestation of the acute disease (b1% of cases), but likely the most severe form of it [1,2]. We present, to our knowledge, the first cardiovascular magnetic resonance imaging (MRI) of a patient with acute Coxiella burnetii myocarditis. He fully recovered under levofloxacin treatment. A previously healthy 23-year-old man presented to the emergency department complaining of severe, steady retrosternal pain of abrupt onset and two hours duration. He had been well until 1 day earlier, when malaise, chills, and fever occurred. He lived in a rural area but denied having contact with animals, occupational exposure or raw cheese consumption. At admission, the patient had pyrexia of 38.5 °C, a heart rate of 92 beats/min, a respiratory rate of 18 breaths/min, and blood pressure of 109/62 mm Hg. Physical examination was unremarkable. The initial electrocardiogram revealed sinus rhythm and diffuse ST-segment elevation, most evident in leads II, ☆ All authors had access to the data included in this work and a role in writing the manuscript. ⁎ Corresponding author. Tel.: + 34 942 638500; fax: + 34 942 607876. E-mail address:
[email protected] (M.F. Carrascosa). 0167-5273/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2011.10.042
III, and aVF. Laboratory tests results showed a normal leukocyte count, a platelet count of 125 × 109 cells/L, an ASAT level of 114 IU/L (normal level, b37 IU/L), an ALAT level of 177 IU/L (normal level, b41 IU/L), and increased serum level of both creatine kinase MB fraction (up to 45·32 ng/mL, normal ≤ 6) and troponin T (up to 6·55 ng/mL, normal b0·1). Chest radiography showed a left-sided lower lobe consolidation. Two sequential transthoracic echocardiograms as well as an abdominal ultrasonography displayed no abnormalities. Serological tests for Legionella pneumophila, Mycoplasma pneumoniae, Coxiella burnetii, hepatitis B and C viruses, herpesvirus, cytomegalovirus, Epstein–Barr virus, and HIV were negative; standard blood cultures grew no organisms. On T2-weighted (Fig. 1A, arrows) and T1-weighted (Fig. 1B and C, arrows) cardiovascular MRI scans there were subepicardial abnormalities indicating myocardial edema and inflammation, respectively. Contrast enhancement was not found originating from the subendocardial portion of the wall, as would be typical for myocardial infarction. In addition, the pericardium showed a normal appearance. A diagnosis of acute myocarditis with associated pneumonia and subclinical hepatitis was done and he was given levofloxacin (500 mg daily for 16 days). On the third hospital day, a self-limited, non-sustained ventricular tachycardia was evident. He did not develop congestive heart failure during his stay and was discharged asymptomatic on the tenth hospital day. Acute Q fever was diagnosed on the basis of a positive serologic test performed 2 weeks later, with titers of 1:400 and 1:100 for IgG and IgM to phase II Coxiella burnetii, respectively (indirect immunofluorescence assay). At a follow-up visit 1 month after discharge, he was well and a new echocardiography revealed normal findings. Platelet count and level of liver enzymes were within normal limits and electrocardiographic as well as chest X-ray abnormalities have resolved. The most frequent clinical syndrome associated with acute Q fever is a self-limited “flu-like” illness with varying degrees of pneumonia and hepatitis [1,4]. Other less common presentations include cutaneous, neurologic, gastrointestinal, and cardiac involvement [1,4]. Myocarditis complicating acute Coxiella burnetii disease has been rarely reported. In a series of 1276 patients with acute Q fever, myocarditis was diagnosed in 8 (0.6%) [2]. Seven of them presented dilated cardiomyopathy, and 2 died from severe heart failure despite appropriate treatment (one of the deceased patients had undergone heart transplantation). Five patients evolved favorably after receiving antibiotic therapy and recovered a
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M.F. Carrascosa et al. / International Journal of Cardiology 158 (2012) e17–e19
Fig. 1. Cardiovascular MRI of a 23-year old man with acute Coxiella burnetii myocarditis.
normal cardiac function in the following months. Another patient was scheduled for heart transplantation owing to persistent myocardial hypokinesis. In contrast to acute Q fever as a whole, which entails a case fatality rate of 1–2% [4], acute Coxiella burnetii myocarditis has a worse prognosis than most other manifestations of the disease (25% mortality in the aforementioned series). Nowadays, there is no single clinical, laboratory, or imaging feature that confirms the presence of myocarditis with definitive certainty. Even though endomyocardial biopsy with immunohistochemistry still remains the accepted diagnostic standard [6], it also has several limitations (restricted availability, risk of severe complications, limited sensitivity, non-homogeneous and widely accepted diagnostic criteria, indication confined to patients with heart failure, and others) [6]. In consequence, an integrated approach including history, clinical evaluation, laboratory tests, and imaging studies, should be used to diagnose the disorder and guide therapy. Cardiovascular MRI, which offers a combination of safety, clarity of anatomical observation, and interobserver consistency [6], is now established as the first-line tool for noninvasive diagnosis and assessment of myocarditis [5,6]. In this setting, a combination of T1-weighted and T2weighted images has been reported to have the best combination of sensitivity and specificity [6,7].
Although most frequently caused by common viral infections [8], specific forms of myocarditis may result from other organisms. Since myocarditis is the most serious manifestation of acute Q fever and given the availability of a suitable antibiotic therapy (firstly, doxycycline), Coxiella burnetii should be taken into account in the management of all patients with suspected acute myocardial inflammation. As shown in this report, cardiac MRI can help demonstrate accurately the presence of myocarditis, even though its findings are not pathognomonic of acute Q fever or other specific etiologies. Axial T2-weighted nonenhanced image shows subepicardial high signal intensity of the lateral ventricular wall indicating regional edema (Fig. 1A, arrows). T1-weighted images show subepicardial late gadolinium enhancement revealing myocardial inflammation in both a four-chamber view (Fig. 1B, arrows) and a short axis view (Fig. 1C, arrows). References [1] Raoult D, Tissot-Dupont H, Foucault C, et al. Q fever 1985–1998: clinical and epidemiologic features of 1,383 infections. Medicine 2000;79:109–23. [2] Fournier PE, Etienne J, Harle JR, Habib G, Raoult D. Myocarditis, a rare but severe manifestation of Q fever: report of 8 cases and review of the literature. Clin Infect Dis 2001;32:1440–7.
M.F. Carrascosa et al. / International Journal of Cardiology 158 (2012) e17–e19 [3] Chevalier P, Vandenesch F, Brouqui P, et al. Fulminant myocardial failure in a previously healthy young man. Circulation 1997;95:1654–7. [4] Parker NR, Barralet JH, Bell AM. Q fever. Lancet 2006;367:679–88. [5] Pennell DJ. Cardiovascular magnetic resonance. Circulation 2010;121:692–705. [6] Friedrich MG, Sechtem U, Schulz-Menguer J, et al. Cardiovascular magnetic resonance in myocarditis: a JACC white paper. J Am Coll Cardiol 2009;53:1475–87.
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[7] Abdel-Aty H, Boyé P, Zagrosek A, et al. Diagnostic performance of cardiovascular magnetic resonance in patients with suspected acute myocarditis: comparison of different approaches. J Am Coll Cardiol 2005;45:1815–22. [8] Cooper LT. Myocarditis. N Engl J Med 2009;360:1526–38.
