A post-menopausal lady with severe babesiosis developed a basal-type stress-induced cardiomyopathy.
Left ventricular function normalized at three months. We believe this is the first
reported case of stress cardiomyopathy complicating severe babesiosis. Cardiac biomarker
elevation disproportionate to the area of myocardial dysfunction, electrocardiographic changes,
the patient&#8217;s clinical condition, and close follow-up of left ventricular function parameters are
all vital in diagnosing stress cardiomyopathy and may exclude the need for coronary angiography.
There may be a possible association between severe babesiosis and stress cardiomyopathy.
(Cardiol J 2011; 18, 1: 83-86

Dodson, John

Odigie-Okon, Esosa

Okon, Emmanuel

Vorobiof, Gabriel

English

Via Medica Journals

www.cardiologyjournal.org 83CASE REPORTCardiology Journal2011, Vol. 18, No. 1, pp. 83–86Copyright © 2011 Via MedicaISSN 1897–5593Address for correspondence: Esosa Odigie-Okon, MD, MSc, Bridgeport Hospital, 267 Grant St, Bridgeport, CT 06610, USA,tel.: 781 706 10 02, fax: 203 384 42 94, e-mail: sesky146@yahoo.comReceived: 30.10.2009 Accepted: 3.12.2009Stress-induced cardiomyopathycomplicating severe babesiosisEsosa Odigie-Okon1, Emmanuel Okon2, John Dodson3, Gabriel Vorobiof31Department of Medicine, Yale University (Bridgeport Hospital), Bridgeport, CT, USA2Department of Medicine, New Milford Hospital(New York Presbyterian Healthcare System), New Milford, CT, USA3Departments of Cardiology and Diagnostic Radiology, Yale University School of Medicine, New Haven, CT, USAAbstractA post-menopausal lady with severe babesiosis developed a basal-type stress-induced cardio-myopathy. Left ventricular function normalized at three months. We believe this is the firstreported case of stress cardiomyopathy complicating severe babesiosis. Cardiac biomarkerelevation disproportionate to the area of myocardial dysfunction, electrocardiographic changes,the patient’s clinical condition, and close follow-up of left ventricular function parameters areall vital in diagnosing stress cardiomyopathy and may exclude the need for coronary angiogra-phy. There may be a possible association between severe babesiosis and stress cardiomyopathy.(Cardiol J 2011; 18, 1: 83–86)Key words: stress-induced cardiomyopathy, tako-tsubo, babesiosisIntroductionBabesiosis is a hemolytic protozoan illnesscaused most commonly by Babesia microti specie inthe United States. It is transmitted to humans via thetick vector Ixodes scapularis, and less often via bloodtransfusion. We describe a case of stress-induced car-diomyopathy (SCM) that occurred in association withsevere babesiosis. To the best of our knowledge, thisis the first report of SCM complicating babesiosis.Case and resultsA 62 year-old Caucasian lady with hyperten-sion, hypercholesterolemia, and no significant fam-ily or social history, presented initially to her PMD’soffice complaining of fevers up to 102.9° F, chills,nausea and headaches. Approximately seven weeksprior to this admission, she had a nine day hospitalstay for surgery involving resection of a left-sidedretroperitoneal liposarcoma, left kidney, adrenalgland, ovary, hemi-diaphragm and a splenectomy.She received two units of packed red blood cellsfollowing a post-operative drop in hematocrit from32.1% to 20.7%. Approximately three and a halfweeks after her discharge, she was readmitted fornine days for management of nosocomial pneumoniaand malnutrition. She was discharged home on totalparenteral nutrition (TPN) via a peripherally insertedcentral (PICC) line. She presented ten days later.Physical examination in the office revealed a fati-gued lady with laboratory investigations significantfor a platelet count  of 70,000/mL. Blood cultureswere drawn, a dose of vancomycin and cefepime wasgiven, and she was admitted to the hospital for fur-ther management. In the hospital, she was in milddistress and febrile, with a temperature of 102.7o F.Blood pressure was 100/70 mm Hg, heart rate 104 bpmand oxygen saturation was 100% on room air. Othersignificant findings included decreased breathsounds at the left lung base and a normal cardio-vascular exam.84Cardiology Journal 2011, Vol. 18, No. 1www.cardiologyjournal.orgThe patient was admitted to the medical unit,and placed on vancomycin and piperacillin-tazo-bactam. On day one, significant laboratory resultsrevealed leucocytosis (WBC count 15,000/mL), nor-mocytic anemia (hemoglobin 9.9 g/dL), thrombocy-topenia (platelet count 83,000/mL), aspartate ami-notransferase (AST) 119 U/L; alanine aminotrans-ferase (ALT) 65 U/L; alkaline phosphatase 224 U/L,unconjugated hyperbilirubinemia 2.12 mg/dL andnormal renal function. On day two, hemoglobindropped to 7 g/dL, reticulocyte count was 13.5%,and lactate dehydrogenase 1770 µ/L (normal range313–618 µ/L), suspicious for ongoing hemolysis.Coagulation work-up was negative for consumptivecoagulopathy. Blood smear was positive for intra-erythrocyte parasites consistent with babesia.Babesia polymerase chain reaction was positive andthe parasite load was 7%. Clindamycin and quininewere started and exchange blood transfusion wasperformed with seven units of packed red bloodcells. Subsequent parasite load monitored over oneweek remained less than 1%. In addition, bloodcultures grew methicillin-sensitive staphylococcusaureus and torulopsis glabrata. She was treated withoxacillin and anidulafungin.On day four, she became progressively short ofbreath and hypoxic. Chest X-ray showed pulmonaryedema, unresponsive to furosemide. She was intubat-ed and transferred to the intensive care unit. An elec-trocardiogram revealed sinus tachycardia, ST eleva-tions and Q-waves in leads aVL, V2–V4 (Fig. 1).Three sets of cardiac biomarkers over thecourse of 24 hours showed mildly elevated tropon-in-I levels from 0.28–0.44 ng/mL and creatinine ki-nase-MB fraction (CK-MB) from 2.8–4.3 ng/mL, brainnatriuretic peptide was 1,860 pg/mL. An echocardio-gram showed an overall decrease in left ventricular(LV) systolic function, estimated ejection fraction of30%, a hypokinetic mid antero-septum and anteriorwall, extending to and involving the entire apex, witha global hypokinesis of all other segments. Right ven-tricular function was normal, and trace mitral and tri-cuspid regurgitations were noted (Fig. 2).A diagnosis of stress-induced cardiomyopathywas entertained, and a decision was made not toproceed with invasive coronary angiography asa true anterior wall myocardial infarction would haveresulted in far greater elevations of the cardiac bio-markers than the area of myocardial injury visibleon echocardiography. She was diuresed and extu-bated after 48 hours.Repeat echocardiogram six days later revealedimprovement of the left ventricular function to anestimated left ventricular ejection fraction of 45%,normal left ventricular cavity size, normal leftventricular wall thickness, hypokinetic mid septumand mid inferior segment, and significantlyimproved anterior and anteroseptal wall motionabnormalities. She was discharged on day elevento complete a five week course of atovaquone andazithromycin for babesiosis, and chronicmanagement with lisinopril, furosemide andaspirin. She was seen three months later in thecardiology clinic, and a follow-up echocardiogramshowed a normal left ventricular systolic functionwithout wall motion abnormalities.Figure 1. Electrocardiogram showing Q waves in leads aVL, V2–V4.85Esosa Odigie-Okon et al., Babesiosis and stress-induced cardiomyopathywww.cardiologyjournal.orgDiscussionPrompted by the rarity in Japan of a peculiarpattern of contrast left ventriculogram, consisting ofhypokinesis or akinesis from the mid-portion to theapical area and hyperkinesis of the basal area, com-bined with an end-systolic left-ventriculogram simi-lar to a ‘tako-tsubo’ (a contraption used for trappingoctopuses in Japan), the term ‘tako-tsubo left ven-tricular dysfunction’ was coined [1]. Over time, rec-ognition of similar pathogenetic mechanisms has giv-en rise to the term ‘stress-induced cardiomyopathy’.SCM is a syndrome of unclear etiology, charac-terized by a transient contractile dysfunction of themid-LV segments with or without apical involve-ment, extending beyond a single epicardial vasculardistribution; absence of obstructive coronary diseaseor angiographic evidence of acute plaque rupture;new electrocardiographic abnormalities (either ST--segment elevation, T-wave inversion, or both) ormodest elevation in cardiac troponin; and the absenceof a pheochromocytoma or myocarditis [2]. Variantsof this syndrome are increasingly recognized includ-ing a mid-ventricular and basal ballooning pattern ofLV dysfunction. Various mechanisms of SCM havebeen proposed, including neurogenic myocardialstunning, excessive catecholamines, microvasculardysfunction and myocarditis [3, 4]. In babesiosis,infected erythrocytes cause vascular stasis, leadingto microvascular obstruction, tissue anoxia andischemia [5]. Animal models have specifically de-scribed cases of cardiomegaly, myocarditis, andmultifocal coagulation cardiac necrosis [6, 7]. Wehypothesize that there may be an association of SCMin cases of severe babesiosis. Research into thepathophysiology is warranted.The incidence of SCM is uncertain, perhapsdue to the complexities involved in its presentationand the requirement for a diagnosis to be made af-ter excluding an acute myocardial infarction. None-theless, evidence suggests it is more common inwomen than men [8] and also seems to have a highincidence in medical intensive care units [9, 10].Observed complications have ranged from pulmonaryedema (as in our patient) to cardiogenic shock anddeath [11]. Treatment of this illness is largely sup-portive and based on the overall clinical condition ofthe patient. Empiric therapy favors the use of stand-ard medications for left ventricular systolic dysfunc-tion including angiotensin-converting enzyme inhibi-tors, beta-blockers and diuretics [12]. The appropri-ate duration of therapy remains unknown.The events in this patient’s illness occurredbetween September and November, outside thetypical tick-bite summer months which peak in July.However, our patient’s recent hospital stay madeit unlikely that her babesiosis infection was the re-sult of a tick-bite.  As such, circumstantial evidencepoints to the post-operative blood transfusion as thesource of her babesiosis. In contrast to the 1–6 weekincubation period following a tick bite, post-trans-fusion disease typically has a 6–9 week incubationperiod [13]. In the hospital setting, where bloodproducts have seemingly undergone rigorousscreening processes, physicians are prone to for-get the inadequacy of screening blood products forbabesiosis [14, 15]. A broad index of suspicionshould be the ‘rule’ in patients with a recent histo-ry of blood transfusion presenting with a febrile ill-ness and hemolytic anemia.In conclusion, this is the first known case dem-onstrating that SCM may be a complication of se-Figure 2. A. Parasternal long axis still shot in diastole; B. Parasternal long axis still shot in systole.A B86Cardiology Journal 2011, Vol. 18, No. 1www.cardiologyjournal.orgvere babesiosis with high parasitemia counts. Cluesto the diagnosis are: cardiac biomarker elevation outof proportion to the area of myocardial dysfunction;typical electrocardiographic findings; the patient’sclinical context; and close follow-up of global andregional LV function.AcknowledgementsThe authors declare no conflicts of interest.References1. Kurisu S, Sato H, Kawagoe T et al. Tako-tsubo-like left ven-tricular dysfunction with ST-segment elevation: A novel cardiacsyndrome mimicking acute myocardial infarction. Am Heart J,2002; 143:448-455.2. Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome(Tako-Tsubo or stress cardiomyopathy): A mimic of acute myo-cardial infarction. Am Heart J, 2008; 155: 408–417.3. Kurowski V, Kaiser A, von Hof K et al. Apical and midventricu-lar transient left ventricular dysfunction syndrome (tako-tsubocardiomyopathy): Frequency, mechanisms, and prognosis. Chest,2007; 132: 809–816.4. Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes.Circulation, 2008; 118: 397–409.5. Dao AH, Eberhard ML. Pathology of acute fatal babesiosis inhamsters experimentally infected with the WA-1 strain of Babesia.Lab Invest, 1996; 74: 853.6. Oz HS, Hughes WT. Acute fulminating babesiosis in hamstersinfected with Babesia microti. Int J Parasitol, 1996; 26: 667––670.7. Wozniak EJ, Lowenstine LJ, Hemmer R, Robinson T, Conrad PA.Comparative pathogenesis of human WA1 and Babesia microtiisolates in a Syrian hamster model. Lab Anim Sci, 1996; 46:507–515.8. Wittstein IS, Thiemann DR, Lima JAC et al. Neurohumoral fea-tures of myocardial stunning due to sudden emotional stress.N Engl J Med, 2005; 352: 539.9. Park JH, Kang SJ, Song JK et al. Left ventricular apical ballooningdue to severe physical stress in patients admitted to the medicalICU. Chest, 2005; 128: 296–302.10. Dec GW. Recognizing the apical ballooning syndrome in theintensive care unit. Intensive Care Med, 2006, 32: 962–964.11. Donahue D, Movahed MR. Clinical characteristics, demogra-phics and prognosis of transient left ventricular apical ballooningsyndrome. Heart Fail Rev, 2005; 10: 311–316.12. Bybee KA, Prasad A, Barsness GW et al. Clinical characteristicsand thrombolysis in myocardial infarction frame counts in wom-en with transient left ventricular apical ballooning syndrome.Am J Cardiol, 2004; 94: 343–346.13. Villar BF, White DJ, Benach JL. Human babesiosis. Prog ClinParasitol, 1991; 2: 129.14. Leiby DA, Chung AP, Gill JE et al. Demonstrable parasitemiaamong Connecticut blood donors with antibodies to Babesiamicroti. Transfusion, 2005; 45: 1804–1810.15. McQuiston JH, Childs JE, Chamberland ME, Tabor E. Trans-mission of tick-borne agents of disease by blood transfusion:A review of known and potential risks in the United States.Transfusion, 2000; 40: 274–284.

Stress-induced cardiomyopathy complicating severe babesiosis

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Stress-induced cardiomyopathy complicating severe babesiosis

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