CASE REPORT

Restrictive cardiomyopathy due to myocardial cysticercosis

Rodrigo Morel Vieira de Melo; Almiro Vieira de Melo Neto; Luís Cláudio L. Corrêa; Almiro Vieira de Melo Filho

Universidade Federal da Bahia - UFBA – Salvador, BA - Brazil

Mailing Address

ABSTRACT

There is no description of cysticercosis affecting heart function. In the present report, the authors describe the case of a 46-year-old woman with cardiac cysticercosis and heart failure, presenting with echocardiographic findings suggestive of restrictive cardiomyopahy and myocardial microcalcifications suggestive of cardiac infiltration by the disease.

Cysticercosis is a disease caused by aninfestation of the larval form of Taenia solium. In humancysticercosis, the person is an accidental intermediate host. Theinfection is caused by the ingestion of eggs containing viableoncospheres that invade the intestine, enter the vasculatorysystem and lodge in tissues. The global prevalence ofcysticercosis caused by cisticerco cellulosae has beenestimated at three hundred thousandpeople¹.

Although any organ or tissue can house the cysts, the most commonly affected areas are the brain, skeletal musculature and subcutaneous tissue. While the topic of neurocysticercosis has been documented in numerous reports, cardiac cysticercosis and particularly myocardial cysticercosis are rare and consequently few studies have been conducted.

CASE REPORT

The patient is a 46 year old female born in the city of Jacobina – BA, with a history of seizures since 1970, believed to be caused from epilepsy, using phenobarbital on a regular basis. In 1996, a simple x-ray of soft tissues revealed microcalcifications (fig.1). Examination of the cerebrospinal fluid revealed a positive hemagglutination reaction of 1:4 for cysticercosis and a positive ELISA reaction for the detection of the antibody Cysticercus cellulosae. A CT scan of the brain revealed cerebral and right cerebellar calcifications which are also compatible with neurocysticercosis (fig.2). As such, the patient was diagnosed with neurocysticercosis.

In 1998 she began to present dyspnea while performing out-of-the-ordinary exertions and palpitations. An electrocardiogram revealed a sinus rhythm, strain on the left ventricle (LV), secondary alterations of repolarization and supraventricular ectopic activity.

In 2001, the dyspnea progressed to ordinary exertions, fatigue, edema in the lower limbs, ascites and hepatomegaly. The Doppler echocardiogram revealed normal LV systolic function and restrictive diastolic impairment. The Doppler did not reveal any mitral valve respiratory flow variations and there was no paradoxal movement of the interventricular septum. The unusual aspect of the diffusion of myocardial microcalcifications in both ventricles called attention, in view of the aspect of other sites attacked by the disease (fig. 3). Additionally, a concentric increase in the LV wall thickness was observed and slight dilation of the left atrium.

A hemodynamic study andangiocardiography showed normal coronaries. The diagnosis wastherefore confirmed as diastolic heart failure as a result ofrestrictive cardiomyopathy and due to the pattern ofcalcification is probably secondary to myocardialcysticercosis.

DISCUSSION

The clinical picture presented by thepatient starting in 2001 indicated a syndromic diagnosis of heartfailure. The Doppler echocardiogram revealed alterationscompatible with a restrictive cardiomyopathy and presence ofmicrocalcifications suggestive of cysticercosis. In this case amyocardial biopsy was not performed to confirm the diagnosis,however, the lesions found on the echocardiogram are verysuggestive of cysticercosis since they correspond to thecalcification pattern in other areas.

There are other possible causes of thediastolic impairment that could be suggested, such as:hypertensive heart disease, constrictive pericarditis,endomyocardial fibrosis and Loeffler's idiopathichypereosinophilic syndrome.

Hypertensive heart disease is unlikelysince the patient did not present a prior history of systemichypertension. In reference to constrictive pericarditis, theDoppler echocardiogram did not reveal any indicative signs ofthis disease, such as mitral valve respiratory flow variations,paradoxal movement of the interventricular septum ormorphological alterations of the pericardium.

The increased thickness of the LV wallsand the absence of signs of endocardial fibrosis on theechocardiogram, such as abnormal echoes in the left ventricleapical region, inflow pathway or apex of the right ventricle didnot substantiate a diagnosis of endomyocardial fibrosis orLoeffler's idiopathic hypereosinophilicsyndrome².

The distribution of topographiclocations of cysticercosis varies among different papers on thesubject. Nevertheless, there is a relative consensus that theencephalic and muscular skeletal forms have a greaterprevalence.

Reports in medical literature arecontroversial regarding the prevalence of cardiac cysticercosis.Gobbi et al³ and Lino et al^.4 discoveredcysticerci in the hearts of 26% and 22% of cysticercosisautopsies, respectively, while Vianna et al. discovered them inonly 8%⁵.

The cardiac variety can cause functionaldiastolic alteration which is a minor symptom in the majority ofcases^3,6-9.

Most cases related in medical literatureof myocardial cysticercosis consist of anatomical pathologicalstudies of autopsy⁸ series and there are few dataabout the functional importance of these alterations and clinicalevolution of these patients' condition.

The patient's condition progressed withsignificant clinical improvement after specific treatment forrestrictive cardiomyopathy and was referred to a cardiologist foroutpatient treatment.

The relevance of this clinical case isthe significant clinical manifestation of cardiac disease in thecase of myocardial cysticercosis; there are no documented casesin medical literature of restrictive cardiomyopathy associatedwith this disease. Additionally, medical literature lacks dataabout echocardiograms for myocardial cysticercosis and this caseillustrates these alterations.

CONCLUSION

Cardiac cysticercosis presents anunusual echocardiograph aspect and can provoke a significantmanifestation of diastolic heart failure.

REFERENCES

1. Nascimento E. Teníase e cisticercose. In: Neves DP. Parasitologia Humana. 8ª ed. São Paulo: Atheneu, 1991: 230-42.        [ Links ]

2. Acquatella H, Schiller NB, Puigbo JJ et al. Value of two-dimensional echocardiography in endomyocardial disease with and without eosinophilia. Circulation 1983; 67:1219-26.        [ Links ]

3. Gobbi H, Adad SJ, Neves RR, Almeida HO. Ocorrência de cisticercose (Cysticercus cellulosae) em pacientes necropsiados em Uberaba, MG. Rev Patol Trop 1980; 9: 51-9.        [ Links ]

4. Lino RS, Reis MA, Teixeira VPA. Ocorrência de cisticercose (Cysticercus cellulosae) encefálica e cardíaca em necropsias. Rev Saúde Públ 1999; 33: 495-8.         [ Links ]

5. Vianna LG, Macedo V, Costa JM. Cisticercose músculo-cutânea e visceral – Doença rara? Rev Inst Med Trop S Paulo 1991; 33: 129-36.        [ Links ]

6. García HH, Gonzales AE, Evans CAW et al. Taenia solium cysticercosis. Lancet 2003; 362:547–56.        [ Links ]

7. Agapejev S. Epidemiology of neurocysticercosis in Brazil. Rev Inst Med Trop S Paulo 1996; 38: 207-16.        [ Links ]

8. Lino RS, Ribeiro PM, Antonelli EJ. Developmental characteristics of Cysticercus cellulosae in the human brain and heart. Rev Soc Bras Med Trop 2002; 35: 617-22.        [ Links ]

9. Garcia HH, Del Brutto OH. Taenia solium cysticercosis. Infect Dis Clin North Am 2000; 14:97-119.        [ Links ]

Mailing Address:
Rodrigo Morel Vieira de Melo
Rua Martagão Gesteira, 274/501
40150-390 Salvador, BA - Brazil
E-mail: rodimorel@yahoo.com.br

Received on 01/14/05
Accepted on 07/01/05