Viral Studies

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The presence of myocardial inflammation in more than two-thirds of cases has suggested that some pathologic features of ARVC/D may be considered a sequela of infective myocarditis [33]. Thus, fibro-fatty infiltration may, in part, be viewed as a healing phenomenon in the setting of chronic myocarditis. Enterovirus was first investigated on the basis of an experimental model in which a BALB/C mice infected with Coxsackievirus B3 developed selective right ventricular myocardial cell death, acute mononuclear cell infiltration, and right ventricular aneurysm formation [34]. Several researchers have evaluated ARVC/D patients for the presence of enteroviral genome in the myocardium [17, 35-40] and controversial results have been reported, possibly reflecting different patient selection (Table 9.2).

In 1997, Heim et al. [37] reported the identification of enterovirus RNA in endomyocardial biopsies obtained from two male patients (15 and 26 years old, respectively) by use of in situ hybridization. One of these patients had a strong family history of ARVC/D. In both of these patients, fibrosis was identified in the myocardium, supporting the hypothesis that ARVC/D is a sequela of enterovirus myocarditis.

In another study involving eight patients, en-teroviral RNA was identified in myocardial specimens with homology to coxsackievirus type B found in three subjects [17]. A negative study of viral genome was reported by Calabrese et al. in which there was a high rate of familial ARVC/D cases (50%) and only enteroviral genome was evaluated [38].

Table 9.2 • Molecular investigation in ARVC/D

First Author, year [Ref]

Sex

Mean age yrs

Family history

Methods

Viruses screened

Molecular finding

Kearney, 1995 [35]

2F

Not specified

Yes (2 cases)

PCR

EV, RSV, INVA-B, AV, CMV, HSV, EBV

None

Heim, 1997 [36]

4M, 2F

51

Not specified

N-PCR

EV

3 EV

Heim, 1997 [37]

2M

20

Yes (1 case)

ISH

EV

2 EV

Grumbach, 1998 [17]

4M,4F

44

No

PCR

EV

3 EV

Calabrese,2000 [38]

11M,9F

40

Yes (9 cases)

PCR

EV

None

Bowles, 2002 [39]

7M,12F

19

No

PCR

EV, RSV, INVA-B, AV, CMV, HSV, PV, EBV

5 EV, 2 AV

Chimenti, 2004 [40]

5M,4F

29

No

PCR

EV, INV A-B, AV, CMV, HSV, PV, EBV, HCV

None

^Adenovirus; CMV,Cytomegalovirus; EßV,Ebstein Barr Virus; £V,Enterovirus; HCV, F,female; Hepatitis C Virus; HSV,Herpes Simplex Virus; /NV/4-ß,Influenza virus A and B; /SH,in situ hybridization; M,male; yrs,years; N-PCR,nested-PCR; PCR,polimerase chain reaction; PV, Parvovirus B 19; RSV, Respiratory Syncitial virus

The role of other cardiotrophic viruses was reported by Bowles et al. [39]. The study involved 12 ARVC/D patients, who were considered sporadic cases after a pedigree analysis and a clinical screening of family members. Viruses were detected in 58% (7 out of 12): including enterovirus in five and adenovirus type 5 in two patients, respectively.

The presence of viruses and their role in ARVC/D patients was investigated by Chimenti et al. [40]. They studied 30 patients who were diagnosed with ARVC/D on the basis of having either two major criteria or one major plus at least two minor criteria [41]. At histology, ARVC/D was confirmed in nine patients, whereas the remaining met the Dallas criteria for myocarditis. The molecular investigation detected viral genome in four patients with myocarditis and in none with ARVC/D.

In Italy, our recent experience using molecular viral screening, both PCR and RT-PCR, confirmed the presence of different viral genomes in seven (19%) of 36 cases with clinical and histological evidence of ARVC/D (unpublished data) (Fig. 9.2).

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