Fulminant myocarditis demonstrating uncommon morphology?a report of two autopsy cases

Abstract

Two autopsy cases of fulminant myocarditis demonstrating uncommon morphology were studied. Subjects included two male patients: a 42-year-old (case 1) and a 39-year-old (case 2). Both cases had fever, chest or epigastric pain, electrocardiographic abnormalities, prominent elevation of serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, lactic dehydrogenase and creatine phosphokinase. They were treated with intra-aortic balloon pumping and percutaneous cardiopulmonary support, and they died at 3 days and 4 days after admission (total course of 10 days and 9 days), respectively. Case 1 showed focal necrosis, severe myocardial dystrophic calcification positive for Kossa stain, inflammatory edema, lymphocyte and macrophage infiltration and extravasation of erythrocytes. Case 2 showed acute inflammation and severe myocardial necrosis with neutrophilic abscess, lymphocyte and macrophage infiltration, cell debris and purulent exudate. Calcified, degenerative and necrotic cardiac myocytes and macrophages were reacted with anti-Enterovirus antibody (clone 5-D8/1), which recognizes an epitope on the VP1 peptide of most Coxsackievirus, echovirus, poliovirus and enterovirus strains. Therefore, the present two cases may be compatible with fulminant enterovirus-associated myocarditis. Using reverse transcriptase-semi-nested polymerase chain reaction, picornaviral RNA was detected in the amplified products extracted from the paraffin-embedded myocardial sample of case 1 but not in case 2.

Targeting of the Osteoclastogenic RANKL–RANK Axis Prevents Osteoporotic Bone Loss and Soft Tissue Calcification in Coxsackievirus B3–Infected Mice

“…This was confirmed by an increase in the myeloid lineage population that can differentiate into osteoclasts as well as higher recruitment of lymphocytes and macrophages to the heart and pancreas of CVB3-infected mice (Supplemental Fig. 2D, 2E), which is consistent with previous reports (12,13). Based on these results, we propose that an increase in inflammatory cytokines and osteoclast progenitors in the virus-infected mice contributes to the stimulation of osteoclast differentiation and function, eventually leading to a reduction in bone mass.…”

“…Such infection in humans has also been found to result in various inflammatory conditions, including myocarditis, pancreatitis, respiratory disease, gastroenteritis, hepatitis, meningitis, and encephalitis (9)(10)(11). Moreover, case reports have described individuals infected with CVB3 who manifest symptoms of calcification in the heart or liver, resulting in premature death, and with the tissue surrounding calcified lesions being found to be infiltrated with lymphocytes, macrophages, and neutrophils (12,13). In acute viral myocarditis, CVB3 infection results in the migration and subsequent infiltration of NK cells into the heart, followed by a second wave of infiltration by Th cells and CTLs (14).…”

Genetic Determinants of Virulence in the Group B Coxsackieviruses

“…When inoculated intraperitoneally into mice, the TD CVB3 strains can persist in hearts for up to 5 months post-inoculation. The relevance of this persistence mechanism for human cardiomyopathic disease has been confirmed by the detection, sequence analysis and molecular cloning of similar TD genomes in heart muscle of a human case of myocarditis [32], the only case to date in which the 5´-terminus of a persisting enteroviral genome in a human being has been examined [Kim K-S, Tracy S, Oka K, Chapman NM, Unpublished Data]. This finding demonstrates how a replicating enterovirus can remain in heart muscle for long periods of time in a form that is difficult to detect: standard cell culture techniques that depend upon cytopathic effects are inadequate due to the slow replication rate and must be carefully performed due to low RNA copy number RT-PCR.…”

An Unusual Case of Allograft Neutrophilic Myocarditis Mimicking Acute Myocardial Infarction in a Post–Heart Transplant Patient

“…Myocarditis with neutrophilic infiltration is extremely rare and has been reported in the setting of acute fulminant myocarditis 22 with necrosis and abscess, as well as in animals with severe streptococcal myocarditis. 23 It is important to recognize that identifying the pathologic distinction between myocarditis and severe acute rejection may be difficult 24 ; furthermore, these two processes may occur at the same time.…”