Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enteroviral infection can cause an acquired form of dilated cardiomyopathy. We recently reported that dystrophin is cleaved, functionally impaired, and morphologically disrupted in vitro as well as in vivo during infection with coxsackievirus B3. Genetic dystrophin truncations lead to a marked decrease in dystrophin-associated glycoproteins, whereas expression of only the naturally occurring dystrophin carboxyl terminus, Dp-71, restores the sarcolemmal association of the dystrophin-associated glycoproteins. We sought to determine whether acute cleavage of dystrophin leads to a dissociation of the carboxyl-terminal dystrophin fragment and of the sarcoglycans from the sarcolemma during coxsackievirus B3 infection. We found that in cultured cardiac myocytes and murine hearts infected with coxsackievirus B3, the sarcolemmal localization of the dystrophin carboxyl terminus is lost. The dystrophin-associated glycoproteins alpha-, beta-, gamma-, and delta-sarcoglycan and beta-dystroglycan were markedly decreased in the membrane fraction of infected cells in culture, and the typical sarcolemmal localization for each of these proteins was lost in coxsackievirus-B3-infected cardiomyocytes in vivo. Furthermore, sucrose gradient ultracentrifugation demonstrated that delta-sarcoglycan was physically dissociated from dystrophin within the membrane fraction. In vivo, the sarcolemmal integrity was functionally impaired with Evans blue dye uptake even though there was no generalized disruption of the sarcolemma of infected myocytes evidenced by intact wheat germ agglutinin staining. In analogy to hereditary sarcoglycanopathies, this disintegration of the sarcoglycan complex may, in addition to the dystrophin cleavage, play an important role in the pathogenesis of enterovirus-induced cardiomyopathy. These results imply a potential role for disruption of the sarcoglycans in an acquired form of heart failure.
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PMID:Dissociation of sarcoglycans and the dystrophin carboxyl terminus from the sarcolemma in enteroviral cardiomyopathy. 1098 41

Enterovirus infections are common in the neonatal period. Newborns are at a higher risk of severe disease including meningoencephalitis, sepsis syndrome, cardiovascular collapse, or hepatitis. The mechanism of heart failure in patients with enterovirus infection remains unknown. Early diagnosis may help clinicians predict complications in those infants initially presenting with severe disease. An 11-day-old male newborn was admitted to our neonatal intensive care unit because of tachycardia and crises of cyanosis. His elder brother had febrile illness. The newborn was cyanotic, in respiratory distress, with tachycardia, low blood pressure and prolonged capillary refilling time. Limb pulse oximeter was around 85%. During the first day of hospitalization, the newborn had one febrile episode. Laboratory data: elevated transaminases, markers of inflammation negative, all bacterial cultures negative. Enterovirus RNA was detected in blood sample. Other blood findings were without significant abnormalities. Electrocardiogram showed tachycardia, with narrow QRS complexes (atrial tachycardia) and heart rate up to 280/min. In order to convert the rhythm, the patient was administered adenosine and amiodarone. In the further course of hospitalization, the patient was in good general condition, eucardiac and eupneic. Newborns with tachycardia and a family history of febrile illness should be suspected to have enterovirus infection. Enterovirus infection is a highly contagious and potentially life-threatening infection if not detected early. The use of sensitive molecular-based amplification methods offers potential benefits for early diagnosis and timely treatment.
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PMID:Tachycardia in a newborn with enterovirus infection. 2497 73