Adenovirus infection, which has been known to mimic Kawasaki disease (KD), is one of the most frequent conditions observed during differential diagnosis when considering KD. Accordingly, it is essential to being able to differentiate between these two diseases. Therefore, we performed multiplex reverse transcriptase- polymerase chain reaction and tissue-Doppler echocardiography to distinguish between adenovirus patients and KD patients.

A total of 113 adenoviral infection patients (female 48, male 65) diagnosed from January 2010 to June 2016 were evaluated. We divided adenoviral infection patients into two groups: group 1, which consisted of individuals diagnosed with KD according to the KD American Heart Association criteria (n=62, KD with adenovirus infection); and group 2, which comprised individuals only diagnosed with adenovirus infection (n=51). Laboratory data were obtained from each patient including N-terminal pro-brain natriuretic peptide. Echocardiographic measurements were compared between two groups. In addition, reverse transcriptase-polymerase chain reaction was performed using nasopharyngeal secretions to diagnose adenoviral infection.

Conjunctival injection, cervical lymphadenopathy, polymorphous skin rash, abnormalities of the lip or oral mucosa and abnormalities of extremities were significantly higher in group 1 than group 2. Moreover, group 1 had significantly higher C-reactive protein and alanine aminotransferase levels, as well as lower platelet counts and albumin levels than group 2. Coronary artery diameter was significantly greater in group 1 than group 2.

In patients with adenoviral infection with unexplained prolonged fever, echocardiography and C-reactive protein can be used to differentiate KD with adenoviral infection from adenoviral infection alone.

Simvastatin has been reported to attenuate the development of pulmonary hypertension through increased apoptosis as well as reduced proliferation of smooth muscle cells in obstructive vascular lesions. Microarray experiment can accomplish many genetic tests in parallel. The purpose of this study is to evaluate altered expressions of gene in rat hearts with monocrotaline (MCT)-induced pulmonary arterial hypertension after simvastatin treatment.

Six-week-old male rats were grouped as follows: control group (C group, saline injection), M group (MCT 60 mg/kg), and S group (MCT 60 mg/kg plus 10 mg/kg/day simvastatin by gavage during 28 days). Body weight, right ventricular pressure and right ventricular/left ventricle+septum ratio in each group were measured. The rats were sacrificed after 28 days. Total RNA was extracted from the rat heart tissue and microarray analysis was performed.

Administration of simvastatin significantly inhibited the progression of right ventricular hypertrophy at day 28 in the S group than in the M group. Compared with the C group, MCT was associated with a significant difference in expression of genes related to biosynthesis and with the regulation of heart contraction rate. Simvastatin treatment resulted in a significantly changed expression of genes about the regulation of progression through cell cycle and system development compared to the M group. The expressions of nitric oxide synthase and brain natriuretic peptide were significantly decreased after simvastatin treatment.

Administration of simvastatin exerted inhibitory effects on right ventricular hypertrophy during the development of MCT-induced pulmonary arterial hypertension in rats. Simvastatin changes the expression of genes associated with various functions.