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Abstract Background Henoch-Schonlein purpura is the most common vasculitis in childhood, usually triggered by an upper respiratory tract infection and rarely observed in infective endocarditis patients. Abiotrophia defectiva is a rare causative agent of infective endocarditis associated with pre-existing heart disease, immunocompromised and prosthetic valves. Dental procedures are also a common predisposing factor. Case presentation We present the first pediatric congenital heart disease case of infective endocarditis caused by Abiotrophia defectiva combined with recurrent Henoch-Schonlein purpura. A 10-year-old girl with uncorrected congenital heart defects and Henoch-Schonlein purpura developed a purple petechial rash again. Transthoracic echocardiography evaluation revealed multiple irregular vegetations on the right ventricular side of the ventricular septal defect and on the tricuspid valve leaflets. Blood cultures grew Abiotrophia defectiva. The girl received cardiac surgery for vegetation resection as well as congenital heart defect correction and tricuspid valve replacement. Five months after the surgery, the patient was in satisfactory condition without any signs of endocarditis or valve insufficiency and her purpuric rash disappeared. Conclusions The coexistence of recurrent Henoch-Schonlein purpura and infective endocarditis is possible. Abiotrophia defectiva belongs to the streptococcus with a high virulence. In addition, cardiovascular surgery is often required for pediatric infective endocarditis associated with Abiotrophia defectiva, and bioprosthetic valve replacement is considered feasible for irreparable tricuspid valve in children.

Increasing evidence has revealed that humid heat stress (HHS) causes considerable damage to human health. The cardiovascular system has been suggested to be the primary target of heat stress, which results in serious cardiovascular diseases. However, there is still a lack of effective approaches for the prevention and treatment of cardiovascular diseases induced by HHS.Heat-shock proteins (Hsps), especially Hsp70, are reported to provide effective cytoprotection under various stress stimuli. In the present study, we evaluated the cytoprotective effect of geranylgeranylacetone (GGA), which was previously been reported to induce Hsp70 expression in cardiomyocytes under HHS.Using a mouse model of HHS, we showed that the pretreatment of GGA enhanced Hsp70 expression under HHS, as examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. We then examined the effect of GGA pretreatment on the cardiomyocyte apoptosis induced by HHS using terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL) staining, and found that GGA pretreatment inhibited mitochondria-mediated apoptosis. GGA pretreatment could reverse the effect of HHS on cell apoptosis by increasing expression of Bcl-2, decreasing cytochrome c in cytosol, and increasing cytochrome c in mitochondria. However, GGA pretreatment had no effect on the oxidative stress induced by HHS as determined by levels of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH).We have demonstrated that GGA pretreatment suppressed HHS-induced apoptosis of cardiomyocytes through the induction of Hsp70 overexpression.