A case report of Vancomycin in the treatment of Q fever endocarditis.

The patient, a 43-year-old male, was admitted to the hospital with gradually aggravated exertional palpitations and chest tightness over a 2-day period. Upon hospital admission, a cardiac ultrasound revealed aortic valve redundancy, however multiple blood culture investigations came back negative. Blood mNGS was perfected, revealing Coxiella burnetii, and the diagnosis of Q fever (query fever) was established. The temperature and inflammatory indices of the patient were all normal with the treatment of vancomycin before cardiac surgery. But for the potential liver damage of and the Coxiella burnetii was still positive in the anti-phase II IgG titer, the doxycycline and hydroxychloroquine instead of vancomycin were applied for the patient. Despite receiving standardized anti-infective therapy of doxycycline combined with hydroxychloroquine, this patient had fever and increased leukocytes following surgery. After the addition of vancomycin as an anti-infective treatment, the temperature and leukocytes improved quickly. During the treatment of vancomycin, a discovery of liver injury may have resulted. These findings provide new therapy options for future professionals.

Comparison and analysis of statins drug use in the treatment of diastolic dysfunction in patients.

Statins have multiple anti lipid effects, such as anti-inflammatory, anti-oxidation and anti arteriosclerosis, which are beneficial to improve cardiac function. Statins can effectively improve left ventricular remodeling and protect ventricular diastolic function. In this study, the effects of statin therapy on diastolic function and BNP level and exercise tolerance after exercise were observed by statins in patients with diastolic dysfunction. The results showed that after atorvastatin treatment, the exercise BNP decreased in the treatment group, which was significantly different from that before treatment and in the control group (P<0.05). This study demonstrated that atorvastatin was used to treat patients with diastolic dysfunction and exercise hypertension by lowering blood pressure and reducing exercise SBP, anti-inflammatory and improving vascular endothelial function.

Effect of doxycycline and atorvastatin on improving exercise tolerance in patients with angina pectoris.

The therapeutic effect of statins on the stabilization of atherosclerotic plaques has been affirmed. In recent years, the inhibition of matrix metalloproteinases (MMPS) of tetracycline drug doxycycline has attracted more and more attention. In this paper, we observed the effect of atorvastatin and doxycycline on exercise tolerance in patients with stable angina pectoris. The results showed that there was no significant difference in the clinical efficacy of the two groups and the effect on the exercise tolerance (P<0.05). There were 4 cases of mild gastrointestinal reaction in the doxycycline group and no other serious adverse reactions. The total effective rate of treatment in the doxycycline group was 93.3%. Doxycycline treatment significantly reduced the frequency of angina pectoris and the incidence of cardiovascular events, and the treatment effect was better. To sum up, we think doxycycline is a safe, cheap, therapeutic drug to stabilize plaque.

Sphingomyelin phosphodiesterase 1 (SMPD1) mediates the attenuation of myocardial infarction-induced cardiac fibrosis by astaxanthin.

Uncontrolled cardiac fibrosis following myocardial infarction (MI) is a critical pathological change leading to heart failure. Current pharmacotherapies are limited by unsatisfactory efficacy and undesired systemic side effects. Astaxanthin (ASX) is a natural carotenoid with strong antioxidant and anti-inflammatory activities. The effects of ASX on MI-induced cardiac fibrosis and the underlying mechanisms remain largely unknown. In this study, after the establishment of MI model, mice were administrated with ASX (200 mg/kg⋅d) for 4 weeks. We found that ASX treatment attenuated cardiac fibrosis and improved heart function following MI, as evidenced by reduced collagen I/III ratio, hydroxyproline content and left ventricular end diastolic pressure (LVEDP). Lipidomic analysis revealed the overaccumulation of myocardial ceramides in mice with cardiac fibrosis, which was normalized by ASX treatment. Molecular docking analysis showed that ASX produced a tight fit in the pocket of sphingomyelin phosphodiesterase 1 (SMPD1), a key enzyme in the production of ceramides. Western blot analysis confirmed the significant inhibition of SMPD1 expression by ASX. Furthermore, MI-induced overexpression of transforming growth factor ß1 (TGF-ß1) and phosphorylated SMAD2/3 were attenuated by ASX administration. SMPD1 knockout (KO) abrogated the beneficial effect of ASX. Taken together, our results suggest that the cardioprotective effects of ASX are mediated by SMPD1 through the indirection inhibition of TGF- ß1/SMAD signaling cascade.

Hsp27 reduces cold ischemia-reperfusion injury in heart transplantation through regulation of NF-κB and PUMA signaling.

BACKGROUND AND OBJECTIVE: Global myocardial ischemia-reperfusion (I/R) injury after heart transplantation is believed to impair graft function and aggravate episodes of both acute and chronic rejection. The 27-kDa heat shock protein (Hsp27) has a potent ability to alleviate I/R after cardiac transplantation. The aim of this study was to investigate the anti-I/R injury effect of Hsp27 to elucidate the underling mechanisms. METHODS: Heart grafts from BALB/c mice were preserved in University of Wisconsin (UW) solution (control) or UW solution containing pAAV-Hsp27 (Hsp27 solution) at 4°C for 48 h and subsequently transplanted into syngeneic recipients for 72 h. The heart grafts were then collected for histopathological and gene expression analyses. An in vitro I/R model (H9c2 cells or H9c2/Hsp27 cells) was constructed. Then, protein and mRNA expression of Hsp27, p65, p53 upregulated modulator of apoptosis (PUMA), interleukin (IL)-6, IL-1ß, and tumor necrosis factor (TNF)-α in heart tissues and H9c2 cells were detected with western blot and reverse transcription polymerase chain reaction analyses. Caspase-3 activity was detected using a commercial assay, while protein levels of IL-6, IL-1ß, and TNF-α were detected using specific enzyme-linked immunosorbent assays. NF-κB activity was detected with an electrophoretic mobility shift assay. Cell apoptosis was detected with the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay and flow cytometric analysis. RESULTS: Cold I/R caused severe morphologic myocardial injury of heart grafts from wild type C57BL/c mice, whereas grafts from Hsp27 preservation showed less damage as demonstrated by decreased cell apoptosis/death and the preservation of the normal structure of the heart. Hsp27 inhibited I/R-induced injury as indicated by the reduction in cardiac troponin I activities and decreased cardiac tissue levels of the proinflammatory factors TNF-α, IL-1ß, and IL-6. Hsp27 was further demonstrated to significantly inhibit nuclear translocation of p65 and p53 upregulated modulator of apoptosis (PUMA) expression. CONCLUSIONS: These results suggested that the cardioprotective effect of Hsp27 could be due to the suppression of the myocardial inflammatory response and apoptosis by blocking the NF-κB-dependent pro-inflammatory and NF-κB-dependent PUMA signaling pathways.