Cardiac rupture (CR) is a potentially fatal mechanical complication of ST-elevation myocardial infarction (STEMI). We aimed to determine the incidence and risk factors of CR in Chinese STEMI patients. A total of 9798 consecutive STEMI patients from four centers in China were retrospectively analyzed, among which 178 patients had CR. STEMI patients without CR were chosen as a control group. Clinical characteristics were compared between STEMI patients with CR and those without CR. The incidence of CR in STEMI patients was 1.82%, and the 30-d mortality was up to 61.2%. CR patients were significantly older, more female, and associated with a longer time from onset of pain to hospital admission than their non-CR counterparts (P<0.001). More patients with anterior myocardial infarction (82.1%) were found in the CR group, and CR patients had significantly higher heart rates than the control group ((91±19) bpm vs. (71±16) bpm; P<0.001). In multiple-adjusted models, the independent risk factors of CR were advanced age, female gender, anaemia, increased heart rate, anterior myocardial infarction, increased white blood cell (WBC) count, delayed admission, and renal dysfunction. The level of hemoglobin remained a significant determinant factor of CR (OR (95% CI): 0.82 (0.75-0.89); P<0.001) after adjusting for various potential confounding factors. Counts of WBC also remained a significant determinant of the CR (OR (95% CI): 1.08 (1.04-1.12); P<0.001). A number of variables were independently related to CR. This study indicated, for the first time, that both hemoglobin and WBC levels were independently correlated with occurrence of CR.

Inflammation serves an important role in myocardial infarction (MI). Ginsenoside Rg3 (Rg3), an activator of sirtuin 1 (SIRT1), has been identified to elicit anti-inflammatory effects via the NF-κB pathway. However, the function of Rg3 in MI remains unknown. In the present study, a MI rat model was established by coronary artery ligation and treated with Rg3 to explore whether Rg3 could inhibit inflammation in MI rats by inhibiting the SIRT1/NF-κB pathway. At 28 days post-MI, it was identified that Rg3 not only decreased the ST-segment ECG values in MI rats, but also significantly decreased serum LDH, CK-MB and cTnI levels in MI rats. In addition, Rg3 also significantly decreased serum tumor necrosis factor α (TNFα), interleukin (IL)-1β and IL-6 levels and increased serum IL-10 levels in MI rats. In the heart tissues of the MI rats, Rg3 attenuated myocardial pathological changes and cell apoptosis caused by MI, decreased the gene expression levels of TNF-α, IL-1β and IL-6, but increased the gene expression level of IL-10. In addition, the expression levels of the SIRT1 and transcription factor RelB proteins were significantly increased following Rg3 treatment, and the expression level of p-p65/p65 protein was significantly decreased in the heart tissues of MI rats with Rg3 treatment compared with that in heart tissues of MI rats without Rg3 treatment. In conclusion, Rg3 alleviates inflammation in a rat model of MI via the SIRT1/NF-κB pathway.

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