Clinical risk factors and outcomes of young patients with acute ST segment elevation myocardial infarction: a retrospective study.

BACKGROUND: This study aimed to analysis the clinical characteristics and prognosis of acute STEMI in patients aged ≤ 45 years. METHODS: Seven hundred and one patients with STEMI from Liaocheng People's Hospital from January 2018 to March 2021 were included in this study. Clinical characteristics, management, and outcomes (average follow-up: 11.5 months) were compared between patients aged ≤ 45 years and those aged > 45 years. RESULTS: Of the patients with STEMI who underwent primary percutaneous coronary intervention, 108 (15.4%) were aged ≤ 45 years. Compared to the older group, the younger patient group included more males, current smokers, and those with alcohol use disorder (AUD) or a family history of ischaemic heart disease (IHD). The culprit vessel in young patients was the left anterior descending (LAD) artery (60% vs. 45.9%, P = 0.031), which may have been due to smoking (odds ratio, 3.5; 95% confidence interval: 1.12-10.98, P = 0.042). Additionally, young patients presented with higher low-density lipoprotein and lower high-density lipoprotein levels than older patients; uric acid levels were also significantly higher in younger patients than that in the older group. Diabetes showed a trend toward major adverse cardiovascular events (MACE) in both groups; age and sex were both independent predictors of MACE in older patients. CONCLUSION: More patients who were smokers, had AUD, or a family history of IHD were present in the young patient group. Hyperuricaemia (but not dyslipidaemia) was a prevalent risk factor in patients aged ≤ 45 years. Diabetes should be controlled to reduce cardiovascular events in young patients.

HGF Reduces Disease Severity and Inflammation by Attenuating the NF-κB Signaling in a Rat Model of Pulmonary Artery Hypertension.

The purpose of the present study was to investigate the anti-inflammatory effect of hepatocyte growth factor (HGF) on pulmonary artery hypertension (PAH) in a rat model and underlying mechanisms. Wistar rats were treated with monocrotaline intravenously to induce PAH and then treated with vehicle or HGF for 2 weeks, respectively. The mean pulmonary artery pressure (mPAP), the index of right heart ventricular hypertrophy (RHVI), pathological changes, and inflammation in the lungs of individual rats were measured. The levels of serum inflammatory interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and high mobility group protein B1 (HMGB1) and the relative levels of IκBα and NF-κB p65 expression in the lungs of individual rats were determined by methods of enzyme-linked immunosorbent assay (ELISA) and Western blot. The levels of mPAP and RVHI in the HGF group were significantly lower than that in the PAH group (P < 0.05), but remained significantly higher than that of the control group (P < 0.05). Similar patterns of inflammatory scores and the levels of serum IL-6, TNF-α, ICAM-1, and HMGB1 were detected among the different groups of rats. Furthermore, the relative levels of IκBα expression in the lungs of the HGF group of rats were significantly higher than that in the control group, which were significantly higher than that in the PAH group. In contrast, the relative levels of NF-kB p65 expression in the HGF group were significantly lower than that in the PAH group (P < 0.05). HGF treatment significantly mitigated the severity of PAH and inhibited inflammation by attenuating the NF-kB signaling in the lungs of PAH rats.

Impact of acute pulmonary embolism on plasma and tissue hepatocyte growth factor: an experimental study.

This study was designed to investigate the impact of acute pulmonary embolism (PE) on plasma and tissue hepatocyte growth factor (HGF). PE was established in 16 New Zealand white rabbits by intravenous injection of autologous blood clots. Another 16 sham-operated rabbits were used as control. Plasma HGF levels and tissue HGF expression was measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry, respectively. The plasma HGF levels in the PE group were elevated 1 hour after PE (P < .01). In the lung tissue samples, the positive HGF expression ratio was 91.7% and 20.8%, respectively, in the PE and the control group (P < .01). The positive HGF expression ratio in the right ventricular tissue samples in the PE group was higher than in the control group (75.0% versus 20.9%; P < .01). The positive HGF expression ratio in the liver samples in the PE and the control groups was 33.3% and 16.7%, respectively (P < .05). In conclusion, acute PE was associated with a significant increase in plasma HGF. Acute PE was also associated with an enhanced HGF expression in the lungs, the right ventricle, and the liver.