Associations between various lipid components and premature myocardial infarction: a cross-sectional study / 中华心血管病杂志

Objective: Hyperlipidemia is closely related to premature acute myocardial infarction (AMI). The present study was performed to explore the correlation between various blood lipid components and the risk of premature AMI. Methods: This is a cross-sectional retrospective study. Consecutive patients with acute ST-segment elevation myocardial infarction (STEMI), who completed coronary angiography from October 1, 2020 to September 30, 2022 in our hospital, were enrolled and divided into premature AMI group (male<55 years old, female<65 years old) and late-onset AMI group. Total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), non-HDL-C, lipoprotein (a) (Lp (a)), apolipoprotein B (ApoB), apolipoprotein A-1 (ApoA-1), non-HDL-C/HDL-C and ApoB/ApoA-1 were analyzed. The correlation between the above blood lipid indexes and premature AMI was analyzed and compared by logistic regression, restricted cubic spline and receiver operating characteristic curve (ROC). Results: A total of 1 626 patients with STEMI were enrolled in this study, including 409 patients with premature AMI and 1 217 patients with late-onset AMI. Logistic regression analysis showed that the risk of premature AMI increased significantly with the increase of TG, non-HDL-C/HDL-C, non-HDL-C, ApoB/ApoA-1, TC and ApoB quintiles; while LDL-C, ApoA-1 and Lp (a) had no significant correlation with premature AMI. The restricted cubic spline graph showed that except Lp (a), LDL-C, ApoA-1 and ApoB/ApoA-1, other blood lipid indicators were significantly correlated with premature AMI. The ROC curve showed that TG and non-HDL-C/HDL-C had better predictive value for premature AMI. Inconsistency analysis found that the incidence and risk of premature AMI were the highest in patients with high TG and high non-HDL-C/HDL-C. Conclusion: TG, non-HDL-C/HDL-C and other blood lipid indexes are significantly increased in patients with premature AMI, among which TG is the parameter, most closely related to premature AMI, and future studies are needed to explore the impact of controlling TG on incidence of premature AMI.

Three-dimensional architecture of intraosseous vascular anatomy of the hamate: a micro-computed tomography study / 北京大学学报(医学版)

OBJECTIVE@#To obtain three-dimensional intraosseous artery of the hamate and to provide the vascular anatomy basis of hamate fracture fixation.@*METHODS@#PbO (lead monoxide, Sinopharm Chemical Reagent Beijing Co. Ltd) was ground into particles less than 40 μm and suspended in turpentine oil (Chemical Reagent Beijing Co. Ltd) at ratios of 1 g : 1.5 mL, 1 g : 1 mL and 1 g : 0.5 mL. Three specimens were investigated. Brachial arteries were cannulated and perfused with lead-based contrast agent. Hamates were harvested and scanned using micro-computed tomography (microCT). The acquisition protocols were as follows: CT scan setup: total rotation [Degrees], 360; rotation steps, 360; X-ray detector setup: transaxial, 2048; axial, 2048; exposure time, 1 500 ms, Binning, 1; system magnification: high-med. X-ray tube setup: 80 kV, 500 mA current. The down-sampling factor used in the reconstruction was 2. The effective voxel size of the final image was 27.30 μm. The three-dimensional model of the hamate was generated and the distribution and pattern of vessels were evaluated.@*RESULTS@#There were abundant extraosseous vessels around the hamate. They were mainly running in the tendons and ligaments around the hamate. Four vascular zones were identified on the hamate surface. They were on the palmar platform of the hamate body, on the dorsal side, on the ulnar side and on the tip of hamulus, namely. There were anastomoses among 4 vascular zones. We did not observe any vessels penetrating through the articular cartilage. The extraosseous vessels of the vascular zones gave a number of intraosseous branches into the hamate. The hamate body received intraosseous blood supply from the dorsal, palmar and ulnar while the hamulus from the palmar, ulnar and hamulus tip. There were some intraosseous branches anastomosing with each other.@*CONCLUSION@#The extraosseous and intraosseous vessels of the hamate were more than what used to be considered. The hamate body and hamulus received blood supply from multiple directions and arteries anastomosed extensively both outside and inside the hamate, making it possible that the intraosseous perfusion survived after fracture. It is likely that the nonunion after the hamate fracture is not caused by the vascular damage but the malalignment of the fragments.

Presence of Severe Stenosis in Most Culprit Lesions of Patients with ST-segment Elevation Myocardial Infarction / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Previous studies revealed that culprit vessels of ST-segment elevation myocardial infarction (STEMI) were often related to mild or moderate stenosis. However, recent studies suggested that severe stenosis was primarily found in culprit lesions. The objective of this study was to analyze the stenosis severity of culprit lesions in STEMI patients and to clarify the paradoxical results.</p><p><b>METHODS</b>A total of 489 consecutive STEMI patients who underwent primary percutaneous coronary intervention were retrospectively studied from January 2012 to December 2014. The patients were divided into three groups based on stenosis severity using quantitative coronary analysis: Group A, 314 cases, stenosis ≥70%; Group B, 127 cases, stenosis 50-70%; and Group C, 48 cases, stenosis ≤50%. The clinical, demographic, and angiographic data of all groups were analyzed.</p><p><b>RESULTS</b>Patients in Group A exhibited a significantly higher prevalence of history of angina pectoris (95.9% vs. 62.5%, P< 0.001), multivessel disease (73.2% vs. 54.2%, P = 0.007), and lower cardiac ejection fraction (53.3 ± 8.6 vs. 56.8 ± 8.4, P= 0.009) than those in Group C. Multivariable analysis revealed that history of angina pectoris (odds ratio [OR]: 13.89, 95% confidence interval [CI]: 6.21-31.11) and multivessel disease (OR: 2.32, 95% CI: 1.25-4.31) were correlated with severe stenosis of the culprit lesion in Group A.</p><p><b>CONCLUSIONS</b>Most culprit lesions in STEMI patients were severe stenosis. These patients exhibited a higher prevalence of angina history and multivessel diseases.</p>