目的 探讨老年冠心病患者PCI后血脂谱变化跟性别交互作用与支架内膜增生的关联.方法 选择行PCI成功置入支架的老年冠心病患者385例,女性130例,男性255例.其中支架内膜轻度增生190例、中度增生137例和重度增生58例.分别于PCI前、复查冠状动脉造影前检测TC、TG、LDL-C、HDL-C水平,其中非HDL-C为TC与HDL-C的差值.用多因素logistic回归模型分析内膜增生的影响因素.结果 女性TC、TG、LDL-C、HDL-C和非HDL-C水平均显著高于男性(P＜0.05,P＜0.01).全体、轻度增生、中度增生患者随访TC、LDL-C和非HDL-C水平较基线明显降低(P＜0.01);重度增生患者非HDL-C水平较基线明显降低(P＜0.05,P＜0.01).多因素logistic回归模型调整混杂因素后,女性内膜增生风险较男性减少50.0％(OR=0.500);TC和非HDL-C每下降 1 mmol/L,内膜增生风险可分别减少63.7％(OR=0.333)和58.2％(OR=0.418);HDL-C 每下降 1 mmol/L,内膜增生风险可增加76.7％(OR=1.767).TC、TG和非HDL-C降低对女性内膜增生保护效能最高(P交互作用＜0.01),老年男性HDL-C水平未降低者内膜增生程度更高(P交互作用＜0.01).结论 老年患者血脂谱跟性别交互作用与PCI后内膜增生程度相关,降低TC、非HDL-C水平和保持HDL-C水平对防治PCI后内膜增生有性别差异.

Objective. Panax ginseng is used widely for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of P. ginseng. We aimed to investigate the protective effect of ginsenoside Re on isoproterenol-induced myocardial fibrosis and heart failure in rats. Methods. A model of myocardial fibrosis and heart failure was established by once-daily subcutaneous injection of isoproterenol (5 mg/kg/day) to rats for 7 days. Simultaneously, rats were orally administrated ginsenoside Re (5 or 20 mg/kg) or vehicle daily for 4 weeks. Results. Isoproterenol enhanced the heart weight, myocardial fibrosis, and hydroxyproline content in rat hearts. Ginsenoside Re inhibited (at least in part) the isoproterenol-induced increase in heart weight, myocardial fibrosis, and hydroxyproline content. Compared with the isoproterenol group, treatment with ginsenoside Re ameliorated changes in left ventricular systolic pressure, left ventricular end diastolic pressure, and the positive and negative maximal values of the first derivative of left ventricular pressure. Ginsenoside Re administration also resulted in decreased expression of transforming growth factor (TGF)-β1 in serum and decreased expression of Smad3 and collagen I in heart tissue. Conclusion. Ginsenoside Re can improve isoproterenol-induced myocardial fibrosis and heart failure by regulation of the TGF-β1/Smad3 pathway.

在过去50年间,随着医疗技术的革新及发展,急性心肌梗死( AMI)的诊断及治疗预后也得到长足改善,其中心电图、心血管疾病重症监护、冠状动脉造影、再灌注治疗、高敏肌钙蛋白检测等发挥了重要作用.临床中,AMI患者冠状动脉造影结果中,冠状动脉明显阻塞(狭窄程度>50% )的患者约占90% ,但剩余约10%的患者造影狭窄程度<50% ,即冠状动脉非阻塞性心肌梗死( MINOCA,几项大规模注册研究显示为1% ~13%)[1,2].

1病例资料 例1,男,62岁,40min前因心前区疼痛伴有左臂及背部放射痛入院.体检:血压128/72 mmHg(1 mmHg=0.133 kPa),心率95次/min,心律齐,各瓣膜听诊区未闻及额外心音.心电图:Ⅱ、Ⅲ、avF导联ST段呈下斜型压低2 mV,V1～V3导联呈QS波,V4～V6导联ST呈上斜型压低,T波高尖对称.急检结果:肌红蛋白＞500 ng/ml,肌钙蛋白Ⅰ(cTnI)1.08 ng/ml,肌酸激酶同工酶(CK-MB)28.80 ng/ml,钾离子4.05 mmol/L,三酰甘油0.52mmol/L,胆固醇4.86 mmol/L.冠状动脉造影示:前降支近段闭塞.给予血运重建后,复查心电图:V1～V4呈QS波,V4～V6其ST段明显回落接近基线.见图1～3.

PURPOSETo investigate the effect of alprostadil on myocardial ischemia/reperfusion (I/R) in rats.METHODSRats were subjected to myocardial ischemia for 30 min followed by 24h reperfusion. Alprostadil (4 or 8 μg/kg) was intravenously administered at the time of reperfusion and myocardial infarct size, levels of troponin T, and the activity of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) in the serum were measured. Antioxidative parameters, nitric oxide (NO) content and phosphorylated endothelial nitric oxide synthase 3 (p-eNOS) expression in the left ventricles were also measured. Histopathological examinations of the left ventricles were also performed.RESULTSAlprostadil treatment significantly reduced myocardial infarct size, serum troponin T levels, and CK-MB and LDH activity (P<0.05). Furthermore, treatment with alprostadil significantly decreased malondialdehyde (MDA) content (P<0.05) and markedly reduced myonecrosis, edema and infiltration of inflammatory cells. Superoxide dismutase and catalase activities (P<0.05), NO level (P<0.01) and p-eNOS (P<0.05) were significantly increased in rats treated with alprostadil compared with control rats.CONCLUSIONThese results indicate that alprostadil protects against myocardial I/R injury and that these protective effects are achieved, at least in part, via the promotion of antioxidant activity and activation of eNOS.

心血管疾病在许多国家成为第一位致死原因,其中急性心肌梗死( AMI)是目前致死率及致残率最高的疾病之一. 对于急性ST段抬高型心肌梗死( STEMI )患者的治疗,欧洲心脏病学会( ESC)指南推荐首选急诊直接经皮冠状动脉介入治疗[1]. 然而,AMI患者在接受介入治疗时,都会出现心肌缺血-再灌注损伤( MI-RI) ,特别是再灌注心律失常,且这些患者AMI后心力衰竭及死亡的主要原因与 MIRI 有着密不可分的关系[2]. 缺血后适应( IPostC)在改善冠脉血流、保护冠脉微血管、减少心肌细胞凋亡、缩小心肌梗死面积等方面有着重要作用,同时由于IPostC在现实中便于临床操作,从而在改善MIRI方面有了一个新的治疗策略.

Objective. Panax ginseng is widely used for treatment of cardiovascular disorders in China. Ginsenoside Re is the main chemical component of Panax ginseng. This study aimed to investigate the protective effect of Ginsenoside Re on isoproterenol-induced myocardial injury in rats. Methods. Male Wistar rats were orally given Ginsenoside Re (5, 20 mg/kg) daily for 7 days. Isoproterenol was subcutaneously injected into the rats for two consecutive days at a dosage of 20 mg/kg/day (on 6th and 7th day). Six hours after the last isoproterenol injection, troponin T level and creatine kinase-MB (CK-MB) activity were assayed. Histopathological examination of heart tissues was performed. The levels of malondialdehyde (MDA) and glutathione (GSH) in heart tissues were measured. The nuclear factor erythroid 2-related factor 2 (Nrf2) content in nucleus and the proteins of glutathione cysteine ligase catalytic subunit (GCLC) and glutathione cysteine ligase modulatory subunit (GCLM) in heart tissues were assayed by western blotting method. Results. Treatment with Ginsenoside Re at dose of 5, 20 mg/kg reduced troponin T level and CK-MB activity of rats subjected to isoproterenol. The cardioprotective effect of Ginsenoside Re was further confirmed by histopathological examination which showed that Ginsenoside Re attenuated the necrosis and inflammatory cells infiltration. Ginsenoside Re inhibited the increase of MDA content and the decrease of GSH in heart tissues. Moreover, the Nrf2 content in nucleus and the expressions of GCLC and GCLM were significantly increased in the animals treated with Ginsenoside Re. Conclusion. These findings suggested that Ginsenoside Re possesses the property to attenuate isoproterenol-induced myocardial ischemic injury by regulating the antioxidation function in cardiomyocytes.

经皮冠状动脉介入(PCI)治疗已广泛应用于冠心病的临床治疗,随着介入治疗技术的不断进步、器械材料的不断改进和药物洗脱支架的出现,PCI 治疗的指征不断扩大,越来越多的患者从中获益,但仍有少部分患者由于各种因素导致术后不良事件的发生.有研究显示,随着冠心病危险因素的升高,PCI术后不良反应也随之升高〔1〕,因此,明确接受PCI治疗术患者术后死亡率与自身冠心病危险因素的关系,对相关危险因素进行早期干预及预防有重要意义.本文仅针对冠心病常见危险因素进行讨论,揭示常见危险因素与术后死亡率之间的关系.

心肌淀粉样变性(CA)是由于原发性或继发性因素致使淀粉样物质沉积于心肌组织,从而引起心脏舒缩功能和(或)传导系统障碍,具有典型限制性心肌病临床表现的一组疾病.所谓的淀粉样物质是前体蛋白以异常的β折叠形式沉积在细胞外的某种自体蛋白纤维,经过刚果红染色在偏振光显微镜下,呈现苹果绿双折射,在电镜观察下,可见直径7.5~10.0 nm无分支皱褶结构排列.目前,已经确定31种前体蛋白可形成淀粉样纤维蛋白,其中11种可导致心脏受累〔1,2〕.基于前体蛋白、治疗、预后等,目前多将CA分为原发性(AL)、继发性(AA)、遗传性、老年系统性或孤立性心房淀粉样变〔3~6〕.AL是由意义不明的单克隆性丙种球蛋白血症或多发性骨髓瘤或其他疾病所致κ或λ轻链等免疫球蛋白片段所形成的淀粉样物质沉积所致〔7,8〕.遗传性、老年系统性淀粉样变性为突变型或野生型转甲状腺素蛋白(TTR)异常折叠形成淀粉样蛋白沉积所致,AA由慢性感染或炎性疾病所致,为血清蛋白A沉积所致,一般很少影响心脏,即使累及临床表现亦较轻.孤立性心房淀粉样变性与心房钠尿肽沉积相关,目前临床意义并不明确,可能与心房颤动发生相关.另外,一些较少见前体蛋白亦可形成淀粉样纤维蛋白,包括突变型载脂蛋白A1、纤维蛋白原、肌动蛋白等.

Aims A longevity gene, Sirtuin 1 (SIRT1) and energy sensor AMP-activated protein kinase (AMPK) have common activators such as caloric restriction, oxidative stress, and exercise. The objective of this study is to characterize the role of cardiomyocyte SIRT1 in age-related impaired ischemic AMPK activation and increased susceptibility to ischemic insults. Methods and results Mice were subjected to ligation of left anterior descending coronary artery for in vivo ischemic models. The glucose and fatty acid oxidation were measured in a working heart perfusion system. The cardiac functions by echocardiography show no difference in young wild-type C57BL/6 J (WT, 4-6 months), aged WT C57BL/6 J (24-26 months), and young inducible cardiomyocyte-specific SIRT1 knockout (icSIRT1 KO) (4-6 months) mice under physiological conditions. However, after 45 mins ischaemia and 24-h reperfusion, the ejection fraction of aged WT and icSIRT1 KO mice was impaired. The aged WT and icSIRT1 KO hearts vs. young WT hearts also show an impaired post-ischemic contractile function in a Langendorff perfusion system. The infarct size of aged WT and icSIRT1 KO hearts was larger than that of young WT hearts. The immunoblotting data demonstrated that aged WT and icSIRT1 KO hearts vs. young WT hearts had impaired phosphorylation of AMPK and downstream acetyl-CoA carboxylase during ischaemia. Intriguingly, AMPK upstream LKB1 is hyper-acetylated in both aged WT and icSIRT1 KO hearts; this could blunt activation of LKB1, leading to an impaired AMPK activation. The working heart perfusion results demonstrated that SIRT1 deficiency significantly impaired substrate metabolism in the hearts; fatty acid oxidation is augmented and glucose oxidation is blunted during ischaemia and reperfusion. Adeno-associated virus (AAV9)-Sirt1 was delivered into the aged hearts via a coronary delivery approach, which significantly rescued the protein level of SIRT1 and the ischemic tolerance of aged hearts. Furthermore, AMPK agonist can rescue the tolerance of aged heart and icSIRT1 KO heart to ischemic insults. Conclusions Cardiac SIRT1 mediates AMPK activation via LKB1 deacetylation, and AMPK modulates SIRT1 activity via regulation of NAD+ level during ischaemia. SIRT1 and AMPK agonists have therapeutic potential for treatment of aging-related ischemic heart disease.

近些年来,情绪障碍与身体健康之间的关系越来越受到人们的重视,成为当今的热门话题.心血管疾病尤其是冠心病是威胁人类生命和健康的主要疾病,其发病率和死亡率均非常高,并发症严重且多样,而焦虑、抑郁障碍是心血管疾病常见的两个临床并发症.在双心医学领域,冠心病在精神障碍患者中的患病率非常高,尤其是存在焦虑抑郁障碍的患者.事实上,冠心病与焦虑抑郁障碍是相互关联的.两种疾病相互影响各自的发生、发展及预后.多项研究表明,冠心病患者并发焦虑、抑郁等情绪障碍的比例很高,焦虑症、抑郁症是冠心病病理生理进展中的一个独立危险因素〔1〕,其贯穿于疾病治疗、康复和预防的整个过程,同时增加冠心病患者的死亡风险〔2〕.

冠状动脉介入治疗已成为冠心病的主要治疗手段. 借助生物医学工程技术,从最初的单纯经皮冠状动脉腔内成形术(PTCA)到裸金属支架(BMS)置入术再到药物洗脱支架(DES)置入术,再狭窄的发生率得到明显改善,但DES仍存在5%左右的再狭窄率. 另外,诸如小血管病变、分叉病变等特殊冠脉病变的介入治疗也无一致且优效的处理手段,仍然困扰着广大介入医生. 近年来,一种以球囊为药物载体的临床新技术——药物涂层球囊( DCB)的出现备受关注. 其在球囊膨胀时可迅速将抗细胞增殖药物转移至靶病变血管,使药物被冠状动脉组织吸收,有效避免血管再狭窄. 同药物支架相比,其不在血管中留下永久性置入物,发生后续炎性反应及正性重塑的风险低. DCB的出现无疑为冠脉介入治疗拓展了治疗的适应证、提供了新的选择. 本文就DCB的技术发展及其在冠脉介入治疗中的应用进行综述.

Background— There are no reports on a large-scale randomized trial exploring optimal dual antiplatelet therapy (DAPT) duration after biodegradable polymer sirolimus-eluting stent implantation. We sought to report the outcomes of a randomized substudy of the prospective Evaluate Safety and Effectiveness of the Tivoli DES and the Firebird DES for Treatment of Coronary Revascularization (I-LOVE-IT 2) trial. Methods and Results— In the prospective noninferiority randomized I-LOVE-IT 2 trial, 1829 patients allocated to the biodegradable polymer sirolimus-eluting stent group were also randomized to receive either 6-month (n=909) or 12-month DAPT (n=920). The primary end points of this noninferiority substudy were 12-month target lesion failure (composite of cardiac death, target vessel myocardial infarction or clinically indicated target lesion revascularization), and the major secondary end points were 12-month net adverse clinical and cerebral events (composite of all-cause death, all myocardial infarction, stroke, or major bleeding [Bleeding Academic Research Consortium type ≥3]). The 12-month target lesion failure in 6-month DAPT group was comparable with the 12-month DAPT group (6.8% versus 5.9%; difference and 95% confidence interval, 0.87% [−1.37% to 3.11%], P for noninferiority=0.0065). Further follow-up at 18 months showed that incidence of target lesion failure and net adverse clinical and cerebral events were similar between the 2 groups (7.5% versus 6.3%, log-rank P =0.32; 7.8% versus 7.3%, log-rank P =0.60; respectively), as well as their individual end point components. Conclusions— This study indicated noninferiority in safety and efficacy of 6-month versus 12-month DAPT after implantation of a novel biodegradable polymer sirolimus-eluting stent. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01681381.

目前，冠心病最有效、最直接的治疗策略是经皮冠脉介入治疗（PCI），而分叉病变约占所有冠脉介入治疗病例的10％～20％〔1〕。分叉病变介入治疗的过程中技术操作难度大，接受放射线量多，手术成功率相对低而再狭窄率高，近期及远期主要心脏不良事件发生率高，因此分叉病变一直是介入医生面临的挑战之一。分叉病变介入治疗过程中发生“铲雪”效应、分支痉挛或血管夹层等均可导致分支狭窄或闭塞，然而每个患者、每处病变都有其特殊性，所以没有两个完全相同的分叉病变，也没有一种可适用于所有分叉病变的手术方法。选择最合适的治疗策略、最优的手术技术才会达到最理想的即刻临床效果及远期预后，现对分叉病变的治疗策略及手术技术进行简要综述。

Pyruvate dehydrogenase (PDH) plays a key role in aerobic energy metabolism and occupies a central crossroad between glycolysis and the tricarboxylic acid cycle. We generated inducible cardiac-specific PDH E1α knockout (CreER(T2)-PDH(flox/flox)) mice that demonstrated a high mortality rate. It was hypothesized that PDH modulating cardiac glucose metabolism is crucial for heart functions under normal physiological and/or stress conditions. The myocardial infarction was conducted by a ligation of the left anterior descending coronary arteries. Cardiac PDH E1α deficiency caused large myocardial infarcts size and macrophage infiltration in the hearts (P < .01 vs wild-type [WT]). Wheat germ agglutinin and Masson trichrome staining revealed significantly increased hypertrophy and fibrosis in PDH E1α-deficient hearts (P < .05 vs WT). Measurements of heart substrate metabolism in an ex vivo working heart perfusion system demonstrated a significant impairment of glucose oxidation in PDH E1α-deficient hearts during ischemia/reperfusion (P < .05 vs WT). Dichloroacetate, a PDH activator, increased glucose oxidation in WT hearts during ischemia/reperfusion and reduced myocardial infarct size in WT, but not in PDH E1α-deficient hearts. Immunoblotting results demonstrated that cardiac PDH E1α deficiency leads to an impaired ischemic AMP-activated protein kinase activation through Sestrin2-liver kinase B1 interaction which is responsible for an increased susceptibility of PDH E1α-deficient heart to ischemic insults. Thus, cardiac PDH E1α deficiency impairs ischemic AMP-activated protein kinase signaling and sensitizes hearts to the toxicological actions of ischemic stress.

1临床资料男性，55岁，因“发热20天，心前区闷痛3天”入院。20天前无明显诱因出现发热，最高体温达39.1℃，伴寒战、干咳，当地诊断为“感冒”，给予静脉应用左氧氟沙星（0.2 g，2次/d）、青霉素（400万单位，2次/d）治疗5天后体温恢复正常。2天后患者再次出现发热，间断口服布洛芬，体温可降至正常。3天前无明显诱因突发胸部闷痛，以左侧为著，呈持续性，与体位、呼吸无关，活动后胸闷略有加重，当地医院急诊行胸片提示球型心，腹部彩色超声见肝左叶117 mm×76 mm的占位性病变，为进一步诊治来我院就诊。

Diabetic complications are the major cause of mortality for the patients with diabetes. Oxidative stress and inflammation have been recognized as important contributors for the development of many diabetic complications, such as diabetic nephropathy, hepatopathy, cardiomyopathy, and other cardiovascular diseases. Several studies have established the anti-inflammatory and oxidative roles of bioactive constituents in Magnolia bark, which has been widely used in the traditional herbal medicines in Chinese society. These findings have attracted various scientists to investigate the effect of bioactive constituents in Magnolia bark on diabetic complications. The aim of this review is to present a systematic overview of bioactive constituents in Magnolia bark that induce the prevention of obesity, hyperglycemia, hyperlipidemia, and diabetic complications, including cardiovascular, liver, and kidney.

Objectives. Ginsenoside Rg3 is one of the ginsenosides which are the main constituents isolated from Panax ginseng. Previous study demonstrated that ginsenoside Rg3 had a protective effect against myocardial ischemia/reperfusion- (I/R-) induced injury. Objective. This study was designed to evaluate the effect of ginsenoside Rg3 on cardiac function impairment induced by myocardial I/R in rats. Methods. Sprague-Dawley rats were subjected to myocardial I/R. Echocardiographic and hemodynamic parameters and histopathological examination were carried out. The expressions of P53, Bcl-2, Bax, and cleaved caspase-3 and the levels of TNF-α and IL-1β in the left ventricles were measured. Results. Ginsenoside Rg3 increased a left ventricular fractional shortening and left ventricular ejection fraction. Treatment with ginsenoside Rg3 also alleviated increases of left ventricular end diastolic pressure and decreases of left ventricular systolic pressure and ±dp/dt in myocardial I/R-rats. Ginsenoside Rg3 decreased apoptosis cells through inhibiting the activation of caspase-3. Ginsenoside Rg3 also caused significant reductions of the contents of TNF-α and IL-1β in left ventricles of myocardial I/R-rats. Conclusion. The findings suggested that ginsenoside Rg3 possessed the effect of improving myocardial I/R-induced cardiac function impairment and that the mechanism of pharmacological action of ginsenoside Rg3 was related to its properties of antiapoptosis and anti-inflammation.

目的：探讨Stanford B型主动脉夹层（AD）急性期内行胸主动脉腔内修复术（TEVAR）的有效性和安全性。<br>　　目的：探讨冠脉分叉病变采用单支架术不同介入策略的临床效果，以期为冠脉分叉病变的介入治疗积累更多的临床依据。

目的：探讨冠状动脉（冠脉）支架置入术后患者血脂水平、降低程度及其与冠脉支架内膜增生程度之间的相关性。