Emerging evidence for the role of cardiotrophin-1 in cardiac repair in the infarcted heart

Ischemic heart disease is the most common cause of mortality worldwide. Cardiac fibroblasts and myofibroblasts, i.e., the hypersecretory, muscular, and contractile fibroblastic phenotype variant, play an important role in myocardial healing and are responsible for accumulation of collagen in the infarct scar as well as in viable myocardium. Thus, cardiac fibroblasts and myofibroblasts directly contribute to cardiac stiffness, altered performance, and ultimately to the onset of systolic and diastolic heart failure. Cardiotrophin-1 (CT-1) is a member of the IL-6 superfamily and is elevated in the serum of patients with ischemic heart disease and valvular heart disease; it is also known to induce cardiomyocyte hypertrophy in vitro. The recent, burgeoning awareness of the functions of IL-6 superfamily of cytokines within cardiovascular diseases predicates this summary of CT-1's effect in cardiac wound healing, and particularly after the induction of myocardial infarction. Further, we summarize recent results of cardiac CT-1 expression post-myocardial infarction (post-MI) as well as the effect of CT-1 on cultured primary adult rat cardiac fibroblasts with respect to proliferation and collagen secretion. It would appear that CT-1 plays an important and heretofore largely unrecognized role in infarct scar formation and angiogenesis in the rat model of chronic MI. Further work is required to determine factors that induce CT-1 expression, its interplay with other mediators of cardiac infarct wound healing in the setting of acute cardiac ischemia and chronic post-MI heart failure, and ultimately whether it confers a beneficial effect or contributes to maladaptive cardiac fibrosis.     

OSAHS与冠状动脉粥样硬化性心脏病的研究进展

阻塞性睡眠呼吸暂停低通气综合征(OSAHS)由于睡眠时气道塌陷而引起反复缺氧、白天嗜睡等症状,且与高血压、心律失常、冠状动脉粥样硬化性心脏病(CHD)和心力衰竭等心血管疾病关系密切。OSAHS在促进心血管疾病发生、发展过程中起到重要作用,目前OSAHS作为CHD的重要危险因素逐渐受到重视。本文就OSAHS引起CHD的发病机制,OSAHS与冠状动脉狭窄程度之间的联系,OSAHS合并CHD的不良预后及持续气道正压通气对该类患者预后的影响作一综述。     

Endothelins in health and disease

Endothelins are powerful vasoconstrictor peptides that also play numerous other roles. The endothelin (ET) family consists of three peptides produced by a variety of tissues. Endothelin-1 (ET-1) is the principal isoform produced by the endothelium in the human cardiovascular system, and it exerts its actions through binding to specific receptors, the so-called type A (ET(A)) and type B (ET(B)) receptors. ET-1 is primarily a locally acting paracrine substance that appears to contribute to the maintenance of basal vascular tone. It is also activated in several diseases, including congestive heart failure, arterial hypertension, atherosclerosis, endothelial dysfunction, coronary artery diseases, renal failure, cerebrovascular disease, pulmonary arterial hypertension, and sepsis. Thus, ET-1 antagonists are promising new agents. They have been shown to be effective in the management of primary pulmonary hypertension, but disappointing in heart failure. Clinical trials are needed to determine whether manipulation of the ET system will be beneficial in other diseases.     

白介素-18与心血管疾病

心血管疾病在现代社会中严重威胁人类健康,死亡率高。近年来,随着基因组学、蛋白质学和生物学的研究发展,确定心血管疾病的生物学标志物已经成为一种迫切需要,因为其能够客观反映生物学进程、发病机制和药理学改变,并可能成为可测定或评估的特征性指标。白介素-18（interleukin-18,IL-18）是近年来发现的具有多种生物学特性的炎性细胞因子,其作为细胞因子的重要成员在炎症过程中起重要作用。越来越多的实验和临床证据表明,IL-18在心血管疾病的发生、发展、预后及并发症中扮演着重要的角色。本文就IL-18与冠心病、高血压病、心力衰竭、房颤的关系作简要综述。     

白介素-18与心血管疾病

心血管疾病在现代社会中严重威胁人类健康,死亡率高。近年来,随着基因组学、蛋白质学和生物学的研究发展,确定心血管疾病的生物学标志物已经成为一种迫切需要,因为其能够客观反映生物学进程、发病机制和药理学改变,并可能成为可测定或评估的特征性指标。白介素-18(interleukin-18,IL-18)是近年来发现的具有多种生物学特性的炎性细胞因子,其作为细胞因子的重要成员在炎症过程中起重要作用。越来越多的实验和临床证据表明,IL-18在心血管疾病的发生、发展、预后及并发症中扮演着重要的角色。本文就IL-18与冠心病、高血压病、心力衰竭、房颤的关系作简要综述。     

肥胖悖论与心血管疾病

超重或肥胖与2型糖尿病、高脂血症和高血压等多种心血管危险因素密切相关。但近年的观察研究表明,已确诊心血管疾病的肥胖患者与患相同心血管疾病的正常体重和消瘦患者相比,具有生存优势。早期肥胖悖论研究主要集中于心力衰竭和冠心病,但最近的数据也表明肥胖悖论还涉及其他心血管疾病,如高血压、心房颤动、肺动脉高压和先天性心脏病。尽管许多研究结果都显示出肥胖悖论,然而关于肥胖悖论的依据以及它是否能让肥胖的心血管疾病患者获益,仍存在大量争论。本综述旨在整理支持和反对肥胖悖论的依据,回顾关于心血管疾病肥胖悖论的假定机制和最新证据,并讨论观察性研究中存在的混杂因素和偏见。     

肾上腺髓质素与心血管系统研究进展

肾上腺髓质素是从人的嗜铬细胞瘤组织中发现并分离的一种心血管活性多肽,具有多种生物学活性,广泛分布于全身各系统(其中心血管组织是肾上腺髓质素的重要来源).以自分泌、旁分泌或内分泌形式参与这些系统的生理调节和多种疾病的病理生理过程,可能在高血压、冠状动脉粥样硬化性心脏病、慢性心力衰竭等疾病的临床治疗方面具有潜在的应用价值.     

肠道菌群与心血管疾病

肠道菌群是一个数量庞大种类繁多的复杂生态系统,参与调节物质和能量代谢、机体免疫、组织器官发育等重要的生理过程,其结构和功能的稳态失调参与高血压、动脉粥样硬化、冠心病、心肌梗死、心力衰竭以及心律失常等心血管疾病的发生发展。本文旨在阐明肠道菌群及相关代谢产物与心血管疾病研究的新进展,为心血管疾病的防治提供新的思路,为未来开展肠道菌群与心血管疾病的研究指明发展方向。     

阻塞性睡眠呼吸暂停与心血管疾病的关系及发病机制探讨

阻塞性睡眠呼吸暂停的发病率有逐年增高趋势,越来越多的研究表明阻塞性睡眠呼吸暂停与心血管疾病（如高血压、肺动脉高压、冠心病、心律失常、心力衰竭等）的发生率与病死率关系密切;为有助于加深心血管病医生对阻塞性睡眠呼吸暂停与心血管疾病的认识,进一步探索阻塞性睡眠呼吸暂停的发病机制,从而提高疾病的防控水平;现就阻塞性睡眠呼吸暂停与心血管病的关系,导致疾病的可能发病机制作一综述。     

Role of urotensin II in atherosclerotic cardiovascular diseases

Urotensin II (U-II) is a powerful vasoconstrictor peptide with a potency greater than that of endothelin 1. Its plasma level correlates positively with body weight and is raised in diabetes, renal failure, hypertension, and other cardiovascular diseases, including congestive heart failure and carotid atherosclerosis. Experimental and clinical studies have revealed increased expression of U-II and U-II receptor (UT) in animals with experimentally induced myocardial infarction, heart failure, and in patients with hypertension, atherosclerosis, and diabetes, suggesting a potential role for U-II in coronary artery disease. Peptide and nonpeptide UT ligands have been shown to be effective in antagonizing the effects of U-II in the cardiovascular system. This article aims to review recent advances in physiology and pathophysiology of U-II with particular reference to its role in atherosclerotic cardiovascular diseases.     

铁代谢与心血管疾病

铁代谢异常与多种心血管疾病密切相关。慢性心力衰竭、肺动脉高压常与铁缺乏并存,铁超负荷可促进冠心病的发生发展。现简要综述常见心血管疾病中铁代谢异常的表现特征及可能的机制。     

氧化三甲胺与心血管疾病的研究新进展

越来越多的证据表明,肠道菌群结构紊乱与心血管疾病的发生密切相关。氧化三甲胺作为肠道菌群的代谢产物,在心血管疾病的发生和发展中起重要作用。现就氧化三甲胺与冠心病、心力衰竭、高血压、心房颤动和心肌纤维化的关系及其可能的机制做一综述,为心血管疾病的防治提供新靶点。     

miR-126与心血管疾病关系的研究进展

微小核糖核酸(microRNAs,miRNA)是一类内源性高度保守的非编码小分子RNA,其可通过降解信使RNA并抑制其翻译在转录水平调控靶基因的表达,参与细胞生长、发育、分化和增殖等多个生命过程。MicroRNAs-126(miR-126)是一种内皮特异性miRNA,与高血压、动脉粥样硬化、冠心病、心力衰竭等心血管疾病密切相关。近期研究表明,miR-126能显著影响心血管疾病的发生、发展和疾病的预后。本文就miR-126与心血管疾病的关系进行综述。     

高血压视网膜病在心血管疾病中的意义

高血压视网膜病是多种因素引起的以视网膜血管病变为特征的疾病,高血压视网膜病征与高血压、心肌肥厚、冠心病、心力衰竭等多种心血管疾病密切相关,能够独立于传统的危险因素预测心血管疾病。     

gp130 signaling pathways: Recent advances and implications for cardiovascular disease

gp130 was initially identified as a signal-transducing receptor component that associates with the interleukin 6 receptor (IL-6R) when the receptor is occupied by interleukin 6 (IL-6). It has been revealed that the receptor complexes for IL-6, IL-11, leukemia inhibitory factor (LIF), oncostatin M (OM), and ciliary neurotrophic factor (CNTF) utilize this gp130 protein as a common signal-transducing component, explaining how these cytokines mediate overlapping biological function. Recent observations with mice lacking gp130 or having continuously activated gp130 protein have disclosed an important biological function of gp130 in cardiovascular system: the former mice show extremely hypoplastic development of the ventricular myocardium at 16.5 days postcoitum (dpc), and the latter exhibit hypertrophy of myocardium. These cardiovascular abnormalities are considered to be the results of the perturbation of gp130, which also transduces the signal of cardiotrophin-1 (CT-1), a recently isolated factor causing hypertrophy in cultured cardiomyocytes and having sequence similarity with IL-6, IL-11, LIF, CNTF, and OM. In fact, CT-1 shares gp130 with these cytokines as a critical signaling component. Besides various well-established mechanisms by which cardiac growth and development are regulated, a gp130 signaling may be a newly discovered mechanism that regulates these events.     

Obesity and target organ damage: the heart

In most patients, coronary atherosclerosis or congestive heart failure develop as an integrated response to multiple cardiovascular risk factors. Obesity increases the prevalence of most cardiovascular risk factors and is the predominant cause of diabetes mellitus and arterial hypertension. Moreover, obesity shifts the manifestation of these risk factors to younger age groups, such that subsequent damage results prematurely in clinically overt cardiac diseases. In addition, due to clustering of obesity-related risk factors, obesity may amplify the risk by synergistic mechanisms acting in parallel. Finally, an elevated body mass index (BMI) results in an increase in heart rate and blood volume, as well as increased systolic and diastolic blood pressure. These changes affect cardiac geometry and mass in addition to the alterations of the coronary vasculature. At the population level, the role of obesity in promoting multiple risk factors and, subsequently, the development of heart diseases cannot be underestimated. In individual patients, however, the clinical presentation may be dominated by obesity-related hypertension, diabetes, metabolic and inflammatory derangements or clinical symptoms of heart failure or coronary artery disease. Weight reduction remains a crucial component of the therapeutic strategy to ameliorate insulin resistance, hypertension and left ventricular hypertrophy, among other risk factors, with profound implications for the individual's prognosis.     

Diabetic Cardiovascular Disease: Getting to the Heart of the Matter

Diabetes is a major risk factor for heart disease, and heart disease is responsible for substantial morbidity and mortality among people living with diabetes. The diabetic metabolic milieu predisposes to aggressive obstructive coronary artery disease that causes heart attacks, heart failure, and death. Furthermore, diabetes can be associated with heart failure, independent of underlying coronary artery disease, hypertension, or valve abnormalities. The pathogenesis of the vascular and myocardial complications of diabetes is, as yet, incompletely understood. Although a number of medical and surgical approaches can improve outcomes in diabetic patients with cardiovascular disease, much remains to be learned in order to optimize approaches to these critical complications.     

心血管合并症对慢阻肺患者急性加重及死亡率影响的1年随访观察

目的探讨心血管合并症对慢性阻塞性肺疾病(简称慢阻肺)患者1年内急性加重及死亡率的影响。方法本研究入选600例C级、D级慢阻肺患者,其中无心血管合并症慢阻肺患者(A组)167例,合并心血管疾病慢阻肺患者(B组)433例(其中心力衰竭亚组98例、冠心病亚组142例、心律失常亚组115例、高血压亚组78例),两组患者均随访1年,随访期间每3月复查肺功能、动脉血气、心脏彩超、血清脑钠肽(brain natriuretic peptide,BNP)。结果 B组患者1年内平均急性加重次数[(4.51±0.75)次]明显多于A组患者[(2.68±0.45)次],差异有统计学意义(P0.05);B组患者1年内死亡率为8.8%,明显高于A组患者的3.6%,差异有统计学意义(P0.05)。B组心力衰竭亚组、冠心病亚组1年内急性加重次数及死亡率均明显高于A组及B组心律失常亚组、高血压亚组(P均0.05)。随访1年后,A组患者及B组各亚组患者FEV1均明显下降(P0.05);B组心力衰竭亚组患者血清BNP浓度、Pa CO2、肺动脉收缩压明显升高、而左室EF值、Pa O2明显下降(P0.05);B组冠心病亚组患者血BNP浓度明显升高(P0.05);B组高血压亚组患者平均动脉压无明显变化。结论心血管合并症明显增加慢阻肺患者1年内急性加重次数及死亡率,心力衰竭、冠心病是导致慢阻肺患者死亡率升高、急性加重次数增加的两个重要原因。     

Headache and cardiovascular disease: old symptoms, new proposals

Evidence of a link between headache symptoms and cardiovascular disease has rapidly grown in recent years and it is of utmost importance for the cardiologist and neurologist to be aware of this intimate connection. A brief overview of different cardiovascular diseases (namely hypertension, stroke, coronary heart disease, patent foramen ovale, atrial septal defects, atrial septal aneurisms, mitral valve prolapse, and aortic and carotid disease) that may be related to headache is presented in this article. Proposed pathophysiological mechanisms for this association and landmark studies are reviewed and discussed.     

Sleep apnea and cardiovascular risk

Sleep apnea is evident in approximately 10% of adults in the general population, but in certain cardiovascular diseases, and in particular those characterized by sodium and water retention, its prevalence can exceed 50%. Although sleep apnea is not as yet integrated into formal cardiovascular risk assessment algorithms, there is increasing awareness of its importance in the causation or promotion of hypertension, coronary artery disease, heart failure, atrial arrhythmias, and stroke, and thus, not surprisingly, as a predictor of premature cardiovascular death.Sleep apnea manifests as two principal phenotypes, both characterized by respiratory instability: obstructive (OSA), which arises when sleep-related withdrawal of respiratory drive to the upper airway dilator muscles is superimposed upon a narrow and highly compliant airway predisposed to collapse, and central (CSA), which occurs when the partial pressure of arterial carbon dioxide falls below the apnea threshold, resulting in withdrawal of central drive to respiratory muscles.The present objectives are to: (1) review the epidemiology and patho-physiology of OSA and CSA, with particular emphasis on the role of renal sodium retention in initiating and promoting these processes, and on population studies that reveal the long-term consequences of untreated OSA and CSA; (2) illustrate mechanical, autonomic, chemical, and inflammatory mechanisms by which OSA and CSA can increase cardiovascular risk and event rates by initiating or promoting hypertension, atherosclerosis, coronary artery disease, heart failure, arrhythmias, and stroke; (3) highlight insights from randomized trials in which treating sleep apnea was the specific target of therapy; (4) emphasize the present lack of evidence that treating sleep apnea reduces cardiovascular risk and the current clinical equipoise concerning treatment of asymptomatic patients with sleep apnea; and (5) consider clinical implications and future directions of clinical research and practice.