The Cardioprotective Potential of von Willebrand Disease in Ischemic Heart Disease

von Willebrand factor (vWF) aids coagulation at sites of vessel injury. Elevated vWF levels have been associated with an increased risk of ischemic heart disease (IHD); however, it is unclear whether vWF deficiency, seen in patients with von Willebrand disease (vWD), protects people against IHD. We determined and compared the prevalence and risk of IHD in patients with versus without vWD by using data from the National Inpatient Sample (2009–2014), excluding patients younger than 18 and older than 75 years. The primary outcome was the odds ratio (OR) of IHD in patients with versus without vWD. Secondary outcomes were major medical comorbidities and demographic characteristics in patients with vWD.Of 224,475,443 weighted hospital-discharge samples, we identified 82,809 patients with a vWD diagnosis. The odds of IHD were lower in patients with vWD than in those without (OR=0.54; 95% CI, 0.52–0.56). After multivariable logistic regression analysis and adjustment for age, sex, and typical IHD risk factors (hypertension, smoking, diabetes, hyperlipidemia, chronic kidney disease, obesity, and family history of IHD), the likelihood of IHD remained lower in patients with vWD than in patients without (OR=0.65; 95% CI, 0.63–0.67). Our study shows that vWF deficiency, as seen in patients with vWD, is associated with a decreased prevalence of IHD. Further investigation may confirm these findings.     

慢性心力衰竭病人QRS综合波幅值及形态的变化

探讨慢性心力衰竭 (CHF)病人QRS综合波幅值及形态的变化与意义。使用常规、高频及动态心电图分别采集 6 0例不同病因CHF病人QRS综合波幅度、QRS切迹与扭挫、室性心律失常等体表心电信息。结果 :QRS幅度的缺血性心脏病 (IHD)与扩张型心肌病 (DCM)较对照组 (1.76± 0 .2 7,1.5 7± 0 .14vs 2 .2 3± 0 .32mV ,P均 <0 .0 5 )降低。IHD、高血压性心脏病 (HHD)与DCM的QRS切迹数的较对照组 (5 .43± 0 .2 5 ,4.36± 0 .19,7.2 3± 0 .46vs 0 .6 4± 0 .11mV)增多 ;各组室性异位搏动显著增加。上述改变随CHF加重愈趋明显。结论 :由QRS综合波幅值及形态变化所反映的心脏电活动异常 ,可能是导致CHF病人心律失常的电生理基础     

Impact of lung‐function measures on cardiovascular disease events in older adults with metabolic syndrome and diabetes

Background

Individuals with metabolic syndrome (MetS) and diabetes (DM) are more likely to have decreased lung function and are at greater risk of cardiovascular disease (CVD).

Hypothesis.

Lung‐function measures can predict CVD events in older persons with MetS, DM, and neither condition.

Methods

We followed 4114 participants age ≥ 65 years with and without MetS or DM in the Cardiovascular Health Study. Cox regression examined the association of forced vital capacity (FVC) and 1‐second forced expiratory volume (FEV₁; percent of predicted values) with incident coronary heart disease and CVD events over 12.9 years.

Results

DM was present in 537 (13.1%) and MetS in 1277 (31.0%) participants. Comparing fourth vs first quartiles for FVC, risk of CVD events was 16% (HR: 0.84, 95% CI: 0.59–1.18), 23% (HR: 0.77, 95% CI: 0.60–0.99), and 30% (HR: 0.70, 95% CI: 0.58–0.84) lower in DM, MetS, and neither disease groups, respectively. For FEV₁, CVD risk was lower by 2% (HR: 0.98, 95% CI: 0.70–1.37), 26% (HR: 0.74, 95% CI: 0.59–0.93), and 31% (HR: 0.69, 95% CI: 0.57–0.82) in DM. Findings were strongest for predicting congestive heart failure (CHF) in all disease groups. C‐statistics increased significantly with addition of FEV₁ or FVC over risk factors for CVD and CHF among those with neither MetS nor DM.

Conclusions

FEV₁ and FVC are inversely related to CVD in older adults with and without MetS, but not DM (except for CHF); however, their value in incremental risk prediction beyond standard risk factors is limited mainly to metabolically healthier persons.     

Prognostic Significance of QTc Interval for Predicting Total,Cardiac, and Ischemic Heart Disease Mortality in Community‐Based Cohort from Warsaw Pol‐MONICA Population

Background: QT interval in resting electrocardiogram (ECC) is a sum of ventricular depolarization and repolarization time. Its prolongation is associated with a worse prognosis for survival due to a high incidence of severe ventricular arrhythmias. Methods: The random sample of the Warsaw Pol‐MONICA population consisting of 2646 men and women, aged 35–64, screened in 1984, was followed‐up until 1996. All deaths and their causes were registered based on death certificate diagnosis. QT interval was measured manually in three consecutive QRST complexes in each ECG and corrected using Bazett's formula (QT corrected: QT_c). For statistical analyses the mean value of 3 QT_c measurements were used. To assess the relationship between QT_c and mortality, the Cox proportional hazards model with stepwise selection of variables was used. Results: Out of the screened sample, 459 persons died (309 men, 150 women), 226 due to cardiovascular diseases (CVD) (162 men, 64 women), and 81 due to ischemic heart disease (IHD) (59 men, 22 women). Both men and women who died were significantly older at baseline and had significantly longer mean QTc as compared to survivors (men: 457 ms vs 446 ms, P = 0.0001; women: 469 ms vs 459 ms, P = 0.001). Among men, after adjustment for confounding variables, mean QT_c was significantly associated with total and CVD mortality, and in women, with CVD and IHD mortality. The risk of death rose with an increase in QT_c duration. In men, with every increase in QT_c by 20 ms, the risk of all causes of death rose by 11% (95% CI: 1.04–1.18), CVD death by 9% (95% Cl: 1.01–1.19), and IHD death by 11 % (95%: 0.97–1.28). In women, the risk of all‐cause death increased by 9% (95% CI: 0.98–1.21), CVD death by 21% (95% Cl: 1.02–1.43), and IHD death by 41% (95% Cl: 1.08–1.85). Conclusion: QTc interval was significantly related to all cause, cardiovascular and ischemic heart disease. The risk of death increased with longer QTc duration. A.N.E. 2000;5(4):322–329     

Activation of the Ergoreceptors in Cardiac Patients With and Without Heart Failure

BackgroundThe presence of ergoreflex activity and its current relationship to hyperventilation and prognosis in cardiac patients is unclear. Therefore, we evaluated ergoreflex activity in cardiac patients with and without heart failure (CHF) as well as in healthy subjects, and we examined how ergoreceptor activity was related to a mortality risk score in CHF (MAGGIC).Methods and ResultsTwenty-five healthy subjects and 76 patients were included, among whom were 25 with ischemic heart disease (IHD), 24 with stable CHF, and 27 with unstable CHF. Ergoreflex activity was measured with a dynamic handgrip exercise, followed by post-handgrip regional circulatory occlusion (PH-RCO). Ergoreflex activity contributed significantly to ventilation (median [interquartile range] %V) in unstable CHF (81 [73-91] %V without PH-RCO, 92 [82–107] %V with PH-RCO, and 11 [6–20] difference in %V; P < .001) and was positively correlated with the MAGGIC risk score (Spearman ρ = 0.431; P = .002). No ergoreflex activity was observed in healthy subjects (−4 [−10 to 5] difference in %V), IHD (0 [−8 to 3] Diff in %V) and stable CHF (−3 [−11 to 6] difference in %V).ConclusionsErgoreflex activity contributes to hyperventilation, but only in CHF patients with persistent symptoms, and is closely related to the MAGGIC risk score. Ergoreflex activity was not present in patients with IHD or stable CHF, suggesting other reasons for the increased ventilatory drive in those patients.     

Hypertension is the Most Important Component of Metabolic Syndrome in the Association With Ischemic Heart Disease in Taiwanese Type 2 Diabetic Patients

Background To evaluate the association between components of metabolic syndrome (MS) and ischemic heart disease (IHD) in Taiwanese patients with type 2 diabetes mellitus (T2DM). Methods and Results A total of 1,296 (604 men and 692 women) subjects with T2DM aged 62.5+/-11.7 (14-87) years were studied. MS was defined using the World Health Organization modified criteria and included more than 2 of hypertension, obesity, dyslipidemia and microalbuminuria. IHD was diagnosed through history or ischemic electrocardiogram according to the Minnesota codes. Results showed that MS was present in 76.2% and IHD in 36.3% of the patients, respectively. MS increased with age for both sexes, but there was no difference between men and women in the age groups of <45, 45-54 and 55-64 years. However, the prevalence of MS was significantly higher in women (87.7% vs 78.0%) in the age group >/=65 years. IHD prevalence was significantly higher in patients with MS, hypertension, dyslipidemia and obesity (p<0.01), and was higher with borderline significance for microalbuminuria (0.05相似文献   

Apolipoprotein E genotype: epsilon32 women are protected while epsilon43 and epsilon44 men are susceptible to ischemic heart disease: the Copenhagen City Heart Study

OBJECTIVES: We tested the hypothesis that risk of ischemic heart disease (IHD) differs as a function of apolipoprotein E (APOE) genotype in women and men. BACKGROUND: Apolipoprotein E genotype influences lipids and lipoproteins and, therefore, possibly the risk of IHD. METHODS: We genotyped 9,241 white women and men from the general population and 940 white women and men with IHD. RESULTS: Test of interaction suggested that APOE genotype may influence risk of IHD differently in women and men (p = 0.07). After age adjustment, the odds ratio (OR) for IHD for epsilon32 versus epsilon33 women was 0.57 (95% confidence interval [CI]: 0.35 to 0.94) while epsilon43 and epsilon44 versus epsilon33 men had ORs of 1.16 (0.96 to 1.41) and 1.58 (1.01 to 2.45). After adjustment for age and other conventional cardiovascular risk factors, the equivalent ORs were for epsilon32 women 0.38 (0.18 to 0.79), for epsilon43 men 1.35 (1.02-1.78) and for epsilon44 men 1.58 (0.80 to 3.08). Equivalent ORs for epsilon43 and epsilon44 versus epsilon33 women and for epsilon32 versus epsilon33 men were all close to 1.0 and nonsignificant. Of the total risk of IHD relative to the epsilon33 genotype, the fraction attributed to epsilon32 in women was -9%, while the fractions attributed to epsilon43 and epsilon44 in men were +8% and +2%. CONCLUSIONS: Relative to epsilon33 individuals, epsilon32 women are protected while epsilon43 and epsilon44 men are particularly susceptible to IHD.     

Heart Failure Epidemiology in Patients With Diabetes Mellitus Without Coronary Heart Disease

Background

Epidemiology of patients with comorbid heart failure (HF) and diabetes mellitus (DM) without coronary heart disease (CHD) is not well described.

Contribution of congestive heart failure and ischemic heart disease to excess mortality in rheumatoid arthritis

OBJECTIVE: Although mortality among patients with rheumatoid arthritis (RA) is higher than in the general population, the relative contribution of comorbid diseases to this mortality difference is not known. This study was undertaken to evaluate the contribution of congestive heart failure (CHF) and ischemic heart disease (IHD), including myocardial infarction, to the excess mortality in patients with RA, compared with that in individuals without RA. METHODS: We assembled a population-based inception cohort of individuals living in Rochester, Minnesota, in whom RA (defined according to the criteria of the American College of Rheumatology [formerly, the American Rheumatism Association]) first developed between 1955 and 1995, and an age- and sex-matched non-RA cohort. All subjects were followed up until either death, migration from the county, or until 2001. Detailed information from the complete medical records was collected. Statistical analyses included the person-years method, cumulative incidence, and Cox regression modeling. Attributable risk analysis techniques were used to estimate the number of RA deaths that would be prevented if the incidence of CHF was the same in patients with RA and non-RA subjects. RESULTS: The study population included 603 patients with RA and 603 subjects without RA. During followup, there was an excess of 123 deaths among patients with RA (345 RA deaths occurred, although only 222 such deaths were expected). The mortality rates among patients with RA and non-RA subjects were 39.0 and 29.2 per 1,000 person-years, respectively. There was a significantly higher cumulative incidence of CHF (but not IHD) in patients with RA compared with non-RA subjects (37.1% versus 27.7% at 30 years of followup, respectively; P < 0.001). The risk of death associated with either CHF or IHD was not significantly different between patients with RA and non-RA subjects. If the risk of developing CHF was the same in patients with RA and individuals without RA, the overall mortality rate difference between RA and non-RA hypothetically would be reduced from 9.8 to 8.0 excess deaths per 1,000 person-years; that is, 16 (13%) of the 123 excess deaths could be prevented. CONCLUSION: CHF, rather than IHD, appears to be an important contributor to the excess overall mortality among patients with RA. CHF contributes to this excess mortality primarily through the increased incidence of CHF in RA, rather than increased mortality associated with CHF in patients with RA compared with non-RA subjects. Eliminating the excess risk of CHF in patients with RA could significantly improve their survival.     

The Dietary Approaches to Stop Hypertension (DASH) Diet Pattern and Incident Heart Failure

BackgroundThe Dietary Approaches to Stop Hypertension (DASH) diet pattern has shown some promise for preventing heart failure (HF), but studies have been conflicting.ObjectiveTo determine whether the DASH diet pattern was associated with incident HF in a large biracial and geographically diverse population.Methods and ResultsAmong participants in the REasons for Geographic And Racial Differences in Stroke (REGARDS) cohort study of adults aged ≥45 years who were free of suspected HF at baseline in 2003–2007, the DASH diet score was derived from the baseline food frequency questionnaire. The main outcome was incident HF defined as the first adjudicated HF hospitalization or HF death through December 31, 2016. We estimated hazard ratios for the associations of DASH diet score quartiles with incident HF, and incident HF with reduced ejection fraction and HF with preserved ejection fraction using the Lunn–McNeil extension to the Cox model. We tested for several prespecified interactions, including with age. Compared with the lowest quartile, individuals in the second to fourth DASH diet score quartiles had a lower risk for incident HF after adjustment for sociodemographic and health characteristics: quartile 2 hazard ratio, 0.69 (95% confidence interval [CI], 0.56–0.85); quartile 3 hazard ratio, 0.71 (95% CI, 0.58–0.87); and quartile 4 hazard ratio, 0.73 (95% CI, 0.58–0.92). When stratifying results by age, quartiles 2–4 had a lower hazard for incident HF among those age <65 years, quartiles 3–4 had a lower hazard among those age 65–74, and the quartiles had similar hazard among those age ≥75 years (P_interaction = .003). We did not find a difference in the association of DASH diet with incident HF with reduced ejection fraction vs HF with preserved ejection fraction (P = .11).ConclusionsDASH diet adherence was inversely associated with incident HF, specifically among individuals <75 years old.     

Bone Marrow-Derived Progenitor Cells Are Functionally Impaired in Ischemic Heart Disease

To determine whether the presence of ischemic heart disease (IHD) per se, or rather the co-presence of heart failure (HF), is the primum movens for less effective stem cell products in autologous stem cell therapy, we assessed numbers and function of bone marrow (BM)-derived progenitor cells in patients with coronary artery disease (n?=?17), HF due to ischemic cardiomyopathy (n?=?8), non-ischemic HF (n?=?7), and control subjects (n?=?11). Myeloid and erythroid differentiation capacity of BM-derived mononuclear cells was impaired in patients with underlying IHD but not with non-ischemic HF. Migration capacity decreased with increasing IHD severity. Hence, IHD, with or without associated cardiomyopathy, is an important determinant of progenitor cell function. No depletion of hematopoietic and endothelial progenitor cells (EPC) within the BM was observed, while circulating EPC numbers were increased in the presence of IHD, suggesting active recruitment. The observed myelosuppression was not driven by inflammation and thus other mechanisms are at play.     

Ischemic Heart Disease and Vascular Risk Factors Are Associated With Accelerated Brain Aging

BackgroundIschemic heart disease (IHD) has been linked with poor brain outcomes. The brain magnetic resonance imaging–derived difference between predicted brain age and actual chronological age (brain-age delta in years, positive for accelerated brain aging) may serve as an effective means of communicating brain health to patients to promote healthier lifestyles.ObjectivesThe authors investigated the impact of prevalent IHD on brain aging, potential underlying mechanisms, and its relationship with dementia risk, vascular risk factors, cardiovascular structure, and function.MethodsBrain age was estimated in subjects with prevalent IHD (n = 1,341) using a Bayesian ridge regression model with 25 structural (volumetric) brain magnetic resonance imaging features and built using UK Biobank participants with no prevalent IHD (n = 35,237).ResultsPrevalent IHD was linked to significantly accelerated brain aging (P < 0.001) that was not fully mediated by microvascular injury. Brain aging (positive brain-age delta) was associated with increased risk of dementia (OR: 1.13 [95% CI: 1.04-1.22]; P = 0.002), vascular risk factors (such as diabetes), and high adiposity. In the absence of IHD, brain aging was also associated with cardiovascular structural and functional changes typically observed in aging hearts. However, such alterations were not linked with risk of dementia.ConclusionsPrevalent IHD and coexisting vascular risk factors are associated with accelerated brain aging and risk of dementia. Positive brain-age delta representing accelerated brain aging may serve as an effective communication tool to show the impact of modifiable risk factors and disease supporting preventative strategies.     

Association between variants in the genes for leptin, leptin receptor, and proopiomelanocortin with chronic heart failure in the Czech population

Patients with chronic heart failure (CHF) express enhanced catabolic metabolism finally resulting in overall weight loss, whereas adipokines might play a crucial role in signaling among tissues. The aim of this study was to investigate the possible associations of defined variability in leptin (dbSNP ID rs7799039), proopiomelanocortin (dbSNP ID rs3754860 and dbSNP ID rs1009388), and leptin receptor gene (dbSNP rs1137101) with CHF and evaluate their potential as the CHF susceptibility genes. The case-control study comprised a total of 372 patients of Caucasian origin with chronic heart failure (New York Heart Association [NYHA] functional classes II–IV, ejection fraction (EF) <40%) and 407 healthy controls. They were genotyped for the leptin (LEP) −2548 G/A, leptin receptor (LEPR) Gln223Arg, and proopiomelanocortin (POMC) RsaI (5′-untranslated region) and C1032G variants (intron 1) using PCR-based methodology. No case-control differences in genotype as well as allele frequencies were observed between CHF patients and controls. We constructed POMC RsaI/C1032G haplotypes, having found no significant association with body mass index (BMI), left ventricle ejection fraction (LVEF), left ventricle hypertrophy (LVH) and diabetes mellitus (DM). Multivariate regression analyses revealed an approximately 2-fold risk for NYHA class IV associated with the LEPR Gln223Arg (P = 0.0000001, odds ratio [OR] = 2.10, 95% confidence interval [CI] = 1.56−2.84); it also displayed an independent prediction role for LVEF in heart failure cases of all etiologies (P = 0.002, OR = 4.05, 95% CI = 1.36−10.06). In subanalyses according to CHF etiology the LEPR Gln223Arg showed an independent prediction role for NYHA IV in IHD patients (P = 0.0001, OR = 2.50, 95% CI = 1.69−3.82) and both for NYHA IV(P = 0.007, OR = 2.04, 95% CI = 1.20−3.84) and LVEF (P = 0.004, OR = 11.87, 95% CI = 2.08−55.6) in DCMP patients. The role of the polymorphic variants in the genes encoding for adipokines as potential CHF susceptibility genes is unclear. Based on our findings, the LEPR Gln223Arg polymorphism could be considered a disease susceptibility modulating factor both in ischemic heart disease or dilated cardiomyopathy patients.     

Targeting Sleep Disordered Breathing to Prevent Heart Failure: What is the Evidence?

Cardiovascular disease (CVD) contributes to risk of dementia by either enhancing the development and progression of brain vascular disease and subsequent neurodegeneration and Alzheimer's disease (AD) pathology, ie, amyloid plaques and neurofibrillary tangles, acts as a precipitant of dementia in older individuals with preexisting subclinical neuropathology of dementia. Atrial fibrillation, congestive heart failure (CHF), stroke, and myocardial infarction are associated with increased risk of dementia. All older individuals age 65–70+ can be considered to be at very high risk of vascular disease and dementia and candidates for aggressive CV preventive therapies, such as lipid lowering, antihypertensive therapy, increased physical activity, antidiabetic therapies, smoking cessation, etc to prevent heart attacks subsequent CHF, atrial fibrillation, stroke, frailty, and dementia. Furthermore, preventing or delaying dementia should be a primary outcome of all CV trials in older individuals.     

Diabetes and Prior Coronary Heart Disease are Not Necessarily Risk Equivalent for Future Coronary Heart Disease Events

Background

For more than a decade, the presence of diabetes has been considered a coronary heart disease (CHD) “risk equivalent”.

Objective

The objective of this study was to revisit the concept of risk equivalence by comparing the risk of subsequent CHD events among individuals with or without history of diabetes or CHD in a large contemporary real-world cohort over a period of 10 years (2002 to 2011).

Design

Population-based prospective cohort analysis.

Participants

We studied a cohort of 1,586,061 adult members (ages 30–90 years) of Kaiser Permanente Northern California, an integrated health care delivery system.

Main Measurements

We calculated hazard ratios (HRs) from Cox proportional hazard models for CHD among four fixed cohorts, defined by prevalent (baseline) risk group: no history of diabetes or CHD (None), prior CHD alone (CHD), diabetes alone (DM), and diabetes and prior CHD (DM + CHD).

Key Results

We observed 80,012 new CHD events over the follow-up period (~10,980,800 person-years). After multivariable adjustment, the HRs (reference: None) for new CHD events were as follows: CHD alone, 2.8 (95 % CI, 2.7–2.85); DM alone 1.7 (95 % CI, 1.66–1.74); DM + CHD, 3.9 (95 % CI, 3.8–4.0). Individuals with diabetes alone had significantly lower risk of CHD across all age and sex strata compared to those with CHD alone (12.2 versus 22.5 per 1000 person-years). The risk of future CHD for patients with a history of either DM or CHD was similar only among those with diabetes of long duration (≥10 years).

Conclusions

Not all individuals with diabetes should be unconditionally assumed to be a risk equivalent of those with prior CHD.KEY WORDS: coronary heart disease, diabetes, epidemiology     

Hepatic lipase mutations,elevated high-density lipoprotein cholesterol,and increased risk of ischemic heart disease: the Copenhagen City Heart Study

OBJECTIVES: We investigated associations between single nucleotide polymorphisms (SNPs) in the hepatic lipase promoter, levels of high-density lipoprotein (HDL), and risk of ischemic heart disease (IHD). Our primary hypothesis was that these SNPs associate with IHD after adjustment for HDL levels. BACKGROUND: Hepatic lipase influences HDL metabolism, and may thus affect reverse cholesterol transport and consequently risk of IHD. METHODS: We genotyped 9,121 white subjects aged 20 to 93 years from the Copenhagen City Heart Study, 456 of whom had incident IHD, as well as 921 Danish patients with IHD for the -216, -480, and -729 SNPs in the hepatic lipase promoter. RESULTS: Frequencies of wild-type, triple heterozygotes, and triple mutation homozygotes in the general population were 61%, 33%, and 5%, respectively. Compared with wild-type, HDL cholesterol levels were 4% (0.06 mmol/l) and 10% (0.15 mmol/l) higher in heterozygotes and mutation homozygotes; the equivalent values for apolipoprotein A1 were 3% and 7% higher. In prospective and case-control studies, mutation homozygotes versus wild-type had relative risk (RR) and odds ratio (OR) for IHD of 1.5 (95% confidence interval [CI]: 1.0 to 2.2) and 1.4 (CI: 1.1 to 1.9) when adjusted for age, gender, and HDL cholesterol. In individuals with the epsilon43 apolipoprotein E genotype, RR and OR for IHD in mutation homozygotes versus wild-type was 2.9 (CI: 1.5 to 5.6) and 2.0 (CI: 1.2 to 3.2). CONCLUSIONS: Hepatic lipase promoter SNPs are associated with increased HDL cholesterol and, paradoxically, an increased risk of IHD after adjustment for HDL cholesterol, and particularly in individuals with apolipoprotein E epsilon43 genotype. Implications are that increased HDL levels may in certain situations be not protective, but rather associated with increased IHD risk.     

凝血纤溶指标的变化与缺血性心脏病的关系

目的：探讨缺血性心脏病患者的凝血、纤溶变化及其临床意义，并对部分患者跟踪观察。方法：用高效液相色谱仪测定２６例急性心肌梗死患者，２６例不稳定性心绞痛患者，以及２０例正常人的尿纤维蛋白肽Ａ（ＦＰＡ）；并用相应方法同步测定了血浆Ｄ－二聚体（Ｄ－ｄｉｍｅｒ）含量、组织型纤溶酶原激活物（ｔＰＡ）及其抑制剂（ＰＡＩ）活性。结果：急性心肌梗死、不稳定性心绞痛患者较正常对照组尿纤维蛋白肽Ａ值增高，血浆Ｄ－二聚体水平、ＰＡＩ活性升高，ｔＰＡ活性降低。且急性心肌梗死与不稳定性心绞痛患者之间上述指标也存在显著性差异。结论：研究结果提示凝血纤溶系统的变化在缺血性心脏病的发生、发展中起着重要作用，研究凝血、纤溶指标对探讨其发病机制及判断预后可能有一定帮助。     

Biomarkers of endothelial dysfunction are elevated and related to prognosis in chronic heart failure patients with diabetes but not in those without diabetes

BACKGROUND: Biomarkers of endothelial dysfunction, such as soluble E-selectin, and von Willebrand factor (vWf) are elevated in patients with chronic heart failure (CHF). The impact of diabetes mellitus (DM) on these biomarkers, and their relation to prognosis remains unknown. AIMS: to investigate the impact of DM on plasma levels and the prognostic value of E-selectin and vWf in patients with CHF. METHODS AND RESULTS: Plasma levels of E-selectin and vWf were measured in 195 CHF patients with (n=48, 24.5%), and without DM, and in 116 age-matched healthy controls. Compared with controls, median plasma E-selectin levels were higher in CHF patients with DM (P=0.012), but not in CHF patients without DM (P=0.45); vWf levels were also higher in CHF patients with DM (P<0.001), but not without DM (P=0.108). E-selectin was associated with risk of recurrent ischaemic cardiovascular events among CHF patients with DM (HR 2.60; P=0.009), but not among patients without DM (HR 1.09; P=0.60) per 1 SD increment in log transformed variable. vWf was not related with outcome in CHF patients with or without DM. CONCLUSIONS: Plasma levels of E-selectin and vWf are elevated in CHF patients with DM but not in those without DM. High E-selectin levels may be associated with ischaemic events in patients with DM.     

Adaptive Servo-ventilation Therapy Results in the Prevention of Arrhythmias in Patients with Heart Failure Due to Ischemic Heart Disease

Objective Whether or not adaptive servo-ventilation (ASV) is effective in preventing arrhythmias in patients with heart failure (HF) due to ischemic heart disease (IHD) is unclear. This study estimated the effects of ASV therapy on arrhythmias in patients with HF due to IHD. Methods One hundred and forty-one consecutive hospitalized patients with HF due to IHD (mean age: 74.9±11.9 years old) were retrospectively assessed in this study. Of the 141 patients, 75 were treated with ASV (ASV group), and 66 were treated without ASV (Non-ASV group). We estimated the incidence of arrhythmias, including paroxysmal atrial fibrillation (PAF) and ventricular tachycardia (VT), during one-year follow-up in both groups using multivariable logistic regression models. Results Men accounted for 55.3% of the study population. There were no significant differences in the baseline clinical characteristic data between the ASV and Non-ASV groups with respect to age, sex, heart rate, risk factors, oral medication, or laboratory data, including the estimated glomerular filtration rate (eGFR), brain natriuretic peptide, and left ventricular ejection fraction. ASV therapy was associated with a reduced incidence of arrhythmia after adjusting for demographic and cardiovascular disease risk factors (odds ratio, 0.27; 95% confidence interval, 0.11 to 0.63; p<0.01; compared to the Non-ASV group). In addition, at the 1-year follow-up, an improvement (increase) in the eGFR was found in the ASV group but not in the Non-ASV group. Conclusion ASV therapy was able to prevent arrhythmias, including PAF and VT, with short-term improvements in the renal function in patients with HF due to IHD.     

Plasma Cardiotrophin‐1 Levels are Associated With Hypertensive Heart Disease: A Meta‐Analysis

Cardiotrophin‐1 (CT‐1) is a member of the interleukin 6 cytokine superfamily. Plasma CT‐1 levels have been associated with heart failure and hypertension in small independent studies. Whether plasma CT‐1 levels are associated with progression of hypertensive heart disease is poorly understood. The authors carried out a meta‐analysis using published studies and electronic databases. Relevant data were extracted using standardized algorithms. Additional data were obtained directly from investigators when indicated. A total of 18 studies were included that reported on association between CT‐1 level and hypertension (n=8), cardiac hypertrophy (n=9), and heart failure (HF) (n=10). The serum levels of CT‐1 were significantly higher in patients with hypertension (standard mean difference [SMD], 0.85; 95% confidence interval [CI], 0.64–1.06 fmol/mL), left ventricular hypertrophy (SMD, 0.88; 95% CI 0.60–1.17 fmol/mL), or HF (SMD, 0.66; 95% CI, 0.51–0.80 fmol/mL) compared with controls. Subgroup analysis revealed CT‐1 levels to be highest in patients with hypertension‐induced hypertrophy with HF, followed by patients with hypertension‐induced left ventricular hypertrophy without HF (SMD, 0.52; 95% CI, 0.30–0.75 fmol/mL), patients with hypertension without left ventricular hypertrophy (SMD, 0.67; 95% CI, 0.46–0.88 fmol/mL) as compared with normotensive patients (SMD, 0.74; 95% CI, 10.45–1.04 fmol/mL). Increased plasma CT‐1 levels are associated with risk for HF in hypertensive patients. CT‐1 may serve as a novel biomarker in determining prognosis in hypertensive patients.