Sepsis Protects the Heart of Alcoholic Rats from Ischemia-Reperfusion Injury

We have previously shown that administration of Escherichia coli to a rat induces cardiac dysfunction, but also prevents the myocardium from being further damaged by total ischemia. We have also previously shown that induction of sepsis in a rat that has consumed alcohol as 36% of its caloric intake for 8–10 weeks, results in a potentiation of the cardiac depression resulting from sepsis. In this study, we determined if administration of Gram-negative bacteria to a chronically alcoholic rat would still protect the heart from ischemia-reperfusion injury. We tested the protective effect of sepsis using an in vitro, isovolumically contracting heart preparation. Global ischemia was maintained for 35 min, followed by 25-min reperfusion. In the present experiments, sepsis produced a 40% decrease in cardiac performance, but was also protective of hearts made ischemic the next day. Hearts from septic and alcoholic septic rats recovered 100% of preischemic ventricular function after 35-min ischemia, whereas hearts from the control and alcohol groups recovered only 80% of preischemic left ventricular performance. Whereas preischemic function was significantly decreased in the septic groups compared with the two nonseptic groups, postishemic function was no longer significantly different in the four groups. Thus, sepsis resulted in development of protection of the hearts from ischemia-reperfusion injury, even in hearts that were severely compromised by the combination of chronic alcoholism and Gram-negative sepsis.     

Systolic Right Ventricular Function in Children and Young Adults with Pulmonary Artery Hypertension Secondary to Congenital Heart Disease and Tetralogy of Fallot: Tricuspid Annular Plane Systolic Excursion (TAPSE) and Magnetic Resonance Imaging Data

Objective. The tricuspid annular plane systolic excursion (TAPSE), as echocardiographic index to assess right ventricular (RV) systolic function, has not been investigated thoroughly in children and young adults with tetralogy of Fallot (TOF) and pulmonary artery hypertension secondary to congenital heart disease (PAH‐CHD). Patients. TAPSE values of 49 patients with PAH‐CHD and 156 patients with TOF were compared with age‐matched normal subjects. TAPSE values were also compared with RV ejection fraction (RVEF) and RV indexed end‐diastolic volume (RVEDVi) determined by magnetic resonance imaging in PAH‐CHD and TOF patients. Results. Patients with a PAH‐CHD showed a positive correlation between TAPSE with RVEF (r= 0.81; P < 0.001) and a negative correlation between TAPSE with RVEDVi (r=?0.67; P < 0.001). Similarly, in our TOF patients, a positive correlation between TAPSE with RVEF (r= 0.65; P < 0.001) and a negative correlation between TAPSE with RVEDVi (r=?0.42; P < 0.001) was seen. Conclusions. Significant pressure overload in PAH‐CHD patients and volume overload in TOF patients lead to a decreased systolic RV function, determined by TAPSE and magnetic resonance imaging and to increased RVEDVi values, determined by MRI, with time.     

糖尿病大鼠心肌梗死后易发心力衰竭的机制

目的研究STZ诱导的血糖不加控制的糖尿病大鼠急性心肌梗死（AMI）后易发心力衰竭（HF）的机制。方法217只SD大鼠随机分组，糖尿病组经腹腔内注射链脲酶素（STZ，65mg／kg）诱导糖尿病，10周后所有AMI组结扎冠状动脉左前降支建立AMI模型。确定AMI前和AMI后1天，7天，14天，28天，56天做为实验观察时间点，观察大鼠的生存率，心肌超微结构的变化，进行心脏超声检测、心肌纤维化测定及左心肥厚的评估。结果结扎左冠状动脉前降支后，糖尿病大鼠的死亡率、左心功能恶化及左室重构的速度均较非糖尿病大鼠显著。在早期阶段，糖尿病与非糖尿病大鼠心肌纤维化相似，而1月后却出现显著差别。结论糖尿病加速了STZ诱导的糖尿病大鼠AMI后心脏重构的进展。     

血浆降钙素基因相关肽与冠心病患者冠状动脉病变严重程度及左心室功能的关系

为探讨血浆降钙素基因相关肽浓度与冠心病患者冠状动脉病变严重程度及左心室功能的关系 ,应用放射免疫法检测 42例选择性冠状动脉造影主要分支狭窄≥ 70 %的患者和 15例正常人的血浆降钙素基因相关肽浓度 ,并作Leaman冠状动脉记分 ,左心室造影测左心室射血分数 ,研究血浆降钙素基因相关肽浓度与Leaman冠状动脉记分及左心室射血分数之间的关系。结果发现 ,冠心病患者血浆降钙素基因相关肽浓度明显低于正常对照者(2 76 .12± 16 4.75ng/L比 411.44± 110 .32ng/L ,P <0 .0 1) ;血浆降钙素基因相关肽浓度与Leaman记分呈显著负相关 (r=- 0 .6 1,P <0 .0 0 1) ,而与左心室射血分数呈显著正相关 (r=0 .5 7,P <0 .0 0 1) ;患者全组Leaman记分与左心室射血分数无明显相关 ,但在血浆降钙素基因相关肽浓度 <2 5 0ng/L的亚组 ,Leaman记分与左心室射血分数呈显著负相关 (r=- 0 .49,P <0 .0 5 )。结果提示 ,血浆降钙素基因相关肽水平与冠心病患者的冠状动脉病变严重程度和左心室功能均有一定关系 ;血浆降钙素基因相关肽水平降低的冠心病患者左心室功能随冠状动脉病变的加重而减退。血浆降钙素基因相关肽浓度变化可能在冠状动脉粥样硬化的发生发展及冠心病患者左心室功能降低的发病机制中有一定意义。     

Relationships between Depressive Symptoms, Anxiety, Alcohol Consumption, and Blood Pressure: Results from the CARDIA Study

Objectives : We examined cross-sectional relationships among depressive symptoms, anxiety, alcohol intake, and blood pressure. Test hypotheses were that: (1) alcohol intake, depressive symptoms, and anxiety would be positively related to blood pressure; (2) depressive symptoms and anxiety would have a stronger association with alcohol intake in Blacks than in Whites; and (3) adjustment for differences in depressive symptoms, anxiety, and alcohol intake would reduce Black-White blood pressure differences. Methods : Study hypotheses were tested in a sample of 4,352 Black and White adults, participating in the CARDIA study. Hypotheses were tested using multiple linear regression. Results : Alcohol intake was positively related to systolic ( p = 0.0001) and diastolic ( p = 0.0004) blood pressure in men, but not in women. Depressive symptoms and anxiety were unrelated to blood pressure. The relationship between alcohol intake and depressive symptoms differed by race/ethnicity in men ( p = 0.0719) and in women ( p = 0.0002). Alcohol intake increased with increasing levels of depressive symptoms, but the increase was greater in Blacks than in Whites. After accounting for alcohol intake, body mass index, and other variables, Black-White blood pressure differences were reduced in men, but not in women; most of the reduction was caused by body mass index. Conclusions : Blacks may respond differently than Whites to psychological distress.     

Increased comorbidities in heart failure patients ≥ 85 years but declined from > 90 years: Data from the Swedish Heart Failure Registry

Objectives

Epidemiological studies of elderly heart failure (HF) patients (≥ 85 years) are limited with inconsistent findings. Our objective is to confirm and extend epidemiological study in elderly (≥ 85 years) patients using the Swedish Heart Failure Registry database.

Methods

This retrospective study included 8,347 HF patients aged ≤ 65 years and 15,889 HF patients aged ≥ 85 years. Elderly population was further divided into two subgroups: 11,412 patients were 85–90 years and 4,477 patients were > 90 years.

Results

The ≥ 85 year group was characterized by more women, higher systolic blood pressure (SBP), lower body-mass index (BMI), more than twice as many HF with normal left ventricular ejection fraction (HFNEF), higher incidence of cardiovascular and non-cardiovascular comorbidities and less use of proven therapeutics compared with the ≤ 65 year group. Compared with the 85–90 year subgroup, the > 90 year subgroup had a decline in cardiovascular and non-cardiovascular comorbidities except renal insufficiency and anaemia which continued to increase with ageing (p < 0.01). Tendency was the same regardless of gender but slightly different between systolic HF (SHF) and HFNEF. In the group with HFNEF, there were more women, higher SBP, lower N-terminal pro-B-type natriuretic peptide levels, less ischaemic heart disease, more hypertension and left bundle branch block regardless of age. Atrial fibrillation was more frequent in patients with HFNEF than with SHF in the elderly group (p < 0.01). Patients with HFNEF in the > 90 year subgroup had increasing incidence of ischaemic heart disease compared to 85–90 year group (p < 0.01).

Conclusions

HF patients ≥ 85 years had increased cardiovascular and non-cardiovascular comorbidities but with a decline from > 90 years.     

Clinical effects of early angiotensin-converting enzyme inhibitor treatment for acute myocardial infarction are similar in the presence and absence of aspirin : Systematic overview of individual data from 96,712 randomized patients

OBJECTIVES

We sought to determine whether the clinical effects of early angiotensin-converting enzyme (ACE) inhibitor (ACEi) treatment for acute myocardial infarction (MI) are influenced by the concomitant use of aspirin (ASA).

BACKGROUND

Aspirin and ACEi both reduce mortality when given early after MI. Aspirin inhibits the synthesis of vasodilating prostaglandins, and, in principle, this inhibition might antagonize some of the effects of ACEi. But it is uncertain whether, in practice, this influences the effects of ACEi on mortality and major morbidity after MI.

METHODS

This overview sought individual patient data from all trials involving more than 1,000 patients randomly allocated to receive ACEi or control starting in the acute phase of MI (0–36 h from onset) and continuing for four to six weeks. Data on concomitant ASA use were available for 96,712 of 98,496 patients in four eligible trials (and for none of 1,556 patients in the one other eligible trial).

RESULTS

Overall 30-day mortality was 7.1% among patients allocated to ACEi and 7.6% among those allocated to control, corresponding to a 7% (standard deviation [SD], 2%) proportional reduction (95% confidence interval 2% to 11%, p = 0.004). Angiotensin-converting enzyme inhibitor was associated with similar proportional reductions in 30-day mortality among the 86,484 patients who were taking ASA (6% [SD, 3%] reduction) and among the 10,228 patients who were not (10% [SD, 5%] reduction: chi-squared test of heterogeneity between these reductions = 0.4; p = 0.5). Angiotensin-converting enzyme inhibitor produced definite increases in the incidence of persistent hypotension (17.9% ACEi vs. 9.4% control) and of renal dysfunction (1.3% ACEi vs. 0.6% control), but there was no good evidence that these effects were different in the presence or absence of ASA (chi-squared for heterogeneity = 0.4 and 0.0, respectively; both not significant). Nor was there good evidence that the effects of ACEi on other clinical outcomes were changed by concomitant ASA use.

CONCLUSIONS

Both ASA and ACEi are beneficial in acute MI. The present results support the early use of ACEi in acute MI, irrespective of whether or not ASA is being given.