Outdoor air pollution, mortality, and hospital admissions from coronary heart disease in Sheffield, UK: a small-area level ecological study.

AIMS: To examine the hypothesis that coronary heart disease mortality and emergency hospital admission rates are higher in areas with higher outdoor air pollution levels. METHODS AND RESULTS: Modelled nitrogen oxides (NO(x)), particulate matter (PM(10)), and carbon monoxide (CO) levels were interpolated to 1030 census enumeration districts using an ecological study design. Results, based on 6857 deaths and 11,407 admissions from 1994-98 and a population of 199,682 aged >or=45 years, were adjusted for age, sex, deprivation, and smoking prevalence. Mortality rate ratios were 1.17 (95% CI 1.06-1.29), 1.08 (95% CI 0.96-1.20), and 1.05 (95% CI 0.95-1.16) in the highest relative to the lowest NO(x), PM(10), and CO quintile categories, respectively. Corresponding admission rate ratios were 1.00 (95% CI 0.90-1.10), 1.01 (95% CI 0.90-1.14), and 0.88 (95% CI 0.79-0.98). CONCLUSION: The results are consistent with an excess risk of coronary heart disease mortality in areas with high outdoor NO(x), a proxy for traffic-related pollution, but residual confounding cannot be ruled out. If causality were assumed, 6% of coronary heart disease deaths would have been attributable to outdoor NO(x,) and targeting pollution reduction measures at high pollution areas would be an option for coronary mortality prevention.     

Acute effect of ambient air pollution on heart failure in Guangzhou,China

Background

Heart failure (HF) is a global public health problem of increasing importance. The association between acute exposure to air pollution and HF has been well established in developed countries, but little evidence was available in developing countries where air pollution levels were much higher. We conducted a time-series study to investigate the short-term association between air pollution and overall emergency ambulance dispatches (EAD) due to HF in Guangzhou, China.

Methods

Daily data of EAD due to HF from 1 January 2008 to 31 December 2012 were obtained from Guangzhou Emergency Center. We applied the over-dispersed Poisson generalized addictive model to analyze the associations after controlling for the seasonality, day of the week and weather conditions.

Results

We identified a total of 3375 EAD for HF. A 10-μg/m³ increase in the present-day concentrations of particulate matter with an aerodynamic diameter of less than 10 μm, sulfur dioxide and nitrogen dioxide corresponded to increases of 3.54% [95% confidence interval (CI): 1.35%, 5.74%], 5.29% (95% CI: 2.28%, 8.30%) and 4.34% (95% CI: 1.71%, 6.97%) in daily EAD for HF, respectively. The effects of air pollution on acute HF were restricted on the concurrent day and in the cool seasons.

Conclusions

Our results provided the first population-based evidence in Mainland China that outdoor air pollution could trigger the exacerbation of HF.     

Particulate air pollution and hospital admissions for congestive heart failure in seven United States cities

The association between short-term elevations in ambient particulate air pollution and increased cardiovascular morbidity and mortality is well documented. Ambient particles may also trigger acute decompensation in patients with congestive heart failure (CHF), but this hypothesis has not been evaluated in a systematic manner. This study evaluated the association between daily levels of respirable particulate matter of aerodynamic diameters < or =10 microm (PM10) and the rate of hospitalization from the emergency room for CHF in Medicare recipients (age > or = 65 years) in 7 United States cities from 1986 and 1999. The time-stratified case-crossover design was used to separately estimate the effect of a 10 microg/m3 increase in PM10 in each city. A combined random-effects estimate was then obtained from the city-specific effect estimates. There were 292,918 admissions with primary diagnoses of CHF during the observation period. Overall, a 10 microg/m3 increase in PM10 was associated with a 0.72% (95% confidence interval 0.35% to 1.10%) increase in the rate of admission for CHF on the same day. The effect of PM10 appeared to be less in patients with secondary diagnoses of hypertension. There was no consistent effect modification by age, gender, race, or any other secondary diagnosis evaluated. In conclusion, these results support the hypothesis that elevated levels of particulate air pollution, below the current limits set by the United States Environmental Protection Agency, are associated with an increase in the rate of hospital admission for exacerbation of CHF.     

Air pollution and heart failure: Relationship with the ejection fraction

AIM: To study whether the concentrations of particulate matter in ambient air are associated with hospitaladmission due to heart failure in patients with heart failure with preserved ejection fraction and reduced ejection fraction. METHODS: We studied 353 consecutive patients admitted into a tertiary care hospital with a diagnosis of heart failure. Patients with ejection fraction of ≥ 45% were classified as having heart failure with preserved ejection fraction and those with an ejection fraction of < 45% were classified as having heart failure with reduced ejection fraction. We determined the average concentrations of different sizes of particulate matter (< 10, < 2.5, and < 1 μm) and the concentrations of gaseous pollutants (carbon monoxide, sulphur dioxide, nitrogen dioxide and ozone) from 1 d up to 7 d prior to admission. RESULTS: The heart failure with preserved ejection fraction population was exposed to higher nitrogen dioxide concentrations compared to the heart failure with reduced ejection fraction population (12.95 ± 8.22 μg/m 3 vs 4.50 ± 2.34 μg/m 3 , P < 0.0001). Multivariate analysis showed that nitrogen dioxide was a significant predictor of heart failure with preserved ejection fraction (odds ratio ranging from (1.403, 95%CI: 1.003-2.007, P = 0.04) to (1.669, 95%CI: 1.043-2.671, P = 0.03). CONCLUSION: This study demonstrates that shortterm nitrogen dioxide exposure is independently associated with admission in the heart failure with preserved ejection fraction population.     

心肌肌钙蛋白I水平联合Tilburg量表对高龄心力衰竭患者预后的判断价值

目的 探讨心肌肌钙蛋白(cardiac troponin,cTn)I及Tilburg衰弱量表（tilburg frailty scale,TFI）对老年慢性心力衰竭（chronic heart failure,CHF）患者预后的评估价值。 方法 选取2014年9月～2017年8月我院心内科收治的经确诊为老年CHF患者280例作为研究对象,根据NYHA心功能分级将患者分为四组,比较各组cTnI及TFI评分水平。再根据患者随访期间是否发生主要不良心血管事件(major adverse cardiovascular events,MACE)分为MACE组（n=92）和非MACE组（n=188）,收集患者一般临床资料、入院第2天血液生化指标、cTnI及TFI评分,采用COX比例风险模型分析cTnI及TFI评分与MACE的关系,并根据ROC曲线下cTnI及TFI评分的最佳临界值对老年CHF患者进行危险分组,经Kaplan-Meier生存分析法分析各组间MACE平均发生时间的差异。 结果 cTnI及TFI评分水平随NYHA心功能分级的增高呈明显上升,差异有统计学意义（P<0.05）;与非MACE组比较,MACE组患者cTnI及TFI评分更高,差异均具有统计学意义（P<0.05）;cTnI及TFI评分的ROC曲线下面积分别为0.722、0.761,具有较高的诊断价值,最佳临界值分别为8.36ng/ml、8分;COX分析结果显示,cTnI>8.36ng/ml、TFI评分>8分是老年CHF患者发生MACE的独立危险因素;以cTnI及TFI评分的最佳临界值将患者分层,Kaplan-Meier生存曲线分析结果显示,低危组、中危组、高危组三组患者发生MACE的平均生存时间分别为14.37个月、9.39个月、7.29个月,差异有统计学意义（P<0.05）。 结论 老年CHF患者cTnI、TFI评分随着心功能增加明显升高,同时二者是老年CHF患者发生MACE的独立预测因子,二者联用可提高老年CHF患者3年MACE发生的预测效率,具有潜在临床诊断价值。     

Genetic variation in the natriuretic peptide system and heart failure

Heart failure (HF) is a modern epidemic and is one of the few cardiovascular diseases which is increasing in prevalence. The growing importance of the Natriuretic Peptide (NP) system in HF is well recognized. Laboratory tests for B-type Natriuretic Peptide (BNP) have proven value as diagnostic and prognostic tools in HF and are now part of routine clinical care. Furthermore, recombinant atrial natriuretic peptide (ANP) (carperitide) and BNP (nesiritide) and are approved HF therapies in Japan and the US, respectively and additional natriuretic peptides (e.g., CNP, urodilatin, and designer NPs) are under investigation for use in HF. Common genetic sequence variants are increasingly being recognized as determinants of disease risk or drug response and may help explain a portion of the inter-individual variation in the human NP system. This review describes current knowledge of NP system genetic variation as it pertains to HF as well as ongoing studies and where the field is expected to progress in the near future. To briefly summarize, NP system genetic variants have been associated with alterations in gene expression, NP levels, and cardiovascular disease. The next step forward will include specific investigations into how this genetic variation can advance ‘Personalized Medicine’, such as whether they impact the utility of diagnostic BNP testing or effectiveness of therapeutic NP infusion. This is already in progress, with pharmacogenetic studies of nesiritide currently underway. We expect that within 5 years there should be a reasonable idea of whether NP system genetic variation will have important clinical implications.     

ICU层流病房空气质量影响因素的探讨与管理

目的探讨ICU层流病房空气质量影响因素及管理对策。方法采用平板暴露采样法,对不同人员数及活动状态、不同湿度、回风口过滤网不同清洗时间的细菌菌落数进行对比研究。结果①相对静止状态细菌菌落数少于活动状态时,两组有显著性差异(P<0.05)。②在不同湿度状态下湿度控制在40%~50%和50%~70%两组对比细菌菌落数差异无显著性(P>0.05)。③清洗回风口过滤网后第7、14、21、28d采样,结果过滤网清洗时间细菌菌落数无显著性差异(P>0.05)。结论对ICU进行科学的工作流程和管理是保持室内空气洁净的有效方法。     

Direct implication of carbon monoxide in the development of heart failure in rats with cardiac hypertrophy subjected to air pollution

Pollution is known to particularly affect patients with respiratory insufficiency and right ventricle abnormalities. We therefore hypothesized that carbon monoxide (CO) at low dose could be involved in cardiovascular disorders in patients with chronic hypoxic pulmonary hypertension secondary to chronic hypoxia. Ten-week-old male and female healthy Dark Agouti rats were randomly divided into two series—untrained (U) and trained (T)—of four groups of 18 animals each. Both U and T series were continuously exposed to ambient air (U_AIR, and T_AIR; n=16) or air plus 50 ppm CO (U_AIR+CO and T_AIR+CO; n=18). Similarly, rats initially subjected to right ventricle hypertrophy secondary to chronic hypoxia (H) were continuously exposed to ambient air (TH_AIR, and UH_AIR; n=18) or air plus 50 ppm CO (UH_AIR+CO, and TH_AIR+CO; n=18). Doppler-echocardiography and hemodynamic studies performed at rest both indicated that CO had no significant effect on cardiac morphology or functions in control rats (U_AIR+CO vs U_AIR). In contrast, cardiac dilation and large decreases in left ventricular ejection fraction, mitral early diastolic rapid inflow (E) deceleration, E/atrial contraction filling (A) ratio, +dP/dt, and −dP/dt were found in TH_AIR+CO compared with TH_AIR. After exposure, heart rate variability was unaffected in U_AIR+CO, whereas total power spectra were markedly decreased and low frequency/high frequency power ratio was increased in TH_AIR+CO rats. CO pollution could be directly involved in cardiac disorders of patients with pre-existent hypertrophic cardiomyopathies.     

Psychometric characteristics of the mutuality scale in heart failure patients and caregivers

Background

Higher patient-caregiver mutuality is associated with improved patient and caregiver outcomes, but no studies have tested the psychometric characteristics of the mutuality scale (MS) in heart failure (HF) patient and caregiver population.

小剂量前列腺素E1对严重充血性心力衰竭及内皮素的影响

为探讨小剂量前列腺素Ｅ１（ＰＧＥ１）对重度充血性心力衰竭及内皮素（ＥＴ）水平的影响,对２０例经传统治疗无效的心衰患者小剂量静滴ＰＧＥ１１周,观察治疗前后临床症状、血流动力学及ＥＴ变化。结果发现,临床总有效率为９５％。肺动脉压（ＰＡＰ）、肺毛细血管嵌楔压（ＰＣＷＰ）比治疗前明显下降（４．９３±０．５３对４．００±０．５３ｋＰｓ,Ｐ＜０．０１;３．４７±０．５３对２．５３±０．４０ｋＰａ,Ｐ＜０．０１）,体循环阻力指数（ＳＶＲＩ）下降（２０４．８±２１．３对１５０．６±１．３ｋＰａ·ｓ·Ｌ－１·ｍ－２,Ｐ＜０．０５）,心指数（ＣＩ）上升（２．２±０．１对２．８±０．２Ｌ·ｍｉｎ－１·ｍ－２,Ｐ＜０．０５）。内皮素明显降低（１５４．５６±４．４０对１１８．１３±２．２４ｎｇ／Ｌ,Ｐ＜０．０１）。提示ＰＧＥ１可降低ＥＴ水平并通过多种机制对心衰产生有益的作用。     

Growth hormone, acromegaly, and heart failure: an intricate triangulation

Short‐term GH or IGF‐I excess provides a model of physiological cardiac growth associated with functional advantage. The physiological nature of cardiac growth is accounted for by the following: (i) the increment in cardiomyocyte size occurs prevalently at expense of the short axis. This is the basis for the concentric pattern of left ventricular (LV) hypertrophy, with consequent fall in LV wall stress and functional improvement; (ii) cardiomyocyte growth is associated with improved contractility and relaxation, and a favourable energetic setting; (iii) the capillary density of the myocardial tissue is not affected; (iv) there is a balanced growth of cardiomyocytes and nonmyocyte elements, which accounts for the lack of interstitial fibrosis; (v) myocardial energetics and mechanics are not perturbed; and (vi) the growth response is not associated with the gene re‐programming that characterizes pathologic cardiac hypertrophy and heart failure. Overall, the mechanisms activated by GH or IGF‐I appear to be entirely different from those of chronic heart failure. Not to be neglected is also the fact that GH, through its nitric oxide (NO)‐releasing action, contributes to the maintenance of normal vascular reactivity and peripheral vascular resistance. This particular kind of interaction of GH with the cardiovascular system accounts for: (i) the lack of cardiac impairment in short‐term acromegaly; (ii) the beneficial effects of GH and IGF‐I in various models of heart failure; (iii) the protective effect of GH and IGF‐I against post‐infarction ventricular remodelling; (iv) the reversal of endothelial dysfunction in patients with heart failure treated with GH; and (v) the cardiac abnormalities associated with GH deficiency and their correction after GH therapy. If it is clear that GH and IGF‐I exert favourable effects on the heart in the short term, it is equally undeniable that GH excess with time causes pathologic cardiac hypertrophy and, if it is not corrected, eventually leads to cardiac failure. Why then, at one point in time in the natural history of acromegaly, does physiological cardiac growth become maladaptive and translate into heart failure? Before this transition takes places, the acromegalic heart shares very few features with other models of chronic heart failure. None of the mechanisms involved in the progression of heart failure is clearly operative in acromegaly, save for the presence of insulin‐resistance and mild alterations of lipoproteins and clot factors. Is this enough to account for the development of heart failure? Probably not. On the other hand, it must be stressed that GH and IGF‐I activate several mechanisms that play a protective role against the development of heart failure. These include ventricular unloading, deactivation of neurohormonal components, antiapoptotic effect and enhanced vascular reactivity. Ultimately, all data available concur to hypothesize that acromegalic cardiomyopathy represents a progressive model of cardiac hypertrophy in which the cardiotoxic and pro‐remodelling effect is intrinsic to the excessive and unrestrained myocardial growth.     

Pattern of heart failure in Abuja,Nigeria: an echocardiographic study

Aim

Despite heart failure having been identified in subjects in sub-Saharan Africa over the last 60 years, there is still a dearth of data, especially echocardiographic data on heart failure. We therefore set out to analyse the clinical and echocardiographic features of all consecutive subjects presenting with heart failure in a tertiary institution in Nigeria.

Methods

Three hundred and forty subjects with heart failure, according to the guidelines of the European Society of Cardiology, were studied. Each patient had two-dimensional guided transthoracic echocardiography.

Results

The mean age of the patients was 50.60 ± 15.29 years, and 50.9% of the study population were males while 49.1% were females. The commonest cause of heart failure identified was hypertension in 61.5% of the patients; 75.5% had systolic heart failure, whereas 23.5% had heart failure with preserved ejection fraction.

Conclusions

Untreated hypertension has been identified as the leading cause of heart failure in Abuja, Nigeria, which is similar to that in many other parts of sub-Saharan Africa. Coronary artery disease is a rare cause of heart failure in this population group.     

Perfusion/ventilation mismatch during exercise in chronic heart failure: an investigation of circulatory determinants.

BACKGROUND--The ventilatory cost of carbon dioxide (CO2) elimination on exercise (VE/VCO2) is increased in chronic heart failure (CHF). This reflects increased physiological dead space ventilation secondary to mismatching between perfusion and ventilation during exercise. The objectives of this study were to investigate the relation of this increased VE/VCO2 slope to the syndrome of CHF or to limitation of the exercise related increase of pulmonary blood flow, or both. PATIENTS AND METHODS--Maximal treadmill exercise tests with respiratory gas analysis were performed in 45 patients with CHF (defined as resting left ventricular ejection fraction < 40% on radionuclide scan); 15 normal controls; 23 patients with coronary artery disease and normal resting left ventricular function; and 13 pacemaker dependent patients (six with and seven without CHF) directly comparing exercise responses in rate responsive and fixed rate mode. RESULTS--Patients with CHF had a steeper VE/VCO2 slope than normal controls: this was related inversely to peak VO2 below 20 mol/min/kg. In patients with coronary artery disease in whom peak VO2 (at respiratory exchange ratio > 1) was as limited as in the patients with CHF but resting left ventricular function was normal, the VE/VCO2 slope was normal. In pacemaker dependent patients fixed rate pacing resulted in lower exercise capacity and peak VO2 than rate responsive pacing; the VE/VCO2 slope was normal in patients without CHF but steeper than normal in patients with CHF; the VE/VCO2 slope was steeper during fixed rate than during rate responsive pacing in these patients with CHF. CONCLUSIONS--These findings suggest that the perfusion/ventilation mismatch during exercise in CHF is related to the chronic consequences of the syndrome and not directly to limitation of exercise related pulmonary flow. Only when the syndrome of CHF is present can matching between perfusion and ventilation be acutely influenced by changes in pulmonary flow.