***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Chronic obstructive pulmonary disease ( COPD ) often coexists with other chronic diseases and comorbidities that can markedly influence patients ' health status and prognosis . This is particularly true for cardiovascular disease ( CVD ) . However , there have been no trials assessing the effect of COPD medications on CVD in patients with both diseases . The “ Study to Underst and Mortality and Morbidity in COPD ” ( SUMMIT ) aims at determining the impact of fluticasone furoate/vilanterol combination and the individual components on the survival of patients with moderate COPD and either a history of CVD or at increased risk for CVD . SUMMIT is a multicentre , r and omised , double-blind , parallel-group , placebo-controlled trial of 16 000 patients with moderate COPD r and omly assigned to once daily treatment with fluticasone furoate/vilanterol ( 100/25 & mgr;g ) , fluticasone furoate ( 100 & mgr;g ) , vilanterol ( 25 & mgr;g ) or matched placebo ; mortality is the primary end-point . The study is an event-driven trial powered by the comparison of furoate/vilanterol versus placebo . Secondary end-points are decline in forced expiratory volume in 1 s and effect on a composite cardiovascular end-point . This article describes the design of the SUMMIT study Background Low serum magnesium has been implicated in cardiovascular mortality , but results are conflicting and the pathway is unclear . We studied the association of serum magnesium with  coronary heart disease ( CHD ) mortality and sudden cardiac death ( SCD ) within the prospect i ve population ‐based Rotterdam Study , with adjudicated end points and long‐term follow‐up . Methods and Results Nine‐thous and eight‐hundred and twenty participants ( mean age 65.1 years , 56.8 % female ) were included with a median follow‐up of 8.7 years . We used multivariable Cox proportional hazard models and found that a 0.1 mmol/L increase in serum magnesium level was associated with a lower risk for CHD mortality ( hazard ratio : 0.82 , 95 % CI 0.70–0.96 ) . Furthermore , we divided serum magnesium in quartiles , with the second and third quartile combined as reference group ( 0.81–0.88 mmol/L ) . Low serum magnesium ( ≤0.80 mmol/L ) was associated with an increased risk of CHD mortality ( N=431 , hazard ratio : 1.36 , 95 % CI 1.09–1.69 ) and SCD ( N=217 , hazard ratio : 1.54 , 95 % CI 1.12–2.11 ) . Low serum magnesium was associated with accelerated sub clinical atherosclerosis ( expressed as increased carotid intima‐media thickness : + 0.013 mm , 95 % CI 0.005–0.020 ) and increased QT‐interval , mainly through an effect on heart rate ( RR‐interval : −7.1 ms , 95 % CI −13.5 to −0.8 ) . Additional adjustments for carotid intima‐media thickness and heart rate did not change the associations with CHD mortality and SCD . Conclusions Low serum magnesium is associated with an increased risk of CHD mortality and SCD . Although low magnesium was associated with both carotid intima‐media thickness and heart rate , this did not explain the relationship between serum magnesium and CHD mortality or SCD . Future studies should focus on why magnesium associates with CHD mortality and SCD and whether intervention reduces these risks Background Because chronic obstructive pulmonary disease ( COPD ) is a heterogeneous condition , the identification of specific clinical phenotypes is key to developing more effective therapies . To explore if the persistence of systemic inflammation is associated with poor clinical outcomes in COPD we assessed patients recruited to the well-characterized ECLIPSE cohort ( NCT00292552 ) . Methods and Findings Six inflammatory biomarkers in peripheral blood ( white blood cells ( WBC ) count and CRP , IL-6 , IL-8 , fibrinogen and TNF-α levels ) were quantified in 1,755 COPD patients , 297 smokers with normal spirometry and 202 non-smoker controls that were followed-up for three years . We found that , at baseline , 30 % of COPD patients did not show evidence of systemic inflammation whereas 16 % had persistent systemic inflammation . Even though pulmonary abnormalities were similar in these two groups , persistently inflamed patients during follow-up had significantly increased all-cause mortality ( 13 % vs. 2 % , p<0.001 ) and exacerbation frequency ( 1.5 ( 1.5 ) vs. 0.9 ( 1.1 ) per year , p<0.001 ) compared to non-inflamed ones . As a descriptive study our results show associations but do not prove causality . Besides this , the inflammatory response is complex and we studied only a limited panel of biomarkers , albeit they are those investigated by the majority of previous studies and are often and easily measured in clinical practice . Conclusions Overall , these results identify a novel systemic inflammatory COPD phenotype that may be the target of specific research and treatment Background —A prolonged QT interval is associated with a risk for life-threatening events . However , little is known about prognostic implication s of the reverse — a short QT interval . Several members of 2 different families were referred for syncope , palpitations , and resuscitated cardiac arrest in the presence of a positive family history for sudden cardiac death . Autopsy did not reveal any structural heart disease . All patients had a constantly and uniformly short QT interval at ECG . Methods and Results —Six patients from both families were su bmi tted to extensive noninvasive and invasive work-up , including serial resting ECGs , echocardiogram , cardiac MRI , exercise testing , Holter ECG , and signal-averaged ECG . Four of 6 patients underwent electrophysiological evaluation including programmed ventricular stimulation . In all subjects , a structural heart disease was excluded . At baseline ECG , all patients exhibited a QT interval ≤280 ms ( QTc ≤300 ms ) . During electrophysiological study , short atrial and ventricular refractory periods were documented in all and increased ventricular vulnerability to fibrillation in 3 of 4 patients . Conclusions —The short QT syndrome is characterized by familial sudden death , short refractory periods , and inducible ventricular fibrillation . It is important to recognize this ECG pattern because it is related to a high risk of sudden death in young , otherwise healthy subjects Regulation of magnesium balance is poorly understood . However , hypomagnesaemia has been reported in patients in clinical situations where circulating catecholamines are raised including myocardial infa rct ion , cardiac surgery and insulin-induced hypoglycaemia stress tests . The effects of L-adrenaline infusions , sufficient to achieve pathophysiological levels of adrenaline , and of therapeutic intravenous infusions of salbutamol , a beta 2-agonist , on plasma magnesium , plasma potassium , plasma glucose and plasma insulin levels were studied in a placebo-controlled design in eight normal subjects .  Plasma magnesium levels fell significantly during the adrenaline infusion and also during the salbutamol infusion , though more slowly . In a 1 h period of observation after cessation of the infusions no recovery of plasma magnesium levels was seen . Significant falls in plasma potassium levels were also observed during both infusions with spontaneous recovery within 30 min after the infusions . No significant changes in plasma insulin levels occurred with either salbutamol or L-adrenaline compared with control . Plasma glucose levels rose significantly during the adrenaline infusion . The study suggests that both L-adrenaline and salbutamol cause shifts in plasma magnesium which are not mediated by insulin . We propose that intracellular shifts of magnesium occur as a result of beta-adrenergic stimulation IMPORTANCE Risk stratification of patients with nonischemic dilated cardiomyopathy is primarily based on left ventricular ejection fraction ( LVEF ) . Superior prognostic factors may improve patient selection for implantable cardioverter-defibrillators ( ICDs ) and other management decisions . OBJECTIVE To determine whether myocardial fibrosis ( detected by late gadolinium enhancement cardiovascular magnetic resonance [ LGE-CMR ] imaging ) is an independent and incremental predictor of mortality and sudden cardiac death ( SCD ) in dilated cardiomyopathy . DESIGN , SETTING , AND PATIENTS Prospect i ve , longitudinal study of 472 patients with dilated cardiomyopathy referred to a UK center for CMR imaging between November 2000 and December 2008 after presence and extent of midwall replacement fibrosis were determined . Patients were followed up through December 2011 . MAIN OUTCOME MEASURES Primary end point was all-cause mortality . Secondary end points included cardiovascular mortality or cardiac transplantation ; an arrhythmic composite of SCD or aborted SCD ( appropriate ICD shock , nonfatal ventricular fibrillation , or sustained ventricular tachycardia ) ; and a composite of HF death , HF hospitalization , or cardiac transplantation . RESULTS Among the 142 patients with midwall fibrosis , there were 38 deaths ( 26.8 % ) vs 35 deaths ( 10.6 % ) among the 330 patients without fibrosis ( hazard ratio [ HR ] , 2.96 [ 95 % CI , 1.87 - 4.69 ] ; absolute risk difference , 16.2 % [ 95 % CI , 8.2%-24.2 % ] ; P < .001 ) during a median follow-up of 5.3 years ( 2557 patient-years of follow-up ) . The arrhythmic composite was reached by 42 patients with fibrosis ( 29.6 % ) and 23 patients without fibrosis ( 7.0 % ) ( HR , 5.24 [ 95 % CI , 3.15 - 8.72 ] ; absolute risk difference , 22.6 % [ 95 % CI , 14.6%-30.6 % ] ; P < .001 ) . After adjustment for LVEF and other conventional prognostic factors , both the presence of fibrosis ( HR , 2.43 [ 95 % CI , 1.50 - 3.92 ] ; P < .001 ) and the extent ( HR , 1.11 [ 95 % CI , 1.06 - 1.16 ] ; P < .001 ) were independently and incrementally associated with all-cause mortality . Fibrosis was also independently associated with cardiovascular mortality or cardiac transplantation ( by fibrosis presence : HR , 3.22 [ 95 % CI , 1.95 - 5.31 ] , P < .001 ; and by fibrosis extent : HR , 1.15 [ 95 % CI , 1.10 - 1.20 ] , P < .001 ) , SCD or aborted SCD ( by fibrosis presence : HR , 4.61 [ 95 % CI , 2.75 - 7.74 ] , P < .001 ; and by fibrosis extent : HR , 1.10 [ 95 % CI , 1.05 - 1.16 ] , P < .001 ) , and the HF composite ( by fibrosis presence : HR , 1.62 [ 95 % CI , 1.00 - 2.61 ] , P = .049 ; and by fibrosis extent : HR , 1.08 [ 95 % CI , 1.04 - 1.13 ] , P < .001 ) . Addition of fibrosis to LVEF significantly improved risk reclassification for all-cause mortality and the SCD composite ( net reclassification improvement : 0.26 [ 95 % CI , 0.11 - 0.41 ] ; P = .001 and 0.29 [ 95 % CI , 0.11 - 0.48 ] ; P = .002 , respectively ) . CONCLUSIONS AND RELEVANCE Assessment of midwall fibrosis with LGE-CMR imaging provided independent prognostic information beyond LVEF in patients with nonischemic dilated cardiomyopathy . The role of LGE-CMR in the risk stratification of dilated cardiomyopathy requires further investigation OBJECTIVES Our aim was to utilize a community-based approach to identify sex-related differences in risk factors for  sudden cardiac arrest ( SCA ) . BACKGROUND There are significant sex-based differences in prevalence and manifestation of SCA . Any differences related to predictors of SCA in women versus men are likely to have implication s for risk stratification and prevention . METHODS The Ore-SUDS ( Oregon Sudden Unexpected Death Study ) is an ongoing prospect i ve investigation of SCA in the Portl and , Oregon , metropolitan area ( population approximately 1 million ) . All cases meeting criteria for SCA were ascertained using multiple sources . Medical records were review ed to identify clinical conditions that may contribute to SCA risk , and comparisons were made between male and female SCA cases using Pearson 's chi-square tests for categorical variables , t tests for continuous variables , and multivariate logistic regression analysis . RESULTS During 2002 to 2007 , 1,5 
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In these studies , COPD was associated with a prolonged and shortened QT interval .
In patients with a myocardial infa rct ion ( MI ) , COPD was associated with an increased risk of ventricular arrhythmias and decreased survival .
COPD was a risk factor for SCD both in cardiovascular patient groups and in community-based studies , independent from cardiovascular risk profile .
In conclusion , cumulating evidence associates COPD with an increased risk of SCD .
Asystole and pulseless electric activity could be more common than VT/VF in deaths associated with COPD .