***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: Background — Few prospect i ve studies have examined quantitative cigarette consumption and smoking cessation on sudden cardiac death ( SCD ) risk with long-term follow-up . Methods and Results — We prospect ively examined the association between cigarette smoking and smoking cessation on the risk of SCD among 101 018 women participating in the Nurses ’ Health Study without known coronary heart disease , stroke , and cancer at baseline 1980 . During 30 years of follow-up , we identified 351 SCD events . Compared with never smokers , current smokers had a 2.44-fold ( 95 % CI , 1.80–3.31 ) increased risk of SCD after controlling for coronary risk factors . In multivariable analyses , quantity of cigarettes smoked daily ( P value for trend , < 0.0001 ) and smoking duration ( P value for trend , < 0.0001 ) were linearly associated with SCD risk among current smokers . Small-to-moderate amounts of cigarette consumption ( 1–14 per day ) were associated with a significant 1.84-fold ( 95 % CI , 1.16–2.92 ) increase in SCD risk and every 5 years of continued smoking was associated with an 8 % increase in SCD risk ( hazard ratio , 1.08 ; 95 % CI , 1.05–1.12 ; P<0.0001 ) . The SCD risk linearly decreased over time after quitting and was equivalent to that of a never smoker after 20 years of cessation ( P value for trend , < 0.0001 ) . Conclusions — In this large prospect i ve cohort of women without coronary heart disease at baseline , a strong dose – response relationship between cigarette smoking and SCD risk was observed , and smoking cessation significantly reduced and eventually eliminated excess SCD risk . This suggests efforts to prevent SCD among women should include aggressive strategies for smoking cessation Sudden cardiac death ( SCD ) generally refers to an unexpected death from a cardiovascular cause in a person with or without preexisting heart disease . The specificity of this definition varies depending on whether the event was witnessed ; however , most studies include cases that are associated with a witnessed collapse , death occurring within 1 hour of an acute change in clinical status , or an unexpected death that occurred within the previous 24 hours.1–3 Further , sudden cardiac arrest describes SCD cases with resuscitation records or aborted SCD cases in which the individual survived the cardiac arrest . The incidence of SCD in the United States ranges between 180 000 and 450 000 cases annually.4 These estimates vary owing to differences in SCD definitions and surveillance methods for case ascertainment.4,5 In recent prospect i ve studies using multiple sources in the United States,6,7 Netherl and s,8 Irel and , 9 and China,10 SCD rates range from 50 to 100 per 100 000 in the general population .3 Despite the need for multiple sources of surveillance to provide a more accurate estimate of SCD incidence , it is clear that the overall burden in the population remains high . Although improvements in primary and secondary prevention have result ed in substantial declines in overall coronary heart disease ( CHD ) mortality over the past 30 years,11,12 SCD rates specifically have declined to a lesser extent.13–16 SCD still accounts for > 50 % of all CHD deaths and 15 % to 20 % of all deaths.17,18 For some segments of the population , rates are not decreasing19 and may actually be increasing.14,19 As a result , SCD prevention represents a major opportunity to further reduce mortality from CHD . Despite major advances in cardiopulmonary resuscitation20 and postresuscitation care , survival BACKGROUND Cigarette smoking is a known risk factor for cardiovascular disease ( CVD ) , but its relationship to the development of hypertension is unclear . Previous epidemiological studies have shown inconsistent results , having demonstrated inverse and positive associations between cigarette smoking and the development of hypertension . METHODS We analyzed 13,529 male participants from the Physicians ' Health Study free of baseline hypertension and CVD who provided information about smoking status . Smoking status was categorized as never , past , or current < 20 cigarettes/day , or current > or = 20 cigarettes/day .  Incident hypertension was defined as either the initiation of antihypertensive treatment , self-reported systolic blood pressure ( BP ) > or = 140 mm Hg , or diastolic BP > or = 90 mm Hg . RESULTS Over a median follow-up of 14.5 years , 4,904 men developed hypertension .  We modeled the risk of developing hypertension by baseline smoking status adjusting for known risk factors for hypertension or CVD . In a fully adjusted Cox proportional hazards model , we found that compared with never smokers , past smokers and current smokers had corresponding relative risks ( RRs ) of 1.08 and 1.15 of developing hypertension . The risk for smokers did not appear to differ based on number of cigarettes smoked daily . Further , the RR of hypertension was higher for men with normal vs. prehypertensive levels of systolic ( SBP ) or diastolic BP ( DBP ) . CONCLUSIONS This prospect i ve cohort data suggests that cigarette smoking may be a modest but important risk factor for the development of hypertension BACKGROUND Sudden death was found to share the same set of usual risk factors as coronary events and therefore could not be specifically predicted in the population . It appears , however , that parental history of sudden death has not been investigated yet as a risk factor for sudden death . Therefore , we assessed risk factors , including parental sudden death , associated with the occurrence of sudden death in a long-term cohort study . METHODS AND RESULTS We included 7746 men employed by the city of Paris who were 43 to 52 years of age in 1967 to 1972 in the Paris Prospect i ve Study I. Each subject underwent a physical examination and an ECG , provided blood for laboratory tests , and answered question naires administered by trained interviewers who paid particular attention to family medical history .  Men with known ischemic cardiac disease were further excluded from analysis . For 95.5 % of the men , vital status was obtained from specific inquiries until retirement , then by death certificates . Resting heart rate , systolic or diastolic blood pressure , tobacco consumption , body mass index , diabetes status , serum cholesterol , and parental history of sudden death were independent factors associated with sudden death during follow-up ( 23 years on average ) . When adjusted for confounding variables , including parental history of myocardial infa rct ion , relative risk of sudden death associated with parental sudden death was 1.80 ( 95 % CI , 1.11 to 2.88 ) . CONCLUSIONS Parental sudden death is an independent risk factor for sudden death in middle-aged men . The existence of familial risk factors for sudden death may help provide better identification of subjects at high risk of and early prevention of sudden death Background —There are few data regarding the determinants of sudden cardiac death ( SCD ) in women , primarily because of their markedly lower rate of SCD compared with men . Nonetheless , existing data , although sparse , suggest possible gender differences in risk factors for SCD . Methods and Results —In this prospect i ve cohort of 121 701 women aged 30 to 55 years at baseline , SCD was defined as death within 1 hour of symptom onset . From 1976 to 1998 , 244 SCDs were identified . Although the risk of SCD increased markedly with age , the percentage of cardiac deaths that were sudden decreased . Most ( 69 % ) women who suffered a SCD had no history of cardiac disease before their death . However , almost all of the women who died suddenly ( 94 % ) had reported at least 1 coronary heart disease risk factor . Smoking , hypertension , and diabetes conferred markedly elevated ( 2.5- to 4.0-fold ) risk of SCD , similar to that conferred by a history of nonfatal myocardial infa rct ion ( relative risk , 4.1 ; 95 % confidence interval , 2.9 to 6.7 ) . Family history of myocardial infa rct ion before age 60 years and obesity were associated with moderate ( 1.6-fold ) elevations in risk . With regard to mechanism , 88 % of SCDs were classified as arrhythmic . In 76 % of these , the first rhythm documented was ventricular tachycardia or ventricular fibrillation . Conclusions —These prospect i ve data suggest that , as in men , coronary heart disease risk factors predict risk of SCD in women and that SCD is usually an arrhythmic death . Therefore , prevention of atherosclerosis or ventricular arrhythmias may reduce the incidence of SCD in women Summary Background Women born around 1940 in countries such as the UK and USA were the first generation in which many smoked substantial numbers of cigarettes throughout adult life . Hence , only in the 21st century can we observe directly the full effects of prolonged smoking , and of prolonged cessation , on mortality among women in the UK . Methods For this prospect i ve study , 1·3 million UK women were recruited in 1996–2001 and resurveyed postally about 3 and 8 years later . All were followed to Jan 1 , 2011 , through national mortality records ( mean 12 woman-years , SD 2 ) . Participants were asked at entry whether they were current or ex-smokers , and how many cigarettes they currently smoked . Those who were ex-smokers at both entry and the 3-year resurvey and had stopped before the age of 55 years were categorised by the age they had stopped smoking . We used Cox regression models to obtain adjusted relative risks that compared categories of smokers or ex-smokers with otherwise similar never-smokers . Findings After excluding 0·1 million women with previous disease , 1·2 million women remained , with median birth year 1943 ( IQR 1938–46 ) and age 55 years ( IQR 52–60 ) . Overall , 6 % ( 66 489/1 180 652 ) died , at mean age 65 years ( SD 6 ) . At baseline , 20 % ( 232 461 ) were current smokers , 28 % ( 328 417 ) were ex-smokers , and 52 % ( 619 774 ) were never-smokers . For 12-year mortality , those smoking at baseline had a mortality rate ratio of 2·76 ( 95 % CI 2·71–2·81 ) compared with never-smokers , even though 44 % ( 37 240/85 256 ) of the baseline smokers who responded to the 8-year resurvey had by then stopped smoking . Mortality was tripled , largely irrespective of age , in those still smoking at the 3-year resurvey ( rate ratio 2·97 , 2·88–3·07 ) . Even for women smoking fewer than ten cigarettes per day at baseline , 12-year mortality was doubled ( rate ratio 1·98 , 1·91–2·04 ) . Of the 30 most common causes of death , 23 were increased significantly in smokers ; for lung cancer , the rate ratio was 21·4 ( 19·7–23·2 ) . The excess mortality among smokers ( in comparison with never-smokers ) was mainly from diseases that , like lung cancer , can be caused by smoking . Among ex-smokers who had stopped permanently at ages 25–34 years or at ages 35–44 years , the respective relative risks were 1·05 ( 95 % CI 1·00–1·11 ) and 1·20 ( 1·14–1·26 ) for all-cause mortality and 1·84 ( 1·45–2·34 ) and 3·34 ( 2·76–4·03 ) for lung cancer mortality . Thus , although some excess mortality remains among these long-term ex-smokers , it is only 3 % and 10 % of the excess mortality among continuing smokers . If combined with 2010 UK national death rates , tripled mortality rates among smokers indicate 53 % of smokers and 22 % of never-smokers dying before age 80 years , and an 11-year lifespan difference . Interpretation Among UK women , two-thirds of all deaths of smokers in their 50s , 60s , and 70s are caused by smoking ; smokers lose at least 10 years of lifespan . Although the hazards of smoking until age 40 years and then stopping are substantial , the hazards of continuing are ten times greater . Stopping before age 40 years ( and preferably well before age 40 years ) avoids more than 90 % of the excess mortality caused by continuing smoking ; stopping before age 30 years avoids more than 97 % of it . Funding Cancer Research UK , Medical Research Council BACKGROUND Risk factors specific to sudden cardiac death ( SCD ) , ie , death within 1 hour after onset of symptoms , have been poorly identified , although recent findings from the present study incriminate heavy drinking and elevated heart rate . This paper examines the relations between a wide range of established and potential risk factors for ischemic heart disease ( IHD ) and SCD to identify independent risk factors for SCD and factors that might particularly or specifically relate to SCD . METHODS AND RESULTS We present a prospect i ve study of a cohort that was drawn from general 
    Output:
    
These results confirm that smoking increases the risk of sudden cardiac death .