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Chronic obstructive pulmonary disease and sudden cardiac death: the Rotterdam study
Aims Both sudden cardiac death (SCD) and chronic obstructive pulmonary disease (COPD) are common conditions in the elderly. Previous studies have identified an association between COPD and cardiovascular disease, and with SCD in specific patient groups. Our aim was to investigate whether there is an association between COPD and SCD in the general population.
Methods and results The Rotterdam study is a population-based cohort study among 14 926 subjects aged 45 years and older with up to 24 years of follow-up. Analyses were performed with a (time dependent) Cox proportional hazard model adjusted for age, sex, and smoking. Of the 13 471 persons included in the analysis; 1615 had a diagnosis of COPD and there were 551 cases of SCD. Chronic obstructive pulmonary disease was associated with an increased risk of SCD (age- and sex-adjusted hazard ratio, HR, 1.34, 95% CI 1.06–1.70). The risk particularly increased in the period 2000 days (5.48 years) after the diagnosis of COPD (age- and sex-adjusted HR 2.12, 95% CI 1.60–2.82) and increased further to a more than three-fold higher risk in COPD subjects with frequent exacerbations during this period (age- and sex-adjusted HR 3.58, 95% CI 2.35–5.44). Analyses restricted to persons without prevalent myocardial infarction or heart failure yielded similar results.
Conclusion Chronic obstructive pulmonary disease is associated with an increased risk for SCD. The risk especially increases in persons with frequent exacerbations 5 years after the diagnosis of COPD. This risk indicator could provide new directions for better-targeted actions to prevent SCD.
- Comorbidity
- Cardiovascular mortality
- General population
- Sudden cardiac death
Translational perspective
Sudden cardiac death (SCD) is a major health problem; however, risk stratification remains difficult and probably not all risk indicators have been identified. Chronic obstructive pulmonary disease (COPD) has been associated with an increased risk of cardiovascular disease and with SCD in specific high-risk patient populations. This study shows that COPD is a risk indicator for SCD in the general population and that the risk increases with COPD severity. This provides directions for further measures to prevent SCD.
Sudden cardiac death (SCD) forms a substantial part of cardiovascular mortality, which is the leading cause of death globally,1 with a currently estimated incidence of 4–5 million cases worldwide per year.2 Sudden cardiac death is primarily caused by ventricular arrhythmias3 and risk factors for SCD include male sex, increasing age,2 a history of heart failure or cardiac ischaemia, cardiomyopathies, channelopathies, and alcohol and drug use.4 However, SCD is a heterogeneous outcome with multiple aetiological pathways of which many have not been established. This complicates an adequate risk assessment and prevention plan for SCD.
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death.5 Chronic obstructive pulmonary disease is characterized by a progressive airflow limitation and is associated with a chronic inflammatory response in the airways and lungs.6 Besides these local pulmonary manifestations, systemic effects and comorbidities are frequently present and determine the prognosis of patients with COPD.7,8 Patients with COPD have a two- to three-fold higher risk of developing cardiovascular disease and half of COPD deaths can be attributed to cardiovascular disease.9 Although the underlying mechanisms for this high cardiovascular morbidity and mortality in patients with COPD are not fully established to date, a role for the accompanied hypoxia and hypoxaemia,6 higher heart rate,10 systemic inflammation,6 or recurrent exacerbations has been suggested. Moreover, patients with COPD suffer more frequently from ventricular arrhythmias than controls.11,12 In patients hospitalized for an exacerbation of COPD, atrial fibrillation and ventricular arrhythmias are independent predictors of death at 1 year.13 Furthermore, COPD has also been shown to be an independent predictor of SCD in high-risk patients after a percutaneous coronary intervention and coronary artery bypass graft13,14 and in patients with myocardial infarction.15 However, this association has not yet been assessed in the general population. Therefore, our objective was to assess whether COPD is an independent risk factor for SCD in the general population, and whether COPD, exacerbations, and systemic inflammation modify the association between COPD and SCD.
The Rotterdam study is a prospective population-based cohort study in 14 926 people aged ≥45 years, which started in 1990.16 In addition to regular follow-up examinations at the research facility, participants are continuously monitored for morbidity and mortality through general practitioners and municipality records. The Rotterdam study was approved by the medical ethics committee and all participants gave written informed consent. This study complies with the Declaration of Helsinki.
Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease was diagnosed by an obstructive spirometry (FEV1/FVC < 70%) performed at the research centre visit or, if not available, by a physician based on the combination of clinical history, physical examination, and spirometry.17 The severity of COPD was determined by the forced expiratory volume in 1 s (FEV1), expressed as percentage predicted, according to the modified global initiative for chronic obstructive lung disease (GOLD) criteria (2007): mild COPD (GOLD I, FEV1 ≥ 80%), moderate COPD (GOLD II, 50% ≤ FEV1<80%), and severe COPD (GOLD III, FEV1 < 50%).18 Asthma patients were excluded. The date of incident COPD was defined as the date of obstructive lung function measurement, the date of COPD diagnosis in the medical records or the date of a first COPD medication prescription in someone with established COPD, whichever came first. Medication use was obtained through pharmacy-filled prescription data from seven pharmacies in the region which are all on one computer network. Moderate exacerbations were defined as needing a course of steroids and/or antibiotics and severe exacerbations as needing hospitalization. Frequent exacerbators were defined as COPD participants who had during follow-up on average two or more moderate or severe exacerbations a year.19
Sudden cardiac death
Sudden cardiac death cases were validated independently by two researchers and confirmed by a cardiologist through details from the medical records. In witnessed deaths, SCD was diagnosed according to Myerburg's definition endorsed by the European Society of Cardiology: 'a natural death due to cardiac causes, heralded by abrupt loss of consciousness within one hour from onset of acute symptoms; preexisting heart disease may have been known to be present, but the time and mode of death are unexpected'.20,21 Unwitnessed deaths were coded as SCD if death was unexpected in persons found death, while they were in a stable medical condition 24 h before they were found and without evidence of a non-cardiac cause.22
Statistical analysis
Differences between subjects with and without COPD were studied using Mann–Whitney U and χ2 tests. In SPSS (IBM Corp., Somers, NY, USA), time-dependent cox proportional hazard models were performed to assess the association between COPD and SCD. Follow-up time was determined as the time between study entry or incident COPD date and death or end of study (1 January 2011). We also performed a sensitivity analysis adding the time between cohort entry and incident COPD to the non-COPD follow-up time. All models were adjusted for age and sex, and additionally for all biologically plausible covariates according to the previous literature which changed the risk estimate by >10%. Potential confounders were age (years), sex, height (cm), weight (kg), body mass index (kg/m²), smoking behaviour, pack-years, myocardial infarction, heart failure, coronary revascularisation procedures, systolic blood pressure (mmHg), diastolic blood pressure (mmHg), hypertension, total serum cholesterol (mmol/L), diabetes mellitus, atrial fibrillation, and heart rate corrected QT interval (ms) according to Bazett's formula. As high-sensitivity C-reactive protein (hsCRP) might be an important effect modifier, we investigated this variable in a separate analysis. High-sensitivity C-reactive protein serum levels (mg/L) were categorized as high vs. moderate/low, based on the American Heart Association classification.23 We constructed cumulative survival curves using the Kaplan–Meier method. With regard to the competing risk of non-SCD, we performed a sensitivity analysis using the data augmentation method and unstratified model described by Lunn & McNeil to estimate the hazard ratio (HR) of SCD in comparison with non-SCD.24 More details on the methods including the performed sensitivity analyses are provided in Supplementary material online.
General characteristics
Table 1 shows the baseline characteristics of the study population (n = 13 471) with a median age of 64 years (interquartile range, IQR = 16) at the start of follow-up. Chronic obstructive pulmonary disease subjects were older, more often male, more (current) smokers, had a slightly lower body mass index, higher levels of hsCRP at baseline and had more frequently a medical history of myocardial infarction and coronary artery bypass graft. During a median follow-up of 3229 days (8.84 years; IQR = 3651 days; total of 123 024 person years of follow-up), 5197 (39%) of the participants died of whom 551 died suddenly. Eighty-two (5%) COPD subjects and 469 (4%) subjects without COPD died due to SCD (Figure 1). The SCDs were witnessed in about half of the cases (54%) and the ratio of witnessed vs. unwitnessed SCD was not different for COPD subjects vs. subjects without COPD (P = 0.975). The time of SCD was divided into three equal parts of 8 h and registered in 380 (69%) of 551 SCDs. The data show that SCD subjects with COPD died more frequently during night time (0–8 h; 53%) than SCD subjects without COPD (36%; P = 0.023) (Supplementary material online, Figure S1).
|COPD (n = 1615)
|No COPD (n = 11 856)
|Age (years)
|70 (13)
|63 (15)
|Males (%)
|909 (56)
|4727 (40)
|Smoking status
|Never smoker (%)
|251 (16)
|4361 (38)
|Former smoker (%)
|689 (44)
|4903 (43)
|Current smoker (%)
|632 (40)
|2209 (19)
|Pack-years cigarette smoking
|26 (37)
|3 (23)
|Height (cm)
|170 (13)
|167 (14)
|Weight (kg)
|74.9 (17.0)
|74.6 (17.8)
|BMI (kg/m²)
|25.8 (4.7)
|26.4 (4.9)
|hsCRP (mg/L)
|1.9 (3.0)
|1.5 (2.5)
|Myocardial infarction (%)
|118 (7)
|581 (5)
|Heart failure (%)
|52 (3)
|235 (2)
|Coronary revascularization
|57 (4)
|334 (3)
|CABGa (%)
|41 (3)
|212 (2)
|PTCAa (%)
|19 (1)
|155 (1)
|Systolic blood pressure (mmHg)
|137 (29)
|137 (29)
|Diastolic blood pressure (mmHg)
|75 (16)
|77 (16)
|Total serum cholesterol (mmol/L)
|6.2 (1.6)
|6.1 (1.6)
|Hypertension (%)
|741 (55)
|5344 (56)
|Atrial fibrillation (%)
|71 (5)
|438 (4)
|QTc interval (ms)
|430 (31)
|429 (30)
|Diabetes mellitus (%)
|154 (10)
|1196 (10)
|Potassium (mmol/L)
|4.2 (0.4)
|4.2 (0.4)
|GFR (sex specific ml/min/1.73 m²)
|74.8 (19.5)
|73.6 (19.2)
|Diuretic use
|511 (31.6%)
|1966 (16.6%)
Categorical variables are expressed as numbers (percentage). Values of continuous variables are expressed as median (IQR).There were missings in baseline smoking status (n = 426), pack-years (n = 728), height (n = 1447), weight (n = 1438), BMI (n = 1455), hsCRP (n = 1922), myocardial infarction (n = 161), heart failure (n = 297), coronary revascularization (n = 583), systolic/ diastolic blood pressure (n = 1317), cholesterol (n = 1439), hypertension (n = 2547), atrial fibrillation (n = 1876), QTc interval (n = 1659), potassium (n = 3282), and GFR (n = 3325).
BMI, body mass index; CABG, coronary artery bypass graft; COPD, chronic obstructive pulmonary disease; GFR, glomerular filtration rate; hsCRP, high-sensitivity C-Reactive Protein; QTc, heart rate corrected QT interval according to Bazett's formula; PTCA, percutaneous transluminal coronary angioplasty.
aNumbers overlap.
Association between chronic obstructive pulmonary disease and sudden cardiac death
Figure 2 illustrates the higher probability of SCD for COPD subjects compared with subjects without COPD. Adjusted for age and sex, COPD was significantly associated with an increased risk of dying due to SCD (HR 1.34, 95% CI 1.06–1.70). A stratified analysis in patients without prevalent myocardial infarction nor heart failure nor CABG nor PCI resulted in a comparable age- and sex-adjusted HR of 1.38 (95% CI 1.03–1.85). An additional analysis only including subjects with a study acquired spirometry resulted in an age- and sex-adjusted HR of 3.32 (95% CI 1.77–6.22) of SCD for COPD subjects with an obstructive spirometry compared with subjects with normal spirometry. Supplementary material online, Table S1 demonstrates the risk of SCD according to the severity of airflow limitation. A sensitivity analysis using the stratified Lunn–McNeil method to model the competing risk effect of other causes of death, resulted in an age- and sex-adjusted HR of COPD on SCD of 1.43; 95% CI 1.19–1.67. The cumulative incidence function (CIF) in Supplementary material online represents the higher incidence of SCD and other causes of death for subjects with COPD compared with subjects without COPD (see Supplementary material online, Figure S2). The CIFs for COPD vs. no COPD were statistically significant for SCD (Gray's test; P = 0.0006) and for non-SCD (Gray's test; P < 0.0001). Another sensitivity analysis adding the time between cohort entry and incident COPD to the control follow-up time did not substantially change the estimate.
Figure 2 further illustrates that the distinction of SCD risk according to COPD status occurred ∼2000 days (5.48 years) after the study start (incident COPD date or cohort entry for participants without incident COPD), while the difference for other causes of death was seen much earlier (Supplementary material online, Figure S2). Since the proportional hazard assumption was violated, we evaluated the effect of COPD on SCD using a time-dependent Cox regression analysis stratifying time in more or <2000 days after COPD diagnosis. Within these strata, the proportional hazards assumption was satisfied and adjusted for age and sex, the HR for the period before 2000 days was non-significant (HR 0.66, 95% CI 0.43–1.02), whereas the HR for the period after 2000 days was significantly increased (HR 2.12, 95% CI 1.60–2.82; Table 2). We additionally adjusted the model for covariables which changed the risk estimate by >10%, i.e. only pack-years of cigarette smoking. Chronic obstructive pulmonary disease was associated with an almost two-fold increased risk to develop SCD, independent of age, sex, and pack-years of cigarette smoking (HR 1.93, 95%CI 1.44-2.59; Table 2). The other potential confounders (i.e. height, weight, body mass index, myocardial infarction, heart failure, coronary revascularisation procedure, blood pressure, hypertension, total cholesterol, diabetes mellitus, atrial fibrillation, and heart rate corrected QT interval) did not significantly influence the effect. We did not observe any significant interactions with sympathomimetic respiratory drugs or with cardiac treatment.
|Categorical, all vs. no COPD
|Model 1
|Model 2
|COPD without frequent exacerbations
|COPD with frequent exacerbations
Model 1: age and sex adjusted.
Model 2: adjusted for age, sex, and pack-years of cigarette smoking. The other potential confounders (i.e. height, weight, body mass index, myocardial infarction, heart failure, coronary revascularisation procedure, blood pressure, hypertension, total cholesterol, diabetes mellitus, atrial fibrillation, and heart rate corrected QT interval) did not significantly influence the association.
Time-dependent Cox regression analysis for the period >2000 days of follow-up.
Frequent exacerbations were defined as having at least two moderate or severe exacerbations a year, averaged over the total years of follow-up.
CI, confidence interval; COPD, chronic obstructive pulmonary disease; HR, hazard ratio.
Influence of exacerbations
Regarding the influence of COPD exacerbations, 366 (23%) of 1615 COPD subjects had frequent exacerbations. Thirty-three (9%) frequent exacerbators compared with 49 (4%) COPD subjects without frequent exacerbations died due to SCD. The Kaplan–Meier curve for SCD in Figure 3 illustrates the poorer survival for COPD subjects with frequent exacerbations (log-rank P < 0.001). Adjusted for age, sex, and pack-years of cigarette smoking, the COPD frequent exacerbator phenotype was significantly associated with a more than three-fold increased risk of developing SCD (HR 3.21; 95% CI: 2.08–4.95; Table 2). A sensitivity analysis using the stratified Lunn–McNeil method to model the competing risk effect of other causes of death, resulted in an age- and sex-adjusted HR of the frequent exacerbators on SCD of 2.51 (95% CI: 2.15–2.86). Finally, the cumulative incidence of SCD was significantly higher when COPD subjects had frequent exacerbations (Supplementary material online, Figure S3).
Influence of baseline systemic inflammation
Of the 13 471 subjects, 11 549 (85.7%) had a baseline hsCRP measurement. A linear regression model adjusted for age and sex, demonstrated that the natural logarithm of hsCRP concentration was significantly increased in subjects with COPD and SCD compared with subjects with COPD without SCD (P < 0.05). When stratified according to the level of baseline systemic inflammation, the HR for SCD was significantly increased in COPD subjects with frequent exacerbations having an hsCRP level >3 mg/L (HR 3.67; 95% CI 1.97–6.85; Table 3). In contrast, in all subjects with a low-to-moderate degree of systemic inflammation, the HR for SCD was significantly increased in COPD subjects without frequent exacerbations (HR 1.84; 95% CI 1.16–2.91; Table 3).
|Model 1
|Model 2
|hsCRP ≤ 3 mg/L
|COPD without frequent exacerbations
|COPD with frequent exacerbations
|hsCRP > 3 mg/L
|COPD without frequent exacerbations
|COPD with frequent exacerbations
Model 1: age and sex adjusted.
Model 2: adjusted for age, sex, and pack-years of cigarette smoking. The other potential confounders at baseline (i.e. height, weight, body mass index, myocardial infarction, heart failure, coronary revascularisation procedure, blood pressure, hypertension, total cholesterol, diabetes mellitus, atrial fibrillation, and heart rate corrected QT interval) did not significantly influence the association.
Time-dependent Cox regression analysis for the period >2000 days of follow-up.
Frequent exacerbations were defined as having at least two moderate or severe exacerbations a year, averaged over the total years of follow-up.
CI, confidence interval; COPD, chronic obstructive pulmonary disease; hsCRP, high-sensitivity C-reactive protein; HR, hazard ratio.
In this population-based study in community-dwelling middle-aged and elderly persons, we showed an ∼30% increased risk of SCD in subjects with COPD. The risk almost doubled in the period 2000 days (5.48 years) after the diagnosis of COPD, a trend which was not observed for other causes of death. Among subjects with a higher degree of baseline systemic inflammation, COPD patients with frequent exacerbations had a 3.7-fold increase in the risk of SCD.
An increased risk of SCD in patients with COPD has been previously described in specific patient populations at high risk of SCD.13 Our prospective cohort study demonstrated for the first time that COPD is associated with an increased risk of SCD in the general population, even when the already increased risk of COPD on all-cause mortality was taken into account. There are several factors in persons with COPD that could play a role in the mechanism which ultimately leads to SCD. Chronic obstructive pulmonary disease has been associated with an increased risk of ventricular arrhythmias11,12 and a prolongation of the QTc interval,25 currently the most well-known electrocardiogram-derived risk indicator for SCD.26 QTc prolongation in COPD patients can originate from different mechanisms. First, COPD is associated with autonomic neuropathy, which is associated with QTc prolongation.25 Also, common comorbidities in COPD patients, such as coronary heart disease and heart failure are associated with a prolonged QTc.27 Other factors that are present in persons with COPD are a higher resting heart rate,10 hypoxia and hypoxaemia,6 cardiac ischaemia,4,9 and heart failure4,28 which are all known risk factors for SCD. Although information on time of SCD was incomplete, our data suggest that patients with COPD die more frequently during night time, potentially due to the reduced ventilation and blunted responses to hypercapnia resulting in more ventricular ectopic episodes while they are sleeping.29,30 Since baseline cardiovascular diseases did not have a substantial impact on the association between COPD and SCD, our data suggest that preexisting cardiovascular disease in patients with COPD does not explain the observed association. Moreover, our data suggest that mechanisms through which COPD might raise the risk of SCD act in a severity- or duration-dependent manner since the estimate increased by duration of COPD. One mechanism could be that COPD leads to hyperinflation, followed by remodelling, pulmonary hypertension, cardiac arrhythmias, and subsequently SCD.
Exacerbations could provide another mechanism through which SCD is caused. Suissa et al. recently described that with every exacerbation both the risk of subsequent COPD exacerbations and the risk of mortality increased.31 Elevated biomarkers of cardiovascular morbidity, such as troponine,32 midregional-pro atrial natriuretic peptide,33 and N-terminal-pro brain natriuretic peptide34 (the latter two are both indicators of heart failure) are associated with exacerbation mortality and a higher risk of myocardial infarction and stroke after a COPD exacerbation has been observed.35 Wedzicha et al. described that COPD exacerbations may lead to increased cardiovascular morbidity through systemic inflammation.36 This hypothesis is endorsed by another study that showed increased levels of C-reactive protein (CRP) and interleukin-6 following COPD exacerbations.37 Systemic inflammation in patients with COPD can be evaluated using CRP levels, an acute phase protein.38 C-reactive protein is strongly associated with cardiovascular disease in general,39,40 and SCD41 and COPD specifically.17,38 Our results demonstrate that the effect of frequent exacerbations was modified by the baseline degree of systemic inflammation. Similar to the subgroup of COPD patients with persistent inflammation which demonstrated high incidence of exacerbations and worse survival, the risk of SCD was minimally affected by the degree of airflow limitation.42 Possibly, COPD patients with substantial systemic inflammation develop more atherosclerosis, increasing the risk of coronary heart disease whereby each exacerbation further increases the risk of SCD.
The association between COPD and SCD provides various directions for further research. The first is to unravel the underlying mechanisms. Secondly, effective strategies to reduce the risk of SCD in COPD patients are needed. In addition to increased awareness of COPD as a risk factor for SCD, preventive options such as medical treatment (e.g. β-blockers), placement of implantable cardioverter defibrillator (ICD) or withdrawing QTc-prolonging drugs, should be investigated.
Our study has several strengths and some limitations. First, in previous studies, the association between COPD and SCD has been assessed only in specific patient populations who already had an increased risk of SCD, but not in a general population setting with adjustment for all known confounders. Second, SCD was validated by research physicians blinded to the COPD status of the subject. Another strength of this study is that we have prospectively gathered data on morbidity and mortality events, and on covariables, limiting the risk of information bias. However, some potential misclassification may have occurred by inclusion of unwitnessed deaths, though the percentage of unwitnessed deaths in our study was not different for COPD subjects compared with subjects without COPD. A first limitation is that autopsies and electrocardiography at time of death were rarely performed,2 hampering the evaluation of exact causes of death. However, we applied a universal definition, which is the best method for identification of SCD cases in a population-based study and indicates similar data validity.22 By exclusion of non-cardiac causes in all sudden deaths, we refined sudden deaths to only those of cardiac origin. Secondly, we do not have information on successful resuscitations. Importantly, numbers of subjects with ICD placement were very low, implicating that use of ICD could not distort our results. Another limitation is that lung function measurements were not performed in all study participants at baseline. However, a sensitivity analysis in subjects with spirometry, confirmed the increased risk of SCD in subjects with an obstructive lung function compared with subjects with a normal lung function. Finally, it has previously been suggested that participants in a prospective cohort study are more healthy than non-participants.43 The Rotterdam Study has an overall response rate of 72%. Persons with more severe COPD could have had lower participation rates. However, in our study this would have only resulted in an underestimation of the effect.
In conclusion, our study demonstrated that COPD is a risk factor for SCD in the general population, especially in the period more than 5 years after the diagnosis of COPD. The risk further increases in COPD patients with frequent exacerbations having a higher degree of baseline systemic inflammation. These data could facilitate accurate risk stratification and pave the path to targeted preventive actions for patients with COPD.
Supplementary material
Supplementary material is available at European Heart Journal online.
This work was supported by grants from the Fund for Scientific Research Flanders (FWO) project G035014N, the Netherlands Organisation for Health Research and Development (ZonMw) (Priority Medicines Elderly 113102005 to M.E. and P.R.R.; and DoelmatigheidsOnderzoek 80-82500-98-10208 to B.H.S.). L.L. is the recipient of a Belgian Thoracic Society Fellowship. O.H.F. works in ErasmusAGE, a centre for aging research across the life course funded by Nestlé Nutrition (Nestec Ltd.); Metagenics Inc.; and AXA. The Rotterdam Study is supported by the Erasmus MC and Erasmus University Rotterdam; the Netherlands Organisation for Scientific Research (NWO), the Netherlands Organisation for Health Research and Development (ZonMw), the Research Institute for Diseases in the Elderly (RIDE), the Netherlands Genomics Initiative (NGI), the Ministry of Education, Culture and Science, the Ministry of Health Welfare and Sports, the European Commission (DG XII), and the Municipality of Rotterdam.
The authors thank the study participants, the staff from the Rotterdam Study, and the participating pharmacists and general practitioners.
Conflict of interest: none declared.
- Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: email@example.com.


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...And suddenly everything became complicated.
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Join Date: Jan 2011
Location: Transsexual, Transylvania
Posts: 2
...And suddenly everything became complicated.
So, to start off, I am currently in a relationship with a wonderful, handsome young man, who I am very much in love with. He is also quite polyphobic due to some personal issues. At the beginning of the relationship I told him that I was polycurious, but that it probably wouldn't be much of a problem for me to be monogamous.
But of course, that didn't really turn out to be true, or I wouldn't be posting it here.
Somewhere around the same time that I met my current boyfriend, I also met another person, who I was also somewhat attracted to. When I started a relationship, however, I decided that the best thing to do would be to put such thoughts out of my mind.
Well, that didn't actually work so well. Last night, I was chatting on Facebook with the other boy, and discovered that my feelings for him were, and still are, mutual. Now things are a little more complicated. It was a lot easier to ignore my feelings while I wasn't sure whether or not he felt the same.
I have told my boyfriend about these newly resurfaced feelings, and he's understanding, and has told me that he wants to try to work out his issues about polyamory. However, I know that he's quite scared of this new situation. I don't want to ignore the feelings I have, but I want to wait until my current boyfriend is absolutely comfortable with whatever arrangement we decide on. The other boy has told me that he is willing to wait until this happens.
So, I guess I'm mostly looking for advice for this situation, about how I can support him, and how I can make him feel more comfortable.
Thanks for reading, and thanks in advance for any advice. I'd be really grateful for it.
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X5 Superlite
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Loving It So Far....Ive owned the X5 for about a month now - and its great. The best part about it is how light weight it is. My hand used to get tired mid-way through drying my hair. It also gets super hot, which is great for my thick hair. I cant say that the drying time has been cut down much - but my hair does look more shiny (yet with volumn), and I no longer need to use a flat iron/curling iron after blow drying to get that shine. I have mid-lenght, wavy thick hair. I picked the X5 honestly because after a lot of research I couldnt really tell the difference between the different features - I went with the X5 simply because Glamour Magazine had given it high reviews. Good luck finding the perfect hair dryer for you.Aug 22, 2007Rebecca / NYC
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Great For Frizzy HairI love this dryer. I hate blow drying my hair because its super thick and frizzy. But this dryer made it MUCH easier. It drys fast and I can even go without having to use a flat iron after which I have NEVER been able to do. The dryer is really light weight too.Jul 19, 2007Sandy / Hermosa Beach, CAHAIR TYPEDry Hair
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Property Location
With a stay at Best Western Elko Inn in Elko, you'll be in the entertainment district and minutes from Elko Convention Center, and close to Northeastern Nevada Museum. This hotel is within close proximity of Great Basin College and Western Folklife Center.
Make yourself at home in one of the 109 air-conditioned rooms featuring refrigerators and microwaves. Flat-screen televisions with cable programming provide entertainment, while complimentary wireless Internet access keeps you connected. Private bathrooms with shower/tub combinations feature complimentary toiletries and hair dryers. Conveniences include desks and complimentary weekday newspapers, and housekeeping is provided daily.
Don't miss out on the many recreational opportunities, including a 24-hour health club, an indoor pool, and a spa tub. This hotel also features complimentary wireless Internet access, a picnic area, and barbecue grills.
A complimentary hot/cold buffet breakfast is included.
Business, Other Amenities
Featured amenities include a business center, express check-out, and complimentary newspapers in the lobby. Free self parking is available onsite.
You must present a photo ID when checking in. Your credit card is charged at the time you book. Bed type and smoking preferences are not guaranteed.Your reservation is prepaid and is guaranteed for late arrival. The total charge includes all room charges and taxes, as well as fees for access and booking. Any incidental charges such as parking, phone calls, and room service will be handled directly between you and the property.


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Estimated delivery date: 3 (based on standard shipping).
We offer free shipping on orders over $99, and free returns and exchanges for up to 30 days.


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Check in from 14h / Check out prior to 11h
Beppuwan Royal Hotel: Find photos, reviews, information, amenities and compare prices for 4 stars hotels in Hiji, Japan.
Beppuwan Royal Hotel features a mineral bath, an outdoor pool and a bike service. Popular facilities, such as a swimming pool and a sauna, ensure a satisfying stay in Hiji.
Hotel description
Beppuwan Royal Hotel Oita provides 287 air conditioned rooms filled with all the necessities to ensure a comfortable stay. A refrigerator, cable/satellite channels and a hair dryer are also provided.
Beppuwan Royal Hotel is less than a 45-minute drive from Oita Airport. It is also a short car ride from Beppu and Oita.
Hotel features
Restaurant, Air Conditioned, Refrigerator, Cable / Satellite TV, Hair Dryer, TV
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4.3 km


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HUMBOLDT – Harold H. Hinners, 81, of rural Humboldt passed away October 11, 2013. Funeral services will be 10:30 a.m. Wednesday at the Oak Hill Baptist Church with Pastor Doug Wolter officiating. Interment will be in Union Cemetery, Humboldt with full military rites by the Adams American Legion Post 119 and Sathers-Odgaard VFW Post 5240. Visitation is from 5-8 p.m. Tuesday at the Mason-Lindhart Funeral Home in Humboldt.
Harold is survived by his beloved wife of 52 years, Anita Hinners of Humboldt; children, Julie Fridolfson of Fort Dodge, Joan "Joni" (Dan) Noack of Waukee, and Wade (Lauri) Hinners of Ames; grandchildren, Brittani Rucker of West Des Moines, Rebekah Noack of Winona Lake, IN, Bethany Noack of Waukee, Benjamin Hinners and Sarah Hinners both of Ames; sisters-in-law, Marilyn Hinners of Humboldt, Marilyn Hundertmark of Humboldt, Donna (Ralph) Olson of Humboldt, Bev Solbeck of Humboldt; and his nieces and nephews who often thought of him as a father. He was preceded in death by his parents; sisters, Junis (Frank) Rezabek, Hazel (Leonard) Madsen, Irene (Zeb) Hamilton, and Esther (Ken) Cudd; and his brother, Ernest Hinners; brothers-in-law, Norval Hundertmark and Bob Solbeck.


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Juicy Enlightenment
Monday, January 27, 2014 from 7:00 PM to 10:00 PM (PST)
Who's Going
San Francisco, California
London, United Kingdom
Florence, Italy
Event Details
Many years ago Reid Mihalko came up with this genius playshop and tonight he is allowing us to "borrow" the format for YOUR viewing pleasure.....
Watch and Learn as Real Sex Educators Go Head To Head and Reveal Their Best Bedroom Moves...
What better way to learn about practical sex education that you can actually use than to watch two sex educators literally go head to head?
Let's face it, sex is one of the few things we're not allowed to learn by watching others. You go to a fancy dinner. You don't know which spoon to use. You watch to see what spoon everyone else uses... But don't know what to do how in the bedroom, or want to add a few tricks to your repertoire? No such luck!
Until now...
Tonight's Iron Slut Sex Educators:
Monique Darling
Lawrence Lanoff
Sabrina Morgan
Charlie Glickman
(maybe a surprise or two)
COST: $30 advanced, on-line tickets, $25 each for twosomes, for Threesomes and Moresomes! $40 day-of at the door
Suite number will be given to attendees only. Free parking and BART accessible!
Show up to this Rated-R and NC-17 workshop designed to empower adults around their sex lives and get folks smiling!
Show up to this fun-filled, 3 hour workshop and learn:
- What sex educators do under the covers and how
- Their best tips and tricks (and probably not the kind you read about in Cosmo)
- Their favorite, black belt sexy-sexy time moves!
- And much, much more...
We can't promise you badly dubbed voice-overs or high-jinx dramma like television's Iron Chef, but we can promise you some down-to-earth, applicable sex and relationship education. The only theme ingredient is education!
Iron Slut is a wealth of sex geekery and informative experience that you don't want to miss.
If you were a big fan of "I'll show you mine, if you show me yours" as a kid, or you always wished there was a reality show called "Shagging With the Stars," then this workshop might be for you. Tell your friends. Bring a date. Bring a note book, too, while you're at it!
Because of this workshop's explicit and frank nature and live demonstrations, no one under 18 admitted. Please try to arrive on time. And, as with all of Reid's workshops, you can always leave early.
About Your World Renowned Sex Educators Extraordinaire:
Lawrence Lanoff, Sedona, AZ, one of the most fascinating people on the teaching landscape is Lawrence Lanoff. Truly a renaissance man, Lawrence is a film director, photographer, author… and a deeply enlightened healer and teacher. He calls himself a "rubber meets the road kinda guy" as he applies this practical essence to his artistic and spiritual skills over a 20 year span, to an amazing array of disciplines, starting with a couple of dream jobs – the directing of movies and as a photographer for Playboy Magazine.
Over the past several years, Lawrence has been in a process of refining his radical teachings, leading people into a new kind of freedom, literally deprogramming them from the sleep imposed by cults and religions. What is slowly evolving is a revolutionary new theory of consciousness that incorporates evolution, symbolism, metaphor, neurobiology, and their relationship to healing, spiritual evolution, and neuro-economics — the neural pathways that influences our deepest feelings about self worth and money, and, of course, sex and relationships. www.lawrencelanoff.com
Monique Darling, San Diego, CA, is the founder of Divine Interludes which provides workshops and experiential play-shops in the art of Tantra and conscious loving. She has studied and taught with renowned Tantra teachers and extraordinary workshop facilitators since 1990 and is a certified Cuddly Party Facilitator. She has been featured on TLC and The Dr's and has been interviewed by magazines across the USA. Monique is dedicated to empowering others utilizing her vast repertoire of cutting-edge teachings. She specializes is helping others reclaim their power and natural sensuality by transmuting fear and repression into courage, self-love and freedom. She guides from a place of understanding and her natural exuberance is infectious! She is available for private sessions, experiential workshops and Cuddle Parties. www.divineinterludes.com
Charlie Glickman PhD is a sex coach, a certified sexuality educator, and an internationally-acclaimed speaker. He's certified by the American Association of Sexuality Educators, Counselors, and Therapists, and has been working in this field for over 20 years. His areas of focus include sex & shame, sex-positivity, queer issues, masculinity & gender, communities of erotic affiliation, and many sexual & relationship practices. Charlie is also the co-author of The Ultimate Guide to Prostate Pleasure(http://www.prostatepleasureguide.net/). Find out more about him on his website (www.charlieglickman.com) or on Twitter (www.twitter.com/charlieglickman) and Facebook (www.facebook.com/charlie.glickman).
Sabrina Morgan, Oakland, CA, is a kink educator, sex worker advocate, and workshop facilitator. Working directly with others' sexuality has given her a deft sensitivity to the needs of those exploring new facets of their selves and an understanding of the power of hands-on sex and kink education for adults. She speaks regularly at conferences and presents workshops internationally on topics such as kink, sex work advocacy and conscious sexuality. She is available for both couples and one-on-one sessions as well as distance coaching. Follow Sabrina on Twitter (@SabrinaMorgan) and Facebook ( http://facebook.com/ms.sabrina.morgan), or keep up at http://www.sabrinamorgan.com/
When & Where
1080 23rd Ave
Monday, January 27, 2014 from 7:00 PM to 10:00 PM (PST)
Add to my calendar


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Pension San Joaquin: Find photos, reviews, information, amenities and compare prices for 2 stars hotels in Granada, Spain.
Pension San Joaquin offers a charming setting when in Granada. It is close to Monastery of Saint Jerome, eateries and shops.
Hotel description
Pensión San Joaquín has luggage storage, a ticket service and a 24-hour reception. Wi-Fi is also available.
Pension San Joaquin Granada has 40 comfortable rooms that are ideal for travellers on a budget. Disabled access rooms are available on request.
San Joaquín is ideally situated for discovering Granada with Granada Cathedral within walking distance. Castril Palace and Plaza Nueva are also within 20 minutes' walk.
Hotel features
Disabled Access, Air Conditioned, Non-Smoking Rooms, TV, Disabled Accessible Rooms, En suite, Private Bathroom, Vending Machines
Elevator / Lift, 24 Hour Reception, Safe-Deposit Box, Meeting Rooms, Photocopier, Ticket Service, Luggage Storage
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Internet Connection (wireless)
Private Toilet, Gay/Lesbian Friendly
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50 Cent Rolls Into SXSW
Rapper confirms a Music Conference interview
By Kevin Curtin,
1:00PM, Tue. Mar. 5, 2013
Having already announced appearances by hip-hop kings (Master P), princes (Kendrick Lamar), and crusaders (Killer Mike), South by Southwest now puts forth rap enforcer 50 Cent, slated for a SXSW Interview on Saturday, March 16, at the Austin Convention Center.
On his recent single "Major Distribution," off the long delayed Street King Immortal LP (now slated for a spring release), Fif comes off defensive:
"I'm a rap tycoon/ Make a hundred mil by June/ Now who the fuck said I can't rap, Jack?"
No matter, the 37-year-old Queens native's mic skills have become increasingly secondary in the scope of his massive brand extensions, which include acting, a signature Vitamin Water flavor, his SMS headphones company, and authoring several books including his latest, Formula 50: A 6-Week Workout and Nutrition Plan That Will Transform Your Life, in which the hulking rapper shares bodybuilding and dieting techniques.
Expect talk about the possibility of a G-Unit reunion with original members Lloyd Banks and Tony Yayo, which has become a hot topic in the hip-hop press after 50 gave fans hope in a recent interview with ESPN. These SXSW sit-downs, which in the last two years have featured tenured rappers Nas and Chamillionaire, may be as up close and personal as anyone gets to these mad MCs.
Of course 50 Cent attended SXSW last year, performing his Get Rich or Die Tryin' album in its entirety at the Shady Records 2.0 showcase, joined by label boss Eminem on the song "Patiently Waiting." While the bulletproof vested MC has no scheduled musical performances this year, don't rule it out.
This is, after all, SXSW.
Abby Johnston, May 30, 2014
Chase Hoffberger, March 12, 2014
Jan. 19, 2017
Jan. 20, 2017
50 Cent, Master P, Kendrick Lamar, Killer Mike, Nas, Chamillionaire, G Unit, Lloyd Banks, Tony Yayo, Eminem


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UKIP's tactical error during referendum came at a huge cost
UKIP will spend the next few weeks engaged in a leadership battle following the resignation of Nigel Farage.
The future prospects of the party itself are unclear; some had argued that a narrow Remain victory would have boosted UKIP's electoral fortunes in the same way that the close "No" vote in the Scottish referendum had benefited the SNP. Instead the battle to leave the EU has been won, raising the question over what the People's Army will now be fighting for. Farage himself has said the party will in the future "attract a significant vote" and that "UKIP's best days may be yet to come."
Despite this, UKIP faces uncertain times for at least three reasons. First, it must replace the irreplaceable Nigel Farage. Say what you like about him – and everyone does – but there is no doubt that he has proven himself to be an outstanding politician. It is because of him that UKIP started polling high enough to threaten scores of Conservative-held marginal seats, forcing the Tories to promise an EU referendum in an (ultimately successful) attempt to pull back support. Sorry, but Steven Woolfe, Diane James and Neill Hamilton just don't come close.
Second, their electoral power base and source of significant funding – their 22 MEPs – will disappear along with the UK's membership of the European Union.
Third, UKIP has been fighting internal battles for some time. One of its most able media performers, Suzanne Evans, has been suspended after falling out with the party leadership while its only MP, Douglas Carswell, has been ostracized. Both have been blocked from running for leader by recently amended party rules.
All of these problems are compounded the huge tactical error UKIP made in the midst of the EU referendum campaign.
The Electoral Commission was handed the task of designating an official "Remain" and "Leave" campaign, both of which would be handed £600,000 of public money, the right to contact each elector by Royal Mail freepost and prime-time TV slots for referendum broadcasts. UKIP's error was to try and win the prize of officially-designated "Leave" campaign for itself – initially in the guise of Leave.EU and then as Grassroots Out. While claiming to have cross-party support, this merely amounted to a handful of backbench Conservative and Labour MPs. Vote Leave was backed by nearly 150 MPs including Cabinet Ministers, Labour MPs and even UKIP's only MP. Vote Leave's organisational ability, campaign experience and fund-raising capacity was in a different league to Grassroots Out. Most of this seemed to be overlooked by the Electoral Commission which found Vote Leave only slightly better suited to being the official campaign. Despite the cack-handed approach of the much-discredited elections watchdog, the truth is that the UKIP-backed Grassroots Out was never going to get the nod ahead of Vote Leave.
In seeking to win the designation for itself, UKIP missed the opportunity to entrench itself within the official campaign. The personality clash at the top of the rival campaigns between UKIP's Farage and Aaron Banks, and Vote Leave's Dominic Cummings and Matthew Elliott, has been well reported. But this isn't the level of the campaign that I'm referring to. UKIP should have tried to have as many of its own regional staff and county/constituency volunteers in corresponding positions within Vote Leave. This would have given them access to something far more valuable than £600k and some TV time: data. Vote Leave collected large amounts of data on volunteers and electors. Access and management of this data was tightly controlled by Vote Leave and prevented anyone except senior volunteers using it. Those who could use it found sometimes hundreds of volunteers in each constituency (from all parties, and none) at their disposal. Many of Vote Leave's co-ordinators came from UKIP – but there were plenty of UKIP volunteers who stayed with Grassroots Out or UKIP itself. I expect those from UKIP reading this who disagree with me probably don't put the same value on volunteer and elector data that I do. Having this data post-referendum would have been an enormous boost to a party that doesn't have the historic data that more established parties do. In my view, seeking to head up the official campaign instead of controlling it from the neck down was a tactical error that came with a huge opportunity cost.
I predicted in 2012 that UKIP wouldn't win any parliamentary seats and I think they look even less likely to win any in 2020 – unless they get lucky. UKIP's electoral fortunes will rise significantly if the Conservatives fail to make a success of Brexit negotiations and Labour's civil war leaves it ill-prepared to fight off UKIP in northern seats. Given how unpredictable politics has been in the past three weeks, it's difficult to say with any certainty what will happen over the next four years.
10 reasons you shouldn't bet against Zac Goldsmith winning London
A poll for LBC this week has a 10 point lead for Labour's Sadiq Khan in the race to become Mayor of London. Trailing 55-45 is the Conservatives' Zac Goldsmith, with James Kirkup listing four reasons he'd bet £50 against the Richmond MP succeeding Boris Johnson. More damning was Alice Thomson in The Times (£), arguing that not only would Goldsmith lose but that the Tory high command wouldn't shed a tear if he did; a Labour win would help Jeremy Corbyn survive until the 2020 general election – a price worth paying, some might say.
To all of that, I say don't go down the bookies just yet. Here's 10 reasons not to bet against Zac Goldsmith being the next Mayor of London.
1. Turnout
The lower the turnout, the harder it is to predict the result. In 2012, Boris went toe-to-toe with fellow political heavyweight Ken Livingstone. Having faced each other in 2008, this was round two and the gloves were off. Despite impressive ground campaigns on both sides, huge media coverage and millions spent, the turnout was a ridiculously low 38%. It may be lower for Goldsmith vs Khan, and therefore it's anyone's game.
2. Zac may steal second preferences of Green voters from Labour
Green peer Baroness Jenny Jones told the Standard last May, "Most, though not all, Greens would usually vote Labour in a second vote in an election like the London mayoralty. But if Zac Goldsmith is standing, it's a different scenario. Many of us very much like that he comes across as very green and committed and passionate."
3. And Lib Dem second preferences too
In just five years, he reduced the Liberal Democrat vote share in his Richmond Park and North Kingston constituency from 43% to 19%. Brutal.
4. As well as capturing UKIP second preferences
Well, he will if he takes the right stance on the EU referendum. Despite a strong track-record of Euroscepticism, he has only gone has far as to say (on the Today programme earlier this week) that "It may be that [Cameron] comes back with reforms that are not adequate for people who are sceptical of the EU. If that is the case I will, along with those other people, vote to come out."
5. Policy platform yet to be set out
While rival Sadiq Khan has been firing off policies on housing (50% affordable housing target, London Living Rent) and transport (four year rail fares freeze, first year cut and then freeze in bus fares), the Goldsmith campaign has until now kept its powder dry.
6. The united nations of London
The Daily Mail recently highlighted that residents originally from India dominate ten of the capital's 32 boroughs, while research of voting patterns at the general election found that among Hindus, 49% supported the Conservatives compared to 41% who voted Labour.
7. The best there is
The Goldsmith campaign is headed by CTF Partners. Lynton Crosby's firm not only masterminded last year's stunning Conservative election victory but was also behind Boris Johnson's two successful mayoral campaigns. While the Times article above is right to point out that "the newly knighted Wizard of Oz… will not be personally involved in this contest", the campaign is being headed by Mark Fullbrook, who with pollster Mark Textor makes up the trio that is CTF. Deputy Director of the 2012 Mayoral campaign, Goldsmith has hired the best there is.
8. Closeness to Corbyn – motivating Conservatives
Dame Tessa Jowell was the initial favourite to win the Labour nomination, but a wave of hard-left supporters who had signed up to support Corbyn also swept Khan to victory. Khan nominated Corbyn for Labour leader (although he voted for Andy Burnham) and owes his current position to Corbyn supporters. The Tory campaign will play on this – even though Corbyn's support in London is strong – because anti-Corbyn sentiment is even stronger among Tories in the capital; motivating them on a low turnout will be crucial.
9. Distance from Corbyn – demotivating Labour activists
The more the Tories seek to lump Khan in with Corbyn, the more he will try to move away. He's been doing this from day one of his campaign. He slated Jez for not singing the national anthem and his comments about condoning terrorism as "particularly dangerous in London" were interpreted as a savage rebuke to Corbyn and co. How this will go down with the rank and file remains to be seen.
10. Top Tories want Goldsmith to win. Many Labour MPs do too
Toasting a silver lining is not the same as welcoming a black cloud. Yes, a Labour victory would help bolster the embattled Corbyn – good news for the Tories in the long term. But any suggestion that the Conservative Party is tempted to soft peddle for Zac Goldsmith is a great exaggeration. A loss in May would be followed by the tumult of the EU referendum and, later on, what could be a bruising battle to choose a new party leader. The Tories, including those at the top, want a win in London. The same can't be said for those many moderate Labour MPs in London who may use a Mayoral defeat to oust Corbyn in the hope of saving their party in time for 2020.
Of all of these reasons, number one is the most important. It's all to play for.


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International factory productivity gains in 2006
September 28, 2007
Manufacturing labor productivity increased in 2006 in 15 of the 16 economies under comparison.
The Republic of Korea and Taiwan had the largest productivity increases (+10.8 and +6.9 percent, respectively).
The U.S. productivity increase of 2.4 percent placed it eleventh among the 16 economies compared, and was less than the average annual growth rate since 2000.
Manufacturing output increased in 14 of the 16 economies in 2006. Korea, Sweden, and Taiwan continued to be the leaders in the growth of output, as they have been for the last decade. In 2006, growth in manufacturing output in Germany, Norway and Denmark was also noticeably higher than their average annual rates of increase over the 1979-2006 period. The U.S. increase of 3.3 percent was also above its average annual increase since 1979 of 2.9 percent.
While 14 of the economies had increases in output in 2006, 9 economies had reductions in total hours worked in manufacturing. The United Kingdom had the greatest decline in hours in 2006, followed by Korea and France. Total hours worked increased in the United States by 0.9 percent, and by over 2 percent in Japan and Italy.
These data are from the Foreign Labor Statistics program. Data are subject to revision. Additional information is available in "International Comparisons of Manufacturing Productivity and Unit Labor Cost Trends, 2006" (PDF) (TXT), news release USDL 07-1456.
Bureau of Labor Statistics, U.S. Department of Labor, The Economics Daily, International factory productivity gains in 2006 on the Internet at https://www.bls.gov/opub/ted/2007/sept/wk4/art05.htm (visited January 21, 2017).
Recent editions of Spotlight on Statistics
Workplace injuries and illnesses and employer costs for workers' compensation
Workplace injury and illness data and the costs to employers for workers' compensation in natural resources, construction, and maintenance occupations.
A look at the future of the U.S. labor force to 2060
Projected long-term trends in the growth, size, and composition of the labor force.
Union membership in the United States
Historical trends in union membership among employed wage and salary workers; union membership by a variety of demographic characteristics.
A look at healthcare spending, employment, pay, benefits, and prices
Spending on healthcare, current and projected employment in the industry, employer-provided healthcare benefits, healthcare prices, and pay for workers in healthcare occupations.
Self-employment in the United States
Trends in self-employment by various demographic and socioeconomic characteristics, including both the unincorporated and the incorporated self-employed, as well as data on paid employees who work for the self-employed.


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qoutation marks
where should the period be at the end of this qoutation, after the qoutation mark or before?
See example:
For example, Participant 9 described that a supervisor had initiated the idea and "so I took it on as part of my job."
2 answers
Please read my full post as referenced by Lewis. I will, however, summarize here:
The American style is to always place commas and periods inside the quotation mark. The British style is to place commas and periods outside unless the original text being quoted includes a comma or period.
Both the American and British styles agree on the placement of other punctuation, such as colons, semi colons, exclamation points, and question marks. These are placed outside unless the original included the punctuation.
I hope this helps.
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|answered Oct 12 '12 at 03:26 Jeff Pribyl Grammarly Fellow
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|answered Mar 27 '16 at 16:24 Keniesha Johnson New member
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