Coronary Heart Disease Hazard Ratio Research Articles

A sialoadenectomy is associated with an increased risk of coronary heart disease: A three-year follow-up study.

Little is known regarding the long-term adverse effects of a sialoadenectomy. The purpose of this study was to estimate the risk of coronary heart disease (CHD) among patients receiving a sialoadenectomy procedure by utilizing a cohort study based on a population-based database in Taiwan. This study retrieved data of the study sample from the Longitudinal Health Insurance Database 2005. This retrospective cohort study included 608 patients who underwent a sialoadenectomy and 1824 propensity score-matched comparison patients. We individually tracked each sampled patient for a 3-year period from their index date to discriminate those who subsequently received a diagnosis of CHD during the follow-up period. We found that respective incidence rates of CHD during the 3-year follow-up period were 3.87 (95% confidence interval (CI): 3.01–4.91) and 1.79 (95% CI: 1.45–2.18) per 100 person-years for patients who did and those who did not undergo a sialoadenectomy. The stratified Cox proportional analysis revealed that the hazard ratio of CHD during the 3-year follow-up period was 2.43 (95% CI: 1.77–3.33) than comparison patients. This study demonstrates an association between sialoadenectomy and CHD.

Cardiovascular disease mortality in relation to physical activity during adolescence and adulthood in Japan: Does school-based sport club participation matter?

We examined potential associations of sport club participation during adolescence and sports-related physical activity during adulthood with mortality from cardiovascular diseases (CVD) in a Japanese population. Between 1988 and 1990, 29,526 men and 41,043 women aged 40–79 years responded to a questionnaire including questions about the frequency of sports participation at baseline and sport club participation during junior/senior high school. Subjects were followed-up until the end of 2009, and 4230 cardiovascular deaths (870 CHD, 1859 stroke) were identified. Cox proportional-hazard regression models were used to estimate hazard ratios (HR). During the first-two thirds of the follow-up – where the proportional hazards assumption was met – the multivariate-adjusted HR (95% confidence interval) for total CVD mortality was 0.77 (0.61–0.98) among men and 0.82 (0.61–1.10) among women who were physically active at baseline (≥5 h/week versus 1–2 h/week). The corresponding HRs for coronary heart disease (CHD) mortality were 0.65 (0.39–1.07) and 0.40 (0.17–0.91), respectively. The combined associations of sports participation during adulthood and adolescence were also examined. Among men who participated in sports for ≥5 h/week at baseline, the multivariate-adjusted HR for those who also engaged in sport club activities during adolescence was 0.89 (0.61–1.30) for total CVD mortality and 0.24 (0.08–0.71) for CHD mortality when compared to non-participants. Among women, no statistically significant differences were found between sport club participants and non-participants. In conclusion, participating in sport clubs during adolescence might lead to a more pronounced risk-reduction for CHD mortality among men who also participate in sport activities during adulthood.

Use of BMI as the marker of adiposity in a metabolic syndrome severity score: Derivation and validation in predicting long-term disease outcomes

BackgroundEstimates of adiposity in evaluating the metabolic syndrome (MetS) have traditionally utilized measures of waist circumference (WC), whereas body mass index (BMI) is more commonly used clinically. Our objective was to determine if a MetS severity Z-score employing BMI as its measure of adiposity (MetS-Z-BMI) would perform similarly to a WC-based score (MetS-Z-WC) in predicting future disease. MethodsTo formulate the MetS-Z-BMI, we performed confirmatory factor analysis on a sex- and race/ethnicity-specific basis on MetS-related data for 6870 adult participants of the National Health and Nutrition Survey 1999–2010. We then validated this score and compared it to MetS-Z-WC in assessing correlations with future coronary heart disease (CHD) and Type 2 diabetes mellitus (T2DM) using Cox proportional hazard analysis of 13,094 participants of the Atherosclerosis Risk in Communities study and Jackson Heart Study. ResultsLoading factors, which represent the relative contribution of each component to the latent MetS factor, were lower for BMI than for WC in formulating the two respective scores (MetS-Z-BMI and MetS-Z-WC). Nevertheless, MetS-Z-BMI and MetS-Z-WC exhibited similar hazard ratios (HR) toward future disease. For each one standard-deviation-unit increase in MetS-Z-BMI, HR for CHD was 1.76 (95% confidence interval [CI]: 1.65, 1.88) and HR for T2DM was 3.39 (CI 3.16, 3.63) (both p < 0.0001). There were no meaningful differences between the MetS-Z-WC and MetS-Z-BMI scores in their associations with future CHD and T2DM. ConclusionsA MetS severity Z-score utilizing BMI as its measure of adiposity operated similarly to a WC-based score in predicting future CHD and T2DM, suggesting overall similarity in MetS-based risk as estimated by both measures of adiposity. This indicates potential clinical usefulness of MetS-Z-BMI in assessing and following MetS-related risk over time.

Meat intake and incidence of cardiovascular disease in Japanese patients with type 2 diabetes: analysis of the Japan Diabetes Complications Study (JDCS).

Excessive meat intake has been researched as a major cause of cardiovascular disease (CVD) among healthy adults, but data on this topic in Asian patients with diabetes are sparse. The quantity and variety of available meats vary widely between Asian and Western countries. As part of a nationwide cohort study we investigated the relationship between meat intake and incidence of CVD in Japanese patients with type 2 diabetes aged 40-70 years with HbA1c ≥ 6.5%. Analyzed were 1353 responders to a baseline dietary survey assessed by the Food Frequency Questionnaire based on food groups. Primary outcome was the 8-year risk of a CVD event, including coronary heart disease (CHD) and stroke. Cox regression analyses estimated hazard ratios (HRs) for dietary intake adjusted for age, gender, body mass index, HbA1c, smoking, energy intake, and other confounders. Mean meat intake in quartiles ranged from 9.9 to 97.7g/day. After adjusting for confounders, HRs of CHD in the 2nd, 3rd, and 4th quartiles for meat intake compared with the 1st quartile were 2.84 (95% confidence interval 1.29-6.24, p = 0.01), 3.02 (1.36-6.70, p < 0.01), and 2.99 (1.35-6.65, p = 0.01), respectively. In two groups according to meat intake, patients consuming ≥ 20g/day of meat had a 2.94-fold higher risk of CHD than those consuming < 20g/day (p < 0.01). There was no significant association of stroke with meat intake. An elevated incidence of CHD in Japanese patients with type 2 diabetes was associated with high meat intake.

Abstract MP054: Associations of Monounsaturated Fat From Plant and Animal Sources With Coronary Heart Disease Risk

Background: The association between monounsaturated fat (MUFA) intake and coronary heart disease (CHD) risk remains unclear. We aimed to investigate whether MUFA from plant foods (MUFA-P) and animal foods (MUFA-A) show different associations with CHD risk in two large prospective studies of U.S. men and women. Method: We calculated MUFA-P and MUFA-A among 60,931 women in the Nurses’ Health Study (1990-2012), and 28,445 men in the Health Professionals Follow-Up Study (1990-2010). Diet was assessed by validated food-frequency questionnaire every 4 years. CHD incidence was self-reported and confirmed by review of medical records or death certificates. Result: MUFA-A (median intake: 5.8-6.1% energy) was highly correlated with saturated fat (SFA; spearman correlation [ r ] =0.81-0.83) but not polyunsaturated fat (PUFA, r =0.04 -0.19), whereas MUFA-P intake (median: 5.3-5.4.9% energy) was strongly correlated with PUFA(r=0.61 for both cohorts) but not SFA ( r =0.20-0.21; All P&lt;0.001). In multivariate models adjusted for demographic, lifestyle, and dietary factors, hazard ratios of CHD (HR, 95% confidence interval[95%CI]) from low to high total MUFA quintiles were 1 (reference), 0.92 (0.83, 1.02), 1.03 (0.93, 1.05), 0.89 (0.79,1.00). 0.95(0.873, 1.08; P trend =0.42). For MUFA P these were 1(reference), 0.98 (0.89, 1.07), 0.90 (0.82, 0.99), 0.85 (0.77, 0.93), and 0.86 (0.78, 0.94; P trend &lt;0.001) and for MUFA-A 1(reference), 1.09 (0.99, 1.20), 1.22 (1.11, 1.35), 1.26 (1.13, 1.39), and 1.33 (1.19, 1.48; P trend &lt;0.001). In the energy-density model, CHD risk was lower when MUFA-P iso-calorically replaced 1% energy from total SFA (HR [95%CI]: 0.96[0.92, 1.00]; P=0.03), with no significant changes when MUFA-A replacing SFA (HR [95%CI]: 1.01[0.95, 1.07]; P=0.76). When grouping fat intake as the sum of animal MUFA plus saturated fat and the sum of plant MUFA plus PUFA, the HR (95%CI) of CHD was 0.96 (0.95, 0.98; P&lt;0.001) for replacing 1% energy from the former with the latter. Conclusion: Because MUFA compositions of animal and plant origins are largely similar, our data suggested other components in plant and animal foods may lead to the observed different associations of MUFA-P and MUFA-A with CHD risk. These findings provided a possible explanation on current controversies regarding MUFA intake and CHD risk, and further support health benefit of MUFA intake.

D-dimer and the Risk of Stroke and Coronary Heart Disease

D-dimer, a biomarker of coagulation, is higher in blacks than in whites and has been associated with stroke and coronary heart disease (CHD). It was our objective to assess the association of higher D-dimer with stroke and CHD in blacks and whites. REGARDS recruited 30,239 black and white participants across the contiguous US and measured baseline D-dimer in stroke (n=646) and CHD (n=654) cases and a cohort random sample (n=1,104). Cox models adjusting for cardiovascular risk factors determined the hazard ratio (HR) for increasing D-dimer for cardiovascular disease with bootstrapping to assess the difference in HR for CHD versus stroke by race. D-dimer was higher with increasing age, female sex, diabetes, hypertension, pre-baseline cardiovascular disease and higher C-reactive protein (CRP). Accounting for cardiovascular risk factors, each doubling of D-dimer was associated with increased stroke (hazard ratio [HR] 1.15; 95 % confidence interval [CI] 1.01, 1.31) and CHD (HR 1.27; 95 % CI 1.11, 1.45) risk. The difference in the HR between CHD and stroke was 0.20 (95 % CI >0.00, 0.58) for blacks and 0.02 (95 % CI -0.30, 0.27) for whites. CRP mediated 22 % (95 % CI 5 %, 41 %) of the association between D-dimer and CHD and none of the association with stroke. Higher D-dimer increased the risk of stroke and CHD independent of cardiovascular risk factors and CRP, with perhaps a stronger association for CHD versus stroke in blacks than whites. These findings highlight potential different pathophysiology of vascular disease by disease site and race suggesting potential further studies targeting haemostasis in primary prevention of vascular disease.

Serum bicarbonate concentration and the risk of cardiovascular disease and death in type 2 diabetes: the Fremantle Diabetes Study.

BackgroundSerum bicarbonate is associated with mortality, heart failure (HF) and progression of renal failure in studies of healthy people and patients with chronic kidney disease, but the significance of these observations in unselected patients with diabetes in the general population is unknown. The aim of this study was to determine whether serum bicarbonate was associated with mortality and cardiovascular disease risk in type 2 diabetes.MethodsBaseline serum bicarbonate was available for 1283 well-characterized community-based patients (mean ± SD age 64.1 ± 11.3 years, 48.7 % males) from the longitudinal observational Fremantle Diabetes Study followed for a mean of 12 years. Associations between serum bicarbonate and mortality, coronary heart disease (CHD) and incident HF were analysed using Cox proportional hazards regression.ResultsSerum bicarbonate was independently and negatively associated with incident CHD. For each 1 mmol/L increase in bicarbonate, the hazard ratio for CHD was 0.95 (95 % confidence interval 0.92–0.99) after adjustment for age as time scale, age at baseline, sex, English fluency, diabetes duration, loge(serum triglycerides), loge(urinary albumin: creatinine ratio), peripheral sensory neuropathy and peripheral arterial disease. There were no independent associations between serum bicarbonate and all-cause mortality [0.98 (0.95–1.004)] or incident HF [0.99 (0.95–1.03)].ConclusionsSerum bicarbonate was a significant independent predictor of incident CHD but not death or HF in community-based patients with type 2 diabetes. This supports intervention trials of bicarbonate replacement in type 2 patients at risk of CHD and who have a low serum bicarbonate concentration.Electronic supplementary materialThe online version of this article (doi:10.1186/s12933-016-0462-x) contains supplementary material, which is available to authorized users.

Nephrectomy Type Was Not Associated with a Subsequent Risk of Coronary Heart Disease: A Population-Based Study.

Previous studies investigated the impacts of a partial nephrectomy (PN) or radical nephrectomy (RN) on cardiovascular events and death. However, the association between the type of nephrectomy (PN vs. RN) and cardiovascular disease is still equivocal. This retrospective cohort study aimed to compare the risk of coronary heart disease (CHD) between patients who underwent a PN and those who underwent an RN. We used data from the Taiwan Longitudinal Health Insurance Database 2005. In total, 60 patients who underwent a PN and 545 patients who underwent an RN were included. Each patient was tracked for 1-, 2-, 3-, and 5-year periods to identify those who were subsequently diagnosed with CHD. Cox proportional hazard regression analyses were used to calculate hazard ratios (HRs) for CHD during 1-, 2-, 3-, and 5-year follow-up periods between these two cohorts. For the 1-year follow-up period, the adjusted HR was 0.39 (95% CI: 0.05~2.90, p = 0.355) for patients who underwent a PN compared to those who underwent an RN. Additionally, the adjusted HRs of CHD in patients who underwent a PN for 2-, 3- and 5-year follow-up periods were 1.40 (95% CI: 0.62~3.16, p = 0.417), 1.09 (95% CI: 0.52~2.31, p = 0.814), and 1.02 (95% CI: 0.48~2.18, p = 0.961), respectively, compared to those who underwent an RN. We concluded that there was no significant difference in the risk of CHD between patients who underwent a PN and those who underwent an RN.

Lead-Related Genetic Loci, Cumulative Lead Exposure and Incident Coronary Heart Disease: The Normative Aging Study.

BackgroundCumulative exposure to lead is associated with cardiovascular outcomes. Polymorphisms in the δ-aminolevulinic acid dehydratase (ALAD), hemochromatosis (HFE), heme oxygenase-1 (HMOX1), vitamin D receptor (VDR), glutathione S-transferase (GST) supergene family (GSTP1, GSTT1, GSTM1), apolipoprotein E (APOE),angiotensin II receptor-1 (AGTR1) and angiotensinogen (AGT) genes, are believed to alter toxicokinetics and/or toxicodynamics of lead.ObjectivesWe assessed possible effect modification by genetic polymorphisms in ALAD, HFE, HMOX1, VDR, GSTP1, GSTT1, GSTM1, APOE, AGTR1 and AGT individually and as the genetic risk score (GRS) on the association between cumulative lead exposure and incident coronary heart disease (CHD) events.MethodsWe used K-shell-X-ray fluorescence to measure bone lead levels. GRS was calculated on the basis of 22 lead-related loci. We constructed Cox proportional hazard models to compute adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for incident CHD. We applied inverse probability weighting to account for potential selection bias due to recruitment into the bone lead sub-study.ResultsSignificant effect modification was found by VDR, HMOX1, GSTP1, APOE, and AGT genetic polymorphisms when evaluated individually. Further, the bone lead-CHD associations became larger as GRS increases. After adjusting for potential confounders, a HR of CHD was 2.27 (95%CI: 1.50–3.42) with 2-fold increase in patella lead levels, among participants in the top tertile of GRS. We also detected an increasing trend in HRs across tertiles of GRS (p-trend = 0.0063).ConclusionsOur findings suggest that lead-related loci as a whole may play an important role in susceptibility to lead-related CHD risk. These findings need to be validated in a separate cohort containing bone lead, lead-related genetic loci and incident CHD data.

Green tea consumption is associated with reduced incident CHD and improved CHD-related biomarkers in the Dongfeng-Tongji cohort.

Prospective studies on the association of green tea with risk of coronary heart disease (CHD) incidence were scarce. This study examined whether green tea can reduce CHD incidence and have a beneficial effect on CHD-related risk markers in middle-aged and older Chinese population. We included 19 471 participants who were free of CHD, stroke or cancer at baseline from September 2008 to June 2010, and were followed until October 2013. Cox proportional hazard models were used to examine the hazard ratios (HR) of CHD incidence in relation to green tea consumption. Linear regression models were used to evaluate the effect of green tea on 5-year changes of CHD-related biomarkers. Compared with non-green tea consumers, the multivariable-adjusted HR for CHD was 0.89 (95% CI, 0.81-0.98) in green tea consumers. Particularly, the reduced risk of CHD incidence with green tea consumption was more evident among participants who were male, more than 60 years old, overweight, or with diabetes mellitus. In addition, green tea consumption improved multiple CHD-related risk markers including total cholesterol, HDL-cholesterol, triglycerides, mean platelet volume, and uric acid. In conclusion, green tea consumption was associated with a reduced risk of CHD incidence in the middle-aged and older Chinese populations, and the association might be partly due to altered CHD-related biomarkers.

No increased risk of coronary heart disease for patients receiving androgen deprivation therapy for prostate cancer in Chinese/Taiwanese men

The relationship between androgen deprivation therapy (ADT) and coronary heart disease (CHD) remains controversial. Furthermore, the majority of such studies focused on Caucasian populations, and there is still a paucity of studies among Asian populations. This population-based study aimed to investigate the relationship between ADT and CHD in an ethnic Chinese (i.e., Taiwanese) population. We used data sourced from the Taiwan 'Longitudinal Health Insurance Database'. This study included 1278 patients with prostate cancer in the study group and 1278 subjects without prostate cancer in the comparison group. Each patient was individually tracked for a 3-year period to identify those who had subsequently received a diagnosis of CHD. The results showed that the incidence rate of CHD during the 3-year follow-up period was 4.69 (95% CI: 2.99-5.48) per 100 person-years and 2.67 (95% CI: 2.15-3.27) per 100 person-years for the study and comparison cohort, respectively. The Cox proportional hazard regression showed that the hazard ratio for CHD during the 3-year follow-up period for prostate cancer patients was 1.65 (95% confidence interval (CI) = 1.25-2.16) compared with comparison subjects after adjusting for patients' geographic location, monthly income, urbanization level, hypertension, diabetes, hyperlipidemia, and stroke. However, we failed to find a significant difference in the adjusted hazard of CHD during the 3-year follow-up period between prostate cancer patients who did and those who did not receive ADT (hazard ratio = 1.12, 95% CI = 0.79-1.59). We concluded that prostate cancer but not ADT was significantly associated with CHD. In addition, a common cause of prostate cancer and coronary heart disease could exist.

Association of Serum Lipids and Coronary Heart Disease in Contemporary Observational Studies.

The use of statins increased among US adults with high coronary heart disease (CHD) risk after publication of the 2001 cholesterol treatment guidelines. We analyzed the association between lipids and CHD among 9578 REasons for Geographic And Racial Differences in Stroke (REGARDS) study participants and 346,595 Kaiser Permanente Southern California (KPSC) members with baseline lipid measurements in 2003 to 2007. We performed the same analyses among 14,590 Atherosclerosis Risk In Communities (ARIC) study participants with lipid measurements in 1987 to 1989. Analyses were restricted to blacks and whites 45 to 64 years of age without CHD who were not taking statins at baseline. Total cholesterol, high-density lipoprotein cholesterol, and triglycerides were measured at baseline. Low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and ratios of total to high-density lipoprotein cholesterol and triglycerides to high-density lipoprotein cholesterol were calculated. The prevalence of diabetes mellitus, history of stroke, and antihypertensive medication use increased at higher low-density lipoprotein cholesterol in ARIC but not in REGARDS or KPSC. Over 8.9 years of follow-up, 225 CHD events occurred in REGARDS, 6547 events in KPSC, and 583 events in ARIC. After multivariable adjustment, less favorable lipid levels were associated with higher hazard ratios for CHD in ARIC. These associations were attenuated in REGARDS and KPSC. For example, the hazard ratio associated with the highest versus lowest quartile of low-density lipoprotein cholesterol (≥ 146 versus ≤ 102 mg/dL) was 1.89 (95% confidence interval, 1.42-2.51) in ARIC, 1.25 (95% confidence interval, 0.81-1.92) in REGARDS, and 1.49 (95% confidence interval, 1.38-1.61) in KPSC. The association between lipids and CHD in contemporary studies may be attenuated by the preferential use of statins by high-risk individuals.

Coronary Heart Disease and Stroke in Adults Born Preterm - The Helsinki Birth Cohort Study.

Adults born preterm have increased risk factors for cardiovascular disease. We studied the cumulative incidence of manifest coronary heart disease (CHD) and stroke in adults born preterm. We studied 19 015 people born in Helsinki, Finland, during 1924-44. Of them, 137 (0.7%) were born early (<34 weeks) and 1006 (5.3%) late preterm (34 to <37 weeks). We ascertained CHD and stroke from the National Hospital Discharge and Death Registers and estimated hazard ratios (HRs) by Cox regression. A total of 3027 subjects (15.9%) had CHD and 1805 (9.5%) stroke. HRs for CHD were 1.17 (95% confidence interval 0.83, 1.65) for early and 0.99 (0.85, 1.14) for late preterm. For stroke, they were 0.84 (0.50, 1.39) and 0.86 (0.71, 1.06). HRs were little changed when adjusted for childhood and adult socio-economic position and birthweight for gestation standard deviation score. They were similar for first-ever events before or after 65 years, for haemorrhagic and thrombotic stroke, and for men and women, except that the HR for CHD for women born early preterm was 1.98 (1.18, 3.30). We found no increased risk of CHD or stroke up to old age in people born preterm, although women born early preterm had a higher rate of CHD. There is a discrepancy between increased risk factors in younger generations born preterm and little or no increase in manifest disease in older age. Uncovering reasons underlying this discrepancy may give important insights into the prevention of cardiovascular disease.

The sex-specific association between BMI and coronary heart disease: a systematic review and meta-analysis of 95 cohorts with 1·2 million participants

The risk of developing coronary heart disease differs by sex, and accumulating evidence suggests that sex differences exist in the effect of coronary risk factors on vascular risk. So far, the existence of a sex difference in the association between BMI and coronary heart disease has not been systematically studied. Since sexual dimorphisms in body composition exist, we postulated that the association between BMI and coronary heart disease would differ between women and men. We did systematic searches of PubMed and Embase up to Feb 20, 2015, for studies of the longitudinal association between BMI and coronary heart disease in women and men from population-based cohorts. We excluded studies if they contained duplicate data from the same study, reported estimates only for Z scores or percentiles of BMI, did not report estimate uncertainty, did not report sex-specific estimates, recruited mainly individuals with a previous history of cardiovascular disease or from within selected populations, and those for which the full text was not available in English. We also included individual participant data from four large studies. Study results were pooled using random-effect models with inverse variance weighting. Our predefined primary endpoint was the pooled women-to-men ratio of the age-adjusted hazard ratios (HRs), or equivalent, relating (continuous and categorical) BMI to coronary heart disease. We reviewed a total of 8561 original entries twice for inclusion in the analysis, of which 32 published studies were eligible for inclusion. Data from 95 cohorts, 1,219,187 participants, and 37,488 incident cases of coronary heart disease were included. Higher BMI was significantly associated with age-adjusted coronary heart disease: for a one-unit (kg/m(2)) increment in BMI; the HR was 1·04 (95% CI 1·03-1·05) in women and 1·05 (1·04-1·07) in men. Compared with people of a normal weight, the age-adjusted HR of coronary heart disease for the underweight group was 1·25 (1·05-1·49) in women and 1·09 (0·91-1·23) in men; for the overweight group 1·20 (1·12-1·29) in women and 1·22 (1·12-1·32) in men; and for the obese group 1·61 (1·42-1·82) in women and 1·60 (1·43-1·79) in men. Overall, these associations did not differ between the sexes. The women-to-men ratios of the HRs were 0·99 (95% CI 0·98-1·00) for a one-unit increment in BMI, 1·10 (0·91-1·32) for the underweight group, 0·99 (0·92-1·07) for the overweight group, and 1·06 (0·95-1·17) for the obese group, relative to the normal weight group. Similar results were obtained after multiple adjustment and in a range of sensitivity analyses. Increased BMI, measured either continuously or categorically, has the same deleterious effects on the risk of coronary heart disease in women and men across diverse populations. None.

Cigarette smoking and cardiovascular events: role of inflammation and subclinical atherosclerosis from the MultiEthnic Study of Atherosclerosis.

To examine the contemporary effect of smoking in a multiethnic sample, and to explore the respective contributions of inflammation and subclinical atherosclerosis to the cardiovascular consequences of smoking. We studied 6814 participants free of cardiovascular disease and coronary heart disease (CHD) from the Multiethnic Study of Atherosclerosis. Smoking status and cumulative exposure were determined by self-report and confirmed by urinary cotinine. Multivariable Cox regression was used to estimate the association between smoking parameters and all-cause cardiovascular disease, all-cause CHD, and hard CHD events. We further adjusted for high-sensitivity C-reactive protein and coronary artery calcium (CAC) in hierarchical Cox models. We identified 3218 never smokers, 2607 former smokers, and 971 current smokers. Median follow-up was 10.2 years. Compared with never smokers, adjusted hazard ratios in current smokers were 1.7 (95% confidence interval, 1.3-2.2) for all-cause cardiovascular disease, 1.6 (1.1-2.1) for all-cause CHD, and 1.7 (1.2-2.4) for hard CHD. Similarly, among current smokers, hazard ratios were higher in the 4th versus 1st quartile of pack-years (eg, all-cause CHD hazard ratio=2.7 [1.1-6.6]). Both CAC>100 and high-sensitivity C-reactive protein ≥3 mg/L identified higher relative risk among current smokers (eg, all-cause CHD hazard ratio of 3.0 [1.5-6.0, compared with CAC=0] and 2.6 [1.4-4.8, compared with high-sensitivity C-reactive protein <2 mg/L], respectively). However, CAC was a stronger mediator of events and adversely modified the effect of smoking on events (eg, P-interaction=0.02 for hard CHD). Compared with never smokers, former smokers (median cessation interval=22 years) had similar adjusted hazard for events. In this multiethnic cohort, current smoking and cumulative exposure remain important modifiable determinants of cardiovascular disease. Both high-sensitivity C-reactive protein ≥3 mg/L and, particularly, CAC>100 identified high-risk smokers who may benefit from more intensive smoking-cessation efforts.

BMI and coronary heart disease risk among low-income and underinsured diabetic patients.

OBJECTIVEThe association between obesity and coronary heart disease (CHD) risk remains debatable, and no studies have assessed this association among diabetic patients. The aim of our study was to investigate the association between BMI and CHD risk among patients with type 2 diabetes.RESEARCH DESIGN AND METHODSThe sample included 30,434 diabetic patients (10,955 men and 19,479 women) 30–95 years of age without a history of CHD or stroke in the Louisiana State University Hospital-Based Longitudinal Study.RESULTSDuring a mean follow-up period of 7.3 years, 7,414 subjects developed CHD. The multivariable-adjusted hazard ratios for CHD across levels of BMI at baseline (18.5–24.9, 25–29.9, 30–34.9, 35–39.9, and ≥40 kg/m2) were 1.00, 1.14 (95% CI 1.00–1.29), 1.27 (1.12–1.45), 1.54 (1.34–1.78), and 1.42 (1.23–1.64) (Ptrend < 0.001) in men and 1.00, 0.95 (0.85–1.07), 0.95 (0.84–1.06), 1.06 (0.94–1.20), and 1.09 (1.00–1.22) (Ptrend < 0.001) in women, respectively. When we used an updated mean or last visit value of BMI, the positive association between BMI and CHD risk did not change in men. However, the positive association of BMI with CHD changed to a U-shaped association in women when we used the last visit value of BMI.CONCLUSIONSOur study suggests that there is a positive association between BMI at baseline and during follow-up with the risk of CHD among patients with type 2 diabetes. We indicate a U-shaped association between BMI at the last visit and the risk of CHD among women with type 2 diabetes.

Impact of age and gender on the prevalence and prognostic importance of the metabolic syndrome and its components in Europeans. The MORGAM Prospective Cohort Project.

ObjectiveTo investigate the influence of age and gender on the prevalence and cardiovascular disease (CVD) risk in Europeans presenting with the Metabolic Syndrome (MetS).MethodsUsing 36 cohorts from the MORGAM-Project with baseline between 1982–1997, 69094 men and women aged 19–78 years, without known CVD, were included. During 12.2 years of follow-up, 3.7%/2.1% of men/women died due to CVD. The corresponding percentages for fatal and nonfatal coronary heart disease (CHD) and stroke were 8.3/3.8 and 3.1/2.5.ResultsThe prevalence of MetS, according to modified definitions of the International Diabetes Federation (IDF) and the revised National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATPIII), increased across age groups for both genders (P<0.0001); with a 5-fold increase in women from ages 19–39 years to 60–78 years (7.4%/7.6% to 35.4%/37.6% for IDF/NCEP-ATPIII) and a 2-fold increase in men (5.3%/10.5% to 11.5%/21.8%). Using multivariate-adjusted Cox regressions, the associations between MetS and all three CVD events were significant (P<0.0001). For IDF/NCEP-ATPIII in men and women, hazard ratio (HR) for CHD was 1.60/1.62 and 1.93/2.03, for CVD mortality 1.73/1.65 and 1.77/2.06, and for stroke 1.51/1.53 and 1.58/1.77. Whereas in men the HRs for CVD events were independent of age (MetS*age, P>0.05), in women the HRs for CHD declined with age (HRs 3.23/3.98 to 1.55/1.56; MetS*age, P = 0.01/P = 0.001 for IDF/NCEP-ATPIII) while the HRs for stroke tended to increase (HRs 1.31/1.25 to 1.55/1.83; MetS*age, P>0.05).ConclusionIn Europeans, both age and gender influenced the prevalence of MetS and its prognostic significance. The present results emphasise the importance of being critical of MetS in its current form as a marker of CVD especially in women, and advocate for a redefinition of MetS taking into account age especially in women.

Aggressive Blood Pressure Control Increases Coronary Heart Disease Risk Among Diabetic Patients

OBJECTIVEBlood pressure control can reduce the risk of coronary heart disease (CHD) among diabetic patients; however, it is not known whether the lowest risk of CHD is among diabetic patients with the lowest blood pressure level.RESEARCH DESIGN AND METHODSWe performed a prospective cohort study (2000–2009) on diabetic patients including 17,536 African Americans and 12,618 whites. Cox proportional hazards regression models were used to estimate the association of blood pressure with CHD risk.RESULTSDuring a mean follow-up of 6.0 years, 7,260 CHD incident cases were identified. The multivariable-adjusted hazard ratios of CHD associated with different levels of systolic/diastolic blood pressure at baseline (<110/65, 110–119/65–69, 120–129/70–80, and 130–139/80–90 mmHg [reference group]; 140–159/90–100; and ≥160/100 mmHg) were 1.73, 1.16, 1.04, 1.00, 1.06, and 1.11 (P trend <0.001), respectively, for African American diabetic patients, and 1.60, 1.27, 1.08, 1.00, 0.95, and 0.99 (P trend<0.001) for white diabetic patients, respectively. A U-shaped association of isolated systolic and diastolic blood pressure at baseline as well as blood pressure during follow-up with CHD risk was observed among both African American and white diabetic patients (all Ptrend <0.001). The U-shaped association was present in the younger age-group (30–49 years), and this U-shaped association changed to an inverse association in the older age-group (≥60 years).CONCLUSIONSOur study suggests that there is a U-shaped or inverse association between blood pressure and the risk of CHD, and aggressive blood pressure control (blood pressure <120/70 mmHg) is associated with an increased risk of CHD among both African American and white patients with diabetes.

Bladder pain syndrome/interstitial cystitis increase the risk of coronary heart disease

Vascular factor was proposed as being involved in the etiology of bladder pain syndrome/interstitial cystitis (BPS/IC). However, few studies have attempted to investigate the relationship between BPS/IC and cardiovascular disease. This study aimed to investigate the risk of coronary heart disease (CHD) among BPS/IC subjects during a 3-year follow-up period. Data for this retrospective matched-cohort study were retrieved from the Taiwan "Longitudinal Health Insurance Database 2000." There were 752 BPS/IC female subjects in the study cohort and 3,760 randomly selected female subjects in the comparison cohort. We individually tracked each subject for 3 years and identified each subject that received a subsequent diagnosis of CHD during that follow-up period. Results showed that incidence rates of CHD during the 3-year follow-up period were 19.50 (95% confidence interval (CI): 14.35-25.95) and 8.87 (95% CI: 7.25-10.74) per 1,000 person-years for the study and comparison cohorts, respectively. The Cox proportional hazards regression suggested that the hazard ratio for CHD in subjects with BPS/IC was 1.65 (95% CI: 1.09-2.48) within the 3-year follow-up period following the index date compared to the comparison subjects after adjusting for monthly income, geographic region, hypertension, diabetes, hyperlipidemia, chronic kidney disease, bladder outlet obstruction, urinary tract infection, chronic pelvic pain, overactive bladder, and number of physician visits during the 3-year follow up period. Our study demonstrated an association between BPS/IC and a subsequent CHD diagnosis. We advise clinicians to screen subjects with BPS/IC for modifiable risk factors for CHD.

Time-dependent propensity score and collider-stratification bias: an example of beta2-agonist use and the risk of coronary heart disease

Stratification and conditioning on time-varying cofounders which are also intermediates can induce collider-stratification bias and adjust-away the (indirect) effect of exposure. Similar bias could be expected when one conditions on time-dependent PS. We explored collider-stratification and confounding bias due to conditioning or stratifying on time-dependent PS using a clinical example on the effect of inhaled short- and long-acting beta2-agonist use (SABA and LABA, respectively) on coronary heart disease (CHD). In an electronic general practice database we selected a cohort of patients with an indication for SABA and/or LABA use and ascertained potential confounders and SABA/LABA use per three month intervals. Hazard ratios (HR) were estimated using PS stratification as well as covariate adjustment and compared with those of Marginal Structural Models (MSMs) in both SABA and LABA use separately. In MSMs, censoring was accounted for by including inverse probability of censoring weights.The crude HR of CHD was 0.90 [95 % CI: 0.63, 1.28] and 1.55 [95 % CI: 1.06, 2.62] in SABA and LABA users respectively. When PS stratification, covariate adjustment using PS, and MSMs were used, the HRs were 1.09 [95 % CI: 0.74, 1.61], 1.07 [95 % CI: 0.72, 1.60], and 0.86 [95 % CI: 0.55, 1.34] for SABA, and 1.09 [95 % CI: 0.74, 1.62], 1.13 [95 % CI: 0.76, 1.67], 0.77 [95 % CI: 0.45, 1.33] for LABA, respectively. Results were similar for different PS methods, but higher than those of MSMs. When treatment and confounders vary during follow-up, conditioning or stratification on time-dependent PS could induce substantial collider-stratification or confounding bias; hence, other methods such as MSMs are recommended.