Objective: To compare the early and late outcomes of primary percutaneous transluminal coronary angioplasty (PTCA) with fibrinolytic treatment among diabetic patients with acute myocardial infarction (AMI). Design: Retrospective observational study with data obtained from prospective registries. Setting: Tertiary cardiovascular institution with 24 hour acute interventional facilities. Patients: 202 consecutive diabetic patients with AMI receiving reperfusion treatment within six hours of symptom onset. Interventions: Fibrinolytic treatment was administered to 99 patients, and 103 patients underwent primary PTCA. Most patients undergoing PTCA received adjunctive stenting (94.2%) and glycoprotein IIb/IIIa inhibition (63.1%). Main outcome measures: Death, non-fatal reinfarction, and target vessel revascularisation at 30 days and one year were assessed. Results: Baseline characteristics were similar in these two treatment groups except that the proportion of patients with Killip class III or IV was considerably higher in those treated with PTCA (15.5% v 6.1%, p = 0.03) and time to treatment was significantly longer (103.7 v 68.0 minutes, p < 0.001). Among those treated with PTCA, the rates for in-hospital recurrent ischaemia (5.8% v 17.2%, p = 0.011) and target vessel revascularisation at one year (19.4% v 36.4%, p = 0.007) were lower. Death or reinfarction at one year was also reduced among those treated with PTCA (17.5% v 31.3%, p = 0.02), with an adjusted relative risk of 0.29 (95% confidence interval 0.15 to 0.57) compared with fibrinolysis. Conclusion: Among diabetic patients with AMI, primary PTCA was associated with reduced early and late adverse events compared with fibrinolytic treatment. E ven with the widespread availability of fibrinolytic treatment, diabetes mellitus remains an important adverse prognostic factor in patients with acute myocardial infarction (AMI).1-3 Although recent evidence from randomised trials has shown that primary percutaneous transluminal coronary angioplasty (PTCA) provides significantly better clinical outcomes than fibrinolysis for AMI in general, 4-9 its effect on diabetic patients remains unclear. A post hoc subgroup analysis of the GUSTO-IIb (global use of strategies to open occluded coronary arteries in acute coronary syndromes) angioplasty substudy found modest improvements in short and long term outcomes in diabetic patients treated with primary PTCA compared with fibrinolysis.

Objective: To determine the ethnic variation of short and long term female vulnerability after an acute coronary event in a population of Chinese, Indians, and Malays. Design: Population based registry. Patients: Residents of Singapore between the ages of 20-64 years with coronary events. Case identification and classification procedures were modified from the MONICA (monitoring trends and determinants in cardiovascular disease) project. Main outcome measures: Adjusted 28 day case fatality and long term mortality. Results: From 1991 to 1999, there were 16 320 acute coronary events, including 3497 women. Age adjusted 28 day case fatality was greater in women (51.5% v 38.6%, p , 0.001), with a larger sex difference evident among younger Malay patients. This inequality between the sexes was observed in both the pre-hospitalisation and post-admission periods. Among hospitalised patients, women were older, were less likely to have suffered from a previous Q wave or anterior wall myocardial infarction, and had lower peak creatine kinase concentrations. Case fatality was higher among women, with adjusted hazard ratios of 1.64 (95% confidence interval (CI) 1.43 to 1.88) and 1.50 (95% CI 1.37 to 1.64) for 28 day and mean four year follow up periods. There were significant interactions of sex and age with ethnic group (p = 0.017). The adjusted hazards for mortality among Chinese, Indian, and Malay women versus men were 1.30, 1.71, and 1.96, respectively. The excess mortality among women diminished with age. Conclusion: In this multiethnic population, both pre-hospitalisation and post-admission case fatality rates were substantially higher among women. The sex discrepancy in long term mortality was greatest among Malays and in the younger age groups. W hile acute myocardial infarction (MI) occurs more commonly among men, several studies have shown that short term mortality after the event is higher among women.1 2 A review of 27 studies concluded that the reasons for increased early mortality among women were older age and the presence of other unfavourable baseline clinical characteristics.3 Long term survival was shown to be better for women after adjusting for differences in age and other covariates in large MI population registries.3 Subsequent investigators found an interaction between sex and age, 4-7 with a female excess of mortality among younger patients (, 50 years of age) that diminished with age. Survival was similar between the sexes among the elderly (. 70 years of age).The higher early mortality among hospitalised women may also be attributed to a difference in survival pattern after an acute coronary event. Among those who died within 28 days in the Scottish MONICA (monitoring trends and determinants in cardiovascular disease) population of Glasgow, 8 men were more likely to die out of hospital (74.3% v 67.8%; p = 0.0004). After hospitalisation, women were more likely to die, resulting in a similar 28 day case fatality rate between men (49.8%) and women (48.5%). However, in the MONICA project of 37 populati...

Clinical observations have linked tobacco smoking with increased type 2 diabetes risk. Mendelian randomization analysis has recently suggested smoking may be a causal risk factor for type 2 diabetes. However, this association could be mediated by additional risk factors correlated with smoking behavior, which have not been investigated. We hypothesized that body mass index (BMI) could help to explain the association between smoking and diabetes risk. First, we confirmed that genetic determinants of smoking initiation increased risk for type 2 diabetes (OR = 1.21, 95% CI: 1.15–1.27, P = 1 × 10−12) and coronary artery disease (CAD; OR = 1.21, 95% CI: 1.16–1.26, P = 2 × 10−20). Additionally, 2-fold increased smoking risk was positively associated with increased BMI (~0.8 kg/m2, 95% CI: 0.54–0.98 kg/m2, P = 1.8 × 10−11). Multivariable Mendelian randomization analyses showed that BMI accounted for nearly all the risk smoking exerted on type 2 diabetes (OR 1.06, 95% CI: 1.01–1.11, P = 0.03). In contrast, the independent effect of smoking on increased CAD risk persisted (OR 1.12, 95% CI: 1.08–1.17, P = 3 × 10−8). Causal mediation analyses agreed with these estimates. Furthermore, analysis using individual-level data from the Million Veteran Program (MVP) independently replicated the association of smoking behavior with CAD (OR 1.24, 95% CI: 1.12–1.37, P = 2 × 10−5), but not type 2 diabetes (OR 0.98, 95% CI: 0.89–1.08, P = 0.69), after controlling for BMI. Our findings support a model whereby genetic determinants of smoking increase type 2 diabetes risk indirectly through their relationship with obesity. Smokers should be advised to stop smoking to limit type 2 diabetes and CAD risk. Therapeutic efforts should consider pathophysiology relating smoking and obesity.

To illustrate methods for assessing environmental exposures associated with lung cancer risk, we investigated anthropogenic based air pollutant data in a major metropolitan area using United States-Environmental Protection Agency (US-EPA) Toxic Release Inventory (TRI) (1987–2017), and PM2.5 (1998–2016) and NO2 (1996–2012) concentrations from NASA satellite data. We studied chemicals reported according to the following five exposome features: (1) International Agency for Research on Cancer (IARC) cancer grouping; (2) priority EPA polycyclic aromatic hydrocarbons (PAHs); (3) component of diesel exhaust; (4) status as a volatile organic compound (VOC); and (5) evidence of lung carcinogenesis. Published articles from PubChem were tallied for occurrences of 10 key characteristics of cancer-causing agents on those chemicals. Zone Improvement Plan (ZIP) codes with higher exposures were identified in two ways: (1) combined mean exposure from all features, and (2) hazard index derived through a multi-step multi-criteria decision analysis (MMCDA) process. VOCs, IARC Group 1 carcinogens consisted 82.3% and 11.5% of the reported TRI emissions, respectively. ZIP codes along major highways tended to have greater exposure. The MMCDA approach yielded hazard indices based on imputed toxicity, occurrence, and persistence for risk assessment. Despite many studies describing environmental exposures and lung cancer risk, this study develops a method to integrate these exposures into population-based exposure estimates that could be incorporated into future lung cancer screening trials and benefit public health surveillance of lung cancer incidence. Our methodology may be applied to probe other hazardous exposures for other cancers.