Surgery for rheumatic heart disease in the Northern Territory, Australia, 1997-2016: what have we gained?

BACKGROUND: Between 1964 and 1996, the 10-year survival of patients having valve replacement surgery for rheumatic heart disease (RHD) in the Northern Territory, Australia, was 68%. As medical care has evolved since then, this study aimed to determine whether there has been a corresponding improvement in survival. METHODS: A retrospective study of Aboriginal patients with RHD in the Northern Territory, Australia, having their first valve surgery between 1997 and 2016. Survival was examined using Kaplan-Meier and Cox regression analysis. FINDINGS: The cohort included 281 adults and 61 children. The median (IQR) age at first surgery was 31 (18-42) years; 173/342 (51%) had a valve replacement, 113/342 (33%) had a valve repair and 56/342 (16%) had a commissurotomy. There were 93/342 (27%) deaths during a median (IQR) follow-up of 8 (4-12) years. The overall 10-year survival was 70% (95% CI: 64% to 76%). It was 62% (95% CI: 53% to 70%) in those having valve replacement. There were 204/281 (73%) adults with at least 1 preoperative comorbidity. Preoperative comorbidity was associated with earlier death, the risk of death increasing with each comorbidity (HR: 1.3 (95% CI: 1.2 to 1.5), p<0.001). Preoperative chronic kidney disease (HR 6.5 (95% CI: 3.0 to 14.0) p≤0.001)), coronary artery disease (HR 3.3 (95% CI: 1.3 to 8.4) p=0.012) and pulmonary artery systolic pressure>50 mm Hg before surgery (HR 1.9 (95% CI: 1.2 to 3.1) p=0.007) were independently associated with death. INTERPRETATION: Survival after valve replacement for RHD in this region of Australia has not improved. Although the patients were young, many had multiple comorbidities, which influenced long-term outcomes. The increasing prevalence of complex comorbidity in the region is a barrier to achieving optimal health outcomes.

Nicotine yesterday, today, and tomorrow: a global review.

This intentionally selective global review reflects the views and frustrations of a public health physician with 45 years of frontline experience in tobacco control. In particular, it focuses on the nexus between research and policy and the long periods between relevant discoveries and application as policy. Consideration is given to the relative neglect of the possibility of reducing the carcinogenicity and toxicity of the cigarette on the grounds that it is the preferred source of nicotine for the global majority of nicotine users. Although the outcome of such change is unquantifiable, there is much in cigarette smoke that can be changed to make it less carcinogenic and less toxic. It is difficult to think of excuses for accepting the status quo.

Research required for the effective implementation of the framework convention on tobacco control, articles 9 and 10.

This paper is part of a series of articles intended to set out the research questions that are relevant to the successful implementation of the various provisions of the Framework Convention on Tobacco Control (FCTC). This paper focuses on issues affecting Articles 9 and 10 of the FCTC. This paper focuses on the research that is most important for most countries, rather than on what is desirable in countries with high levels of research capacity. Articles 9 and 10 of the FCTC address the regulation of contents and emissions of tobacco products and regulation of tobacco product disclosure. Such regulation will be essential if the long-term objective of reducing the danger of tobacco products is to be achieved. There are many components of tobacco and tobacco smoke that are excessively toxic and dangerous to the user. Many of these components are carcinogenic and addictive and can be removed or reduced substantially with current known technology. The fact that these components remain in tobacco and tobacco smoke at levels that are unnecessarily dangerous is precisely the reason why the successful implementation of Articles 9 and 10 of the FCTC is important to tobacco control. This paper discusses the scientific challenges involved in successfully implementing Articles 9 and 10 of the FCTC, which focuses on regulating carcinogens and toxins in tobacco and tobacco smoke, the abuse liability of tobacco products, and the additives and engineering features in tobacco products that make tobacco products appealing to future consumers. The research issues we focus on are those required to support the early stages of regulation. As regulation proceeds, new and more sophisticated research questions will undoubtedly emerge.

Do changes in cigarette design influence the rise in adenocarcinoma of the lung?

BACKGROUND: Incidence rates for adenocarcinoma of the lung are increasing and are higher in the United States than in many other developed countries. We examine whether these trends may be associated with changes in cigarette design. METHODS: Lung cancer risk equations based on observations during 1960-1972 from the American Cancer Society Cancer Prevention Study I are applied to 5-year birth cohort-specific estimates of changes in smoking behaviors to predict birth cohort-specific rates of squamous cell carcinoma and adenocarcinoma of the lung among US White men for the period 1973-2000. These expected rates are compared to observed rates for the same birth cohorts of White men in the US Surveillance, Epidemiology and End Results (SEER) data. RESULTS: Changes in smoking behaviors over the past several decades adequately explain the changes in squamous cell carcinoma rates observed in the SEER data. However, predicted rates for adenocarcinoma do not match the observed SEER data without inclusion of a term increasing the risk for adenocarcinoma with the duration of smoking after 1965. CONCLUSION: The risk of developing squamous cell carcinoma from smoking appears to have remained stable in the United States over the past several decades; however, the risk of adenocarcinoma has increased substantially in a pattern temporally associated with changes in cigarette design.

Has the lung cancer risk from smoking increased over the last fifty years?

BACKGROUND: We examine whether the lung cancer risk due to smoking has increased over time. METHODS: Lung cancer risk equations based on prospective mortality data collected from 1960 to 1972 were applied to 5-year birth-cohort-specific estimates of smoking behaviors among white males to estimate lung cancer mortality rates for U.S. white males from 1960 to 2000. These estimated rates were compared to U.S. white male mortality rates for the same birth cohorts. RESULTS: Observed birth-cohort-specific U.S. lung cancer mortality rates are substantially higher than those expected from changes in smoking behaviors, and the proportional difference increases with advancing calendar year. This trend persisted even when the duration term was increased in the risk equation. However, adjusting for changes in cigarette design over time by adding a term for the duration of smoking after 1972 resulted in the predicted rates closely approximating the observed U.S. mortality rates. CONCLUSION: Lung cancer risk estimates observed during the 1960s under predict current lung cancer mortality rates in U.S. white males. Adjustment for the duration of smoking after 1972 results in estimates that reasonably approximate the observed U.S. lung cancer mortality, suggesting that lung cancer risks from smoking are increasing in the United States coincident with changes in cigarette design.

Smokeless tobacco and cancer.

Use of smokeless tobacco products is common worldwide, with increasing consumption in many countries. Although epidemiological data from the USA and Asia show a raised risk of oral cancer (overall relative risk 2.6 [95% CI 1.3-5.2]), these are not confirmed in northern European studies (1.0 [0.7-1.3]). Risks of oesophageal cancer (1.6 [1.1-2.3]) and pancreatic cancer (1.6 [1.1-2.2]) have also increased, as shown in northern European studies. Results on lung cancer have been inconsistent, with northern European studies suggesting no excess risk. In India and Sudan, more than 50% of oral cancers are attributable to smokeless tobacco products used in those countries, as are about 4% of oral cancers in US men and 20% of oesophageal and pancreatic cancers in Swedish men. Smokeless tobacco products are a major source of carcinogenic nitrosamines; biomarkers of exposure have been developed to quantify exposure as a framework for a carcinogenesis model in people. Animal carcinogenicity studies strongly support clinical results. Cancer risk of smokeless tobacco users is probably lower than that of smokers, but higher than that of non-tobacco users.

The consequences of the unregulated cigarette.

This article considers changes in cigarette design in relation to the concept of "dose", drawing attention to the observation that there is not one smoking related epidemic of lung cancer, but at least two. Squamous carcinoma is declining in parallel with smoking prevalence while adenocarcinoma is increasing in the face of declining smoking prevalence. It is concluded that the adenocarcinoma epidemic is unnecessary and is due substantially to cigarette design changes, including increases in tobacco specific nitrosamines, manipulation of droplet size and ventilated filters. The need for regulation of smoke constituents is emphasised.