Innovative methodologies for elucidating bushfire smoke-induced pathophysiological mechanism.

<i>Circulation</i> Editors’ Picks

Bushfires in Australia: a serious health emergency under climate change

Since the initial scientific statement on Secondary Prevention of Coronary Heart Disease (CHD) in the Elderly was published in 2002,1 several trends have continued that make an update highly appropriate. First, the graying of the US population and those of other industrialized countries has progressed unabated because more adults are surviving into their senior years. The number of Americans aged ≥75 years was estimated at 18.6 million in 2010, representing ≈6% of the population,2 and it is expected to double by 2050. The population aged ≥85 years is growing the most rapidly, with numbers expected to reach 19.5 million by 2040. In 2008, 67% of the 811 940 cardiovascular deaths in the United States occurred in people aged ≥75 years.3 In parallel to this increase in the older adult demographic, the number of Americans with CHD has increased to an estimated 16.3 million, more than half of whom are >65 years of age.3 Similarly, 7 million have had a stroke, the incidence of which approximately doubles with successive age decades after 45 to 54 years.3 Peripheral artery disease (PAD) affects 8 to 10 million Americans, the majority of whom are >65 years of age. Between 2015 and 2030, annual US costs related to atherosclerotic cardiovascular disease (ASCVD) are projected to increase from $84.8 billion to $202 billion.3 Moreover, given that ASCVD often undermines functional capacity and independence and increases reliance on long-term care, indirect expenses related to ASCVD are also expected to increase. Thus, the need for effective secondary prevention measures in the older adult population with known ASCVD has never been greater. Notably, the 2011 American Heart Association (AHA)/American College of Cardiology Foundation (ACCF) updated guidelines for secondary prevention of CHD broadened …

COPD 2020: new directions needed.

Chronic respiratory diseases (CRDs) are diseases of the respiratory tract and are among the most prominent causes of disability and mortality globally(1). Chronic obstructive pulmonary disease (COPD) and lung cancer are among the leading cause of death among all CRDs(2). Evidence showed that diet, particularly ultra-processed foods (UPFs) are strongly associated with cardiovascular disease, diabetes, cancer, and depression(3). However, the link between UPFs intake and CRDs has rarely been investigated. we aimed to examine the association between UPF consumption and risk of mortality due to CRDs overall, COPD and lung cancer among adults in the USA. A total of 96,607 participants aged 55 years and over were obtained from Prostate, Lung, Colorectal and Ovarian (PLCO) cancer study, a randomised trial designed to investigate the effects of screening on cancer-related mortality. However, data collected also afforded the opportunity to examine the relationships between UPF intake and mortality caused by respiratory diseases. Dietary history of participants was collected at baseline using a validated food frequency questionnaire as was the presence of respiratory diseases. Food items were grouped into one of the four NOVA food classification system(4). Cox regression was fitted to estimate the risk of all-cause mortality and cause-specific mortality due to increased consumption of UPFs over time. Competing risk regression was used to account for the competing risks events and effect of participant loss. During the follow-up period of 1,379,655.5 person-years (median 16.8 years), 28700 all-cause, 4,901 all respiratory, 2,015 lung cancer and 1,536 COPD mortalities occurred. A dose-response association was found between higher UPF intake and mortality from all respiratory diseases and COPD, but not lung cancer. After considering competing events, higher intake of UPF increased the risk of mortality from all respiratory diseases by 10% (HR: 1.10; 95% CI: 1.01, 1.21) and COPD by 20% (HR: 1.20; 95% CI: 1.02, 1.42). After imputation for missing data, the risk of lung cancer increased by 25% among participants in the highest quintile of UPF intake. The PLCO trial data highlighted that consumption of UPF increased respiratory mortality, among those with COPD, however further mechanistic studies are recommended to further clarify the link between UPF and lung cancer. This study also indicated that a high intake of UPF generally increases the risk of mortality of those with respiratory diseases and contributes to a large body of evidence indicating that higher UPF consumption increases the overall risk of mortality.

Cardiovascular disease and cancer are the two leading causes of morbidity and mortality in patients with chronic obstructive pulmonary disease. The epidemiological and mechanistic evidence linking these disorders, however, is uncertain. In patients with mild chronic obstructive pulmonary disease, cardiovascular disease accounts for nearly 50% of all hospitalizations and over 20% of all deaths, whereas lung cancer accounts for about a third of all mortality. Collectively, cancer is responsible for over 50% of all deaths in mild chronic obstructive pulmonary disease. In general, chronic obstructive pulmonary disease increases the risk of cardiovascular disease and lung cancer by two-fold, with increasing risk as the disease progresses. The mechanisms linking these disorders have not been well worked out. Shared genetic risk factors, and perturbations in the inflammatory, oxidative and neurohumoral responses, are implicated. Epidemiological studies suggest that anti-inflammatory drugs may reduce the risk of cardiovascular disease and lung cancer but have not been confirmed. Cardiovascular diseases and lung cancer are major sources of morbidity and mortality in chronic obstructive pulmonary disease. Patients should be assessed carefully for additional risk factors and be treated aggressively with interventions to mitigate the risk of cardiovascular disease and lung cancer.

The Impact of APOL1 on Chronic Kidney Disease and Hypertension.

APOL1 renal risk variants are strongly associated with chronic kidney disease in Black adults, but reported associations with cardiovascular disease (CVD) have been conflicting. We examined associations of APOL1 with incident coronary heart disease (n=323), ischemic stroke (n=331), and the composite CVD outcome (n=500) in 10 605 Black participants of the REGARDS study (Reasons for Geographic and Racial Differences in Stroke). Primary analyses compared individuals with APOL1 high-risk genotypes to APOL1 low-risk genotypes in Cox proportional hazards models adjusted for CVD risk factors and African ancestry. APOL1 high-risk participants were younger and more likely to have albuminuria at baseline than APOL1 low-risk participants. The risk of incident stroke, coronary heart disease, or composite CVD end point did not significantly differ by APOL1 genotype status in multivariable models. The association of APOL1 genotype with incident composite CVD differed by diabetes mellitus status (Pinteraction=0.004). In those without diabetes mellitus, APOL1 high-risk genotypes associated with greater risk of incident composite CVD (hazard ratio, 1.67; 95% confidence interval, 1.12-2.47) compared with those with APOL1 low-risk genotypes in multivariable adjusted models. This latter association was driven by ischemic strokes (hazard ratio, 2.32; 95% confidence interval, 1.33-4.07), in particular, those related to small vessel disease (hazard ratio, 5.10; 95% confidence interval, 1.55-16.56). There was no statistically significant association of APOL1 genotypes with incident CVD in subjects with diabetes mellitus. The APOL1 high-risk genotype was associated with higher stroke risk in individuals without but not those with chronic kidney disease in fully adjusted models. APOL1 high-risk status is associated with CVD events in community-dwelling Black adults without diabetes mellitus.

J-curve for DBP and cardiovascular mortality in coronary artery disease patients

T he cardiovascular disease (CVD) risk associated with diabetes mellitus (DM) has become increasingly evident, accounting for Ϸ80% of deaths among patients with this disease 1 and making CVD risk modification a key therapeutic objective in diabetic patients.2][3][4] The rapidly increasing global burden of DM, 5 coupled with the associated CVD risk, underscores the imperative for continued generation and application of evidence-based therapies to reduce CVD risk in this high-risk cohort.In this 2-part series, we first review the CVD effects of the thiazolidinedione medications, the most broadly investigated class of antihyperglycemic drugs evaluated in the context of CVD risk.In the second part, we review the modulators of the incretin axis that have most recently achieved US Food and Drug Administration approval, with a focus on CVD considerations; introduce selected drugs in advanced development; summarize glucose control strategies for cardiovascular patients; and discuss the regulatory review of glucose-lowering medications.

Annals for Educators - 21 August 2018.

Heated tobacco products (HTPs) have become popular recently. People with chronic disease, such as diabetes, cardiovascular disease (CVD), chronic obstructive pulmonary disease (COPD) and cancer, should quit smoking for treatment and recurrence of tobacco-related diseases. However, they have difficulty in quitting smoking, and they may start HTPs use to quit smoking. The purpose of this study is to examine the use of HTPs in people with chronic disease. We used data from an internet study, the Japan Society and New Tobacco Internet Survey (JASTIS). We analyzed 9,008 respondents aged 15–73 years in 2019 using logistic regression. Current use of tobacco products was defined as use within the previous 30 days. Prevalence of current HTP use including dual use and dual use with cigarettes was 9.0% and 6.1% respectively in total. By disease: hypertension 10.2% and 7.4%, diabetes 15.9% and 12.3%, CVD 19.2% and 15.7%, COPD 40.5% and 33.3%, and cancer 17.5% and 11.9%. Diabetes, CVD, COPD, and cancer were positively associated with current use of HTPs (odds ratios (ORs) and 95% confidence intervals (CIs): 1.48 (1.06, 2.07), 2.29 (1.38, 3.80), 3.97(1.73, 9.11), and 3.58(1.99, 6.44), respectively) and dual use of cigarettes and HTPs (ORs and 95% CIs: 2.23 (1.61, 3.09), 3.58 (2.29, 5.60), 7.46 (3.76, 14.80), and 2.57 (1.46, 4.55), respectively) after adjusting for confounders. People with chronic disease were more likely to use HTPs and HTPs together with cigarettes. Further research on the smoking situation of HTPs in patients with chronic diseases is necessary.

As early and effective antiretroviral therapy has become more widespread, HIV has transitioned from a progressive, fatal disease to a chronic, manageable disease marked by elevated risk of chronic comorbid diseases, including cardiovascular diseases (CVDs). Rates of myocardial infarction, heart failure, stroke, and other CVD manifestations, including pulmonary hypertension and sudden cardiac death, are significantly higher for people living with HIV than for uninfected control subjects, even in the setting of HIV viral suppression with effective antiretroviral therapy. These elevated risks generally persist after demographic and clinical risk factors are accounted for and may be partly attributed to chronic inflammation and immune dysregulation. Data on long-term CVD outcomes in HIV are limited by the relatively recent epidemiological transition of HIV to a chronic disease. Therefore, our understanding of CVD pathogenesis, prevention, and treatment in HIV relies on large observational studies, randomized controlled trials of HIV therapies that are underpowered to detect CVD end points, and small interventional studies examining surrogate CVD end points. The purpose of this document is to provide a thorough review of the existing evidence on HIV-associated CVD, in particular atherosclerotic CVD (including myocardial infarction and stroke) and heart failure, as well as pragmatic recommendations on how to approach CVD prevention and treatment in HIV in the absence of large-scale randomized controlled trial data. This statement is intended for clinicians caring for people with HIV, individuals living with HIV, and clinical and translational researchers interested in HIV-associated CVD.

Systemic arterial hypertension affects 72 million US adults and an additional hundreds of millions of persons worldwide.1,2 Most of these are candidates for pharmacological treatment to reduce risk of cardiovascular disease (CVD) events, based primarily on a very large body of epidemiological and intervention research in humans. Because of this high prevalence and the cardiovascular consequences of untreated or inadequately treated hypertension, the selection of drugs for initial and continuing, long-term treatment has large public health and economic implications. Fortunately, such decisions and the expert recommendations that seek to guide them can call on evidence from 4 decades of randomized multicenter clinical trials evaluating effects of treatment on clinical CVD. We summarize that evidence in this article, in approximate chronological order, and we comment on the related treatment guidelines. We close with some of the major clinical questions yet to be resolved. Response by Messerli et al p 2705 Before the current era beginning in the early 1990s of emphasis on positive-control trials, which directly compare different drug regimens, there were 3 decades of trials that compared an active regimen with placebo or, in a few cases, “usual care.” For most of this period, the mainstay of treatment was generally a thiazide-type diuretic (hereinafter called thiazides) or, to a lesser extent, a β-adrenergic blocker (termed β-blockers). With few exceptions, these trials, especially those with high statistical power and thiazide-based regimens, showed benefit for CVD outcomes.3–8 This evidence, which provided a basis for recommending thiazides or β-blockers as first-step drugs in most editions of US guidelines through 1997,9 needs to continue to be given due weight in practice and practice guidelines. The largest and most consistent benefits from the earlier trials were for stroke and (where reported) heart failure. Benefits for coronary heart disease (CHD) were less clear, …

The Framingham Heart Study has contributed importantly to understanding of the causes of coronary heart disease (CHD), stroke, and other cardiovascular diseases. Framingham research has helped define the quantitative and additive nature of these causes or, as they are now called, “cardiovascular risk factors.”1 The National Cholesterol Education Program (NCEP)2 3 has made extensive use of Framingham data in developing its strategy for preventing CHD by controlling high cholesterol levels. The NCEP guidelines2 3 adjust the intensity of cholesterol-lowering therapy with absolute risk as determined by summation of risk factors. The National High Blood Pressure Education Program (NHBPEP) has set forth a parallel approach for blood pressure control. In contrast to the NCEP,2 however, earlier NHBPEP reports issued through the Joint National Committee4 did not match the intensity of therapy to absolute risk for CHD. “Normalization” of blood pressure is the essential goal of therapy regardless of risk status. Blood pressure–lowering therapy is carried out as much for prevention of stroke and other cardiovascular complications as for reduction of CHD risk. Nonetheless, risk assessment could be important for making decisions about type and intensity of therapy for hypertension. Thus, the most recent Joint National Committee report5 gives more attention to risk stratification for adjustment of therapy for hypertension. Although Framingham data have already been influential in the development of national guidelines for risk factor management, the opportunity may exist for both cholesterol and blood pressure programs to draw more extensively from Framingham results when formulating improved risk assessment guidelines and recommending more specific strategies for risk factor modification. The American Heart Association has previously used Framingham risk factor data to prepare charts for estimating CHD risk. Framingham investigators of the National Heart, Lung, and Blood Institute prepared the original charts and have now revised …