Global burden of cardiovascular diseases and risk factors, 1990–2019: update from the GBD 2019 study

Cardiovascular diseases (CVDs), principally ischemic heart disease (IHD) and stroke, are the leading cause of global mortality and a major contributor to disability. This paper reviews the magnitude of total CVD burden, including 13 underlying causes of cardiovascular death and 9 related risk factors, using estimates from the Global Burden of Disease (GBD) Study 2019. GBD, an ongoing multinational collaboration to provide comparable and consistent estimates of population health over time, used all available population-level data sources on incidence, prevalence, case fatality, mortality, and health risks to produce estimates for 204 countries and territories from 1990 to 2019. Prevalent cases of total CVD nearly doubled from 271 million (95% uncertainty interval [UI]: 257 to 285 million) in 1990 to 523 million (95% UI: 497 to 550 million) in 2019, and the number of CVD deaths steadily increased from 12.1 million (95% UI:11.4 to 12.6 million) in 1990, reaching 18.6 million (95% UI: 17.1 to 19.7 million) in 2019. The global trends for disability-adjusted life years (DALYs) and years of life lost also increased significantly, and years lived with disability doubled from 17.7 million (95% UI: 12.9 to 22.5 million) to 34.4 million (95% UI:24.9 to 43.6 million) over that period. The total number of DALYs due to IHD has risen steadily since 1990, reaching 182 million (95% UI: 170 to 194 million) DALYs, 9.14 million (95% UI: 8.40 to 9.74 million) deaths in the year 2019, and 197 million (95% UI: 178 to 220 million) prevalent cases of IHD in 2019. The total number of DALYs due to stroke has risen steadily since 1990, reaching 143 million (95% UI: 133 to 153 million) DALYs, 6.55 million (95% UI: 6.00 to 7.02 million) deaths in the year 2019, and 101 million (95% UI: 93.2 to 111 million) prevalent cases of stroke in 2019. Cardiovascular diseases remain the leading cause of disease burden in the world. CVD burden continues its decades-long rise for almost all countries outside high-income countries, and alarmingly, the age-standardized rate of CVD has begun to rise in some locations where it was previously declining in high-income countries. There is an urgent need to focus on implementing existing cost-effective policies and interventions if the world is to meet the targets for Sustainable Development Goal 3 and achieve a 30% reduction in premature mortality due to noncommunicable diseases

A geospatial assessment of the relationship between reef flat community calcium carbonate production and wave energy

The ability of benthic communities inhabiting coral reefs to produce calcium carbonate underpins the development of reef platforms and associated sedimentary landforms, as well as the fixation of inorganic carbon and buffering of diurnal pH fluctuations in ocean surface waters. Quantification of the relationship between reef flat community calcium carbonate production and wave energy provides an empirical basis for understanding and managing this functionally important process. This study employs geospatial techniques across the reef platform at Lizard Island, Great Barrier Reef, to (1) map the distribution and estimate the total magnitude of reef community carbonate production and (2) empirically ascertain the influence of wave energy on community carbonate production. A World-View-2 satellite image and a field data set of 364 ground referencing points are employed, along with data on physical reef characteristics (e.g. bathymetry, rugosity) to map and validate the spatial distribution of the four major community carbonate producers (live coral, carbonate sand, green calcareous macroalgae and encrusting calcified algae) across the reef platform. Carbonate production is estimated for the complete reef platform from the composition of these community components. A synoptic model of wave energy is developed using the Simulating WAves Nearshore (SWAN) two-dimensional model for the entire reef platform. The relationship between locally derived measures of carbonate production and wave energy is evaluated at both the global scale and local scale along spatial gradients of wave energy traversing the reef platform. A wave energy threshold is identified, below which carbonate production levels appear to increase with wave energy and above which mechanical forcing reduces community production. This implies an optimal set of hydrodynamic conditions characterized by wave energy levels of approximately 300 J m, providing an empirical basis for management of potential changes in community carbonate production associated with climate change-driven increases in wave energy

Low doses of Celecoxib attenuate gut barrier failure during experimental peritonitis

The intestinal barrier becomes compromised during systemic inflammation, leading to entry of luminal bacteria into the host and gut origin sepsis. Pathogenesis and treatment of inflammatory gut barrier failure is an important problem in critical care. In this study we examined the role of cyclooxygenase-2 (COX-2), a key enzyme in the production of inflammatory prostanoids, in gut barrier failure during experimental peritonitis in mice. I.p. injection of LPS or cecal ligation and puncture (CLP) increased the levels of COX-2 and its product prostaglandin E(2) (PGE(2)) in the ileal mucosa, caused pathologic sloughing of the intestinal epithelium, increased passage of FITC-dextran and bacterial translocation across the barrier, and increased internalization of the tight junction-associated proteins JAM-A and ZO-1. Luminal instillation of PGE(2) in an isolated ileal loop increased transepithelial passage of FITC-dextran. Low doses (0.5–1 mg/kg), but not a higher dose (5 mg/kg) of the specific COX-2 inhibitor Celecoxib partially ameliorated the inflammatory gut barrier failure. These results demonstrate that high levels of COX-2-derived PGE(2) seen in the mucosa during peritonitis contribute to gut barrier failure, presumably by compromising tight junctions. Low doses of specific COX-2 inhibitors may blunt this effect while preserving the homeostatic function of COX-2-derived prostanoids. Low doses of COX-2 inhibitors may find use as an adjunct barrier-protecting therapy in critically ill patients

ESICM LIVES 2016: part two : Milan, Italy. 1-5 October 2016.

Meeting abstrac