After decades of robust growth, the rise in US life expectancy stalled after 2010. Explanations for the stall have focused on rising drug-related deaths. Here we show that a stagnating decline in cardiovascular disease (CVD) mortality was the main culprit, outpacing and overshadowing the effects of all other causes of death. The CVD stagnation held back the increase of US life expectancy at age 25 y by 1.14 y in women and men, between 2010 and 2017. Rising drug-related deaths had a much smaller effect: 0.1 y in women and 0.4 y in men. Comparisons with other high-income countries reveal that the US CVD stagnation is unusually strong, contributing to a stark mortality divergence between the US and peer nations. Without the aid of CVD mortality declines, future US life expectancy gains must come from other causes—a monumental task given the enormity of earlier declines in CVD death rates. Reversal of the drug overdose epidemic will be beneficial, but insufficient for achieving pre-2010 pace of life expectancy growth.
Impressive decreases in cardiovascular mortality have been achieved through risk factor reduction and clinical intervention, yet cardiovascular disease remains a leading cause of death nationally.To estimate up-to-date preventable fractions of cardiovascular mortality associated with elimination and reduction of 5 leading risk factors nationally and by state in the United States.Cross-sectional and cohort studies.Nationally representative and state-representative samples of the U.S. population.Adults aged 45 to 79 years.Self-reported risk factor status in the BRFSS (Behavioral Risk Factor Surveillance System) 2009-2010 was corrected to approximate clinical definitions. The relative hazards of cardiovascular death (International Classification of Diseases, 10th Revision, codes I00 to I99) associated with risk factors were estimated using data from NHANES (National Health and Nutrition Examination Survey) (1988-1994 and 1999-2004, followed through 2006).The preventable fraction of cardiovascular mortality associated with complete elimination of elevated cholesterol levels, diabetes, hypertension, obesity, and smoking was 54.0% for men and 49.6% for women in 2009 to 2010. When the more feasible target of reducing risk factors to the best achieved levels in the states was considered, diabetes (1.7% and 4.1%), hypertension (3.8% and 7.3%), and smoking (5.1% and 4.4%) were independently associated with the largest preventable fractions among men and women, respectively. With both targets, southern states had the largest preventable fractions, and western states had the smallest.Self-reported state data; mortality hazards relied on baseline risk factor status.Major modifiable cardiovascular risk factors collectively accounted for half of cardiovascular deaths in U.S. adults aged 45 to 79 years in 2009 to 2010. Fewer than 10% of cardiovascular deaths nationally could be prevented if all states were to achieve risk factor levels observed in the best-performing states.Robert Wood Johnson Foundation.
Nonalcoholic hepatic steatosis, also known as fatty liver, is a uniform response of the liver to hyperlipidic-hypercaloric diet intake. However, the post-ingestive signals and mechanistic processes driving hepatic steatosis are not well understood. Emerging data demonstrate that protein kinase C beta (PKCβ), a lipid-sensitive kinase, plays a critical role in energy metabolism and adaptation to environmental and nutritional stimuli. Despite its powerful effect on glucose and lipid metabolism, knowledge of the physiological roles of hepatic PKCβ in energy homeostasis is limited. The floxed-PKCβ and hepatocyte-specific PKCβ-deficient mouse models were generated to study the in vivo role of hepatocyte PKCβ on diet-induced hepatic steatosis, lipid metabolism, and mitochondrial function. We report that hepatocyte-specific PKCβ deficiency protects mice from development of hepatic steatosis induced by high-fat diet, without affecting body weight gain. This protection is associated with attenuation of SREBP-1c transactivation and improved hepatic mitochondrial respiratory chain. Lipidomic analysis identified significant increases in the critical mitochondrial inner membrane lipid, cardiolipin, in PKCβ-deficient livers compared to control. Moreover, hepatocyte PKCβ deficiency had no significant effect on either hepatic or whole-body insulin sensitivity supporting dissociation between hepatic steatosis and insulin resistance. The above data indicate that hepatocyte PKCβ is a key focus of dietary lipid perception and is essential for efficient storage of dietary lipids in liver largely through coordinating energy utilization and lipogenesis during post-prandial period. These results highlight the importance of hepatic PKCβ as a drug target for obesity-associated nonalcoholic hepatic steatosis.
Abstract Objectives Reductions in U.S. cardiovascular disease (CVD) mortality have stagnated. While other high life expectancy countries (HLCs) have also recently experienced a stall, the stagnation in CVD mortality in the United States appeared earlier and has been more pronounced. The reasons for the stall are unknown. We analyze cross-national variations in mortality trends to quantify the U.S. exceptionality and provide insight into its underlying causes. Methods Data are from the World Health Organization (2000–2016). We quantified differences in levels and trends of CVD mortality between the United States and 17 other HLCs. We decomposed differences to identify the individual contributions of major CVD subclassifications (ischemic heart disease [IHD], stroke, other heart diseases). To identify potential behavioral explanations, we compared trends in CVD mortality with trends in other causes of death related to obesity, smoking, alcohol, and drugs. Results Our study has four central findings: (a) U.S. CVD mortality is consistently higher than the average of other HLCs; (b) the U.S.–HLC gap declined until around 2008 and increased thereafter; (c) the shift from convergence to divergence was mainly driven by slowing IHD and stroke mortality reductions and increasing mortality from other CVD causes; (d) among the potential risk factors, only obesity- and alcohol-related mortality showed age-specific temporal changes that are similar to those observed for cardiovascular mortality. Discussion The exceptional changes in U.S. CVD mortality are driven by a distinct pattern of slowing reductions in IHD and stroke mortality and deteriorating mortality from other CVD causes. Obesity and alcohol abuse appear to be interrelated factors.
Los efectos tanto del descenso de la fecundidad como el aumento de la longevidad han acelerado la tasa de envejecimiento de la población en distintas partes del mundo. A diferencia de otros países, Puerto Rico también está experimentando niveles de emigración de la población en edad laboral sin precedentes. El impacto total de la elevada emigración en la demografía puertorriqueña no se conoce en su totalidad. Por ello, situar el proceso de envejecimiento de Puerto Rico en un contexto internacional es útil a la hora de identificar el papel que la emigración está teniendo en el envejecimiento acelerado de la sociedad puertorriqueña. Utilizando las estimaciones de 2019 del World Population Prospects, se comparan el patrón de envejecimiento acelerado encontrado en Puerto Rico con las trayectorias de otros seis países con altos porcentajes de población mayor de 65 años en el Asia, Europa y el Caribe de 1960 a 2020. Antes de 2010, el proceso de envejecimiento poblacional en Puerto Rico era comparable al de los otros países. Sin embargo, después de 2010, el porcentaje de la población mayor de 65 años en Puerto Rico casi se duplicó, pasando del 13.1% al 21%. La casi duplicación del porcentaje de adultos mayores no se observa en ninguno de los otros países incluidos en este estudio comparativo. Observamos que el rápido envejecimiento de Puerto Rico, caracterizado por el cambio de una tendencia lineal a una exponencial, es el resultado de la aceleración de los niveles de emigración que se concentraron en la población en edad laboral.
: Mitral regurgitation (MR) is a common cause of morbidity worldwide and an accepted indication for interventional therapies which aim to reduce or resolve adverse clinical outcomes associated with MR. Cardiac magnetic resonance (CMR) provides highly accurate means of assessing MR, including a variety of approaches that can measure MR based on quantitative flow. Additionally, CMR is widely accepted as a reference standard for cardiac chamber quantification, enabling reliable detection of subtle changes in cardiac chamber size and function so as to guide decision-making regarding timing of mitral valve directed therapies. Beyond geometric imaging, CMR enables tissue characterization of ischemia and infarction in the left ventricular (LV) myocardium as well as within the mitral valve apparatus, thus enabling identification of structural substrates for MR. This review provides an overview of established and emerging CMR approaches to measure valvular regurgitation, including relative utility of different approaches for patients with primary or secondary MR. Clinical outcomes studies are discussed with focus on data demonstrating advantages of CMR for guiding diagnosis, risk stratification, and management of patients with known or suspected MR. Comparative data is reviewed with focus on diagnostic performance of CMR in comparison to conventional assessment via echocardiography (echo). Emerging literature is reviewed concerning potential new approaches that utilize CMR tissue characterization to guide clinical decision-making in order to improve therapeutic outcomes and clinical prognosis for patients with MR.