Equity and length of lifespan are not the same.

Efforts to understand the dramatic declines in mortality over the past century have focused on life expectancy. However, understanding changes in disparity in age of death is important to understanding mechanisms of mortality improvement and devising policy to promote health equity. We derive a novel decomposition of variance in age of death, a measure of inequality, and apply it to cause-specific contributions to the change in variance among the G7 countries (Canada, France, Germany, Italy, Japan, the United Kingdom, and the United States) from 1950 to 2010. We find that the causes of death that contributed most to declines in the variance are different from those that contributed most to increase in life expectancy; in particular, they affect mortality at younger ages. We also find that, for two leading causes of death [cancers and cardiovascular disease (CVD)], there are no consistent relationships between changes in life expectancy and variance either within countries over time or between countries. These results show that promoting health at younger ages is critical for health equity and that policies to control cancer and CVD may have differing implications for equity.

Efficacy and Safety of Transcatheter Aortic Valve Implantation in Aortic Stenosis Patients With Extreme Age.

OBJECTIVES: To investigate the in-hospital and long-term outcomes of patients at extreme age with severe symptomatic aortic stenosis (AS) who underwent transcatheter aortic valve implantation (TAVI). METHODS: A total of 276 consecutive patients with a mean age of 82.2 ± 5.0 years with severe symptomatic AS underwent TAVI at our institute. We evaluated periprocedural, in-hospital, and long-term outcomes in all patients aged ≥87 years (the highest 20th percentile of age distribution) and compared them with the less elderly patients. RESULTS: The extremely aged group included 58 patients (21%) ≥87 years (mean age, 89.0 ± 1.9 years; 67.2% women). Baseline EuroSCOREs and STS scores were 19.6 ± 11.2% and 9.4 ± 5.0%, respectively. Nineteen patients (34.5%) were considered frail. Following TAVI, all patients regained New York Heart Association class 1-2 functional capacity. The main periprocedural and in-hospital complications were minor vascular complications, bleeding requiring blood transfusions, and the need for permanent pacemaker. None of the patients suffered from clinical stroke. In comparison to the less elderly patients, there were no significant differences in the rates of periprocedural, in-hospital complications or long-term survival (log rank, 0.87). CONCLUSIONS: Meticulously selected patients at extreme age benefit from TAVI with a reasonable overall risk, which does not impact the overall survival or functional status.

Clopidogrel response up to six months after acute myocardial infarction.

High on-treatment platelet reactivity (HTPR) despite clopidogrel therapy is associated with adverse cardiac events after acute myocardial infarction (AMI). Most studies to date have assessed clopidogrel response at a single time point before or after percutaneous coronary intervention (PCI). It is unclear, however, whether the HTPR phenotype is stable over time. Therefore, we aimed to examine response to clopidogrel in patients with AMI treated with PCI over a 6-month period. Patients (n = 57) with AMI treated with PCI were assessed for response to clopidogrel at 3 time points: in hospital, 30 days, and 6 months after index hospitalization. Response to clopidogrel was determined by the VerifyNow P2Y12 assay (reported as P2Y12 response units) and multiple electrode aggregometry (MEA; reported as aggregation units). HTPR was defined as ≥235 P2Y12 response units or ≥47 aggregation units. Patients' mean age was 54.5 ± 10.9 years, 91% were men, 19% had diabetes, and 74% were admitted with ST-segment elevation MI. HTPR based on MEA was observed in 22.8% of patients in hospital, 26.3% at 30 days, and 17.5% at 6 months (p = NS). HTPR based on the VerifyNow assay was observed in 38.6% of patients in hospital, 28.1% at 30 days, and 33.3% at 6 months (p = NS). Individual HTPR phenotypic assignment at baseline was stable in 73.7% (based on MEA) and 70.2% (based on VerifyNow) of patients at 6-month follow-up. In conclusion, this is the first study evaluating the stability of clopidogrel response over time after AMI. Rates of HTPR to clopidogrel therapy appear to be relatively stable up to 6 months after AMI.

Circulating endothelial progenitor cells in patients with dysfunctional versus normally functioning congenitally bicuspid aortic valves.

Patients with bicuspid aortic valve (BAV) may gradually develop significant valve dysfunction, whereas others remain free of dysfunction. Factors that determine the prognosis of BAV remain unclear. Because endothelial progenitor cells (EPCs) have a role in the repair of endothelial surfaces after injury, we hypothesized that EPCs may also be involved in preventing BAV degeneration. Accordingly, we compared EPC level and function in patients with BAV with versus without valve dysfunction. The study group included 22 patients with BAV and significant valve dysfunction (at least moderate aortic regurgitation and/or at least moderate aortic stenosis). The control group included 28 patients with BAV without valve dysfunction. All patients had 1 blood sample taken. Proportion of peripheral mononuclear cells expressing vascular endothelial growth factor receptor 2, CD133 and CD34 was evaluated by flow cytometry. EPC colony-forming units (CFUs) were grown from peripheral mononuclear cells, characterized, and counted after 7 days of culture. The 2 groups had similar clinical characteristics except for higher prevalence of hypertension in the dysfunctional valve group. Number of EPC CFUs was smaller in the dysfunctional valve group (32 CFUs/plate, 15 to 42.5, vs 48 CFUs/plate, 30 to 62.5, respectively, p = 0.01), and the migratory capacity of the cells in this group was decreased. In addition, the proportion of cells coexpressing vascular endothelial growth factor receptor 2, CD133, and CD34 tended to be smaller in the dysfunctional valve group. In conclusion, patients with BAV and significant valve dysfunction appear to have circulating EPCs with impaired functional properties. These findings require validation by further studies.

Circulating endothelial progenitor cell levels and function in patients who experienced late coronary stent thrombosis.

AIMS: The pathogenesis of late coronary stent thrombosis may be related to impaired arterial healing. Endothelial progenitor cells (EPCs) have been shown to play an important role in repair and re-endothelialization following vascular injury. We hypothesized that patients who develop late stent thrombosis may have reduced or dysfunctional EPCs, and aimed to compare EPC level and function in patients who experienced stent thrombosis vs. matched controls. METHODS AND RESULTS: Patients who developed late (> 30 days) stent thrombosis within the past 3 years were compared with matched patients who underwent stenting and did not develop stent thrombosis. All patients had blood samples taken ≥ 3 months from the stent thrombosis or index procedure. The proportion of peripheral mononuclear cells (PMNCs) expressing vascular endothelial growth factor receptor 2 (VEGFR-2), CD133, and CD34 was evaluated by flow cytometry. Endothelial progenitor cell colony forming units (CFUs) were grown from PMNCs, characterized and counted following 7 days of culture. The two groups (n = 30 each) were well-matched (93.3% men, mean age 60-62 years, 33.3% diabetes, 73-80% DESs). The proportion of cells co-expressing VEGFR-2, CD133, and CD34 was lower in the stent thrombosis group compared with the control [VEGFR-2(+)CD133(+): 0.18% (0.03-0.41%) vs. 0.47% (0.16-0.66%), P = 0.01; VEGFR-2(+)CD34(+): 0.32% (0.22-0.70%) vs. 0.66% (0.24-1.1%), P = 0.03]. The number of EPC CFUs was also lower in the stent thrombosis group [3.9% (3.2-5.5%) vs. 8.3% (6.5-13.4%) colonies/well, respectively, P < 0.0001]. CONCLUSION: Patients who suffered late coronary stent thrombosis appear to have reduced levels of circulating EPCs and impaired functional properties of the cells. These findings require validation by further studies, but may contribute to understanding the pathogenesis of late stent thrombosis.