Productivity loss and indirect costs in the year following acute coronary events in Switzerland

Acute coronary syndrome (ACS) is highly prevalent in Switzerland and a leading cause of death. Associated productivity loss and indirect costs have rarely been studied. We investigated these factors in the first year after ACS in 24 Swiss patients (mean (SD) age 56 (8) years, 79% male). Data on patient productivity loss, absenteeism, presenteeism and caregiver assistance, were collected with the Productivity Cost Questionnaire during a routine cardiologist visit 3 to 12 months after hospitalisation for ACS and at least 4 weeks after patients returned to work. To estimate costs, lost hours were converted into 8-hour workdays, pro-rated to 1 year, combined with time off work due to initial hospitalisation and sick leave, and valued at Swiss labour costs. Additional data came from medical records. ACS patients lost on average (SD, range) 79 (81, 0.3–294) workdays; 38 (36, 0.3–153) days due to the initial hospitalisation and sick leave, 37 (75, 0–243) due to absenteeism after patients returned to work, and 4 (11, 0–41) due to presenteeism. Caregivers lost 10 (23, 0–90) additional workdays. The total indirect costs amounted to CHF 43,205 (44,026, 122–148,648); including CHF 18,514 (17,507, 122-74,619) for initial hospitalisation and sick leave and CHF 17,988 (36,394, 122–143,277) and CHF 1,849 (5181, 0–20,158) for absenteeism and presenteeism after patients returned to work, respectively. Costs of caregiver assistance amounted to CHF 4,855 (11,015, 0–43,843). This study showed that ACS patients lost on average 36% of their annual productive time. Caregivers lost an additional 5%. Lost work time was associated with substantial indirect costs that exceeded estimates of direct costs for ACS during 1 year. This suggests that costs and burden could be reduced through better risk reduction management.

Cocaine consumption and acute coronary syndromes: a cross sectional study from the Swiss registry AMIS Plus

INTRODUCTION Cocaine abuse is a relevant public health issue which causes medical, psychological and social drawbacks. Only limited data are currently available on outcomes of acute coronary syndromes (ACS) in cocaine-addicted patients. The aim of this study was to evaluate the cardiovascular impact of cocaine in a population of patients enrolled in the Swiss nationwide AMIS Plus registry, with a focus on in-hospital outcomes. METHODS We retrospectively analysed data of patients enrolled in the Swiss AMIS Plus registry from 1 January 2007 to 31 December 2018. Baseline and in-hospital data of ACS patients with self-reported regular cocaine abuse were compared with the remaining AMIS Plus population and a sex and age-matched group of non-cocaine user ACS patients (ratio 1:5, 540 patients). Primary endpoints were in-hospital death and major adverse cardiac and cardiovascular events (MACCEs). RESULTS A total of 20,036 patients were included in the AMIS Plus registry for ACS in the study period, of whom 110 (0.5%) reported regular cocaine abuse. As compared with the remaining AMIS population, cocaine users were significantly younger (46.4 ± 10.8 vs 66.4 ± 13.2 years, p <0.001), presented more frequently with out-of-hospital cardiac arrest (11.8% vs 4.7%, p <0.001) and ST-elevation myocardial infarction (68.2% vs 54.7%, p = 0.007). Of the traditional cardiovascular risk factors, there was a higher incidence of positive family history and active smoking, but a lower incidence of arterial hypertension, diabetes and obesity. In-hospital mortality (3.6% vs 4.4%, p = 1) and MACCEs (5.4% vs 5.5%, p = 0.83) were comparable. When compared with an age-matched non-cocaine user ACS population, cocaine users were more frequently smokers (87.6% vs 63.6%, p <0.001) but less frequently obese (10.4% vs 25.6%, p = 0.001). Clinical presentation was comparable between the two groups. However, cocaine abuse was associated with a higher incidence of in-hospital death (3.7% vs 0.7%, p <0.05) and MACCEs (5.6% vs 1.3%, p <0.05). CONCLUSION Cocaine abuse increases the risk of mortality by a factor of 5 and the risk of major adverse cardiac and cardiovascular events by a factor of 4 as compared with a sex and age-matched population hospitalised after an acute coronary syndrome.

Clinical value of soluble suppression of tumourigenicity 2 (sST2) in addition to NTproBNP measurements in a general cardiac outpatient population

BACKGROUND AND AIMS: The soluble form of suppression of tumourigenicity 2 (sST2), a recently introduced biomarker, is a strong and NTproBNP-independent predictor of outcome in heart failure patients. This study sought to evaluate the added clinical value of sST2 in addition to NTproBNP in a heterogeneous cardiac outpatient population. METHODS: A total of 297 all-comer patients visiting the outpatient clinic of Heart Clinic Zurich, Switzerland, from January to December 2018 were included. Patients were divided into four groups depending on their sST2 and NTproBNP levels: group 1 (n = 91, 30.6% of all patients) with normal levels of both biomarkers, group 2 (n = 41, 13.8%) with isolated elevation of sST2 but normal NTproBNP, group 3 (n = 97, 32.7%) with elevated NTproBNP but normal sST2 levels, and group 4 (n = 68, 22.9%) with elevation of both biomarkers. Differences between groups, Spearman’s correlations and linear and multiple regression analysis for sST2 were calculated. RESULTS: The median age was 74 ± 19 years and 41.8% were women. NTproBNP levels continuously increased across the groups (medians in pg/ml: group 1 123.0, group 2 152.0, group 3 990.0 and group 4 2610.0), whereas sST2 levels did not (medians in ng/ml: 28.7, 58.9, 28.4 and 63.7 for groups 1 to 4, respectively). In patients with normal NTproBNP (groups 1 and 2), elevation of sST2 (group 2) was associated with significantly higher rates of coronary artery disease, peripheral vascular disease and renal dysfunction. In patients with elevated NTproBNP (groups 3 and 4), the additional elevation of sST2 (group 4) was associated with clinical signs of heart failure, higher EuroScore II and worse left ventricular ejection fraction (LVEF group 3 58.0% vs group 4 53.3%, p = 0.022). Correlation of sST2 was overall weak and weaker than of NTproBNP with most clinical variables. Soluble ST2 significantly correlated with EuroScore II (R = 0.280), kidney function (R = −0.259), C-reactive protein (R = 0.248), right ventricular function (R = 0.213) and left atrial volume (R = 0.199), all p ≤0.001. In multiple regression analysis, left atrial volume was the strongest independent predictor of sST2 elevation (p = 0.002). CONCLUSION: In this all-comer cardiology population, the added clinical value of sST2 measurements in addition to NTproBNP was small. In patients with elevated NTproBNP, the simultaneous elevation of sST2 was associated with clinical signs of heart failure. Soluble ST2 measurements could thus be beneficial in patients with uncertain signs of heart failure and confounding factors for NTproBNP elevation. Surprisingly, this study found elevated sST2 levels in a substantial number of a patients with normal NTproBNP levels, pointing to an additional pathway of sST2 elevation independent of heart failure.

Co-repressing immunometabolic processes in atherosclerosis

Cardiovascular disease is the primary cause of mortality in the world, and tightly associated with the metabolic syndrome, which is a cluster of interconnected metabolic dysfunctions including insulin resistance, obesity, hypertension and dyslipidaemias. These dysfunctions increase the risk of developing atherosclerosis and consequent cardiovascular diseases, such as myocardial infarction and stroke. Atherosclerosis is primarily triggered by increased plasma cholesterol levels and can be classified as an immunometabolic disease, a chronic disease that is affected by both metabolic and inflammatory triggers and/or mediators. These triggers and mediators activate common downstream pathways, including nuclear receptor signalling. Interestingly, specific cofactors that bind to these complexes act as immunometabolic integrators. This review provides examples of such co-regulator complexes, including nuclear sirtuins, nuclear receptor co-repressor 1 (NCOR1), nuclear receptor interacting protein 1 (NRIP1), and prospero homeobox 1 (PROX1). Their study might provide novel insight into mechanistic regulations and the identification of new targets to treat atherosclerosis.