Long-term effects of coronavirus disease 2019 on the cardiovascular system, CV COVID registry: A structured summary of a study protocol

COVID-19; Cardiologia; PronòsticCOVID-19; Cardiología; PronósticoCOVID 19; Cardiology; PrognosisBackground Patients presenting with the coronavirus-2019 disease (COVID-19) may have a high risk of cardiovascular adverse events, including death from cardiovascular causes. The long-term cardiovascular outcomes of these patients are entirely unknown. We aim to perform a registry of patients who have undergone a diagnostic nasopharyngeal swab for SARS-CoV-2 and to determine their long-term cardiovascular outcomes. Study and design This is a multicenter, observational, retrospective registry to be conducted at 17 centers in Spain and Italy (ClinicalTrials.gov number: NCT04359927). Consecutive patients older than 18 years, who underwent a real-time reverse transcriptase-polymerase chain reaction (RT-PCR) for SARS-CoV2 in the participating institutions, will be included since March 2020, to August 2020. Patients will be classified into two groups, according to the results of the RT-PCR: COVID-19 positive or negative. The primary outcome will be cardiovascular mortality at 1 year. The secondary outcomes will be acute myocardial infarction, stroke, heart failure hospitalization, pulmonary embolism, and serious cardiac arrhythmias, at 1 year. Outcomes will be compared between the two groups. Events will be adjudicated by an independent clinical event committee. Conclusion The results of this registry will contribute to a better understanding of the long-term cardiovascular implications of the COVID19.SB. Research grant (COV20/00040) from the Carlos III Institute, Madrid, Spain

One-year cardiovascular outcomes after coronavirus disease 2019: The cardiovascular COVID-19 registry

COVID 19; Arrhythmia; Ischemic strokeCOVID 19; Arrítmia; Ictus isquèmicCOVID-19; Arritmia; Ictus isquémicoBackground: The long-term cardiovascular (CV) outcomes of COVID-19 have not been fully explored. Methods: This was an international, multicenter, retrospective cohort study conducted between February and December 2020. Consecutive patients ≥18 years who underwent a real-time reverse transcriptase-polymerase chain reaction (RT-PCR) for SARS-CoV2 were included. Patients were classified into two cohorts depending on the nasopharyngeal swab result and clinical status: confirmed COVID-19 (positive RT-PCR) and control (without suggestive symptoms and negative RT-PCR). Data were obtained from electronic records, and clinical follow-up was performed at 1-year. The primary outcome was CV death at 1-year. Secondary outcomes included arterial thrombotic events (ATE), venous thromboembolism (VTE), and serious cardiac arrhythmias. An independent clinical event committee adjudicated events. A Cox proportional hazards model adjusted for all baseline characteristics was used for comparing outcomes between groups. A prespecified landmark analysis was performed to assess events during the post-acute phase (31-365 days). Results: A total of 4,427 patients were included: 3,578 (80.8%) in the COVID-19 and 849 (19.2%) control cohorts. At one year, there were no significant differences in the primary endpoint of CV death between the COVID-19 and control cohorts (1.4% vs. 0.8%; HRadj 1.28 [0.56-2.91]; p = 0.555), but there was a higher risk of all-cause death (17.8% vs. 4.0%; HRadj 2.82 [1.99-4.0]; p = 0.001). COVID-19 cohort had higher rates of ATE (2.5% vs. 0.8%, HRadj 2.26 [1.02-4.99]; p = 0.044), VTE (3.7% vs. 0.4%, HRadj 9.33 [2.93-29.70]; p = 0.001), and serious cardiac arrhythmias (2.5% vs. 0.6%, HRadj 3.37 [1.35-8.46]; p = 0.010). During the post-acute phase, there were no significant differences in CV death (0.6% vs. 0.7%; HRadj 0.67 [0.25-1.80]; p = 0.425), but there was a higher risk of deep vein thrombosis (0.6% vs. 0.0%; p = 0.028). Re-hospitalization rate was lower in the COVID-19 cohort compared to the control cohort (13.9% vs. 20.6%; p = 0.001). Conclusions: At 1-year, patients with COVID-19 experienced an increased risk of all-cause death and adverse CV events, including ATE, VTE, and serious cardiac arrhythmias, but not CV death.This research was funded by Carlos III Health Institute (Madrid, Spain) and co-funded by the European Union, grant number COV20/00040. Dr. Bikdeli is supported by the Scott Schoen and Nancy Adams IGNITE Award from the Mary Horrigan Connors Center for Women’s Health and Gender Biology at Brigham and Women’s Hospital and a Career Development Award from the American Heart Association (#938814)

Extended use of dual antiplatelet therapy among older adults with acute coronary syndromes and associated variables: a cohort study

Acute coronary syndromes; Dual antiplatelet therapy; ElderlySíndromes coronàries agudes; Teràpia antiplaquetària dual; Gent granSíndromes coronarios agudos; Terapia antiplaquetaria dual; Personas mayoresBackground Current guidelines recommend extending the use of dual antiplatelet therapy (DAPT) beyond 1 year in patients with an acute coronary syndrome (ACS) and a high risk of ischaemia and low risk of bleeding. No data exist about the implementation of this strategy in older adults from routine clinical practice. Methods We conducted a Spanish multicentre, retrospective, observational registry-based study that included patients with ACS but no thrombotic or bleeding events during the first year of DAPT after discharge and no indication for oral anticoagulants. High bleeding risk was defined according to the Academic Research Consortium definition. We assessed the proportion of cases of extended DAPT among patients 65 ≥ years that went beyond 1 year after hospitalisation for ACS and the variables associated with the strategy. Results We found that 48.1% (928/1,928) of patients were aged ≥ 65 years. DAPT was continued beyond 1 year in 32.1% (298/928) of patients ≥ 65; which was a similar proportion as with their younger counterparts. There was no significant correlation between a high bleeding risk and DAPT duration. Contrastingly, there was a strong correlation between the extent of coronary disease and DAPT duration (p < 0.001). Other variables associated with extended DAPT were a higher left ventricle ejection fraction, a history of heart failure and a prior stent thrombosis. Conclusion There was no correlation between age and extended use of DAPT beyond 1 year in older patients with ACS. DAPT was extended in about one-third of patients ≥ 65 years. The severity of the coronary disease, prior heart failure, left ventricle ejection fraction and prior stent thrombosis all correlated with extended DAPT.This work was supported by the “Instituto de Salud Carlos III” and “Fondos Europeos de Desarrollo Regional FEDER” [grant numbers JR/21/00041, PI20/00637 and CIBERCV16/11/00486] and by Conselleria de Educación – Generalitat Valenciana (PROMETEO/2021/008)

Evaluation of the Use of Dual Antiplatelet Therapy beyond the First Year after Acute Coronary Syndrome

Acute coronary syndrome; Dual antiplatelet therapy; Ischemic riskSíndrome coronario agudo; Terapia antiplaquetaria dual; Riesgo isquémicoSíndrome coronària aguda; Teràpia antiplaquetària dual; Risc isquèmicClinical practice guidelines recommend extending dual antiplatelet therapy (DAPT) beyond 1 year after acute coronary syndrome (ACS) in patients with high ischemic risk and without high bleeding risk. The aim of this study was to identify variables associated with DAPT prolongation in a cohort of 1967 consecutive patients discharged after ACS without thrombotic or hemorrhagic events during the following year. The sample was stratified according to whether DAPT was extended beyond 1 year, and the factors associated with this strategy were analyzed. In 32.2% of the patients, DAPT was extended beyond 1 year. Overall, 770 patients (39.1%) were considered candidates for extended treatment based on PEGASUS criteria and absence of high bleeding risk, and DAPT was extended in 34.4% of them. The presence of a PEGASUS criterion was associated with extended DAPT in the univariate analysis, but not history of bleeding or a high bleeding risk. In the multivariate analysis, a history of percutaneous coronary intervention (odds ratio (OR) = 1.8, 95% confidence interval (CI) 1.4–2.4), stent thrombosis (OR = 3.8, 95% CI 1.7–8.9), coronary artery disease complexity (OR = 1.3, 95% CI 1.1–1.5), reinfarction (OR = 4.1, 95% CI 1.6–10.4), and clopidogrel use (OR = 1.3, 95% CI 1.1–1.6) were significantly associated with extended use. DAPT was extended in 32.2% of patients who survived ACS without thrombotic or hemorrhagic events. This percentage was 34.4% when the candidates were analyzed according to clinical guidelines. Neither the PEGASUS criteria nor the bleeding risk was independently associated with this strategy.This work was supported by “Instituto de Salud Carlos III” and “Fondos Europeos de Desarrollo Regional FEDER” [grant numbers JR/21/00041, PI20/00637 and CIBERCV16/11/00486] and by Conselleria de Educación – Generalitat Valenciana (PROMETEO/2021/008)

Hospital and 4-year mortality predictors in patients with acute pulmonary edema with and without coronary artery disease

Long-term prognosis of acute pulmonary edema () remains ill defined. We evaluated demographic, echocardiographic, and angiographic data of 806 consecutive patients with with () and without coronary artery disease (non-) admitted from 2000 to 2010. Differences between hospital and long-term mortality and its predictors were also assessed. patients (n=638) were older and had higher incidence of diabetes and peripheral vascular disease than non- (n=168), and lower ejection fraction. Hospital mortality was similar in both groups (26.5% vs 31.5%; P =0.169) but recurrence was higher in patients (17.3% vs 6.5%; P <0.001). Age, admission systolic blood pressure, recurrence of , and need for inotropics or endotracheal intubation were the main independent predictors of hospital mortality. In contrast, overall mortality (70.0% vs 57.1%; P =0.002) and readmission for nonfatal heart failure after a 45-month follow-up (10-140; 17.3% vs 7.6%; P =0.009) were higher in than in non- patients. Age, peripheral vascular disease, and peak creatine kinase during index hospitalization, but not ejection fraction, were the main independent predictors of overall mortality, whereas coronary revascularization or valvular surgery were protective. These interventions were mostly performed during hospitalization index (294 of 307; 96%) and not intervened patients showed a higher risk profile. Long-term mortality in is high and higher in than in non- patients. Considering the different in-hospital and long-term mortality predictors herein described, which do not necessarily involve systolic function, it is conceivable that a more aggressive interventional program might improve survival in high-risk patients

Diabetic retinopathy as an independent predictor of subclinical cardiovascular disease: baseline results of the PRECISED study

Type 2 diabetes; Diabetic retinopathy; Subclinical cardiovascular diseaseDiabetis tipus 2; Retinopatia diabètica; Malalties cardiovasculars subclíniquesDiabetes tipo 2; Retinopatía diabética; Enfermedades cardiovasculares subclínicasObjective Detection of subclinical cardiovascular disease (CVD) has significant impact on the management of type 2 diabetes. We examined whether the assessment of diabetic retinopathy (DR) is useful for identifying patients at a higher risk of having silent CVD. Research design and methods Prospective case–control study comprising 200 type 2 diabetic subjects without history of clinical CVD and 60 age-matched non-diabetic subjects. The presence of subclinical CVD was examined using two parameters: (1) calcium coronary score (CACs); (2) composite of CACs >400 UA, carotid plaque ≥3 mm, carotid intima–media thickness ratio >1, or the presence of ECG changes suggestive of previous asymptomatic myocardial infarction. In addition, coronary angio-CT was performed. DR was assessed by slit-lamp biomicroscopy and retinography. Results Type 2 diabetic subjects presented higher CACs than non-diabetic control subjects (p400 (area under the receiver operating characteristic curve (AUROC) 0.76). In addition, an inverse relationship was observed between the degree of DR and CACs <10 AU. The variables independently associated with the composite measurement of subclinical CVD were age, diabetes duration, the glomerular filtration rate, microalbuminuria, and the presence of DR (AUROC 0.71). In addition, a relationship (p<0.01) was observed between the presence and degree of DR and coronary stenosis. Conclusions The presence and degree of DR is independently associated with subclinical CVD in type 2 diabetic patients. Our results lead us to propose a rationalized screening for coronary artery disease in type 2 diabetes based on prioritizing patients with DR, particularly those with moderate–severe degree.This work was supported by an Integrative Excellence Project by the Spanish Institute of Health, Instituto de Salud Carlos III, grant PIE 2013/27, CIBER CV, CIBERDEM, and the European Regional Development Fund (ERDF-FEDER). The Neurovascular Research Laboratory is part of the Spanish Stroke Research Network INVICTUS+ (RD16/0019/0021)

Long-term effects of coronavirus disease 2019 on the cardiovascular system, CV COVID registry: A structured summary of a study protocol

Background: Patients presenting with the coronavirus-2019 disease (COVID-19) may have a high risk of cardiovascular adverse events, including death from cardiovascular causes. The long-term cardiovascular outcomes of these patients are entirely unknown. We aim to perform a registry of patients who have undergone a diagnostic nasopharyngeal swab for SARS-CoV-2 and to determine their long-term cardiovascular outcomes. Study and design: This is a multicenter, observational, retrospective registry to be conducted at 17 centers in Spain and Italy (ClinicalTrials.gov number: NCT04359927). Consecutive patients older than 18 years, who underwent a real-time reverse transcriptase-polymerase chain reaction (RT-PCR) for SARS-CoV2 in the participating institutions, will be included since March 2020, to August 2020. Patients will be classified into two groups, according to the results of the RT-PCR: COVID-19 positive or negative. The primary outcome will be cardiovascular mortality at 1 year. The secondary outcomes will be acute myocardial infarction, stroke, heart failure hospitalization, pulmonary embolism, and serious cardiac arrhythmias, at 1 year. Outcomes will be compared between the two groups. Events will be adjudicated by an independent clinical event committee. Conclusion: The results of this registry will contribute to a better understanding of the long-term cardiovascular implications of the COVID19

Efectos de la contaminación atmosférica sobre la incidencia, mortalidad y arritmias ventriculares en el síndrome coronario agudo con elevación del ST

Antecedentes. El conocimiento del papel de la contaminación atmosférica (CA) como desencadenante del síndrome coronario agudo con elevación del ST (SCAEST) es escaso y controvertido. Por otra parte no se conoce el efecto de la CA sobre la gravedad en la fase aguda del SCAEST en términos de mortalidad y arritmias ventriculares. Objetivo: determinar si la CA incrementa la incidencia, mortalidad y arritmias ventriculares en el SCAEST. Métodos. El estudio se ha realizado en la Regió Sanitària de Barcelona entre enero de 2010 y diciembre de 2011. De forma prospectiva, a través del Registro Codi IAM se han obtenido las series temporales del número de SCAEST, y su mortalidad y arritmias ventriculares asociadas. Las variables meteorológicas y las concentraciones de los principales contaminantes atmosféricos han sido también representadas mediante series temporales. Se han definido tres cohortes con criterios geográficos y temporales para minimizar el sesgo de exposición. La magnitud de las asociaciones se ha estimado mediante un modelo de regresión de Poisson autorregresiva. Se han obtenido medidas de asociación y de impacto. Los análisis se han realizado utilizando el software RStudio 0.97.551. Resultados. El número diario de SCAEST se asoció con incrementos en 10 unidades (microgramos por metro cúbico, excepto plomo que fue medido en nanogramos por metro cúbico) de las concentraciones de materia particulada (PM) 2.5 con un riesgo relativo (RR) de 1.005 [intervalo de confianza (IC) 95%: 1.001-1.010] , PM 10 con un RR de 1.004 (IC 95%: 1.000-1.007), dióxido de nitrógeno con un RR de 1.002 (IC 95%: 1.000-1.003), plomo con un RR de 1.0260 (IC 95%: 1.0027-1.0480) y monóxido de nitrógeno con un RR de 1.0140 (IC 95%: 1.0009-1.0270). La mortalidad se asoció a incrementos en 10 unidades de PM 2.5 y PM 10 con un RR de 1.042 (IC 95%: 1.012-1.070) y RR de 1.036 (IC 95%: 1.011-1.059), respectivamente. Las arritmias ventriculares se asociaron con incrementos en 10 unidades de PM 2.5 con un RR de 1.016 (IC 95%: 1.003-1.028). La proporción de riesgo atribuible alcanzó un 4.58% en la exposición al plomo para desencadenar un SCAEST, y un 11.9% y un 3.76% en la exposición a PM 2.5 y su relación con la mortalidad y las arritmias ventriculares respectivamente. Conclusiones. La exposición a corto plazo de PM2.5, PM 10, monóxido y dióxido de nitrógeno y plomo incrementa la incidencia de SCAEST. La exposición a PM 2.5 y PM 10 incrementa la mortalidad en fase aguda y PM 2.5 incrementa el riesgo de presentar arritmias ventriculares. La proporción de complicaciones graves en fase aguda de un SCAEST que se podrían evitar alcanza un máximo de 11.9% en reducción de mortalidad si se evitase la exposición a PM 2.5. A señalar que PM 2.5 resulta ser el contaminante más dañino por lo que los esfuerzos sociopolíticos deberían dirigirse a disminuir sus concentraciones ambientales en primer lugar.Background. Knowledge of the role of air pollution (AP) as a trigger for ST elevation acute coronary syndrome (STEACS) is scarce and controversial. On the other hand, the effect of AP on severity in the acute phase of STEACS in terms of mortality and ventricular arrhythmias is not known. Objective: To determine if AP increases the incidence, mortality and ventricular arrhythmias in the STEACS. Methods. The study was carried out in the Regió Sanitària of Barcelona between January 2010 and December 2011. In a prospective way, through the Codi IAM Registry, the time series of the number of STEACS and their mortality and associated ventricular arrhythmias were obtained. The meteorological variables and the concentrations of the main air pollutants have also been represented by time series. Three cohorts with geographic and temporal criteria have been defined to minimize exposure bias. The magnitude of the associations has been estimated using an autoregressive Poisson regression model. Association and impact measures have been obtained. The analyzes were performed using the software RStudio 0.97.551. Results. The daily number of STEACS was associated with increments of 10 units (micrograms per cubic meter, except lead measured in nanograms per cubic meter) of particulate matter (PM) 2.5 with a relative risk (RR) of 1.005 [ confidence interval (CI) 95%: 1.001-1.010], PM 10 with RR of 1.004 (95% CI: 1.000-1.007), nitrogen dioxide with RR of 1.002 (95% CI: 1.000-1.003), lead with a RR of 1.0260 (95% CI: 1.0027-1.0480) and nitrogen monoxide with an RR of 1.0140 (95% CI: 1.0009-1.0270). Mortality was associated with increases in 10 units of PM 2.5 and PM 10 with an RR of 1.042 (95% CI: 1012-1.070) and RR of 1.036 (95% CI: 1011-1.059), respectively. Ventricular arrhythmias were associated with increments in 10 units of PM 2.5 with a RR of 1.016 (95% CI: 1.003-1.028). The proportion of attributable risk reached 4.58% in lead exposure to trigger a STEACS, and 11.9% and 3.76% in exposure to PM 2.5 and its relationship with mortality and ventricular arrhythmias respectively. Conclusions. Short-term exposure to PM2.5, PM 10, monoxide and dioxide nitrogen and lead increases the incidence of STEACS. Exposure to PM 2.5 and PM 10 increases acute phase mortality and PM 2.5 increases the risk of ventricular arrhythmias. The proportion of severe acute phase STEACS complications that could be prevented reaches a maximum of 11.9% in reducing mortality if exposure to PM 2.5 is avoided. It should be noted that PM 2.5 turns out to be the most harmful pollutant so that sociopolitical efforts should be directed at lowering their environmental concentrations in the first place

Efectos de la contaminación atmosférica sobre la incidencia, mortalidad y arritmias ventriculares en el síndrome coronario agudo con elevación del ST /

Antecedentes. El conocimiento del papel de la contaminación atmosférica (CA) como desencadenante del síndrome coronario agudo con elevación del ST (SCAEST) es escaso y controvertido. Por otra parte no se conoce el efecto de la CA sobre la gravedad en la fase aguda del SCAEST en términos de mortalidad y arritmias ventriculares. Objetivo: determinar si la CA incrementa la incidencia, mortalidad y arritmias ventriculares en el SCAEST. Métodos. El estudio se ha realizado en la Regió Sanitària de Barcelona entre enero de 2010 y diciembre de 2011. De forma prospectiva, a través del Registro Codi IAM se han obtenido las series temporales del número de SCAEST, y su mortalidad y arritmias ventriculares asociadas. Las variables meteorológicas y las concentraciones de los principales contaminantes atmosféricos han sido también representadas mediante series temporales. Se han definido tres cohortes con criterios geográficos y temporales para minimizar el sesgo de exposición. La magnitud de las asociaciones se ha estimado mediante un modelo de regresión de Poisson autorregresiva. Se han obtenido medidas de asociación y de impacto. Los análisis se han realizado utilizando el software RStudio 0.97.551. Resultados. El número diario de SCAEST se asoció con incrementos en 10 unidades (microgramos por metro cúbico, excepto plomo que fue medido en nanogramos por metro cúbico) de las concentraciones de materia particulada (PM) 2.5 con un riesgo relativo (RR) de 1.005 [intervalo de confianza (IC) 95%: 1.001-1.010] , PM 10 con un RR de 1.004 (IC 95%: 1.000-1.007), dióxido de nitrógeno con un RR de 1.002 (IC 95%: 1.000-1.003), plomo con un RR de 1.0260 (IC 95%: 1.0027-1.0480) y monóxido de nitrógeno con un RR de 1.0140 (IC 95%: 1.0009-1.0270). La mortalidad se asoció a incrementos en 10 unidades de PM 2.5 y PM 10 con un RR de 1.042 (IC 95%: 1.012-1.070) y RR de 1.036 (IC 95%: 1.011-1.059), respectivamente. Las arritmias ventriculares se asociaron con incrementos en 10 unidades de PM 2.5 con un RR de 1.016 (IC 95%: 1.003-1.028). La proporción de riesgo atribuible alcanzó un 4.58% en la exposición al plomo para desencadenar un SCAEST, y un 11.9% y un 3.76% en la exposición a PM 2.5 y su relación con la mortalidad y las arritmias ventriculares respectivamente. Conclusiones. La exposición a corto plazo de PM2.5, PM 10, monóxido y dióxido de nitrógeno y plomo incrementa la incidencia de SCAEST. La exposición a PM 2.5 y PM 10 incrementa la mortalidad en fase aguda y PM 2.5 incrementa el riesgo de presentar arritmias ventriculares. La proporción de complicaciones graves en fase aguda de un SCAEST que se podrían evitar alcanza un máximo de 11.9% en reducción de mortalidad si se evitase la exposición a PM 2.5. A señalar que PM 2.5 resulta ser el contaminante más dañino por lo que los esfuerzos sociopolíticos deberían dirigirse a disminuir sus concentraciones ambientales en primer lugar.Background. Knowledge of the role of air pollution (AP) as a trigger for ST elevation acute coronary syndrome (STEACS) is scarce and controversial. On the other hand, the effect of AP on severity in the acute phase of STEACS in terms of mortality and ventricular arrhythmias is not known. Objective: To determine if AP increases the incidence, mortality and ventricular arrhythmias in the STEACS. Methods. The study was carried out in the Regió Sanitària of Barcelona between January 2010 and December 2011. In a prospective way, through the Codi IAM Registry, the time series of the number of STEACS and their mortality and associated ventricular arrhythmias were obtained. The meteorological variables and the concentrations of the main air pollutants have also been represented by time series. Three cohorts with geographic and temporal criteria have been defined to minimize exposure bias. The magnitude of the associations has been estimated using an autoregressive Poisson regression model. Association and impact measures have been obtained. The analyzes were performed using the software RStudio 0.97.551. Results. The daily number of STEACS was associated with increments of 10 units (micrograms per cubic meter, except lead measured in nanograms per cubic meter) of particulate matter (PM) 2.5 with a relative risk (RR) of 1.005 [ confidence interval (CI) 95%: 1.001-1.010], PM 10 with RR of 1.004 (95% CI: 1.000-1.007), nitrogen dioxide with RR of 1.002 (95% CI: 1.000-1.003), lead with a RR of 1.0260 (95% CI: 1.0027-1.0480) and nitrogen monoxide with an RR of 1.0140 (95% CI: 1.0009-1.0270). Mortality was associated with increases in 10 units of PM 2.5 and PM 10 with an RR of 1.042 (95% CI: 1012-1.070) and RR of 1.036 (95% CI: 1011-1.059), respectively. Ventricular arrhythmias were associated with increments in 10 units of PM 2.5 with a RR of 1.016 (95% CI: 1.003-1.028). The proportion of attributable risk reached 4.58% in lead exposure to trigger a STEACS, and 11.9% and 3.76% in exposure to PM 2.5 and its relationship with mortality and ventricular arrhythmias respectively. Conclusions. Short-term exposure to PM2.5, PM 10, monoxide and dioxide nitrogen and lead increases the incidence of STEACS. Exposure to PM 2.5 and PM 10 increases acute phase mortality and PM 2.5 increases the risk of ventricular arrhythmias. The proportion of severe acute phase STEACS complications that could be prevented reaches a maximum of 11.9% in reducing mortality if exposure to PM 2.5 is avoided. It should be noted that PM 2.5 turns out to be the most harmful pollutant so that sociopolitical efforts should be directed at lowering their environmental concentrations in the first place

Hospital and 4-year mortality predictors in patients with acute pulmonary edema with and without coronary artery disease

Long-term prognosis of acute pulmonary edema () remains ill defined. We evaluated demographic, echocardiographic, and angiographic data of 806 consecutive patients with with () and without coronary artery disease (non-) admitted from 2000 to 2010. Differences between hospital and long-term mortality and its predictors were also assessed. patients (n=638) were older and had higher incidence of diabetes and peripheral vascular disease than non- (n=168), and lower ejection fraction. Hospital mortality was similar in both groups (26.5% vs 31.5%; P =0.169) but recurrence was higher in patients (17.3% vs 6.5%; P <0.001). Age, admission systolic blood pressure, recurrence of , and need for inotropics or endotracheal intubation were the main independent predictors of hospital mortality. In contrast, overall mortality (70.0% vs 57.1%; P =0.002) and readmission for nonfatal heart failure after a 45-month follow-up (10-140; 17.3% vs 7.6%; P =0.009) were higher in than in non- patients. Age, peripheral vascular disease, and peak creatine kinase during index hospitalization, but not ejection fraction, were the main independent predictors of overall mortality, whereas coronary revascularization or valvular surgery were protective. These interventions were mostly performed during hospitalization index (294 of 307; 96%) and not intervened patients showed a higher risk profile. Long-term mortality in is high and higher in than in non- patients. Considering the different in-hospital and long-term mortality predictors herein described, which do not necessarily involve systolic function, it is conceivable that a more aggressive interventional program might improve survival in high-risk patients