Preprocedural statin therapy, inflammation, and myocardial injury in low-risk stable coronary artery disease patients submitted to coronary stent implantation.

OBJECTIVE: Evaluate if statin therapy prior to elective coronary stent implantation (CSI) reduces the plasma levels of markers of inflammation and of myocardial necrosis in low-risk stable coronary artery disease patients (CAD). BACKGROUND: The elevation of markers of inflammation and of myocardial necrosis after percutaneous coronary intervention may interfere with clinical outcome. Among acute coronary syndrome patients, statins improve clinical outcomes when used before CSI-mostly due to reduction of CSI-related myocardial infarction. However, little is known concerning preprocedural statin therapy on the reduction of these markers in stable patients at low-risk. METHODS: In this prospective, observational study, 100 patients (n = 50 on statin therapy vs. n = 50 not on statin) with stable coronary artery disease underwent elective CSI. Inflammatory (C-reactive protein [CRP], interleukin [IL]-6, tumor necrosis factor-α and matrix metalloproteinase-9) and myocardial necrosis markers (troponin I and CK-MB) were determined before and 24 hr after CSI. RESULTS: All patients presented a significant increase of CRP and IL-6 after CSI. However, this increase was attenuated in patients on statin therapy prior to CSI than those without statin therapy: 75% vs. 150% (P < 0.001) and 192% vs. 300% (P < 0.01). The other pro-inflammatory markers were similar for both sets of patients. Troponin I and CK-MB did not change after CSI regardless of previous statin therapy or not. CONCLUSIONS: Pretreatment with statin attenuates procedural inflammation, denoted by markedly lower increases of CRP and IL-6 levels, in elective CSI within low-risk stable CAD patients. Periprocedural myocardial injury was irrelevant and was not affected by preprocedural statin therapy in this population.

Natriuretic peptides and long-term mortality in patients with severe aortic stenosis.

BACKGROUND AND AIM OF THE STUDY: The natriuretic peptides, brain natriuretic peptide (BNP) and its N-terminal prohormone (NT-proBNP), can be used as diagnostic and prognostic markers for aortic stenosis (AS). However, the association between BNP, NT-proBNP, and long-term clinical outcomes in patients with severe AS remains uncertain. METHODS: A total of 64 patients with severe AS was prospectively enrolled into the study, and underwent clinical and echocardiographic assessments at baseline. Blood samples were drawn for plasma BNP and NT-proBNP analyses. The primary outcome was death from any cause, through a six-year follow up period. Cox proportional hazards modeling was used to examine the association between natriuretic peptides and long-term mortality, adjusting for important clinical factors. RESULTS: During a mean period of 1,520 +/- 681 days, 51 patients (80%) were submitted to aortic valve replacement, and 13 patients (20%) were medically managed without surgical interventions. Mortality rates were 13.7% in the surgical group and 62% in the medically managed group (p < 0.001). Patients with higher plasma BNP (> 135 pg/ml) and NT-proBNP (> 1,150 pg/ml) levels at baseline had a greater risk of long-term mortality (hazard ratio [HR] 3.2, 95% confidence interval [CI] 1.1-9.1; HR 4.3, 95% CI 1.4-13.5, respectively). After adjusting for important covariates, both BNP and NT-proBNP remained independently associated with long-term mortality (HR 2.9, 95% CI 1.5-5.7; HR 1.8, 95% CI 1.1-3.1, respectively). CONCLUSION: In patients with severe AS, plasma BNP and NT-proBNP levels were associated with long-term mortality. The use of these biomarkers to guide treatment might represent an interesting approach that deserves further evaluation.

Low platelet reactivity in patients with myocardial infarction treated with aspirin plus ticagrelor.

OBJECTIVE: Low platelet reactivity levels are associated with higher risk of bleeding in patients receiving dual antiplatelet therapy relative to patients with optimal platelet blockade. This study set out to evaluate the prevalence of low platelet reactivity in patients with acute myocardial infarction treated with ticagrelor and aspirin. METHODS: Patients admitted with acute myocardial infarction who were already undergoing dual antiplatelet therapy with aspirin and ticagrelor were enrolled. Blood samples were collected 1 hour before and 2 hours after the maintenance dose of ticagrelor to investigate trough and the peak effects of the drug respectively. Platelet reactivity was measured by three methods: Multiplate®, PFA-100® with Innovance® PFA-P2Y cartridge and PFA-100® with Collagen/ADP cartridge. Platelet reactivity was assessed in the presence of peak levels of ticagrelor and defined according to previously validated cut-offs for each method (<19 AUC, >299 seconds and >116 seconds respectively). The level of significance was set at p<0.05. RESULTS: Fifty patients were enrolled (44% with ST-elevation). Median duration of DAPT was 3 days (interquartile range, 2-5 days). On average, peak and trough platelet reactivity were markedly low and did not differ between different methods. Low platelet reactivity was common, but varied according to analytic method (PFA-100®/Innovance®PFA-P2Y: 86%; Multiplate®: 74%; PFA-100®/Collagen/ADP: 48%; p<0.001). CONCLUSION: Low platelet reactivity was very common in patients with acute myocardial infarction submitted to dual antiplatelet therapy with ticagrelor and aspirin. Findings of this study justify the investigation of less intensive platelet inhibition strategies aimed at reducing the risk of bleeding in this population, such as lower dose regimens or monotherapy with P2Y12 inhibitors.

Cluster of climatic and pollutant characteristics increases admissions for acute myocardial infarction: Analysis of 30,423 patients in the metropolitan area of Sao Paulo.

BACKGROUND: The impact of simultaneous adverse climate conditions in the risk of myocardial infarction (MI) was not tested before. The aim of the present study was to investigate the impact of the combination of climate and air pollution features in the number of admissions and mortality due to acute myocardial infarction in 39 municipalities of São Paulo from 2012 to 2015. METHODS: Data about MI admissions were obtained from the Brazilian public health system (DataSUS). Daily information on weather were accessed from the Meteorological Database for Teaching and Research. Additionally, daily information on air pollution were obtained from the Environmental Company of the State of São Paulo. A hierarchical cluster analysis was applied for temperature, rainfall patterns, relative air humidity, nitrogen dioxide, particulate matter 2.5 and particulate matter 10. MI admissions and in-hospital mortality were compared among the clusters. RESULTS: Data analysis produced 3 clusters: High temperature variation-Low humidity-high pollution (n=218 days); Intermediate temperature variation/high humidity/intermediate pollution (n=751 days) and low temperature variation/intermediate humidity-low pollution (n=123 days). All environmental variables were significantly different among clusters. The combination of high temperature variation, dry weather and high pollution resulted in a significant 9% increase in hospital admissions for MI [30.5 (IQR 25.0-36.0)]; patients/day; P<0.01). The differences in weather and pollution did not have impact on in-hospital mortality (P=0.88). CONCLUSION: The combination of atmospheric conditions with high temperature variation, lower temperature, dryer weather and increased inhalable particles was associated with a marked increase of hospital admissions due to MI.

Intensive support recommendations for critically-ill patients with suspected or confirmed COVID-19 infection.

In December 2019, a series of patients with severe pneumonia were identified in Wuhan, Hubei province, China, who progressed to severe acute respiratory syndrome and acute respiratory distress syndrome. Subsequently, COVID-19 was attributed to a new betacoronavirus, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Approximately 20% of patients diagnosed as COVID-19 develop severe forms of the disease, including acute hypoxemic respiratory failure, severe acute respiratory syndrome, acute respiratory distress syndrome and acute renal failure and require intensive care. There is no randomized controlled clinical trial addressing potential therapies for patients with confirmed COVID-19 infection at the time of publishing these treatment recommendations. Therefore, these recommendations are based predominantly on the opinion of experts (level C of recommendation).

Native LDL-cholesterol mediated monocyte adhesion molecule overexpression is blocked by simvastatin.

AIM OF THE STUDY: This study sought to evaluate the effect of nLDL concentrations on monocyte adhesion molecule expression in hypercholesterolemic patients with stable coronary artery disease (CAD) and to determine whether lipid-lowering therapy with simvastatin would change this effect. METHODS: Blood samples from patients with hypercholesterolemia (mean LDL 152 mg/dL) and CAD (HC, n = 23) were collected before and after a 12-week treatment with 40 mg of simvastatin. Healthy individuals (mean LDL 111 mg/dL) were used as controls (CT, n = 15). Isolated nLDL, at a fixed concentration of 100 mg/dL, was added to monocyte suspensions obtained before and after the simvastatin treatment. Monocyte activation was determined by changes in cellular adhesion molecule expression. RESULTS: In response to nLDL, CD11b and CD14 adhesion molecule expression was higher in HC patients than in CT patients before treatment (174.2 +/- 8.4 vs 102.2 +/- 6.3, P < 0.03 and 140.4 +/- 5.0 vs 90.4 +/- 6.7, P < 0.04). After simvastatin treatment, CD11b expression decreased to 116.9 +/- 12.5 (P < 0.03) and CD14 expression to 107.5 +/- 6.2 (P < 0.04). Alternatively, L-selectin expression was lower in HC patients than in CT patients before therapy (46.0 +/- 3.5 vs 62.1 +/- 5.5, P < 0.04), and it increased markedly after lipid reduction to 58.7 +/- 5.0 (P < 0.04 vs baseline). After simvastatin treatment, LDL was reduced to mean 101.5 mg/dL. CONCLUSIONS: These data demonstrate that monocytes from HC patients are more prone to marked nLDL-mediated changes of adhesion molecule expression than monocytes from controls. Simvastatin is capable of inhibiting such nLDL effects. This proinflammatory response to nLDL may have a role in the early onset of atherosclerosis.

Low platelet reactivity in patients with myocardial infarction treated with aspirin plus ticagrelor

ABSTRACT Objective: Low platelet reactivity levels are associated with higher risk of bleeding in patients receiving dual antiplatelet therapy relative to patients with optimal platelet blockade. This study set out to evaluate the prevalence of low platelet reactivity in patients with acute myocardial infarction treated with ticagrelor and aspirin. Methods: Patients admitted with acute myocardial infarction who were already undergoing dual antiplatelet therapy with aspirin and ticagrelor were enrolled. Blood samples were collected 1 hour before and 2 hours after the maintenance dose of ticagrelor to investigate trough and the peak effects of the drug respectively. Platelet reactivity was measured by three methods: Multiplate®, PFA-100® with Innovance® PFA-P2Y cartridge and PFA-100® with Collagen/ADP cartridge. Platelet reactivity was assessed in the presence of peak levels of ticagrelor and defined according to previously validated cut-offs for each method (<19 AUC, >299 seconds and >116 seconds respectively). The level of significance was set at p<0.05. Results: Fifty patients were enrolled (44% with ST-elevation). Median duration of DAPT was 3 days (interquartile range, 2-5 days). On average, peak and trough platelet reactivity were markedly low and did not differ between different methods. Low platelet reactivity was common, but varied according to analytic method (PFA-100®/Innovance®PFA-P2Y: 86%; Multiplate®: 74%; PFA-100®/Collagen/ADP: 48%; p<0.001). Conclusion: Low platelet reactivity was very common in patients with acute myocardial infarction submitted to dual antiplatelet therapy with ticagrelor and aspirin. Findings of this study justify the investigation of less intensive platelet inhibition strategies aimed at reducing the risk of bleeding in this population, such as lower dose regimens or monotherapy with P2Y12 inhibitors.

P2Y12 receptor inhibition with prasugrel and ticagrelor in STEMI patients after fibrinolytic therapy: Analysis from the SAMPA randomized trial.

BACKGROUND: A pharmacodynamic comparison between ticagrelor and prasugrel after fibrinolytic therapy has not yet been performed. METHODS: In the single-center SAMPA trial, 50 consecutive STEMI patients previously treated with clopidogrel and undergoing a pharmacoinvasive strategy were randomized to either a ticagrelor (n=25) 180mg loading dose followed by 90mg bid, or a prasugrel (n=25) 60mg loading dose followed by 10mg/day, initiated after fibrinolytic therapy but before angiography. Platelet reactivity was assessed with the VerifyNow P2Y12 assay at 0, 2, 6, and 24h after randomization. RESULTS: Mean times from fibrinolysis to prasugrel or ticagrelor administration were 11.1±6.9 and 13.3±6.3h, respectively (p=0.24). The values of PRU decreased significantly from baseline to 2h (all p<0.001) and from 2h to 6h (all p<0.001) in both groups. There was no difference in PRU values between 6h and 24h. The mean PRU values at 0, 2, 6, and 24h were 234.9, 127.8, 45.4, and 48.0 in the prasugrel group and 233.1, 135.1, 67.7, and 56.9 in the ticagrelor group, respectively. PRU values did not significantly differ between groups at any time period of the study. CONCLUSIONS: In patients with STEMI treated with fibrinolytic therapy, platelet inhibition after clopidogrel is suboptimal and can be further increased with more potent agents. Ticagrelor and prasugrel demonstrated a similar extent of P2Y12 receptor inhibition within 24h, although maximal platelet inhibition after these potent agents was not achieved for 6h.

Coronary artery disease in women: a review on prevention, pathophysiology, diagnosis, and treatment.

Despite numerous studies on women's cardiac health throughout the past decade, the number of female deaths caused by cardiovascular disease still rises and remains the leading cause of death in women in most areas of the world. Novel studies have demonstrated that cardiovascular disease, and more specifically coronary artery disease presentations in women, are different than those in men. In addition, pathology and pathophysiology of the disease present significant gender differences, which leads to difficulties concerning diagnosis, treatment and outcome of the female population. The reason for this disparity is all steps for female cardiovascular disease evaluation, treatment and prevention are not well elucidated; and an area for future research. This review brings together the most recent studies published in the field of coronary artery disease in women and points out new directions for future investigation on some of the important issues.

Mechanical Ventilation and Clinical Outcomes in Patients with Acute Myocardial Infarction: A Retrospective Observational Study.

PURPOSE: Patients with acute myocardial infarction (AMI) and respiratory impairment may be treated with either invasive or non-invasive mechanical ventilation (MV). However, there has been little testing of non-invasive MV in the setting of AMI. Our objective was to evaluate the incidence and associated clinical outcomes of patients with AMI who were treated with non-invasive or invasive MV. METHODS: This was a retrospective observational study in which consecutive patients with AMI (n = 1610) were enrolled. The association between exclusively non-invasive MV, invasive MV and outcomes was assessed by multivariable models. RESULTS: Mechanical ventilation was used in 293 patients (54% invasive and 46% exclusively non-invasive). In-hospital mortality rates for patients without MV, with exclusively non-invasive MV, and with invasive MV were 4.0%, 8.8%, and 39.5%, respectively (P<0.001). The median lengths of hospital stay were 6 (5.8-6.2), 13 (11.2-4.7), and 28 (18.0-37.9) days, respectively (P<0.001). Exclusively non-invasive MV was not associated with in-hospital death (adjusted HR = 0.90, 95% CI 0.40-1.99, P = 0.79). Invasive MV was strongly associated with a higher risk of in-hospital death (adjusted HR = 3.07, 95% CI 1.79-5.26, P<0.001). CONCLUSIONS: In AMI setting, 18% of the patients required MV. Almost half of these patients were treated with exclusively non-invasive strategies with a favorable prognosis, while patients who needed to be treated invasively had a three-fold increase in the risk of death. Future prospective randomized trials are needed to compare the effectiveness of invasive and non-invasive MV for the initial approach of respiratory failure in AMI patients.

[Negative sestamibi-dipyridamole perfusion imaging in severe coronary artery disease in the preoperative period of correction of abdominal aortic aneurysm]. / Cintilografia com MIBI-dipiridamol negativa em doença coronariana grave no pré-operatório de correção de aneurisma de aorta abdominal.

We report the case of a 73-year-old male patient who was a candidate for correction of an abdominal aortic aneurysm without abnormalities in his first cardiological evaluation. The surgery was postponed because of the need for treatment of epididymitis. Two weeks later, the patient returned to the hospital with thoracic pain, when the angiography showed obstructions in 2 coronary arteries, which were successfully treated with percutaneous transluminal angioplasty and stent implantation. After 45 days, the patient underwent surgery for correction of the abdominal aortic aneurysm under peridural and general anesthesia. The patient evolved without complications.

Acute management of unstable angina and non-ST segment elevation myocardial infarction.

Non-ST segment elevation coronary syndrome usually results from instability of an atherosclerotic plaque, with subsequent activation of platelets and several coagulation factors. Its treatment aims to reduce the ischemic pain, limiting myocardial damage and decreasing mortality. Several antiplatelet and anticoagulation agents have been proven useful, and new drugs have been added to the therapeutic armamentarium in the search for higher anti-ischemic efficacy and lower bleeding rates. Despite the advances, the mortality, infarction and readmission rates remain high.

Heart failure with preserved left ventricular ejection fraction in patients with acute myocardial infarction.

BACKGROUND: The prevalence and clinical outcomes of heart failure with preserved left ventricular ejection fraction after acute myocardial infarction have not been well elucidated. OBJECTIVE: To analyze the prevalence of heart failure with preserved left ventricular ejection fraction in acute myocardial infarction and its association with mortality. METHODS: Patients with acute myocardial infarction (n = 1,474) were prospectively included. Patients without heart failure (Killip score = 1), with heart failure with preserved left ventricular ejection fraction (Killip score > 1 and left ventricle ejection fraction ≥ 50%), and with systolic dysfunction (Killip score > 1 and left ventricle ejection fraction < 50%) on admission were compared. The association between systolic dysfunction with preserved left ventricular ejection fraction and in-hospital mortality was tested in adjusted models. RESULTS: Among the patients included, 1,256 (85.2%) were admitted without heart failure (72% men, 67 ± 15 years), 78 (5.3%) with heart failure with preserved left ventricular ejection fraction (59% men, 76 ± 14 years), and 140 (9.5%) with systolic dysfunction (69% men, 76 ± 14 years), with mortality rates of 4.3%, 17.9%, and 27.1%, respectively (p < 0.001). Logistic regression (adjusted for sex, age, troponin, diabetes, and body mass index) demonstrated that heart failure with preserved left ventricular ejection fraction (OR 2.91; 95% CI 1.35-6.27; p = 0.006) and systolic dysfunction (OR 5.38; 95% CI 3.10 to 9.32; p < 0.001) were associated with in-hospital mortality. CONCLUSION: One-third of patients with acute myocardial infarction admitted with heart failure had preserved left ventricular ejection fraction. Although this subgroup exhibited more favorable outcomes than those with systolic dysfunction, this condition presented a three-fold higher risk of death than the group without heart failure. Patients with acute myocardial infarction and heart failure with preserved left ventricular ejection fraction encounter elevated short-term risk and require special attention and monitoring during hospitalization.

Intensive support recommendations for critically-ill patients with suspected or confirmed COVID-19 infection / Recomendações de suporte intensivo para pacientes graves com infecção suspeita ou confirmada pela COVID-19

ABSTRACT In December 2019, a series of patients with severe pneumonia were identified in Wuhan, Hubei province, China, who progressed to severe acute respiratory syndrome and acute respiratory distress syndrome. Subsequently, COVID-19 was attributed to a new betacoronavirus, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Approximately 20% of patients diagnosed as COVID-19 develop severe forms of the disease, including acute hypoxemic respiratory failure, severe acute respiratory syndrome, acute respiratory distress syndrome and acute renal failure and require intensive care. There is no randomized controlled clinical trial addressing potential therapies for patients with confirmed COVID-19 infection at the time of publishing these treatment recommendations. Therefore, these recommendations are based predominantly on the opinion of experts (level C of recommendation).

RESUMO Em dezembro de 2019, uma série de pacientes com pneumonia grave foi identificada em Wuhan, província de Hubei, na China. Esses pacientes evoluíram para síndrome respiratória aguda grave e síndrome do desconforto respiratório agudo. Posteriormente, a COVID-19 foi atribuída a um novo betacoronavírus, o coronavírus da síndrome respiratória aguda grave 2 (SARS-CoV-2). Cerca de 20% dos pacientes com diagnóstico de COVID-19 desenvolvem formas graves da doença, incluindo insuficiência respiratória aguda hipoxêmica, síndrome respiratória aguda grave, síndrome do desconforto respiratório agudo e insuficiência renal aguda e requerem admissão em unidade de terapia intensiva. Não há nenhum ensaio clínico randomizado controlado que avalie potenciais tratamentos para pacientes com infecção confirmada pela COVID-19 no momento da publicação destas recomendações de tratamento. Dessa forma, essas recomendações são baseadas predominantemente na opinião de especialistas (grau de recomendação de nível C).

[Acute myocardial infarction -- acute coronary syndrome with ST-segment elevation]. / Infarto agudo do miocárdio -- síndrome coronariana aguda com supradesnível do segmento ST.

Cardiovascular diseases continue to be the first cause of death in Brazil -- responsible for almost 32% of all deaths. In addition, they are the third major cause of admission in the country. Among them, acute myocardial infarction is still one of the major causes of morbidity and mortality. Despite of the last decade's therapeutic advances, acute myocardial infarction still shows remarkable rates of mortality, and great part of the patients do not receive the adequate treatment. The opening of the Coronary Care Units and the introduction of reperfusion treatment with fibrinolytics or primary angioplasty were fundamental to reduce mortality and complications related to myocardial infarction. Important beneficial effects to the current treatment include less ventricular dysfunction and better control of ventricular arrhythmias. The need of early reperfusion is crucial for the good prognosis after a myocardial infarction. The objective of this review is to emphasize the modern basic concepts of the pathophysiology, diagnosis and treatment of acute myocardial infarction, according to national and international guidelines.

Diabetes and cardiovascular disease: from evidence to clinical practice - position statement 2014 of Brazilian Diabetes Society.

There is a very well known correlation between diabetes and cardiovascular disease but many health care professionals are just concerned with glycemic control, ignoring the paramount importance of controlling other risk factors involved in the pathogenesis of serious cardiovascular diseases. This Position Statement from the Brazilian Diabetes Society was developed to promote increased awareness in relation to six crucial topics dealing with diabetes and cardiovascular disease: Glicemic Control, Cardiovascular Risk Stratification and Screening Coronary Artery Disease, Treatment of Dyslipidemia, Hypertension, Antiplatelet Therapy and Myocardial Revascularization. The issue of what would be the best algorithm for the use of statins in diabetic patients received a special attention and a new Brazilian algorithm was developed by our editorial committee. This document contains 38 recommendations which were classified by their levels of evidence (A, B, C and D). The Editorial Committee included 22 specialists with recognized expertise in diabetes and cardiology.

Vascular calcification: pathophysiology and clinical implications.

Vascular calcification in coronary artery disease is gaining importance, both in scientific research and in clinical and imaging applications. The calcified plaque is considered the most relevant form of atherosclerosis within the coronary artery tree and is frequently a challenge for percutaneous intervention. Recent studies showed that plaque calcification is dynamic and is strictly related to the degree of vascular inflammation. Several inflammatory factors produced during the different phases of atherosclerosis induce the expression and activation of osteoblastic cells located within the arterial wall, which, in turn, promote the deposit of calcium. The vascular smooth muscle cells have an extraordinary capacity to undergo osteoblastic phenotypical differentiation. There is no doubt that the role of these factors, as well as the elements of genomics and proteomics, could be a vital strategic point in prevention and treatment. Within this context, we conducted an updating review on coronary calcification focused on pathophysiology, experimental models, and clinical implications of vascular calcification.

Increasing doses of simvastatin versus combined ezetimibe/simvastatin: effect on circulating endothelial progenitor cells.

BACKGROUND: Patients with coronary artery disease (CAD) should be treated with statins to attain very low cholesterol levels, in order to reduce cardiovascular adverse events. More than 70% of these patients do not reach the appropriate cholesterol goal despite moderate statin doses. However, it is not known whether therapeutic uptitration with different lipid-lowering strategies has a similar "pleiotropic" effect on atherosclerotic endothelial dysfunction evaluated by measurement of endothelial progenitor cells (EPCs). OBJECTIVE: We sought to compare, in patients with stable CAD and with a low-density lipoprotein cholesterol (LDL-C) >70 mg/dL on treatment with simvastatin 20 mg, the effects on EPCs by increasing simvastatin to 80 mg versus adding ezetimibe 10 mg. METHODS: Patients (n = 68, 63 ± 9 years, 39% men) were randomly allocated to receive ezetimibe 10/simvastatin 20 mg or simvastatin 80 mg for 6 weeks. Circulating EPCs were measured by flow cytometry before and after the treatment. RESULTS: Both strategies presented similar effects on metabolic parameters. The LDLs were equally reduced by ezetimibe 10/simvastatin 20 mg and simvastatin 80 mg (28.9% ± 13% vs 21.1% ± 33%; P = .46, respectively). The levels of EPCs were unaffected by ezetimibe 10/simvastatin 20 mg (median [25th, 75th]: pre- vs posttreatment, 7.0 [2.3; 13.3] vs 3.1 [0.1; 13.2] EPCs/10(4) mononuclear cells; P = .43) or simvastatin 80 mg (pre- vs posttreatment, 6.1 [2.9; 15.2] vs 4.0 [1.4; 10.7] EPCs/10(4) mononuclear cells; P = .5), and there were no differences between the groups on treatment effects (P = .9). CONCLUSIONS: Among stable patients with CAD and with an LDL-C >70 mg/dL on simvastatin 20 mg, increasing simvastatin dose to 80 mg or adding ezetimibe 10 mg promoted similar further cholesterol reduction but did not have incremental effects on circulating EPCs. These data suggest that the effects of simvastatin moderate doses on EPCs are not increased by intensive lipid-lowering strategies (clinicaltrials.gov: NCT00474123).

Effect of implementing an acute myocardial infarction guideline on quality indicators.

OBJECTIVE: To evaluate the compliance rates to quality of care indicators along the implementation of an acute myocardial infarction clinical practice guideline. METHODS: A clinical guideline for acute myocardial infarction was introduced on March 1st, 2005. Patients admitted for acute myocardial infarction from March 1st, 2005 to December 31st, 2012 (n=1,431) were compared to patients admitted for acute myocardial infarction before the implementation of the protocol (n=306). Compliance rates to quality of care indicators (ASA prescription on hospital admission and discharge, betablockers on discharge and door-to-balloon time) as well as the length of hospital stay and in-hospital mortality were compared before and after the implementation of the clinical guideline. RESULTS: The rates of ASA prescription on admission, on discharge and of betablockers were higher after guideline implementation: 99.6% versus 95.8% (p<0.001); 99.1% versus 95.8% (p<0.001); and 95.9% versus 81.7% (p<0.001), respectively. ASA prescription rate increased over time, reaching 100% from 2009 to 2012. Door-to-balloon time after versus before implementation was of 86(32) minutes versus 93(51) (p=0.20). The length of hospital stay after the implementation versus before was of 6(6) days versus 6(4) days (p=0.34). In-hospital mortality was 7.6% (before the implementation), 8.7% between 2005 and 2008, and 5.3% between 2009 and 2012, (p=0.04). CONCLUSION: The implementation of an acute myocardial infarction clinical practice guideline was associated with an increase in compliance to quality of care indicators.