Risk Of Acute Coronary Syndrome Research Articles

The risk for a first acute coronary syndrome in patients treated with different types of antidepressants: A population based nested case-control study

BackgroundTricyclic antidepressants (TCAs) are still used in 30% of anxiety/depression cases and have been related to increased cardiovascular risk. Newer serotonin/norepinephrine reuptake inhibitors (SSRIs/SNRIs) safety remains conflicting. Our aim was to assess the risk of a first acute coronary syndrome (ACS) in patients treated by various types of antidepressants. MethodsStudy was a retrospective nested case-control of 40–80 years old northern-Israeli members of Clalit Health Services (CHS) during 1.1.2003–31.12.2013. Patients with severe psychiatric, cardiac or systemic diseases, or pre-enrollment antidepressants were excluded. Cases that had a first ACS during the study period were matched in 1:30 ratio with controls. The association between antidepressants use and ACS was tested by adjusted multivariable conditional logistic regression. ResultsThe cohort included 535,315 individuals 128,550 of whom met the exclusion/inclusion criteria. 3391 Cases with first ACS, (incidence rate of 24.6/10,000 person years) were matched with 88,016 controls.ACS was not associated with use of either SSRIS/SNRIS or TCAs compared with no antidepressants use. However, treatment by SSRIS/SNRIS was associated with a 36% decreased risk ACS compared to TCAs, OR = 0. 64, 95%CI (0.43–0.95), p = 0.029. Age 40–64 years, male gender and metabolic syndrome associated with reduced risk of ACS among SSRIS/SNRIS compared to TCAs users. ConclusionIn this study of patients without prior cardiovascular disease– neither antidepressant group imposed excess risk for ACS, compared to-no treatment. SSRIs treatment seemed safer compared to TCAs in regard of ACS. This study probably adds to our confidence of preferring SSRIs over TCAs in patients without prior cardiovascular disease.

APOA1 and APOB polymorphisms and apolipoprotein concentrations as biomarkers of risk in acute coronary syndrome: Relationship with lipid-lowering therapy effectiveness

Background and objectiveLipid metabolism alterations contribute to acute coronary syndrome (ACS). rs670, rs5070 and rs693 polymorphisms have shown to modify the risk of cardiovascular disease. Apolipoprotein A-I (ApoA-I) plays a major role in reverse cholesterol transport; apolipoprotein B (ApoB) contributes to accumulation of cholesterol in the plaque. The aim of this study was to investigate the association of rs670 and rs5070 polymorphisms of APOA1 and rs693 polymorphism of APOB with ACS and circulating levels of its proteins and find if ApoB/ApoA-I could be implemented as an independent parameter of risk for cardiovascular disease and as a biomarker of lipid-lowering therapy effectiveness in Mexican population. MethodsThree hundred patients with ACS and 300 control subjects (CS) were included. ResultsNeither genotype nor allele frequencies of rs670, rs5070 and rs693 polymorphisms showed statistical differences between groups. Serum levels of ApoA-I (195 vs. 161.4mg/dL; p<.001) and ApoB (167 vs. 136.9mg/dL; p<.001) were significantly higher in CS compared with ACS; however, there was no genetic association. Unstable angina patients showed the highest ApoA-I levels (males: 176.3mg/dL; females: 209.1mg/dL). ConclusionThe rs670, rs5070 and rs693 polymorphisms are not genetic susceptibility factors for ACS in Mexican population and had no effect on their apolipoprotein concentrations. In our population, ApoA-I, ApoB and HDL-C could be better biomarkers of cardiovascular risk and could indicate if statins doses reduce atherogenic particles properly.

Comparison of clinical risk scores for triaging high-risk chest pain patients at the emergency department

BackgroundMany of the clinical risk scores routinely used for chest pain assessment have not been validated in patients at high risk for acute coronary syndrome (ACS). We performed an independent comparison of HEART, TIMI, GRACE, FRISC, and PURSUIT scores for identifying chest pain due to ACS and for predicting 30-day death or re-infarction in patients arriving through Emergency Medical Services (EMS). Methods and resultsWe enrolled consecutive EMS patients evaluated for chest pain at three emergency departments. A reviewer blinded to outcome data retrospectively reviewed patient charts to compute each risk score. The primary outcome was ACS diagnosed during the primary admission, and the secondary outcome was death or re-infarction within 30-days of initial presentation. Our sample included 750 patients (aged 59 ± 17 years, 42% female), of whom 115 (15.3%) had ACS and 33 (4.4%) had 30-day death or re-infarction. The c-statistics of HEART, TIMI, GRACE, FRISC, and PURSUIT for identifying ACS were 0.87, 0.86, 0.73, 0.84, and 0.79, respectively, and for predicting 30-day death or re-infarction were 0.70, 0.73, 0.72, 0.72, and 0.62, respectively. Sensitivity/negative predictive value of HEART ≥ 4 and TIMI ≥ 3 for ACS detection were 0.94/0.98 and 0.87/0.97, respectively. ConclusionsIn chest pain patients admitted through EMS, HEART and TIMI outperform other scores for identifying chest pain due to ACS. Although both have similar negative predictive value, HEART has better sensitivity and lower rate of false negative results, thus it can be used preferentially over TIMI in the initial triage of this population.

Thrombomodulin can predict the incidence of second events in patients with acute coronary syndrome: Single-center, retrospective cohort study

BackgroundPlasma levels of atherothrombosis-related markers such as endothelial biomarkers have been reported to predict the risk of first acute coronary syndrome (ACS) events. Percutaneous coronary intervention (PCI) by balloon angioplasty and stenting established as a treatment for ACS enabled early discharge and early clinic care. The procedure of PCI, however, may itself be associated with arterial injury with endothelial dysfunction. The clinical significance of those biomarkers for second events in patients after PCI has not yet been completely understood to identify patients who need strict follow-up. MethodsAfter the exclusion of 100 patients (60 deaths during hospitalization, 40 severe renal failure), 400 ACS patients (291 males, 71.1±13.0 years) who had undergone successful PCI followed by biomarker assessment within the first postoperative hour were enrolled. We evaluated atherothrombosis-related biomarkers: thrombomodulin (TM), C-reactive protein (CRP), and D-dimer, prothrombin fragment F1+2, and plasminogen activator inhibitor-1, other than those assessed by routine biochemical tests. The outcome after PCI in ACS patients was assessed by the incidence of major adverse cardiovascular events (MACEs). ResultsMACEs occurred in 112 patients during the follow-up period (813.9±474.8 days). As in previous reports, patients with MACEs showed decreased left ventricular ejection fraction (LVEF) by echocardiography, elevated brain natriuretic peptide and HbA1c than patients without MACEs. Not only these markers but also TM were significantly associated with MACEs in multivariate analysis. There were no significant correlations between MACEs and CRP. The association between TM and MACEs was especially high (odds ratio 2.73) and unaffected by the stage of cardiac (≤40, 40<LVEF≤55, 55<%) or renal function (≤40, 40<creatinine clearance≤75, 75<ml/min). ConclusionsTM is independently associated with MACEs and may be predictive of second events in patients after PCI for ACS. ACS patients with high TM value need strict follow up.

Clinical Challenges of Using Novel Oral Anticoagulants for Stroke Prevention in Patients with Atrial Fibrillation.

Atrial fibrillation (AF) is the most prevalent arrhythmia, and patients with AF have an increased risk of stroke. According to the CHA2DS2-VASc scoring system, stroke risk is greater when these patients are older than 65 years; are female; have systolic heart failure, diabetes mellitus, hypertension, peripheral vascular disease, or a recent myocardial infarction; or have a history of stroke or transient ischemic attack.1 Oral anticoagulants are the mainstay therapy for stroke prevention in AF patients. Drugs called new oral anticoagulants (NOACs) are often prescribed for this purpose and are as effective as warfarin. Currently, 4 NOACs are approved by the U.S. Food and Drug Administration: dabigatran (a direct thrombin inhibitor), rivaroxaban, apixaban, and edoxaban (a direct factor Xa inhibitor). Only dabigatran has a reversal agent. In comparison with warfarin, NOACs have fewer interactions with foods and medications, and routine bloodwork is not required to evaluate patients' anticoagulation levels when they take these drugs.1–3When NOACs are prescribed instead of warfarin, considerations include patients' renal and liver function, and possible drug interactions. A management challenge is to formulate an appropriate plan for NOAC use before noncardiac surgery, with answers to the following questions: should we hold NOACs? When should they be stopped? Do we need to bridge the patient with heparin? When should we restart the NOACs? Other factors to consider are the risk of bleeding associated with the procedure, the patient's individual risk of stroke and bleeding, and the type of NOAC to use.2 Bridging is not typically recommended for NOACs.2 For example, in a patient with persistent AF who is taking apixaban, has a CHA2DS2-VASc score of 3, has normal renal function, and is to undergo transurethral resection of the prostate (associated with a high risk of bleeding), apixaban should be stopped 48 hours preoperatively, without heparin bridging; it can be restarted as soon as the surgeon determines that doing so is safe.Cytochrome P450 subgroup CYP3A4 is important in the metabolism of NOACs,4 P-glycoprotein in their absorption, and renal function in their excretion. Medications that induce or inhibit the functions of CYP3A4 or P-glycoprotein can affect the bioavailability of NOACs and increase the risk of bleeding or thromboembolism.4 One such, an over-the-counter supplement, is St. John's wort. Typically taken as therapy for psychological depression, this herb induces P-glycoprotein and can thus decrease the bioavailability of dabigatran.Therapy with NOACs is limited in patients with valvular heart disease. However, current data suggest that NOACs can decrease stroke risk in patients with nonvalvular AF.1 This condition is defined as AF in the absence of rheumatic mitral valve stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair.1 For instance, in a patient with AF and severe mitral stenosis, the anticoagulant of choice is warfarin. Conversely, in a patient with AF and severe aortic stenosis, a NOAC may be considered.Concomitant oral anticoagulation and dual antiplatelet therapy (DAPT) (aspirin and an adenosine diphosphate inhibitor)—known as triple therapy—greatly increases a patient's bleeding risk; however, NOACs can be used. The expert recommendation is to keep the duration of triple therapy as short as possible in patients who have acute coronary syndrome and AF. It is essential to accurately evaluate the patient's risk of bleeding, thrombosis, or recurrent acute coronary syndrome during triple therapy. Clopidogrel is the adenosine diphosphate inhibitor of choice; conversely, ticagrelor and prasugrel should be avoided.3,5 In DAPT plus warfarin, the target international normalized ratio is 2 to 2.5. In DAPT plus a NOAC, the NOAC prescription should be the lowest dose studied in the relevant clinical trial.3,5 Proton-pump inhibitors are recommended for patients with a risk or history of gastrointestinal bleeding, and their use is encouraged in all patients who are prescribed triple therapy.3,5 For example, in a patient with acute myocardial infarction, persistent AF, and no history of bleeding, the recommended combination would be aspirin, clopidogrel, and either a NOAC (apixaban, 2.5 mg twice daily) or warfarin.To maintain the clinical benefits and minimize the adverse effects of NOACs, clinicians must consider the pharmacologic characteristics of the particular drug, the patient's risk of bleeding, the correct drug combination with antiplatelet therapy, and potential interactions between the NOAC and the patient's other medications. In addition, all patients should be counseled about the potential side effects before they start taking NOACs.

Coronary Events After Dispensing of Ibuprofen: A Propensity Score-Matched Cohort Study Versus Paracetamol in the French Nationwide Claims Database Sample.

Non-steroidal anti-inflammatory drugs are associated with a dose and duration-dependent coronary risk. There is little information concerning analgesic-dose ibuprofen, among the most widely used drugs worldwide. Our objective was to measure the risks of acute coronary syndrome (ACS) after dispensing of ibuprofen, versus paracetamol. Propensity score 1:2-matched cohorts of ibuprofen or paracetamol treatment episodes (TEs) in Echantillon Généraliste de Bénéficiaires (EGB), the 1/97 sample of Système National des Données de Santé (SNDS), the French nationwide claims database, from 2009 to 2014, were compared. Outcomes were hospital admissions for ACS during the 3months after the dispensing of ibuprofen or paracetamol. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated overall and stratified on low-dose aspirin dispensing. A total of 315,269 ibuprofen TEs in 168,400 persons were matched to 630,457 paracetamol TEs in 395,952 patients. Event rates were 50-100 times higher in low-dose aspirin users (27 vs 0.28 per 1000 patient years). Overall there was no difference in risk of ACS at 3months (HR 0.94, 95% CI 0.74-1.20) despite a transient increase in the first 2weeks in ibuprofen users (HR 1.70, 95% CI 1.11-2.59). In the stratified analysis, this short-term risk was only found in aspirin users (5% of population, HR 1.84, 95% CI 1.24-3.24), but not in non-aspirin users (HR 1.09, 95% CI 0.40-2.94). There was no evidence for an increased risk of ACS in patients dispensed ibuprofen compared to paracetamol.

Accuracy of the Canadian new risk score as in hospital prognostic score for the Egyptian patients with acute coronary syndrome

ObjectivesPatients with acute coronary syndrome (ACS) need to be risk stratified to deliver the most appropriate therapy. There is no appropriate score for early-risk stratification at the time of the first medical contact with ACS patients. Canada Acute Coronary Syndrome Risk Score (Canadian-ACS) is a new risk score for early prognostication in acute coronary syndromes. The aim of our study is to evaluate the accuracy and validity of Canadian-ACS risk score as a prognostic score for in-hospital risk stratification of patients with ACS, as compared to TIMI AND GRACE risk scores in the Egyptian patients. MethodsOur study included 79 patients having acute coronary syndrome admitted to CCU. Calculations of The Canada Acute Coronary Syndrome Risk Score (Canadian-ACS) and ranged from 0 to 4, with 1 point assigned for the presence of: age ≥75 years, Killip class >1, systolic blood pressure <100mm Hg, and heart rate >100 beats/min. ResultsIn our study, there is a strong association between Canadian-ACS and TIMI risk score with sensitivity 85.7% and specificity 100.0% and Grace risk score with sensitivity 78.1%% and specificity 85.1%. The negative predictive value of a Canadian-ACS score ≥1 is ≥84.4% for short-term in hospital morbidity and mortality, and for score ≥2 at ≥98%. Conclusionthe Canadian-ACS is a valid accurate and simple prognostic risk score for short-term risk stratification in patients with ACS independent of hypertension, diabetes, smoking and troponin level.

Association of Short term Outcomes of Acute Coronary Syndrome with Prediabetes

The global incidence and prevalence of prediabetes are rapidly increasing with a parallel increase in the proportion of patients suffering from acute coronary ischemic events with prediabetes. Impaired glucose metabolism (IGM), comprising impaired glucose tolerance and impaired fasting glycemia (IFG), is also associated with an increase risk of Acute coronary syndrome (ACS). This study was aimed to assess the adverse outcomes of Acute Coronary Syndrome (ACS) with and without prediabetes. This prospective observational study was conducted with 132 patients admitted in coronary care unit and cardiology departments of Dhaka medical college and NICVD, Dhaka from January 2010 to December 2010. The patients were grouped into prediabetic ACS group (Group A) and non-diabetic ACS group (Group B) by estimating fasting blood glucose and 2 hours postparandial blood glucose. Mean (±SD) age of prediabetic ACS group (56.73±8.19 years) was higher than non-diabetic ACS group (53.16±8.92 years) and it was statistically significant. In this study 85 (64.4%) patients were male and 47 (35.6%) patients were female. The presence of risk factors, such as smoking (65.9% vs 48.9%), dyslipidemia (86.4% vs 68.2%), family history of IHD (20.5% vs 14.8%) and hypertension (65.9% vs 43.2%) was higher in group A study subjects in comparison to group B. Overall final outcome results of study subjects during hospital stay in group A and group B respectively were heart failure 14 (31.8%) and 10 (11.4% (P&lt;0.01), cardiogenic shock 9 (20.5%) and 4 (4.5%) (P&lt;0.01), arrhythmia 4 (9.1%) and 5 (5.7%) (P=0.480), recurrent angina 2 (4.5%) and 0 (0%) (P=0.109), need for urgent revascularization 1 (2.3%) and 0 (0%) (P=0.333), and death 2 (4.5%) and 3 (3.4%) (P=1.000). Significantly higher number of study subjects of group A suffered cardiogenic shock (P&lt;0.01) and heart failure (P&lt;0.01) than those in group B. The study shows that acute coronary syndrome patients with prediabetes have more risk to develop adverse effects like cardiogenic shock and heart failure than non-diabetic ACS patients.Bangladesh J Med Biochem 2016; 9(2): 54-58

Acute coronary syndrome remodels the antiplatelet aggregation properties of HDL particle subclasses

Background Although HDLs have antithrombotic effects by reducing platelet activation, the relationship between HDL levels and the risk of acute coronary syndrome (ACS) is unclear, as HDL particles are heterogeneous in composition and biological properties. Objective To characterize the effects of HDL2 and HDL3 subclasses from ACS patients and non-coronary artery disease (CAD) subjects on platelet activation. Methods We measured platelet aggregation and ex vivo thrombus formation, analyzed signaling pathways by flow cytometry, and performed a targeted lipidomics analysis on HDL subclasses. Results Analysis of human platelet aggregation in suspension, adhesion on von Willebrand factor and thrombus formation on collagen under arterial shear demonstrated that HDL2 from ACS patients had higher antiplatelet potency than HDL3 from ACS patients and HDL from non-CAD subjects. HDL binding to scavenger receptor class B type I was essential for this effect. A lipidomics analysis revealed that HDL2 from ACS patients had more oxidized polyunsaturated fatty acids (PUFAs). An inverse correlation between the concentrations of 9-hydroxyoctadecadienoic acid (9-HODE), 13-hydroxyoctadecadienoic acid (13-HODE), the eicosapentaenoic acid metabolite 18-hydroxyeicosapentaenoic acid (18-HEPE) and hydroxyeicosatetraenoic acid isomers in HDL2 and platelet aggregation was observed. This relationship was further demonstrated by the direct inhibitory effects of 18-HEPE, 9-HODE, 13-HODE, 17-hydroxydocosahexaenoic acid and 14-hydroxydocosahexaenoic acid on collagen-related peptide-induced platelet aggregation, indicating that oxidized PUFAs contribute to the antithrombotic effect of ACS HDL2. Conclusions Our data shed new light on the antiplatelet effects of HDL subclasses, and suggest physiological adaptation through the modulation of HDL properties in ACS patients that may limit their platelet-dependent thrombotic risk.

Abstract 412: Dietary Lectins Cause Coronary Artery Disease via an Autoimmune Endothelial Attack Mediated by Interleukin 16

Interleukin 16 (IL-16) is a chemoattractant released by endothelial and other cells to attract activated T cells. It has previously been shown to have expression in many autoimmune diseases (AI). Based on our previous reports using elevated adiponectin levels of 16 ug/mL to predict lectin sensitivity, and showing an association between lectins and AI causation, we have treated a large pt population with known autoimmune disease (as confirmed by markers). We recently began using the PULS Cardiac Test (GD Biosciences Lab, Irvine, CA) a validated blood test for predicting 5 year risk of acute coronary syndrome (ACS) to examine which measured biomarkers predominate in these patients. 325 consecutive pts aged 25-89 had PULS tested as part of a comprehensive blood panel, which also screens for 14 autoimmune disease markers. The PULS tests ranks 9 biomarkers, including IL-16, MCP-3, Eotaxin, CTACK, sFas, Fas Ligand, HGF for ACS risk, ranking each biomarker from lowest to highest level contributing to risk. 241 pts (74%) were positive for elevated adiponectin, hx of AI, and/or markers for AI. Of these pts, 223 (93%) were positive for IL-16 as the highest PULS risk factor. In contrast, of the other 84 pts without AI or adiponectin elevation, only 5 (6%) had IL-16 recorded as a risk. We conclude that based on IL-16 testing via PULS, that this provides further evidence to support an autoimmune cause of coronary artery disease at the endothelial level via T cell activation and attraction in patients with gluten and lectin sensitivity or known autoimmune disease. It also explains the known high association of autoimmune disease and ACS.

Correlation between malnutrition and acute coronary syndrome in the elderly with comprehensive geriatric assessment

Objective To analyze the influence of malnutrition in the elderly patients with acute coronary syndrome on related factors and short-term prognosis. Methods 415 elderly patients with acute coronary syndrome were selected.Comprehensive geriatric assessment was used to investigate the risk of acute coronary syndrome by examining coexisting diseases and using the NRS2000 score.The mortality and emergency visits were followed up. Results The patients were divided into two groups according to NRS2000 score: malnutrition group (n=179) and non-malnutrition group (n=236). (1) In malnutrition group, the proportions of female, over 85 years old, more than 3 kinds of coexisting diseases were 47.5%(85/179), 11.7%(21/179), 62.6%(112/179), respectively, which were higher than those of the non-malnutrition group[36.9%(87/236), 4.7%(11/236), 41.9%(99/236)](χ2=4.732, 7.152, 17.318, all P<0.05). (2) In malnutrition group, the incidence rates of geriatric syndromes such as uracratia, falls, visual disorder, hearing disorder, constipation, sleep disorders, oral problems were 47.5%(85/179), 30.2%(54/179), 40.2%(72/179), 41.9%(75/179), 54.7%(98/179), 52.0%(93/179), 76.5%(137/179), respectively, which were higher than those of the non-malnutrition group[31.4%(74/236), 14%(33/236), 29.2% (69/236), 29.7% (70/236), 30.5%(72/236), 36.0%(85/236), 53.0%(125/236)](χ2=11.206, 16.092, 5.477, 6.707, 24.732, 10.577, 24.297, all P<0.05). (3) In malnutrition group, the incidence rates of coexisting chronic diseases such as hypertension, chronic obstructive pulmonary disease, heart failure, severe renal insufficiency, cerebrovascular disease, dementia, anemia, osteoporosis were 77.1%(138/179), 16.2% (29/179), 22.9%(41/179), 17.9%(32/179), 46.9%(84/179), 6.7%(12/179), 27.4%(49/179), 26.8%(48/179), respectively, which were higher than those of the non-malnutrition group[61.9%(146/236), 7.6%(18/236), 14.4%(34/236), 7.2%(17/236), 32.2%(76/236), 1.3%(3/236), 13.1%(31/236), 17.4%(41/236)](χ2=10.931, 7.451, 4.965, 11.137, 9.315, 8.624, 13.262, 5.388, all P<0.05). (4)Cox regression analysis showed that malnutrition risk score was the independent risk predictor for all-cause mortality (HR=0.034, 95% CI: 0.072-0.904) and emergency department visits (HR=0.328, 95% CI: 0.197-0.548) in elderly patients with acute coronary syndrome. Conclusion Comprehensive geriatric assessment and nutritional assessment are useful to evaluate the clinical features of acute coronary syndrome in elderly patients.Malnutrition risk score is an independent predictor of all-cause mortality and emergency treatment in elderly patients with acute coronary syndrome. Key words: Coronary disease; Comprehensive geriatric assessment; Aged; Malnutrition

TREML4 affects lesion composition but not calcification in the Apolipoprotein E deficient model of experimental Atherosclerosis

Abstract The Triggering Receptor Expressed on Myeloid cells-like 4 (Treml4) is a member of the TREM receptor family which are recognized fine-tuners of the inflammatory response. We have previously found that Treml4 expression correlates to increased risk of Human Coronary Arterial Calcification and Acute Coronary Syndrome. Moreover, we show that carriage of either one of the eQTL SNPs previously identified to permit Treml4 expression, confers the highest treml4 expression in human inflammatory macrophages when compared to alternative activated macrophages. However, the exact role of Treml4 in the pathogenesis of coronary diseases remains incompletely defined. To elucidate the role of Treml4 in atherosclerosis, we investigated whether treml4 deficiency affected pathogenesis in the Apolipoprotein E knockout mouse (apoe−/−). We found that aortas from apoe−/− mice had increased treml4 expression when compared to wild type and that treatment with either LDL or oxLDL upregulated macrophage treml4 expression in vitro. After a western diet, overall plaque burden and calcification in the aortic sinus of apoe−/−/treml4−/− mice remained unchanged compared to controls. However, we found that treml4 deficiency resulted in less complex lesions as indicated by decreased foam cell content, plaque necrosis and collagen deposition as well as dysregulation of matrix metalloproteinases expression within the plaques. Moreover, less collagenous metaplasia was observed in the brachiocephalic artery of apoe−/−/treml4−/− mice. Taken together, our results suggest that Treml4 contributes to the inflammatory mechanisms and extracellular matrix regulation associated with lesion complexity without affecting lesion burden or calcification.

PERBEDAAN KADAR PROLYLCARBOXYPEPTIDASE DI PASIEN SINDROM KORONER AKUT DENGAN PASIEN ANGINA STABIL (The Difference of Prolylcarboxypeptidase Level in Acute Coronary Syndrom and Stable Angina Patient)

Coronary arterial disease (CAD) is the main cause of mortality across many countries throughout the world. Formation ofatherosclerosis plaque is the early cause for cardiovascular dysfunction in CAD. Detecting of atherosclerosis plaque instability is veryimportant to predict the risk of acute coronary syndrome (ACS). Various biomarkers have been studied to find the good marker fordetecting atherosclerosis and its instability, but until now there is no biomarker meet the requirements to be used in routine clinicaltests. Prolylcarboxypeptidase (PRCP) is the alternative parameter in the detection of atherosclerosis, assessing the degree of its plaqueand instability in CAD patients. The benefits of PRCP level test in serum, compared to angiography that is currently used in the detectionof atherosclerosis plaque is that this test is non-invasive, provides quantitative level information, able to estimate the instability of theplaque and the fact that it is a laboratorial test that can be performed in hospitals with less advance facilities. The aim of this study isto know the different PRCP level between ACS and stable angina patients by determination. This study was held in the period betweenMarch–May 2014, in Rumah Sakit dr. Hasan Sadikin Bandung. The subjects were selected on the basis of consecutive sampling onpatients that are presented in the Emergency Departement and Cardiovascular Clinic. From 88 patients consisted of 44 patients withACS and 44 patients with stable angina, were tested for PRCP level in the serum using the ELISA sandwich method. This study wascarried out by observational design with cross sectional method. The statistical analysis uses the Saphiro Wilk data normality test,Mann Whitney test and Kruskal Wallis test. There was no characteristic difference between the two groups. This research identifiedsignificant difference of PRCP level between the ACS group and stable angina (P=0.005). Prolylcarboxy peptidase level in the ACS group(156,3í—102 pg/mL) is higher compared to the stable angina (143.8í—102pg/mL). PRCP level test hopefully can be recommended asone of the laboratorycal parameter in measuring the degree and instability of atherosclerosis plaque, in the absence of angiography orintravascular ultrasonography test facility.

Increased risk of acute coronary syndrome in patients with bronchiectasis: A population-based cohort study.

There are few studies on the relationship between bronchiectasis and acute coronary syndrome (ACS). We conducted a population-based cohort study to assess whether bronchiectasis was associated with an increased risk of ACS. We identified 3521 patients diagnosed with bronchiectasis between 2000 and 2010 (bronchiectasis cohort) and frequency matched them with 14 084 randomly selected people without bronchiectasis from the general population (comparison cohort) according to sex, age and index year using the Longitudinal Health Insurance Database. Both cohorts were followed until the end of 2010 to determine the ACS incidence. Hazard ratios of ACS were measured. Based on 17 340 person-years for bronchiectasis patients and 73 639 person-years for individuals without bronchiectasis, the overall ACS risk was 40% higher in the bronchiectasis cohort (adjusted hazard ratio (HR) = 1.40; 95% CI: 1.20-1.62). Compared with those in the comparison cohort with one respiratory infection-related emergency room (ER) visit per year, the ACS risk was 5.46-fold greater in bronchiectasis patients with three or more ER visits per year (adjusted HR = 5.46, 95% CI: 4.29-6.96). Patients with bronchiectasis and three or more respiratory infection-related hospitalizations per year had an 8.15-fold higher ACS risk (adjusted HR = 8.15, 95% CI: 6.27-10.61). Bronchiectasis patients, particularly those experiencing frequent exacerbations with three or more ER visits and consequent hospitalization per year, are at an increased ACS risk.

Comparison of Serum Levels of Vitamin D in Patients With and Without Acute Coronary Syndrome

Introduction: Coronary artery disease is one of the most common causes of mortality around the world. The association between vitamin D deficiency and the incidence of diseases, such as hypertension, diabetes, and metabolic syndrome, has been demonstrated previously. There have been studies concerning the relationship between vitamin D deficiency and cardiovascular diseases, which have shown different results. Therefore, this study aimed at determining the association between serum levels of vitamin D and acute coronary syndrome. Methods: In this case-control study, serum levels of vitamin D were compared between 50 patients with acute coronary syndrome and 50 individuals without this syndrome. A checklist, including demographic data of patients, comorbidities, vitamin D levels, lipid profiles, Electrocardiogram (ECG) changes and echocardiography results, was completed during hospitalization. Results: Mean age in the case and control group was 63.26 ± 10.76 and 61.22 ± 10.71 years, respectively. The prevalence of diabetes and high blood pressure in the case group was 32% and 54% versus 10% and 8% in the control group, respectively. Overall, 70% and 18% of subjects were smokers in the control and case groups, respectively. Mean concentration of vitamin D in serum was 20.63 ± 13.90 ng/mL, which was significantly lower than the control group with a mean concentration of 29.54 ± 16.8 ng/mL (P-Value = 0.002). Finally, it was shown that for every one unit increase in vitamin D levels, the risk of acute coronary syndrome was reduced by 7% (P-Value = 0.005). Conclusions: The results of this study showed that the serum levels of vitamin D were significantly lower in patients with acute coronary syndrome compared to those without this disease.

Angiographic severity of coronary artery disease and cardiovascular risk in acute coronary syndrome in patients with metabolic syndrome.

The extent of angiographic lesions, size of infarct, and in-hospital and long-term prognosis in patients with metabolic syndrome (MS) have not been clearly determined. The aim of the study was to investigate the effect of MS on the severity of coronary artery disease (CAD) and cardio-vascular risk evaluated using the GRACE 2.0 risk score and left ventricular ejection fraction (LVEF) in patients with first acute coronary syndrome (ACS) treated with coronary angioplasty. The study was conducted in a group of 160 consecutive patients hospitalised for their first ACS. Coronary angiogra-phy was assessed and an echocardiographic evaluation of LVEF was performed. MS was diagnosed according to the National Cholesterol Education Programme-Adult Treatment Panel III criteria. Cardiovascular risk was evaluated using the GRACE 2.0 score. Statistical analysis was performed using the STATISTICA software version 12.0. Diagnostic criteria for MS were met by 53.5% of the patients. Patients with and without MS did not differ in angio-graphic severity of CAD and cardiovascular risk as evaluated with the GRACE 2.0 score. LVEF was significantly elevated in patients with MS. In the examined group the angiographic severity of CAD correlated positively with age, body mass index (BMI) and the homeostatic model assessment for insulin resistance (HOMA-IR) index. The cardiovascular risk correlated positively with age, BMI, fasting insulin levels, and HOMA-IR, and inversely with blood pressure and triglyceride levels. The multivariable regression model for predicting the LVEF value indicated that the strongest prognostic factor was the type of ACS. The associations between the angiographic severity of CAD and age, BMI, and insulin resistance (IR) confirm the involvement of these parameters in coronary atherosclerosis. The correlations between the estimated cardiovascular risk and IR indicate the prognostic value of metabolic parameters in patients after first ACS. The type of ACS is the strongest predictor of LVEF at discharge in this population.

Risk of acute coronary syndrome in patients with cervical spondylosis

Background and aimsCervical spondylosis (CS) is reported to be associated with increased sympathetic activity and hypertension. However, the cardiovascular (CV) outcomes of patients with CS are largely unknown. MethodsA national insurance claims dataset of 22 million enrollees in Taiwan during 1999–2010 was used as the research database. We identified 27,948 patients with CS and age-, sex-, and comorbidity-matched controls. By using multivariate logistic regression analysis after adjustment for potential cardiovascular (CV) confounders, we calculated odds ratios (ORs) with 95% confidence intervals (CIs) to quantify the association between CS and acute coronary syndrome (ACS). ResultsA total of 744 ACS events were identified among the 27,948 patients with CS. The overall incidence of ACS was 4.27 per 1000 person-years in the CS cohort and 3.90 per 1000 person-years in the non-CS cohort, with an adjusted hazard ratio (aHR) of 1.13 (95% CI = 1.08–1.18). The aHRs of ACS were 1.08 (95% CI = 1.03–1.15) in the CS cohort without myelopathy and 1.20 (95% CI = 1.13–1.28) in the CS cohort with myelopathy, compared with the non-CS cohort. Compared with patients with CS without neurological signs, patients with CS receiving rehabilitation exhibited a 0.67 aHRs of ACS (95% CI = 0.59–0.76), whereas those with neurological signs receiving spinal decompression exhibited 0.73 aHRs of ACS (95% CI = 0.63–0.84). ConclusionsCS is associated with an increased risk of ACS. Receiving treatment for CS, either rehabilitation or spinal decompression, is associated with less risk of ACS.

Outcomes of non-invasive diagnostic modalities for the detection of coronary artery disease: network meta-analysis of diagnostic randomised controlled trials

ObjectiveTo evaluate differences in downstream testing, coronary revascularisation, and clinical outcomes following non-invasive diagnostic modalities used to detect coronary artery disease.DesignSystematic review and network meta-analysis.Data sourcesMedline, Medline in process, Embase,...

Acute Kidney Injury and mortality prognosis in Acute Coronary Syndrome patients: A meta-analysis.

The aim of this study is to provide a robust estimate of mortality risk in acute coronary syndrome (ACS)-associated acute kidney injury (AKI) to inform clinical practice and policy. A meta-analysis of cohort studies evaluating outcomes of ACS and which reported AKI and AKI-associated mortality. Studies were excluded if they incorporated patients not admitted through the emergency department (i.e. for elective procedures), were limited to cardiogenic shock or cardiac arrest, or relied on registry data for outcomes without further adjudication. The predictor was ACS-associated AKI and outcomes early (30day or in-hospital) mortality and late-mortality (post-hospital discharge). Thirty-six studies with 37 unique cohorts comprising 100476 patients were included. The pooled rate of ACS-associated AKI was 15.8%. In 32 cohorts reporting early mortality, the crude early mortality rate was 15.0% amongst those with AKI compared with 2.0% amongst those without AKI. The pooled estimate of the relative risk of AKI-associated early mortality was 4.1 (95% confidence interval: 3.3 to 5.0) with high heterogeneity between studies (I 2 =84% (61% to 88%)). When heterogeneity was accounted for mathematically using credibility ceilings, the risk of mortality was lower, but still clinically significant (3.1 (2.6 to 3.6)). In 19 cohorts reporting late mortality (1 to 10years), the relative risk of AKI-associated mortality was 2.6 (2.0 to 3.3) with moderate heterogeneity (I 2 =65% [35% to 88%]). Following application of credibility ceiling relative risk estimate dropped to 2.2 (1.9 to 2.6). Acute coronary syndrome-associated AKI is associated with more than a three-fold increase in early mortality and more than two-fold in long-term mortality.

Perivascular Epicardial Fat Stranding at Coronary CT Angiography: A Marker of Acute Plaque Rupture and Spontaneous Coronary Artery Dissection.

Purpose To evaluate the frequency and implications of perivascular fat stranding on coronary computed tomography (CT) angiograms obtained for suspected acute coronary syndrome (ACS). Materials and Methods This retrospective registry study was approved by the institutional review board. The authors reviewed the medical records and images of 1403 consecutive patients (796 men, 607 women; mean age, 52.8 years) who underwent coronary CT angiography at the emergency department from February 2012 to March 2016. Fat attenuation, length and number of circumferential quadrants of the affected segment, and attenuation values in the unaffected epicardial and subcutaneous fat were measured. "Cases" were defined as patients with perivascular fat stranding. Patients with significant stenosis but without fat stranding were considered control subjects. Baseline imaging characteristics, ACS frequency, and results of subsequent downstream testing were compared between cases and control subjects by using two-sample t, Mann-Whitney U, and Fisher tests. Results Perivascular fat stranding was seen in 11 subjects, nine with atherosclerotic lesions and two with spontaneous coronary artery dissections, with a mean fat stranding length of 19.2 mm and circumferential extent averaging 2.9 quadrants. The mean attenuation of perivascular fat stranding, normal epicardial fat, and normal subcutaneous fat was 17, -93.2, and -109.3 HU, respectively (P < .001). Significant differences (P < .05) between cases and control subjects included lower Agatston score, presence of wall motion abnormality, and initial elevation of serum troponin level. ACS frequency was 45.4% in cases and 3.8% in control subjects (P = .001). Conclusion Recognition of perivascular fat stranding may be a helpful additional predictor of culprit lesion and marker of risk for ACS in patients with significant stenosis or spontaneous coronary artery dissection. © RSNA, 2018 Online supplemental material is available for this article.