Differential expression of osteopontin, and osteoprotegerin mRNA in epicardial adipose tissue between patients with severe coronary artery disease and aortic valvular stenosis: association with HDL subclasses.

BACKGROUND: Previous studies suggest a relationship of the epicardial adipose tissue (EAT) with progression and calcification of the atherosclerotic plaque; however, it is unknown if this tissue expresses genes that may participate on these processes and if the expression of these genes is regulated by high-density lipoprotein (HDL) subclasses. METHODS: To explore this possibility, we determined the mRNA expression by qPCR of a pro-calcifying gene (osteopontin (OPN)), and two anti-calcifying genes (osteoprotegerin (OPG) and osteonectin (ON)), in biopsies of EAT obtained from 15 patients with coronary artery disease (CAD) determined by angiography, and 15 patients with diagnostic of aortic valve stenosis but without CAD as control group. We determined the distribution and composition of HDL subclasses by electrophoresis and their statistical relationship with the gene expression in EAT. RESULTS: EAT from CAD patients showed a higher expression level of OPN and OPG than control group, whereas ON expression was similar between groups. Large HDL subclasses were cholesterol-poor in CAD patients as estimated by the cholesterol-to-phospholipid ratio. A linear regression model showed an independent association of OPN expression with HDL3a-cholesterol, and OPG expression with the relative proportion of HDL3b protein. Logistic analysis determined that OPN expression was positively associated with the presence of atherosclerotic plaque CONCLUSION: OPN, ON, and OPG genes are transcribed in EAT; to the exception of ON, the level of expression was different in CAD patients and control group, and correlated with some HDL subclasses, suggesting a new role of these lipoproteins.

The variant rs8048002 T>C in intron 3 of the MHC2TA gene is associated with risk of developing acute coronary syndrome.

Recently, an intronic single nucleotide polymorphism (rs8048002) in the MHC class II transactivator gene (MHC2TA) was shown to be associated with increased susceptibility to several inflammatory diseases. The aim of the present study was to test for an association between this MHC2TA gene polymorphism and susceptibility to the risk of developing acute coronary syndromes (ACS) in a group of Mexicans patients. The single nucleotide polymorphism (rs8048002) of the MHC2TA gene was analyzed by 5' exonuclease TaqMan genotyping assays in a group of 452 patients with ACS and 456 healthy controls. The C allele and TC genotype were associated with risk of developing ACS (OR=4.55, pC=6×10(-4) and OR=4.41, pC=1.5×10(-3), respectively). Multiple logistic analysis was used for estimate risk between ACS patients and controls adjusted by cardiovascular risk factors (gender, age, hypertension, dyslipidemia, smoking, diabetes, body mass index and alcohol consumption). In this analysis, the TC+CC genotypes were significantly associated with increased risk of ACS as compared to TT genotype (OR=4.56, pC=0.004). In summary, our data suggest that the MHC2TA rs8048002 C>T gene polymorphism plays an important role in the risk of developing ACS.

Acute left main coronary artery thrombosis as the first manifestation of systemic lupus erythematosus and catastrophic antiphospholipid syndrome.

Most coronary events in young adults are related to atherosclerosis; however, approximately 20% of coronary heart disease in young adults is related to nonatherosclerotic factors such as coronary abnormalities, connective tissue disorders, and autoimmune diseases. Different initial manifestations of systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) have been reported. Myocardial infarction is observed in patients with SLE in all age groups; it appears during the course of the disease; and it is unusual in the APS. We present a unique case of a 28-year-old young man previously healthy who has an ST-elevation myocardial infarction by total acute thrombosis of the left main coronary artery. Laboratory studies demonstrated the presence of antibodies for SLE and APS. The patient was treated successfully with percutaneous coronary intervention. He developed catastrophic APS despite an adequate anticoagulation and was treated with intravenous steroids and plasmapheresis. Clinical evolution was satisfactory, and he discharged from the hospital. This case highlights the importance of considering in the emergency department, the prothrombotic states such as SLE and APS in young patients presenting with acute myocardial infarction caused by an unexplained intracoronary thrombosis. Early diagnosis of catastrophic APS and aggressive therapies are essential to help such patients from succumbing to this potentially fatal condition.

Intramyocardial hemorrhage in spontaneously reperfused myocardial infarction.

OBJECTIVE. The presence of intramyocardial hemorrhage (IMH) is frequent in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PPCI). We aim for the presence IMH using cMRI in patients who presented AMI and did not undergo PPCI or thrombolysis. Cardiac magnetic resonance has proven to be a highly sensitive method for detect its presence in the ischemic damaged tissue. MATERIAL AND METHODS. Patients admitted with diagnosis of ST elevation myocardial infarction > 24 h after initial presentation and without reperfusion therapy were enrolled in the study. All patients underwent cardiac magnetic resonance for detecting edema, microvascular obstruction and intramyocardial hemorrhage, followed by coronary angiography. RESULTS. Seven male patients, with median age of 53 years, were enrolled. Cardiac magnetic resonance showed that all patients had microvascular obstruction and edema. Two of them had intramyocardial hemorrhage in association with spontaneous reperfusion demonstrated by angiography. CONCLUSION. The results of our study show that in patients with acute myocardial infarction, intramyocardial hemorrhage occurs not only after therapeutic, but also after spontaneous reperfusion. This is the first time that its presence is demonstrated by cardiac magnetic resonance.

Effectiveness and Safety of Extracorporeal Shockwave Myocardial Revascularization in Patients With Refractory Angina Pectoris and Heart Failure.

Extracorporeal shockwave myocardial revascularization (ESMR) is a therapy for refractory angina pectoris. Our aim was to assess the efficacy and safety of ESMR in the management of patients with stable coronary artery disease (CAD) and heart failure as well as its effects on inflammation and angiogenesis. In this single-arm prospective trial, we included 48 patients with CAD, myocardial ischemia assessed by radionuclide imaging, echocardiographic evidence of left ventricular systolic dysfunction and without revascularization options. Changes in angina grading score, myocardial perfusion, left ventricular ejection fraction, and six-minute walk test after ESMR therapy were used for efficacy assessment. Changes of inflammation and angiogenesis biomarkers were also evaluated. ESMR therapy was performed using a commercially available cardiac shockwave generator system (Cardiospec; Medispec). After 9 weeks of ESMR therapy, a significant improvement was found regarding the initial angina class, severity of ischemia, left ventricular ejection fraction, and six-minute walk test in most patients. No deleterious side effects after treatment were detected. Regarding biomarkers, endothelial progenitor cells and angiopoietin-3 were significantly increased whereas IL-18 and TGF-ß were significantly decreased after ESMR in the total group. Notably, VEGF, IL-1ß, and lipoxin A4 levels were significantly increased only in patients with myocardial ischemia improvement. In conclusion, ESMR therapy is safe and effective in most but not all patients with CAD and heart failure. ESMR is associated with increased markers of angiogenesis and decreased markers of inflammation. Myocardial ischemia improvement after ESMR is associated with increased markers of angiogenesis and pro-resolving mediators.

Clinical phenotypes, aetiologies, management, and mortality in acute heart failure: a single-institution study in Latin-America.

AIMS: Little is known regarding acute heart failure (AHF) clinical characteristics and its hospital outcome in Latin America. This study sought to assess the prevalence of, and identify differences among, in-hospital outcomes in patients hospitalized for AHF who were stratified by clinical phenotype at a hospital in Latin America. METHODS AND RESULTS: This is a retrospective cohort study of patients with AHF who were hospitalized in the coronary care unit of a Latin American teaching hospital from January 2006 to December 2018. Cox regression analysis was used to identify predictors of mortality. Of 21 042 patients admitted, 7759 (36.6%) had AHF. Their median age was 62 years, and 35% were women. De novo heart failure was seen in 39.4% of patients. Most common was AHF-associated acute coronary syndromes (ACS-HF) in 43.0%, decompensated heart failure (DHF) in 33.7%, hypertensive heart failure (HT-HF) in 11.8%, and cardiogenic shock (CS) in 5.2%. Pulmonary oedema (PO) (3.3%) and right heart failure (RHF) (3.0%) were least frequent. Coronary artery disease was the most frequent aetiology in 56.5% of patients, valvular heart disease in 22.4%, and cardiomyopathies in 12.3%. Other less frequent aetiology included adult congenital heart disease (2.5%), lung diseases (2.1%), acute aortic syndromes (1.4%), pericardial diseases (0.8%), and intracardiac tumours (0.3%). Aetiology could not be established in 1.6% of patients. Before admission, patients with worsening chronic heart failure and reduced ejection fraction were treated with renin-angiotensin system blockers (60.4%), beta-blockers (42.5%), or spironolactone (34.4%). The percentages of patients given in-hospital management with intravenous diuretics, vasodilators, inotropes, and vasopressors were 81.2%, 33.4%, 18.9%, and 20.4%, respectively. The overall in-hospital mortality was 17.9% (71.3%, 43.9%, 23.8%, 14.9%, 13.6%, and 10.1% for CS, PO, RHF, DHF, ACS-HF, and HT-HF, respectively; P < 0.0001). Multivariate analysis revealed that PO (hazard ratio [HR] 2.68, 95% confidence interval [CI] 1.73-4.14, P < 0.0001) and CS (HR 3.37, 95% CI 2.12-5.35, P < 0.0001) were independent predictors of in-hospital mortality. Use of intravenous diuretics was linked to reduction of in-hospital mortality (HR 0.70, 95% CI 0.59-0.59, P < 0.0001). By contrast, increased in-hospital mortality was associated with the use of intravenous inotrope or vasopressor (HR 1.49, 95% CI 1.27-1.76 and HR 2.91, 95% CI 2.41-3.51, P < 0.0001, respectively). CONCLUSIONS: Real-world evidence from a university hospital in Latin America shows that the high mortality among patients with AHF may depend, among other factors, on patients' AHF clinical phenotypes. The clinical characteristics and aetiologies of AHF appear to differ between these data from Mexico and those from European and US registries.

Cardiogenic Shock Among Patients with and without Acute Myocardial Infarction in a Latin American Country: A Single-Institution Study.

Background: Latin America has limited information about the full spectrum cardiogenic shock (CS) and its hospital outcome. This study sought to examine the temporal trends, clinical features and outcomes of patients with CS in a coronary care unit of single Mexican institution. Methods: This was a retrospective study of consecutive patients hospitalized with CS in a Mexican teaching hospital between 2006-2019. Patients were classified according to the presence or absence of acute myocardial infarction (AMI). Results: Of 22,747 admissions, 833 (3.7%) exhibited CS. Among patients with AMI (n = 12,438), 5% had AMI-CS, and in patients without AMI (n = 10,309), 2.3% developed CS (non-AMI-CS). Their median age was 63 years and 70.5% were men. Cardiovascular risk factors were more frequent among the AMI-CS group, whereas a history of heart failure was greater in non-AMI-CS patients (70.1%). In AMI-CS patients, the median delay time was 17.2 hours from the onset of AMI symptoms to hospital admission. Overall, the median left ventricular ejection fraction (LVEF) was 30%. Patients with CS at admission showed end-organ dysfunction, evidenced by lactic acidosis, renal impairment, and elevated liver transaminases. Of the 620 AMI-CS patients, the main cause was left ventricular dysfunction in 71.3%, mechanical complications in 15.2% and right ventricular infarction in 13.5%. Among the 213 non-AMI-CS patients, valvular heart disease (49.3%) and cardiomyopathies (42.3%) were the most frequent etiologies. In-hospital all-cause mortality rates were 69.7% and 72.3% in the AMI-CS and non-AMI-CS groups, respectively. Among AMI-CS patients, renal dysfunction, diabetes, older age, depressed LVEF, absence of revascularization and the use of mechanical ventilation were independent predictors of in-hospital mortality. However, in the non-AMI-CS group, only low LVEF and high lactate levels proved significant. Conclusions: This study demonstrates differences in the epidemiology of CS compared to high-income countries; the high mortality reflects critically ill patients and the lack of contemporary effective therapies in the population studied.

Integrating the STOP-BANG Score and Clinical Data to Predict Cardiovascular Events After Infarction: A Machine Learning Study.

BACKGROUND: OSA conveys worse clinical outcomes in patients with coronary artery disease. The STOP-BANG score is a simple tool that evaluates the risk of OSA and can be added to the large number of clinical variables and scores that are obtained during the management of patients with myocardial infarction (MI). Currently, machine learning (ML) is able to select and integrate numerous variables to optimize prediction tasks. RESEARCH QUESTION: Can the integration of STOP-BANG score with clinical data and scores through ML better identify patients who experienced an in-hospital cardiovascular event after acute MI? STUDY DESIGN AND METHODS: This is a prospective observational cohort study of 124 patients with acute MI of whom the STOP-BANG score classified 34 as low (27.4%), 30 as intermediate (24.2%), and 60 as high (48.4%) OSA-risk patients who were followed during hospitalization. ML implemented feature selection and integration across 47 variables (including STOP-BANG score, Killip class, GRACE score, and left ventricular ejection fraction) to identify those patients who experienced an in-hospital cardiovascular event (ie, death, ventricular arrhythmias, atrial fibrillation, recurrent angina, reinfarction, stroke, worsening heart failure, or cardiogenic shock) after definitive MI treatment. Receiver operating characteristic curves were used to compare ML performance against STOP-BANG score, Killip class, GRACE score, and left ventricular ejection fraction, independently. RESULTS: There were an increasing proportion of cardiovascular events across the low, intermediate, and high OSA risk groups (P = .005). ML selected 7 accessible variables (ie, Killip class, leukocytes, GRACE score, c reactive protein, oxygen saturation, STOP-BANG score, and N-terminal prohormone of B-type natriuretic peptide); their integration outperformed all comparators (area under the curve, 0.83 [95% CI, 0.74-0.90]; P < .01). INTERPRETATION: The integration of the STOP-BANG score into clinical evaluation (considering Killip class, GRACE score, and simple laboratory values) of subjects who were admitted for an acute MI because of ML can significantly optimize the identification of patients who will experience an in-hospital cardiovascular event.

Derivation and validation of a simple inflammation-based risk score system for predicting in-hospital mortality in acute coronary syndrome patients.

BACKGROUND: Accurate assessment of inflammatory status of patients during acute coronary syndrome (ACS) has become of great importance in their risk classification and in the research of new anti-inflammatory therapies. METHOD: The study cohort included 7396 patients with ACS. We sought to derive and internally validate an inflammation-based score that included high-sensitivity C-reactive protein, white blood cell count, and serum albumin level at admission to evaluate the predictive role of systemic inflammation in the clinical outcome of these patients. We randomly assigned patients into derivation (66.6%) and validation (33.4%) cohorts. A total of four categories of systemic inflammation were defined. RESULTS: Assessed individually, the three biomarkers were associated with a higher rate of in-hospital mortality. When we combined them into an inflammation score, in-hospital mortality was significantly different across the four categories of inflammation in the derivation cohort (1.8%, 2.8%, 4.1%, and 13.8% for without, mild, moderate, and severe inflammation, respectively; p<0.0001, C-statistic, 0.71). These results were similar in the validation cohort (1.1%, 2.9%, 5.2%, and 12.6%, respectively; p<0.0001, C-statistic, 0.71). After multivariate adjustment, only the category of severe systemic inflammation was associated with a threefold increased risk of in-hospital mortality (odds ratios 3.02, p<0.0001) and was the most powerful predictor of mortality. In the whole cohort, after subsetting patients based on GRACE risk score, the severe inflammation category was associated with a significant increase of in-hospital mortality across all sub-groups, mainly in patients with higher GRACE risk score. The inflammation-based risk score reclassified 25.3% of the population. The net reclassification index was 8.2% (p=0.001). CONCLUSION: A risk score system based on biomarkers of inflammation readily available at admission in patients with ACS, could better assess the inflammatory status and predict in-hospital mortality, as well as severe systemic inflammation that contributes to a worse outcome independently of clinical risk factors.

Combined clot fragmentation and aspiration in patients with acute pulmonary embolism.

BACKGROUND: Massive angiographic pulmonary embolism (PE) with right ventricular dysfunction (RVD) is associated with a high early mortality rate. The therapeutic alternatives for this condition include thrombolysis, surgical embolectomy, or percutaneous mechanical thrombectomy (PMT). We describe our experience using PMT in patients with massive PE and RVD with unsuccessful thrombolysis, increased bleeding risk, or major contraindications for thrombolytic therapy. METHODS: Clinical, hemodynamic, and angiographic parameters prior to and following PMT were evaluated. Our primary objective was to describe the incidence of in-hospital cardiovascular death, and of major and minor complications. Mid-term outcomes included analysis of occurrence of cardiovascular death, recurrent pulmonary embolism, change of New York Heart Association functional class, and hospital readmission. RESULTS: From July 2004 to May 2007, 69 patients were referred to the cardiac catheterization laboratory with a diagnosis of acute PE, 18 of whom met the criteria for massive PE and are the subject of this study. All patients underwent thrombus fragmentation using a pigtail catheter that was complemented in 13 patients with thrombus aspiration. A percutaneous thrombectomy device (Aspirex; Straub Medical; Wangs, Switzerland) was used in 11 patients. Hemodynamic, angiographic, and blood oxygenation parameters improved after the procedure. A significant increase was observed for systolic systemic BP (74.3+/-7.5 mm Hg vs 89.4+/-11.3 mm Hg, p=0.001) [mean+/-SD], as was a decrease in mean pulmonary artery pressure (37.1+/-8.5 mm Hg vs 32.3+/-10.5 mm Hg , p=0.0001). The in-hospital major complications rate was 11.1%; one patient died from refractory shock, and one patient had intracerebral hemorrhage with minor neurologic sequelae. No cardiovascular deaths or recurrent pulmonary thromboembolism were documented during clinical follow-up (12.3+/-9.4 months). CONCLUSIONS: In patients with massive PE, RVD and major contraindications to thrombolytic therapy, increased bleeding risk, failed thrombolysis, or unavailable surgical thrombectomy, PMT appears to be a useful therapeutic alternative.

A proposed functional clinical classification predicts in-hospital and long-term survival in the setting of acute right ventricular infarction.

BACKGROUND: The objectives of the present investigation were to validate the prognostic role of a proposed Clinical Classification [CC], to evaluate the TIMI risk score [RS] and to establish whether the TIMI-RS should incorporate points for patients with acute right ventricular infarction [TIMI-RS-RVI]. METHODS AND RESULTS: A total of 523 RVI patients were classified on clinical and functional basis as: A, without right ventricular failure [RVF], B with RVF and C with cardiogenic shock. The CC was evaluated prospectively among 98 patients with RVI and retrospectively in 425 RVI patients. The TIMI-RS was evaluated prospectively among 622 patients with STEMI [anterior:277, inferior:247, RVI:98], and retrospectively in 425 RVI patients. The CC established differences among the 3-RVI Classes for in-hospital mortality [prospectively and retrospectively; p<0.01, p<0.001, respectively] that were maintained at 8 years [p < 0.001]. Patients with anterior and inferior STEMI, but not those with RVI revealed an association between outcome and TIMI-RS [p<0.001]. Testing for TIMI-RS-RVI did not result a good prognostic tool [ROC=0.9; excellent discrimination, but with a very poor "clinical calibration"]. CONCLUSIONS: The proposed CC allowed prediction of mortality at short- and long-term in the setting of acute RVI. The role of the TIMI-RS should be reevaluated prospectively as a prognostic tool in the scenario of RVI patients.

[Prevention and treatment of hypertension and coronary heart disease]. / Prevención y tratamiento de la hipertensión arterial sistémica en el paciente con enfermedad arterial coronaria.

The association between arterial systemic hypertension arterial coronary disease has been demonstrated by cumulated evidence of several epidemiological studies. Hypertension is an important independent risk factor for the development of coronary artery disease, vascular cerebral disease and nephropathy. Important advances exist in the knowledge of neurohumoral and hemodynamic factors that come together in the pathophysiology of the hypertension and in the development of coronary disease that allow to establish better strategies not only of treatment, but also of prevention, with the purpose of diminishing the cardiovascular mortality. The spectrum of the coronary artery disease secondary to atherosclerosis is wide and the strategies of treatment of hypertension must be adapted to each particular case. The treatment of both conditions needs of specific limits of agreement to the conditions of the patient and the form of presentation of each one of these disease.

[Extreme elevation of the blood pressure (hypertensive crisis): recommendations for its clinical-therapeutic approach]. / Elevación extrema de la presión arterial (crisis hipertensiva): recomendaciones para su abordaje clínico-terapéutico.

From beginnings of last century the hypertensive emergency was defined as the association of acutely elevation from the arterial pressure and the appearance of damage to end organ. At present is recognized the effects of the hypertensive emergency, the aspects of its patophysiology in which are included phenomenon of vasomotricity and the participation of different substances with vasoactives properties. The clinical presentation includes not only the manifestations of the increase of the arterial pressure, the end organ damage too; for this reason the hypertensive emergency needs the immediate reduction of the arterial tension to prevent the damage to specific organs. The treatment in every case will have to be individualized, with a wide knowledge of the characteristics of every medicament to obtain the best results. The diagnosis and treatment of the hypertensive emergencies needs often of the attention of its complications if they have appeared and later, of a treatment of support for the arterial hypertension.

[Influence of rosuvastatin in endothelial function and oxidative stress, in patients with acute coronary syndrome]. / Impacto del uso de rosuvastatina en los primeros días de un síndrome coronario agudo en la fiunción endotelial y el poder oxidativo.

PURPOSE: The endothelial function is the cornerstone of several cardiovascular disease. In this trial we compared how the Nitric Oxide (NO) and Oxidative Stress (OS) serum levels, as surrogate markers of endothelial function, change in patients who received (or not) rosuvastatin during the first seven days of an acute coronary syndrome (ACS). METHODS: Twenty-two patients with ACS (age:66 +/- 9 years, gender: ten female and 12 male) were randomized in two groups. Patients in the first group (G1) received the conventional treatment for an ACS, plus placebo. The other group (G2) additionally received a daily oral dose of 40 mg of rosuvastatin. We measured the blood levels of nitrates and OS in both groups twice: at baseline (admission to Intensive care unit) and seven days after. The statistical analysis was performed using the paired t-test or the Chi2 test depending of the variables. Statistical significance was considered with a p < 0.05. RESULTS: Groups (G1 and G2) differed statistically on age (G1=71 years +/- 10 vs. G2 63 +/- 9 years, p=0.04). After 7 days of the ACS onset, ON levels diminished on 21% (p=0.17) in G1, but raised on 24% in the group who re- ceived rosuvastatin (p=0.005), with statistically difference between groups (p=0.005). On the other hand, the OS, augmented statistically on both groups: G1 (17%, p<0.001) and G2 (13%, p<0.001), without any difference between groups (p=0.77). CONCLUSION: The endothelial dysfunction in the first days of an ACS is accentuated, but with the use of rosuvastatina, the endothelial function improves. In contrast, the OS increase in both groups, without differences between groups.

Reperfusion of myocardial infarction in India: Notions for México.

In India and México, cardiovascular diseases are the first cause of death and potential years of life lost. Close similarities exist between these two countries when facing the difficulties to establish a universal reperfusion program for ST elevation myocardial infarction (STEMI). This paper describes the situation of STEMI treatment in both countries, and examines the lessons that Mexico's health care system could adopt from the recent advances accomplished by the STEMI initiative in India.

[Pharmacologic combination in the treatment of the acute myocardial infarction with ST elevation]. / Combinación farmacológica en el tratamiento del infarto agudo del miocardio con elevación del segmento ST. Análisis de la literatura y experiencia en la Unidad Coronaria del Instituto Nacional de Cardiología "Dr. Ignacio Chávez".

The evolution of reperfusion treatment has permitted an improvement in the prognosis and survival of patients with Acute myocardial infarction with ST elevation. The benefit of thrombolitic therapy was demonstrated clearly starting with the first trials of ISIS 2. It was also demonstrated this benefit is greater when the thrombolitic is combined with aspirin. Other trials have arisen like GUSTO I and TIMI 14, which have continued with the search for the best strategy of reperfusion, demonstrating that the pharmacologic combination with fibrinolitic, antiplatelet and antithrombinics provides the best results regarding permeability of the epicardic artery and transmiocardic reperfusion. Finally the mechanical reperfusion has managed to improve the results obtained with the pharmacologic treatment. Nevertheless it is probably that the Angioplasty with fibrinolitic and antiplatelet therapy is a useful treatment strategy, available for the patient with acute coronary syndrome with ST elevation. In light of the latest studies we must be very cautious, but based on the knowledge of the physiopathology of these syndromes, we think there is still much to discover.

Prognostic Implications of Serum Albumin Levels in Patients With Acute Coronary Syndromes.

Hypoalbuminemia is a long-term risk factor for incident of both myocardial infarction and heart failure. We assessed whether serum albumin levels at admission are associated with new-onset heart failure and in-hospital mortality in patients with acute coronary syndrome (ACS). The study included 7,192 patients with ACS with no previous history of heart failure. Patients were divided into quartiles according to serum albumin levels (Q1: ≤3.50 g/dl; Q2: 3.51 to 3.80 g/dl; Q3: 3.81 to 4.08 g/dl; and Q4: >4.08 g/dl). Logistic regressions were used to explore the relations among serum albumin quartiles, new-onset heart failure, and in-hospital mortality. Serum albumin levels were negatively correlated with both high-sensitivity C-reactive protein and white blood cell count at admission. The unadjusted rate for both new-onset heart failure (37.7%, 20.2%, 14.7%, and 11.4% for Q1, Q2, Q3, and Q4, respectively; p <0.0001) and in-hospital mortality (9.8%, 3.4%, 2.0%, and 1.7% for Q1, Q2, Q3, and Q4, respectively; p <0.0001) were higher at lower serum albumin levels. Multivariate analysis demonstrated that serum albumin level ≤3.50 g/dl is an important and independent predictor of both the development of new-onset heart failure (odds ratio 2.31, 95% CI 1.87 to 2.84, p <0.0001) and in-hospital mortality (odds ratio 1.88, 95% CI 1.23 to 2.86, p = 0.003). In conclusion, albumin level ≤3.50 g/dl is an independent predictor of new-onset heart failure and in-hospital mortality in patients with ACS. The inflammatory state may be a mechanism underlying hypoalbuminemia in this clinical setting.

The NLRP3 and CASP1 gene polymorphisms are associated with developing of acute coronary syndrome: a case-control study.

The protein products of NLRP3 and CASP1 genes are involved in the cleavage of pro-IL-1B and pro-IL-18 leading to the active cytokines, which play an important role in the development of the acute coronary syndrome (ACS). The aim of the present study was to evaluate whether NLRP3 and CASP1 gene polymorphisms are biomarkers of ACS susceptibility in Mexican population. Two polymorphisms of the CASP1 gene [G+7/in6A (rs501192) and A10370-G Exon-6 (rs580253)] and one of the NLRP3 gene [UTR'3 G37562-C (rs10754558)] were genotyped by 5' exonuclease TaqMan assays in a group of 617 patients with ACS and 609 control individuals. Under recessive model, the CASP1 G+7/in6A polymorphism was associated with an increased risk of developing ACS when compared to healthy controls (OR = 1.76, 95% CI 1.08-2.86, P Res  = 0.022). In the same way, under recessive model, the CASP1 A10370-G was associated with increased risk of ACS (OR = 1.75, 95% CI 1.07-2.85, P Res  = 0.025). Moreover, under co-dominant, dominant, over-dominant, and additive models, the NLRP3 UTR'3 G37562-C was associated with a decreased risk of ACS (OR = 0.45, 95%CI 0.22-0.92, P Co-dom  = 0.006; OR = 0.61, 95%CI 0.44-0.84, P Dom  = 0.002; OR = 0.67, 95%CI 0.48-0.94, P Over-dom  = 0.02; and OR = 0.65, 95%CI 0.50-0.94, P Add  = 0.02, respectively). In summary, this study demonstrates that the G+7/in6A and A10370-G polymorphisms of the CASP1 gene are associated with increased risk of developing ACS, whereas the UTR'3 G37562-C polymorphism of the NLRP3 gene is associated with a decreased risk of developing ACS in Mexican population.