miR-196a2 (rs11614913) polymorphism is associated with coronary artery disease, but not with in-stent coronary restenosis.

OBJECTIVE: The aim of the study was to evaluate the association of miRNA-146a G/C (rs2910164), and miRNA-196a2 C/T (rs11614913) polymorphisms with the presence of coronary artery disease (CAD) and/or restenosis in patients with coronary stent. MATERIALS AND METHODS: The polymorphisms were determined in 218 patients with CAD who underwent coronary artery stenting (66 with restenosis and 152 without restenosis) and 611 healthy controls using 5' exonuclease TaqMan assays. RESULTS: The distribution of both polymorphisms was similar in patients with and without restenosis. However, when the whole group of patients (with and without restenosis) was compared to healthy controls, under co-dominant, dominant and additive genetic models, the T allele of the miRNA-196a2 C/T (rs11614913) polymorphism was associated with increased risk of CAD (OR = 2.18, Pco-dom = 0.006, OR = 1.86, Pdom = 0.002, and OR = 1.52, Padd = 0.002, respectively). All models were adjusted for age, type 2 diabetes mellitus, dyslipidemia, hypertension and smoking habit. The "GT" haplotype was associated with increased risk of developing CAD (OR = 1.36, P = 0.046). CONCLUSIONS: Our data suggests that the T allele of the miRNA-196a2 C/T (rs11614913) polymorphism is associated with the risk of developing CAD, but no association with restenosis was observed.

Primary thrombosis of the anterior descending in a patient with antiphospholipid antibody syndrome / Trombosis primaria de la descendente anterior en un paciente con síndrome de anticuerpos antifosfolípidos

Antiphospholipid antibody syndrome is a heterogeneous clinical and biochemical entity. We present the case of a young male with history of venous thromboembolism. This time he presents because of chest ischemic pain associated with ST segment elevation. He was taken to the cath lab to perform a primary percutaneous coronary intervention and a total occlusion of the left anterior descending artery was noted. Successful thrombus aspiration was performed. No stent was deployed. He was taken to the cath lab for a second look angiography and no atherosclerotic lesions were observed, which was confirmed by intravascular ultrasound.

El síndrome de anticuerpos antifosfolípidos es una situación clínica y bioquímica heterogénea. Presentamos el caso de un varón joven con antecedente de tromboembolia venosa que se presentó en esta ocasión por dolor precordial, con elevación del ST en el electrocardiograma. Fue llevado a sala de angiografía para realizar angioplastia primaria y se observó una oclu- sión total ostial de la descendente anterior. Se realizó aspiración manual del trombo. No se realizó angioplastia con balón ni stent. En la angiografía de control a las 48 horas se observó ausencia de trombo y de placas aterosclerosas, lo cual se co- rroboró mediante ultrasonido intracoronario.

The T29C (rs1800470) polymorphism of the transforming growth factor-ß1 (TGF-ß1) gene is associated with restenosis after coronary stenting in Mexican patients.

The aim of the present study was to establish the role of IL-6 and TGF-ß1 gene polymorphisms in the risk of developing in-stent restenosis. Two IL-6 [rs1800796 (-572 G>C), rs2069827 (-1426 T>G)] and two TGF-ß1 [rs1800469 (-509 T>C), rs1800470 (T29C)] gene polymorphisms were analyzed by 5' exonuclease TaqMan genotyping assays in a group of 244 patients, who underwent coronary artery stenting. Basal and procedure coronary angiography were analyzed, looking for angiographic predictors of restenosis and follow-up angiography was performed to screen for binary restenosis. Under the dominant and additive models adjusted for hypertension, stable angina, stent used, and diameter of stent, the TGF-ß1 T29C (rs1800470) polymorphism was significantly associated with an increase risk of restenosis when compared to patients without restenosis (OR=2.06, 95% CI: 1.03-4.11, P(Dom)=0.034 and OR=1.64, 95% CI: 1.09-2.45, PAdd=0.016). TGF-ß1 polymorphisms were in linkage disequilibrium and one haplotype (TT) was significantly increased in patients with restenosis when compared to patients without restenosis (OR=2.03, P=0.041). In summary, our results suggest that the TGF-ß1 T29C gene polymorphism could be involved in the risk of developing restenosis after coronary stent placement.

The C4280A (rs5705) gene polymorphism of the renin (REN) gene is associated with risk of developing coronary artery disease, but not with restenosis after coronary stenting.

The aim of the present study was to evaluate the role of AGT and REN gene polymorphisms as susceptibility markers for coronary artery disease (CAD) and/or restenosis after coronary stent placement in a group of Mexican patients. Five polymorphisms of the AGT (rs699, rs4762, rs5051, rs5049, rs5046) and two of the REN (rs5707, rs5705) genes were analyzed by 5' exonuclease TaqMan genotyping assays in 240 patients with CAD who underwent coronary artery stenting (76 with restenosis and 164 without restenosis). A group of 610 individuals without clinical and familial antecedents of cardiovascular diseases were included as controls. The results showed that the distribution of AGT and REN polymorphisms were similar in patients with and without restenosis. However, when the whole group of patients (with and without restenosis) was compared to healthy controls, under co-dominant, dominant, heterozygous and additive models, the REN A4280C (rs5705) polymorphism was associated with increased risk of CAD (OR=1.76, PCo-dom=0.006, OR=1.81, PDom=0.001, OR=1.75, PHet=0.003 and OR=1.59, PAdd=0.003, respectively). All models were adjusted for age, gender, diabetes, dyslipidemia, hypertension and smoking habit. The TC haplotype of the REN gene was associated with increased risk of CAD (OR=1.53, P=0.014). The data suggest that the REN C4280A (rs5705) polymorphism plays an important role in the risk of developing CAD with the highest risk for C allele, but do not support its role as a risk factor for developing restenosis after coronary stenting.

Haplotypes of the angiotensin-converting enzyme (ACE) gene are associated with coronary artery disease but not with restenosis after coronary stenting.

The aim of the present study was to establish the role of ACE gene polymorphisms in the risk of developing in-stent restenosis and/or coronary artery disease (CAD). Eight ACE gene polymorphisms were genotyped by 5' exonuclease TaqMan genotyping assays in 236 patients with CAD who underwent coronary artery stenting. Basal and procedure coronary angiographies were analyzed searching for angiographic predictors of restenosis and follow-up angiography was analyzed looking for binary restenosis. A group of 455 individuals without clinical and familial antecedents of cardiovascular diseases were included as controls. Haplotypes were constructed after linkage disequilibrium analysis. Distribution of ACE polymorphisms was similar in patients with and without restenosis. Similar results were observed when the analysis was made comparing the whole group of patients (with and without restenosis) and healthy controls. Six out of eight polymorphisms were in high linkage disequilibrium and were included in five haplotypes (AAAGCA, GGGATG, GAGATG, AGAGCA and AAGACA). The distribution of these haplotypes was similar in patients with and without restenosis. However, CAD patients showed an increased frequency of the AAAGCA haplotype (OR=1.31, 95% CI: 1.04-1.66, P=0.018) and decreased frequencies of GAGATG (OR=0.47, 95% CI: 0.25-0.88, P=0.011) and AGAGCA (OR=0.15, 95% CI: 0.02-0.65, P=0.002) haplotypes when compared to healthy controls. Haplotypes of the ACE gene could be a genetic factor related to coronary artery disease in the Mexican individuals, but do not support its role as a risk factor for developing restenosis after coronary stenting.

Distribution of ABCB1, CYP3A5, CYP2C19, and P2RY12 gene polymorphisms in a Mexican Mestizos population.

The aim of the present study was to establish the gene frequency of six polymorphisms of the ABCB1, CYP3A5, CYP2C19, and P2RY12 genes in a population resident of Mexico City. The proteins encoded by these genes have been associated with the absorption, and biotransformation of clopidogrel. The ABCB1 T3435C, CYP3A5 V3 A6986G, P2RY12 G52T, P2RY12 C34T, CYP2C19 V2 and V3 (positions G681A and G636A, respectively), polymorphisms were analyzed by 5' exonuclease TaqMan genotyping assays in a group of 269 healthy unrelated Mexican Mestizo individuals. The CYP2C19 V3 G636A polymorphism was not detected in the Mexican Mestizos population. However, the studied population presented significant differences (P < 0.05) in the distribution of the T3435C, A6986G, G681A, G52T and C34T polymorphisms when compared to reported frequencies of Amerindian of South America, Caucasian, Asian, and African populations. In summary, the distribution of the ABCB1, CYP3A5, CYP2C19, and P2RY12 gene polymorphisms distinguishes to the Mexican Mestizos population from other ethnic groups.

The T29C polymorphism of the transforming growth factor-ß1 (TGF-ß1) gene is associated with genetic susceptibility to acute coronary syndrome in Mexican patients.

Inflammation plays an essential role in the development and progression of atherosclerotic lesions, and plaque disruption. The TGF-ß1 plays an important role in the anti-inflammatory process. The aim of the present study was to evaluate the role of TGF-ß1 gene polymorphisms as susceptibility markers for acute coronary syndrome (ACS). Two polymorphisms (TGF-ß -509T>C and TGF-ß T29C) of the TGF-ß gene were analyzed by 5' exonuclease TaqMan genotyping assays in a group of 426 patients with coronary acute syndrome and 551 healthy unrelated controls. A significant difference was observed in the distribution of TGF-ß T29C polymorphism between ACS patients and healthy controls (P<10(-3)). According to the co-dominant model, individuals with the TGF-ß 29 TT genotype have a 2.5-fold increased risk of developing ACS (P<10(-3)). Multiple logistic analysis showed that the largest risk factor for developing ACS was given by smoking habit, diabetes, hypertension, dyslipidemia, and the TGF-ß1 29 TT genotype. The analysis of linkage disequilibrium showed one haplotype (TT) with increased frequency and one haplotype (CC) with decreased frequency in ACS patients when compared to healthy controls. The results suggest that TGF-ß1 T29C gene polymorphism could be involved in the risk of developing ACS in Mexican individuals.

Lipoprotein(a) and homocysteine potentiate the risk of coronary artery disease in male subjects.

BACKGROUND: Lipoprotein (Lp(a)) and homocysteine (Hcy) are independent risk factors for coronary artery disease (CAD). Hcy promotes the release of free apo(a) from Lp(a). The high fibrin affinity of free apo(a) inhibits plasminogen binding and plasmin generation. Hyperhomocysteinemia can result from a less active variant of methylene tetrahydrofolate reductase (variant C677T). Because the C677T genotype is estimated to be present in 32.2% of the Mexican population, we took advantage of this prevalence to determine the possible potentiating effect between high plasma Lp(a) and Hcy for increasing the risk of CAD in male patients. METHODS AND RESULTS: First, 222 male patients admitted for coronary angiography were recruited and classified as CAD+ or CAD-. Anthropometric measurements, traditional risk factors, and plasma total Hcy (tHcy) and Lp(a) levels were recorded in both groups. We performed a conditional logistic regression model adjusted for conventional risk factors of CAD and it became clear that Lp(a) ≥30mg/dl was a risk factor for CAD (odds ratio [OR] 5.06, 95% confidence interval [CI] 1.88-13.51, P=0.001), whereas Hcy was not related to CAD (OR 0.44, 95% CI 0.63-2.90, P=0.44). However, when both factors were considered together in an interaction model, high tHcy and high Lp(a) plasma concentrations showed a potentiated effect (OR 10.52, 95% CI 2.18-50.71, P=0.003). CONCLUSIONS: The combination of high Lp(a) and Hcy levels synergistically increases the likelihood of developing CAD in male patients.

[Cell therapy for ischemic heart disease]. / La terapia celular en la cardiopatía isquémica.

Ischemic heart disease is the leading cause of death and heart failure worldwide. That is why it is important to develop new therapeutic modalities to decrease mortality and long-term complications in these patients. One of the main lines of research worldwide is myocardial regeneration, using progenitor cells in order to improve systolic and diastolic function in patients with ischemic heart disease, as well as to increase their survival. There have been carried out, with great enthusiasm worldwide, human and animal studies to define the usefulness of stem cells in the management of patients with ischemic heart disease. Today, regenerative therapy in ischemic heart disease is considered a novel therapeutic tool, with substantial theoretical benefits and few side effects. Here we present the scientific principles that support the use of this therapy, discuss the current clinical evidence available; and point out the controversial issues still not clarified on its use and usefulness in the short and long term.

The MHC2TA gene polymorphisms are not associated with restenosis after coronary stenting in Mexican patients.

OBJECTIVE: The aim of this study was to test for association between MHC2TA gene polymorphisms and risk for restenosis after coronary stent placement in a group of Mexican patients. METHODS: The MHC2TA-168A>G (rs3087456), 1614C>G (rs4774), and 2536G>A (rs2229320) single nucleotide polymorphisms were genotyped using 5' exonuclease TaqMan genotyping assays in a group of 202 patients, who underwent coronary artery stenting. Basal and procedure coronary angiography were analyzed, looking for angiographic predictors of restenosis and follow-up angiography was performed to screen for binary restenosis. RESULTS: The results obtained in this study showed that the frequency of the three polymorphisms studied was similar in patients with and without restenosis. Univariate analysis showed that the use of drug-eluting stent (DES) reduces the risk of developing restenosis (p<0.001, OR=0.26). In contrast, the diameter<2.5mm of the stent and bifurcations increased the risk of developing restenosis (p=0.049, OR=1.74 and p=0.041, OR=1.8). CONCLUSION: The present study suggests that the MHC2TA polymorphisms are not involved in the risk of developing restenosis after coronary stent placement.

CASP1 Gene Polymorphisms and BAT1-NFKBIL-LTA-CASP1 Gene-Gene Interactions Are Associated with Restenosis after Coronary Stenting.

In the present study, we evaluated the association of the BAT1, NFKBIL, LTA, and CASP1 single nucleotide polymorphisms and the gene−gene interactions with risk of developing restenosis after coronary stenting. The allele and genotype determination of the polymorphisms (BAT1 rs2239527 C/G, NFKBIL1 rs2071592 T/A, LTA rs1800683 G/A, CASP1 rs501192 A/G, and CASP1 rs580253 A/G) were performed by 5'exonuclease TaqMan assays in 219 patients: 66 patients with restenosis and 153 without restenosis. The distribution of rs2239527 C/G, rs2071592 T/A, and rs1800683 G/A polymorphisms was similar in patients with and without restenosis. Nonetheless, under recessive (OR = 2.73, pCRes = 0.031) and additive models (OR = 1.65, pCAdd = 0.039), the AA genotype of the rs501192 A/G polymorphism increased the restenosis risk. Under co-dominant, dominant, recessive, and additive models, the AA genotype of the rs580253 A/G was associated with a high restenosis risk (OR = 5.38, pCCo-Dom = 0.003; OR = 2.12, pCDom = 0.031; OR = 4.32, pCRes = 0.001; and OR = 2.16, 95%CI: 1.33−3.52, pCAdd = 0.001, respectively). In addition, we identified an interaction associated with restenosis susceptibility: BAT1-NFKBIL1-LTA-CASP1 (OR = 9.92, p < 0.001). In summary, our findings demonstrate that the rs501192 A/G and rs580253 A/G polymorphisms, as well as the gene−gene interactions between BAT1-NFKBIL1-LTA-CASP1, are associated with an increased restenosis risk after coronary stenting.

Alleles and haplotypes of the interleukin 10 gene polymorphisms are associated with risk of developing acute coronary syndrome in Mexican patients.

Inflammation plays an important role in the pathogenesis of atherosclerosis and acute coronary syndromes (ACS). Interleukin-10 (IL-10) is a potent anti-inflammatory cytokine that mediates the inflammatory process. The objective of the present study was to evaluate the role of IL-10 gene polymorphisms as susceptibility markers for ACS in Mexican patients. IL-10 promoter polymorphisms (positions -1082, -819, and -592) were analyzed by 5' exonuclease TaqMan genotyping assays in 389 ACS patients and 302 healthy controls. ACS patients showed increased frequencies of IL-10-592 C allele and CC genotype when compared to healthy controls (pC=0.0006, OR=1.48 and pC=0.022, OR=1.56, respectively), whereas the frequencies of the A allele and AA genotype were decreased in patients (pC=0.0006, OR=0.68 and pC=0.006, OR=0.57, respectively). When the distribution of IL-10-592 genotypes was analyzed separately in women and men (patients and healthy controls), a different distribution of alleles and genotypes was observed only in the group of men. In this case, increased frequency of C allele (pC=0.004, OR=1.46) and decreased frequencies of A allele (pC=0.004, OR=0.68) and AA genotype (pC=0.023, OR=0.56) were observed in the group of patients when compared to healthy controls. Multiple logistic analyses by gender showed that male individuals with IL-10-592CC+AC genotypes had 3.54-fold increased risk of developing ACS than individuals with AA genotype (p<0.001). The analysis of linkage disequilibrium showed one (ACC) increased haplotype in patients as compared to healthy controls. The results suggest that IL-10 gene polymorphisms could be involved in the risk of developing ACS in the Mexican population.

Histological and Mechanical Behavior of INC 01 and 02 Bare Metal Stents Against a Commercial Stent: A Preclinical Study in a Porcine Model.

BACKGROUND: PCI is an expensive procedure in our population and it implies a huge cost for the institutions and National Health Service. AIM OF THE STUDY: The main objective was to evaluate the technical and biological success of two stents designed in Mexico. METHODS: Ten York pigs, 4-6 months of age, underwent implantation of the bare metal INC-01 (10 stents) and INC-02 (6 stents) coronary stent in addition to a conventional commercial stent (10 stents). Technical success was evaluated immediately with angiography and Intravascular Ultrasound IVUS, continued by a mean follow-up of 4 month and a final angiographic, IVUS and histological evaluation. RESULTS: Initial technical success, angiography and IVUS between the three stents were not significant. One stent presented restenosis in follow-up (commercial stent), but all other stents presented excellent clinical outcome, satisfactory angiographic and IVUS results. Inflammation, proliferation and endothelialization between the stents had no major differences in histological analysis in a mean of 4 months follow-up. CONCLUSIONS: In this pig model, the INC 01 and INC 02 stents showed the same delivering technical success, angiographic and IVUS features, biological and histological response compared to commercial last generation stents.

Tumor necrosis factor alpha and interleukin 10 promoter polymorphisms in Mexican patients with restenosis after coronary stenting.

To test for an association with risk for restenosis after coronary stent placement, the TNF-alpha and IL-10 polymorphisms were analyzed by 5' exonuclease TaqMan assays in 162 patients who initially underwent coronary stenting. Analysis of basal and procedure coronary angiographies revealed a higher proportion of restenosis in lesions treated with bare metal stents compared with those treated with drug-eluting stents (P < 0.001). Distribution of TNF-alpha genotypes was similar in patients with and without restenosis. The IL-10 polymorphisms showed a moderate protective trend of the -819 TT genotype against restenosis when the lesions were analyzed (P = 0.071, OR = 0.471). Multivariate analysis confirmed a protective role for drug-eluting stents (P < 0.001, OR = 0.199) and the -819 TT genotype (P = 0.037, OR = 0.391). These results suggest the IL-10 -819 TT genotype has a protective role against in-stent restenosis.

The -44 C/G (rs1800972) polymorphism of the ß-defensin 1 is associated with increased risk of developing type 2 diabetes mellitus.

BACKGROUND: The aim of this study was to establish the association of two polymorphisms of the ß-defensin 1 gene (DEFB1, OMIM#602056) with the risk of developing type 2 diabetes mellitus (T2DM) in a group of Mexican patients. METHODS: The 5'UTR -20 G/A, and -44 C/G polymorphisms of DEFB1 gene were genotyped by 5' exonuclease TaqMan assays in a group of 252 patients with T2DM and 522 healthy control. RESULTS: Under dominant and additive models adjusted for the risk factors, the C allele of the -44 C/G polymorphism was associated with increased risk of T2DM (OR = 1.63, 95% CI = 1.07-2.48, pCdom  = 0.021 and OR = 1.42, 95% CI = 1.05-1.91, pCadd  = 0.023, respectively). In addition, the linkage disequilibrium analysis showed that AC haplotype was associated with an increased risk of developing T2DM (OR = 4.39, p = 0.04). The in-silico analysis showed that the -44 C allele produces a binding site for the transcription factor Ikaros (IK). CONCLUSION: This study demonstrates that the C allele of -44 C/G polymorphism, as well as haplotype AC are associated with the presence of T2DM in the Mexican population. The variation in this polymorphism of the DEFB1 gene could increase the migration of the macrophages to pancreatic islets accelerate the ß-cell dysfunction in T2DM.

The interleukin 1B-511 polymorphism is associated with the risk of developing restenosis after coronary stenting in Mexican patients.

Inflammation is the primary response to vessel wall injury caused by stent placement in coronary arteries. Cytokines of the interleukin-1 family are central regulators in immunoinflammatory mechanisms. The objective of this study was to test for association between IL-1 family gene polymorphisms and risk for restenosis after coronary stent placement. The IL-1B-511, IL-1F10.3, RN.4T>C, RN.6/1C>T, RN.6/2C>G, and IL-1RN VNTR polymorphisms were analyzed by 5' exonuclease TaqMan genotyping assays and polymerase chain reaction in a group of 165 patients who underwent coronary artery stenting. Basal and procedure coronary angiography were analyzed in search of angiographic predictors of restenosis and follow-up angiography was analyzed in search of binary restenosis. Patients with IL-1B-511 TT genotype had a 1.89-fold increased risk of developing restenosis. The analysis considering the lesions treated demonstrated that the lesions of patients with IL-1B-511 TT genotype had a 3.44-fold increased risk of developing restenosis. When the analysis considered the type of stent, the risk of developing restenosis was increased in lesions of patients with TT genotype (odds ratio = 4.50) who underwent coronary bare-metal stent implantation. Multiple logistic analysis identified IL-1B-511 TT genotype as an independent predictor for restenosis. The results suggest that IL-1B-511 polymorphism could be involved in the risk of developing restenosis after coronary stent placement.

No association found between the insertion/deletion of a 287-bp alu repeat sequence within intron 16 of the angiotensin-I-converting enzyme (ACE) gene in Mexican patients and binary restenosis after coronary stenting.

BACKGROUND: It has been suggested that the incidence of coronary restenosis after a percutaneous coronary intervention is much higher in patients with a 287-bp alu repeat sequence within intron 16 of the angiotensin-I-converting enzyme (ACE) gene (deletion allele) than in others, but published studies are conflicting. METHODS: The presence (insertion) or absence (deletion) of a 287-bp alu repeat sequence within intron 16 of the ACE gene (I/D polymorphism) was analyzed by polymerase chain reaction in a group of 168 patients with coronary artery disease who underwent coronary artery stenting. Basal and procedure coronary angiographies were analyzed searching for angiographic predictors of restenosis and follow-up angiography was analyzed looking for binary restenosis. RESULTS: Distribution of angiotensin converting enzyme I/D polymorphisms was similar in patients with and without restenosis. Similar results were observed when the analysis was made considering the type of stent implanted. On the other hand, the whole group of coronary artery disease patients showed increased frequencies of the D allele (p=0.00001, OR=2.17, 95% CI=1.49-3.16) and ID genotype (p=0.0002, OR=2.58, 95%CI=1.49-4.47) when compared to healthy controls. CONCLUSIONS: Genetic variations of the ACE gene could be a genetic factor related to coronary artery disease in the Mexican mixed racial ancestry individuals, but do not support its role as a risk factor for developing restenosis after coronary stenting.

CETP and LCAT Gene Polymorphisms Are Associated with High-Density Lipoprotein Subclasses and Acute Coronary Syndrome.

We evaluated whether CETP and LCAT gene polymorphisms are statistically associated with the high-density lipoprotein (HDL) size distribution, the cholesterol level of HDL subclasses, and the acute coronary syndrome (ACS) susceptibility. Two CETP gene polymorphisms (rs4783961 and rs708272) and one LCAT polymorphism (rs2292318) were genotyped by 5' exonuclease TaqMan assays in 619 patients with ACS and 607 control individuals. For HDL analysis, a subgroup of 100 healthy individuals was recruited; the HDL subclasses were separated via ultracentrifugation and polyacrylamide gradient gel electrophoresis under native conditions. Under a dominant model, the G allele of the rs708272 polymorphism was associated with an increased risk of ACS (odds ratios [OR] = 1.45, corrected p-value [pCDom ] = 0.036). The linkage disequilibrium analysis showed that one of the eight possible combinations was associated with the risk of developing ACS (OR = 1.52, pC = 0.02), which suggests that it may contribute to coronary atherosclerosis. The rs708272 G allele carriers had a lower concentration of cholesterol associated with the HDL2a and HDL3a subclasses when compared with subjects carrying the A allele. Carriers of LCAT rs2292318 A allele showed a lower concentration of high-density lipoprotein-cholesterol (HDL-C) in comparison to the GG genotype; the cholesterol associated with the each one of the five HDL subclasses was significantly lower in rs2292318 A than in GG subjects. In summary, this study demonstrates that the rs708272 polymorphism is associated with a heightened risk of developing ACS. In addition, we report the association of the rs708272 and rs2292318 polymorphisms with HDL-C levels and HDL subclasses.

Predictors of mortality and adverse outcome in elderly high-risk patients undergoing percutaneous coronary intervention.

OBJECTIVES: We sought to identify predictors of in-hospital and long-term (> 1 year) mortality and major adverse cardiac events (MACE) in elderly patients referred for percutaneous coronary intervention (PCI). METHODS: Seventy-three patients (> or = 80 years) were included. Clinical and interventional characteristics were collected retrospectively. Primary end points were in-hospital and long-term mortality, and a composite of non-fatal myocardial infarction, target vessel revascularization, urgent coronary artery bypass graft surgery, and death (MACE). RESULTS: Eighty-three percent of the patients had acute coronary syndromes, 43% three-vessel disease, and 42% heart failure. In-hospital mortality and MACE were 16.4% and 19%, respectively. Long-term mortality and MACE were 11.3% and 16.4%, respectively. Univariate characteristics associated with in-hospital mortality and MACE were: Killip Class III-IV, heart failure, cardiogenic shock, TIMI 0-2 flow prior and after intervention, diabetes mellitus, contrast nephropathy, and presence of A-V block or atrial fibrillation (AF). Long term predictors for mortality were the presence of heart failure, cardiogenic shock, diabetes mellitus, TIMI flow 0-2 before and after intervention, and A-V block or AF. CONCLUSION: The identification of the factors previously mentioned may help to predict complications in elderly patients.

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.