A randomized controlled trial of lung ultrasound-guided therapy in heart failure (CLUSTER-HF study).

BACKGROUND: Lung ultrasound (LUS) has emerged as a new tool for the evaluation of congestion in heart failure (HF); incorporation of LUS during follow-up may detect congestion earlier and prompt interventions to prevent hospitalizations. The aim of this study was to test the hypothesis that the incorporation of LUS during follow-up of patients with HF may reduce the rate of adverse events compared with usual care. METHODS: In this single-blinded, randomized controlled trial, patients were randomized into an LUS-guided arm or control arm. Patients were followed in 4 prespecified visits during a 6-month period. LUS was performed in every patient visit in both groups; however, LUS results were available for the treating physician only in the LUS group. The primary outcome was the composite of urgent HF visits, rehospitalization for worsening HF, and death from any cause. RESULTS: One hundred twenty-six patients were randomized to either LUS (n = 63) or control (n = 63) (age 62.5 ±â€¯10 years, median left ventricular ejection fraction 31%). The primary end point occurred in 30 (47.6%) patients in the control group and 20 (31.7%) patients in the LUS group (P = .041). LUS-guided treatment was associated with a 45% risk reduction in the primary end point (hazard ratio 0.55, 95% CI 0.31-0.98, P = .044), mainly driven by a reduction in urgent HF visits (hazard ratio 0.28, 95% CI 0.13-0.62, P = .001). No significant differences in rehospitalizations for HF or death were found. CONCLUSIONS: Incorporation of LUS into clinical follow-up of patients with HF significantly reduced the risk of urgent visits for worsening HF.

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.

Echocardiographic correlates of severe pulmonary hypertension in adult patients with ostium secundum atrial septal defect.

OBJECTIVE: To identify echocardiographic factors that correlate with pulmonary hypertension (PH) in adults with ostium secundum atrial septal defect (ASD). METHODS: Between November 2009 and November 2013, 92 adults with ASD were studied. All had clinical history and transthoracic echocardiogram. RESULTS: Thirty-nine percent of patients had severe PH defined as systolic pulmonary artery pressure (sPAP) of 70 mm Hg or more. The size of ASD (31.84±8.21 mm) and a right-sided tricuspid inflow E-wave to tissue Doppler e'-wave ratio >6.2 correlated with severe PH with AUC of 0.704 (CI 95%=0.59 to 0.818, P<.001) and 0.65 (CI 95%=0.531 to 0.773, P<.014), respectively. Multivariate logistic regression showed that sPAP >70 mm Hg was the variable that most precisely correlated with right ventricular (RV) dysfunction as evidenced by TAPSE <17 mm and RV fractional shortening area (RVFSA) <35%. Left ventricular (LV) diastolic function was also significantly reduced in the group with severe PH with mitral inflow E/A ratio of 0.73±0.23 vs 1.13±0.42 in the group without severe PH (sPAP <70 mm Hg, (P=.001). The pulmonary (Qp) to systemic (Qs) cardiac output ratio (3.09±1.12) and right-sided tissue Doppler S <9.5 cm/s most accurately predicted a Tei index >0.55. CONCLUSIONS: Larger size of ASD using the QP/QS ratio and increased right-sided tricuspid E/e' ratio correlated with severe PH with a sPAP of 70 mm Hg or more. Patients with severe PH had more severe RV dysfunction as evaluated by TAPSE and RVFSA in comparison to those with PH <70 mm Hg. LV diastolic function was also reduced in the severe PH group.

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.

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 DEFB1 gene rs11362 A/G genetic variant is associated with risk of developing CAD: a case-control study.

BACKGROUND: In the present study, we evaluated whether DEFB1 gene polymorphisms are associated with the presence of coronary artery disease (CAD). METHODS: Two rs11362 A/G, and rs1800972 C/G gene polymorphisms of DEFB1 gene were genotyped by 5'exonuclease TaqMan assays in 219 patients with CAD and 522 control individuals. RESULTS: The distribution of rs1800972 C/G polymorphisms was similar in patients with CAD and healthy controls. Nonetheless, under the co-dominant, dominant, recessive, and additive models, the AA genotype of the rs11362 A/G polymorphism was associated with the risk of developing CAD (OR = 1.89 pCCo-Dom = 0.041, OR = 1.46, pCDom = 0.034, OR = 1.69, pCRes = 0.039, and OR = 1.37, pCAdd = 0.012, respectively). In addition, the linkage disequilibrium showed that the 'AG' haplotype was associated with an increased risk of developing CAD (OR = 1.23, p = 0.042). According, with the Genotype-Tissue Expression (GTEx) consortium data, the rs11362 AA genotype is associated with a low mRNA expression of the ß-defensin-1 in tissues, such as artery aorta, artery coronary, heart left ventricle, and heart atrial appendage (p < 0.001). CONCLUSION: This study demonstrates that rs11362 A/G polymorphism of the DEFB1 gene is involved in the risk of developing CAD, and with a low RNA expression of the ß-defensin-1 in heart tissue.

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.

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.

Dual Antiplatelet Therapy Versus Antiplatelet Monotherapy Plus Oral Anticoagulation in Patients with Acute Coronary Syndrome and Coronary Artery Ectasia: Design and Rationale of OVER-TIME Randomized Clinical Trial.

INTRODUCTION: The optimal anti-thrombotic therapy to prevent recurrent ischemic events in patients with acute coronary syndrome and coronary artery ectasia (CAE) remains unclear. AIM: To assess the efficacy and safety of antiplatelet plus anticoagulant therapy versus dual antiplatelet therapy in patients with acute coronary syndromes and coronary artery ectasia. METHODS: OVER-TIME is an investigator initiated, exploratory, open label, single center, randomized clinical trial comparing dual antiplatelet therapy (acetyl-salicylic acid plus a P2Y12 inhibitor) with the combination of an antiplatelet monotherapy (a P2Y12 inhibitor) plus a low dose anticoagulant (rivaroxaban, 15mg oral dose) for the prevention of recurrent ischemic events among patients with CAE. We aim to enroll approximately 60 patients with CAE and acute coronary syndromes. After recruitment, patients are randomized to (a) standard of care (dual antiplatelet regimen) or (b) the combination of antiplatelet monotherapy and low dose anticoagulant. Patients will be followed for at least 12 months. The OVER-TIME study aims to assess the efficacy of the regimen in prevention of major cardiovascular events and its security in bleeding events in acute coronary syndromes among patients with CAE. Expected results and conclusions: OVER-TIME is the first randomized controlled trial to assess different antithrombotic strategies in patients with CAE and acute coronary syndrome, and its results will offer preliminary data for the prevention of major cardiovascular events and bleeding events in this group of patients. TRIAL REGISTRATION NUMBER: NCT05233124 (ClinicalTrials.gov), date of registration: February 10, 2022.

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.

Subepicardial aneurysm: echocardiographic evaluation and evolution.

Subepicardial aneurysms (SEA) are an infrequent and serious form of subacute cardiac rupture complicating myocardial infarction. An early diagnosis and surgical repair may be life saving. SEA comprise an abrupt interruption of the myocardium, with a narrow neck and thin wall containing only the epicardium. It may progress to fatal cardiorrhexis. We describe the echocardiographic evolution of this type of cardiac rupture and the contribution of contrast-enhanced echocardiography. A possible pathophysiological mechanism is proposed.

Dissecting intramyocardial hematoma: clinical presentation, pathophysiology, outcomes and delineation by echocardiography.

BACKGROUND: In large necropsy studies dissecting intramyocardial hematoma (DIH) with serpiginous tracts across the myocardial fibers has been reported in both the septum and the left ventricle free wall. METHODS: We studied 15 patients admitted to the hospital with acute myocardial infarction (AMI) in which DIH was demonstrated by either transthoracic and/or transesophageal and confirmed intraoperatively or by necropsy. RESULTS: In nine patients the hemorrhagic dissection was predominantly in the septum and in the remaining it was in the free wall of the left ventricle (LV). Myocardial infarction involved the left ventricular inferior wall in two, and the anterior wall in 13 patients. The overall mortality was 47%, and in the group with septal hematoma it reached to 78%. Echocardiography disclosed the various acoustic densities of the evolving intramyocardial hematoma, its extension through the hemorrhagic dissection, its spontaneous reabsorption, as well as its communication with the ventricular cavities. CONCLUSIONS: Echocardiography is the method of choice for the noninvasive diagnosis of patients with suspected myocardial rupture and intramyocardial dissection postmyocardial infarction.

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.