Marco Antonio Martínez-Ríos

Acute right ventricular infarction: clinical spectrum, results of reperfusion therapy and short-term prognosis

BackgroundThe role of thrombolytic therapy (TT) and percutaneous coronary interventions (PCIs) in subgroups of patients with right ventricular infarction (RVI) has not been evaluated. Methods and ResultsWe risk-stratified 302 patients with RVI into three subsets upon admission. Class A (n =197) comprised patients without right ventricular (RV) failure, Class B (n =69) with RV failure and Class C (n =36) with cardiogenic shock. All eligible patients in Class A or B received either PCI or TT. Patients in Class C eligible for reperfusion were treated with PCI. All patients were evaluated for in-hospital major adverse cardiac events and short-term mortality. There was a statistically significant difference in in-hospital mortality among the classes. Classes B and C were the strongest indicators of in-hospital mortality. By multivariate analysis TT or PCI did not reduce mortality in Classes A and B, but a clinically favorable trend in mortality reduction was documented: both methods decreased RV dysfunction in Class B (from 97% to 61% with TT and to 28% with PCI;P  < 0.001) and PCI reduced the risk of mortality in Class C (89.5% compared with 58%;P  < 0.05). ConclusionsClassification into types A, B or C allows the prediction of mortality. The use of TT or PCI suggests a clinical favorable trend in the reduction of mortality in Class A, either is beneficial in Class B for decreasing morbidity and PCI appears to be the most appropriate procedure for Class C since it reduced mortality.

C3435T polymorphism of the ABCB1 gene is associated with poor clopidogrel responsiveness in a Mexican population undergoing percutaneous coronary intervention

BACKGROUND Clopidogrel is a pro-drug and its intestinal absorption is limited by the P-glycoprotein encoded by the ABCB1 gene. It is metabolized hepatically by cytochrome P450 enzymes encoded by CYP genes to produce an active metabolite that antagonizes the P2Y12 platelet receptor. Some patients exhibit poor clopidogrel responsiveness due to polymorphisms, resulting in thrombotic events. The aim of this study was to determine the relationship between poor clopidogrel responsiveness and the ABCB1, CYP and P2RY12 gene polymorphisms among patients undergoing percutaneous coronary intervention (PCI). METHODS AND RESULTS Two hundred seventy-six patients who underwent PCI were included in this study. Clopidogrel responsiveness was determined via optical aggregometry in platelet-rich plasma using 10 μM ADP. Patients exhibiting a platelet aggregation response higher than 70% were classified as poor responders. The genetic polymorphisms were analyzed via real-time PCR. Poor responsiveness to clopidogrel was noted in 22.1% of the patients. The TT genotype of the C3435T polymorphism of the ABCB1 gene and omeprazole usage were each associated with poor clopidogrel responsiveness (Exp (β) 2.73, p=0.009 and Exp (β) 3.86, p=0.04, respectively). CONCLUSION Poor clopidogrel responsiveness is associated with the TT genotype of the C3435T polymorphism of the ABCB1 gene.

Apo(a) phenotyping and long-term prognosis for coronary artery disease

OBJECTIVES Identify whether the plasma concentration of Lp(a), apo(a) size or a greater affinity for fibrin predict the likelihood of cardiac death, non-fatal myocardial infarction, unstable angina, the need for additional revascularization, and stroke (MACCE). DESIGN AND METHODS We analyzed the clinical prognosis of 68 patients with coronary artery disease included in a case-controlled study which evaluated Lp(a) concentration, apo(a) size, and Lp(a) fibrin-binding. Cohort was conducted over a median of 8 years. We used Kaplan-Meier survival tables to evaluate cardiovascular and cerebrovascular events in the follow-up period. RESULTS Apo(a) isoforms of small size are predictors of MACCE. We find an association between Lp(a) concentration and apo(a) fibrin-binding with major adverse cardiovascular and cerebrovascular events, although without statistically significant results. CONCLUSIONS Small-sized apo(a) isoforms are an independent risk factor for MACCE in patients with coronary artery disease in follow-up. Lp(a) plasma concentration and apo(a) fibrin-binding were associated, although not significant.

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.

Association between Stable Coronary Artery Disease and In Vivo Thrombin Generation

Background. Thrombin has been implicated as a key molecule in atherosclerotic progression. Clinical evidence shows that thrombin generation is enhanced in atherosclerosis, but its role as a risk factor for coronary atherosclerotic burden has not been proven in coronary artery disease (CAD) stable patients. Objectives. To evaluate the association between TAT levels and homocysteine levels and the presence of coronary artery disease diagnosed by coronary angiography in patients with stable CAD. Methods and Results. We included 95 stable patients admitted to the Haemodynamics Department, including 63 patients with significant CAD and 32 patients without. We measured the thrombin-antithrombin complex (TAT) and homocysteine concentrations in all the patients. The CAD patients exhibited higher concentrations of TAT (40.76 μg/L versus 20.81 μg/L, p = 0.002) and homocysteine (11.36 μmol/L versus 8.81 μmol/L, p < 0.01) compared to the patients without significant CAD. Specifically, in patients with CAD+ the level of TAT level was associated with the severity of CAD being 36.17 ± 24.48 μg/L in the patients with bivascular obstruction and 42.77 ± 31.81 μg/L in trivascular coronary obstruction, p = 0.002. Conclusions. The level of in vivo thrombin generation, quantified as TAT complexes, is associated with the presence and severity of CAD assessed by coronary angiography in stable CAD patients.

Association of the suppressor of cytokine signaling 1 (SOCS1) gene polymorphisms with acute coronary syndrome in Mexican patients

Recent studies provide evidence on the emerging role of the SOCS1 gene in the development and progression of atherosclerotic lesions. This gene encodes for the suppressor of the cytokine signaling-1 protein that interacts directly with the Janus kinases that are essential intracellular mediators of the immune cytokine action. The aim of this study was to test for associations between SOCS1 gene single nucleotide polymorphisms (SNPs) and the risk of developing acute coronary syndromes (ACS) in a group of Mexicans patients. Four SNPs [-3969 C>T (rs243327), -1656 G>A (rs243330), -820 G>T (rs33977706) and +1125 G>C (rs33932899)] of SOCS1 gene were determined for TaqMan genotyping assays in a group of 447 patients with ACS and 622 healthy controls. Under heterozygous model, the -3969 C>T (rs243327) SNP was associated with increased risk of ACS (OR=1.45, P(Het)=0.021). On the other hand, under co-dominant and heterozygous models, the -1656 G/A (rs243330) SNP was associated with increased risk of ACS (OR=1.47, P(Co-dom)=0.038 and OR=1.50, P(Het)=0.013, respectively). Moreover, under co-dominant, dominant, and heterozygous models, the -820T/G (rs33977706) SNP was associated with increased risk of ACS (OR=1.59, P(Co-dom)=0.03, OR=1.48, P(Dom)=0.028 and OR=1.61, P(Het)=0.01). Finally, under co-dominant and heterozygous models, the +1125 G/C (rs33932899) SNP was associated with increased risk of ACS (OR=1.54, P(Co-dom)=0.006, OR=1.58, P(Het)=0.012, respectively). Models were adjusted for gender, age, body index mass, dyslipidemia, alcohol consumption, and smoking. In summary, our data suggests that the four studied polymorphisms of the SOCS1 gene play an important role as susceptibility markers for developing ACS.

Primary angioplasty limited to the culprit vessel in patients with multivessel disease: Impact on clinical outcomes

adverse events in patients with STEMI: meta-analysis of randomised controlled trials. Heart Feb 2012;98(4):303–11. [6] Vorobcsuk A, Konyi A, Aradi D, et al. Transradial versus transfemoral percutaneous coronary intervention in acute myocardial infarction systematic overview and metaanalysis. Am Heart J Nov 2009;158(5):814–21. [7] Lunn DJ, Thomas A, Best N, Spiegelhalter D. WinBUGS — a Bayesian modelling framework: concepts, structure, and extensibility. Stat Comput 2000;10:325–37. [8] Higgins Julian PT, Green Sally. Cochrane Handbook for Systematic Reviews of Interventions. Wiley-Blackwell ed. 2009.

Aortic mineralisation in children with congenital cardiac disease

BACKGROUND Congenital cardiac diseases are the most frequent congenital malformations. In adult patients, the mineralisation of the aorta due to cardiovascular disease is very common, but vascular mineralisation in paediatric cardiopathies is a topic less studied. This study shows that children with a complex congenital cardiopathy show a high degree of vascular mineralisation in the ascending aorta. This can be part of the cardiac failure pathophysiology due to congenital cardiopathies. OBJECTIVE The aim of this study was to determine the presence and degree of vascular mineralisation in samples of the ascending and descending aorta of children with complex congenital cardiopathies. DESIGN We conducted a cross-sectional study. SUBJECTS We obtained 34 vascular tissues from the autopsies of 17 children with congenital cardiac disease. METHODS We used a scanning electron microscope with an energy-dispersive X-ray spectroscopy in order to analyse the vascular tissues. RESULTS The amount of minerals was two times higher in the ascending aorta than in the descending aorta of children with congenital cardiac disease. CONCLUSIONS The study provides evidence that vascular mineralisation can start at an early age, and that it is higher in the ascending aorta than in the descending aorta.

Reperfusion therapy of myocardial infarction in Mexico: A challenge for modern cardiology

Mexico has been positioned as the country with the highest mortality attributed to myocardial infarction among the members of the Organization for Economic Cooperation and Development. This rate responds to multiple factors, including a low rate of reperfusion therapy and the absence of a coordinated system of care. Primary angioplasty is the reperfusion method recommended by the guidelines, but requires multiple conditions that are not reached at all times. Early pharmacological reperfusion of the culprit coronary artery and early coronary angiography (pharmacoinvasive strategy) can be the solution to the logistical problem that primary angioplasty rises. Several studies have demonstrated pharmacoinvasive strategy as effective and safe as primary angioplasty ST-elevation myocardial infarction, which is postulated as the choice to follow in communities where access to PPCI is limited. The Mexico City Government together with the National Institute of Cardiology have developed a pharmaco-invasive reperfusion treatment program to ensure effective and timely reperfusion in STEMI. The model comprises a network of care at all three levels of health, including a system for early pharmacological reperfusion in primary care centers, a digital telemedicine system, an inter-hospital transport network to ensure primary angioplasty or early percutaneous coronary intervention after fibrinolysis and a training program with certification of the health care personal. This program intends to reduce morbidity and mortality associated with myocardial infarction.

Persistent pulmonary hypertension and right ventricular function after percutaneous mechanical thrombectomy in severe acute pulmonary embolism

Acute pulmonary embolism is one of the main causes of death, morbidity and hospitalisation [1, 2]. The most common cause of early death in these patients is right ventricular failure [1–3]. Complete resolution of the pulmonary thrombus at 6 months of evolution is not achieved in 57% of patients, with persistent right ventricular dysfunction (RVD) in 6–8% of patients and persistent pulmonary arterial hypertension (PAH) in 7–13.5% of patients who received treatment with heparin or fibrinolytic agents [4–8]. Percutaneous mechanical thrombectomy (PMT) is accepted as a treatment in patients with high-risk acute pulmonary embolism with contraindications to systemic thrombolysis or when the treatment has failed [1, 2, 9]. Percutaneous mechanical thrombectomy in acute PE restores right ventricle function in most patients at 40 months http://ow.ly/lhTh304sqeY