Biomedical subjects
Publications and source records attributed to Javier Pineda.
Single coronary artery is an extremely rare congenital anomaly with a very low incidence in the general population. We present a 65-year-old woman with atypical chest pain and a single left coronary artery discovered in the cath lab. No coronary lesions were found. Such anomaly has been previously described before only in twelve patients.
Coronary artery spasm is usually defined as a focal constriction of a coronary artery segment, reversible, and causing myocardial ischaemia by coronary blood flow restriction. Sometimes this condition is not focal and can compromise all the coronary tree. This is a very rarely described event. Generally, coronary vasospasm may occur spontaneously or induced, either physically by catheter, physiological manoeuvres (hyperventilation), or by pharmacological agents. It may also occur with or without underlying atheromatous coronary disease. The mechanism of coronary spasm remains unclear but endothelial dysfunction seems to be the main triggering factor in all causes.
Factor XII (FXII) plays a key role in both coagulation and fibrinolysis, thus its role in thrombotic processes is uncertain. Both genetic and environmental factors determine FXII plasma levels. A common C46T polymorphism in the Kozak region of F12 gene disturbs the translation of the protein leading to a significant reduction of FXII levels although its clinical significance is conflictive. We studied the F12 C46T polymorphism in 281 patients who had suffered from an acute myocardial infarction (MI) before 45-year-old and 550 control subjects from the same area. Serum levels of cholesterol, HDL, LDL, triglycerides and C reactive protein (CRP) were assayed in the MI group. The 46T allele slightly increased the risk to suffer from premature MI (OR: 1.64; 95% CI: 1.14-2.37; p = 0.008). Moreover, patients carrying the 46T allele showed increased levels of CRP (p = 0.002). Interestingly, we found that the simultaneous presence of the 46T allele and hypercholesterolemia increases the risk to develop premature MI 2.26 times. The F12 C46T polymorphism, associated with a reduction of plasma FXII levels, seems to play a deleterious effect, predisposing the development of premature MI, especially in hypercholesterolemic patients. This effect could be associated with an increased pro-inflammatory state, as the 46T allele associates with high levels of CRP.
We studied 5 functional hemostatic polymorphisms in 281 patients with premature myocardial infarction and in 530 control subjects. The role of these polymorphisms when analyzed independently is small, if any. However, the simultaneous combination of factor XIII and prothrombin polymorphisms exacerbated the risk. (OR=12.12; p=0.028). Moreover, combinations of factor V Leiden with prothrombin, and factor XII with prothrombin polymorphisms were only identified in patients. Our results support the relevance of gene-gene interactions in myocardial infarction.
BACKGROUND: Atherosclerosis is an inflammatory disease resulting from an injury that leads to an increase in the adhesiveness and permeability of the endothelium to leukocytes or platelets. The selectin family plays a key role initiating the cascade of events. Recently, we have demonstrated the functional relevance of a variable number of tandem repeats polymorphism affecting the P-selectin glycoprotein ligand (PSGL-1). Neutrophils carrying short alleles exhibit a significantly lower capacity to bind activated platelets. These alleles consistently protect against transient ischemic attack. We sought to evaluate the role of this polymorphism in premature myocardial infarction because genetic risk factors have more relevance in the development of disease in young patients. METHODS: We genotyped 219 Caucasian patients who had suffered a premature myocardial infarction (MI) (aged < or =45 years) and 594 control subjects from our Mediterranean area. The role of the PSGL-1 polymorphism was also evaluated according to the additional risk factors of age, sex, smoking history, hypertension, hypercholesterolemia, and diabetes. RESULTS: The frequency of the short alleles (B and C) was significantly lower in patients than in controls (P =.012, odds ratio 0.62; 95% CI 0.42-0.92). Multiple regression analysis revealed that B and C alleles had an independent protective effect on the development of premature MI (P =.034, odds ratio 0.62 95%CI: 0.40-0.96). CONCLUSIONS: We found an interesting association between a functional polymorphism and the risk of MI at a younger age. According to our results, the short B and C PSGL-1 alleles might protect against premature MI, probably because of their lesser adhesive capacity.
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INTRODUCTION AND OBJECTIVES: Annexin V has an anticoagulant effect in vitro that derives from its ability to displace coagulation proteins from phospholipid surfaces, prolonging phospholipid-dependent coagulation reactions. Antiphospholipid antibodies (APL) and annexin V have an affinity for anionic phospholipids, so it has been hypothesized that one of the thrombotic mechanisms of APL may be due to displacement of annexin V from phospholipid surfaces. We studied plasma annexin V levels and analyzed its relationship to risk factors and several blood markers. PATIENTS AND METHOD: We studied 62 patients < 45 years old who had suffered myocardial infarction. The control group comprised 23 healthy subjects of similar age and sex. We analyzed the presence of APL, anti-beta2 glycoprotein I (beta2-GPI), anti-beta2-GPI/phospholipid complexes and anti-annexin V antibodies. We determined plasma annexin V levels. Cholesterol, HDL-cholesterol, triglycerides, antigenic tissue plasminogen activator and its inhibitor, von Willebrand factor, and fibrinogen levels were measured. RESULTS: We detected only 2 patients with positive anti-beta2-GPI/phospholipid complexes and 2 patients with positive anti-annexin V antibodies. We did not detect any positive APL or anti-beta2-GPI antibodies. In the control group there was only 1 patient with positive APL and anti-beta2-GPI antibodies. The myocardial infarction group showed significantly lower levels of annexin V than the control group: 0.640 ng/ml (0.520-0.818 ng/ml) vs 1.570 ng/ml (1.140-2.390 ng/ml), p < 0.01. There were no statistical associations between annexin V levels and other variables. CONCLUSIONS: The low levels of annexin V in young myocardial infarction patients could indicate a procoagulant trend. This hypercoagulable state was unrelated to the presence of APL.