The role of the TERC-63G>A and TERT-1327C>T telomerase polymorphisms in the study of men with acute coronary syndrome.

AIM: Telomerase is a ribonucleoprotein that maintains telomere length. Telomeres and telomerase are involved in cellular ageing and have been connected to some ageing related diseases, like cardiovascular disease. Telomerase dysfunction could be the main underlying mechanism in this connection but this point is still unclear. The aim of this article is to investigate the possible influence of cellular ageing, measured by two telomerase polymorphisms, TERC-63G>A (rs2293607) and TERT-1327C>T (rs2735940), on the whole spectrum of acute coronary artery disease (CAD). METHODS: We studied 150 middle aged men admitted for an acute coronary syndrome (ACS). Cardiovascular risk factors prevalence was collected at admission. Severity variables analyzed were Killip class and number of vessels affected. Telomerase polymorphisms were studied by real time PCR in DNA samples extracted from peripheral blood leukocytes. Clinical follow-up had been developed for more than 600 days and a prognostic combined event was defined. RESULTS: C allele of TERT polymorphism was more prevalent among hypertensive patients (OR: 3.19; 95% CI: 1.37-7.42; P=0.006). None of polymorphisms showed any prognostic value or relation to CAD severity. CONCLUSION: Telomerase dysfunction could be involved in hypertension prevalence. This finding could support new screening strategies in high risk population. The two telomerase polymorphisms analyzed did not show any prognostic value or connection to CAD severity. However, further studies are required to determine the molecular mechanisms responsible for cellular ageing in ACS.

Hyperhomocysteinemia is a risk factor of recurrent coronary event in young patients irrespective to the MTHFR C677T polymorphism.

Despite the well-known pro-coagulant effect of hyperhomocysteinemia, data is limited regarding the result on recurrent coronary event (RCE) in young people. One hundred and forty patients <55 years old with a first acute coronary syndrome (ACS) were prospectively followed for a mean (+/-S.D.) follow-up of 49+/-14 months in order to investigate the relationship between homocysteine levels (tHcy) at admission and the incidence of RCE. The tHcy values were divided into quartiles to examine their relationship with end points. Furthermore, we determined the effect of C677T methylene tetrahydrofolate reductase (MTHFR) polymorphism, as well as other risk factors for developing a RCE. The median plasma homocysteine concentration was 9.6 mumol/L (interquartile range, 3.7). In the screening of MTHFR C677T polymorphism in patients with ACS, the T allele frequency was 0.4 and the genotype frequency distributions were in Hardy-Weinberg equilibrium. At time of final evaluation, 49 (35%) of the 140 valuable patients had developed a RCE. Increasing numbers of RCE were observed for increasing quartiles of tHcy according to Kaplan-Meier survival (Log-rank test=0.0092). The MTHFR C677T polymorphism was not associated with an increased incidence of RCE. In multivariate analysis, the variables independently associated with a higher risk of RCE were age older than 45 years [HR=2.7; (95% CI, 1.3-6.1); p=0.030], body mass index more than 25 [HR=2.6; (95% CI, 1.1-5.9); p=0.034] and tHcy levels into quartile 4 (tHcy>12.37 mumol/L) [HR=2.5; (95% CI, 1.1-4.7); p=0.04]. Elevated plasma homocysteine level at admission is an independent risk factor for RCE after the first episode of ACS in young patients irrespective of the status of MTHFR C677T.

[Mitral prosthesis thrombosis treated by fibrinolysis with accelerated administration of r-TPA]. / Trombosis protésica mitral tratada mediante fibrinólisis con dosis acelerada de r-TPA.

We report the case of a 53-year-old patient with a mitral prosthesis hospitalized for heart failure. Diagnosis of mitral prosthetic thrombosis, led to a therapeutic disjunction between thrombolysis and surgery. Because of the high risk of surgical intervention, the patient was treated with r-TPA (accelerated infusion), showing immediate, successful response.

Tratamiento de la angina de pecho / Treatment of angor pectoris

La angina de pecho es la forma más común de manifestarse la cardiopatía isquémica. El paciente que presenta dolor anginoso es afortunado porque dentro del amplio abanico de manifestaciones de la cardiopatía isquémica, cualquiera de las otras como infarto de miocardio, muerte súbita, insuficiencia cardíaca y arritmias ventriculares, son más graves y porque, además, la presencia del dolor torácico permite poner en marcha todo el sistema diagnósticoterapéutico que redundará finalmente en una reducción del infarto de miocardio y la muerte. El tratamiento de la angina de pecho, tanto en su forma crónica y estable como en la forma aguda e inestable, tiene como objetivos inmediatos controlar el síntoma y prevenir la muerte y el infarto agudo, y como objetivos a medio y largo plazo el control de la enfermedad aterosclerótica coronaria. El plan terapéutico siempre deberá diseñarse según el perfil de riesgo de cada paciente.La angina inestable frecuentemente se estabiliza con tratamiento médico, pero puede presentar inicialmente predictores de mal pronóstico o en la fase pre-alta hospitalaria una prueba de isquemia moderada o severamente positiva, que determinarán una actitud agresiva con angiografía coronaria y eventualmente revascularización. En la angina crónica, el tratamiento médico, que se dirige a controlar síntomas pero también a prevenir infarto y muerte, debe también configurarse atendiendo a tres variables de significación pronóstica, grado de isquemia, estado de la función ventricular y extensión angiográfica de la enfermedad coronaria. Según el perfil pronóstico de cada paciente se decidirá el tipo de tratamiento definitivo. Los casos con mayor riesgo se beneficiarán de un tratamiento revascularizador y la técnica a proponer se establecerá en función de la localización y extensión de las lesiones anatómicas, la severidad de la i quemia y el grado de disfunción ventricular. (AU)