Marcelo Sanmartín

[Influence of shear stress on in-stent restenosis: in vivo study using 3D reconstruction and computational fluid dynamics].

INTRODUCTION AND OBJECTIVES Local factors may influence neointimal proliferation following conventional stent implantation. In this study, the relationship between wall shear stress and luminal loss after coronary stenting was assessed using a combination of angiography, intravascular ultrasound, and computational fluid dynamics. PATIENTS AND METHOD Seven patients with de novo right coronary lesions treated with conventional (i.e., bare metal) stents were included. Realistic three-dimensional geometric reconstructions were generated offline from angiographic and intravascular ultrasound data both immediately after stenting and at 6-month follow-up. A finite-volume model was used to calculate local wall shear stress within the stent and 4 mm proximally and distally to the stent. The mean coronary ostium entry flow velocity was assumed to be 25 cm/s in all cases. RESULTS The mean neointimal thickness was 0.29 (0.21) mm. In five cases, weak negative correlations between wall shear stress and neointimal thickness were found: maximum r value = -0.34, minimum r value = -0.11 (P < .001). The neointimal thickness in segments in which the level of wall shear stress was in the lowest quartile was greater than that in segments in which it was in highest quartile, at 0.34 (0.21) mm and 0.27 (0.24) mm (P < .001) for quartiles 1 and 4, respectively. CONCLUSIONS Low wall shear stress after stenting favors neointimal proliferation both within the stent and at the stents edges.

Incidence, angiographic features and outcomes of patients presenting with subtle ST-elevation myocardial infarction

BACKGROUND Borderline electrocardiograms represent a challenge in ST-segment elevation myocardial infarction (STEMI) management and are associated with inappropriate discharges and delays to intervention. OBJECTIVES To assess angiographic characteristics and outcomes of patients presenting with subtle ST-elevation (STE) myocardial infarction. METHODS A total of 504 consecutive patients with suspected STEMI treated by systematic primary percutaneous coronary intervention were prospectively included. Subtle STE was defined as a maximal preinterventional STE of 0.1 to 1 mm. Angiograms were interpreted by investigators unaware of the electrocardiographic data. RESULTS The proportion of patients with subtle STE was 18.3%, 86% of them presented with Thrombolysis In Myocardial Infarction flow grade 0/1 and 91% underwent percutaneous coronary intervention. Despite having smaller infarcts, subtle STE patients associated more frequent multivessel disease (57% vs 44%, P = .02) and larger delays to reperfusion. During a follow-up of 19.0 ± 4.9 months, the rates of death or reinfarction were similar among groups (10.0% vs 12.6%, P = .467). Subtle STE was not associated with better outcomes neither in univariate nor after adjustment in a multivariate analysis (adjusted hazard ratio 0.79, 95% CI 0.37-1.69, P = .546). CONCLUSIONS Subtle STEMI is frequent in clinical practice and is usually associated with acute total coronary occlusion. Therefore, it should be diagnosed and treated in the same expeditiously manner as marked STEMI.

Seguridad y eficacia de un protocolo de deambulación precoz, con dispositivo de hemostasia Angio-seal, tras angioplastia coronaria

Introduccion y objetivos Con objeto de valorar la seguridad y eficacia de una estrategia de deambulacion precoz (1-2 h) tras angioplastia coronaria mediante la utilizacion de Angio-seal hemos analizado una serie consecutiva de pacientes con dicho dispositivo y contrarrestado los resultados obtenidos con los de un grupo control de referencia coetaneo en el cual el dispositivo utilizado fue el C-clamp. Pacientes y metodos Fueron incluidos en el estudio un total de 207 pacientes sometidos a angioplastia coronaria entre febrero y agosto de 2000. De ellos, 98 fueron tratados con compresion mecanica y 109 con Angio-seal. En todos los casos se realizo un seguimiento clinico, al alta y a los 15 dias. Resultados En el 80% de los pacientes con el dispositivo Angio-seal, la hemostasia fue inmediata ( Conclusion Con nuestro protocolo de actuacion, la estrategia de deambulacion precoz mediante la utilizacion de Angio-seal tras angioplastia coronaria es eficaz y segura.

Ausencia de interferencia entre teléfonos móviles GSM y desfibriladores implantables: estudio in vivo

Introduccion y objetivos El campo electromagnetico generado por los telefonos moviles puede causar disfuncion de marcapasos. Aunque los desfibriladores implantables son tambien susceptibles a ese tipo de interferencia, se han realizado pocos estudios para evaluar ese riesgo y la compatibilidad con la tecnologia GSM no ha sido probada. El objetivo de este estudio es detectar interferencia in vivo entre telefonos moviles GSM y desfibriladores. Material y metodos La poblacion de estudio se compone de 30 pacientes portadores de 8 modelosdistintos de desfibriladores. Veintiseis tenian electrodos endocardicos y 4 epicardicos. Se evaluaron tres telefonos moviles GSM: Siemens S3 COM y Motorola 6200 en todos los casos y Ericsson GA 318 en uno. Las pruebas fueron realizadas bajo monitorizacion electrocardiografica continua. Las formas de terapia eran desactivadas y los parametros de sensibilidad aumentados al maximo valor permitido. Los telefonos se colocaron en contacto proximo con la carcasa y sobre el precordio, en dos angulos distintos. Se estudiaron tres situaciones: establecimiento de llamada, contacto durante 15 s y recepcion de llamada. Se repitio el protocolo durante estimulacion a frecuencias superiores a la basal para evaluar una posible inhibicion del modo de marcapasos. Resultados No se observaron casos de interferencia electromagnetica. Un paciente presento episodios espontaneos de taquicardia ventricular no sostenida durante las pruebas que fueron detectados por el desfibrilador. Conclusiones Los resultados sugieren que la interferencia electromagnetica por telefonos moviles GSM es una causa poco probable de disfuncion de los desfibriladores implantables.

Frailty is an independent prognostic marker in elderly patients with myocardial infarction

Acute coronary syndrome (ACS) patients are increasingly older. Conventional prognostic scales include chronological age but do not consider vulnerability. In elderly patients, a frail phenotype represents a better reflection of biological age.

Effects of Ivabradine on Heart Rate and Hemodynamic Parameters in a Swine Model of Cardiogenic Shock

Cardiogenic shock (CS) after myocardial infarction is associated with elevated mortality. There are few specific treatment options. Catecholamine administration may worsen tachycardia because decreased tissue perfusion may lead to reduced ventricular efficiency and increased oxygen consumption. Preliminary data indicate that ivabradine may offer a benefit in situations of severe tachycardia and shock, probably as a result of lower oxygen consumption and oxidative stress, although the hemodynamic effects of the drug in this context are unknown. For this reason, prior to administration of the drug in a clinical setting, we deemed it appropriate to study whether ivabradine administration may induce hemodynamic changes in a porcine model of CS after myocardial infarction. Ten female large white pigs (mean weight, 32.8 [2.2] kg) were included. The animals were anesthetized with propofol and fentanyl and the anterior descending artery was occluded for 45 minutes by inflation of an angioplasty balloon. To simulate CS after infarction, noradrenalin, dobutamine, and saline solution were administered until a postreperfusion heart rate (HR) of 90 bpm and a pulmonary wedge pressure > 18 mmHg were achieved. Amiodarone was also administered at the same dose in both study groups to prevent ventricular fibrillation, which is a frequent occurrence in porcine models of acute ischemia. Hemodynamic parameters (blood pressure, HR, cardiac output, pulmonary artery pressure, pulmonary wedge pressure, and central venous pressure) were monitored with Swan-Ganz catheters inserted into the aorta via the carotid and jugular approach. After balloon deflation, each animal was stabilized for 15 minutes prior to subsequent open-label randomization to the control group (n = 5) or ivabradine group (n = 5). Ivabradine was administered intravenously as a slow intravenous bolus at a dose of 0.3 mg/kg and was diluted in distilled water at a concentration 12 mg/mL. The placebo group received the equivalent volume of saline solution. The aforementioned hemodynamic parameters were then measured at 15-minute intervals after infusion of drug/placebo. The study variables are expressed as mean SD. The means were compared with the Student t test for independent data with a normal distribution and with the Fisher-Pitman test for independent variables with a nonparametric distribution. Ivabradine administration was associated with a significant decrease in HR (Figure 1; median [confidence interval] absolute reduction in HR at 15 minutes, 21 [21 to 25] vs –1 [–5 to 0] bpm; P = .04), with no change in blood pressure, pulmonary artery pressure, or cardiac output. Tidal volume significantly increased in the ivabradine group (Figure 2; tidal volume at 15 minutes, 63.7 [5.7] vs 43.7 [7.5] mL; P < .01). However, the decrease in HR was not accompanied by a reduction in pulmonary wedge pressure, and an increase in central venous pressure was observed compared with the control group (Figure 1). The numerical differences recorded in the 2 groups before administration of the study drug were not significant for any variables. Although findings indicative of the efficacy and safety of ivabradine in acute heart failure after infarction have been reported, the hemodynamic impact of reducing HR in CS is not known. Our results are in agreement with those of Bakkehaug et al. in a porcine model of CS. The model used by those authors, however, was more invasive than ours—medial sternotomy was performed—and is thus less readily applicable in clinical practice. An additional consideration, at least as important as the type of model, is that the animals in that study were not randomized; rather, the animals were their own control. An effect of spontaneous improvement occurring after induction of ischemia and reperfusion of the infarction cannot therefore be ruled out. In conclusion, ivabradine administered in a porcine model of CS induced by ischemia/reperfusion can reduce HR without significantly compromising cardiac output and can therefore increase tidal volume. However, this reduction in HR does not appear to reduce filling pressures. Before randomized clinical studies are conducted, we believe broader knowledge is required, in particular with a view to establishing whether this pharmacological strategy is of any value in reducing oxidative stress and myocardial damage in CS after myocardial infarction.

USEFULNESS OF RECIPROCAL CHANGES IN THE DIAGNOSIS OF MYOCARDIAL INFARCTION WITH MINIMAL ST-ELEVATION

Minimal ST-elevation (STE) represents a challenge in the diagnosis of myocardial infarction, and is associated with delays to intervention. We sought to analyze the prevalence of reciprocal changes as a diagnostic tool in patients with minimal STE. We conducted a prospective cohort study in a