Coronary heart disease is the leading cause of death in the Spanish population, and acute coronary syndromes are actually the main cause of mortality, morbidity and health care costs in Spain. In ischemic heart disease, much attention has been focused on the study and characterization of the left ventricle (LV), and the prognostic implications that LV dysfunction has in these patients, overshadowing the right ventricle (RV) and considering it dispensable for cardiac function and in consequence, it has been partly ignored. The right ventricle’s blood supply varies according to the coronary artery dominance. In a right-dominant system, the right coronary artery (RCA) distributes blood to most of the RV. Its lateral wall is supplied by the marginal branches, whereas the posterior wall and the inferoseptal region are supplied by the posterior descending artery. The anterior wall and the anteroseptal region are usually supplied by branches of the left anterior descending artery (LAD). The RV has besides, an excellent collateral system that originates from the moderator band, receiving blood supply from the first septal perforator branch which arises from the LAD. This feature, along with its low oxygen consumption and its capability to increase oxygen extraction, gives the RV a certain resistance to irreversible ischemia injury. Cardiac magnetic resonance (CMR) represents a non-invasive technique with increasing applications in acute myocardial infarction, and provides us with a wide range of information such as: identification of myocardial oedema (myocardium at risk), location of transmural necrosis, cuantification of infarct size and salvaged myocardium, and also identifying microvascular obstruction in a highly reproducible manner. Actually, is the gold standard technique for the evaluation of cardiac volumes and systolic function of RV. However, the literature that focuses on right ventricular involvement in the setting of an anterior myocardial infarction assessed by CMR is scarce. Our study was performed in an experimental group and in a group of patients with a first anterior ST segment elevation myocardial infarction (STEMI). Experimental Group: The study was approved by the Animal Care and Use Committee of the University of Valencia and it conforms with the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication No. 85–23, revised 1996). It was performed in nine female domestic pigs employing a percutaneous reversible ischemia technique, after sedation and anesthesia of the animal. A 6-F sheath was introduced into the right femoral artery to measure blood pressure and to access the LAD. An Amplatz left 0.75 guiding catheter and a standard hydrophilic angioplasty wire were also used. Ischaemia was induced by inflating a 2.5 × 10 mm over the wire balloon up to four atmospheres in the mid LAD. Coronary artery occlusion was confirmed by contrast injection and by electrocardiographic ST-segment elevation. After 90 minutes, the LAD balloon was deflated and restoration of normal coronary flow was documented by angiography. After 72 hours, 20 mL of 4% thioflavin-S solution was selectively infused into the mid LAD using the same over the wire balloon. The hearts were then arrested with potassium chloride and excised. The necropsy pieces were incubated in 2% 2,3,5-triphenyltetrazolium chloride solution during 20 minutes at 37ºC. The LAD-perfused area in both, RV and LV, was defined as the percentage of the myocardial volume showing thioflavin-S staining. Infarct size was designated as the percentage of the myocardial volume that failed to stain with 2,3,5-triphenyltetrazolium chloride. The salvaged myocardium was regarded as the percentage of the LAD-perfused area showing 2,3,5-triphenyltetrazolium chloride staining. Group of patients: From January 2008 to December 2012, we prospectively included 106 patients admitted consecutively with a first STEMI, whose repercussion strategy was primary angioplasty and did not show contraindication for CMR. CMR was performed 4 ± 1 and 181 ± 11 days after STEMI. Steady-state free-precession sequences were used for cine and first-pass perfusion imaging, a dark-blood T2-weighted short-tau inversion-recovery turbo-spin echo sequence was applied for determining the area at risk (oedema) and a segmented inversion recovery steady-state free-precession sequence was used for late enhancement imaging. All images were acquired by a phased-array body surface coil during breath-holds and were ECG triggered. The 17-segment model for the LV and the nine-segment model for the RV were applied. In cine images, end-diastolic volume index (mL/m2 ), end-systolic volume index (mL/m2), ejection fraction (%), and left ventricular mass (g/m2) were quantified by manual definition of endocardial and epicardial borders of all short-axis slices. T2-weighted images were used to quantify the area at risk in the RV and LV. Area at risk was defined as the percentage of ventricular mass with signal intensity two standard deviations above the mean signal obtained in the remote non-infarcted myocardium (posterior wall). Increased signal intensity from the blood pool adjacent to the endocardium was excluded. Late enhancement imaging was used to define infarct size in the RV and LV. Infarct size was regarded as the percentage of ventricular mass with signal intensity two standard deviations above the mean signal obtained in the remote non-infarcted myocardium (posterior wall). The salvaged myocardium was regarded as the percentage of the area at risk without late enhancement. For the assessment of the area at risk, area of necrosis and RV systolic function after a first anterior STEMI, 20 patients with an excellent image quality in CMR were included. For the evaluation of the area at risk, area of necrosis and RV systolic function after a first inferior STEMI, 10 patients with an excellent image quality in CMR were included.An experimental model was developed using 9 domestic pigs, and performing a percutaneous model of reversible ischemia based on inflating during 90 minutes an angioplasty balloon in the mid LAD and the subsequent repercussion. During balloon inflation, five pigs developed ventricular fibrillation. Four of them reverted to a stable sinus rhythm after undergoing electrical cardioversion; but one developed a refractory ventricular fibrillation, resulting in asystole and death. None of the animals presented an occlusion or dissection of the LAD after deflation of the angioplasty balloon. Within 72 hours, a new catheterization was performed in order to infuse selectively 20 ml of thioflavin-S to 4% in the LAD, without notable complications. To quantify the area at risk of the right ventricle that depends on the left anterior descending artery. Intracoronary thioflavin-S was the dye used to identify the area at risk, obtaining an excellent staining quality in all cases. Thioflavin-S staining (LAD-perfused area) was detected both in the RV and in the LV in all cases. A large area of the anterior wall of the RV (30  5% of the myocardial volume) was perfused by LAD. In comparison, the LV displayed a significant larger LAD-perfused area (62  15% of the myocardial volume, p< 0.001) comprising all anterior, antero-lateral and antero-septal segments. To quantify the salvaged myocardium and necrosis of the right ventricle resulting from a transient occlusion of the mid left anterior descending artery with the angioplasty balloon. The area of necrosis was evaluated after the incubation of the necropsy pieces in a 2-3-5 triphenyltetrazolium chloride 2% solution at 37ºC during 20 minutes. Areas that showed no staining with 2-3-5 triphenyltetrazolium corresponded to areas of necrosis. The area of necrosis was detected in four cases in the RV (50%) and in eight (100%) in the LV (p= 0.04). A large percentage of salvaged myocardium was observed in the RV; 94  6% of the area supplied by the LAD showed no necrosis after staining with 2-3-5 triphenyltetrazolium, resulting in a very small RV infarction (2  1% of the RV myocardial volume). In comparison, the percentage of salvaged myocardium in the LV was significantly lower (73  11% of the area supplied by the LAD, p<0.001), resulting in a significantly larger infarct size (16  5% of the LV myocardial volume, p<0.001). To determine the area of the right ventricle that is supplied by the right coronary artery. On average, 65 ± 8% of the RV and 30 ± 6% of the LV were supplied by the RCA, showing thioflavin-S staining. This area comprised mainly the inferior and infero-septal segments of the LV, and the inferior and lateral segments of the RV. To analyze right ventricular systolic function by cardiac magnetic resonance in the first week and sixth month after ST segment elevation myocardial infarction, in a consecutive group of patients with a first ST segment elevation myocardial infarction and reperfused by primary angioplasty. In the CMR studies at first week and sixth month after STEMI, we observed a preserved systolic function of the RV at first week CMR (mean RV ejection fraction of 60  8%), which showed a significant improvement at sixth month CMR (62  8%, p=0.03). The patients were categorized in 2 groups according to the location of the infarction: anterior and non-anterior STEMI. We observed no significant differences regarding RV ejection fraction between both groups, neither at first week nor at sixth month CMR (61 ± 9% vs 59 ± 8%, p=0.2 at first week and 63 ± 8% vs 61 ± 8%, p=0.1 at sixth month). When comparing the ejection fraction evolution in both groups, we observed a significant improvement in right ventricular ejection fraction at sixth month in the non-anterior STEMI group (59.8 ± 8% at first week vs 61 ± 8% at sixth month, p=0.022). Patients in the anterior STEMI group showed a similar tendency, although non significant. When classifying our patients according to the reference criteria for RV dysfunction established by Maceira et al. 8 patients (16.7%) with an anterior STEMI and 13 (22.4%) patients with a non-anterior STEMI (p=0.6) showed a depressed RV ejection fraction at first week CMR. This result suggests that patients with a non- anterior STEMI have a tendency of more depressed RV ejection fraction at first week after STEMI. There was a significant decrease in the number of patients with depressed RV ejection fraction in the non-anterior STEMI group at sixth month CMR: first week 13 (22.4%) vs sixth month 4 (6.9%), (p=0.03). The anterior STEMI group showed a similar tendency, although non significant. To assess the area at risk, area of necrosis and the right ventricle systolic function by cardiac magnetic resonance in a group of patients with a first ST segment elevation myocardial infarction due to the thrombotic occlusion of the proximal left anterior descending artery and reperfused by primary angioplasty. All the analysed cases (100%) displayed a certain amount of area at risk in T2-weighted imaging, both in the RV and in the LV. Necrosis (late enhancement) was detected in four cases (40%) in the RV (p<0.001) and in 20 cases (100%) in the LV (p<0.001). A large area of the anterior wall of the RV was at risk (34 ± 13%), owing to a large area of salvaged myocardium (94 ± 10% of the area at risk) and resulting in a small RV infarct size (2 ± 3%). On the other hand, the LV displayed more myocardium at risk (43 ± 12%, p= 0.02). As a consequence of a lesser amount of salvaged myocardium (33 ± 26% of the area at risk, p< 0.001) the resulting infarct size (30 ± 16%, p< 0.001) was larger than in the RV. To assess the area at risk, area of necrosis and right ventricle systolic function by cardiac magnetic resonance in a group of patients with a first ST segment elevation myocardial infarction due to the thrombotic occlusion of the proximal right coronary artery and reperfused by primary angioplasty. All the analysed cases with inferior STEMI (100%) displayed a certain amount of area at risk in T2-weighted imaging, both in the RV and in the LV. The RV exhibited larger area at risk than in the LV (49 ± 9% vs 27 ± 11%, p=0.01). Necrosis (late enhancement) was detected in five cases (50%) in the RV and in 9 cases (90%) in the LV (p<0.001). However, the area of necrosis in the RV (6 ± 5%) was significantly smaller when compared with the area of necrosis in the LV (19± 10%, p=0.01).This was probably the result of the fact that salvaged myocardium was significantly higher in the RV (85 ± 29% of the area at risk) when compared with the LV (28 ± 19%, p=0.01).La afectación del ventrículo derecho (VD) en el seno de un infarto agudo de miocardio de localización inferior, es de sobra conocida. Sin embargo, la vascularización de la cara anterior del VD depende de ramas de la arteria descendente anterior (ADA), siendo escasos los trabajos que estudian la afectación del VD que se produce durante un infarto agudo de miocardio de localización anterior. Evaluamos la afectación del VD que se produce tras la oclusión del ADA en un grupo experimental de 9 cerdos, al que le realizamos un modelo de isquemia-reperfusión percutánea mediante el hinchado de un balón de angioplastia en la ADA media durante 90 minutos, y en un grupo de pacientes con un primera infarto agudo de miocardio de localización anterior secundario a la oclusión trombótica de la ADA proximal, y estudiados mediante resonancia magnética cardiaca (RMC). Valoramos el área en riesgo de VD dependiente de la oclusión con balón de la ADA a partir de la infusión intracoronaria de tioflavina-S, Se consideró área en riesgo aquel porcentaje de volumen de miocardio que mostraba tintinó con tioflavina-S. Se valoró el área de necrosis a partir de la incubación de las piezas de corazón porcino en una solución de cloruro de 2-3-5 trifeniltetrazolio, se cualificaron como áreas de necrosis aquel porcentaje de volumen de miocardio que nos mostraba captación por 2-3-5 trifeniltetrazolio. Se cualificó el miocardio salvado como aquel porcentaje que mostraba tintinó con tioflavina-S y captación por 2-3-5 trifeniltetrazolio. En nuestro grupo de pacientes se valoró el área en riesgo a partir del análisis de las secuencias potenciadas en T2 y el área de necrosis mediante el análisis de las secuencias de realce tardío de gadolinio. Se consideró miocardio sacado aquel porcentaje de masa ventricular con hiperintensidad de señal en las secuencias potenciadas en T2 y que nos mostraba realce tardío de gadolinio. Obtuvimos en nuestro grupo experimental que tanto el VD como el ventrículo izquierdo (VI) mostraban tinción por tioflavina-S, es decir ambos ventrículos recibían irrigación por la ADA La cuantificación del área en riesgo fue del 30% del volumen de miocardio derecho y del 62% para VI. El 50% (4 animales) mostraron necrosis en el VD y el 100% en VI, sin embargo la extensión del área de necrosis de VD fue pequeño, el 2% del volumen de miocardio derecho, obteniendo por tanto una extensa área de miocardio salvado en VD. En nuestro grupo de pacientes, el 100% mostraron área de edema, es decir en riesgo tanto en VD como el VI, con un porcentaje del área en riesgo del 34% de la masa ventricular derecha. El 40% (8 pacientes) mostraron necrosis en VD, sin embargo la extensión del área de necrosis fue pequeña, observan también una extensa área de miocardio salvado, superior al 90% del área en riesgo. Concluimos, que tanto en un grupo experimental como en un grupo real de pacientes la oclusión de la ADA ocasiona un área en riesgo en VD, siendo el tamaño de la necrosis resultante pequeña y obteniendo una extensa área de miocardio salvado, lo que corrobora la resistencia a la isquemia del VD, debido fundamentalmente a su bajo consumo de oxígeno y a su extensa red de colaterales.