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Sin financiación No data JCR 2021 0.385 SJR (2021) Q3, 1499/2489 Medicine (miscellaneous) No data IDR 2021 UEM

El síndrome de Bayés es una nueva entidad clínica, caracterizada por la combinación de bloqueo interauricular (BIA) avanzado en el electrocardiograma de superficie con fibrilación auricular (FA) y otras arritmias auriculares. Este síndrome se asocia con un riesgo incrementado de ictus, demencia y mortalidad. El BIA avanzado se diagnostica con la presencia de una onda P ≥ 120 ms de morfología bifásica (±) en derivaciones de cara inferior. Se produce por un bloqueo completo del haz de Bachmann que causa una despolarización retrógrada de la aurícula izquierda desde zonas cercanas a la unión auriculoventricular. La miocardiopatía auricular fibrótica es el sustrato anatómico del BIA avanzado. La disincronía inducida por el BIA avanzado funciona como desencadenante y mecanismo de mantenimiento de la FA. Esta alteración de la arquitectura auricular produce remodelado auricular, estasis sanguínea e hipercoagulabilidad, lo cual desencadena la cascada trombogénica. El BIA avanzado, incluso sin arritmias auriculares documentadas, también se ha relacionado con FA, ictus, demencia y mortalidad. Sin embargo, todavía no se ha demostrado el beneficio de la anticoagulación para los pacientes sin FA documentada. Por lo tanto, es recomendable una búsqueda proactiva de FA en los pacientes con BIA avanzado. Bayés syndrome is a new clinical entity, characterized by the association of advanced interatrial block (IAB) on surface electrocardiogram with atrial fibrillation (AF) and other atrial arrhythmias. This syndrome is associated with an increased risk of stroke, dementia, and mortality. Advanced IAB is diagnosed by the presence of a P-wave ≥ 120 ms with biphasic morphology (±) in inferior leads. The cause of IAB is complete Bachmann bundle blockade, leading to retrograde depolarization of the left atrium from areas near the atrioventricular junction. The anatomic substrate of advanced IAB is fibrotic atrial cardiomyopathy. Dyssynchrony induced by advanced IAB is a trigger and maintenance mechanism of AF. This alteration of the atrial architecture produces atrial remodeling, blood stasis and hypercoagulability, triggering the thrombogenic cascade. The presence of advanced IAB, even in patients without documented atrial arrhythmias, has also been associated with AF, stroke, dementia, and mortality. However, in these patients, there is no evidence to support the use of anticoagulation. Therefore, in patients with advanced IAB, a proactive search for AF is recommended. Sin financiación 4.753 JCR (2020) Q2, 45/142 Cardiac & Cardiovascular Systems 0.455 SJR (2020) Q3, 202/349 Cardiology and Cardiovascular Medicine No data IDR 2020 UEM

Resumen Introduccion y objetivos La fibrilacion auricular (FA) es la arritmia mas frecuente en la practica clinica. Nuestro objetivo es determinar la asociacion entre la duracion de la onda P y el bloqueo interauricular (BIA) avanzado y la FA. Metodos Estudio de casos y controles anidado en una cohorte (REGICOR: REgistre GIroni del COR) emparejada por edad y sexo. Entre 1999 y 2005 se realizaron 2 estudios transversales en los que participaron 9.380 individuos; entre 2009 y 2013 se invito a todos los participantes a un segundo examen. Se selecciono a los participantes de 25-79 anos que participaron en el segundo examen. Dos observadores determinaron la duracion y la morfologia de la onda P para determinar la presencia de BIA (ausencia, parcial o avanzado). Resultados La mediana de seguimiento fue 7,12 anos. Se incluyo a 80 participantes que sufrieron FA y 160 controles. La duracion de la onda P y la presencia de BIA se asociaron con la FA. Al considerar simultaneamente las 2 variables, solo la duracion de la onda P (≥ 110 ms) se asocio con la aparicion de FA. Las odds ratio de FA para la duracion de la onda P entre 110-119, 120-129 y ≥ 130 ms frente a Conclusiones La duracion de la onda P ≥ 110 ms aumenta el riesgo de FA. No parece que el BIA avanzado aporte un riesgo adicional al de la duracion de la onda P.

A dogma is any point of doctrine that is believed to be unquestionable and certain. In this sense, in electrocardiographic diagnosis, the dogma that there was a posterior wall of the left ventricle and that post-infarction patients in which a tall R wave appeared in V1 through V2 had an infarction of that wall was considered certain and unquestionable. Besides, the presence of QS morphology in VL was considered as a manifestation of a high lateral infarction. Lastly, it was believed, ever since Myers et al1-3 anatomopathologic correlation study, in the 1940s, that the localization of a Q wave infarction was as follows: Q in V1 through V2 indicated septum infarction, V3 through V4 anterior, V5 through V6 low lateral, I through VL high lateral, and II, III, VF inferior.

El diagnostico clinico de los tumores cardiacos es, a menudo, dificil. Presentamos el caso de un paciente de 17 anos en el que se diagnostico un tumor del ventriculo izquierdo a partir del estudio de un sincope. El estudio anatomopatologico confirmo el diagnostico de mixoma. Clinical diagnosis of cardiac tumours is often difficult. We present the case of a 17 year-old boy inwhom a left ventricular tumour was discovered duringon diagnostic work-up for a syncope. The tumourwas removed and histology confirmed thediagnosis of myxoma.

Our study was designed with the primary objective of evaluating the cardiac, overall and sudden mortality in patients with class IV heart failure (NYHA) managed with standard treatment and captopril (50 mg/8 hr. max.).95 consecutive patients were enrolled in 21 hospitals and were followed for 6 months in order to design an interventional clinical trial to reduce sudden death.Death occurred in 14 patients (14.7%; i.c. 8.3% - 23.5%; p0.05). There were no non-cardiovascular deaths in the group. There were 6 sudden death cases (42.9%; i.c. 16.9% - 68.8%, p0.05). Patients who died had a higher baseline end-diastolic (p0.05) and end-systolic (p0.01) diameter of the left ventricle (LV) and lower values of systolic (p0.01) and diastolic (p0.05) blood pressure. During the follow-up phase, heart rate, ventricular premature contraction, blood pressure and LV diameters decreased significantly in the whole group (p0.05, p0.001). We found no any differences during the follow-up phase between the patients who died and those who survived. In the patients who died we found no any differences between sudden death cases and the other death cases.Sudden death was less frequent than we had expected and due to this fact it is impossible for us to design an interventional trial.

A patient with a localized severe stenosis of his lower thoracic aorta is described. He presented a coarctation like syndrome with hypertension, pulseless legs and left ventricular failure. At surgery a biopsy of the lesion and bypass graft were performed. Pathology diagnosed intimal hyperplasia. Twenty eight months later he developed a sarcoma.

To evaluate the characteristics of early ventricular arrhythmias in acute myocardial infarction and their predictive value of ventricular fibrillation.We retrospectively compared 85 patients who presented ventricular fibrillation with a control group of 187 consecutively acute myocardial infarction patients recorded within the first 12 hours after onset of acute myocardial infarction symptoms. Patients in Killip class III-IV were excluded.In the ventricular fibrillation group we observed a high prevalence of inferior site of infarction (69 vs 56%; p0.05), sum of ST in 3 leads (ST-3 leads) with maximal elevation (13 +/- 17 vs 8 +/- 7 mm; p0.005), basic heart rate (97 +/- 23 vs 88 +/- 18 bpm; p0.01), R-on-T phenomenon (16 vs 2%; p0.001). In 22 patients in whom the ventricular fibrillation episode was registered, the basic heart rate preceding the ventricular fibrillation was fast (113 +/- 54 bpm), and the prematurity index (coupling interval/QT) shorter than in the other ventricular arrhythmias (0.9 +/- 0.2 vs 1.2 +/- 0.3 s respectively; p0.005). The prematurity index of ventricular arrhythmias in the ventricular fibrillation group was shorter than in the control group (1.2 +/- 0.3 vs 1.5 +/- 0.3 s respectively; p0.0001) and the heart rate during runs was faster (172 +/- 54 vs 126 +/- 40 bpm; p0.01). The logistic regression analysis showed that R-on-T phenomenon (odds ratio [OR] = 2.8), inferior site of infarct (OR = 3.65), sum of ST-3 leads10 mm (OR = 5.82), and basic heart rate100 bpm (OR = 2.33) were independent risk factors for ventricular fibrillation.Characteristic ventricular arrhythmias were found to precede ventricular fibrillation episodes: R-on-T phenomenon or short prematurity index and fast runs of ventricular tachycardia, with other parameters such a inferior site of infarct, sum of ST-3 leads10 mm and basic heart rate100 bpm.

The hemodynamic response to amrinone was analyzed in 19 patients with severe heart failure (NYHA III or IV). In 17 patients, 2 bolus of amrinone (0.75 mg/kg) were administered with an interval of 30 minutes, while a single bolus only was administered in 2 patients. In all patients the initial bolus was followed by continuous perfusion of Amrinone (10 micrograms/kg/min in 17 patients; 7 and 5 micrograms/kg/min in the remaining two). Cardiac index increased from 1.8 +/- 0.2 to 2.5 +/- 0.4 l/min/m2 (p less than 0.01), and pulmonary capillary wedge pressure and mean right atrial pressure decreased significantly (from 24 +/- 5.2 to 14 +/- 6 mmHg, p less than 0.01; and from 8.7 +/- 6.5 to 3.2 +/- 3.4, p less than 0.05 respectively). There were no significant changes in mean blood pressure (93 +/- 17 versus 88 +/- 13), heart rate (81 +/- 15 versus 84 +/- 14 beats per minute) and systolic work index (26.4 +/- 10.7 versus 37.7 +/- 12.3 g-m/m2). The maximum effect was obtained at 60 minutes and maintained throughout the period of monitoring (8 hours). In the 2 patients who received a single bolus of amrinone the maximum effect was reached at 30 minutes (cardiac index 1.3 +/- 0.1 versus 2.5 +/- 0.1 l/min/m2; pulmonary capillary pressure 24 +/- 5 versus 16.8 +/- 6.5 mmHg; mean right atrial pressure 11 +/- 1 versus 3.5 +/- 3.5 mmHg), and was followed by a progressive loss of efficiency, until effect had totally disappeared and situation basal returned, between the third and fourth hours.(ABSTRACT TRUNCATED AT 250 WORDS)