Maritime transport and regional climate change impacts in large EU islands and archipelagos.

Maritime transport is a vital sector for global trade and the world economy. Particularly for islands, there is also an important social dimension of this sector, since island communities strongly rely on it for a connection with the mainland and the transportation of goods and passengers. Furthermore, islands are exceptionally vulnerable to climate change, as the rising sea level and extreme events are expected to induce severe impacts. Such hazards are anticipated to also affect the operations of the maritime transport sector by affecting either the port infrastructure or ships en route. The present study is an effort to better comprehend and assess the future risk of maritime transport disruption in six European islands and archipelagos, and it aims at supporting regional to local policy and decision-making. We employ state-of-the-art regional climate datasets and the widely used impact chain approach to identify the different components that might drive such risks. Larger islands (e.g., Corsica, Cyprus and Crete) are found to be more resilient to the impacts of climate change on maritime operations. Our findings also highlight the importance of adopting a low-emission pathway, since this will keep the risk of maritime transport disruption similar to present levels or even slightly decreased for some islands because of an enhanced adaptation capacity and advantageous demographic changes. Supplementary Information: The online version contains supplementary material available at 10.1007/s41207-023-00370-6.

Anticoagulation Therapy by Age and Embolic Risk for Nonvalvular Atrial Fibrillation in Mexico, an Upper-Middle-Income Country: The CARMEN-AF Registry.

Background: Documenting the patterns of oral anticoagulation therapy (OAT) is essential to prevent thromboembolic complications of nonvalvular atrial fibrillation (NVAF). Objective: To report the patterns of OAT according to age and thromboembolic risk in patients included in CARMEN-AF, a nationwide registry of NVAF in Mexico, an upper middle-income country. Material and methods: There were 1,423 consecutive patients ≥18 years old and with at least one thromboembolic risk factor enrolled in the CARMEN-AF Registry at their regular clinical visit during a three-year period. They were analyzed according to 1) age, 2) AF type, and 3) CHA2DS2-VASc score. Results: Overall, 16.4% of patients did not receive antithrombotic treatment, 19.4% received antiplatelet drugs (APD), 29.2% vitamin K antagonists (VKA), and 34.6% direct oral anticoagulants (DOAC). With increasing age, the proportion of subjects treated with VKA decreased significantly from 36.2% in subjects <65 years to 22.5% in those ≥75 years old (P <0.0001). Concomitantly, an increase in both APD and no antithrombotic treatment was observed with increasing age. DOAC were prescribed equally among all age groups (34.2% in <65, 36.0% in 65-74, and 33.9% in ≥75). According to the type of AF, VKA use was more common in patients with permanent AF (32.7%). A lower use of DOAC was observed in high thromboembolic risk subjects (33.6% in CHA2DS2-VASc ≥2) compared with the moderate risk group (41% in CHA2DS2-VASc = 1). Conclusions: VKA use for NVAF in Mexico decreased in relation to increasing age. The proportion of DOAC therapy was the same in all age groups. Nevertheless, elderly patients with high thromboembolic risk received a suboptimal thromboprophylaxis. These data could help to improve gaps in the implementation of global guidelines. Clinical trial registration: http://www.clinicaltrials.gov. Unique identifier: NCT02334852. Highlights: CARMEN-AF is a nationwide multi-centric registry seeking to bridge the data gap on anticoagulation therapy for NVAF in Mexico.Elderly patients are more prone to receive suboptimal OAT for NVAF.DOAC were less frequently used in high thromboembolic risk patients (CHA2DS2-VASc ≥2).

Tryptophan supplementation helps totoaba (Totoaba macdonaldi) juveniles to regain homeostasis in high-density culture conditions.

High-density culture brings with it chronic stress situations that affect fish welfare. In order to evaluate the effect of tryptophan (Trp) levels on the response to stress, Totoaba macdonaldi juveniles were stocked at low (13.5 kg m-3) and high (27.0 kg m-3) densities (32.5 and 56.4 kg m-3, respectively, at the end of the experiment) in 100-L tanks and fed for 63 days with experimental diets containing different Trp levels: control diet CD0.42 (0.42%) and three supplemented diets with 0.99, 1.55 and 2.19% (0.99Trp, 1.55Trp and 2.19Trp, respectively) (three tanks × density × diet). The high-density stocking fed with CD0.42 diets showed significantly increased blood parameters. Trp decreased catalase (CAT) activity in low- and high-density stocking, while the superoxide dismutase (SOD) activity showed no difference. Serotonin (5-hydroxytryptamine, 5-HT) content decreased, and the serotonin turnover ratio (5-HIAA:5-HT) increased in the brains of fish fed with the CD0.42 diet. Indeed, Trp-supplemented diets helped to restore homeostasis in high-density growth conditions as evaluated by the hematological and plasma parameters as well as the serotonergic activity. When the fish were provided a diet containing moderate Trp levels, plasma cortisol increased under high-density conditions. However, no differences were observed among stock densities when totoaba were fed with the 2.19Trp diet. Notably, survival was unaffected by both Trp or densities, but weight gain (WG) decreased with the dietary Trp levels in the high density culture. In sum, Trp supplementation decreased the parameter values linked to stress response on totoaba juveniles cultured at high stock densities.

De la tromboembolia pulmonar aguda a la hipertensión pulmonar tromboembólica crónica: implicaciones en la patobiología y fisiopatología / From acute pulmonary embolism to chronic thromboembolic pulmonary hypertension: Pathobiology and pathophysiology

Resumen: La hipertensión pulmonar tromboembólica crónica (HPTEC) es un subtipo de hipertensión pulmonar (HP) caracterizada por la obstrucción mecánica de las arterias pulmonares causada por una tromboembolia pulmonar. Sin tratamiento es una enfermedad progresiva y devastadora, y es el único subgrupo de HP potencialmente curable mediante la endarterectomía pulmonar. La magnitud, así como la recurrencia de la embolia pulmonar, son determinantes y contribuyen al desarrollo de la HPTEC aun cuando está asociada solo a algunos factores trombofílicos. Una hipótesis es que la enfermedad es consecuencia de la resolución incompleta y la organización del trombo, favorecido por fenómenos de inflamación, inmunitarios y/o genéticos que promueven el desarrollo de estenosis de tipo fibroso que culminan con el remodelado vascular oclusivo de vasos proximales y distales. Los mecanismos involucrados en la fallida resolución del trombo aún no están esclarecidos. Los pacientes con HPTEC con frecuencia exhiben HP severa que no puede ser explicada por el grado de obstrucción vascular demostrada en estudios por imagen. En tales casos la arteriopatía pulmonar y las lesiones trombóticas obstructivas, distales al nivel subsegmentario, pueden contribuir al incremento fuera de proporción de las resistencias vasculares pulmonares. Los procesos que llevan al desarrollo de la arteriopatía pulmonar y los cambios microvasculares que ocurren en la HPTEC explican el comportamiento progresivo de la HP y el deterioro clínico gradual con pobre pronóstico para los pacientes, así como también la falta de correlación entre la magnitud de la obstrucción vascular y la medición de parámetros hemodinámicos, aun en ausencia de tromboembolismo venoso recurrente. Esta revisión resume los aspectos más relevantes y actuales de la patobiología y fisiopatología de la HPTEC.

Abstract: Chronic thromboembolic pulmonary hypertension (CTEPH) represents a unique subtype of pulmonary hypertension characterized by the presence of mechanical obstruction of the major pulmonary vessels caused by venous thromboembolism. CTEPH is a progressive and devastating disease if not treated, and is the only subset of PH potentially curable by a surgical procedure known as pulmonary endarterectomy. The clot burden and pulmonary embolism recurrence may contribute to the development of CTEPH however only few thrombophilic factors have been found to be associated. A current hypothesis is that CTEPH results from the incomplete resolution and organization of thrombus modified by inflammatory, immunologic and genetic mechanisms, leading to the development of fibrotic stenosis and adaptive vascular remodeling of resistance vessels. The causes of thrombus non-resolution have yet to be fully clarified. CTEPH patients often display severe PH that cannot be fully explained by the degree of pulmonary vascular obstruction apparent on imaging studies. In such cases, the small vessel disease and distal obstructive thrombotic lesions beyond the sub-segmental level may contribute for out of proportion elevated PVR. The processes implicated in the development of arteriopathy and microvascular changes might explain the progressive nature of PH and gradual clinical deterioration with poor prognosis, as well as lack of correlation between measurable hemodynamic parameters and vascular obstruction even in the absence of recurrent venous thromboembolism. This review summarizes the most relevant up-to-date aspects on pathobiology and pathophysiology of CTEPH.

Mexican registry of pulmonary hypertension REMEHIP / Registro Mexicano de Hipertensión Pulmonar REMEHIP

Abstract: Objective: REMEHIP is a prospective, multicentre registry on pulmonary hypertension. The main objective will be to identify the clinical profile, medical care, therapeutic trends and outcomes in adult and pediatric Mexican patients with well-characterized pulmonary hypertension. Methods: REMEHIP a multicenter registry began in 2015 with a planned recruitment time of 12 months and a 4-year follow-up. The study population will comprise a longitudinal cohort study, collecting data on patients with prevalent and incident pulmonary hypertension. Will be included patients of age >2 years and diagnosis of pulmonary hypertension by right heart catheterization within Group 1 and Group 4 of the World Health Organization classification. The structure, data collection and data analysis will be based on quality current recommendations for registries. The protocol has been approved by institutional ethics committees in all participant centers. All patients will sign an informed consent form. Currently in Mexico, there is a need of observational registries that include patients with treatment in the everyday clinical practice so the data could be validated and additional information could be obtained versus the one from the clinical trials. In this way, REMEHIP emerges as a link among randomized clinical trials developed by experts and previous Mexican experience.

Resumen: Objetivo: REMEHIP es un registro prospectivo, multicéntrico en hipertensión pulmonar. El objetivo principal será identificar el perfil clínico, atención médica, tendencias terapéuticas y evolución en pacientes mexicanos adultos y pediátricos con hipertensión pulmonar bien caracterizada. Métodos: El REMEHIP comenzó en el año de 2015 y se planea un reclutamiento de 12 meses con un seguimiento de 4 años. La población en estudio será una cohorte longitudinal y se obtendrán datos de pacientes prevalentes e incidentes con hipertensión pulmonar. Se incluirán pacientes con edad > 2 años con diagnóstico de hipertensión pulmonar demostrado por cateterismo cardiaco derecho del Grupo 1 y Grupo 4 de la clasificación de la Organización Mundial de la Salud. La estructura, colección de datos y el análisis se establecerá a través de las recomendaciones actuales de calidad para los registros. El protocolo ha sido aprobado por los comités de ética de todos los centros participantes. Todos los pacientes firmarán un consentimiento informado. Actualmente en México existe una necesidad de registros observacionales que incluyan a pacientes con tratamiento en la práctica clínica cotidiana, de tal forma que los datos obtenidos podrían validarse y el resto de la información podría compararse con la derivada de los estudios clínicos. De esta forma REMEHIP surge como un vínculo entre los estudios clínicos aleatorizados conducidos por expertos y la experiencia mexicana previa.

Mexican registry of pulmonary hypertension: REMEHIP.

OBJECTIVE: REMEHIP is a prospective, multicentre registry on pulmonary hypertension. The main objective will be to identify the clinical profile, medical care, therapeutic trends and outcomes in adult and pediatric Mexican patients with well-characterized pulmonary hypertension. METHODS: REMEHIP a multicenter registry began in 2015 with a planned recruitment time of 12 months and a 4-year follow-up. The study population will comprise a longitudinal cohort study, collecting data on patients with prevalent and incident pulmonary hypertension. Will be included patients of age >2 years and diagnosis of pulmonary hypertension by right heart catheterization within Group 1 and Group 4 of the World Health Organization classification. The structure, data collection and data analysis will be based on quality current recommendations for registries. The protocol has been approved by institutional ethics committees in all participant centers. All patients will sign an informed consent form. Currently in Mexico, there is a need of observational registries that include patients with treatment in the everyday clinical practice so the data could be validated and additional information could be obtained versus the one from the clinical trials. In this way, REMEHIP emerges as a link among randomized clinical trials developed by experts and previous Mexican experience.

[From acute pulmonary embolism to chronic thromboembolic pulmonary hypertension: Pathobiology and pathophysiology]. / De la tromboembolia pulmonar aguda a la hipertensión pulmonar tromboembólica crónica: implicaciones en la patobiología y fisiopatología.

Chronic thromboembolic pulmonary hypertension (CTEPH) represents a unique subtype of pulmonary hypertension characterized by the presence of mechanical obstruction of the major pulmonary vessels caused by venous thromboembolism. CTEPH is a progressive and devastating disease if not treated, and is the only subset of PH potentially curable by a surgical procedure known as pulmonary endarterectomy. The clot burden and pulmonary embolism recurrence may contribute to the development of CTEPH however only few thrombophilic factors have been found to be associated. A current hypothesis is that CTEPH results from the incomplete resolution and organization of thrombus modified by inflammatory, immunologic and genetic mechanisms, leading to the development of fibrotic stenosis and adaptive vascular remodeling of resistance vessels. The causes of thrombus non-resolution have yet to be fully clarified. CTEPH patients often display severe PH that cannot be fully explained by the degree of pulmonary vascular obstruction apparent on imaging studies. In such cases, the small vessel disease and distal obstructive thrombotic lesions beyond the sub-segmental level may contribute for out of proportion elevated PVR. The processes implicated in the development of arteriopathy and micro-vascular changes might explain the progressive nature of PH and gradual clinical deterioration with poor prognosis, as well as lack of correlation between measurable hemodynamic parameters and vascular obstruction even in the absence of recurrent venous thromboembolism. This review summarizes the most relevant up-to-date aspects on pathobiology and pathophysiology of CTEPH.

Inhibidores de fosfodiesterasa-5 para el tratamiento de la hipertensión arterial pulmonar / Phosphodiesterase-5 inhibitors for the treatment of pulmonary arterial hypertension

En cardiología clínica y experimental, los inhibidores de fosfodiesterasa-5 (PDE-5) han atraído el interés científico en años recientes como herramienta terapéutica para el tratamiento de la HAP. Las fosfodiesterasas son una superfamilia de enzimas que inactivan el adenosín monofosfato cíclico y el guanosín monofosfato cíclico, los segundos mensajeros de la prostaciclina y del óxido nítrico. El razonamiento para utilizar los inhibidores de PDE-5 en HAP se basa en su relativa selectividad por la circulación pulmonar y en su capacidad para sobreexpresar la vía del óxido nítrico por inhibición de la hidrólisis del guanosín monofosfato cíclico e incrementar sus concentraciones, lo cual produce efectos vasodilatadores, antiproliferativos y proapoptóticos que pueden revertir el remodelado vascular pulmonar. Además, pueden aumentar el inotropismo ventricular derecho al incrementar el adenosín monofosfato cíclico mediado por la inhibición de la fosfodiesterasa tipo 3 sensible al guanosín monofosfato cíclico. El sildenafil, el tadalafil y el vardenafil son 3 inhibidores de PDE-5 actualmente en uso clínico que comparten similar mecanismo de acción aunque presentan algunas diferencias significativas en potencia, selectividad por la PDE-5 y propiedades farmacocinéticas. Para el tratamiento de la HAP en pacientes en clase funcional II y III (NYHA/WHO), el sildenafil fue aprobado por la Food and Drug Administration y la European Medicines Agency en 2005; y tadalafil por la Food and Drug Administration y la European Medicines Agency en 2009. En México, el sildenafil y el tadalafil recibieron la aprobación por parte de la Comisión Federal para la Protección contra Riesgos Sanitarios para la misma indicación en 2010 y 2011 respectivamente.

In experimental and clinical cardiology, phosphodiesterase type 5 (PDE-5) inhibitors have brought scientific interest as a therapeutic tool in pulmonary arterial hypertension (PAH) management in recent years. Phosphodiesterases are a superfamily of enzymes that inactivate cyclic adenosine monophosphate and cyclic guanosine monophosphate, the second messengers of prostacyclin and nitric oxide. The rationale for the use of PDE-5 inhibitors in PAH is based on their capacity to overexpresss the nitric oxide pathway pursued inhibition of cyclic guanosine monophosphate hydrolysis. By increasing cyclic guanosine monophosphate levels it promotes vasodilation, antiproliferative and pro-apoptotic effects that may reverse pulmonary vascular remodeling. There is also evidence that these drugs may directly enhance right ventricular contractility through an increase in cyclic adenosine monophosphate mediated by the inhibition of the cyclic guanosine monophosphate -sensitive PDE-3. Sildenafil, tadalafil and vardenafil are 3 specific PDE-5 inhibitors in current clinical use, which share similar mechanisms of action but present some significant differences regarding potency, selectivity for PDE-5 and pharmacokinetic properties. Sildenafil received approval in 2005 by the Food and Drug Administration and the European Medicines Agency and tadalafil in 2009 by the Food and Drug Administration and the European Medicines Agency for the treatment of PAH in patients classified as NYHA/WHO functional class II and III. In Mexico, sildenafil and tadalafil were approved by Comisión Federal de Protección contra Riesgos Sanitarios for this indication in 2010 and 2011, respectively.

[Phosphodiesterase-5 inhibitors for the treatment of pulmonary arterial hypertension]. / Inhibidores de fosfodiesterasa-5 para el tratamiento de la hipertensión arterial pulmonar.

In experimental and clinical cardiology, phosphodiesterase type 5 (PDE-5) inhibitors have brought scientific interest as a therapeutic tool in pulmonary arterial hypertension (PAH) management in recent years. Phosphodiesterases are a superfamily of enzymes that inactivate cyclic adenosine monophosphate and cyclic guanosine monophosphate, the second messengers of prostacyclin and nitric oxide. The rationale for the use of PDE-5 inhibitors in PAH is based on their capacity to overexpresss the nitric oxide pathway pursued inhibition of cyclic guanosine monophosphate hydrolysis. By increasing cyclic guanosine monophosphate levels it promotes vasodilation, antiproliferative and pro-apoptotic effects that may reverse pulmonary vascular remodeling. There is also evidence that these drugs may directly enhance right ventricular contractility through an increase in cyclic adenosine monophosphate mediated by the inhibition of the cyclic guanosine monophosphate -sensitive PDE-3. Sildenafil, tadalafil and vardenafil are 3 specific PDE-5 inhibitors in current clinical use, which share similar mechanisms of action but present some significant differences regarding potency, selectivity for PDE-5 and pharmacokinetic properties. Sildenafil received approval in 2005 by the Food and Drug Administration and the European Medicines Agency and tadalafil in 2009 by the Food and Drug Administration and the European Medicines Agency for the treatment of PAH in patients classified as NYHA/WHO functional class II and III. In Mexico, sildenafil and tadalafil were approved by Comisión Federal de Protección contra Riesgos Sanitarios for this indication in 2010 and 2011, respectively.

Hipertensión pulmonar asociada a cardiopatías congénitas y síndrome de Eisenmenger / Pulmonary hypertension associated with congenital heart disease and Eisenmenger syndrome

La hipertensión arterial pulmonar es una complicación frecuente de las cardiopatías congénitas (CC). Es reconocido que las CC son las malformaciones más frecuentes al nacimiento con una prevalencia que va de 6 a 8 por 1,000 recién nacidos vivos. En nuestro país se calcula que cada año nacen de 12,000 a 16,000 niños con algún tipo de malformación cardiaca. En los pacientes no corregidos con cortocircuitos de izquierda a derecha el aumento de la presión pulmonar provoca incremento en las resistencias pulmonares y desencadena una disfunción endotelial y remodelación vascular, consecuencia de alteraciones en los mediadores vasoactivos que provocan vasoconstricción, inflamación, trombosis, proliferación y apoptosis celular así como fibrosis. Como consecuencia hay un incremento progresivo de las resistencias pulmonares y de la presión del ventrículo derecho. Finalmente ocurre que el flujo sanguíneo se invierte y se desarrolla el síndrome de Eisenmenger, la forma más avanzada de hipertensión arterial pulmonar consecutiva a CC. La frecuencia de hipertensión arterial pulmonar secundaria a CC ha disminuido en países desarrollados no así en países en vías de desarrollo tanto por un diagnóstico tardío como por falta de infraestructura hospitalaria o de recursos humanos para la atención de los pacientes portadores de CC. Con el advenimiento del tratamiento farmacológico para la hipertensión arterial pulmonar, se han vislumbrado nuevas oportunidades terapéuticas, siendo cada vez más cotidiano que se sumen al tratamiento intervencionista o quirúrgico en pacientes con hipertensión arterial pulmonar secundaria a CC. Se requiere conocer los factores fisiopatológicos involucrados así como llevar a cabo una cuidadosa evaluación para definir la mejor estrategia terapéutica.

Pulmonary arterial hypertension is a common complication of congenital heart disease (CHD). Congenital cardiopathies are the most frequent congenital malformations. The prevalence in our country remains unknown, based on birthrate, it is calculated that 12,000 to 16,000 infants in our country have some cardiac malformation. In patients with an uncorrected left-to-right shunt, increased pulmonary pressure leads to vascular remodeling and endothelial dysfunction secondary to an imbalance in vasoactive mediators which promotes vasoconstriction, inflammation, thrombosis, cell proliferation, impaired apotosis and fibrosis. The progressive rise in pulmonary vascular resistance and increased pressures in the right heart provocated reversal of the shunt may arise with the development of Eisenmenger' syndrome the most advanced form de Pulmonary arterial hypertension associated with congenital heart disease. The prevalence of Pulmonary arterial hypertension associated with CHD has fallen in developed countries in recent years that is not yet achieved in developing countries therefore diagnosed late as lack of hospital infrastructure and human resources for the care of patients with CHD. With the development of targeted medical treatments for pulmonary arterial hypertension, the concept of a combined medical and interventional/surgical approach for patients with Pulmonary arterial hypertension associated with CHD is a reality. We need to know the pathophysiological factors involved as well as a careful evaluation to determine the best therapeutic strategy.

[Pulmonary hypertension associated with congenital heart disease and Eisenmenger syndrome]. / Hipertensión pulmonar asociada a cardiopatías congénitas y síndrome de Eisenmenger.

Pulmonary arterial hypertension is a common complication of congenital heart disease (CHD). Congenital cardiopathies are the most frequent congenital malformations. The prevalence in our country remains unknown, based on birthrate, it is calculated that 12,000 to 16,000 infants in our country have some cardiac malformation. In patients with an uncorrected left-to-right shunt, increased pulmonary pressure leads to vascular remodeling and endothelial dysfunction secondary to an imbalance in vasoactive mediators which promotes vasoconstriction, inflammation, thrombosis, cell proliferation, impaired apotosis and fibrosis. The progressive rise in pulmonary vascular resistance and increased pressures in the right heart provocated reversal of the shunt may arise with the development of Eisenmenger' syndrome the most advanced form de Pulmonary arterial hypertension associated with congenital heart disease. The prevalence of Pulmonary arterial hypertension associated with CHD has fallen in developed countries in recent years that is not yet achieved in developing countries therefore diagnosed late as lack of hospital infrastructure and human resources for the care of patients with CHD. With the development of targeted medical treatments for pulmonary arterial hypertension, the concept of a combined medical and interventional/surgical approach for patients with Pulmonary arterial hypertension associated with CHD is a reality. We need to know the pathophysiological factors involved as well as a careful evaluation to determine the best therapeutic strategy.

[Management of acute pulmonary thromboembolism]. / Tratamiento de tromboembolia pulmonar aguda.

Acute pulmonary embolism (APE) is considered a cardiovascular emergency and is one of the most important causes of morbidity and mortality in hospitalized patients. Pulmonary embolism diagnosis has to be made early in the course of the disease and its management installed immediately. Pulmonary embolism management includes hemodynamic support, anticoagulation, thrombolysis and embolectomy. We present an overview of the treatment of APE.

Tratamiento de tromboembolia pulmonar aguda / Management of acute pulmonary thromboembolism

La tromboembolia pulmonar (TEP) es considerada como una urgencia cardiovascular, representa una de las principales causas de morbilidad y mortalidad en pacientes hospitalizados. El diagnóstico debe realizarse lo más tempranamente posible, y su tratamiento instaurarse de manera inmediata. El manejo de la embolia pulmonar aguda, incluye medidas de soporte, apoyo hemodinámico, utilización de anticoagulantes y en el caso del paciente inestable, trombólisis o embolectomía. En el presente artículo, se revisan las generalidades en el tratamiento de los pacientes con TEP.

Acute pulmonary embolism (APE) is considered a cardiovascular emergency and is one of the most important causes of morbidity and mortality in hospitalized patients. Pulmonary embolism diagnosis has to be made early in the course of the disease and its management installed immediately. Pulmonary embolism management includes hemodynamic support, anticoagulation, thrombolysis and embolectomy. We present an overview of the treatment of APE.

Primera ablación por radiofrecuencia de un flutter auricular / The first radiofrequency catheter ablation for an atrial flutter

La ablación por radiofrecuencia (RF) ha revolucionado el tratamiento de los pacientes con taquicardia supraventricular, ya sea generada por un mecanismo de reentrada en el nodo aurículoventricular o por la presencia de una conexión accesoria aurículoventricular. En los pacientes en los que el sustrato de la taquicardia está confinado en las aurículas y en los que la arritmia o la respuesta ventricular no puedan ser controladas con medicamentos, la ablación por catéter del Haz de His ofrece una opción a considerar. Sin embargo, esta modalidad de tratamiento obliga al implante de un marcapaso permanente sin hacer absolutamente nada por reestablecer la fisiología normal de las aurículas. Por otra parte, el manejo médico de las taquiarritmias auriculares puede ser difícil, en particular después de una cirugía cardiovascular por cardiopatía congénita, pudiendo ser una causa significante de morbi-mortalidad, además de los importantes efectos secundarios producidos por la utilización de medicamentos. Este manuscrito presenta la primera experiencia con éxito en la ciudad capital en la que se realizó ablación por radiofrecuencia de un Flutter (Aleteo) Auricular (FA) posterior al estudio electrofisiológico. Esta experiencia permite afirmar que este método debe ser considerado como una potencial cura para los pacientes con arritmias auriculares, tomando en cosideración la experiencia del operador y del laboratorio de electrofisiología, así como la incidencia de recurrencia de este tipo de patología

Uso de prótesis vasculares coronarias en el tratamiento de la cardiopatía isquémica: Estudio prospectivo con seguimientos clínico y angiográfico predominantemente en lesiones de novo / Use of coronary vascular prothesis in the treatment of ischemic cardiopathy:Prospective study with clinical following and angiography mainly in novo lesions

La angioplastia transluminal constituye un método aceptado para el tratamiento de la arterioesclerosis coronaria desde 1977, con las ventajas de practicarse bajo anestesia local y tener una estadía intrahospitalaria corta; sin embargo, ha encontrado 2 dificultades en su desarrollo, la reestenosis y la oclusión por disección, por lo que se diseñó un método complementario a la angioplastia convencional, el cual consiste en un refuerzo metálico tubular que mantiene permeable al vaso y estabiliza los fragmentos fracturados de la placa ateroesclerótica. Se presentan 66 pacientes a quienes les fueron implantadas 70 prótesis endocoronarias PalmazSchatz desde el 01/09/91 al 21/12/93, en los siguientes segmentos arteriales coronarios: tronco principal izquierdo, 1 caso (1,4 por ciento ); descendente anterior 25 (35,7 por ciento ); coronaria derecha 31 (44,3 por ciento ); circunfleja 7 (10 por ciento ); puentes venosos 6 (8,6 por ciento ). A cinco pacientes se les implantaron 2 prótesis en el mismo vaso y a otros dos pacientes 2 en 2 vasos distintos. Las indicaciones de acuerdo al estado de las lesiones a ser tratadas fueron: lesiones no tratadas previamente, "de novo", 55 (78,6 por ciento ); lesiones previamente dilatadas, reestenosis, 8 (11,4 por ciento ); disección aguda durante angioplastia convencional, 1 (1,4 por ciento ), resultado subóptimo durante angioplastia convencional 6 (8,6 por ciento ). Seguimiento clínico. Se pudo seguir clínicamente a todos los pacientes; antes del implante, 52 (78,8 por ciento ) presentaban angor II-IV y 48 de los 55 pacientes tratados antes de 6 meses (87 por ciento ) estaban en clase I-II (p<0,001). Seguimiento angiográfico cuantificado. De las variables angiográficas determinadas lo más importante fue el diámetro mínimo, la menor dimensión de la estenosis, como el pricipal determinante de la reserva de flujo coronario. Este parámetro se midió antes e inmediatamente después en 55 pacientes (83,3 por ciento ), media 0,9ñ0,39 vs 3,03ñ0,41 mm (p<0,0001). En 25 pacientes, 48 por ciento de los que tenían 6 meses o más del implante se determinó antes, inmediatamente después y posteriormente (6,2ñ1,4 meses), media 0,82ñ0,35vs 2,99ñ0,42vs2,14ñ0,8mm (p<0,0001) entre sí. Cuatro de 28 pacientes en quienes se midió el por ciento de estenosis media en el seguimiento presentaron >50 por ciento (reestenosis de 13 por ciento ) con evidencia de isquemia miocárdica; 3 fueron redilatados y 1 fue revascularizado quirúrgicamente. Complicaciones. 4 pacientes (6,1 por ciento ) presentaron complicaciones hemorrágicas y 1, trombosis de la prótesis, resuelto con trombolisis intracoronaria y redilatación. Se concluye que en pacientes seleccionados la implantación de prótesis coronarias en nuestro medio ofrece una nueva alternativa al tratamiento de arteroesclerosis coronaria con baja incidencia de complicaciones. La alta proporción de pacientes con "lesiones de novo" (78,6 por ciento ) puede explicar la baja incidencia de reestenosis en este estudio (13 por ciento )