In a previous article, we reviewed path physiological concepts of right ventricle considering its importance in cardio respiratory diseases and its behavior was compared with left ventricle. Measurement of right ventricular function is complex due to its pre load dependence. Remarkable progress has been developed in methods to measure anatomy and function. Probably a functional definition might include diverse parameters as geometry, hypertrophy, dilatation, contraction, oxygen supply to muscular wall and ejected volume. In the present review, we describe the behavior of right ventricle in different pathologies. In first place, we analyze its behavior in respiratory diseases and afterwards in diseases, which involves pulmonary circulation and left ventricular failure. Our purpose is to stimulate pulmonary physicians and cardiologists in the study of this common entity. A complete description of the diseases, which causes right ventricular failure, goes beyond the limits of this article.

En una publicación previa¹ actualizamos los conceptos fisiopatológicos, que rigen la función del ventrículo derecho (VD), considerando su importancia en enfermedades cardiorespiratorias, y describimos su comportamiento al compararlo con el ventrículo izquierdo (VI). La función del VD es difícil de medir por su alta dependencia de la precarga, sin embargo, ha habido progresos en los métodos para determinar su anatomía y su función. Es probable que la definición de función deba incluir parámetros diversos, como geometría, hipertrofi a, dilatación, contracción, aporte de oxígeno a la pared y volumen eyectado. En la presente revisión describiremos el comportamiento del VD frente a diversas patologías. En primer lugar analizaremos su comportamiento frente a patologías respiratorias y luego frente a patologías que comprometen la circulación pulmonar y la Insuficiencia cardíaca congestiva (ICC). Nuestro propósito es estimular a la comunidad médica de Enfermedades Respiratorias y Cardiología a profundizar en esta entidad común. La descripción completa de cada uno de los cuadros que causan falla cardíaca derecha, sobrepasa los límites de este artículo.

Right ventricle has traditionally been underemphasized considering the amount of information and investigation about the left ventricle, its pathologies and treatments. Old physiological concepts considered right ventricle as a secondary organ without significance in cardiovascular pathology. The scope of respiratory diseases usually deals with heart involvement or cor pulmonale secondary to pulmonary diseases. Nevertheless, the limited availability of cardiac techniques to evaluate right ventricle has restricted the information about its physiological behavior and diseases. In the last five years, a renewed interest in right ventricle provided significative changes in concepts, methods of evaluation and treatment. In this article, we will review recent physiological concepts about right ventricle, based in up-to-date publications on the mechanisms and pathologies in which it is involved. Right ventricle is different to left ventricle in origin, anatomy, function and recovery capacity. His impedance depends on the pulmonary circulation and its involvement in respiratory diseases. left ventricle preload depends on the right ventricle, emphasizing its importance in left heart failure.

El ventrículo derecho (VD) ha sido tradicionalmente poco valorado, al concentrarse la investigación y el tratamiento de la patología cardíaca en el comportamiento del ventrículo izquierdo (VI). Desde antiguo se suponía que la importancia funcional del VD era secundaria y poco determinante. En el ámbito de las Enfermedades Respiratorias, el concepto de falla cardíaca derecha derivada de patología pulmonar o corazón pulmonar, ha estado siempre vigente, sin embargo, la limitación para efectuar las técnicas de estudio cardíaco, mantuvo distante la información disponible sobre el VD. En los últimos cinco años, ha habido un renovado interés en incrementar el conocimiento sobre el VD, produciéndose cambios significativos en lo conceptual, en los métodos de estudio y en las proyecciones de tratamiento. En este artículo revisaremos conceptos fisiopatológicos recientes, basados en publicaciones actualizadas sobre los mecanismos y patologías que comprometen el VD. Esta cavidad es marcadamente diferente del VI, tanto en su origen, como en su anatomía, función y capacidad de recuperación. Es tributario de la circulación pulmonar y dependiente de la patología respiratoria, la que es capaz de dañarlo. Además, la precarga del ventrículo izquierdo es de su dependencia, convirtiéndolo en un componente importante de su patología y de su capacidad de respuesta.

Pulmonary arterial hypertension (PAH) is a severe and progressive disease. Invasive hemodynamic study (HS) is required to confirm the diagnosis of PAH and to perform the vasodilator test (VT) with adenosine. Vasodilator acute responders (VAR) may have a sustained benefit with diltiazem. There is not national information regarding these issues. All patients with probable PAH were evaluated with HS and VT. VAR were treated with diltiazem and followed up with functional class score (FC) and 6 minute walk test. After 6 months, a second HS was performed. Results: Between 2003 and 2008, 6/54 (11%) were VAR. All were women, 45 ± 14 years oíd, 4 with idiopathic PAH, 4 in FCIII and 2 in FCII. After two years of treatment, all patients clinically improved. Walked distance significantly increased by 83 and 87 m at month 12 and 24 respectively. Hemodynamic parameters also improved. Therapy with diltiazem is effective in VAR patients supporting the convenience to perform the VT.

La Hipertensión Pulmonar Arterial (HAP) es una entidad grave y progresiva. El estudio hemodinámica (EH) permite certificar el diagnóstico y evaluar la vasorreactividad mediante adenosina. Los pacientes vaso-reactivos podrían responder a terapia con diltiazem. No existe información nacional al respecto. En nuestro programa todo paciente con sospecha de HAP es sometido a EH diagnóstico y de vasorreactividad. Los positivos son tratados con diltiazem y seguidos semestralmente según capacidad funcional (CF) y con test de caminata. Al 6º mes se efectúa un 2º EH. Entre 2003-2008, 6/54 (11%) de los pacientes con HAP fueron vasorreactivos. Todas mujeres, 45 ± 14 años, 4 con HPA idiopática, 4 en CFIII y 2 en CFII. A los 2 años, todos mejoraron clínicamente. La distancia recorrida aumentó significativamente en los meses 12 y 24 en 83 y 87 m respectivamente. Todas las variables hemodinámicas mejoraron. La terapia con diltiazem es efectiva en los pacientes vaso-reactivos lo que justifica usar el test de vasorreactividad.

Pulmonary Arterial Hypertension includes a heterogeneous group of disorders with a common genetic, pathological and hemodinamyc origin. It is characterized by a high pulmonary artery pressure due to a primary vascular disease, as a consequence of genetic and environmental factors. The common pathway is a vascular imbalance towards vasoconstriction and proliferation inside the small vessels. According to the World Health Organization, 2003, Pulmonary Arterial Hypertension is classified as idiopathic, familiar or associated to connective tissue diseases, HIV, drugs, porto-pulmonary hypertension, congenital intracardiac shunts and others. The diagnosis is based in hemodynamics. Echocardiogram is a non invasive and right ventricular catheterization is an invasive diagnostic tool. Follow up is based on a clinical and functional assessment through functional class classification, dyspnea scores and 6-minute walking test. The prognosis is historically devastating but new therapies are changing the natural history of the disease. New treatments have demonstrated improvement in symptoms, hemodynamic profiles and survival. Intravenous, subcutaneous or inhaled prostanoids such as Epoprostenol, Treprostinil or Iloprost respectively have been approved for Pulmonary Arterial Hypertension treatment as well as oral endothelial receptor blockers. They are all considered first line treatments for arterial pulmonary hypertensive patients with even better benefits than lung transplantation. Phosphodiesterase inhibitors (Sildenafil), have been recently approved for the treatment of pulmonary arterial hypertension

Background: Pulmonary Arterial Hypertension is a rare, progressive and devastating disease with severe consequences in quality of life and survival. Aim: A clinical, functional and hemodynamic assessment of patients with pulmonary arterial hypertension and categorization according to severity. Material and methods: Prospective registry of patients with arterial pulmonary hypertension, hemodynamically defined. Clinical evaluation was performed using World Health Organization functional score (I to IV) and Borg dyspnea scale. Six minute walking test, echocardiography and right heart catheterization were used for functional and hemodynamic assessment. Intravenous Adenosine was used to assess vascular reactivity during the hemodynamic evaluation. Results: Twenty nine patients were included (25 women, age range 16-72 years). Pulmonary hypertension was idiopathic in 11, associated to connective tissue disease in seven, associated to congenital heart disease in nine and associated to chronic thromboembolism in two. The mean lapse of symptoms before assessment was 2.9 years and 100% had dyspnea (Borg 5.1). Functional class I, II, III and IV was observed in 0, 5, 21 and 3 patients respectively. Six minutes walking test was 378±113 m. Mean pulmonary pressure was 59.4±12.2 mmHg, cardiac index was 2.57±0.88 and pulmonary vascular resistance index: 1798.4±855 (dyne.sec)/cm5. Nine patients had a mean pulmonary arterial pressure >55 mmHg and a cardiac index <2.1, considered as bad prognosis criteria. Adenosine test was positive in 17%. Conclusions: This group of patients with Pulmonary Arterial Hypertension was mainly conformed by young females, with a moderate to severe disease