RESUMEN
OBJECTIVES: The flow velocity-pressure gradient (v-dp) relation is clinically used to assess coronary stenoses. This in vitro study aimed to investigate the ability to determine the impact of each individual stenosis in the setting of two consecutive stenoses, the effect of variable stenosis reference diameters and the impact of one or two wires in a stenosis, on the v-dp relation. METHODS: The model consisted of a reservoir and different sized tubes and stenoses. Pressure gradient and flow velocity were assessed with a pressure and a Doppler wire. By plotting flow velocity and pressure gradient on an X-Y plot, the v-dp relation was determined. RESULTS: The v-dp relation of a proximal stenosis was not influenced by a distal stenosis. The diameter of the segment where flow velocity was measured influenced the v-dp relation. This could be corrected by substituting flow velocity with volume flow. The presence of one or two wires in a stenosis made the v-dp relation substantially steeper. CONCLUSIONS: The v-dp relation can be used to determine the significance of each individual stenosis in arteries with consecutive stenoses, provided that the distance between the stenoses is large enough. The diameter of the segment where flow velocity is measured and the presence of one or two wires substantially affect the v-dp relation. (Neth Heart J 2008;16:156-62.).
RESUMEN
Since systemic sclerosis (SSc) also involves the heart, the aim of the present study was to evaluate possible differences in right ventricular (RV) pump function between SSc-associated pulmonary arterial hypertension (PAH; SScPAH) and idiopathic PAH (IPAH). In 13 limited cutaneous SScPAH and 17 IPAH patients, RV pump function was described using the pump function graph, which relates mean RV pressure ((RV)) and stroke volume index (SVI). Differences in pump function result in shift or rotation of the pump function graph. (RV) and SVI were measured using standard catheterisation. The hypothetical isovolumic (RV) ((RV,iso)) was estimated using a single-beat method. The pump function graph was approximated by a parabola: (RV) = (RV,iso)[1-(SVI/SVI(max))(2)], where SVI(max )is the hypothetical maximal SVI at zero (RV), enabling calculation of SVI(max). There were no differences in SVI and SVI(max). Both (RV) and (RV,iso) were significantly lower in SScPAH than in IPAH ((RV) 30.7+/-8.5 versus 41.2+/-9.4 mmHg; (RV,iso) 43.1+/-12.4 versus 53.5+/-10.0 mmHg). Since higher pressures were found at similar SVI, the difference in the pump function graph results from lower contractility in SScPAH than in IPAH. Right ventricular contractility is lower in systemic sclerosis-associated pulmonary arterial hypertension than in idiopathic pulmonary arterial hypertension.
Asunto(s)
Hipertensión Pulmonar/fisiopatología , Contracción Miocárdica , Esclerodermia Sistémica/fisiopatología , Disfunción Ventricular Derecha/fisiopatología , Adulto , Anciano , Anciano de 80 o más Años , Estudios de Cohortes , Femenino , Hemodinámica , Humanos , Hipertensión Pulmonar/etiología , Masculino , Persona de Mediana Edad , Esclerodermia Sistémica/complicaciones , Volumen Sistólico , Disfunción Ventricular Derecha/diagnósticoAsunto(s)
Hipertensión Pulmonar/tratamiento farmacológico , Piperazinas/uso terapéutico , Vasodilatadores/uso terapéutico , Femenino , Humanos , Hipertensión Pulmonar/sangre , Hipertensión Pulmonar/fisiopatología , Masculino , Péptido Natriurético Encefálico/metabolismo , Fragmentos de Péptidos/metabolismo , Purinas , Citrato de Sildenafil , Sulfonas , Remodelación VentricularAsunto(s)
Vasoespasmo Coronario/etiología , Drenaje/efectos adversos , Mediastino , Complicaciones Posoperatorias/etiología , Angiografía Coronaria/métodos , Vasoespasmo Coronario/diagnóstico por imagen , Drenaje/instrumentación , Femenino , Humanos , Persona de Mediana Edad , Complicaciones Posoperatorias/diagnóstico por imagenRESUMEN
Pulmonary arterial hypertension (PAH) is a disease characterised by an increased pulmonary artery pressure. The precapillary pulmonary arteries show distinct pathobiological changes, i.e. medial hypertrophy, intimal fibrosis, microthrombi and plexiform lesions. Although the pathogenesis is not completely understood, pulmonary vascular proliferation and remodelling, due to a variety of mediators, is believed to play the pathogenetic key role. Genetic research reveals molecular deformities and gene mutations associated with phenotypic PAH. This article covers novel insights into pathobiology, pathogenesis and genes of PAH, which led to a novel classification system and a diagnostic work-up, emanated from the World Health Organisation Symposium on Pulmonary Hypertension in Venice in June 2003.
RESUMEN
Medical therapy for pulmonary arterial hypertension (PAH) focuses on pulmonary vascular remodelling and smooth muscle cell proliferation. This article covers the drugs which are approved or are in sight and the evidence-based treatment strategies that target the different pathobiological pathways, emanated from the World Health Organisation Symposium on Pulmonary Hypertension in Venice, June 2003. In addition we briefly look at the 'Venice consensus' on surgical treatment. In the past five and a half years more than 360 patients were seen for pulmonary hypertension in the Free University Medical Centre (VUmc). Present-day treatment, research studies and novel treatment strategies in the VUmc will be reviewed. Future treatments will be on the basis of insights into pathobiology, pathogenesis and genes in PAH and should focus on drug combinations, which theoretically target different or similar pathobiological pathways.