10. Etiología de la HAP tiene impacto en sobrevida 0 1 2 3 4 5 Mc Laughlin ACCP guidelines CHEST 2004 - Galiè ESC guidelines EHJ 2004 % sobrevida 1 0.8 0.6 0.4 0.2 0 ECC iPAH ECV VIH
11. HAP: una enfermedad de evolución rápida I Preclínica/ Sin síntomas II Sintomática / Estable III -IV Progresión / Declive Nivel Tiempo Presión pulmonar Gasto cardíaco Años Meses Ventana terapéutica Función de VD
13. EC ONS ONítrico GMPc RELAJACIÓN ANTI-PROLIFERACIÓN PGI2 AMPc ENDOTELINA-1 CONTRACCIÓN PROLIFERACIÓN ET A ET B G I Pre-pro-ET ET ET B ECE L-arginina L-citrulina Ácido araquidónico PGI 2 PGI 2 -S endopeptidasa SMC VASODILATADORES VASOCONSTRICTORES
59. EC ONS ONítrico GMPc RELAJACIÓN ANTI-PROLIFERACIÓN PGI2 AMPc ENDOTELINA-1 CONTRACCIÓN PROLIFERACIÓN ET A ET B G I Pre-pro-ET ET ET B ECE L-arginina L-citrulina Ácido araquidónico PGI 2 PGI 2 -S endopeptidasa SMC VASODILATADORES VASOCONSTRICTORES
63. HAP Idiopática Familiar Relacionada Asociada con PVOD/HVCP* Hipertensión venosa pulm Falla cardíaca izquierda Enf. Valvular cavidades izq HAP asociada con enf. pulmonar y/o hipoxemia HAP debida a TEC Obstrucción proximal Obstrucción distal Misceláneos (Bloq canales Ca:BCC) Prostanoides, ARE, Inhibidores PDE5 ? * Mucho cuidado en este grupo Diuréticos, nitratos, BCC, BetaB, IECAs O2 crónico Tromboendarterectomía Similar a iHAP? Sin recomendaciones
64.
65.
Editor's Notes
PAH is characterized by remodeling of precapillary PA … The effect of this remodeling is to increase progressively PAP and PVR. At a certain point heart will fail and cardiac output will decrease. This will cause a rapid decrease in patient exercise capacity.
Endothelium injury is probably at the origin of an imbalance between vasodilators who are decreased and vasocontrictors who are increased in patients with PH. However these vasoactive agents are also very active on vascular cell proliferation. PGI2 and NO are anti-proliferative agents and endothelin …
What is happening with the pulmonary vessels? The initial hypothesis was that repeated vasocontriction would lead to SMC hypertrophy and vessel wall remodeling. However, there is now evidence of early vascular remodeling. The current hypothesis is that PH is the consequence of combined genetic susceptibility and triggering factors causing vascular injury as high flow (Eisenmenger) and inflammation (CTD)
Figure 2. The Cumulative Incidence of CTPH after a First Episode of Pulmonary Embolism without Prior Deep-Vein Thrombosis.
Also with echo-Doppler
Endothelium injury is probably at the origin of an imbalance between vasodilators who are decreased and vasocontrictors who are increased in patients with PH. However these vasoactive agents are also very active on vascular cell proliferation. PGI2 and NO are anti-proliferative agents and endothelin …
What is happening with the pulmonary vessels? The initial hypothesis was that repeated vasocontriction would lead to SMC hypertrophy and vessel wall remodeling. However, there is now evidence of early vascular remodeling. The current hypothesis is that PH is the consequence of combined genetic susceptibility and triggering factors causing vascular injury as high flow (Eisenmenger) and inflammation (CTD)
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