The role of pulmonary pressure/cardiac index to identify pulmonary hemodynamic responders to acute oxygen breathing pulmonary hypertension COPD patients / La utilidad de la relación presión arterial pulmonar - índice cardiaco para identificar respondedores hemodinámicos a la administración aguda de oxígeno en sujetos con enfermedad pulmonar obstructiva crónica e hipertensión pulmonar

Objectives: We sought to analyze exercise-derived mean pulmonary artery pressure (Mpap) - cardiac index (CI) - relationship to expand the concepts regarding its nature and to better identify pulmonary hemodynamic responders to acute oxygen breathing (AOB - 99.5%) in pulmonary hypertension (PH) - COPD patients. Methods: mPAP/CI and extrapolated pressure (Pext) to zero flow were obtained breathing room air (BRA) and under AOB - 99.5% in 40 stable COPD patients with rest and exercise PH. Hemodynamic characteristics were analyzed for the entire cohort and separate for cases those with resting < or > 30 mmHg mPAP (cohort - A and B, respectively). Results: mPAP/CI abnormal location, slope (Sp: 5.77; 95% CI: 5.02 - 6.52 mmHg/L min/m²) and Pext values (15.8 mmHg) were associated with hypoxemia/decreased mixed venous - PO2 and lung mechanics abnormalities. Hemodynamic conditions that did not change for Sp (5.47; 95% CI: 3.64 - 7.3 mmHg/L min/m², p = 0.4) and Pext (15.7 mmHg, p = 0.2) associated with a mPAP/CI significantly decrease in parallel during AOB - 99.5%. For cohort - A, an average-mPAP decline (12.3 mmHg, p <0.004) associated with a slope decrease (from 6.02; 95% CI: 4.04 - 8 to 4.3; 95% CI: 4.11 - 4.49 mmHg/L min/m², (p <0.008), mPAP/CI - 95% CI down-ward displacement and Pext decrease (from 8.58 ± 3 to 4.7 ± 1.4 mmHg, p <0.01) in relation to BRA were observed. For cohort-B, average-mPAP and mPAP/CI - 95% CI location did not change, Sp show a trend to decrease (p = 0.08) and Pext significantly increase (from 12 ± 2.9 to 20.6 ± 4.9 mmHg, p <0.03) in relation to BRA. Under AOB - 99.5%, significant differences for mPAP/ CI - 95% CI location, average-mPAP (A: 19.5 ± 6 vs. B: 41.2 ± 11.5 mmHg, p <0.001) and Pext (A: 4.7 ± 1.4 vs. B: 20.6 ± 4.9 mmHg, p <0.001), without Sp change between cohorts A and B were documented. Conclusions: When exercise derived mPAP/CI is analyzed, valuable information for linear-pulmonary vascular resistance - (LPVR) could be obtained for PH - COPD patients. mPAP/CI abnormalities not always reflect "pure arteriolar" increased LPVR for all PH-COPD patients. Hemodynamic benefit on the pulmonary circulation and right ventricular afterload could be expected with long-term oxygen therapy in resting <30 mmHg mPAP-PH-COPD patients.

Objetivos: En esta investigación clínica-hemodinámica, analizamos la relación que se establece entre la presión arterial pulmonar media (PAPm) con la del índice cardiaco (IC), obtenida durante el ejercicio, con miras a expandir los conceptos relacionados con su propia naturaleza. Con ello, tratar de identificar mejor a los sujetos portadores de EPOC que se han caracterizado por ser respondedores durante la administración aguda de oxígeno (AAO2 - 99.5%). Métodos: Se obtuvieron la PAPm/IC y la presión extrapolada a cero flujo (Pext = bo)en 40 sujetos con EPOC y portadores de hipertensión pulmonar (HP) clínicamente estables, respirando aire ambiental (RAA) y bajo la influencia de la AAO2 - 99.5% en las condiciones de reposo y durante el ejercicio. Las características hemodinámicas se analizaron para toda la cohorte y para aquellos sujetos con PAPm en resposo < o > de 30 mmHg (Cohorte A y B, respectivamente). Resultados: La ubicación anormal de la PAPm/IC, de la pendiente (Sp: 5.77; 95% IC: 5.02 - 6.52 mmHg/L min/m²) y la de los valores para Pext (15.8 mmHg) se asociaron con: hipoxemia/ disminución de la presión venosa mezclada del O2, así como con anormalidades de la mecánica pulmonar. Condiciones hemodinámicas que no se modificaron para la Sp (5.47; 95% IC: 3.64 - 7.3 mmHg/L min/m², p = 0.4) y la Pext (15.7 mmHg, p = 0.2); sin embargo, sí se vieron asociadas a una disminución significativa en paralelo de la PAPm/IC durante la AAO2 99.5%. Observaciones hemodinámicas que para la cohorte A, se caracterizaron por una reducción de la PAPm promedio (12.3 mmHg, p <0.004), por una disminución de la Sp de 6.02; 95% CI: 4.04 - 8 a 4.3; 95% CI: 4.11 - 4.49 mmHg/L min/m², (p <0.008) y por el descenso de Pext de 8.58 ± 3 a 4.7 ± 1.4 mmHg, p <0.01, al compararse con las documentadas RAA. En cambio, para la cohorte B, la PAPm promedio y la PAPm/IC no se modificaron, Sp mostró sólo tendencia a disminuir (p = 0.08) y Pext aumento de 12 ± 2.9 a 20.6 ± 4.9 mmHg, (p <0.03) en relación a las registradas RAA. Bajo la AAO2 - 99.5%, se observaron diferencias significativas para la PAPm/ IC - 95% IC en su localización, para la PAPm promedio (A: 19.5 ± 6 vs. B: 41.2 ± 11.5 mmHg, p <0.001) y Pext (A: 4.7 ± 1.4 vs. B: 20.6 ± 4.9 mmHg, p <0.001) y sin cambios en la Sp, entre la cohorte A y la B. Conclusiones: Cuando se analiza la PAPm/IC, se obtiene información que es valiosa para interpretar la resistencia vascular pulmonar linear en sujetos con EPOC e H P. Sin embargo, las anormalidades de la PAPm/IC, no necesariamente reflejan aumento exclusivo de la resistencia arteriolar pulmonar para sujetos con EPOC e H P. De acuerdo con las observaciones agudas de este estudio, posiblemente solo sea de esperarse beneficio con la oxigenoterapia a largo plazo sobre la circulación pulmonar y la post-carga del ventrículo derecho, para aquellos portadores de EPOC e HP cuando la PAPm en el reposo sea <30 mmHg.

Pulmonary embolism as a cause of death in patients with heart disease: an autopsy study.

STUDY OBJECTIVE: To establish the prevalence of pulmonary embolism (PE) in autopsy material at a tertiary cardiac referral center and its importance as a cause of death in patients with heart disease (HD). DESIGN: Case series. SETTING: National Heart Institute, Mexico City. PATIENTS: One thousand thirty-two patients who died at our institution from 1985 to 1994 in whom an autopsy study was performed. MEASUREMENTS AND RESULTS: Of the 1,032 autopsies reviewed, 231 cases (24.4%) of PE were found; 100 of these patients had a diagnosis of massive PE. Massive PE (obstruction of either of the main pulmonary arteries or more than two lobar arteries) was found to be the third cause of death in this HD population. By age-group distribution, the global prevalence of massive events was higher in patients < 10 years old. Clinical suspicion (premortem) was raised in only 18% of the cases. CONCLUSIONS: PE was a frequent cause of morbidity and mortality in patients with HD who underwent autopsies. The incidence of massive PE was high in children.