Polymorphisms C677T and A1298C of MTHFR Gene: Homocysteine Levels and Prothrombotic Biomarkers in Coronary and Pulmonary Thromboembolic Disease.

The activity of the enzyme methylenetetrahydrofolate reductase (MTHFR) determines homocysteine (Hcy) levels, and polymorphisms in its gene affect the activity of the enzyme. Changes in the enzyme's activity may lead to a higher susceptibility to develop arterial and venous thromboembolic disease. The aim was to analyze the relationship between the C677T and A1298C polymorphisms of MTHFR, Hcy levels, and prothrombotic biomarkers in pulmonary embolism (PE) and acute myocardial ischemia (AMI). Clinical files of patients with thromboembolic diseases having complete data and whose doctor had requested an assay to determine the polymorphisms of the MTHFR gene, Hcy levels, and prothrombotic biomarkers were studied to search for the correlation between mutations of the MTHFR gene and Hcy levels in the different diseases. We included 334 files: 158 were from women and 176 from men (51 [19 SD] years). Sixty-three percent have had thrombosis, 8% AMI, and 31% PE. Patients with thrombosis had elevated frequency of the C677T polymorphism. The CC genotype was higher than the TT genotype ( P = .003) and CT versus the TT ( P = .009). In patients with PE, the CC genotype was higher than the TT genotype ( P = .038). Pulmonary embolism with massive and submassive events had predominant genotypes 677 TT ( P = .003) and the AA 1298 ( P = .017). Elevated Hcy levels in the presence of the T allele in the C677T gene and of the A allele in the A1298C gene are associated with AMI and massive and submassive PE.

Prevalence of Congenital Heart Disease and Pulmonary Hypertension in Down's Syndrome: An Echocardiographic Study.

BACKGROUND: Down's syndrome (DS) is a genetic anomaly, which undergoes increased morbidity and mortality when associated with congenital heart disease (CHD). The aims of the study were to determine the prevalence of CHD and pulmonary hypertension (PH) in DS. METHODS: One hundred twenty-seven patients with DS living in Mexico City were evaluated by physical exam, electrocardiogram and echocardiogram. RESULTS: CHD was found in 40%. In 80% (n = 102) PH was present [systolic pulmonary artery pressure (SPAP) of 47 ± 19 mm Hg and mean pulmonary artery pressure (MPAP) of 32 ± 11 mm Hg]. Patients with CHD and PH were classified as having 1) no shunt (n = 18) with SPAP of 37 ± 9 mm Hg and MPAP of 25 ± 6 mm Hg and 2) with shunt (n = 26) with PASP of 57 ± 29 mm Hg and MPAP of 38 ± 19 mm Hg (p ≤ 0.001). In those without CHD or with CHD without shunt (n = 76), SPAP was 37 ± 19 mm Hg and the MPAP 25 ± 6 mm Hg. The prevalence of PH in DS was 5.9% at one year and 15% at 10 years. The odds ratio of PH in DS with CHD was 7.3 vs. 3 without CHD. CONCLUSION: DS has a high prevalence of CHD and PH. PH prevalence increases when it is associated with CHD. The pathophysiology of PH in DS without CHD should be studied in the near future. Echocardiography is an indispensible tool for evaluation of DS.

Left atrial cardiac myxoma. Two unusual cases studied by 3D echocardiography.

We describe two patients with cardiac tumors in the left atrium, which by their association and histopathological lineage, are extremely rare. The clinical, echocardiographic and pathological findings were analysed. The first case was asymptomatic, but in the control studies of colon adenocarcinoma, an intracardiac mass was found by chest computed tomography (CT). A transesophageal 3D (TEE 3D) echocardiogram revealed a left atrial mass attached to the interatrial septum. The mass was surgically removed and histopathologic findings showed myxoma. The second had history of chronic intermittent diarrhea. A thoraco-abdominal CT showed a left atrial mass. The TEE 3D echocardiography reported an intracardiac mass attached to the roof of the left atrium. The mass was surgically removed and the histopathogical findings showed a myxoma, with dystrophic ossification and extramedullary hematopoiesis. TEE 3D echocardiography provides an acceptable morphological characterisation of intracardiac masses, with good correlation with surgery.

Primary reperfusion in acute right ventricular infarction: An observational study.

AIM: To investigate the impact of primary reperfusion therapy (RT) on early and late mortality in acute right ventricular infarction (RVI). METHODS: RVI patients (n = 679) were prospectively classified as without right ventricular failure (RVF) (class A, n = 425, 64%), with RVF (class B, n = 158, 24%) or with cardiogenic shock (CS) (class C, n = 96, 12%). Of the 679 patients, 148 (21.7%) were considered to be eligible for thrombolytic therapy (TT) and 351 (51.6%) for primary percutaneous coronary intervention (PPCI). TIMI 3-flow by TT was achieved for A, B and C RVI class in 65%, 64% and 0%, respectively and with PPCI in 93%, 91% and 87%, respectively. RESULTS: For class A without RT, the mortality rate was 7.9%, with TT was reduced to 4.4% (P < 0.01) and with PPCI to 3.2% (P < 0.01). Considering TT vs PPCI, PPCI was superior (P < 0.05). For class B without RT the mortality was 27%, decreased to 13% with TT (P < 0.01) and to 8.3% with PPCI (P < 0.01). In a TT and PPCI comparison, PPCI was superior (P < 0.01). For class C without RT the in-hospital mortality was 80%, with TT was 100% and with PPCI, the rate decreased to 44% (P < 0.01). At 8 years, the mortality rate without RT for class A was 32%, for class B was 48% and for class C was 85%. When PPCI was successful, the long-term mortality was lower than previously reported for the 3 RVI classes (A: 21%, B: 38%, C: 70%; P < 0.001). CONCLUSION: PPCI is superior to TT and reduces short/long-term mortality for all RVI categories. RVI CS patients should be encouraged to undergo PPCI at a specialized center.

The role of pulmonary pressure/cardiac index to identify pulmonary hemodynamic responders to acute oxygen breathing pulmonary hypertension COPD patients.

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 averagemPAP 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 linearpulmonary 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.

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.

Left and right ventricular power: outputs are the strongest hemodynamic correlates to allow identification of acute responders to vasodilator treatment in idiopathic pulmonary arterial hypertension.

INTRODUCTION: Despite the prognostic importance of traditionally derived measurements, the significance of right heart catheterization (RHC) remains controversial. Thus, a continued search for hemodynamic markers that define better responsive patients is required. Since, right ventricular failure is the most fatal pathway, right (RVPO) and left (LVPO) ventricular power output are parameters that could provide input for a better understanding of the hemodynamics involved in idiopathic pulmonary artery hypertension (IPAH). METHOD: We retrospectively analyzed how demographics and outcome correlate with hemodynamics to identify responders among IPAH patients. RESULTS: Ninety patients fulfilled the following criteria for inclusion in this study: (1) complete RHC at baseline; (2) an acute evaluation for vasodilators (AEFV, including a positive response, that is, an increase in CO, a decrease in both mPAP and pulmonary vascular resistance (≥ 20% from baseline, respectively); and (3) a long-term follow-up under accepted IPAH treatments. If RVPO decreased (p < 0.001) and LVPO increased (p < 0.012) during AEFV, it is considered that these findings reinforce our ability to identify responders; that is, patients that remained as responders after 6.4 ± 3 years under nifedipine treatment (37.7% of the studied IPAH population). After multivariate analysis, age, RVPO, and LVPO remained as independent variables (OR = 0.927, 95%CI: 0.87-0.98, p = 0.01; OR = 0.114, 95%CI: 0.00-0.91, p = 0.045; and OR = 171.5, 95% CI: 5.3-549, p = 0.004, respectively) when estimating the probability of being a responder. On this basis, an equation was derived to identify responders among IPAH patients, where the probability of being a responder = 1.0196-0.0631 (age) - 4.7693 (RVPO) + 3.8152 (LVPO), ROC: 0.76, 95% CI: 0.63-0.89; p = 0.001. CONCLUSION: based on the proposed equation, LVPO and RVPO could be used for the identification of responders among IPAH patients.

Left and right ventricular power: outputs are the strongest hemodynamic correlates to allow identification of acute responders to vasodilator treatment in idiopathic pulmonary arterial hypertension / El poder del ventrículo derecho y del izquierdo: son parámetros hemodinámicos que correlacionan con la posibilidad de ser respondedor durante el reto agudo con vasodilatadores en la hipertensión arterial pulmonar idiopática

Introduction: Despite the prognostic importance of traditionally derived measurements, the significance of right heart catheterization (RHC) remains controversial. Thus, a continued search for hemodynamic markers that define better responsive patients is required. Since, right ventricular failure is the most fatal pathway, right (RVPO) and left (LVPO) ventricular power output are parameters that could provide input for a better understanding of the hemodynamics involved in idiopathic pulmonary artery hypertension (IPAH). Method: We retrospectively analyzed how demographics and outcome correlate with hemodynamics to identify responders among IPAH patients. Results: Ninety patients fulfilled the following criteria for inclusion in this study: (1) complete RHC at baseline; (2) an acute evaluation for vasodilators (AEFV, including a positive response, that is, an increase in CO, a decrease in both mPAP and pulmonary vascular resistance ≥ 20% from baseline, respectively); and (3) a long-term follow-up under accepted IPAH treatments. If RVPO decreased (p < 0.001) and LVPO increased (p < 0.012) during AEFV, it is considered that these findings reinforce our ability to identify responders; that is, patients that remained as responders after 6.4 ± 3 years under nifedipine treatment (37.7% of the studied IPAH population). After multivariate analysis, age, RVPO, and LVPO remained as independent variables (OR = 0.927, 95%CI: 0.87-0.98, p = 0.01; OR = 0.114, 95%CI: 0.00-0.91, p = 0.045; and OR = 171.5, 95% CI: 5.3-549, p = 0.004, respectively) when estimating the probability of being a responder. On this basis, an equation was derived to identify responders among IPAH patients, where the probability of being a responder = 1.0196-0.0631 (age) - 4.7693 (RVPO) + 3.8152 (LVPO), ROC: 0.76, 95% CI: 0.63-0.89; p = 0.001. Conclusion:based on the proposed equation, LVPO and RVPO could be used for the identification of responders among IPAH patients.

Introducción: A pesar de la importancia y del significado pronóstico que tienen las mediciones directas y las derivadas del cateterismo cardiaco derecho, éstas permanecen hasta el día de hoy en el terreno académico de la controversia. Por lo tanto, se requiere la continua búsqueda de marcadores hemodinámicos para estratificar a los enfermos con hipertensión arterial pulmonar idiopática. Particularmente, cuando la disfunción contráctil del ventrículo derecho es la vía final más común de esta patología. En esta circunstancia, la determinación del poder del ventrículo derecho y del ventrículo izquierdo representa parámetros que pudieran ser de utilidad para lograr un mejor entendimiento en la hemodinámica de la hipertensión arterial pulmonar idiopática. Método: De manera retrospectiva, analizamos los aspectos demográficos, los hemodinámicos y la sobrevivencia, y si éstos se vieron asociados a la posibilidad de ser enfermos respondedores entre los portadores de hipertensión arterial pulmonar idiopática. Resultados: Noventa enfermos llenaron los siguientes criterios para ser incluidos en el estudio: 1. Contar con cateterismo cardiaco derecho basal; 2. Tener valoración aguda con adenosina, en donde quedó definida una respuesta "positiva aguda" como: aumento del gasto cardíaco, disminución de la presión arterial pulmonar media y de la resistencia vascular pulmonar calculada (≥ 20% de la basal, respectivamente) y; 3. Contar con un seguimiento a largo plazo bajo la influencia de los tratamientos modernos aceptados para enfermos con hipertensión arterial pulmonar idiopática. Sí, el poder del ventrículo derecho disminuyó (p < 0.001) y el poder ventrículo izquierdo aumentó (p < 0.012) durante el reto vasodilatador agudo se consideró que éstos hallazgos reforzaban la habilidad para detectar a los sujetos respondedores con hipertensión arterial pulmonar idiopática; población de enfermos que guardó ese comportamiento hemodinámico durante 6.4 ± 3 años bajo la influencia de nifedipina (37% de la totalidad de la población con hipertensión arterial pulmonar idiopática). Después de efectuar un análisis multivariado, la edad, el poder del ventrículo derecho y del ventrículo izquierdo permanecieron como variables independientes (OR = 0.927, 95%IC: 0.87-0.98, p = 0.01; OR = 0.114, 95%IC: 0.00-0.91, p = 0.045; y OR = 171.5, 95%IC: 5.3-549, p = 0.004, respectivamente) para ser considerados "respondedores". Como resultado, se derivó una ecuación donde la probabilidad de ser respondedor = 1.0196-0.0631 (edad) - 4.7693 (poder del ventrículo derecho) + 3.8152 (poder del ventrículo izquierdo), ROC: 0.76, 95%CI: 0.63 - 0.89; p = 0.001. Conclusión: Con fundamento en los hallazgos de este estudio, la ecuación propuesta, el poder del ventrículo derecho y el ventrículo izquierdo pueden ser utilizados para identificar "respondedores" entre los enfermos con hipertensión arterial pulmonar idiopática.

[Pressure-flow relationships interpretation in idiopathic pulmonary arterial hypertension]. / Interpretación de la relación presión-flujo en la hipertensión arterial pulmonar idiopática.

OBJECTIVES: We analyze exercise-derived mean pulmonary artery pressure/cardiac index relationship to expand the concepts regarding its nature and to better identify "responders" in idiopathic pulmonary arterial hypertension patients. METHODS: Mean pulmonary artery pressure/cardiac index relationship and extrapolated pressure to zero flow were obtained in 40 patients' breathing room air, oxygen 99.5% and hydralazine. The hemodynamic characteristics were analyzed for the cohort and separate for responders (n = 20) and non responders (n = 20) according to the acute response to vasodilator. We tested this previous criteria versus the Task Force on diagnosis and treatment prescribed by the European Society of Cardiology. RESULTS: The mean pulmonary arterial pressure-flow diagram of the total cohort (p < 0.01). No alterations in gas exchange or lung mechanics. For patients responders versus non-responders, the slope was abnormal 2.2(95%CI: 1.1-3.3) vs 5.89 (95% CI: 4.69 - 7.11), mmHg/L min/m2 and increased extrapolated pressure to zero flow (38.2 + 7.5 to 66.3 + 7.5 mmHg, p < 0.01). Without difference with oxygen 99.5%. With vasodilator effect, mean pulmonary arterial pressure decreased (52.1+9.5 a 40 + 5.5 mm Hg, p< 0.01) versus it did not change (96.2 + 8.5 vs 90 + 7.5 mmHg, p = 0.3), slope 1.15 (95% CI: 0.68 - 1.62) vs. 1.28 (95% CI: 0.78-1.78) mmHg/L min/m2, the extrapolated pressure to zero flow did not change (69.4 + 7.8 a 85.1 + 8.5 mmHg), p < 0.01 compared to control. In non-responders with vasodilator, mean pulmonary arterial pressure/cardiac index (90 + 7.5 mmHg, pendiente: 1.28, 95%IC: 0.78 - 1.78 mmHg/L min/m2) was different between responders 40 mm Hg mean pulmonary arterial pressure. Pressure were 34 + 3 vs 45 + 4 mm Hg and slopes 1.14 (95%IC: 0.67 - 1.61 vs 2.22 (95%IC: 1.35 - 3.09 mm Hg/L min/m2) p < 0.01 respectively. CONCLUSIONS: Abnormalities of the mean pulmonary arterial pressure/cardiac index relationship exercise-derived seems to reflect "mainly arteriolar" increased lineal pulmonary vascular resistance in idiopathic pulmonary arterial hypertension patients. Both acute vasodilator response criteria are useful to identify responders and not responders in this patient population.

Interpretación de la relación presión-flujo en la hipertensión arterial pulmonar idiopática / Pressure-flow relationships interpretation in idiopathic pulmonary arterial hypertension

Objetivo: Conocer más de la relación presión arterial pulmonar media/índice cardiaco y sus perfiles en enfermos con hipertensión arterial pulmonar idiopática. Métodos: La presión arterial pulmonar media/índice cardiaco y la presión extrapolada al eje de cero flujo se obtuvo en 40 enfermos respirando aire ambiente, oxígeno 99.5% e hidralazina. Se obtuvieron dos grupos de acuerdo a criterios de "respuesta vasodilatadora aguda", respondedores (n = 20) y no respondedores (n = 20). Se analizó este criterio versus el propuesto por la Task Force de la Sociedad Europea de Cardiología en la población respondedora. Resultados: La presión arterial pulmonar media/Índice cardiaco se ubicó de forma anormal en el diagrama de presión-flujo de la cohorte total, (p < 0.01). Sin alteraciones en el intercambio gaseoso o mecánica pulmonar. Para los enfermos respondedores versus no respondedores, la pendiente fue anormal 2.2 (95%IC:1.1-3.3) vs. 5.89 (95%IC:4.69-7.11) mm Hg/L min/m² e incremento de la presión extrapolada al eje de cero flujo (38.2 ± 7.5 a 66.3 ± 7.5 mm Hg, p < 0.01). Sin diferencias con oxígeno al 99.5%. Con vasodilatador, la presión arterial pulmonar media disminuyó (52.1 ± 9.5 a 40 ± 5.5 mm Hg, p < 0.01) vs. no se modificó (96.2 ± 8.5 vs. 90 ± 7.5 mmHg, p = 0.3), pendiente 1.15 (95%IC:0.68-1.62) vs. 1.28 (95%IC:0.78-1.78) mmHg/Lmin/m², la presión extrapolada al eje de cero flujo no cambió vs. incrementó (69.4 ± 7.8 a 85.1 ± 8.5 mm Hg, p < 0.01), en relación al control. En no respondedores con vasodilatador, la presión arterial pulmonar media/índice cardiaco (90 ± 7.5 mmHg, pendiente:1.28; 95%IC: 0.78 - 1.78 mm Hg/L min/m²) fue diferente al comparar respondedores con menor o mayor de 40 mm Hg de presión arterial pulmonar media. Presiones 34 ± 3 vs. 45 ± 4 mm Hg y pendientes 1.14 (95%IC: 0.67 -1.61 vs. 2.22 (95%IC: 1.35 - 3.09 mm Hg/L min/m²), respectivamente p < 0.01. Conclusiones: Las anormalidades de la relación presión arterial pulmonar media/Índice cardiaco reflejan el incremento de las resistencias vasculares pulmonares reales a nivel arteriolar pulmonar en enfermos con hipertensión arterial pulmonar idiopática. Ambos criterios de respuesta vasodilatadora aguda son de utilidad para identificar respondedores y no, en esta población de enfermos.

Objectives: We analyze exercise-derived mean pulmonary artery pressure/cardiac index relationship to expand the concepts regarding its nature and to better identify "responders" in idiopathic pulmonary arterial hypertension patients. Methods: Mean pulmonary artery pressure/cardiac index relationship and extrapolated pressure to zero flow were obtained in 40 patients' breathing room air, oxygen 99.5% and hydralazine. The hemodynamic characteristics were analyzed for the cohort and separate for responders (n = 20) and non responders (n = 20) according to the acute response to vasodilator. We tested this previous criteria versus the Task Force on diagnosis and treatment prescribed by the European Society of Cardiology. Results: The mean pulmonary arterial pressure/cardiac index was located abnormally in the pressure-flow diagram of the total cohort (p < 0.01). No alterations in gas exchange or lung mechanics. For patients responders versus non-responders, the slope was abnormal 2.2 (95% CI:1.1-3.3) vs. 5.89 (95% CI: 4.69 - 7.11), mm Hg/L min/m² and increased extrapolated pressure to zero flow (38.2 ± 7.5 to 66.3 ± 7.5 mm Hg, p <0.01). Without difference with oxygen 99.5%. With vasodilator effect, mean pulmonary arterial pressure decreased (52.1 ± 9.5 to 40 ± 5.5 mm Hg, p <0.01) versus it did not change (96.2 ± 8.5 versus 90 ± 7.5 mm Hg, p=0.3), slope 1.15 (95% CI: 0.68 - 1.62) vs. 1.28 (95% CI: 0.78-1.78) mmHg/L min/m², the extrapolated pressure to zero flow did not change (69.4 ± 7.8 to 85.1 ± 8.5 mm Hg), p <0.01, compared to control. In non-responders with vasodilator, mean pulmonary arterial pressure/cardiac index (90 ± 7.5 mmHg, slope: 1.28, 95% CI :0.78 - 1.78 mm Hg/L min/m²) was different between responders < or > 40 mmHg mean pulmonary arterial pressure. Pressures were 34 ± 3 vs. 45 ± 4 mm Hg and slopes 1.14 (95% CI: 0.67 - 1.61) vs. 2.22(95% CI: 1.35 - 3.09) mm Hg/L min/m², p <0.01, respectively.. Conclusions: Abnormalities of the mean pulmonary arterial pressure/cardiac index relationship exercise-derived seems to reflect "mainly arteriolar" increased lineal pulmonary vascular resistance in idiopathic pulmonary arterial hypertension patients. Both acute vasodilator response criteria are useful to identify responders and not responders in this patient population.

[Clinical interpretation for the pressure-flow relationships in extrinsic allergic alveolitis and in interstitial lung disease pulmonary hypertension patients. Should we care for the lung, the pulmonary artery pressure or both?]. / Interpretación clínica de la relación presión-flujo en enfermos con alveolitis alérgica extrínseca con neumopatía intersticial crónica e hipertensión pulmonar. Debemos tratar la hipertensión, la patología pulmonar o ambas?

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 (AO2B-99.5%) and to hydralazine (H) in extrinsic allergic alveolitis (EAA) and chronic interstitial lung disease (CILD) pulmonary hypertension (PH) patients. MATERIAL AND METHODS: mPAP/CI and extrapolated pressure (Pext) to zero flow were obtained while breathing room air (BRA) and under AO2B-99.5% in 38 stable (EAA (n = 14) and CILD (n = 24)) patients with resting and exercising PH. Hemodynamic characteristics were analyzed for the entire cohort and separate for EAA and CILD patients. AO2B-99.5% was tested in cohorts, H only in CILD and the effect of long-term corticosteroid treatment in EAA patients. Lung biopsies (LB) were obtained to evaluate the inflammatory-fibrosis stage and the degree of vascular lesion in the entire cohort. RESULTS: LB studies reveal a predominant stage of inflammation associated with grade-I vascular lesion for EAA patients. A predominant stage for fibrosis (although moderate) over inflammation associated with grade-II vascular lesions were documented for CILD patients. mPAP/CI abnormal location were associated with hypoxemia/decreased mixed venous-PO2 and lung mechanics abnormalities for both cohorts. An abnormal slope (Sp: 4.13; 95% CI: 3.42-4.84 mmHg/L/min/m2) and a normal Pext value (7 +/- 1.9 mmHg) were found for EAA patients. On the contrary, a normal slope (Sp: 1.22; 95% CI: 0.47-1.99 mmHg/L/min/m2) and an abnormal Pext value (19.7 +/- 3.5 mmHg) were found for CILD patients. Hemodynamic conditions that did not change for the Sp (4.0; 95% CI: 3.18-4.82 mmHg/L/min/m2); however, were associated with a statistical significant decrease in parallel for mPAP/CI during AO2B-99.5% when compared to BRA (p < 0.01), although not to normal slope values (0.96; 95% CI: 0.41-1.37) or mPAP/CI location. For CILD patients, during AO2B-99.5% no change for the slope, for Pext and mPAP/CI location in relation to BRA were observed. Under the effect of H, no change for the previous mentioned hemodynamic findings were found in relation to the control condition for CILD patients. After long-term corticosteroid treatment, normalization for mPAP/CI location and for the slope value (1.6; 95% CI: 0.91-2.29 mmHg/L/min/m2) were associated with lung mechanics and blood-gas exchange normalization were documented in EAA patients. CONCLUSIONS: When mPAP/CI exercise derived is analyzed, valuable information for linear-pulmonary vascular resistance-(LPVR) could be obtained for EAA and CILD-PH patients. mPAP/CI-r abnormalities not always reflect "pure arteriolar" increased LPVR for EAA and CILD patients. H is not useful as an adjunct vasodilator therapy for CILD-PH patients. AO2B-99.5% decrease right ventricular afterload for EAA patients, although not to normal. Complete reversibility for PH could result after long-term corticosteroid treatment. We conclude that treatment should focus mainly on the lung and not in the pulmonary artery pressure in interstitial lung disease PH patients.

Interpretación clínica de la relación presión-flujo en enfermos con alveolitis alérgica extrínseca con neumopatía intersticial crónica e hipertensión pulmonar: ¿debemos tratar la hipertensión, la patología pulmonar o ambas? / Clinical interpretation for the pressure-flow relationships in extrinsic allergic alveolitis and in interstitial lung disease pulmonary hypertension patients: should we care for the lung, the pulmonary artery pressure or both?

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 (AO2B-99.5%) and to hydralazine (H) in extrinsic allergic alveolitis (EAA) and chronic interstitial lung disease (CILD) pulmonary hypertension (PH) patients. MATERIAL AND METHODS: mPAP/CI and extrapolated pressure (Pext) to zero flow were obtained while breathing room air (BRA) and under AO2B-99.5% in 38 stable (EAA (n = 14) and CILD (n = 24)) patients with resting and exercising PH. Hemodynamic characteristics were analyzed for the entire cohort and separate for EAA and CILD patients. AO2B-99.5% was tested in cohorts, H only in CILD and the effect of long-term corticosteroid treatment in EAA patients. Lung biopsies (LB) were obtained to evaluate the inflammatory-fibrosis stage and the degree of vascular lesion in the entire cohort. RESULTS: LB studies reveal a predominant stage of inflammation associated with grade-I vascular lesion for EAA patients. A predominant stage for fibrosis (although moderate) over inflammation associated with grade-II vascular lesions were documented for CILD patients. mPAP/CI abnormal location were associated with hypoxemia/decreased mixed venous-PO2 and lung mechanics abnormalities for both cohorts. An abnormal slope (Sp: 4.13; 95% CI: 3.42-4.84 mmHg/L/min/m2) and a normal Pext value (7 +/- 1.9 mmHg) were found for EAA patients. On the contrary, a normal slope (Sp: 1.22; 95% CI: 0.47-1.99 mmHg/L/min/m2) and an abnormal Pext value (19.7 +/- 3.5 mmHg) were found for CILD patients. Hemodynamic conditions that did not change for the Sp (4.0; 95% CI: 3.18-4.82 mmHg/L/min/m2); however, were associated with a statistical significant decrease in parallel for mPAP/CI during AO2B-99.5% when compared to BRA (p < 0.01), although not to normal slope values (0.96; 95% CI: 0.41-1.37) or mPAP/CI location. For CILD patients, during AO2B-99.5% no change for the slope, for Pext and mPAP/CI location in relation to BRA were observed. Under the effect of H, no change for the previous mentioned hemodynamic findings were found in relation to the control condition for CILD patients. After long-term corticosteroid treatment, normalization for mPAP/CI location and for the slope value (1.6; 95% CI: 0.91-2.29 mmHg/L/min/m2) were associated with lung mechanics and blood-gas exchange normalization were document...

A proposed functional clinical classification predicts in-hospital and long-term survival in the setting of acute right ventricular infarction / Propuesta de una clasificación funcional y clínica para predecir la sobrevida intrahospitalaria y a largo plazo de enfermos con infarto agudo del ventrículo derecho

BACKGROUND: The objectives of the present investigation were to validate the prognostic role of a proposed Clinical Classification [CC], to evaluate the TIMI risk score [RS] and to establish whether the TIMI-RS should incorporate points for patients with acute right ventricular infarction [TIMI-RS-RVI]. METHODS AND RESULTS: A total of 523 RVI patients were classified on clinical and functional basis as: A, without right ventricular failure [RVF], B with RVF and C with cardiogenic shock. The CC was evaluated prospectively among 98 patients with RVI and retrospectively in 425 RVI patients. The TIMI-RS was evaluated prospectively among 622 patients with STEMI [anterior:277, inferior:247, RVI:98], and retrospectively in 425 RVI patients. The CC established differences among the 3-RVI Classes for in-hospital mortality [prospectively and retrospectively; p<0.01, p<0.001, respectively] that were maintained at 8 years [p < 0.001]. Patients with anterior and inferior STEMI, but not those with RVI revealed an association between outcome and TIMI-RS [p<0.001]. Testing for TIMI-RS-RVI did not result a good prognostic tool [ROC=0.9; excellent discrimination, but with a very poor [quot ]clinical calibration[quot ]]. CONCLUSIONS: The proposed CC allowed prediction of mortality at short- and long-term in the setting of acute RVI. The role of the TIMI-RS should be reevaluated prospectively as a prognostic tool in the scenario of RVI patients.

A proposed functional clinical classification predicts in-hospital and long-term survival in the setting of acute right ventricular infarction.

BACKGROUND: The objectives of the present investigation were to validate the prognostic role of a proposed Clinical Classification [CC], to evaluate the TIMI risk score [RS] and to establish whether the TIMI-RS should incorporate points for patients with acute right ventricular infarction [TIMI-RS-RVI]. METHODS AND RESULTS: A total of 523 RVI patients were classified on clinical and functional basis as: A, without right ventricular failure [RVF], B with RVF and C with cardiogenic shock. The CC was evaluated prospectively among 98 patients with RVI and retrospectively in 425 RVI patients. The TIMI-RS was evaluated prospectively among 622 patients with STEMI [anterior:277, inferior:247, RVI:98], and retrospectively in 425 RVI patients. The CC established differences among the 3-RVI Classes for in-hospital mortality [prospectively and retrospectively; p<0.01, p<0.001, respectively] that were maintained at 8 years [p < 0.001]. Patients with anterior and inferior STEMI, but not those with RVI revealed an association between outcome and TIMI-RS [p<0.001]. Testing for TIMI-RS-RVI did not result a good prognostic tool [ROC=0.9; excellent discrimination, but with a very poor "clinical calibration"]. CONCLUSIONS: The proposed CC allowed prediction of mortality at short- and long-term in the setting of acute RVI. The role of the TIMI-RS should be reevaluated prospectively as a prognostic tool in the scenario of RVI patients.

Optimización de los recursos de la imagenología en la cardiopatía isquémica / Staging imagenology in coronary syndromes

For the physician, it should stand out very clearly that the clinical and rationale analysis of the symptoms observed in every patient suffering from stable chronic ischemic cardiopathy (SCIC) or acute coronary ischemic syndrome (ACIS), are the starting point to apply the available resources in imagenology, in order to apply in an optimized and sequential manner to stratify, without forgetting its inherent limitations, or identify its risk. This approach may be based on the ethics, with special emphasis on the patient economy, which may promote the use of indissoluble medical principles regarding never damaging, but improving, the survival. SCIC and ACIS prevalence is still very high in its actually recognized clinical-pathological avenues.

La autorregulación homeométrica: el efecto Anrep: su posible importancia en la patofisiología en los aumentos de la postcarga del ventrículo derecho / Homeometric autoregulation in the heart: the Anrep effect: its possible role in increased right ventricular afterload pathophysiology

One type of intrinsic response exhibited by the isolated and non-isolated heart is the well-known Frank-Starling mechanism, which endows the ventricles with performance characteristics such that the heart ejects whatever volume is put into it [heterometric autoregulation]. A second type of autoregulation in the isolated and no-isolated heart, one which apparently does not utilize the Frank-Starling mechanism, will be the main subject of this review. It requires at least a few beats to develop fully after an increase in activity. The ventricle then exhibits performance characteristics such that its end-diastolic pressure and fiber length tend to be maintained because of an increase in myocardial contractility. It will, therefore be referred to as homeometric autoregulation or Anrep effect. Assessment of ventricular load-independent parameters, including myocardial contractility, is important to better understand the pathophysiology of acute and right ventricular increased afterload. The role of the Anrep effect, in right ventricular dysfunction in patients with primary or secondary forms of pulmonary artery hypertension with chronic cor pulmonale, is analyzed and presented as an hypothesis to be considered in the pathophysiology in acute and in chronic states of right ventricular afterload.