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Copyright of Archivos de Cardiología de México is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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 pul-monary 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 - P02 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. Forcohort-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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Copyright of Archivos de Cardiología de México is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archivos de Cardiología de México is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archivos de Cardiología de México is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archivos de Cardiología de México is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Archivos de Cardiología de México is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Acute pulmonary embolism (APE) is considered a cardiovascular emergency and is one of the most important causes of morbidity and mortality in hospitalized patients. Pulmonary embolism diagnosis has to be made early in the course of the disease and its management installed immediately. Pulmonary embolism management includes hemodynamic support, anticoagulation, thrombolysis and embolectomy. We present an overview of the treatment of APE.

Maternal mortality is still high in the world. Pulmonary thromboembolism as a cause of death is the second in developed countries. The frequency of reported events in Latin-American is 0.6%, which contrasts with that reported for developed countries (14.9%). This difference may be related to information bias. A review of the current information about this topic is presented, and we report a short case of a pregnant woman who presented pulmonary thromboembolism event at 30 weeks of pregnancy. Appropriate therapy allowed maternal and fetal survival.

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.

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.

Objective: Capillary blood gas test has had ample use in the infantile population. In the adult population, the information is limited and controversial. The agreement between capillary-arterial gases seems to parallel the pH and the carbon dioxide pressure in different studied populations. In order to know the degree of agreement between these gases, we evaluate them at breathing room air and at 100% of oxygen fractions at 2,240 meters above sea level., Methods: We obtained capillary-arterial blood gases simultaneously from subjects with stable cardiopulmonary disease in both conditions of inspired oxygen. Demographic, hemodynamic, diagnostic, and laboratory variables were gathered., Statistical Analysis: agreement was analyzed with the intraclass correlation coefficient and the Bland-Altman procedure., Results: We studied 101 subjects, 48 men and 53 women, whose respective ages were 55 +/- 16 and 56 +/- 16. Mean systemic arterial pressure was 94.96 +/- 10.57 mmHg. Hemoglobin was 15.94 +/- 2.48 g/dl. The agreement between the variables with the inspired oxygen fractions, 21%, 100%, and the mean difference in parenthesis was respectively: potential hydrogen, 0.94 (0.0091), 0.94 (0.0039); oxygen pressure, 0.90 (2.94), 0.84 (74.99); carbon dioxide pressure, 0.97 (0.079), 0.97 (0.179); bicarbonate, 0.93 (-0.067), 0,96 (0.262); total dissolved carbon dioxide, 0.94 (-0.142), 0.93 (0.161); base excess: 0.94, (-0.125), 0.92 (0.235); oxygen saturation, 0.98 (0.764), 0.97(0.202)., Conclusions: Capillary blood gas test could be a useful alternative to the arterial one, nevertheless, it is limited by its low agreement with the oxygen pressure in both oxygen inspired fractions.

Unlabelled: Obesity and Eisenmenger's syndrome are entities widely studied. However, its association is unusual and has not been reported. A wide range of gas exchange abnormalities have been describe in both groups. In the severe obese patients this abnormalities are attributed to a ventilation/perfusion mismatch and to an increase pulmonary venous-arterial shunt, that correlates with the lung volume. In severe obese patients with the Eisenmenger's syndrome, this correlation is unknown., Methods: We studied 28 obese subjects paired by body mass index > 30 kg/m2. Assigned to two groups, obese with Eisenmenger's syndrome and obese without the syndrome. Clinical variables, respiratory function, echocardiography and gas exchange pre and post-deep breathing maneuver were obtained., Statistical Analysis: The variables are expressed with mean+/-standard deviation. Student t test for paired groups and Pearson correlation coefficient were gathered for the differences and associations between groups. A p-value <0.05 was considered significant., Result: Age was 48.57 +/- 10.32 vs 60.86 +/- 10.47 y.o. respectively, p < 0.004. Systolic pulmonary arterial pressure 104.36 +/- 37 vs 50.1 +/- 12 mm Hg, p < 0.001. The arterial oxygen pressure at rest and during the deep breathing maneuver in each group was: 51.64 +/- 6.38 vs 57.14 +/- 11, p < 0.188 and 56.29 +/- 11.15 vs 72 +/- 11.83, p < 0.001; venous-arterial shunt 12.79 +/- 3.66 vs 13.07 +/- 4.84, p < 0.767 and 9.21 +/- 3.77 vs 6.5 +/- 2.28, p < 0.001; alveolar arterial oxygen difference 271.14 +/- 79.92 vs 243.79 +/- 92.07, p < 0.001, respectively., Conclusion: Obese subjects with Eisenmenger's syndrome, did not have significant improvement of gas exchange with the deep breathing maneuver.

Massive pulmonary embolism is associated with an increased mortality. It is secondary to migration of a venous thrombus to the right atrium or ventricle (thrombus in transit) towards the pulmonary circulation. The hemodynamic performance depends on the baseline cardiopulmonary status of the patient and the extent of obstruction. Right ventricular dysfunction will appear as a direct consequence of a major obstruction and hemodynamic collapse. The treatment of choice is thrombolysis, either intravenous in a peripheral vein, or local administration associated with percutaneous thrombus fragmentation or surgical embolectomy. We present the clinic case of a woman with massive pulmonary embolism. The transthoracic echocardiogram showed the presence of three auricular thrombus, right ventricular dysfunction and pulmonary hypertension. A right side catheterization and angiography demonstrated the pulmonary artery obstruction and right ventricular dysfunction. The troponin-I was elevated as a result of right ventricular strain. Mechanical thrombectomy was made using a pigtail catheter and thrombolysis into the pulmonary artery using recombinant tisular plasminogen activator. There was an immediate hemodynamic improvement and the post-thrombolysis angiography performed after 24-h demonstrated an improvement of the pulmonary circulation as well as decreased pulmonary artery pressures.

Right ventricular hypertension (RVH) is an entity that could be expected in various cardiopulmonary diseases. Mechanical obstruction to the right ventricle outflow tract is a cause of RVH. We present the case of a 69 year-old male with a history of hepatocarcinoma previously treated. The developed RVH due to mechanical obstruction secondary to metastatic infiltration of the right ventricle. The clinical syndrome was characterized by systemic venous hypertension. Non-invasive studies, such as electrocardiogram and computed tomography scan limited the metastasis to the right ventricle; the diagnosis was confirmed by cardio-angiography and endocardial biopsy. The studies did not demonstrate neoplastic activity at any other level.