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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
Eulo Lupi-Herreraa, Julio Sandovalb, Javier Figueroaa, Arturo Carrillob, Rebeca Aguirrec, Luis Efren Santos-Martínezd, Tomás Pulidob
a Sub-Direction of Clinical-Research.
b Cardiopulmonary-Department, Instituto Nacional de Cardiología Ignacio Chávez.
c Epidemiology-Department, School of Medicine, UNAM.
d Cardiopulmonary-Department, Instituto Nacional de Cardiología Ignacio Chávez. UMAE Cardiología Centro Médico Nacional Siglo XXI, IMSS.
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          "en" => "90024005fig5&#46;jpg&#34; width&#61;&#34;991&#34; height&#61;&#34;637&#34; alt&#61;&#34;Figure 1&#46; LVPO&#47;RVPO behavior for responders and non-responders at baseline &#40;B&#41;&#44; during acute vasodilating &#40;AV&#41; and at long-term &#40;LT&#41; RHC&#46; Differences are noted between B&#44; AV trial&#44; and at LT for the responder cohort&#59; also between responders and non-responders at B&#44; AV&#44; and LT RHC&#46; Lamda-Wilkin"
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Abbreviations&#58; <br></br></span>CO &#61; cardiac output<br></br> CPO &#61; cardiac power output <br></br> CCB &#61; calcium channel blockers <br></br> iNO &#61; inhaled nitric oxide <br></br> IPAH &#61; idiopathic pulmonary artery hypertension <br></br> LVPO &#61; left ventricular power output <br></br> mPWP &#61; mean pulmonary wedge pressure <br></br> mPAP &#61; mean pulmonary artery pressure <br></br> mRAP &#61; mean right atrial pressure <br></br> mSAP &#61; mean systemic arterial pressure <br></br> PAH &#61; pulmonary artery hypertension <br></br> PVR &#61; pulmonary vascular resistance <br></br> PVR&#47;SVR &#61; pulmonary vascular-to-systemic resistance ratio <br></br> RHC &#61; right heart catheterization <br></br> RVPO &#61; right ventricular power output <br></br> SVR &#61; systemic vascular resistance</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Introduction</span></p><p class="elsevierStylePara">The criteria to define a responder or non-responder based on changes in mean pulmonary artery pressure &#40;mPAP&#41; and pulmonary vascular resistance &#40;PVR&#41; during an acute vasodilation challenge have been questioned in recent years in idiopathic pulmonary artery hypertension &#40;IPAH&#41;&#46;<span class="elsevierStyleSup">1-8</span> Instead&#44; a positive acute vasoreactive response is now defined as a reduction of the mPAP &#8805; 10 mmHg to an absolute value of mPAP &#8804; 40 mmHg&#44; with increased&#47; unchanged cardiac output &#40;CO&#41;&#46;<span class="elsevierStyleSup">8</span> Accordingly&#44; only about 6 to 15&#37; of the IPAH population fulfills these criteria based on a retrospective experience&#44; derived from hemodynamic characteristics of patients who benefited from long-term calcium channel blockers &#40;CCBs&#41; treatment&#46;<span class="elsevierStyleSup">8&#44;9</span></p><p class="elsevierStylePara">Despite significant advances in IPAH&#44; right ventricular failure &#40;RVF&#41; remains the common fatal pathway and consequence of PAH&#46;<span class="elsevierStyleSup">1-8</span> The principles used to determine the external work of the heart can be applied to measure either the hydraulic energy associated with blood flow at &#34;<span class="elsevierStyleItalic">any point in the circulation</span>&#34; or the energy dissipated by flow through a particular vascular bed&#46;<span class="elsevierStyleSup">10</span> Thus&#44; for the RV and pulmonary vascular circuit&#44; it will be the product of flow output and pulmonary artery pressure&#44; the rate of useful work done&#44; or right ventricular power output &#40;RVPO&#41;&#46;<span class="elsevierStyleSup">10-12</span> Therefore&#44; by coupling the mPAP and CO domains of the cardiopulmonary system&#44; we will obtain a measure of the RV performance in IPAH&#46; Besides&#44; some studies have shown that left ventricular power output &#40;LVPO&#41; is a good indicator of cardiac function&#46;<span class="elsevierStyleSup">10&#44;11</span> On this functional basis&#44;<span class="elsevierStyleSup">10-12</span> we previously found differences in RVPO in a small cohort of IPAH patients who were considered to be responders or non-responders&#46;<span class="elsevierStyleSup">13</span> To extend this limited hemodynamic observation&#44; the objective of our present study was to investigate the definitive role for RVPO and LVPO to identify better responders among IPAH patients&#46; </p><p class="elsevierStylePara"><span class="elsevierStyleBold">Method</span></p><p class="elsevierStylePara">Our protocol was approved by the institutional ethics review commission&#46; All patients were born and raised at an altitude of 2240 m and were permanent residents of Mexico City&#46; The IPAH diagnosis was based on both clinical and hemodynamic criteria and by excluding other conditions known to cause PAH&#58; 1&#41; PAH associated with anorexigens&#44; connective tissue disease&#44; congenital heart disease&#44; portal hypertension&#44; or HVI infection&#59; 2&#41; chronic thromboembolic pulmonary hypertension&#59; and&#44; 3&#41; other chronic respiratory diseases&#46;<span class="elsevierStyleSup">1-4&#44;8 </span>Pulmonary hypertension was defined by a resting mPAP &#8805; 25 mmHg during RHC&#44; with a mean pulmonary wedge pressure &#40;mPWP&#41; &#8804; 15 mmHg and a PVR greater than three Wood units&#46;<span class="elsevierStyleSup">14&#44;15 </span></p><p class="elsevierStylePara">We retrospectively studied the medical records of 134 consecutive adult patients hospitalized in our institution between 1997 and 2007&#44; with a diagnosis of IPAH&#46; A total of 90 patients fulfilled the following criteria for inclusion in the study&#58; &#40;1&#41; a complete RHC at baseline&#44; &#40;2&#41; an acute I&#46;V&#46; vasodilator-drug challenge to assess vasodilator response&#44; and &#40;3&#41; chronic oral nifedipine therapy was initiated in patients who displayed significant acute pulmonary vasodilatation&#46; </p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Hemodynamic measurements&#58; </span>Our procedure for RHC has been described previously&#46;<span class="elsevierStyleSup">2&#44;13&#44;16&#44;17</span> The following measurements were obtained&#58; mean right atrial pressure &#40;mRAP&#41;&#44; mPAP&#44; mPWP&#44; CO &#40;was measured by triplicate by the thermodilution method&#41;&#44;<span class="elsevierStyleSup">2&#44;13&#44;16&#44;17</span> and mean systemic arterial pressure &#40;mSAP&#41;&#46; The following parameters were derived using traditional equations&#58; PVR&#44; systemic vascular resistance &#40;SVR&#41;&#44; and pulmonary vascular-to-systemic resistance ratio &#40;PVR&#47;SVR&#41;&#46; LVPO was calculated as mSAPxCO&#47;451 and RVPO was calculated as mPAPxCO&#47;451&#46;<span class="elsevierStyleSup">12</span></p><p class="elsevierStylePara">As an important part of our catheterization protocol&#44; we routinely assess the response to oxygen breathing to exclude the role of alveolar hypoxia in the genesis of PAH &#40;our definition of IPAH at our moderate altitude includes the absence of a positive response to 99&#46;9&#37;O<span class="elsevierStyleInf">2</span> breathing&#41;&#46;<span class="elsevierStyleSup">16&#44;17</span></p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Acute Vasodilating Trial&#58; </span>For acute vasodilating testing we used adenosine&#44; supported by the studies of Schrader<span class="elsevierStyleSup">18</span> and Sandoval&#44;<span class="elsevierStyleSup">19 </span>who observed a significant correlation between the reduction in PVR resulting from adenosine and that achieved by the administration of nifedipine&#46; Furthermore&#44; adenosine is considered today an acceptable alternative to the preferred vasodilator&#58; inhaled nitric oxide &#40;iNO&#41;&#46;<span class="elsevierStyleSup">14&#44;15</span></p><p class="elsevierStylePara">Based on the hemodynamic response&#44; we separated the patients into two groups&#58; responders and non-responders&#46; Our criteria for an &#34;<span class="elsevierStyleItalic">acute positive response</span>&#34; to vasodilators included&#58; 1&#41; a decrease in mPAP&#44; 2&#41; an increase in CO&#59; and&#44; 3&#41; a decrease in PVR &#40;&#8805; 20&#37; from baseline&#44; respectively&#41;&#46;<span class="elsevierStyleSup">2&#44;16 </span>When the above criteria were met&#44; a patient was considered for treatment with nifedipine&#46; <span class="elsevierStyleItalic">&#34;Responder</span>&#34; patients were administered oral doses of nifedipine &#40;10 mg 3-4 times&#47;day&#41;&#59; then&#44; daily doses were titrated to 20 mg&#44; 3-4 times&#47;day&#44; provided the patient did not exhibit side effects&#46;<span class="elsevierStyleSup">4</span> Long-term nifedipine responders were defined as patients with hemodynamic improvement &#40;a sustained decrease in mPAP and an increase in CO &#8805; 20&#37;&#41; with at least &#8805; 12 months on nifedipine without addition of other modern modalities of therapy for IPAH&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Data analysis&#58; </span>We&#58; 1&#41; analyzed the clinical and hemodynamic characteristics of our patients for the whole group &#40;n &#61; 90&#41; and separately for those considered to be responders &#40;n &#61; 34&#41; or non-responders &#40;n &#61; 56&#41;&#59; 2&#41; evaluated the ability for LVPO&#44; RVPO&#44; and their ratio to identify responders&#59; 3&#41; compared the Task Force criteria &#40;a decrease in mean PAP by at least 10 mmHg to an absolute of less than 40 mmHg without a decrease in CO&#41;<span class="elsevierStyleSup">8&#44;14&#44;15</span> with our acute positive criteria to identify responders&#59; 4&#41; compared both criteria among responders&#59; and 5&#41; assessed the long-term response to nifedipine&#46; </p><p class="elsevierStylePara">Data are expressed as mean &#177; SD&#44; median &#40;min&#44;max&#41; and frequencies &#40;percentages&#41; as appropriate&#46; A Student <span class="elsevierStyleItalic">t </span>test&#44; 1-way-ANOVA &#40;Bonferroni&#39;s-test for multiple comparison&#41;&#44; <span class="elsevierStyleItalic">chi square</span>&#44; or Fisher exact test was used as appropriate&#46; Univariate analysis based on the logistic regression model was used to examine the relation between responders or non-responders and selected demographics&#44; medical history&#44; and hemodynamic variables that were measured at initial RHC&#46; Results are expressed as odds ratio with 95&#37; CI&#46; Upon completion of the univariate analysis&#44; any variable whose univariate test produced a value of <span class="elsevierStyleItalic">p</span> &#60; 0&#46;25 was considered a candidate for the multivariate model&#46; Inclusions in the final multivariate logistic regression model were determined by those variables associated with a significance level of <span class="elsevierStyleItalic">p</span> &#60; 0&#46;05 in a stepwise elimination process&#46; After the predictor variables in the regression model had been finalized&#44; two statistical tests were performed to assess the model performance&#58; the Hosmer-Lemeshow statistics and the ROC curve&#46; Analyses were performed using SPSS-13 software&#46; </p><p class="elsevierStylePara"><span class="elsevierStyleBold">Results</span></p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Demographic&#47;clinical characteristics&#58; </span>According to the NYHA&#47;WHO classification&#44; there were no class IIIIV responders and no class-I non-responders &#40;<span class="elsevierStyleBold">Table 1</span>&#41;&#46; Treatments&#44; such as subcutaneous treprostinil &#40;n &#61; 12&#41;&#44; sitaxsentan &#40;n &#61; 8&#41;&#44; bosentan &#40;n &#61; 10&#41;&#44; ambrisentan &#40;n &#61; 5&#41; and sildenafil &#40;n &#61; 21&#41;&#44; were only distributed in nonresponders&#46; Fourteen non-responders in classes III-IV were electively sent for graded atrial septostomy&#46;<span class="elsevierStyleSup">17</span> Mortality associated to sudden death occurred in one responder and two non-responders and to refractory RVF in seven nonresponders&#46; </p><p class="elsevierStylePara"><img src="293v81n02-90024005fig1.jpg" alt="Table 1&#46; Clinical and demographic data&#46;"></img></p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Baseline hemodynamics</span>&#58; When we compared responders and non-responders&#44; no differences in mPAP &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;07&#41;&#44; CO &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;7&#41;&#44; mPWP &#40;0&#46;87&#41;&#44; PVR &#40;0&#46;08&#41;&#44; and PVR&#47; SVR ratio &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;08&#41; were observed&#46; Differences were observed for mRAP&#44; LVPO&#44; RVPO and LVPO&#47;RVPO &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#59; for all measurements&#44; <span class="elsevierStyleBold">Table 2</span>&#41;&#46; </p><p class="elsevierStylePara"><img src="293v81n02-90024005fig2.jpg" alt="Table 2&#46; Hemodynamic data at baseline and during acute vasodilation testing&#46;"></img></p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Acute response to vasodilating&#58; </span>The following changes in hemodynamic parameters were observed in the responders &#40;34&#47;90&#44; 37&#46;7&#37;&#41;&#58; a decrease from baseline mRAP&#44; mPAP&#44; and PVR values &#40;-20&#37;&#44; <span class="elsevierStyleItalic">p </span>&#60; 0&#46;045&#59; - 31&#46;5&#37;&#44; <span class="elsevierStyleItalic">p </span>&#60; 0&#46;001&#59; - 45&#37;&#44; <span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#44; respectively&#41;&#44; no change in mPWP &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;901&#41;&#44; an increase in CO &#40;&#43; 36&#46;9&#37;&#44; <span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41;&#44; and a decrease in PVR&#47;SVR ratio &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#44; Table 2&#41;&#46; During the vasodilator trial&#44; RVPO <span class="elsevierStyleItalic">decreased</span> &#40;<span class="elsevierStyleItalic">p </span>&#60; 0&#46;001&#41;&#44; LVPO &#40;<span class="elsevierStyleItalic">p </span>&#61; 0&#46;012&#41; <span class="elsevierStyleItalic">increased</span> and LVPO&#47;RVPO <span class="elsevierStyleItalic">increased</span>&#46; No differences from baseline mPAP &#40;fall&#41;&#44; RVPO &#40;decrease&#41;&#44; LVPO &#40;increase&#41;&#44; and LVPO&#47; RVPO &#40;increase&#41; reached during acute vasodilator testing among responders were observed when the Task Force<span class="elsevierStyleSup">8&#44;14</span> and our criteria were compared &#40;<span class="elsevierStyleBold">Table 3</span>&#41;&#46; </p><p class="elsevierStylePara"><img src="293v81n02-90024005fig3.jpg" alt="Table 3&#46; Hemodynamic values reached during vasodilator testing in acute responders according to the task force and our criteria&#46;"></img></p><p class="elsevierStylePara">For the non-responders &#40;56&#47;90&#44; 62&#46;2&#37;&#41;&#44; mRAP &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;275&#41;&#44; mPAP &#40;<span class="elsevierStyleItalic">p </span>&#61; 0&#46;222&#41;&#44; PVR &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;37&#41;&#44; and mPWP &#40;<span class="elsevierStyleItalic">p </span>&#61; 0&#46;81&#41; did not change&#59; CO increased &#40;&#43; 12&#37;&#44; <span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41;&#59; mSAP decreased &#40;<span class="elsevierStyleItalic">p </span>&#60; 0&#46;002&#41;&#59; and the PVR&#47;SVR ratio did not change &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;243&#41;&#46; During the acute vasodilator trial&#44; RVPO <span class="elsevierStyleItalic">increased</span> &#40;p &#60; 0&#46;001&#41;&#44; LVPO &#40;p &#61; 0&#46;125&#41; and LVPO&#47;RVPO &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;467&#41; <span class="elsevierStyleItalic">did not change</span>&#46; </p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Hemodynamics and NYHA classes&#58; </span>mRAP was different among classes &#40;class I&#58; 5&#46;5 &#177; 3&#46;4&#44; class II&#58; 9&#46;9 &#177; 4&#46;2&#44; class III&#58; 11&#46;4 &#177; 3&#44; and class IV&#58; 18 &#177; 0&#46;1 mmHg&#59; <span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41;&#46; For mPAP&#44; CO&#44; PVR&#44; RVPO&#44; LVPO&#44; and LVPO&#47;RVPO no differences were documented among classes&#46; </p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Long-term evaluation&#58; </span>Was performed by a repeat RHC in 30 responders under chronic nifedipine &#40;this cohort includes 16 patients who did not fulfill the Task Force criteria<span class="elsevierStyleSup">8&#44;15</span> at the initial RHC&#41; and in 42 non-responders treated with the other forms of therapy &#40;<span class="elsevierStyleBold">Table 4</span>&#41;&#46; Long-term nifedipine-treated responders&#44; according to the Task Force<span class="elsevierStyleSup">8&#44;15</span> or our criteria&#44; did not differ in terms of treatment regimen&#58; the mean daily doses of nifedipine were 59 &#177; 15 mg &#40;range 40-80 mg&#44; n &#61; 14&#41;&#44; 62 &#177; 14 mg &#40;range 40-80&#44; n &#61; 16&#41;&#44; <span class="elsevierStyleItalic">p</span> &#61; 0&#46;27&#59; and nifedipine therapy duration &#40;6&#46;4 &#177; 3&#46;5 <span class="elsevierStyleItalic">versus</span> 6&#46;3 &#177; 2&#46;9 years&#44; <span class="elsevierStyleItalic">p</span> &#61; 0&#46;85&#44; respectively&#41;&#46;</p><p class="elsevierStylePara"><img src="293v81n02-90024005fig4.jpg" alt="Table 4&#46; Long-term hemodynamic evaluation&#46;"></img></p><p class="elsevierStylePara">For responders&#44; mRAP &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;05&#41; and mPAP &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41; remained low&#59; CO was still <span class="elsevierStyleItalic">increased</span> &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;002&#41;&#59; the PVR&#47;SVR ratio &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;01&#41; and RVPO &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;04&#41; remained <span class="elsevierStyleItalic">decreased</span> and LVPO <span class="elsevierStyleItalic">increased</span> &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41; after 6&#46;4 &#177; 3&#46;1 years of follow-up &#40;<span class="elsevierStyleBold">Table 4</span>&#41;&#46; For the LVPO&#47;RVPO&#44; a further increase was documented in comparison to the acute evaluation among responders &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41;&#46; For this group&#44; the patients remained in I-II classes&#46; </p><p class="elsevierStylePara">For non-responders&#44; mPAP &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;473&#41;&#44; mRAP &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;494&#41;&#44; CO &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;121&#41;&#44; RVPO &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;1&#41;&#44; LVPO &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;193&#41;&#44; and LVPO&#47;RVPO did not change&#46; The same initial abnormal hemodynamic profile was observed after 6&#46;1 &#177; 3&#46;2 years&#46; In this group&#44; the patients remained in classes II-III&#46; When we compared the hemodynamic evolution over time of the responders versus the non-responders&#44; the responders displayed a <span class="elsevierStyleItalic">decreased</span> mRAP &#40;<span class="elsevierStyleItalic">p </span>&#60; 0&#46;001&#41;&#44; mPAP &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41; and RVPO &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;01&#41; and an<span class="elsevierStyleItalic"> increased </span>CO &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41;&#44; LVPO &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41;&#44; and LVPO&#47;RVPO &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#44; <span class="elsevierStyleBold">Figure 1</span>&#41;&#46; </p><p class="elsevierStylePara"><img src="293v81n02-90024005fig5.jpg" alt="Figure 1&#46; LVPO&#47;RVPO behavior for responders and non-responders at baseline &#40;B&#41;&#44; during acute vasodilating &#40;AV&#41; and at long-term &#40;LT&#41; RHC&#46; Differences are noted between B&#44; AV trial&#44; and at LT for the responder cohort&#59; also between responders and non-responders at B&#44; AV&#44; and LT RHC&#46; Lamda-Wilkins &#40;F &#61; 75&#46;87&#59; p &#60; 0&#46;001&#41;&#46; U-Man-Whitney test&#46;"></img></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Figure 1&#46; </span>LVPO&#47;RVPO behavior for responders and non-responders at baseline &#40;B&#41;&#44; during acute vasodilating &#40;AV&#41; and at long-term &#40;LT&#41; RHC&#46; Differences are noted between B&#44; AV trial&#44; and at LT for the responder cohort&#59; also between responders and non-responders at B&#44; AV&#44; and LT RHC&#46; Lamda-Wilkins &#40;F &#61; 75&#46;87&#59; <span class="elsevierStyleItalic">p </span>&#60; 0&#46;001&#41;&#46; U-Man-Whitney test&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Univariate analysis&#58; </span>Variables associated with an acute responder included&#58; age &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;03&#41;&#44; estimated symptom duration &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;02&#41;&#44; mRAP &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41;&#44; mPAP &#40;<span class="elsevierStyleItalic">p</span> &#60; 0&#46;001&#41;&#44; RVPO &#40;<span class="elsevierStyleItalic">p </span>&#61; 0&#46;007&#41;&#44; and LVPO &#40;<span class="elsevierStyleItalic">p</span> &#61; 0&#46;036&#41; &#40;<span class="elsevierStyleBold">Table 5</span>&#41;&#46; </p><p class="elsevierStylePara"><img src="293v81n02-90024005fig7.jpg" alt="Table 5&#46; Univariate variables entered into the multivariate model to be an acute responder&#46;"></img></p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Multivariate analysis&#58; </span>Age&#44; RVPO&#44; and LVPO remained as independent variables &#40;OR &#61; 0&#46;927&#44; 95&#37; CI&#58; 0&#46;87-0&#46;98&#44; <span class="elsevierStyleItalic">p</span> &#61; 0&#46;01&#59; OR &#61; 0&#46;114&#44; 95&#37; CI&#58; 0&#46;00-0&#46;91&#44; <span class="elsevierStyleItalic">p</span> &#61; 0&#46;045&#59; and OR &#61; 171&#46;5&#44; 95&#37; CI&#58; 5&#46;3-549&#44; <span class="elsevierStyleItalic">p</span> &#61; 0&#46;004&#44; respectively&#41; for estimating the probability of being a responder&#46; According to the logistic multivariate analysis&#44; the following equation was derived for identifying responders among patients &#61; 1&#46;0196-0&#46;0631 &#40;age&#41; -4&#46;7693&#40;RVPO&#41;&#44; &#43;3&#46;8152 &#40;LVPO&#41;&#44; ROC&#58; 0&#46;76&#44; 95&#37; CI&#58; 0&#46;63-0&#46;89&#59; <span class="elsevierStyleItalic">p</span> &#61; 0&#46;001&#46; According to the results of the Hosmer-Lemeshow test &#40;X<span class="elsevierStyleSup">2</span>&#58; 9&#46;234&#44; DF &#61; 8&#44; <span class="elsevierStyleItalic">p</span> &#61; 0&#46;323&#41; and the area value for the ROC curve &#40;0&#46;76&#44; 95&#37; CI&#58; 0&#46;63-0&#46;89&#44; <span class="elsevierStyleItalic">p</span>&#61; 0&#46;001&#41;&#44; the derived model can be used to estimate the probability of being an acute responder among IPAH patients &#40;<span class="elsevierStyleBold">Figure 2</span>&#41;&#46; </p><p class="elsevierStylePara"><img src="293v81n02-90024005fig6.jpg" alt="Figure 2&#46; The probability to be an acute responder patient when the model is applied to a value of 0&#46;5 W for LVPO&#46; For a patient aged 30 years with RVPO of 0&#46;4 W&#44; the probability to be a responder is 30&#37;&#46;"></img></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Figure 2&#46; </span>The probability to be an acute responder patient when the model is applied to a value of 0&#46;5 W for LVPO&#46; For a patient aged 30 years with RVPO of 0&#46;4 W&#44; the probability to be a responder is 30&#37;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Discussion </span></p><p class="elsevierStylePara">A critical reason for considering an &#34;<span class="elsevierStyleItalic">acute positive</span>&#34; response in IPAH is to identify patients whose response at entry RHC appears to predict better long-term prognoses&#46;<span class="elsevierStyleSup">1-5</span> However&#44; this also has important economic consequences &#40;low price oral vasodilators <span class="elsevierStyleItalic">vs&#46;</span> other expensive modern therapies&#41;&#46; Thus&#44; a continued search for hemo-dynamic markers that define better responsive patients is required&#46; By using the proposed criteria from the Task Force<span class="elsevierStyleSup">8&#44;14</span> or our criteria to identify responders among IPAH patients&#44; it is possible to achieve this important goal in this population&#46; However&#44; using the Task Force criteria&#44;<span class="elsevierStyleSup">8&#44;14</span> responders will be identified in 17&#46;7&#37;&#44; whereas our criteria identify 37&#46;7&#37; of the total IPAH patients&#44; and among responders the Task Force criteria<span class="elsevierStyleSup">8&#44;14</span> would identify only 53&#37; of them&#46; Consequently&#44; the question arises as to which hemodynamic criteria are the most appropriate for achieving this important goal&#46; If analyzed as a group&#44; the responders could reach 38&#46;2 mmHg&#44; although a stringent cut-off value of 40 mmHg was not always achieved in association with a &#62;20&#37; increase in CO&#46; Although&#44; we must emphasize that we also observed a decrease in &#62;10 mmHg for mPAP in our responders&#46;<span class="elsevierStyleSup">8&#44;14</span> In addition&#44; the different hemodynamic behavior of the responders and non-responders in regard to RVPO&#44; LVPO&#44; and LVPO&#47;RVPO reinforces our ability to identify responders among IPAH population&#46; In our study we demonstrated a <span class="elsevierStyleItalic">decrease</span> in RVPO associated with an <span class="elsevierStyleItalic">increase</span> in LVPO and LVPO&#47;RVPO for responder patients&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">NYHA&#47;WHO-classification influence on the proportion of responders&#58; </span>In our study&#44; the acute response rate appears higher than other reported for adult IPAH patients&#46;<span class="elsevierStyleSup">9</span> This may be explained&#44; in part&#44; by differences in the proportional NYHA classes distribution of the studied populations&#46; In the cohort studied by Sitbon<span class="elsevierStyleSup">9</span> &#40;n &#61; 557&#41;&#44; only 19&#37; &#40;n &#61; 70&#41; were class I-II patients&#46; Thus&#44; a low proportion of classes I-II were included compared to classes III-IV patients in the Sitbon study&#46;<span class="elsevierStyleSup">9</span> On the contrary&#44; in our series&#44; 78&#46;8&#37; &#40;71&#47;90&#41; were in classes I-II at initial RHC&#46; </p><p class="elsevierStylePara">Consequently&#44; we should emphasize that whenever responder patients are examined in IPAH studies&#44; we must take into consideration the total of class I-II patients who are evaluated in the acute vasodilator challenge&#46; Thus&#44; differences in the acute response rate not only could result from the applied criteria&#44; but also from the number of class I-II patients tested in relation to the number of class III-IV patients tested in an acute trial&#46; </p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Long-term measurements&#58; </span>The significant differences noted between responders and non-responders for RVPO&#44; LVPO&#44; and LVPO&#47;RVPO at the initial RHC were confirmed at the RHC long-term follow-up&#46; For patients under chronic nifedipine therapy&#44; the RVPO <span class="elsevierStyleItalic">decreased</span> further&#44; and LVPO <span class="elsevierStyleItalic">increased</span> to 1&#46;15 &#177; 0&#46;27 W&#44; which is close to the resting normal values&#46;<span class="elsevierStyleSup">10</span> These data suggest a persistent predominant vasodilator effect in the pulmonary vasculature and translates a sustained good RV pumping performance&#46; For non-responders&#44; a persistent abnormal elevation in mPAP&#44; decreased CO&#44; <span class="elsevierStyleItalic">increased</span> RVPO&#44; and a <span class="elsevierStyleItalic">low abnormal resting</span> LVPO &#40;0&#46;67 &#43; 0&#46;15 W&#41; were documented&#44; resulting in a sustained hemodynamic profile that eventually must worsen the cardiac pumping ability&#46; This condition could explain why a low long-term mortality was not associated in non-responders&#44; but was related in the responder cohort &#40;<span class="elsevierStyleBold">Table 1</span>&#41;&#46; The hemodynamic findings for the coupling of RV-pulmonary circulation observed at long-term RHC further underscores the validity of our criteria of &#34;<span class="elsevierStyleItalic">acute positive response</span>&#34; applied at the initial RHC for the IPAH patients studied&#46; Stibon<span class="elsevierStyleSup">9</span> was able to retrospectively define more stringent criteria at baseline&#44; which identified the responders who would have sustained long-term benefit from CCBs&#46; We were unable to demonstrate that such criteria at baseline predict the change from responder to non-responder status in 58&#37; &#40;14&#47;24&#41; of patients&#59; our responders remained as responders at least up to 6&#46;4 &#177; 3 years under nifedipine &#40;<span class="elsevierStyleBold">Table 4</span>&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">The model&#58; </span>To test the proposed model&#44; we examined Rich&#39;s<span class="elsevierStyleSup">4</span> study&#46; The rate of responders obtained by Rich<span class="elsevierStyleSup">4</span> after the vasodilating test was 26&#37;&#46; When we applied our model to estimate the proportion of responders&#44; among IPAH patients&#44; the derived value was close to 30&#37;&#46; Thus&#44; our model to predict an acute positive response is in reasonable agreement with previous information on the proportion of responders who have been observed with a similar age&#44; tested acutely for vasodilation with nifedipine and long-term treated with CCBs&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Overall evaluation&#58; </span>Based on our results&#44; we propose that the hemodynamic behavior of RVPO and LVPO should be incorporated&#44; in addition to the proposed criteria for the definition of a &#34;<span class="elsevierStyleItalic">positive</span>&#34; response to vasodilators&#46; In this regard&#44; there are several pathophysiological reasons to include RVPO for such clinical&#47;hemodynamic stratification&#46; As PAH develops&#44; the distensibility of the elastic arteries decreases&#46;<span class="elsevierStyleSup">8&#44;20</span> Consequently&#44; a larger amount of RV work must be expended to distend the stiff pulmonary arteriolar vessels&#46; As a consequence&#44; the pulsatile arterial power generated by the RV is an important proportion &#40;35-40&#37;&#41; of the total external power&#46;<span class="elsevierStyleSup">10</span> If we include only PVR&#44; we are missing part of the RV load&#59; whereas by determining RVPO&#44; we obtain an approximate calculation of the pressure work generated by the RV&#44; which is determined by flow output and the pulmonary arterial load&#46;<span class="elsevierStyleSup">10</span></p><p class="elsevierStylePara">Our findings for the proposed markers support that RVF is the main resulting cause of death in these patients&#46;<span class="elsevierStyleSup">1-3&#44;5&#44;8</span> In non-responders with lower likelihood of survival&#44; the behavior of RVPO and LVPO indicates that these patients are hemodynamically characterized with a reduced reserve of the pulmonary circulation associated with decreased RV function&#44; resulting in an inappropriate RV-pulmonary arterial coupling and an inappropriate ventricular interaction&#46;<span class="elsevierStyleSup">1&#44;3&#44;5</span></p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Limitations&#58; </span>Are essentially associated with the fact that the information is from a single cardiovascular referral center&#44; located at moderate altitude&#46; Although&#44; we should emphasize that alveolar hypoxia was ruled out &#40;as part of our IPAH definition&#41;&#59;<span class="elsevierStyleSup">14</span> thus&#44; our findings could be generalized for IPAH patients&#46; Moreover&#44; the number of patients included for testing RVPO and LVPO can be considered large because IPAH is a rare disease&#46;<span class="elsevierStyleSup">1&#44;5</span> We are aware that the retrospective nature of the study potentially introduces a selection bias&#46; However&#44; the information collected at the first RHC for the RVPO and LVPO was reproducible for all the patients at long-term follow-up RHC&#46; We are also aware that 1&#41; instantaneous &#40;pulsatile&#41; data on pressure and flow are essential for an accurate calculation of external ventricular work and an error using mPAP in combination with CO &#40;instead of measured flow&#41; will underestimate the true RVPO-LVPO in our RHC studies&#46;<span class="elsevierStyleSup">10</span> 2&#41; perhaps we cannot compare exactly the acute response to adenosine with that obtained with iNO or epoprostenol in class III-IV IPAH patients&#59;<span class="elsevierStyleSup">14&#44;15 </span>and&#44; 3&#41; due to the small number of deaths in the studied population&#44; a mortality prognostic value could not be derived for RVPOLVPO&#46; Mortality prognostic value for RVPO-LVPO that in the near future should be investigated in a larger population IPAH patients&#46; </p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conclusions</span></p><p class="elsevierStylePara">RVPO is a novel hemodynamic-derived measure that gives better insight into the RV-pulmonary arterial coupling nature and&#44; in conjunction with LVPO and LVPO&#47;RVPO&#44; for the overall hemodynamics in IPAH&#46; RVPO and LVPO result in good hemodynamic tools that should be added to the existing ones to identify responders among IPAH patients&#46; </p><hr></hr><p class="elsevierStylePara"><span class="elsevierStyleItalic">Corresponding author&#58;</span> Eulo Lupi Herrera&#46; <br></br> Director de la L&#237;nea de Servicio de la Divisi&#243;n Cardiovascular Centro M&#233;dico ABC&#46; Sur 136 N&#176; 116&#46; Col&#46; Las Am&#233;ricas&#44; 01120&#44; M&#233;xico&#44; D&#46;F&#46; M&#233;xico&#46; <br></br> Telephone&#58; 52 308 000 Extension&#58; 3762&#46; <span class="elsevierStyleItalic"><br></br> E-mail&#58;</span><a href="mailto&#58;elupih&#64;abchospital&#46;com" class="elsevierStyleCrossRefs">elupih&#64;abchospital&#46;com</a>&#44; <a href="mailto&#58;eulolupiherrera&#64;hotmail&#46;com" class="elsevierStyleCrossRefs">eulolupiherrera&#64;hotmail&#46;com</a></p> Received on April 16&#44; 2009&#59; <br></br> accepted on September 28&#44; 2010&#46; "
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            0 => "Hipertensi&#243;n pulmonar idiop&#225;tica&#59; Poder del ventr&#237;culo derecho&#59; Poder del ventr&#237;culo izquierdo&#59; Respondedores&#59; M&#233;xico"
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        "resumen" => "Introduction&#58; Despite the prognostic importance of traditionally derived measurements&#44; the significance of right heart catheterization &#40;RHC&#41; remains controversial&#46; Thus&#44; a continued search for hemodynamic markers that define better responsive patients is required&#46; Since&#44; right ventricular failure is the most fatal pathway&#44; right &#40;RVPO&#41; and left &#40;LVPO&#41; ventricular power output are parameters that could provide input for a better understanding of the hemodynamics involved in idiopathic pulmonary artery hypertension &#40;IPAH&#41;&#46; Method&#58; We retrospectively analyzed how demographics and outcome correlate with hemodynamics to identify responders among IPAH patients&#46; Results&#58; Ninety patients fulfilled the following criteria for inclusion in this study&#58; &#40;1&#41; complete RHC at baseline&#59; &#40;2&#41; an acute evaluation for vasodilators &#40;AEFV&#44; including a positive response&#44; that is&#44; an increase in CO&#44; a decrease in both mPAP and pulmonary vascular resistance &#8805; 20&#37; from baseline&#44; respectively&#41;&#59; and &#40;3&#41; a long-term follow-up under accepted IPAH treatments&#46; If RVPO decreased &#40;p &#60; 0&#46;001&#41; and LVPO increased &#40;p &#60; 0&#46;012&#41; during AEFV&#44; it is considered that these findings reinforce our ability to identify responders&#59; that is&#44; patients that remained as responders after 6&#46;4 &#177; 3 years under nifedipine treatment &#40;37&#46;7&#37; of the studied IPAH population&#41;&#46; After multivariate analysis&#44; age&#44; RVPO&#44; and LVPO remained as independent variables &#40;OR &#61; 0&#46;927&#44; 95&#37;CI&#58; 0&#46;87-0&#46;98&#44; p &#61; 0&#46;01&#59; OR &#61; 0&#46;114&#44; 95&#37;CI&#58; 0&#46;00-0&#46;91&#44; p &#61; 0&#46;045&#59; and OR &#61; 171&#46;5&#44; 95&#37; CI&#58; 5&#46;3-549&#44; p &#61; 0&#46;004&#44; respectively&#41; when estimating the probability of being a responder&#46; On this basis&#44; an equation was derived to identify responders among IPAH patients&#44; where the probability of being a responder &#61; 1&#46;0196-0&#46;0631 &#40;age&#41; - 4&#46;7693 &#40;RVPO&#41; &#43; 3&#46;8152 &#40;LVPO&#41;&#44; ROC&#58; 0&#46;76&#44; 95&#37; CI&#58; 0&#46;63-0&#46;89&#59; p &#61; 0&#46;001&#46; Conclusion&#58; based on the proposed equation&#44; LVPO and RVPO could be used for the identification of responders among IPAH patients&#46;"
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        "resumen" => "Introducci&#243;n&#58; A pesar de la importancia y del significado pron&#243;stico que tienen las mediciones directas y las derivadas del cateterismo cardiaco derecho&#44; &#233;stas permanecen hasta el d&#237;a de hoy en el terreno acad&#233;mico de la controversia&#46; Por lo tanto&#44; se requiere la continua b&#250;squeda de marcadores hemodin&#225;micos para estratificar a los enfermos con hipertensi&#243;n arterial pulmonar idiop&#225;tica&#46; Particularmente&#44; cuando la disfunci&#243;n contr&#225;ctil del ventr&#237;culo derecho es la v&#237;a final m&#225;s com&#250;n de esta patolog&#237;a&#46; En esta circunstancia&#44; la determinaci&#243;n del poder del ventr&#237;culo derecho y del ventr&#237;culo izquierdo representa par&#225;metros que pudieran ser de utilidad para lograr un mejor entendimiento en la hemodin&#225;mica de la hipertensi&#243;n arterial pulmonar idiop&#225;tica&#46; M&#233;todo&#58; De manera retrospectiva&#44; analizamos los aspectos demogr&#225;ficos&#44; los hemodin&#225;micos y la sobrevivencia&#44; y si &#233;stos se vieron asociados a la posibilidad de ser enfermos respondedores entre los portadores de hipertensi&#243;n arterial pulmonar idiop&#225;tica&#46; Resultados&#58; Noventa enfermos llenaron los siguientes criterios para ser incluidos en el estudio&#58; 1&#46; Contar con cateterismo cardiaco derecho basal&#59; 2&#46; Tener valoraci&#243;n aguda con adenosina&#44; en donde qued&#243; definida una respuesta &#34;positiva aguda&#34; como&#58; aumento del gasto card&#237;aco&#44; disminuci&#243;n de la presi&#243;n arterial pulmonar media y de la resistencia vascular pulmonar calculada &#40;&#8805; 20&#37; de la basal&#44; respectivamente&#41; y&#59; 3&#46; Contar con un seguimiento a largo plazo bajo la influencia de los tratamientos modernos aceptados para enfermos con hipertensi&#243;n arterial pulmonar idiop&#225;tica&#46; S&#237;&#44; el poder del ventr&#237;culo derecho disminuy&#243; &#40;p &#60; 0&#46;001&#41; y el poder ventr&#237;culo izquierdo aument&#243; &#40;p &#60; 0&#46;012&#41; durante el reto vasodilatador agudo se consider&#243; que &#233;stos hallazgos reforzaban la habilidad para detectar a los sujetos respondedores con hipertensi&#243;n arterial pulmonar idiop&#225;tica&#59; poblaci&#243;n de enfermos que guard&#243; ese comportamiento hemodin&#225;mico durante 6&#46;4 &#177; 3 a&#241;os bajo la influencia de nifedipina &#40;37&#37; de la totalidad de la poblaci&#243;n con hipertensi&#243;n arterial pulmonar idiop&#225;tica&#41;&#46; Despu&#233;s de efectuar un an&#225;lisis multivariado&#44; la edad&#44; el poder del ventr&#237;culo derecho y del ventr&#237;culo izquierdo permanecieron como variables independientes &#40;OR &#61; 0&#46;927&#44; 95&#37;IC&#58; 0&#46;87-0&#46;98&#44; p &#61; 0&#46;01&#59; OR &#61; 0&#46;114&#44; 95&#37;IC&#58; 0&#46;00-0&#46;91&#44; p &#61; 0&#46;045&#59; y OR &#61; 171&#46;5&#44; 95&#37;IC&#58; 5&#46;3-549&#44; p &#61; 0&#46;004&#44; respectivamente&#41; para ser considerados &#34;respondedores&#34;&#46; Como resultado&#44; se deriv&#243; una ecuaci&#243;n donde la probabilidad de ser respondedor &#61; 1&#46;0196-0&#46;0631 &#40;edad&#41; - 4&#46;7693 &#40;poder del ventr&#237;culo derecho&#41; &#43; 3&#46;8152 &#40;poder del ventr&#237;culo izquierdo&#41;&#44; ROC&#58; 0&#46;76&#44; 95&#37;CI&#58; 0&#46;63 - 0&#46;89&#59; p &#61; 0&#46;001&#46; Conclusi&#243;n&#58; Con fundamento en los hallazgos de este estudio&#44; la ecuaci&#243;n propuesta&#44; el poder del ventr&#237;culo derecho y el ventr&#237;culo izquierdo pueden ser utilizados para identificar &#34;respondedores&#34; entre los enfermos con hipertensi&#243;n arterial pulmonar idiop&#225;tica&#46;"
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          "en" => "90024005fig5&#46;jpg&#34; width&#61;&#34;991&#34; height&#61;&#34;637&#34; alt&#61;&#34;Figure 1&#46; LVPO&#47;RVPO behavior for responders and non-responders at baseline &#40;B&#41;&#44; during acute vasodilating &#40;AV&#41; and at long-term &#40;LT&#41; RHC&#46; Differences are noted between B&#44; AV trial&#44; and at LT for the responder cohort&#59; also between responders and non-responders at B&#44; AV&#44; and LT RHC&#46; Lamda-Wilkin"
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          "en" => "The probability to be an acute responder patient when the model is applied to a value of 0&#46;5 W for LVPO&#46; For a patient aged 30 years with RVPO of 0&#46;4 W&#44; the probability to be a responder is 30&#37;&#46;"
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es en pt

¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?

Você é um profissional de saúde habilitado a prescrever ou dispensar medicamentos