Clinical up-date
Pulmonary hypertension and hepatic cirrhosis
Hipertensión pulmonar y cirrosis hepática
L. Téllez Villajos
, J. Martínez González, V. Moreira Vicente, A. Albillos Martínez
Corresponding author
Servicio de Gastroenterología, Hospital Universitario Ramón y Cajal, Madrid, Spain
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Téllez Villajos, J. Martínez González, V. Moreira Vicente, A. Albillos Martínez" "autores" => array:4 [ 0 => array:4 [ "nombre" => "L." "apellidos" => "Téllez Villajos" "email" => array:1 [ 0 => "luistevilla@gmail.com" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] 1 => array:2 [ "nombre" => "J." "apellidos" => "Martínez González" ] 2 => array:2 [ "nombre" => "V." "apellidos" => "Moreira Vicente" ] 3 => array:2 [ "nombre" => "A." "apellidos" => "Albillos Martínez" ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Servicio de Gastroenterología, Hospital Universitario Ramón y Cajal, Madrid, Spain" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Hipertensión pulmonar y cirrosis hepática" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 955 "Ancho" => 2090 "Tamanyo" => 130684 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Normal values for cardiopulmonary pressures in a right cardiac catheterization using Swan–Ganz catheter.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Background</span><p id="par0005" class="elsevierStylePara elsevierViewall">A 56-year-old woman, drinker of 40<span class="elsevierStyleHsp" style=""></span>g of alcohol daily, smoker of 40 packs/year and a history of breast carcinoma, was treated with lumpectomy and hormone therapy a year ago. Following a first episode of ascites, the woman was diagnosed with hepatic cirrhosis and started taking diuretics, which were discontinued due to acute renal failure. The patient required 6 evacuative paracentesis of considerable volume to control the ascites. The decision was therefore made to place a coated transjugular intrahepatic portosystemic shunt (TIPS), with a satisfactory clinical response. Three years later, the patient visited for the reappearance of ascites, leg edema and moderate effort dyspnea. Laboratory tests revealed preserved hepatic function with BNP level of 1032<span class="elsevierStyleHsp" style=""></span>pg/mL (<500<span class="elsevierStyleHsp" style=""></span>pg/mL) and severe respiratory failure with PaO<span class="elsevierStyleInf">2</span> level of 57<span class="elsevierStyleHsp" style=""></span>mmHg (85–100<span class="elsevierStyleHsp" style=""></span>mmHg). Based on the suspicion of TIPS dysfunction, abdominal Doppler ultrasonography was performed, which showed preserved flow through the TIPS. A hemodynamic study was also performed of the porto-caval circulation in which the pressures in the inferior vena cava, atrium and porta were similar and high (25, 25 and 28<span class="elsevierStyleHsp" style=""></span>mmHg, respectively). The echocardiogram revealed considerable dilation of the right cavities, severe tricuspid regurgitation and moderate pericardial effusion. There was no observable passage of microbubbles from the right cavities to the left of the heart after the injection of agitated saline. The left ventricular ejection fraction was normal, and the systolic pressures of the right ventricle were high (59<span class="elsevierStyleHsp" style=""></span>mmHg). Cardiopulmonary catheterization showed pulmonary hypertension (PH), with a mean pulmonary arterial pressure (mPAP) of 46<span class="elsevierStyleHsp" style=""></span>mmHg, pulmonary vascular resistances (PVR) of 582<span class="elsevierStyleHsp" style=""></span>dyn<span class="elsevierStyleHsp" style=""></span>s/cm<span class="elsevierStyleSup">5</span>, cardiac output (CO) of 8.1<span class="elsevierStyleHsp" style=""></span>bpm and a negative vasodilator test. Other causes of PH were ruled out through spirometry and chest CT angiography.<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><p id="par0010" class="elsevierStylePara elsevierViewall">Are these symptoms of portopulmonary hypertension (PPH)?</p></li><li class="elsevierStyleListItem" id="lsti0010"><p id="par0015" class="elsevierStylePara elsevierViewall">What role has the TIPS played in this patient?</p></li><li class="elsevierStyleListItem" id="lsti0015"><p id="par0020" class="elsevierStylePara elsevierViewall">Would an echocardiogram prior to the placement of the TIPS have changed anything?</p></li></ul></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">The clinical problem</span><p id="par0025" class="elsevierStylePara elsevierViewall">PH is present in up to 0.5–5% of patients with portal hypertension, with or without hepatic cirrhosis.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">1</span></a> Liver transplantation was initially considered contraindicated due to the high risk of respiratory distress in the anesthesia induction and right heart failure after the hepatic reperfusion phase.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">2</span></a> However, the increased pulmonary pressures in patients with cirrhosis can be the result of several conditions, some of which should be interpreted as the body's physiological response to the advanced stages of cirrhosis. It is therefore essential to establish a proper differential diagnosis given that the therapeutic implications differ in each scenario. Undoubtedly, the clinical picture that has traditionally related hepatic diseases to PH is PPH.</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Clinical guidelines and areas of uncertainty</span><p id="par0030" class="elsevierStylePara elsevierViewall">Although we currently have clear diagnostic criteria, such as those proposed by Cartin-Ceba,<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">3</span></a> the limited experience in treating these patients means that we have no clear therapeutic guidelines that enable physicians to guide the management of these conditions based on a good level of evidence. It is tempting to take for granted the association between cirrhosis and PH under the epigraph “portopulmonary hypertension”. Experienced physicians should, however, know how to direct their diagnosis so that it can establish, practically and simply, a proper differential diagnosis that results in the patient undergoing the correct treatment. Nevertheless, there are numerous difficulties, questions and areas of uncertainty that open up when studying and treating patients with cirrhosis and PH: should we suspect PPH in all patients with cirrhosis and PH? Is an echocardiogram sufficient to reach a diagnosis? On what data and tests should we focus to establish a proper differential diagnosis? Are all patients with PH and cirrhosis treated equally? Are patients with PPH treated the same as those with primary PH?</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Pulmonary hypertension and cirrhosis</span><p id="par0035" class="elsevierStylePara elsevierViewall">PH is a relatively common phenomenon in patients with cirrhosis and portal hypertension and generally occurs in the advanced stages of the disease. PH is present in up to 6–9% of patients who are evaluated as candidates for liver transplantation.<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">2</span></a> In general, the definition of PH includes patients who have an mPAP level >25<span class="elsevierStyleHsp" style=""></span>mmHg, measured through right cardiac catheterization.<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">4</span></a> In order to facilitate diagnosis and establish prognostic and therapeutic groups, the World Health Organization (WHO) recently proposed a new classification based on 5 groups: group 1: arterial PH, which includes PPH; group 2: PH secondary to left heart failure; group 3: PH secondary to lung disease or hypoxemia; group 4: PH due to chronic thromboembolic disease; and group 5: PH by multifactorial mechanisms.<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">5</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">In cirrhosis, PH can be due to several conditions, which can be encompassed by the various PH groups. The characteristic syndrome that relates PH to portal hypertension is PPH, which fits within group 1 of the classification proposed by the WHO, due to its similar behavior and histological findings to primary or idiopathic PH. However, the increase in mPAP is a common occurrence in patients with advanced hepatic disease and is not always related to PPH; there are other conditions that can cause it. Thus, for patients with cirrhosis, we need other hemodynamic parameters, such as PVR, CO and pulmonary capillary pressure (PCP) (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>) and echocardiographic data, to help us establish a proper differential diagnosis.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0045" class="elsevierStylePara elsevierViewall">To understand the pathophysiology of the various scenarios with cirrhosis, we should understand that pulmonary circulation is a closed circuit in which the blood circulates under low pressure. Thus, if we apply the formula that relates pressure and flow, we see that the change in pressure (Δ<span class="elsevierStyleItalic">P</span>) is directly proportional to flow (<span class="elsevierStyleItalic">Q</span>) and resistance (<span class="elsevierStyleItalic">R</span>), i.e., Δ<span class="elsevierStyleItalic">P</span><span class="elsevierStyleHsp" style=""></span>=<span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleItalic">Q</span><span class="elsevierStyleHsp" style=""></span>×<span class="elsevierStyleHsp" style=""></span><span class="elsevierStyleItalic">R</span>. Therefore an increase in flow, i.e., a greater blood supply through the right circulation of the heart will cause increased pressure, which can also occur if the resistances in pulmonary microcirculation increase or if there is a difficulty in pulmonary venous drainage, as occurs in left heart failure. Hemodynamic disorders and changes in the endothelium and myocardium of patients with hepatic cirrhosis can generate increased pulmonary pressure through each of the 3 previously mentioned mechanisms, in the context of highly characteristic conditions such as hyperdynamic circulation, PPH and diastolic dysfunction of patients with cirrhosis. These hemodynamic changes can also be affected by the introduction of an external element such as TIPS. In the following sections, we analyze each of the potential scenarios that have a common denominator: presenting high mPAP.</p><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Hyperdynamic circulation in cirrhosis</span><p id="par0050" class="elsevierStylePara elsevierViewall">One of the key events in the progression of chronic liver disease is the onset of portal hypertension, which occurs in the more advanced phases of cirrhosis and corresponds to the development of most episodes of clinical decompensation, such as varicose vein hemorrhaging, ascites, encephalopathy, renal failure and systemic infections. The increase in intrahepatic vascular resistance caused by the fibrotic changes of the cirrhotic liver has traditionally been considered the main mechanism generating the increase in portal vein pressure and the subsequent development of collateral circulation. However, the mechanisms that lead to portal hypertension transcend the purely mechanical event, given that there is a very important functional component that is also potentially reversible. The increase in nitric oxide levels and those of other substances at the splanchnic level causes vasodilation in this territory, which also favors the development of collaterals.<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">6</span></a> These phenomena facilitate an excess of blood in the splanchnic circulation, which translates into an effective hypovolemia, hypoperfusion of target organs such as the kidneys and activation of vasoactive systems, such as the renin-angiotensin-aldosterone and sympathetic nervous systems. The hemodynamic translation of these changes is what we know as hyperdynamic circulation, in which there is an increase in heart rate and CO, with a reduction in peripheral vascular resistances, which clinically manifests with a tendency toward hypotension and tachycardia.<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">7</span></a> The increase in CO (in our case this is the indirect measure of pulmonary flow), which is more apparent in conditions of hypervolemia (such as after the infusion of albumin or fluids),<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">8</span></a> can cause increased mPAP, which in this case should be interpreted as a physiological response. PVR will be <240<span class="elsevierStyleHsp" style=""></span>dyn<span class="elsevierStyleHsp" style=""></span>cm/s<span class="elsevierStyleSup">5</span>, a fact that will provide us with the differential diagnosis from other severe conditions such as PPH.</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Portopulmonary hypertension</span><p id="par0055" class="elsevierStylePara elsevierViewall">PPH is a rare disorder that occurs in up to 4.5% of patients with advanced hepatic cirrhosis who are candidates for liver transplantation.<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">3</span></a> Its diagnosis is established using hemodynamic criteria. It is therefore essential to perform a right cardiac catheterization using a Swan–Ganz catheter and, if possible, a hemodynamic study of the hepatic veins to measure the portal pressure gradient, which can easily be performed in the same act.<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">9</span></a> The diagnosis of PPH is achieved by measuring mPAP levels >25<span class="elsevierStyleHsp" style=""></span>mmHg and PVR levels >240<span class="elsevierStyleHsp" style=""></span>dyn<span class="elsevierStyleHsp" style=""></span>s/cm<span class="elsevierStyleSup">5</span>, in the presence of a portal pressure gradient >10<span class="elsevierStyleHsp" style=""></span>mmHg.<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">10</span></a> Additionally, the hemodynamic study helps establish the severity of the condition based on the mPAP (mild: 25–35<span class="elsevierStyleHsp" style=""></span>mmHg; moderate: 35–45<span class="elsevierStyleHsp" style=""></span>mmHg; and severe >45<span class="elsevierStyleHsp" style=""></span>mmHg). The pathophysiology of PPH is not adequately known. In patients with advanced cirrhosis, the endothelial damage secondary to pulmonary hyperflow (due to increased CO by the hyperdynamic circulation) is coupled with the arrival of vasoactive substances in the pulmonary microcirculation from the splanchnic circulation through portosystemic communications. This combination results in vasoconstrictor stimulation, a proliferation of the arteriolar tunica media and even local phenomena of microthrombosis.<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">11</span></a> The histological findings are similar to those observed in idiopathic PH and are mostly irreversible. The hemodynamic characteristic of PPH is the presence of very high PVR, greater than 240<span class="elsevierStyleHsp" style=""></span>dyn<span class="elsevierStyleHsp" style=""></span>s/cm<span class="elsevierStyleSup">5</span>. The CO in PPH is usually high. However, if vasoconstriction in the lungs is significant, the increase in right ventricular afterload results in normalized CO. Therefore, cases of PPH with very high PVR and normal or low CO are very severe and seldom respond adequately to medical treatment.<a class="elsevierStyleCrossRef" href="#bib0205"><span class="elsevierStyleSup">8</span></a> PCP is another potentially useful parameter for differentiating this condition. PCP reports the pressures in the left cavities; it rises in cases of left heart failure and hydrostatic edema and should therefore be normal in cases of PPH with no left heart disease. PPH has traditionally been considered a contraindication for liver transplantation. However, patients with PPH should be carefully assessed by an experienced transplantation team. Although perioperative mortality is greater for these cases, the 5-year survival rates with transplantation are greater than 50%,<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">12</span></a> which are comparable to other indications for liver transplantation. Given that the mortality for patients with PPH on waiting lists is greater than that of patients with a similar degree of hepatocellular insufficiency and based on the post-transplantation results, we are faced with a dilemma as to whether PPH should be included as an item for waiting list prioritization, as supported by the main consensus conferences, or whether we should only consider transplantation for highly selected patients.<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">13</span></a> The therapeutic arsenal for primary PH is large. However, patients with cirrhosis are excluded from most clinical trials and studies. There are therefore very few studies that have analyzed the utility of these drugs on this patient subgroup. The result is that most current evidence comes from the extrapolation of results obtained in primary PH. Of the vasodilator drugs currently in use, endothelin inhibitors, phosphodiesterase inhibitors, prostanoids and combinations of these drugs have been shown to be useful in reducing mPAP levels. However, more studies are needed to determine their true impact on survival. Of these drugs, epoprostenol has the most available evidence. The drug is a systemic and pulmonary artery vasodilator, which also has an antiplatelet effect. Although it has shown a clinical and hemodynamic benefit by decreasing PAP by 25% and PVR by 52%, the administration route (endovenous, at a dosage of 4<span class="elsevierStyleHsp" style=""></span>ng/kg/min) and the high number of adverse effects makes this drug a suboptimal tool.<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">14</span></a> Therefore, the use of oral drugs such as bosentan and ambrisentan, which are endothelin receptor antagonists, is considered attractive. However, these drugs are contraindicated in the presence of moderate-severe hepatic impairment and are not exempt from adverse effects.<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">15</span></a> Although the utility of sildenafil for mild PPH has been researched, the drug has not extended patient survival.<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">16</span></a> There are preliminary data that point to the future of PPH management with combined therapies.<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">17</span></a> There are also several clinical trials underway that will help establish strong therapy recommendations in the coming years. What does appear to be established is that the histological changes in patients with PPH are usually irreversible. It is therefore rare that drug treatment can be dispensed with after transplantation. At the practical level, we should understand that the use of noncardioselective beta blockers such as propranolol and nadolol is contraindicated for this patient group, given that they have been shown to worsen the functional class without producing any hemodynamic benefit. The withdrawal of these drugs (or at least their noninitiation) should be assessed for patients who undergo preventive treatment for bleeding esophageal varices.<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">18</span></a> Due to its beneficial effect on cardiac remodeling, the use of carvedilol might be safe for these patients, although there is currently insufficient evidence.<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">19</span></a></p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Cardiac dysfunction and cirrhosis</span><p id="par0060" class="elsevierStylePara elsevierViewall">It has traditionally been considered that the main origin of heart disease for patients with cirrhosis lies in the toxic effects of alcohol. However, progress in diagnostic methods and the study of other types of liver disease have demonstrated that patients with cirrhosis more frequently present specific cardiac disorders. In addition to the previously mentioned hyperdynamic circulation, the hearts of patients with cirrhosis can present defects more often than those of the general population. These include defects in systolic and diastolic function,<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">20</span></a> associated or not with electrocardiographic disorders, as well as Qt interval prolongation, which is present in up to 50% of patients with cirrhosis.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">21</span></a> Hyperdynamic circulation undoubtedly plays a key role in the development of these cardiac disorders, although we still do not know precisely the pathophysiological mechanisms that lead to this condition. Two decades ago, it was proposed that a reduction in the density of β-adrenergic receptors could be an initial step affecting the basic functions of heart contraction–relaxation in patients with cirrhosis.<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">22</span></a> Other hormonal regulators such as nitric oxide,<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">23</span></a> carbon monoxide<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">24</span></a> and endocannabinoids could be involved.<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">25</span></a> Changes in cardiac function are not usually obvious in the initial assessment of patients with cirrhosis, even when these patients are in advanced stages of the disease. These changes become patent in conditions of stress or overload, induced either pharmacologically or as the body's response to a noxious agent/event such as infection, hemorrhaging, the placement of a TIPS and after a large-volume paracentesis. The development of diastolic dysfunction is an earlier event in these patients and is related to the reduction in left ventricular compliance and relaxation, which creates an abnormal pattern of ventricular filling, with greater atrial contribution in the late phase of filling.<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">21</span></a> The most widely used diagnostic method in practice to assess diastolic function is the Doppler echocardiogram, which has been perfected in recent years with the introduction of tissue Doppler echocardiography (TDI). The calculation of the 3 parameters (<span class="elsevierStyleItalic">E</span>-wave, <span class="elsevierStyleItalic">A</span>-wave and deceleration time) is fundamental for the diagnosis. The <span class="elsevierStyleItalic">E</span> peak reports on the rapid ventricular filling, while the <span class="elsevierStyleItalic">A</span>-wave reflects the late atrial contribution. Under normal circumstances, the <span class="elsevierStyleItalic">E</span>/<span class="elsevierStyleItalic">A</span> ratio is greater than 1. In the presence of diastolic dysfunction, however, rapid ventricular filling is reduced due to inadequate ventricular distension. The atrial contribution will therefore be greater, which translates into an inversion of the <span class="elsevierStyleItalic">E</span>/<span class="elsevierStyleItalic">A</span> ratio. The deceleration time increases, causing dilation of the left atrium. Doppler echocardiography, however, has significant limitations, given that there is a pattern of diastolic dysfunction known as pseudonormal in which the E/A ratio is not inverted. This is when TDI plays a role.<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">26</span></a> TDI enables the calculation of the early diastolic transmitral velocity (<span class="elsevierStyleItalic">e</span>′). It has been shown that the increase in the <span class="elsevierStyleItalic">E</span>/<span class="elsevierStyleItalic">e</span>′ ratio helps identify patients with diastolic dysfunction and normal <span class="elsevierStyleItalic">E</span>/<span class="elsevierStyleItalic">a</span> ratios.<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">27</span></a> In conditions of stress such as those mentioned earlier, the hearts of patients with cirrhosis cannot adequately respond, generating hydrostatic pulmonary edema in a retrograde manner, which translates hemodynamically into an increase in PCP. The mPAP increases under these circumstances, which in turn produces PH, which we can encompass within group 2 as proposed by the WHO. Eliminating triggers and adding diuretics in the event of fluid overload would be the most appropriate treatment. In terms of the differential diagnosis with the other previously mentioned conditions, the PVR will be normal. A PCP reading ≥15<span class="elsevierStyleHsp" style=""></span>mmHg would therefore be the most revealing hemodynamic parameter, along with the echocardiographic findings.</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Hemodynamic changes after transjugular intrahepatic portosystemic shunt placement</span><p id="par0065" class="elsevierStylePara elsevierViewall">As patients with cirrhosis and/or portal hypertension progress, they might require the placement of a TIPS to manage conditions such as acute variceal bleeding, recurrence and refractory ascites.<a class="elsevierStyleCrossRefs" href="#bib0305"><span class="elsevierStyleSup">28,29</span></a> Hemodynamic changes secondary to the placement of a TIPS have been the object of study in recent years. Establishing direct communication between the splanchnic and systemic circulation using TIPS produces an increase in the preload, that is, a hyperflow of blood in the right heart cavities. This phenomenon, coupled with the arrival of vasodilatory substances from the splanchnic to the systemic circulation, triggers a reduction in systemic vascular resistances and an increase in CO. This worsening of the hyperdynamic circulation is reflected in significant pulmonary hyperflow, which translates into increased mPAP.<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">30</span></a> As a reaction to this, PVR also increases.<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">31</span></a> These hemodynamic changes are temporary, and most patients recover a few months after the placement of the TIPS.<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">32</span></a> However, if the patient previously presents diastolic dysfunction in the left ventricle (as described above), the hemodynamic changes that blood hyperflow causes might be incomplete. The left ventricle would then be incapable of achieving a sufficient preload to provide for the high cardiac output required by the systemic arteries with high capacity for peripheral vasodilation, thereby raising PCP in a retrograde manner and precipitating heart failure conditions.<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">30</span></a> However, this explanation contrasts with the relatively low incidence of heart failure after TIPS placement.<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">33</span></a> There are currently no clear recommendations as to which patients should be contraindicated TIPS. A risk-benefit analysis should always be conducted and should take into account not only the echocardiographic and hemodynamic parameters but also the indication. Placing a TIPS for severe recurrent variceal bleeding refractory to endoscopic and drug therapy should not have the same implications as placing one for controlling refractory ascites, for which there are other treatments. We do know that left atrial dilation and the presence of high PCP and PVR are associated with an increased risk of developing heart failure after TIPS.<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">30</span></a> In the future, we might have firm results that enable us to use Doppler and tissue Doppler echocardiography to stratify the risk of these patients based on a correct assessment and indication of TIPS.</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Interpreting cardiopulmonary catheterization</span><p id="par0070" class="elsevierStylePara elsevierViewall">As we have shown, patients with cirrhosis can have a wide range of conditions with a common denominator: increased mPAP. Some of these conditions respond to physiological hemodynamic changes; others can be temporary, such as those that occur after TIPS placement. In addition, true conditions of pulmonary arterial hypertension can occur, such as portopulmonary syndrome. We should therefore insist on the correct interpretation of results from the hemodynamic studies on these patients and have the support of a proper echocardiography study. This will enable us to rule out structural heart disease and shed light on a possible diastolic dysfunction whose incidence is higher in this patient group. In order to simplify the differential diagnosis as much as possible for clinicians who face these highly complex scenarios, we have listed the main hemodynamic characteristics of each of the previously specified conditions in <a class="elsevierStyleCrossRef" href="#tbl0005">Table 1</a>.</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia></span></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Conclusions</span><p id="par0075" class="elsevierStylePara elsevierViewall">PH in patients with cirrhosis is a more common phenomenon than it initially appears. The differential diagnosis between the various conditions that lead to increased mPAP can be complicated if the hemodynamic parameters obtained after cardiopulmonary catheterization and the echocardiographic findings are not analyzed in depth. It is essential to properly understand the scenario, given that it is pivotal to critical decisions for the patient such as the indication or contraindication for liver transplantation, TIPS placement, the starting of a specific treatment or the suspension of other treatments. Thus, we emphasize the need for a very careful clinical assessment of these patients, who should be evaluated as much as possible by multidisciplinary teams consisting of the physicians who treat the patient, experts in hepatic hemodynamics, cardiologists, pulmonologists, internists, hepatologists, anesthesiologists and surgeons.</p><p id="par0080" class="elsevierStylePara elsevierViewall">In the case presented at the start of this article, the patient's PH could be due to several reasons. It is highly likely that prior to the TIPS placement the patient presented some type of myocardial or pulmonary disorder that induced the subsequent development of PH and right heart failure after TIPS placement. Thus, we can see the importance of requesting a prior echocardiogram, especially in highly suspicious cases due to cardiovascular risk factors. Pulmonary hyperflow in the context of high CO caused stress on the pulmonary endothelium, which in turn translated into increased PVR and mPAP. Given that a response was not observed in the vasodilator test, the decision was made not to start drug treatment for the PH. There is, however, considerable controversy on this point, and there is currently no study that enables us to establish the most appropriate procedure in these cases. Finally, given that the patient had mPAP levels >45<span class="elsevierStyleHsp" style=""></span>mmHg, liver transplantation was ruled out. The patient's functional class significantly improved with diuretics, and the ascites, dyspnea and edema remained under good control.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:11 [ 0 => array:3 [ "identificador" => "xres538278" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec558035" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres538279" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec558034" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Background" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "The clinical problem" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Clinical guidelines and areas of uncertainty" ] 7 => array:3 [ "identificador" => "sec0020" "titulo" => "Pulmonary hypertension and cirrhosis" "secciones" => array:5 [ 0 => array:2 [ "identificador" => "sec0025" "titulo" => "Hyperdynamic circulation in cirrhosis" ] 1 => array:2 [ "identificador" => "sec0030" "titulo" => "Portopulmonary hypertension" ] 2 => array:2 [ "identificador" => "sec0035" "titulo" => "Cardiac dysfunction and cirrhosis" ] 3 => array:2 [ "identificador" => "sec0040" "titulo" => "Hemodynamic changes after transjugular intrahepatic portosystemic shunt placement" ] 4 => array:2 [ "identificador" => "sec0045" "titulo" => "Interpreting cardiopulmonary catheterization" ] ] ] 8 => array:2 [ "identificador" => "sec0050" "titulo" => "Conclusions" ] 9 => array:2 [ "identificador" => "xack182374" "titulo" => "Acknowledgments" ] 10 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2014-12-06" "fechaAceptado" => "2015-02-23" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec558035" "palabras" => array:6 [ 0 => "Portal hypertension" 1 => "Pulmonary hypertension" 2 => "Diastolic dysfunction" 3 => "Portopulmonary syndrome" 4 => "Cirrhosis" 5 => "Hyperdynamic circulation" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec558034" "palabras" => array:6 [ 0 => "Hipertensión portal" 1 => "Hipertensión pulmonar" 2 => "Disfunción diastólica" 3 => "Síndrome portopulmonar" 4 => "Cirrosis" 5 => "Circulación hiperdinámica" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Pulmonary hypertension is a relatively common phenomenon in patients with hepatic cirrhosis and can appear through various mechanisms. The most characteristic scenario that binds portal and pulmonary hypertension is portopulmonary syndrome. However, hyperdynamic circulation, TIPS placement and heart failure can raise the mean pulmonary artery pressure without increasing the resistances. These conditions are not candidates for treatment with pulmonary vasodilators and require a specific therapy. A correct assessment of hemodynamic, ultrasound and clinical variables enables the differential diagnosis of each situation that produces pulmonary hypertension in patients with cirrhosis.</p></span>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">La hipertensión pulmonar es un fenómeno relativamente frecuente en los enfermos con cirrosis hepática y puede aparecer por diversos mecanimos. El escenario más característico que une la hipertensión portal y la hipertensión pulmonar es el síndrome portopulmonar. Sin embargo, la circulación hiperdinámica, la colocación de un TIPS o la insuficiencia cardíaca pueden elevar la presión media de la arteria pulmonar sin incremento de las resistencias. Estas situaciones no serán candidatas a tratamiento con vasodilatadores pulmonares y requieren una terapéutica específica. Una correcta valoración de variables hemodinámicas, ecográficas y clínicas permite el diagnóstico diferencial entre cada situación que produce hipertensión pulmonar en los pacientes cirróticos.</p></span>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: Téllez Villajos L, Martínez González J, Moreira Vicente V, Albillos Martínez A. Hipertensión pulmonar y cirrosis hepática. Rev Clin Esp. 2015;215:324–330.</p>" ] ] "multimedia" => array:2 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 955 "Ancho" => 2090 "Tamanyo" => 130684 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Normal values for cardiopulmonary pressures in a right cardiac catheterization using Swan–Ganz catheter.</p>" ] ] 1 => array:7 [ "identificador" => "tbl0005" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "tabla" => array:2 [ "leyenda" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleItalic">Abbreviations</span>: CO, cardiac output; mPAP, mean pulmonary arterial pressure; PCP, pulmonary capillary pressure; PVR, pulmonary vascular resistance; TIPS, transjugular intrahepatic portosystemic shunt.</p>" "tablatextoimagen" => array:1 [ 0 => array:2 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="table-head " align="" valign="top" scope="col" style="border-bottom: 2px solid black"> \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">mPAP \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">PVR \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">CO \t\t\t\t\t\t\n \t\t\t\t</th><th class="td" title="table-head " align="left" valign="top" scope="col" style="border-bottom: 2px solid black">PCP \t\t\t\t\t\t\n \t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Normal \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">15–24<span class="elsevierStyleHsp" style=""></span>mmHg \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top"><240<span class="elsevierStyleHsp" style=""></span>dyn<span class="elsevierStyleHsp" style=""></span>s/cm<span class="elsevierStyleSup">5</span> \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">4–8<span class="elsevierStyleHsp" style=""></span>l/min \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">6–14<span class="elsevierStyleHsp" style=""></span>mmHg \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Portopulmonary \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High/normal/low \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Normal \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Fluid overload/heart failure \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Normal/high \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">After TIPS placement \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High/normal \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="table-entry " align="left" valign="top">Hyperdynamic circulation in cirrhosis \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High/normal \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Normal \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">High \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="table-entry " align="left" valign="top">Normal \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] "imagenFichero" => array:1 [ 0 => "xTab864967.png" ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Interpretation of cardiopulmonary catheterization and differential diagnosis between the various conditions that raise mean pulmonary pressure in cirrhosis.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:33 [ 0 => array:3 [ "identificador" => "bib0170" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Pulmonary hypertension in liver diseases" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "L. Savale" 1 => "C. Sattler" 2 => "O. Sitbon" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.lpm.2014.07.010" "Revista" => array:6 [ "tituloSerie" => "Presse Med" "fecha" => "2014" "volumen" => "43" "paginaInicial" => "970" "paginaFinal" => "980" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/25148949" "web" => "Medline" ] ] ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib0175" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "MELD exception for liver transplantation in portopulmonary hypertension: current implementation and future considerations" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "M. Porres-Aguilar" 1 => "S.D. Bartolome" 2 => "A. Duarte-Rojo" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Ann Hepatol" "fecha" => "2014" "volumen" => "13" "paginaInicial" => "719" "paginaFinal" => "721" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/25332257" "web" => "Medline" ] ] ] ] ] ] ] ] 2 => array:3 [ "identificador" => "bib0180" "etiqueta" => "3" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Portopulmonary hypertension" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "R. Cartin-Ceba" 1 => "M.J. Krowka" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.cld.2014.01.004" "Revista" => array:6 [ "tituloSerie" => "Clin Liver Dis" "fecha" => "2014" "volumen" => "18" "paginaInicial" => "421" "paginaFinal" => "438" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/24679504" "web" => "Medline" ] ] ] ] ] ] ] ] 3 => array:3 [ "identificador" => "bib0185" "etiqueta" => "4" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Definitions and diagnosis of pulmonary hypertension" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "M.M. Hoeper" 1 => "H.J. Bogaard" 2 => "R. Condliffe" 3 => "R. Frantz" 4 => "M. Kurzyna" 5 => "D. Langleben" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.jacc.2013.10.032" "Revista" => array:5 [ "tituloSerie" => "J Am Coll Cardiol" "fecha" => "2013" "volumen" => "62" "paginaInicial" => "D42" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/24355641" "web" => "Medline" ] ] ] ] ] ] ] ] 4 => array:3 [ "identificador" => "bib0190" "etiqueta" => "5" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Updated clinical classification of pulmonary hypertension" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "G. Simonneau" 1 => "M.A. Gatzoulis" 2 => "I. Adatia" 3 => "D. Celermajer" 4 => "C. Denton" 5 => "R.F. Machado" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.jacc.2013.10.029" "Revista" => array:5 [ "tituloSerie" => "J Am Coll Cardiol" "fecha" => "2013" "volumen" => "62" "paginaInicial" => "D34" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/24355639" "web" => "Medline" ] ] ] ] ] ] ] ] 5 => array:3 [ "identificador" => "bib0195" "etiqueta" => "6" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Endotelial dysfunction and decreased production of nitric oxide in the intrahepatic microcirculation of cirrhotic rats" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "T.K. Gupta" 1 => "M. Toruner" 2 => "M.K. Chung" 3 => "R.J. Groszmann" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1002/hep.510280405" "Revista" => array:6 [ "tituloSerie" => "Hepatology" "fecha" => "1998" "volumen" => "28" "paginaInicial" => "926" "paginaFinal" => "931" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/9755227" "web" => "Medline" ] ] ] ] ] ] ] ] 6 => array:3 [ "identificador" => "bib0200" "etiqueta" => "7" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "M. Bolognesi" 1 => "M. Di Pascoli" 2 => "A. Verardo" 3 => "A. Gatta" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.3748/wjg.v20.i10.2555" "Revista" => array:6 [ "tituloSerie" => "World J Gastroenterol" "fecha" => "2014" "volumen" => "20" "paginaInicial" => "2555" "paginaFinal" => "2563" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/24627591" "web" => "Medline" ] ] ] ] ] ] ] ] 7 => array:3 [ "identificador" => "bib0205" "etiqueta" => "8" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Pathophysiological basis of albumin use in cirrhosis" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "V. Arroyo" 1 => "J. Fernandez" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:7 [ "tituloSerie" => "Ann Hepatol" "fecha" => "2011" "volumen" => "10" "numero" => "Suppl. 1" "paginaInicial" => "S6" "paginaFinal" => "S14" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/21566249" "web" => "Medline" ] ] ] ] ] ] ] ] 8 => array:3 [ "identificador" => "bib0210" "etiqueta" => "9" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The clinical use of HVPG measurements in chronic liver disease" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "J. Bosch" 1 => "J.G. Abraldes" 2 => "A. Berzigotti" 3 => "J.C. García-Pagan" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1038/nrgastro.2009.149" "Revista" => array:6 [ "tituloSerie" => "Nat Rev Gastroenterol Hepatol" "fecha" => "2009" "volumen" => "6" "paginaInicial" => "573" "paginaFinal" => "582" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/19724251" "web" => "Medline" ] ] ] ] ] ] ] ] 9 => array:3 [ "identificador" => "bib0215" "etiqueta" => "10" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Portopulmonary hypertension: an update" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "Z. Safdar" 1 => "S. Bartolome" 2 => "N. Sussman" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Liver Transplant" "fecha" => "2012" "volumen" => "18" "paginaInicial" => "881" "paginaFinal" => "891" ] ] ] ] ] ] 10 => array:3 [ "identificador" => "bib0220" "etiqueta" => "11" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Portopulmonary hypertension: state of art" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "M. Porres-Aguilar" 1 => "M.J. Zuckerman" 2 => "J.B. Figueroa-Casas" 3 => "M.J. Krowka" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Ann Hepatol" "fecha" => "2008" "volumen" => "7" "paginaInicial" => "321" "paginaFinal" => "330" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/19034231" "web" => "Medline" ] ] ] ] ] ] ] ] 11 => array:3 [ "identificador" => "bib0225" "etiqueta" => "12" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The impact of treatment of portopulmonary hypertension on survival following liver transplantation" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "M. Ashfaq" 1 => "S. Chinnakotla" 2 => "L. Rogers" 3 => "K. Ausloos" 4 => "S. Saadeh" 5 => "G.B. Klintmalm" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Am J Transplant" "fecha" => "2007" "volumen" => "125" "paginaInicial" => "8" "paginaFinal" => "64" ] ] ] ] ] ] 12 => array:3 [ "identificador" => "bib0230" "etiqueta" => "13" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Exceptions to model for end-stage liver disease in prioritizing liver transplantation" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "L. Lladó" 1 => "J. Bustamante" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1016/j.gastrohep.2013.06.011" "Revista" => array:6 [ "tituloSerie" => "Gastroenterol Hepatol" "fecha" => "2014" "volumen" => "37" "paginaInicial" => "83" "paginaFinal" => "91" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/24290253" "web" => "Medline" ] ] ] ] ] ] ] ] 13 => array:3 [ "identificador" => "bib0235" "etiqueta" => "14" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Long term follow up of portopulmonary hypertension: effect of treatment with epoprostenol" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:4 [ 0 => "O.K. Fix" 1 => "N.M. Bass" 2 => "T. de Marco" 3 => "R.B. Merriman" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Liver Transplant" "fecha" => "2007" "volumen" => "13" "paginaInicial" => "875" "paginaFinal" => "885" ] ] ] ] ] ] 14 => array:3 [ "identificador" => "bib0240" "etiqueta" => "15" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Experience with inhaled iloprost and bosentan in portopulmonary hypertension" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "M.M. Hoeper" 1 => "H.J. Seyfarth" 2 => "G. Hoeffken" 3 => "H. Wirtz" 4 => "E. Spiekerkoetter" 5 => "M.W. Pletz" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1183/09031936.00032407" "Revista" => array:6 [ "tituloSerie" => "Eur Respir J" "fecha" => "2007" "volumen" => "30" "paginaInicial" => "1096" "paginaFinal" => "1102" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/17652314" "web" => "Medline" ] ] ] ] ] ] ] ] 15 => array:3 [ "identificador" => "bib0245" "etiqueta" => "16" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Sildenafil monotherapy in portopulmonary hypertension can facilitate liver transplantation" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "A.R. Hemnes" 1 => "I.M. Robbins" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Liver Transplant" "fecha" => "2009" "volumen" => "15" "paginaInicial" => "15" "paginaFinal" => "19" ] ] ] ] ] ] 16 => array:3 [ "identificador" => "bib0250" "etiqueta" => "17" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Portopulmonary hypertension: formidable dual threat versus hopeful dual therapy" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "M.J. Krowka" 1 => "R. Cartin-Ceba" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Liver Transplant" "fecha" => "2014" "volumen" => "20" "paginaInicial" => "365" "paginaFinal" => "366" ] ] ] ] ] ] 17 => array:3 [ "identificador" => "bib0255" "etiqueta" => "18" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Deleterious effects of beta-blockers on exercise capacity and hemodynamics in patients with portopulmonary hypertension" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "S. Provencher" 1 => "P. Herve" 2 => "X. Jais" 3 => "D. Lebrec" 4 => "M. Humbert" 5 => "G. Simonneau" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1053/j.gastro.2005.10.013" "Revista" => array:6 [ "tituloSerie" => "Gastroenterology" "fecha" => "2006" "volumen" => "130" "paginaInicial" => "120" "paginaFinal" => "126" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16401475" "web" => "Medline" ] ] ] ] ] ] ] ] 18 => array:3 [ "identificador" => "bib0260" "etiqueta" => "19" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Treatment of group I pulmonary arterial hypertension with carvedilol is safe" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "D. Grinnan" 1 => "H.J. Bogaard" 2 => "J. Grizzard" 3 => "B. Van Tassell" 4 => "A. Abbate" 5 => "C. DeWilde" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1164/rccm.201311-2025LE" "Revista" => array:6 [ "tituloSerie" => "Am J Respir Crit Care Med" "fecha" => "2014" "volumen" => "189" "paginaInicial" => "1562" "paginaFinal" => "1564" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/24930531" "web" => "Medline" ] ] ] ] ] ] ] ] 19 => array:3 [ "identificador" => "bib0265" "etiqueta" => "20" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Cirrhotic cardiomyopathy: a cardiologist's perspective" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "N. Gassanov" 1 => "E. Caglayan" 2 => "N. Semmo" 3 => "G. Massenkeil" 4 => "F. Er" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.3748/wjg.v20.i42.15492" "Revista" => array:6 [ "tituloSerie" => "World J Gastroenterol" "fecha" => "2014" "volumen" => "20" "paginaInicial" => "15492" "paginaFinal" => "15498" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/25400434" "web" => "Medline" ] ] ] ] ] ] ] ] 20 => array:3 [ "identificador" => "bib0270" "etiqueta" => "21" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Cirrhotic cardiomyopathy" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "S. Moller" 1 => "J.H. Henriksen" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "J Hepatol" "fecha" => "2010" "volumen" => "52" "paginaInicial" => "179" "paginaFinal" => "190" ] ] ] ] ] ] 21 => array:3 [ "identificador" => "bib0275" "etiqueta" => "22" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Evidence for down-regulation of beta-2-adrenoceptors in cirrhotic patients with severe ascites" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "A.L. Gerbes" 1 => "J. Remien" 2 => "D. Jüngst" 3 => "T. Sauerbruch" 4 => "G. Paumgartner" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Lancet" "fecha" => "1986" "volumen" => "1" "paginaInicial" => "1409" "paginaFinal" => "1411" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/2884499" "web" => "Medline" ] ] ] ] ] ] ] ] 22 => array:3 [ "identificador" => "bib0280" "etiqueta" => "23" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Contribution of nitric oxide to the pathogenesis of cirrhotic cardiomyopathy in bile duct-ligated rats" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "H. Liu" 1 => "Z. Ma" 2 => "S.S. Lee" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Gastroenterology" "fecha" => "2000" "volumen" => "118" "paginaInicial" => "937" "paginaFinal" => "944" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/10784593" "web" => "Medline" ] ] ] ] ] ] ] ] 23 => array:3 [ "identificador" => "bib0285" "etiqueta" => "24" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The heme oxygenase-carbon monoxide system: a regulator of hepatobiliary function" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "M. Suematsu" 1 => "Y. Ishimura" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1002/hep.510310102" "Revista" => array:6 [ "tituloSerie" => "Hepatology" "fecha" => "2000" "volumen" => "31" "paginaInicial" => "3" "paginaFinal" => "6" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/10613719" "web" => "Medline" ] ] ] ] ] ] ] ] 24 => array:3 [ "identificador" => "bib0290" "etiqueta" => "25" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Role of endocannabinoids in the pathogenesis of cirrhotic cardiomyopathy in bile duct-ligated rats" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "S.A. Gaskari" 1 => "H. Liu" 2 => "L. Moezi" 3 => "Y. Li" 4 => "S.K. Baik" 5 => "S.S. Lee" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1038/sj.bjp.0706331" "Revista" => array:6 [ "tituloSerie" => "Br J Pharmacol" "fecha" => "2005" "volumen" => "146" "paginaInicial" => "315" "paginaFinal" => "323" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16025138" "web" => "Medline" ] ] ] ] ] ] ] ] 25 => array:3 [ "identificador" => "bib0295" "etiqueta" => "26" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "S.F. Nagueh" 1 => "K.J. Middleton" 2 => "H.A. Kopelen" 3 => "W.A. Zoghbi" 4 => "M.A. Quiñones" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "J Am Coll Cardiol" "fecha" => "1997" "volumen" => "30" "paginaInicial" => "1527" "paginaFinal" => "1533" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/9362412" "web" => "Medline" ] ] ] ] ] ] ] ] 26 => array:3 [ "identificador" => "bib0300" "etiqueta" => "27" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Cardiac dysfunction in cirrhotic portal hypertension with or without ascites" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "S. Dadhich" 1 => "A. Goswami" 2 => "V.K. Jain" 3 => "A. Gahlot" 4 => "G. Kulamarva" 5 => "N. Bhargava" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Ann Gastroenterol" "fecha" => "2014" "volumen" => "27" "paginaInicial" => "244" "paginaFinal" => "249" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/24974920" "web" => "Medline" ] ] ] ] ] ] ] ] 27 => array:3 [ "identificador" => "bib0305" "etiqueta" => "28" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Transjugular intrahepatic portosystemic shunt: indications, contraindications, and patient work-up" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "A. Copelan" 1 => "B. Kapoor" 2 => "M. Sands" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1055/s-0034-1382790" "Revista" => array:6 [ "tituloSerie" => "Semin Intervent Radiol" "fecha" => "2014" "volumen" => "31" "paginaInicial" => "235" "paginaFinal" => "242" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/25177083" "web" => "Medline" ] ] ] ] ] ] ] ] 28 => array:3 [ "identificador" => "bib0310" "etiqueta" => "29" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "The transjugular intrahepatic portosystemic shunt for the management of cirrhotic refractory ascites" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "G. Garcia-Tsao" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1038/ncpgasthep0523" "Revista" => array:6 [ "tituloSerie" => "Nat Clin Pract Gastroenterol Hepatol" "fecha" => "2006" "volumen" => "3" "paginaInicial" => "380" "paginaFinal" => "389" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/16819501" "web" => "Medline" ] ] ] ] ] ] ] ] 29 => array:3 [ "identificador" => "bib0315" "etiqueta" => "30" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Cardiac and renal effects of a transjugular intrahepatic portosystemic shunt in cirrhosis" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "T.M. Busk" 1 => "F. Bendtsen" 2 => "S. Moller" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1097/MEG.0b013e32835d09fe" "Revista" => array:6 [ "tituloSerie" => "Eur J Gastroenterol Hepatol" "fecha" => "2013" "volumen" => "25" "paginaInicial" => "523" "paginaFinal" => "530" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/23325273" "web" => "Medline" ] ] ] ] ] ] ] ] 30 => array:3 [ "identificador" => "bib0320" "etiqueta" => "31" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Pulmonary hypertension after transjugular intrahepatic portosystemic shunt: effects on right ventricular function" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => "P. Van der Linden" 1 => "O. Le Moine" 2 => "M. Ghysels" 3 => "M. Ortinez" 4 => "J. Devière" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Hepatology" "fecha" => "1996" "volumen" => "23" "paginaInicial" => "928" "paginaFinal" => "937" ] ] ] ] ] ] 31 => array:3 [ "identificador" => "bib0325" "etiqueta" => "32" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Haemodynamic adaptation two months after transjugular intrahepatic portosystemic shunt (TIPS) in cirrhotic patients" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "L.A. Colombato" 1 => "L. Spahr" 2 => "J.P. Martinet" 3 => "M.P. Dufresne" 4 => "M. Lafortune" 5 => "D. Fenyves" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "Gut" "fecha" => "1996" "volumen" => "39" "paginaInicial" => "600" "paginaFinal" => "604" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/8944572" "web" => "Medline" ] ] ] ] ] ] ] ] 32 => array:3 [ "identificador" => "bib0330" "etiqueta" => "33" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Transjugular intrahepatic portosystemic shunting versus paracentesis plus albumin for refractory ascites in cirrhosis" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "P. Ginès" 1 => "J. Uriz" 2 => "B. Calahorra" 3 => "G. Garcia-Tsao" 4 => "P.S. Kamath" 5 => "L.R. del Arbol" ] ] ] ] ] "host" => array:1 [ 0 => array:2 [ "doi" => "10.1053/gast.2002.37073" "Revista" => array:6 [ "tituloSerie" => "Gastroenterology" "fecha" => "2002" "volumen" => "123" "paginaInicial" => "1839" "paginaFinal" => "1847" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/12454841" "web" => "Medline" ] ] ] ] ] ] ] ] ] ] ] ] "agradecimientos" => array:1 [ 0 => array:4 [ "identificador" => "xack182374" "titulo" => "Acknowledgments" "texto" => "<p id="par0085" class="elsevierStylePara elsevierViewall">The authors thank Victor Moreira for demonstrating on a daily basis that a job well done and humility are the only paths to excellence.</p>" "vista" => "all" ] ] ] "idiomaDefecto" => "en" "url" => "/22548874/0000021500000006/v2_201508011306/S2254887415000600/v2_201508011306/en/main.assets" "Apartado" => array:4 [ "identificador" => "1904" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Clinical Up-Date" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/22548874/0000021500000006/v2_201508011306/S2254887415000600/v2_201508011306/en/main.pdf?idApp=WRCEE&text.app=https://revclinesp.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2254887415000600?idApp=WRCEE" ]
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| 2023 March | 3 | 3 | 6 |
| 2018 February | 5 | 0 | 5 |
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