Involvement of systemic venous congestion in heart failure

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Source: Adapted from Kazory et al.<a class="elsevierStyleCrossRef" href="#bib0690">69</a>" ] ] ] "textoCompleto" => "Concept of venous congestionTaking into account strictly hemodynamic criteria, systemic venous congestion is defined as an increase in pulmonary wedge pressure >12mmHg or an increase in left ventricular diastolic pressure >16mmHg, measured through catheterization of the right-sided heart chambers.<a class="elsevierStyleCrossRef" href="#bib0350">1</a> However, the definition is of little practical use due to the methods’ invasiveness. Systemic venous congestion in heart failure (HF) results from the increase in intravascular volume caused by an increase in ventricular diastolic pressure. Moreover, the increase in ventricular end-diastolic pressure is the direct result of 2 conditions: direct myocardial damage (as in ischemic heart disease or cardiomyopathies) and the increase in preload associated with prior ventricular dysfunction, which causes an increase in central venous pressure (CVP). HF is produces in both conditions, and, depending on the left ventricular ejection fraction (LVEF), we talk of HF with preserved ejection fraction for LVEF >50%; intermediate for 40–49% and reduced if LVEF <40%.<a class="elsevierStyleCrossRef" href="#bib0355">2</a>Identifying congestion in acute HF (AHF) is of primary importance. Up to 66% of patients in the Acute Decompensated Heart Failure National Registry (ADHERE)<a class="elsevierStyleCrossRef" href="#bib0360">3</a> presented some degree of systemic congestion at admission.Symptomatology of congestionClassically, congestion is detected via a physical examination revealing the presence of the following classic signs: jugular venous distention, hepatomegaly, superficial collateral venous circulation, ascites and edema in dependent regions. Pulmonary congestion is defined mainly by the increase in respiratory effort or rate and the auscultation of end-inspiratory crackles.<a class="elsevierStyleCrossRef" href="#bib0365">4</a>The signs of congestion and the degree of skin perfusion configure the 4 clinical phenotypes of patients with AHF (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>), with clear connotations for the prognosis and treatment.<a class="elsevierStyleCrossRef" href="#bib0370">5</a> Patients who present more signs of congestion during the examination have higher wedge pressure in the pulmonary artery and a poorer prognosis.<a class="elsevierStyleCrossRefs" href="#bib0360">3–7</a> However, despite its usefulness, the physical examination has little sensitivity for detecting or ruling out the presence of congestion, especially the subclinical grades.<a class="elsevierStyleCrossRef" href="#bib0365">4</a> Quantifying or measuring the degree of congestion is difficult to determine using the physical examination.<elsevierMultimedia ident="fig0005"></elsevierMultimedia>In recent years and thanks to advances in technology, more objective complementary examinations have been developed to detect and measure venous congestion in HF, such as impedance audiometry,<a class="elsevierStyleCrossRef" href="#bib0385">8</a> pulmonary ultrasonography<a class="elsevierStyleCrossRefs" href="#bib0390">9,10</a> and the measurement of the diameter and collapse of the inferior vena cava (IVC)<a class="elsevierStyleCrossRef" href="#bib0400">11</a> (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>). Thus, systemic congestion is considered when the ultrasound diameter of the IVC is >21mm in inspiration, and the collapse is <50% of the baseline diameter.<a class="elsevierStyleCrossRef" href="#bib0400">11</a> Patients with systemic congestion estimated by this method have a poorer prognosis at 6 months of discharge from an episode of AHF.<a class="elsevierStyleCrossRefs" href="#bib0405">12–14</a> Another ultrasound technique that assesses pulmonary congestion is pulmonary ultrasonography to visualize the Kerley B lines (sign of the comet tail).<a class="elsevierStyleCrossRef" href="#bib0420">15</a> This new approach to the ultrasound examination of the lungs has high sensitivity (94%) and specificity (92%) for detecting interstitial edema and helps differentiate between cardiogenic and respiratory dyspnea. The approach also helps quantify the intensity of the congestion, because there is a correlation between the number of artifacts in the various lung fields and NT-proBNP concentrations and the echocardiographic quotient E/e’ (of vital importance for assessing HF with preserved LVEF).<a class="elsevierStyleCrossRefs" href="#bib0390">9,10,16</a> Lastly, pulmonary impedance audiometry, built into pacemaker technology, has helped reduce the rate of readmissions of patients with chronic HF, as shown by the IMPEDANCE-HF study.<a class="elsevierStyleCrossRef" href="#bib0430">17</a><elsevierMultimedia ident="fig0010"></elsevierMultimedia>Despite these techniques, determining a patient's congestive state remains difficult. A study published in 2007 with 134 patients hospitalized for HF (New York Heart Association functional class III) who were previously telemonitored in their homes through vital sign monitoring and daily weightings, revealed the inability to perform early detection of decompensations.<a class="elsevierStyleCrossRef" href="#bib0435">18</a> This study showed how the week before the admission (i.e., before the patient presented symptoms of decompensation), there was a significant increase in body weight, suggesting that the congestion starts before the clinical manifestations. These results are similar to those from another study in which the authors, by monitoring hemodynamic parameters in a subgroup of the Chronicle Offers Management to Patients with Advanced Signs and Symptoms of Heart Failure (COMPASS-HF) cohort, demonstrated an increase in ventricular diastolic pressure as a phenomenon prior to decompensation by HF.<a class="elsevierStyleCrossRef" href="#bib0440">19</a>To define this oligosymptomatic stage prior to the onset of congestive signs, Gheorghiade et al. introduced the term “congestion hemodynamics” to name the condition in which there is an increase in left ventricular filling pressures without clinical translation. The authors reserved the term “clinical congestion” for the other conditions in which the state of maintained hemodynamic congestion resulted in the onset of dyspnea, orthopnea, crackles, edema and jugular venous distention.<a class="elsevierStyleCrossRef" href="#bib0445">20</a>Despite the better understanding of the concept, of its importance in clinical practice and of the incorporation of a number of techniques for its discovery, the definition, detection and quantification of congestion continue to be a clinical challenge.Prognostic meaning of congestion in heart failureAHF results in approximately a million admissions a year in US hospitals, and 76% of these patients have a history of HF.<a class="elsevierStyleCrossRef" href="#bib0450">21</a> In the ADHERE registry, 66% of the patients showed signs of systemic congestion.<a class="elsevierStyleCrossRef" href="#bib0360">3</a> In a post hoc analysis of the Studies Of Left Ventricular Dysfunction (SOLVD), the authors found a correlation between the presence of jugular venous distention or third heart sound at admission (as surrogate signs of congestion) and the risk of readmission for HF and death.<a class="elsevierStyleCrossRef" href="#bib0455">22</a>In daily practice, treatment response is assessed through the observation of the attenuation or disappearance of congestion, and it is standard procedure to proceed with the discharge when this phenomenon is maintained with stable doses of oral diuretics.<a class="elsevierStyleCrossRefs" href="#bib0355">2,23</a> However, it has been observed that once the congestive symptoms disappear after the first days of treatment, the left ventricle filling pressures can remain high (congestion hemodynamics), with the subsequent increase in the risk of early readmission.<a class="elsevierStyleCrossRef" href="#bib0445">20</a> Up to 48% of patients presented some residual sign of congestion at discharge,<a class="elsevierStyleCrossRefs" href="#bib0470">25,25</a> and it has been shown that patients with 3 or more signs of congestion at discharge have a higher mortality rate than patients with no congestive signs in the first 60 days after discharge.<a class="elsevierStyleCrossRef" href="#bib0465">24</a> In patients with New York Heart Association functional class IV and a mean LVEF of 20%, the absence of congestive symptoms between weeks 4 and 6 after the hospitalization is associated with longer survival.<a class="elsevierStyleCrossRef" href="#bib0475">26</a> Therefore, reaching an optimal state of decongestion before the discharge is a crucial therapeutic objective.Venous congestion is also involved in organ dysfunction, especially of the kidneys. Approximately 30% of patients with AHF have renal function impairment associated with the AHF,<a class="elsevierStyleCrossRef" href="#bib0360">3</a> which results in a poorer prognosis.<a class="elsevierStyleCrossRef" href="#bib0480">27</a> Renal dysfunction resulting from systemic congestion is called congestive renal failure by a number of authors.<a class="elsevierStyleCrossRef" href="#bib0485">28</a> Understanding this condition's pathophysiology could be essential for improved understanding of both organ damage during episodes of decompensation and the diuretic response.Ter Maaten et al. analyzed the rate of readmissions for patients with AHF based on the diuretic response, defined as the weight change in kilograms during the first 72h of treatment for every 40mg of furosemide administered intravenously.<a class="elsevierStyleCrossRef" href="#bib0490">29</a> The authors also used the hemoglobin concentration as a surrogate marker of congestion. The patients with poorer diuretic response who remained hemodiluted, depending on the hemoglobin concentration, had a greater risk of readmission during the 60 days after the discharge. Nuñez et al., using the CA125 biomarker as a surrogate marker of congestion, found a direct association between the changes in renal function (measured by variations in creatinine concentrations) and the intravenous loop diuretic dose.<a class="elsevierStyleCrossRef" href="#bib0495">30</a> The Carbohydrate Antigen 125-guided Therapy in Acute Heart Failure (CHANCE) study confirmed that the use of plasma CA125 concentrations to guide treatment for AHF offers better results than the standard strategy based on signs and symptoms.<a class="elsevierStyleCrossRef" href="#bib0500">31</a>Role of congestion in the cardiorenal interactionCongestion has classically been explained as the consequence of a myocardial aggression that causes reduced cardiac output, with the consequent reduction in intravascular volume, which through the stimulation of various baroreceptors causes the activation of a concerted neurohumoral response. First, the sympathetic nervous system (SNS) causes a redistribution of the blood flow through vasoconstriction of the peripheral circulation and an increased heart rate to compensate for the cardiac output, thereby ensuring the perfusion of vital organs.<a class="elsevierStyleCrossRef" href="#bib0505">32</a> Second, we have the response mediated by the renin-angiotensin-aldosterone system and vasopressin. The former facilitates sodium reabsorption through the distal convoluted tubule and the latter decreases free water excretion in the collecting tubule.<a class="elsevierStyleCrossRefs" href="#bib0505">32,33</a>The activation of these systems enables the recovery of blood volume and maintains the short-term perfusion of vital organs; however, in the medium to long-term, the activation promotes tissue damage, which worsens the cardiac function (maladaptive response). The combined neurohormonal and SNS activation causes an excessive expansion of fluid in the intravascular space, which is stored in the venous system until the maximum possible capacitance is reached. Once this falters, it causes an increase in CVP, with abdominal organ congestion, progressive weight gain, expansion to the interstitial space and onset of classical HF symptoms.<a class="elsevierStyleCrossRef" href="#bib0515">34</a>Systemic congestion can be initially reversed with diuretics.<a class="elsevierStyleCrossRefs" href="#bib0460">23,35</a> In the long term, however, and through complex mechanisms of escape and renal adaptation to the action of diuretics<a class="elsevierStyleCrossRef" href="#bib0525">36</a> and the progression of the disease, a permanent refractory congestive condition develops, as well as signs of organ dysfunction (e.g., renal, hepatic and pulmonary),<a class="elsevierStyleCrossRef" href="#bib0360">3</a> progressive worsening of the quality of life and greater readmissions for HF, which translate into increased mortality.<a class="elsevierStyleCrossRef" href="#bib0465">24</a>Not all patients respond equally to depletive treatment, which shows that congestion is heterogeneous and goes beyond a mere hemodynamic and vascular redistribution problem. Various complex mechanisms that are still not properly understood are likely to act along with the SNS and renin–angiotensin–aldosterone system in perpetuating tissue damage in HF.<a class="elsevierStyleCrossRefs" href="#bib0530">37,38</a> Using an experimental model, Colombo et al. demonstrated the relationship between venous congestion and inflammation.<a class="elsevierStyleCrossRef" href="#bib0530">37</a> The authors produced venous congestion in an arm through extrinsic compression with a sphygmograph and obtained peripheral blood from both arms, the compressed arm (before and after inflating the cuff) and the other taken as a control. The result was a significant increase in the concentrations of interleukin-6, endothelin-1 and angiotensin II in the blood samples extracted from the compressed arm when compared with the control.<a class="elsevierStyleCrossRef" href="#bib0530">37</a> Although this was an experimental model that did not reproduce the pressure conditions achieved inside human vessels, the authors undoubtedly demonstrated the presence of a link between venous congestion and inflammation.Another fundamental factor in the development of congestion in patients with HF is the abdominal circulation and, more specifically, the splanchnic venous network.<a class="elsevierStyleCrossRefs" href="#bib0540">39,40</a> In physiological conditions, the splanchnic venules contain 25% of the total blood volume and can store approximately 65% of the blood volume without repercussion on the patient's hemodynamic state. It has been postulated that when SNS activation is produced (in response to a drop in cardiac output), part of the volume contained in the venules is abruptly poured into the systemic vascular system through the portal vein, simultaneously contributing to systemic venous congestion. This hypothesis partly explains the onset of congestive symptoms in the absence of weight gain.<a class="elsevierStyleCrossRef" href="#bib0540">39</a> This response mechanism, which can keep a healthy individual alive after a hemorrhage, is dysfunctional in patients with HF, given that the chronic SNS stimulation causes hypersensitivity of the splanchnic bed, while simultaneously attenuating the inhibitory response of the baroreceptors.<a class="elsevierStyleCrossRef" href="#bib0540">39</a> Thus, the abrupt activation of the SNS in HF in the presence of relative hypovolemia represented by the drop in cardiac output causes a massive noninhibited mobilization of the blood volume of the splanchnic territory toward the venous circulation through the portal vein.<a class="elsevierStyleCrossRef" href="#bib0540">39</a>The splanchnic venous system is intimately related to the lymphatic system and the interstitial space.<a class="elsevierStyleCrossRef" href="#bib0550">41</a> Molecular biology has revealed that the interstitial space is not an inert space where excess fluid is stored but rather it exerts an active function in the homeostasis of the extracellular volume. The glycosaminoglycans of the interstitium (biopolymers formed by large chains of disaccharides and negatively charged proteins) have a special attraction for the sodium ion. Up to 65% of the body's sodium is stored in the extracellular space. A part of the sodium in this compartment is bound to the glycosaminoglycans of the interstitium where they form a hypertonic environment that can play a highly relevant role in the homeostasis of the body's total sodium content, especially in HF.<a class="elsevierStyleCrossRef" href="#bib0550">41</a> The disruption of this network of hypertonic biopolymers by neurohumoral activation in HF could be one of the key mechanisms involved in congestion during HF exacerbations.<a class="elsevierStyleCrossRef" href="#bib0550">41</a> These biopolymers are also located in the vascular endothelium (glycocalyx), where they play an essential role in the transduction of mechanical and biochemical stimuli in regulatory signals of the endothelial function<a class="elsevierStyleCrossRef" href="#bib0555">42</a> (e.g., the increase in production of nitric oxide when faced with excessive sodium overload, a very common situation for patients with HF).<a class="elsevierStyleCrossRef" href="#bib0550">41</a> However, these molecules are highly sensitive to mechanical changes in their structure. When the point of maximum dilation is reached (caused mainly by volume overload and neurohumoral activation), the molecules lose their functionality, which leads to endothelial dysfunction and the release of sodium into the intravascular space.<a class="elsevierStyleCrossRefs" href="#bib0560">43,44</a>There is therefore a connection between congestion in HF and inflammatory mechanisms, endothelial dysfunction and changes in the protein composition of the interstitium. Although still poorly understood, a number of physiological relationships between the SNS, renin-angiotensin-aldosterone system, natriuretic peptides and the stability of interstitial proteoglycans and the vascular endothelium have been outlined. Their characterization can help expand the pathophysiological understanding of HF decompensations, as well as represent new therapeutic targets for the treatment of HF (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>).<a class="elsevierStyleCrossRefs" href="#bib0540">39–41,45</a><elsevierMultimedia ident="fig0015"></elsevierMultimedia>As has been previously stated, one of the organs most interrelated with the heart during AHF decompensations is the kidneys.<a class="elsevierStyleCrossRef" href="#bib0575">46</a> Although the criteria for defining renal function impairment in the context of acute or chronic HF are the subject of intense review and debate,<a class="elsevierStyleCrossRef" href="#bib0480">27</a> recent HF guidelines consider that there is renal function impairment when the creatinine concentration increases more than 0.3mg/dL or by 25% or if the glomerular filtration rate decreases by more than 20% compared with baseline.<a class="elsevierStyleCrossRef" href="#bib0355">2</a> According to these criteria, up to 30% of patients with HF have renal function impairment,<a class="elsevierStyleCrossRef" href="#bib0360">3</a> which can result in a poorer prognosis in the short, medium and long term.<a class="elsevierStyleCrossRefs" href="#bib0580">47,48</a> The Diuretic Optimization Strategy Evaluation (DOSE) study did not confirm this statement. Therefore, given the lack of clear evidence in the literature, these results should be interpreted with caution.<a class="elsevierStyleCrossRef" href="#bib0590">49</a>The pathophysiological mechanisms that are involved in the cardiorenal interaction are partially known (<a class="elsevierStyleCrossRef" href="#fig0020">Fig. 4</a>).<a class="elsevierStyleCrossRef" href="#bib0595">50</a> Firstly, reducing cardiac output produces a reduction in renal perfusion and a peripheral vasoconstriction, causing a reduction in the glomerular filtration rate, tubular dysfunction and increase in sodium and water reabsorption.<a class="elsevierStyleCrossRef" href="#bib0600">51</a> However, there is no relationship between the degree of renal dysfunction and the objective measures of hypoperfusion, such as LVEF and cardiac output.<a class="elsevierStyleCrossRef" href="#bib0605">52</a> Therefore, there should be independent factors of renal arterial perfusion that propitiate the development of the cardiorenal syndrome. Systemic venous congestion has been postulated as a factor key among these independent factors.<elsevierMultimedia ident="fig0020"></elsevierMultimedia>During the 1930s, various experimental studies performed on mice models with HF revealed renal function impairment after causing venous congestion by compressing the renal vein.<a class="elsevierStyleCrossRef" href="#bib0610">53</a> The increase in CVP produces a reduction in transglomerular pressure, which causes a reduction in the glomerular filtration rate<a class="elsevierStyleCrossRef" href="#bib0615">54</a> and tubular lesions by mechanisms that have not been well described.<a class="elsevierStyleCrossRefs" href="#bib0620">55,56</a> An experimental study on mice with pulmonary hypertension and secondary systemic congestion observed the presence of an increase in creatinine and neutrophil gelatinase-associated lipocalin readings when compared with control mice. The increase in these biomarkers was correlated with a greater degree of cell death in the renal tubular epithelium and myocardium, with increased matrix metallopeptidase 9 protein expression in these tissues.<a class="elsevierStyleCrossRef" href="#bib0630">57</a> In addition, the renal glomerular structure was unaffected, showing that venous congestion causes tubular damage through increased pressure of the renal interstitium and through mechanisms of endothelial inflammation, represented by the increase in neutrophil gelatinase-associated lipocalin and matrix metallopeptidase 9 protein levels, similar to the results obtained in other experimental models.<a class="elsevierStyleCrossRef" href="#bib0530">37</a>Another mechanism that appears to be involved in the congestion-related worsening of the renal function is intestinal bacterial translocation, resulting from intestinal wall edema that is caused during acute decompensation episodes in patients with chronic HF. Peschel et al.<a class="elsevierStyleCrossRef" href="#bib0635">58</a> demonstrated (in patients with HF and New York Heart Association functional class IV) an increase in blood concentrations of endotoxins in samples obtained from suprahepatic veins, compared with those extracted from the left ventricle.<a class="elsevierStyleCrossRef" href="#bib0635">58</a>In addition to these mechanisms, we have the effect of comorbidities. The concomitance of comorbidities with HF is a key issue from the pathophysiological standpoint, especially in HF with persevered LVEF, and contributes to tissue damage “per se” or amplifies the harmful mechanisms triggered by congestion, inflammation and endothelial dysfunction.<a class="elsevierStyleCrossRef" href="#bib0640">59</a>The importance of decongestion in the prognosis of heart failureIn 2009, a retrospective study showed that the increase in CVP during HF exacerbations determined a worsening of renal function and that it was an independent factor for all-cause mortality.<a class="elsevierStyleCrossRef" href="#bib0645">60</a> In 2012, Metra et al. demonstrated that the persistence at discharge of congestive symptoms and renal function impairment during an HF episode were factors related to a poor prognosis.<a class="elsevierStyleCrossRef" href="#bib0650">61</a> This study revealed the importance of achieving a proper level of decongestion, because the increase in creatinine concentration during a decompensation by itself is not associated with more adverse events, unless the congestive condition persists.<a class="elsevierStyleCrossRef" href="#bib0650">61</a> It has been subsequently shown that the increase in creatinine concentrations associated with the titration of some drugs or to an effective decongestion do not constitute signs of a poor prognosis.<a class="elsevierStyleCrossRefs" href="#bib0480">27,47,48</a>In the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE), those patients who lost more weight and had a greater degree of hemoconcentration at discharge had a better prognosis at 180 days of follow-up, regardless of whether their creatinine concentration increased.<a class="elsevierStyleCrossRef" href="#bib0655">62</a> Consequently, a fundamental objective in the treatment of AHF is to achieve effective decongestion, even though this might represent an increase in serum creatinine levels.<a class="elsevierStyleCrossRef" href="#bib0480">27</a>To determine the best strategy for re-establishing the extracellular blood volume in patients with decompensated HF, a clinical trial compared 2 regimens of diuretic, oral or intravenous treatment, at high and low doses. The primary endpoints of safety and efficacy were improvement in the dyspnea (estimated using the visual analog scale) and the variation in serum creatinine concentrations at 72h, respectively. The results showed no significant differences between the various strategies for patients with AHF, in terms of clinical improvement of the congestive symptoms or a worsening of renal function.<a class="elsevierStyleCrossRef" href="#bib0590">49</a>A retrospective analysis of the cohort of the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) concluded that the use of high-dose loop diuretics in patients with persistent congestive symptoms achieved a slight increase in glomerular filtration rate but did not improve the prognosis in terms of survival and readmissions for HF.<a class="elsevierStyleCrossRef" href="#bib0660">63</a> The authors interpreted the results as showing that, despite achieving good symptom control, diuretic treatment might be insufficient from the prognostic standpoint.Decongestion scales as therapeutic toolsWith the objective of having a method for monitoring congestion and guiding treatment, several published studies analyzed the performance of a scoring system based on the patient's symptoms.<a class="elsevierStyleCrossRefs" href="#bib0465">24,64</a>A post hoc study of the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) cohort developed an assessment scale for congestion based on 3 clinical data: orthopnea, edema and jugular venous distention. Each of these items was scored from 0 to 3, in such a way that the score ranged from 0 to 9, considering a score ≥3 as persistent congestion.<a class="elsevierStyleCrossRef" href="#bib0665">64</a> Those patients with persistent congestion (≥3) at discharge or at day 7 of the hospitalization (for those patients who remained hospitalized) had a greater risk of all-cause death and readmissions for HF.<a class="elsevierStyleCrossRef" href="#bib0665">64</a>Another more recent retrospective study, based on the results of the cohorts of the DOSE and Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARRESS-HF) trials, designed a simple scale known as Orthodema, based on the degree of orthopnea and edema.<a class="elsevierStyleCrossRef" href="#bib0465">24</a> Up to 50% of the patients had some degree of congestion at discharge. Of those who reached complete decongestion (score of 0), only 35% remained free of congestive symptoms at 60 days. The persistence of congestion in this period (66% of all patients) meant a poorer prognosis.<a class="elsevierStyleCrossRef" href="#bib0465">24</a>It should be noted that the decongestion scales have obvious limitations, due mainly to subjectivity in the interpretation of the semiological data by the observer, the patient's subjectivity when perceiving the intensity of their symptoms and the absence of objective measures of the diuretic's efficacy.<a class="elsevierStyleCrossRef" href="#bib0670">65</a> In this respect, various definitions have been proposed to reliably quantify the diuretic response, including weight loss in kilograms per 40mg of intravenous furosemide,<a class="elsevierStyleCrossRef" href="#bib0675">66</a> the use of pulmonary ultrasonography<a class="elsevierStyleCrossRefs" href="#bib0390">9,10</a> and the use of impedance audiometry.<a class="elsevierStyleCrossRefs" href="#bib0675">66–68</a>Conflicts of interestThe authors declare that they have no conflicts of interest." "textoCompletoSecciones" => array:1 [ "secciones" => array:12 [ 0 => array:3 [ "identificador" => "xres821245" "titulo" => "Abstract" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0005" ] ] ] 1 => array:2 [ "identificador" => "xpalclavsec818238" "titulo" => "Keywords" ] 2 => array:3 [ "identificador" => "xres821246" "titulo" => "Resumen" "secciones" => array:1 [ 0 => array:1 [ "identificador" => "abst0010" ] ] ] 3 => array:2 [ "identificador" => "xpalclavsec818239" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Concept of venous congestion" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Symptomatology of congestion" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Prognostic meaning of congestion in heart failure" ] 7 => array:2 [ "identificador" => "sec0020" "titulo" => "Role of congestion in the cardiorenal interaction" ] 8 => array:2 [ "identificador" => "sec0025" "titulo" => "The importance of decongestion in the prognosis of heart failure" ] 9 => array:2 [ "identificador" => "sec0030" "titulo" => "Decongestion scales as therapeutic tools" ] 10 => array:2 [ "identificador" => "sec0035" "titulo" => "Conflicts of interest" ] 11 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec818238" "palabras" => array:4 [ 0 => "Heart failure" 1 => "Systemic venous congestion" 2 => "Inflammation" 3 => "Renal function impairment" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec818239" "palabras" => array:4 [ 0 => "Insuficiencia cardíaca" 1 => "Congestión venosa sistémica" 2 => "Inflamación" 3 => "Deterioro de la función renal" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "Systemic venous congestion has gained significant importance in the interpretation of the pathophysiology of acute heart failure, especially in the development of renal function impairment during exacerbations.In this study, we review the concept, clinical characterization and identification of venous congestion. We update current knowledge on its importance in the pathophysiology of acute heart failure and its involvement in the prognosis. We pay special attention to the relationship between abdominal congestion, the pulmonary interstitium as filtering membrane, inflammatory phenomena and renal function impairment in acute heart failure. Lastly, we review decongestion as a new therapeutic objective and the measures available for its assessment." ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "La congestión venosa sistémica ha cobrado mucha importancia en la interpretación de la fisiopatología de la insuficiencia cardíaca aguda, y muy especialmente en el desarrollo del deterioro de la función renal durante las agudizaciones.En el presente trabajo se revisa el concepto, la caracterización clínica y la identificación de la congestión venosa. Se actualiza el conocimiento sobre su importancia en la fisiopatología de la insuficiencia cardíaca aguda y su implicación en el pronóstico. Se presta especial atención a la relación entre la congestión abdominal, el intersticio pulmonar como membrana filtrante, los fenómenos inflamatorios y el deterioro de la función renal en la insuficiencia cardíaca aguda. Por último, se revisa la descongestión como un novedoso objetivo terapéutico y los medios disponibles para su evaluación." ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "Please cite this article as: Rubio Gracia J, Sánchez Marteles M, Pérez Calvo JI. Implicación de la congestión venosa sistémica en la insuficiencia cardíaca. Rev Clin Esp. 2017;217:161–169." ] ] "multimedia" => array:4 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1180 "Ancho" => 1480 "Tamanyo" => 60489 ] ] "descripcion" => array:1 [ "en" => "Description of the 4 patient phenotypes according to the degree of congestion and the degree of skin perfusion. Source: Adapted from Stevenson.<a class="elsevierStyleCrossRef" href="#bib0370">5</a>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 554 "Ancho" => 1397 "Tamanyo" => 83489 ] ] "descripcion" => array:1 [ "en" => "Left: BIVA impedance audiometry. Right: Kerley B lines or “comet tail artefacts”." ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 1133 "Ancho" => 1638 "Tamanyo" => 110951 ] ] "descripcion" => array:1 [ "en" => "Relationship between the interstitium, vascular endothelium and inflammation. Source: Adapted from Nijst et al.<a class="elsevierStyleCrossRef" href="#bib0550">41</a>" ] ] 3 => array:7 [ "identificador" => "fig0020" "etiqueta" => "Figure 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 2008 "Ancho" => 2733 "Tamanyo" => 275141 ] ] "descripcion" => array:1 [ "en" => "Schematic illustrating the various mechanisms involved in renal function impairment during an HF episode. 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Involvement of systemic venous congestion in heart failure

Implicación de la congestión venosa sistémica en la insuficiencia cardíaca

J. Rubio Graciaa,b,

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jorgerubiogracia@gmail.com

Corresponding author.

, M. Sánchez Martelesa,b, J.I. Pérez Calvoa,b,c

a Servicio de Medicina Interna, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain

b Instituto de Investigación Sanitaria de Aragón (IIS Aragón), Zaragoza, Spain

c Facultad de Medicina, Universidad de Zaragoza, Zaragoza, Spain

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        "descripcion" => array:1 [
          "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Schematic illustrating the various mechanisms involved in renal function impairment during an HF episode&#46; <span class="elsevierStyleItalic">Source</span>&#58; Adapted from Kazory et al&#46;<a class="elsevierStyleCrossRef" href="#bib0690"><span class="elsevierStyleSup">69</span></a></p>"
        ]
      ]
    ]
    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Concept of venous congestion</span><p id="par0005" class="elsevierStylePara elsevierViewall">Taking into account strictly hemodynamic criteria&#44; systemic venous congestion is defined as an increase in pulmonary wedge pressure &#62;12<span class="elsevierStyleHsp" style=""></span>mm<span class="elsevierStyleHsp" style=""></span>Hg or an increase in left ventricular diastolic pressure &#62;16<span class="elsevierStyleHsp" style=""></span>mm<span class="elsevierStyleHsp" style=""></span>Hg&#44; measured through catheterization of the right-sided heart chambers&#46;<a class="elsevierStyleCrossRef" href="#bib0350"><span class="elsevierStyleSup">1</span></a> However&#44; the definition is of little practical use due to the methods&#8217; invasiveness&#46; Systemic venous congestion in heart failure &#40;HF&#41; results from the increase in intravascular volume caused by an increase in ventricular diastolic pressure&#46; Moreover&#44; the increase in ventricular end-diastolic pressure is the direct result of 2 conditions&#58; direct myocardial damage &#40;as in ischemic heart disease or cardiomyopathies&#41; and the increase in preload associated with prior ventricular dysfunction&#44; which causes an increase in central venous pressure &#40;CVP&#41;&#46; HF is produces in both conditions&#44; and&#44; depending on the left ventricular ejection fraction &#40;LVEF&#41;&#44; we talk of HF with preserved ejection fraction for LVEF &#62;50&#37;&#59; intermediate for 40&#8211;49&#37; and reduced if LVEF &#60;40&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0355"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Identifying congestion in acute HF &#40;AHF&#41; is of primary importance&#46; Up to 66&#37; of patients in the Acute Decompensated Heart Failure National Registry &#40;ADHERE&#41;<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">3</span></a> presented some degree of systemic congestion at admission&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Symptomatology of congestion</span><p id="par0015" class="elsevierStylePara elsevierViewall">Classically&#44; congestion is detected <span class="elsevierStyleItalic">via</span> a physical examination revealing the presence of the following classic signs&#58; jugular venous distention&#44; hepatomegaly&#44; superficial collateral venous circulation&#44; ascites and edema in dependent regions&#46; Pulmonary congestion is defined mainly by the increase in respiratory effort or rate and the auscultation of end-inspiratory crackles&#46;<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">4</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">The signs of congestion and the degree of skin perfusion configure the 4 clinical phenotypes of patients with AHF &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#44; with clear connotations for the prognosis and treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">5</span></a> Patients who present more signs of congestion during the examination have higher wedge pressure in the pulmonary artery and a poorer prognosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0360"><span class="elsevierStyleSup">3&#8211;7</span></a> However&#44; despite its usefulness&#44; the physical examination has little sensitivity for detecting or ruling out the presence of congestion&#44; especially the subclinical grades&#46;<a class="elsevierStyleCrossRef" href="#bib0365"><span class="elsevierStyleSup">4</span></a> Quantifying or measuring the degree of congestion is difficult to determine using the physical examination&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">In recent years and thanks to advances in technology&#44; more objective complementary examinations have been developed to detect and measure venous congestion in HF&#44; such as impedance audiometry&#44;<a class="elsevierStyleCrossRef" href="#bib0385"><span class="elsevierStyleSup">8</span></a> pulmonary ultrasonography<a class="elsevierStyleCrossRefs" href="#bib0390"><span class="elsevierStyleSup">9&#44;10</span></a> and the measurement of the diameter and collapse of the inferior vena cava &#40;IVC&#41;<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">11</span></a> &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46; Thus&#44; systemic congestion is considered when the ultrasound diameter of the IVC is &#62;21<span class="elsevierStyleHsp" style=""></span>mm in inspiration&#44; and the collapse is &#60;50&#37; of the baseline diameter&#46;<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">11</span></a> Patients with systemic congestion estimated by this method have a poorer prognosis at 6 months of discharge from an episode of AHF&#46;<a class="elsevierStyleCrossRefs" href="#bib0405"><span class="elsevierStyleSup">12&#8211;14</span></a> Another ultrasound technique that assesses pulmonary congestion is pulmonary ultrasonography to visualize the Kerley B lines &#40;sign of the comet tail&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0420"><span class="elsevierStyleSup">15</span></a> This new approach to the ultrasound examination of the lungs has high sensitivity &#40;94&#37;&#41; and specificity &#40;92&#37;&#41; for detecting interstitial edema and helps differentiate between cardiogenic and respiratory dyspnea&#46; The approach also helps quantify the intensity of the congestion&#44; because there is a correlation between the number of artifacts in the various lung fields and NT-proBNP concentrations and the echocardiographic quotient E&#47;e&#8217; &#40;of vital importance for assessing HF with preserved LVEF&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0390"><span class="elsevierStyleSup">9&#44;10&#44;16</span></a> Lastly&#44; pulmonary impedance audiometry&#44; built into pacemaker technology&#44; has helped reduce the rate of readmissions of patients with chronic HF&#44; as shown by the IMPEDANCE-HF study&#46;<a class="elsevierStyleCrossRef" href="#bib0430"><span class="elsevierStyleSup">17</span></a></p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0030" class="elsevierStylePara elsevierViewall">Despite these techniques&#44; determining a patient&#39;s congestive state remains difficult&#46; A study published in 2007 with 134 patients hospitalized for HF &#40;New York Heart Association functional class III&#41; who were previously telemonitored in their homes through vital sign monitoring and daily weightings&#44; revealed the inability to perform early detection of decompensations&#46;<a class="elsevierStyleCrossRef" href="#bib0435"><span class="elsevierStyleSup">18</span></a> This study showed how the week before the admission &#40;<span class="elsevierStyleItalic">i&#46;e&#46;</span>&#44; before the patient presented symptoms of decompensation&#41;&#44; there was a significant increase in body weight&#44; suggesting that the congestion starts before the clinical manifestations&#46; These results are similar to those from another study in which the authors&#44; by monitoring hemodynamic parameters in a subgroup of the Chronicle Offers Management to Patients with Advanced Signs and Symptoms of Heart Failure &#40;COMPASS-HF&#41; cohort&#44; demonstrated an increase in ventricular diastolic pressure as a phenomenon prior to decompensation by HF&#46;<a class="elsevierStyleCrossRef" href="#bib0440"><span class="elsevierStyleSup">19</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">To define this oligosymptomatic stage prior to the onset of congestive signs&#44; Gheorghiade et al&#46; introduced the term &#8220;congestion hemodynamics&#8221; to name the condition in which there is an increase in left ventricular filling pressures without clinical translation&#46; The authors reserved the term &#8220;clinical congestion&#8221; for the other conditions in which the state of maintained hemodynamic congestion resulted in the onset of dyspnea&#44; orthopnea&#44; crackles&#44; edema and jugular venous distention&#46;<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">20</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Despite the better understanding of the concept&#44; of its importance in clinical practice and of the incorporation of a number of techniques for its discovery&#44; the definition&#44; detection and quantification of congestion continue to be a clinical challenge&#46;</p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Prognostic meaning of congestion in heart failure</span><p id="par0045" class="elsevierStylePara elsevierViewall">AHF results in approximately a million admissions a year in US hospitals&#44; and 76&#37; of these patients have a history of HF&#46;<a class="elsevierStyleCrossRef" href="#bib0450"><span class="elsevierStyleSup">21</span></a> In the ADHERE registry&#44; 66&#37; of the patients showed signs of systemic congestion&#46;<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">3</span></a> In a <span class="elsevierStyleItalic">post hoc</span> analysis of the Studies Of Left Ventricular Dysfunction &#40;SOLVD&#41;&#44; the authors found a correlation between the presence of jugular venous distention or third heart sound at admission &#40;as surrogate signs of congestion&#41; and the risk of readmission for HF and death&#46;<a class="elsevierStyleCrossRef" href="#bib0455"><span class="elsevierStyleSup">22</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">In daily practice&#44; treatment response is assessed through the observation of the attenuation or disappearance of congestion&#44; and it is standard procedure to proceed with the discharge when this phenomenon is maintained with stable doses of oral diuretics&#46;<a class="elsevierStyleCrossRefs" href="#bib0355"><span class="elsevierStyleSup">2&#44;23</span></a> However&#44; it has been observed that once the congestive symptoms disappear after the first days of treatment&#44; the left ventricle filling pressures can remain high &#40;congestion hemodynamics&#41;&#44; with the subsequent increase in the risk of early readmission&#46;<a class="elsevierStyleCrossRef" href="#bib0445"><span class="elsevierStyleSup">20</span></a> Up to 48&#37; of patients presented some residual sign of congestion at discharge&#44;<a class="elsevierStyleCrossRefs" href="#bib0470"><span class="elsevierStyleSup">25&#44;25</span></a> and it has been shown that patients with 3 or more signs of congestion at discharge have a higher mortality rate than patients with no congestive signs in the first 60 days after discharge&#46;<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">24</span></a> In patients with New York Heart Association functional class IV and a mean LVEF of 20&#37;&#44; the absence of congestive symptoms between weeks 4 and 6 after the hospitalization is associated with longer survival&#46;<a class="elsevierStyleCrossRef" href="#bib0475"><span class="elsevierStyleSup">26</span></a> Therefore&#44; reaching an optimal state of decongestion before the discharge is a crucial therapeutic objective&#46;</p><p id="par0055" class="elsevierStylePara elsevierViewall">Venous congestion is also involved in organ dysfunction&#44; especially of the kidneys&#46; Approximately 30&#37; of patients with AHF have renal function impairment associated with the AHF&#44;<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">3</span></a> which results in a poorer prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">27</span></a> Renal dysfunction resulting from systemic congestion is called congestive renal failure by a number of authors&#46;<a class="elsevierStyleCrossRef" href="#bib0485"><span class="elsevierStyleSup">28</span></a> Understanding this condition&#39;s pathophysiology could be essential for improved understanding of both organ damage during episodes of decompensation and the diuretic response&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">Ter Maaten et al&#46; analyzed the rate of readmissions for patients with AHF based on the diuretic response&#44; defined as the weight change in kilograms during the first 72<span class="elsevierStyleHsp" style=""></span>h of treatment for every 40<span class="elsevierStyleHsp" style=""></span>mg of furosemide administered intravenously&#46;<a class="elsevierStyleCrossRef" href="#bib0490"><span class="elsevierStyleSup">29</span></a> The authors also used the hemoglobin concentration as a surrogate marker of congestion&#46; The patients with poorer diuretic response who remained hemodiluted&#44; depending on the hemoglobin concentration&#44; had a greater risk of readmission during the 60 days after the discharge&#46; Nu&#241;ez et al&#46;&#44; using the CA125 biomarker as a surrogate marker of congestion&#44; found a direct association between the changes in renal function &#40;measured by variations in creatinine concentrations&#41; and the intravenous loop diuretic dose&#46;<a class="elsevierStyleCrossRef" href="#bib0495"><span class="elsevierStyleSup">30</span></a> The Carbohydrate Antigen 125-guided Therapy in Acute Heart Failure &#40;CHANCE&#41; study confirmed that the use of plasma CA125 concentrations to guide treatment for AHF offers better results than the standard strategy based on signs and symptoms&#46;<a class="elsevierStyleCrossRef" href="#bib0500"><span class="elsevierStyleSup">31</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Role of congestion in the cardiorenal interaction</span><p id="par0065" class="elsevierStylePara elsevierViewall">Congestion has classically been explained as the consequence of a myocardial aggression that causes reduced cardiac output&#44; with the consequent reduction in intravascular volume&#44; which through the stimulation of various baroreceptors causes the activation of a concerted neurohumoral response&#46; First&#44; the sympathetic nervous system &#40;SNS&#41; causes a redistribution of the blood flow through vasoconstriction of the peripheral circulation and an increased heart rate to compensate for the cardiac output&#44; thereby ensuring the perfusion of vital organs&#46;<a class="elsevierStyleCrossRef" href="#bib0505"><span class="elsevierStyleSup">32</span></a> Second&#44; we have the response mediated by the renin-angiotensin-aldosterone system and vasopressin&#46; The former facilitates sodium reabsorption through the distal convoluted tubule and the latter decreases free water excretion in the collecting tubule&#46;<a class="elsevierStyleCrossRefs" href="#bib0505"><span class="elsevierStyleSup">32&#44;33</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">The activation of these systems enables the recovery of blood volume and maintains the short-term perfusion of vital organs&#59; however&#44; in the medium to long-term&#44; the activation promotes tissue damage&#44; which worsens the cardiac function &#40;maladaptive response&#41;&#46; The combined neurohormonal and SNS activation causes an excessive expansion of fluid in the intravascular space&#44; which is stored in the venous system until the maximum possible capacitance is reached&#46; Once this falters&#44; it causes an increase in CVP&#44; with abdominal organ congestion&#44; progressive weight gain&#44; expansion to the interstitial space and onset of classical HF symptoms&#46;<a class="elsevierStyleCrossRef" href="#bib0515"><span class="elsevierStyleSup">34</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Systemic congestion can be initially reversed with diuretics&#46;<a class="elsevierStyleCrossRefs" href="#bib0460"><span class="elsevierStyleSup">23&#44;35</span></a> In the long term&#44; however&#44; and through complex mechanisms of escape and renal adaptation to the action of diuretics<a class="elsevierStyleCrossRef" href="#bib0525"><span class="elsevierStyleSup">36</span></a> and the progression of the disease&#44; a permanent refractory congestive condition develops&#44; as well as signs of organ dysfunction &#40;<span class="elsevierStyleItalic">e&#46;g&#46;</span>&#44; renal&#44; hepatic and pulmonary&#41;&#44;<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">3</span></a> progressive worsening of the quality of life and greater readmissions for HF&#44; which translate into increased mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">24</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Not all patients respond equally to depletive treatment&#44; which shows that congestion is heterogeneous and goes beyond a mere hemodynamic and vascular redistribution problem&#46; Various complex mechanisms that are still not properly understood are likely to act along with the SNS and renin&#8211;angiotensin&#8211;aldosterone system in perpetuating tissue damage in HF&#46;<a class="elsevierStyleCrossRefs" href="#bib0530"><span class="elsevierStyleSup">37&#44;38</span></a> Using an experimental model&#44; Colombo et al&#46; demonstrated the relationship between venous congestion and inflammation&#46;<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">37</span></a> The authors produced venous congestion in an arm through extrinsic compression with a sphygmograph and obtained peripheral blood from both arms&#44; the compressed arm &#40;before and after inflating the cuff&#41; and the other taken as a control&#46; The result was a significant increase in the concentrations of interleukin-6&#44; endothelin-1 and angiotensin II in the blood samples extracted from the compressed arm when compared with the control&#46;<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">37</span></a> Although this was an experimental model that did not reproduce the pressure conditions achieved inside human vessels&#44; the authors undoubtedly demonstrated the presence of a link between venous congestion and inflammation&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">Another fundamental factor in the development of congestion in patients with HF is the abdominal circulation and&#44; more specifically&#44; the splanchnic venous network&#46;<a class="elsevierStyleCrossRefs" href="#bib0540"><span class="elsevierStyleSup">39&#44;40</span></a> In physiological conditions&#44; the splanchnic venules contain 25&#37; of the total blood volume and can store approximately 65&#37; of the blood volume without repercussion on the patient&#39;s hemodynamic state&#46; It has been postulated that when SNS activation is produced &#40;in response to a drop in cardiac output&#41;&#44; part of the volume contained in the venules is abruptly poured into the systemic vascular system through the portal vein&#44; simultaneously contributing to systemic venous congestion&#46; This hypothesis partly explains the onset of congestive symptoms in the absence of weight gain&#46;<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">39</span></a> This response mechanism&#44; which can keep a healthy individual alive after a hemorrhage&#44; is dysfunctional in patients with HF&#44; given that the chronic SNS stimulation causes hypersensitivity of the splanchnic bed&#44; while simultaneously attenuating the inhibitory response of the baroreceptors&#46;<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">39</span></a> Thus&#44; the abrupt activation of the SNS in HF in the presence of relative hypovolemia represented by the drop in cardiac output causes a massive noninhibited mobilization of the blood volume of the splanchnic territory toward the venous circulation through the portal vein&#46;<a class="elsevierStyleCrossRef" href="#bib0540"><span class="elsevierStyleSup">39</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">The splanchnic venous system is intimately related to the lymphatic system and the interstitial space&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">41</span></a> Molecular biology has revealed that the interstitial space is not an inert space where excess fluid is stored but rather it exerts an active function in the homeostasis of the extracellular volume&#46; The glycosaminoglycans of the interstitium &#40;biopolymers formed by large chains of disaccharides and negatively charged proteins&#41; have a special attraction for the sodium ion&#46; Up to 65&#37; of the body&#39;s sodium is stored in the extracellular space&#46; A part of the sodium in this compartment is bound to the glycosaminoglycans of the interstitium where they form a hypertonic environment that can play a highly relevant role in the homeostasis of the body&#39;s total sodium content&#44; especially in HF&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">41</span></a> The disruption of this network of hypertonic biopolymers by neurohumoral activation in HF could be one of the key mechanisms involved in congestion during HF exacerbations&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">41</span></a> These biopolymers are also located in the vascular endothelium &#40;glycocalyx&#41;&#44; where they play an essential role in the transduction of mechanical and biochemical stimuli in regulatory signals of the endothelial function<a class="elsevierStyleCrossRef" href="#bib0555"><span class="elsevierStyleSup">42</span></a> &#40;<span class="elsevierStyleItalic">e&#46;g&#46;</span>&#44; the increase in production of nitric oxide when faced with excessive sodium overload&#44; a very common situation for patients with HF&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">41</span></a> However&#44; these molecules are highly sensitive to mechanical changes in their structure&#46; When the point of maximum dilation is reached &#40;caused mainly by volume overload and neurohumoral activation&#41;&#44; the molecules lose their functionality&#44; which leads to endothelial dysfunction and the release of sodium into the intravascular space&#46;<a class="elsevierStyleCrossRefs" href="#bib0560"><span class="elsevierStyleSup">43&#44;44</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">There is therefore a connection between congestion in HF and inflammatory mechanisms&#44; endothelial dysfunction and changes in the protein composition of the interstitium&#46; Although still poorly understood&#44; a number of physiological relationships between the SNS&#44; renin-angiotensin-aldosterone system&#44; natriuretic peptides and the stability of interstitial proteoglycans and the vascular endothelium have been outlined&#46; Their characterization can help expand the pathophysiological understanding of HF decompensations&#44; as well as represent new therapeutic targets for the treatment of HF &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0540"><span class="elsevierStyleSup">39&#8211;41&#44;45</span></a></p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0100" class="elsevierStylePara elsevierViewall">As has been previously stated&#44; one of the organs most interrelated with the heart during AHF decompensations is the kidneys&#46;<a class="elsevierStyleCrossRef" href="#bib0575"><span class="elsevierStyleSup">46</span></a> Although the criteria for defining renal function impairment in the context of acute or chronic HF are the subject of intense review and debate&#44;<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">27</span></a> recent HF guidelines consider that there is renal function impairment when the creatinine concentration increases more than 0&#46;3<span class="elsevierStyleHsp" style=""></span>mg&#47;dL or by 25&#37; or if the glomerular filtration rate decreases by more than 20&#37; compared with baseline&#46;<a class="elsevierStyleCrossRef" href="#bib0355"><span class="elsevierStyleSup">2</span></a> According to these criteria&#44; up to 30&#37; of patients with HF have renal function impairment&#44;<a class="elsevierStyleCrossRef" href="#bib0360"><span class="elsevierStyleSup">3</span></a> which can result in a poorer prognosis in the short&#44; medium and long term&#46;<a class="elsevierStyleCrossRefs" href="#bib0580"><span class="elsevierStyleSup">47&#44;48</span></a> The Diuretic Optimization Strategy Evaluation &#40;DOSE&#41; study did not confirm this statement&#46; Therefore&#44; given the lack of clear evidence in the literature&#44; these results should be interpreted with caution&#46;<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">49</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">The pathophysiological mechanisms that are involved in the cardiorenal interaction are partially known &#40;<a class="elsevierStyleCrossRef" href="#fig0020">Fig&#46; 4</a>&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0595"><span class="elsevierStyleSup">50</span></a> Firstly&#44; reducing cardiac output produces a reduction in renal perfusion and a peripheral vasoconstriction&#44; causing a reduction in the glomerular filtration rate&#44; tubular dysfunction and increase in sodium and water reabsorption&#46;<a class="elsevierStyleCrossRef" href="#bib0600"><span class="elsevierStyleSup">51</span></a> However&#44; there is no relationship between the degree of renal dysfunction and the objective measures of hypoperfusion&#44; such as LVEF and cardiac output&#46;<a class="elsevierStyleCrossRef" href="#bib0605"><span class="elsevierStyleSup">52</span></a> Therefore&#44; there should be independent factors of renal arterial perfusion that propitiate the development of the cardiorenal syndrome&#46; Systemic venous congestion has been postulated as a factor key among these independent factors&#46;</p><elsevierMultimedia ident="fig0020"></elsevierMultimedia><p id="par0110" class="elsevierStylePara elsevierViewall">During the 1930s&#44; various experimental studies performed on mice models with HF revealed renal function impairment after causing venous congestion by compressing the renal vein&#46;<a class="elsevierStyleCrossRef" href="#bib0610"><span class="elsevierStyleSup">53</span></a> The increase in CVP produces a reduction in transglomerular pressure&#44; which causes a reduction in the glomerular filtration rate<a class="elsevierStyleCrossRef" href="#bib0615"><span class="elsevierStyleSup">54</span></a> and tubular lesions by mechanisms that have not been well described&#46;<a class="elsevierStyleCrossRefs" href="#bib0620"><span class="elsevierStyleSup">55&#44;56</span></a> An experimental study on mice with pulmonary hypertension and secondary systemic congestion observed the presence of an increase in creatinine and neutrophil gelatinase-associated lipocalin readings when compared with control mice&#46; The increase in these biomarkers was correlated with a greater degree of cell death in the renal tubular epithelium and myocardium&#44; with increased matrix metallopeptidase 9 protein expression in these tissues&#46;<a class="elsevierStyleCrossRef" href="#bib0630"><span class="elsevierStyleSup">57</span></a> In addition&#44; the renal glomerular structure was unaffected&#44; showing that venous congestion causes tubular damage through increased pressure of the renal interstitium and through mechanisms of endothelial inflammation&#44; represented by the increase in neutrophil gelatinase-associated lipocalin and matrix metallopeptidase 9 protein levels&#44; similar to the results obtained in other experimental models&#46;<a class="elsevierStyleCrossRef" href="#bib0530"><span class="elsevierStyleSup">37</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">Another mechanism that appears to be involved in the congestion-related worsening of the renal function is intestinal bacterial translocation&#44; resulting from intestinal wall edema that is caused during acute decompensation episodes in patients with chronic HF&#46; Peschel et al&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">58</span></a> demonstrated &#40;in patients with HF and New York Heart Association functional class IV&#41; an increase in blood concentrations of endotoxins in samples obtained from suprahepatic veins&#44; compared with those extracted from the left ventricle&#46;<a class="elsevierStyleCrossRef" href="#bib0635"><span class="elsevierStyleSup">58</span></a></p><p id="par0120" class="elsevierStylePara elsevierViewall">In addition to these mechanisms&#44; we have the effect of comorbidities&#46; The concomitance of comorbidities with HF is a key issue from the pathophysiological standpoint&#44; especially in HF with persevered LVEF&#44; and contributes to tissue damage &#8220;per se&#8221; or amplifies the harmful mechanisms triggered by congestion&#44; inflammation and endothelial dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0640"><span class="elsevierStyleSup">59</span></a></p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">The importance of decongestion in the prognosis of heart failure</span><p id="par0125" class="elsevierStylePara elsevierViewall">In 2009&#44; a retrospective study showed that the increase in CVP during HF exacerbations determined a worsening of renal function and that it was an independent factor for all-cause mortality&#46;<a class="elsevierStyleCrossRef" href="#bib0645"><span class="elsevierStyleSup">60</span></a> In 2012&#44; Metra et al&#46; demonstrated that the persistence at discharge of congestive symptoms and renal function impairment during an HF episode were factors related to a poor prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0650"><span class="elsevierStyleSup">61</span></a> This study revealed the importance of achieving a proper level of decongestion&#44; because the increase in creatinine concentration during a decompensation by itself is not associated with more adverse events&#44; unless the congestive condition persists&#46;<a class="elsevierStyleCrossRef" href="#bib0650"><span class="elsevierStyleSup">61</span></a> It has been subsequently shown that the increase in creatinine concentrations associated with the titration of some drugs or to an effective decongestion do not constitute signs of a poor prognosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0480"><span class="elsevierStyleSup">27&#44;47&#44;48</span></a></p><p id="par0130" class="elsevierStylePara elsevierViewall">In the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness &#40;ESCAPE&#41;&#44; those patients who lost more weight and had a greater degree of hemoconcentration at discharge had a better prognosis at 180 days of follow-up&#44; regardless of whether their creatinine concentration increased&#46;<a class="elsevierStyleCrossRef" href="#bib0655"><span class="elsevierStyleSup">62</span></a> Consequently&#44; a fundamental objective in the treatment of AHF is to achieve effective decongestion&#44; even though this might represent an increase in serum creatinine levels&#46;<a class="elsevierStyleCrossRef" href="#bib0480"><span class="elsevierStyleSup">27</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall">To determine the best strategy for re-establishing the extracellular blood volume in patients with decompensated HF&#44; a clinical trial compared 2 regimens of diuretic&#44; oral or intravenous treatment&#44; at high and low doses&#46; The primary endpoints of safety and efficacy were improvement in the dyspnea &#40;estimated using the visual analog scale&#41; and the variation in serum creatinine concentrations at 72<span class="elsevierStyleHsp" style=""></span>h&#44; respectively&#46; The results showed no significant differences between the various strategies for patients with AHF&#44; in terms of clinical improvement of the congestive symptoms or a worsening of renal function&#46;<a class="elsevierStyleCrossRef" href="#bib0590"><span class="elsevierStyleSup">49</span></a></p><p id="par0140" class="elsevierStylePara elsevierViewall">A retrospective analysis of the cohort of the Controlled Rosuvastatin Multinational Trial in Heart Failure &#40;CORONA&#41; concluded that the use of high-dose loop diuretics in patients with persistent congestive symptoms achieved a slight increase in glomerular filtration rate but did not improve the prognosis in terms of survival and readmissions for HF&#46;<a class="elsevierStyleCrossRef" href="#bib0660"><span class="elsevierStyleSup">63</span></a> The authors interpreted the results as showing that&#44; despite achieving good symptom control&#44; diuretic treatment might be insufficient from the prognostic standpoint&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Decongestion scales as therapeutic tools</span><p id="par0145" class="elsevierStylePara elsevierViewall">With the objective of having a method for monitoring congestion and guiding treatment&#44; several published studies analyzed the performance of a scoring system based on the patient&#39;s symptoms&#46;<a class="elsevierStyleCrossRefs" href="#bib0465"><span class="elsevierStyleSup">24&#44;64</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">A <span class="elsevierStyleItalic">post hoc</span> study of the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan &#40;EVEREST&#41; cohort developed an assessment scale for congestion based on 3 clinical data&#58; orthopnea&#44; edema and jugular venous distention&#46; Each of these items was scored from 0 to 3&#44; in such a way that the score ranged from 0 to 9&#44; considering a score &#8805;3 as persistent congestion&#46;<a class="elsevierStyleCrossRef" href="#bib0665"><span class="elsevierStyleSup">64</span></a> Those patients with persistent congestion &#40;&#8805;3&#41; at discharge or at day 7 of the hospitalization &#40;for those patients who remained hospitalized&#41; had a greater risk of all-cause death and readmissions for HF&#46;<a class="elsevierStyleCrossRef" href="#bib0665"><span class="elsevierStyleSup">64</span></a></p><p id="par0155" class="elsevierStylePara elsevierViewall">Another more recent retrospective study&#44; based on the results of the cohorts of the DOSE and Cardiorenal Rescue Study in Acute Decompensated Heart Failure &#40;CARRESS-HF&#41; trials&#44; designed a simple scale known as Orthodema&#44; based on the degree of orthopnea and edema&#46;<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">24</span></a> Up to 50&#37; of the patients had some degree of congestion at discharge&#46; Of those who reached complete decongestion &#40;score of 0&#41;&#44; only 35&#37; remained free of congestive symptoms at 60 days&#46; The persistence of congestion in this period &#40;66&#37; of all patients&#41; meant a poorer prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0465"><span class="elsevierStyleSup">24</span></a></p><p id="par0160" class="elsevierStylePara elsevierViewall">It should be noted that the decongestion scales have obvious limitations&#44; due mainly to subjectivity in the interpretation of the semiological data by the observer&#44; the patient&#39;s subjectivity when perceiving the intensity of their symptoms and the absence of objective measures of the diuretic&#39;s efficacy&#46;<a class="elsevierStyleCrossRef" href="#bib0670"><span class="elsevierStyleSup">65</span></a> In this respect&#44; various definitions have been proposed to reliably quantify the diuretic response&#44; including weight loss in kilograms per 40<span class="elsevierStyleHsp" style=""></span>mg of intravenous furosemide&#44;<a class="elsevierStyleCrossRef" href="#bib0675"><span class="elsevierStyleSup">66</span></a> the use of pulmonary ultrasonography<a class="elsevierStyleCrossRefs" href="#bib0390"><span class="elsevierStyleSup">9&#44;10</span></a> and the use of impedance audiometry&#46;<a class="elsevierStyleCrossRefs" href="#bib0675"><span class="elsevierStyleSup">66&#8211;68</span></a></p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Conflicts of interest</span><p id="par0165" class="elsevierStylePara elsevierViewall">The authors declare that they have no conflicts of interest&#46;</p></span></span>"
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          "identificador" => "sec0005"
          "titulo" => "Concept of venous congestion"
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          "titulo" => "Symptomatology of congestion"
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        6 => array:2 [
          "identificador" => "sec0015"
          "titulo" => "Prognostic meaning of congestion in heart failure"
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        7 => array:2 [
          "identificador" => "sec0020"
          "titulo" => "Role of congestion in the cardiorenal interaction"
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          "titulo" => "The importance of decongestion in the prognosis of heart failure"
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        9 => array:2 [
          "identificador" => "sec0030"
          "titulo" => "Decongestion scales as therapeutic tools"
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            0 => "Heart failure"
            1 => "Systemic venous congestion"
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          "palabras" => array:4 [
            0 => "Insuficiencia card&#237;aca"
            1 => "Congesti&#243;n venosa sist&#233;mica"
            2 => "Inflamaci&#243;n"
            3 => "Deterioro de la funci&#243;n renal"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Systemic venous congestion has gained significant importance in the interpretation of the pathophysiology of acute heart failure&#44; especially in the development of renal function impairment during exacerbations&#46;</p><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">In this study&#44; we review the concept&#44; clinical characterization and identification of venous congestion&#46; We update current knowledge on its importance in the pathophysiology of acute heart failure and its involvement in the prognosis&#46; We pay special attention to the relationship between abdominal congestion&#44; the pulmonary interstitium as filtering membrane&#44; inflammatory phenomena and renal function impairment in acute heart failure&#46; Lastly&#44; we review decongestion as a new therapeutic objective and the measures available for its assessment&#46;</p></span>"
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        "resumen" => "<span id="abst0010" class="elsevierStyleSection elsevierViewall"><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">La congesti&#243;n venosa sist&#233;mica ha cobrado mucha importancia en la interpretaci&#243;n de la fisiopatolog&#237;a de la insuficiencia card&#237;aca aguda&#44; y muy especialmente en el desarrollo del deterioro de la funci&#243;n renal durante las agudizaciones&#46;</p><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">En el presente trabajo se revisa el concepto&#44; la caracterizaci&#243;n cl&#237;nica y la identificaci&#243;n de la congesti&#243;n venosa&#46; Se actualiza el conocimiento sobre su importancia en la fisiopatolog&#237;a de la insuficiencia card&#237;aca aguda y su implicaci&#243;n en el pron&#243;stico&#46; Se presta especial atenci&#243;n a la relaci&#243;n entre la congesti&#243;n abdominal&#44; el intersticio pulmonar como membrana filtrante&#44; los fen&#243;menos inflamatorios y el deterioro de la funci&#243;n renal en la insuficiencia card&#237;aca aguda&#46; Por &#250;ltimo&#44; se revisa la descongesti&#243;n como un novedoso objetivo terap&#233;utico y los medios disponibles para su evaluaci&#243;n&#46;</p></span>"
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        "etiqueta" => "&#9734;"
        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Rubio Gracia J&#44; S&#225;nchez Marteles M&#44; P&#233;rez Calvo JI&#46; Implicaci&#243;n de la congesti&#243;n venosa sist&#233;mica en la insuficiencia card&#237;aca&#46; Rev Clin Esp&#46; 2017&#59;217&#58;161&#8211;169&#46;</p>"
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          "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Description of the 4 patient phenotypes according to the degree of congestion and the degree of skin perfusion&#46; <span class="elsevierStyleItalic">Source</span>&#58; Adapted from Stevenson&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">5</span></a></p>"
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          "en" => "<p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Left&#58; BIVA impedance audiometry&#46; Right&#58; Kerley B lines or &#8220;comet tail artefacts&#8221;&#46;</p>"
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          "en" => "<p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Relationship between the interstitium&#44; vascular endothelium and inflammation&#46; <span class="elsevierStyleItalic">Source</span>&#58; Adapted from Nijst et al&#46;<a class="elsevierStyleCrossRef" href="#bib0550"><span class="elsevierStyleSup">41</span></a></p>"
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          "en" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Schematic illustrating the various mechanisms involved in renal function impairment during an HF episode&#46; <span class="elsevierStyleItalic">Source</span>&#58; Adapted from Kazory et al&#46;<a class="elsevierStyleCrossRef" href="#bib0690"><span class="elsevierStyleSup">69</span></a></p>"
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Article information

ISSN: 22548874
Original language: English

DOI:10.1016/j.rceng.2016.10.007

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