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• W2776673058 abstract "This article refers to ‘Acutely decompensated heart failure with preserved and reduced ejection fraction present with comparable haemodynamic congestion’ by L.N.L. Van Aelst et al., published in this issue on pages xxx-xxx. Acute heart failure (AHF) is defined as the rapid onset or worsening of symptoms and/or signs of heart failure, requiring urgent evaluation and treatment.1 It imposes a significant burden on both patients and health care systems, due to the high mortality rate (30% one year post-discharge) and need for repeated hospitalizations (20% within 30 days and 50% 6 months post-discharge).2 Under the general definition of AHF is encompassed a wide spectrum of clinical presentations, with varying precipitating factors, underlying aetiology, pathophysiologic mechanisms and clinical outcomes. In several large AHF registries, patients with AHF and reduced (HFrEF) vs. preserved ejection fraction (HFpEF) constitute approximately equal 50% fractions of hospitalized patients. These populations differ in their demographic and clinical characteristics and outcomes.2 Patients with HFrEF are more frequently younger males, with history of chronic heart failure and coronary artery disease. They usually present with normal or low blood pressure, weight gain and signs of systemic venous congestion. On the other hand, HFpEF patients are usually older women with new-onset heart failure and several cardiometabolic co-morbidities, presenting with increased blood pressure, less systemic venous congestion and usually no significant weight gain. Although in-hospital mortality is higher in HFrEF, both groups are equally affected by high rates of post-discharge mortality, unplanned outpatient visits and rehospitalizations.3 Venous congestion is the cardinal manifestation in AHF. Two main pathophysiologic mechanisms have been implicated in the development of congestion: first, rapid redistribution of blood volume from the systemic to the pulmonary venous circulation and, second, intravascular volume accumulation in the setting of chronic cardiorenal dysfunction and impaired sodium and water homeostasis.4 The first mechanism is thought to result from acute reduction of the capacitance of splanchnic venous bed, which in the normal setting serves as a blood reservoir that accommodates approximately 70% of total blood volume.5 Therefore, even small decreases of venous capacitance in a state of increased vasoconstriction could lead to significant blood volume redistribution that acutely increases cardiac preload and may evoke AHF when superimposed on impaired cardiac function. In AHF, sympathetic activation and inflammation-induced endothelial dysfunction may promote venous and arterial vasoconstriction, increasing at the same time cardiac preload and afterload.6 The second mechanism results from impaired sodium and water excretion due to cardiorenal dysfunction, as in pre-existing chronic heart failure.4 In this case, there is rather more gradual development of venous congestion and an absolute increase in total body water and sodium content. Evidence exists that there is cross-talk between the two pathophysiologic mechanisms of AHF, as venous distention caused by congestion may exacerbate endothelial dysfunction by promoting inflammation, increasing oxidative stress and augmenting sympathetic activation, overall further decreasing venous capacitance and promoting blood redistribution.7, 8 It has been suggested previously that each of the two pathophysiologic mechanisms of congestion in AHF is associated with distinct clinical phenotypes of the syndrome.9 Volume redistribution appears to be predominant in AHF presenting with elevated arterial blood pressure. Patients with this profile exhibit mostly pulmonary rather than systemic venous congestion, report less or no weight gain preceding clinical congestion and more frequently have HFpEF. On the other hand, volume overload contributes mostly to AHF presenting with normal arterial blood pressure, is usually accompanied by less prominent clinical and/or radiographical pulmonary congestion but rather by a significant degree of systemic venous congestion. This phenotype is associated with pre-existing chronic heart failure and acute HFrEF. As noted, the association between pathophysiologic mechanisms of congestion and left ventricular ejection fraction phenotype has been based on clinical signs of congestion, as scarce evidence exists in the literature regarding haemodynamic and neurohormonal markers of congestion in different AHF clinical scenarios, as well as in different left ventricular ejection fraction phenotypes. In this issue of the Journal, Van Aelst et al.10 directly compared two populations of AHF patients, either with HFrEF or HFpEF, with respect to clinical, haemodynamic (derived by echocardiography) and neurohormonal markers of venous congestion. The main findings of their study are: (i) there are no differences in clinical signs and echocardiographically derived indexes of peripheral and cardiac venous congestion between HFrEF and HFpEF; (ii) venous endothelial dysfunction induced by venous congestion with resultant stretch of endothelial cells is an important pathophysiologic mechanism in both acute HFrEF and HFpEF, as shown by similarly increased levels of soluble CD146 protein and its correlation with echocardiographic indices of systemic and cardiac congestion in both populations; (iii) cardiorenal interactions play an important role in AHF, whereas mostly in patients with acute HFrEF. Although the study is limited by the relatively small number of patients that could reduce its power to detect statistically significant differences between populations, it highlights that fluid redistribution and fluid accumulation can coexist and additively promote the development of congestion in AHF. In addition, the important pathophysiologic contribution of venous endothelial dysfunction induced by increased stretch in the pathogenesis of AHF, both in HFrEF and HFpEF, is confirmed. However, it is not possible to conclude as to whether endothelial dysfunction was the cause or consequence of congestion in HFrEF and HFpEF, as the assessment was indirect and performed on a single time point in the course of decompensation. Therefore, direct and serial assessments of venous endothelial function will be needed in order to derive firm conclusions regarding the contribution of fluid redistribution and accumulation in the pathogenesis of acute HFrEF vs. HFpEF.11 Lastly, this study has confirmed a significant association between renal dysfunction and echocardiographic indexes of peripheral congestion in patients with acute HFrEF but not HFpEF. This is in accordance with the previously mentioned concept of less contribution of cardiorenal dysfunction and resultant volume overload in acute and chronic HFpEF.4, 12 Indeed, previous studies have shown that chronic HFpEF patients have lower total blood volume or even occult hypovolaemia compared to HFrEF.13, 14 Moreover, larger plasma volume reduction with intravenous diuretics during an acute decompensation is independently associated with worsening renal function only in HFpEF and not HFrEF patients, suggesting absence of excess volume overload in acute HFpEF as compared to acute HFrEF.15 On the other hand, patients with HFpEF are affected in similar rates as HFrEF by chronic renal dysfunction (25–50% co-morbid chronic renal dysfunction in HFpEF depending on definition) as well as by worsening renal function during acute decompensations (incidence of worsening renal function in acute HFpEF reported between 6–15%).16-18 In addition, both chronic renal dysfunction and worsening renal function have been associated with poor outcomes in HFpEF, probably even more than HFrEF.16 Renal venous congestion associated with increased central venous pressure and right ventricular dysfunction, as well as impaired renal blood flow due to reduced cardiac output reserve and blunted renal vascular autoregulation have been implicated in the pathogenesis of renal dysfunction in HFpEF.17, 19 Clearly, further investigation of the role of renal dysfunction in the pathogenesis of acute decompensations in HFpEF is needed. Overall, the study of Van Aelst and colleagues10 puts forward a hypothesis of overlapping pathophysiologic mechanisms of congestion in acute HFrEF and HFpEF, using clinical assessment, comprehensive echocardiography and biomarkers of venous vasculature function and cardiorenal interaction. Further investigation of the time course of pathophysiologic alterations and downstream pathogenetic mechanisms discriminating acute HFrEF and HFpEF is warranted. Conflict of interest: none declared." @default.
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• W2776673058 title "Congestion in acute heart failure with reduced vs. preserved left ventricular ejection fraction: differences, similarities and remaining gaps" @default.
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