Acute heart failure and renal function: an organ interplay not to be underestimated
In “Cardiorenal Syndrome” by Ronco et al. (JACC 2008;52:1527‒39) the authors identified 5 subtypes of cardio-renal syndrome (CRS) with distinctive pathophysiologies and described the nature of the co-dependencies of cardiac and renal dysfunction.
This mattered in 2008 and it matters today because, as Ronco and colleagues noted in their preamble, “A diseased heart has numerous negative effects on kidney function but, at the same time, renal insufficiency can significantly impair cardiac function.”
It matters also because of the numbers of patients affected and the consequences of CRS for patients with acute heart failure. Researchers in the Atherosclerosis Risk in Communities (ARIC) Study Community Surveillance programme have reported that “Severely reduced eGFR (<30 ml/min/1.73m2) was observed in ~30% of acute decompensated heart failure cases”.1 Elsewhere it has been reported that type-1 CRS (kidney injury secondary to acute cardiogenic shock or acute decompensation of chronic heart failure) “accounted for more than half of all mortality”.2 Age or geographical location are no protection from these malign effects.3,4
Both in 2008 and again more recently,5 Dr Ronco and colleagues called attention to the possible conceptual differences between chronic kidney disease and worsening renal function in acute heart failure and suggested that these may represent “different pathophysiological mechanisms in the setting of acute heart failure”. Multiple pathways that might contribute to these differences have been proposed.5,6
All of this is a reminder that the interplay between the acutely compromised heart and the kidneys is complex, with huge scope for variations of relevant pathophysiology between cases. Identifying the optimal treatment for individual cases is a correspondingly complex and demanding task.
In the therapeutic palette, levosimendan seems a reasonable option, in cases where cardiac output is compromised.7 In a tutorial lecture at the recent ESICM-LIVES congress in Vienna, Prof. Sven-Erik Ricksten (Sahlgrenska University Hospital, Gothenburg, Sweden) showed a profound difference in the effects of levosimendan vs dobutamine on glomerular filtration (see here) which would justify the selection of levosimendan as inotrope of choice for treatment of heart failure with concomitant renal failure.
Professor Gerhard Pölzl highlights Hospitalisation for the management of acute decompensation being a critical moment in the trajectory of heart failure (HF) and one that has gloomy prognostic implications for many patients.
There have been some recent achievements in the LEODOR trial including a new website to facilitate administration and communication and submission of a formal study protocol synopsis to the European Journal of Heart Failure.
If we had a way to reduce the risk of life-threatening complications after cardiac surgery would we use it? Of course we would. It is for reason that this blog post highlights the recent work of Dr. Qiang and colleagues. See the details here.
Professor Gerhard Pölzl reports primary results from the LION-HEART study in the management of advanced heart failure where among secondary endpoints, patients treated with levosimendan experienced a reduction in the rate of HF-related hospitalisation compared with placebo.
Professor Cynthia M Dougherty and colleagues outline an array of options for the treatment of advanced heart failure (HF) that create – quite reasonably – the impression that we are in a golden age of therapeutic possibilities for this difficult condition.