What could be worse than heart failure? Perhaps advanced heart failure. The ESC and other expert cardiology groups have produced precise technical definitions of “advanced heart failure” but for many patients affected, those definitions perhaps miss the central experience: every aspect of life as you know and cherish it starts to slide from your grasp as your heart falters repeatedly, and each recovery leaves you weaker and less independent than before.
We are not entirely without options for these critically vulnerable patients. Ivabradine may benefit the patient with tachycardia, even digoxin may retain a role for rate regulation in atrial fibrillation and for symptom relief. For selected patients with a strong renal dimension to their situation rolofylline, empagliflozin or serelaxin may bring benefit, though full characterisation of those drugs and their target populations is desirable.
For acute exacerbations of heart failure we face an emerging alphabet soup of natriuretic peptides (ularitide, cenderitide), beta-arrestin-biased angiotensin II type 1 receptor ligands (TRV120027), nitroxyl donors (CXL-1020, CXL-1427), soluble guanylate cyclase modulators (cinaciguat, vericiguat) and short-acting calcium channel blockers (clevidipine), in addition to familiar names such as nicorandil.
Increasingly there is the option of a left ventricular assist device (LVAD), which in an era when demand consistently exceeds supply is becoming a destination therapy for many patients who might otherwise qualify for a heart transplant.
It remains the case, however, for many patients whose condition continues to deteriorate even though they have “maxed out” on diuretics, beta-blockers and treatments directed at the rennin-angiotensin-aldosterone axis (including perhaps the combined angiotensin receptor blocker and neprilysin inhibitor LCZ696) that inotrope therapy is a key resource in gaining time and preserving quality of life while decisions are taken about heart transplantation, mechanical support or perhaps palliative care.
Conventional inotropes such as dobutamine or milrinone may improve symptom control but appear to do so at the expense of worsened mortality. In this landscape levosimendan stands out as a therapy that preserves or enhances ventricular function in an energy-neutral way and does not make patients choose between more life or a better life – they can have both.
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.