Postinfarct Left Ventricular Remodelling: A Prevailing Cause of Heart Failure

Table 2

Therapies capable of inducing reverse remodelling.

	Mechanism of action	Notes
Class of drugs
ACE inhibitors/ARBs [70, 71]	RAAS antagonism
Antialdosterone diuretics [72]	RAAS antagonism
β-blockers [73]	Reduce cardiotoxic effects of chronic β-adrenergic stimulation and improve heart responsiveness to physiological adrenergic stimulation
NO donors plus hydralazine [74]	Increase cGMP and reduce preload
MMPs inhibitors [75]	Inhibit ECM remodelling	Experimental. No evidences in humans
rNRG-1 [76, 77]	Promotes cardiomyocyte survival pathways	Experimental
Type of mechanical intervention
CRT [44, 78]	Increases GSK-3β activity and improves LV contractility	Eligibility: patients with symptomatic HF and LBBB
LVAD [44, 79]	Reduces LV workload	Eligibility: patients with severe HF as bridge to recovery or bridge to heart transplant
Mitral valve surgery [80]	Reduces LV workload	Eligibility: patients with severe mitral regurgitation
Diastolic cardiac restraint devices [81, 82]	Reduce myocardial wall tension	Experimental

ACE: angiotensin-converting enzyme; ARBs: angiotensin receptor blockers; RAAS: renin-angiotensin-aldosterone system; NO nitric oxide; cGMP: cyclic guanosine monophosphate; MMPs: matrix metalloproteinases; ECM: extracellular matrix; rNRG-1: recombinant human neuregulin-1; CRT: cardiac resynchronization therapy; GSK-3β: glycogen synthase kinase-3β; LV: left ventricle; HF: heart failure; LBBB: left bundle branch block; LVAD: left ventricular assist device.