Can we prevent ventricular remodeling?

Abstract

How could we prevent but also enhance regression of ventricular remodeling. It must not be forgotten that even with today's therapeutic progress a lot of hypertensive patients, with valvular heart disease and foremost myocardial infarction finally do evolve into heart failure having already undergone a step into the stage of Ventricular Remodeling. Especially after an acute anterior myocardial infarction it is estimated that 30% of patients eventually develop remodeling, despite primary angioplasty and all the big 4 families that is angiotensin converting enzyme inhibitors or ARBs, β- blockers, statins and aldoster-one antagonists. It may sound commonplace, but the best way to prevent remodeling is to intervene early. Thus hypertension should be treated as early as possible. Currently, even concentric remodeling without heart failure and probably dys-synchronization around 30% of patients with hypertension might present an early indication of impending remodeling. Valvular heart disease must be operated earlier especially mitral regurgitation as shown by recent publications. Of course the main thrust is after myocardial infarction. We have not made enough progress of the protection of the myocardium during PCI. Fortunately post conditioning both local by deflating the balloon, a difficult process for many interventionists, or remote post conditioning holds promise. Other medications such as opioids may help in diminishing ischemia reperfusion injury although adenosine is not being widely used. A lot of medications are being currently evaluated to prevent or help regress remodeling. Some of the most prominent and clinically used ones are erythropoietin for which there are conflicting reports, metabolic drugs such as metformin, AKAR, or exenatide, valproic acid and some of the widely used antioxidants such as 4-hydroxybiopterin, curcumin, or resveratrol. No large scale human studies are available. Another approach is the electrical - mechanical approach. Thus early application of CRT may prevent remodeling in incipient cardiac dilatation due either to cardiomyopathy or ischemic heart disease. LVAD is a last step approach, might it help, and if its application becomes easier it may be placed earlier. The injection of progenitor cells has been shown to have promise when given early in large anterior infarcts. There is no doubt that what we need is a concerted approach of interventional medical and other techniques. With this in mind we may be able to hope that the incidence of remodeling and ensuing heart failure will decrease.