Hello! You are correct in evaluating types I and III collagens and TGF beta. In our laboratory, when studying cardiac remodeling, we also evaluated the expression of connexin 43, parameters of cellular hypertrophy, and cardiac electrophysiology.

Adverse post-MI LV remodeling can be evaluated at different levels:

- Anatomical level: LV dilatation (increase in LV end-diastolic volume and LV end-systolic volumes), LV hypertrophy (increase in LV mass), architectural / geometrical remodeling (the LV loses its usual elongated, gullet-like shape and acquires a more spherical configuration, you can use sphericity index for this)

- Neurohormonal level: Sympathetic system overdrive (increase in adrenaline/noradrenaline levels), enhancement of RAAS system (higher levels of angiotensin II or aldosterone), raise in BNP (neurohormone marking LV dilatation)

- Histological level in the remote non-infarcted tissue: Cardiomyocyte hypertrophy (using staining for vinculin or wheat hemagglutinin), interstitial fibrosis (staining for picrosirius red), capillary paucity (staining for CD31 or isolectin)

- Molecular level: Activation (phosphorylation) of Akt/ERK/p38 (which drive cardiomyocyte hypertrophy), molecular markers of fibrosis (collagen I/III, CTGF, TGF-beta)

- Metabolism/energetic levels: Healthy myocardium predominantly consumes free fatty acid to generate ATP. There is a shift, however, in cardiac metabolism in remodeled myocardium towards mainly using glucose instead of free fatty acids

Ventricular renodeling mainly refers to geometrical changes in the LV (dilation, sphericity, etc) and functio. Therefore the gold standard is cardiac magentic resonanc Due to costs, echocardiography is the most used method.

For cardiac function (both dyastolic and systoli) the LvEDP ans P-V loop are also use (Millar catheter).

TGF-b and collagen contribute to remodeling but are not surrogants for ventricular remodelin.