Myocardial Fibrosis and Cardiac Decompensation in Aortic Stenosis

Figure 1. Factors Governing the Magnitude of the Hypertrophic Response in Aortic Stenosis Only a modest correlation between the severity of valve narrowing and the magnitude of the hypertrophic response was observed. The other predictor of left ventricular (LV) mass index on multivariate analysis was sex, with men having more hypertrophy than women.

Figure 2. iECV as a Marker of Extracellular Expansion in the Myocardium (A) Regions of interest manually drawn onto native and post-contrast T1 maps are used to calculate indexed extracellular volume (iECV). (B) Histology from a patient with aortic stenosis (AS) with areas of diffuse fibrosis stained with picrosirus red. (C) Excellent correlation between iECV and diffuse myocardial fibrosis on histology. (D) iECV provided good discrimination between disease states. (E) iECV values were higher in patients with replacement fibrosis than patients with normal myocardium or extracellular expansion.

Figure 3. CMR Categorization of Myocardial Fibrosis in Aortic Stenosis Patients with aortic stenosis were categorized into 3 groups based upon cardiac magnetic resonance (CMR) assessments of fibrosis. iECV = indexed extracellular volume; LGE = late gadolinium enhancement.

Figure 4. Progressive LV Decompensation on Moving From Normal Myocardium to Extracellular Expansion to Replacement Fibrosis On moving from normal myocardium to extracellular expansion and then replacement fibrosis, there was a stepwise increase in the following measures: (A) the severity of valve narrowing; (B) the degree of hypertrophy; (C) myocardial injury; (D) left ventricular (LV) performance; and (E) all-cause-mortality. hsTni = high-sensitivity troponin I concentration.