Eccentric hypertrophy occurs due to systolic heart failure, so ejection fraction decreases. Decreased contractility occurs because the volume overload stretches out the myocyte, and this stretching eventually surpasses the ability of the Frank-Starling relationship to increase contractility. Once you've gone beyond that point on the Frank-Starling curve, contractility actually decreases, as actin/myosin interaction sites no longer efficiently overlap due to excess volume-induced stretch.
As for aortic regurg, ejection fraction is initially basically the same because, while you have a greater end-diastolic volume than normal due to the regurgitation, you also have a greater stroke volume because of the aforementioned Frank-Starling relationship. For example, let's say initially you have the textbook normal values of 120 mL EDV and 50 mL ESV for a stroke volume of 70 mL and ejection fraction of 70/120 = 58%. Now let's say you have regurgitant backflow of 20 mL; this extra 20 mL gets pumped out each stroke but also goes back into the ventricle each diastolic cycle. So now you have 140 mL EDV and 50 mL ESV for a stroke volume of 90 mL and ejection fraction of 90/140 = 64%. The ejection fraction has increased, but the important note is that the EF is still normal; problems arise whenever the EF decreases, not increases. Slight increases in EF are a compensatory response to the increased EDV, but decreasing to abnormally low EF indicates that the aortic regurgitation has resulted in volume overload and systolic failure.
