The thickening often happens in the left ventricle that is trying to respond to the poor circulation over time, and that poor circulation is due to the dilation of the left atrium, and possibly due to mitral valve defect, the latter part of the hypertension problem. So, you are correct in that the left atrium expands, and in doing so it most often thins the vessel walls while it expands. Dilation. This weakened structure doesn't fill the left ventricle well, especially if the expansion/dilation stretches the annulus around the mitral valve and affects the closure of that valve. If the valve doesn't sit properly and is kept somewhat open, then when the left ventricle contracts to force blood up into the aorta, it also pushes some of that volume back through the mitral valve and into the left atrium on the other side of the valve. The ventricle is the more powerful of the two, and its force will cause the left atrium, which might be out of sequence in fibrillations or in premature contractions, to balloon. It's bad enough that they often fight each other in fibrillation or in PACs/PVCs when they contract at the same time, but if the atrium is relaxed when the ventricle contracts, and it forces a good bit of blood into the atrium through the defective mitral valve, it can stretch the walls of the left atrium.