This is a condition in which, during the systole of the heart, some portion of the blood passes back into the left auricle instead of the whole being forced into the aorta.

The actual physical conditions are somewhat various, but most of them are related to chronic endocarditis. The commonest is that in which the valvular structures are thickened by the new-formed connective tissue and retracted and shortened from its contraction. This applies to the curtains themselves, but still more to the chords tendineae, which become thickened and shortened, and frequently grow together, so that they hold the curtains rigidly drawn down and do not allow them to go together during the systole of the ventricle (see Fig. 223, p. 457). Again, irregularities of the borders may lead to imperfect apposition of the edges and a certain amount of insufficiency. This, however, although it may lead to a loud murmur during life, can scarcely produce a serious functional disturbance. On the other hand, but more rarely, in acute endocarditis the valve may be perforated, as in the case of valvular aneurysm, or the chords tendines torn so as to allow a portion of the valve to flap upwards through the orifice. Lastly, without much alteration of the curtains, there may be a relative insufficiency of the valve. That is to say, the cavity of the ventricle sometimes enlarges greatly, and produces enlargement of the orifice, which the valve is no longer able to cover. There are some cases of permanent hypertrophy and dilatation of the left ventricle (as from overstrain) where this occurs, but it may be met with where the dilatation is temporary, as in the flabby fatty heart of typhus fever and anasmia. It is not to be supposed that the so-called ansmic murmurs are usually due to this cause, but there is in some cases an actual mitral regurgitation. When recovery occurs, and the heart resumes its former vigour, the valve will again cover the orifice.

The results which follow constant insufficiency of the mitral valve are frequently very serious and far-reaching. At each ventricular systole blood regurgitates into the left auricle, and the most direct result is over-distension of this auricle occurring at successive intervals. The auricle does not usually suffer great enlargement from this cause. There is another result which often follows, apparently from the unduly forcible impact of the blood against the endocardium, and the overstretching of this membrane, namely, a thickening of the endocardium. We may find it generally thickened and opaque, or there may be patches of opacity.

But the results do not confine themselves to the auricle - the abnormal blood-pressure is reflected to the Pulmonary veins which feed the auricle, and they become distended. The distension is further reflected to the pulmonary capillaries and arteries, and finally to the right ventricle. The right ventricle is over-distended, and, as a consequence, Hypertrophy of the right ventricle is a common result of mitral insufficiency. The obstruction to the circulation may extend to the venae cavae, the right ventricle and auricle being over-dilated. In this way General venous engorgement comes about with all the consequences which will be described in the next section in dealing with mitral stenosis.

The amount of blood which the left ventricle sends into the aorta will be diminished in proportion as more or less passes back into the auricle. In consequence, the systemic circulation will be partially starved. In some cases the left ventricle undergoes hypertrophy. This is mainly due to the fact that at each diastole it will receive from the distended auricle an excess of blood, namely, that which would normally arrive from the auricle along with that which regurgitated from the ventricle. The ventricle having thus to deal with an increased mass of blood undergoes dilatation and hypertrophy.