Angina pectoris

Angina pectoris

Department of Reviews and Abstracts Selected Abstracts Keefer, Chester S., and Resnik, William H.: 1928, xli, 769. Angina Pectoris. Arch. Int. ~Ied...

68KB Sizes 2 Downloads 58 Views

Department of Reviews and Abstracts Selected Abstracts Keefer, Chester S., and Resnik, William H.: 1928, xli, 769.

Angina Pectoris.

Arch. Int. ~Ied.,

I n this p a p e r the authors present a theory which explains the attacks of angina peetorls on a basis of localized anoxemia of the myocardium. They believe t h a t the a t t a c k occurs when the oxygen supply to the heart is inadequate to meet the oxygen demands of the heart. In the usual case of angina, the anoxemia is relative, being sufficient for the needs of the heart at rest and insufficient when the work of the heart is increased. In acute coronary occlusion, however, the anoxemia is absoiut% since the oxygen supply is ~nadequate, even when the heart is at rest. Anoxemia of the myoeardimn may exist without causing angina. They point out t h a t under these conditions when anoxemia affects all the tissues of the body as well as the heart, for example in pernicious anemia, or when the heart is uniformly affected so far as one may judge, angina is usnalIy absent. When the heart is affected in sueh eases the symptoms are practically always those of so-called eongestive heart failure. On the other hand, angina tends to appear when in spite of anoxemia being present the contraetural power of the heart remains good, evidenced by more.. or less complete freedom from dyspnea or other symptoms of a failing myoeardihm. These conditions occur most commonly when only a restricted part of the heart muscle suffers from lack of oxygen, as in coronary sclerosis. The remainder is relatively uninvolved and hence the eontraetural power of the heart remains good. Parkinson, ffohn, and Bedford, E. Evan.: Successive Changes in the Electrocardiogram After Cardiac Infarction (Coronary Thrombosis). Heart, xiv, 195. Electrocardiograms are given from twenty-eight cases in which the diagnosis of cardiac infarction was made. Twenty-two patients are still alive and six have died; in four of the latter necropsies were obtained, each confirming the diagnosis. The modifications of the ventrieular complexes of the electrocardiogram following cardiac infaretion are described in detail, and illustrated by serial records. Usually a definite seque~me of changes in the R-T segment and in the T-waves is recorded. Shortly after the onset of symptmns a transient deviation of the R-T segment from the isoelectrie plane occurs. This is followed by a deep inversion of the T-wave in either Lead I or Lead I I I , but not in both, ~nd o~ten by a lesser degree of T inversion in Lead II. Cm'ves obtained after a few weeks conform to one of two main types according to the incidence of T inversion in Lead I or in Lead III. Subsequent T-wave changes in the direction of the normal are recorded, and even complete return to normal occurs. A negative T-wave in Lead I I I alone may be significant of past infarction. T-wave changes seen in clinical curves are comparable with those observed 120