A white man, aged 43, American, married, an embosser, admitted to Bellevue Hospital, Feb. 16, 1922, stated that he had always been in perfect health, never having had a sick day, until February 6. On that day he had a constricting pain over the lower part of his left chest which was diagnosed as indigestion. Following this he had six such attacks in the next ten days, each succeeding one more severe and lasting longer. In the last few the pain radiated to the left supraclavicular region and

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... the ulnar margin of the left fore¬ arm. These spells of sharp pain occurred whether he was active or in bed, and were not relieved by any of the many remedies tried. The attack for which he came into the hos¬ pital was his seventh and had begun the night before, never remitting. The patient was rather well developed and of fair nutri¬ tion. When he reached the ward he was moderately cyanosed, orthopneic, and in marked distress. He groaned constantly and could not lie quietly on his bed. Neither the nitrites nor morphin were of any avail in allaying his terrific dis¬ comfort. The heart was slightly enlarged to the left and right, the apex beat being felt in the fifth left intercostal space, 11 cm. from the midsternal line. No thrills were present, and the apex impulse was localized and of fair strength. The heart sounds were of poor quality. The rate was slow, averaging 72 a minute, and there were no murmurs present. At the base he had an accentuated aortic second sound. The rhythm was peculiarly irregular. About eight beats would occur at a definite, regular rate. This series would be followed quite abruptly by about eight beats at a different rate, but forming a regular unit by themselves. An electrocardiographic record substantiated this finding. It was interpreted by Dr. Cary Eggleston as either a phe¬ nomenon of two foci for stimuli, i. e., a normal sinus and a focus with a slower rate near the sinus, or as an alter¬ nating bradycardia and tachycardia from the same focus. The patient's arteries were thickened and tortuous wherever they could be examined. The blood pressure was : systolic, 170; diastolic, 120. No other physical findings had any bearing on the cardiovascular condition. The course of the disease was short and stormy. The pain was unrelenting. The patient was becoming more dyspneic. A cold perspiration bathed him continually, and he was a picture of utter misery. At 7 p. m., while under observation, the unfortunate man threw his head back, and his face expressed the most extreme anguish. He had a sudden attack of projectile vomiting, became markedly cyanosed, and collapsed. His wrist pulse was imperceptible. He took four deep inspirations about thirty seconds apart, and then died. During these two minutes a stethoscope was clapped to his chest, and over the precordium was heard an extraordinary sound. A continuous, muffled, low pitched, rushing rumble, louder during the expiratory phase, dimmed during the few inspiratory periods, was constantly heard. No heart sounds were evident. All this transpired so quickly that only two auditors could listen to this remarkable murmur. Its sig¬ nificance was not apparent, and at first it was imagined by the observers that the sounds were such as might be heard over a fibrillating ventricle. A necropsy, performed by Dr. Douglas Symmers, revealed an irregular laceration of the wall of the left ventricle in immediate proximity to the interventricular septum, situated midway between the base and apex of the heart. This lacera¬ tion was 3 cm. in length and ran obliquely downward and toward the right directly over the course of the correspond¬ ing coronary artery. The fat tissue covering the upper and * From the Second Medical (Cornell) Division, Bellevue Hospital. outer half of the conus arteriosus was infiltrated by blood, the infiltrated area measuring 5 cm. in length and 3.5 cm. in breadth. From the extreme upper end, a broad linear area of hemorrhage extended upward toward the opening of the corresponding coronary artery. The left coronary artery was opened by the pathologist for a short distance, and presented at a point 1.5 cm. from its origin a calcareous plaque. The laceration extended through the heart muscle and opened into the ventricle. The muscle tissue in the immediate vicinity of the lacerated area was soft, almost fluctuating, for a distance of about 1 cm., and this area of softening extended downward in the general direction of the apex for a distance of 2.5 cm. A transverse section of the heart muscle was made just above the area of laceration. Here the coronary artery was about 2 mm. in diameter and markedly calcified. The lumen could be seen filled with a reddish body about the size of a horsehair, probably a fresh thrombosis. The pericardium was filled with fluid and freshly clotted blood. In the light of the necropsy, the clinical course was thus interpreted : The acute onset of illness, the continuous, agonizing, precordial pain and distress all point to the rather sudden thrombosis of the calcified coronary and the result¬ ing degeneration of the heart muscle. The sudden collapse, projectile vomiting and immediate death were probably coin¬ cident with the rupture of the heart. There can be little doubt that the auscultatory evidence of this dramatic acci¬ dent was the rumble heard as the blood poured into the peri¬ cardium so like the sound of water rushing through a bursting dam.