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To determine the origin of angina pectoris at rest hemodynamic monitoring was performed for 24 to 72 hours in 25 patients with unstable angina who had pacing-induced angina during cardiac catheterization. During the monitoring period, seven patients had spontaneous epidsodes of angina at rest that could be compared with the pain-free periods and periods of pacing-induced angina. At the onset of spontaneous angina, the patients had a significantly lower mean double product (P is less than 0.005) and triple product (P is less than 0.025) than at the onset of pacing-induced angina. The mean double product (heart rate x systolic blood pressure) was 9,411 +/- 2,815 mm Hg/min during pain-free rest, 10,635 +/- 2,587 at the onset of spontaneous angina and 16,623 +/- 3,904 during pacing-induced angina. The mean resting pain-free triple product (heart rate x systolic blood pressure x ejection time) was 3,023 +/- 703 and 3,536 +/- 931 mm Hg/sec per min during, respectively, pain-free rest and spontaneous angina, and 4,350 +/- 938 mm Hg/sec per min during pacing-induced angina. These marked differences in the double and triple products were associated with a mean increase in pulmonary arterial diastolic pressure (from 10.7 mm Hg at rest to 14 mm Hg) at the onset of both spontaneous and pacing-induced angina. Although indirect, these data suggest that transient changes in coronary blood flow, rather than changes in myocardial work, may be primarily responsible for spontaneous angina at rest in certain patients with the syndrome of unstable angina.

Seven patients studied by echocardiography with and without simultaneous phonocardiography for suspected malfunction of a caged mitral valve prosthesis are presented. In case 1, with inaudible prosthetic clicks, thrombosis of the cage and immobility of the ball were suggested by echocardiographic studies and confirmed at surgery. In case 2, simultaneous echocardiographic and phonocardiographic studies demonstrated wide and variable intervals between the aortic second sound the the opening click and also "sticking" of the ball. In case 3 a thrombus prevented full motion of the ball to the apex of the cage, which was seen on the echocardiogram, while in case 4, with a thrombus within the ventricle and prosthesis, the prosthetic opening click was present intermittently and was associated with only subtle echocardiographic changes. In case 5, echocardiographic studies demonstrated abnormal rocking of the cage secondary to severe prosthetic dehiscence. In case 6, dul prosthetic clicks were to be secondary to a low cardiac-output state. In case 7, with multiple valve prostheses, simultaneous echocardiographic and phonocardiographic studies allowed identification of individual valve sounds and abnormal timing of valve opening. Based on these studies, we believe that echocardiography and simultaneous phonocardiography can yield very useful information in the evaluation of patients with suspected malfunction of a caged mitral valve prosthesis.

The first 81 patients who underwent coronary artery bypass surgery at Stanford University Hospital for unstable angina pectoris have been followed up for an average of 18 months. The over-all surgical mortality was 8.6 per cent (seven patients). There have been no operative deaths in last 32 patients, which may be due to over 75 per cent of these patients being stabilized on intensive medical therapy from 24 to 72 hours before study or surgery. There was a 16 per cent (13 patients) perioperative and 15 per cent (12 patients) late incidence of myocardial infarction. Of 74 patients who survived the initial operation 2 died 2 and 3 months postoperatively. Good or complete relief from pain was obtained in 94 per cent (70 patients) of the survivors. Of 57 longterm survivors tested, 49 per cent (28 patients) had a definite ischemic response to treadmill exercise testing. This may reflect the severe nature of the occlusive coronary disease or mechanisms other than increased coronary flow being responsible for the relief of pain. Although coronary bypass surgery appears to be effective in relieving the pain of patients with unstable angina pectoris, the 18 month average follow-up indicates that the incidence of myocardial infarction in surgically treated patients is comparable to that in medically treated patients.

1. In previous studies adenosine has been postulated to be the mediator in coronary blood flow regulation and aminophylline was found to inhibit the coronary vasodilator action of adenosine. The present study was performed to determine whether aminophylline inhibits coronary vasodilatation induced by hypoxia.2. Coronary and systemic haemodynamic and metabolic effects of hypoxia were studied in anaesthetized dogs before and after aminophylline. Aminophylline did not influence coronary vasodilatation induced by hypoxia.3. These results are held not to lend support to the hypothesis that adenosine is the metabolite responsible for the regulation of coronary blood flow.