We conclude that 1) anomalous coronary arteries are associated with a high incidence of hypertension and valvular heart disease in the sample of patients studied; 2) there was a high incidence of palpitations, but this and the other symptoms were difficult to evaluate because of the associated disease; 3) in certain patients with anomalous origin of the left main coronary artery (LM) from the right sinus of Valsalva, myocardial perfusion is probably impaired and may be associated with serious cardiac events whether the initial course of the LM is posterior to the aorta, between the aorta and the pulmonary artery, and/or anterior to the pulmonary artery. Course of the anomalous LM coronary artery between aorta and the pulmonary artery may be associated with sudden death. Atherosclerosis of a single coronary artery proximal to its branching is an additional liability to the anomaly. Since sudden death occurs most commonly in young individuals with anomalous origin of the LM, special care should be taken to evaluate young patients with chest pain resembling angina. A maximal treadmill exercise test should be performed first, and if there is evidence of ischemia, a coronary arteriogram should be performed. Recognition of anomalous origin of coronary arteries and their course also is important in patients undergoing surgery for aortocoronary bypass or for valvular heart disease when perfusion of coronary arteries is needed.MANY VARIATIONS of the aortic origin of one or both coronary arteries exist" 2 and have been considered minor coronary anomalies without clinical significance.' With the increasing use of coronary arteriography, the anomalies are being recognized more frequently and their clinical significance is becoming better appreciated.3 8The variations in the initial course of the coronary arteries with anomalous origin are more important than the anomalous origin itself. Unrecognized coronary anomalies may lead to errors in clinical

Several noninvasive techniques, including radionuclide angiography and Doppler echocardiography, have attempted to measure the regurgitant volume in patients with mitral regurgitation; however, none of these techniques are entirely satisfactory. Utilizing a computerized light pen method for tracing the left atrial endocardial border during systole and diastole in two orthogonal planes (apical four and two chamber views), biplane volume determinations were calculated in 12 normal subjects and 30 patients with nonrheumatic mitral regurgitation. Left atrial emptying volume determinations were performed by subtracting the left atrial end-diastolic volume from the left atrial end-systolic volume. The degree of mitral regurgitation was visually assessed as normal (0, trivial, Group I, 12 patients), mild (1+, Group II, 4 patients), moderate (2+, Group III, 8 patients), moderately severe (3+, Group IV, 12 patients) and severe (4+, Group V, 6 patients) by contrast left ventricular angiography and also quantitatively by regurgitant fraction at cardiac catheterization. All 18 patients with moderately severe (Group IV) and severe (Group V) mitral regurgitation had a left atrial emptying volume greater than 40 ml compared with none of the normal subjects and patients with mild (Group II) or moderate (Group III) mitral regurgitation. There was good correlation between left atrial emptying volume and mitral regurgitant fraction (r = 0.85, p less than 0.01). Thus, in patients with nonrheumatic mitral regurgitation, left atrial emptying volume is useful in separating mild from severe mitral regurgitation.

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SUMMARY We have simplified the Gorlin formula and have compared our measurements of the aortic or mitral valve area, using the original Gorlin formula and the simplified valve formula in 100 consecutive patients. The valve area was measured by the simplified formula as cardiac output (I/min) divided by the square root of pressure differences across the valve.In patients with aortic stenosis of varying severity there was excellent correlation between the original One of the constants is the discharge coefficient that is an empirical constant with an assumed arbitrary value of 1 for the aortic valve and 0.7 for the mitral valve. The second constant is 44.5, which is equal to the square root of twice the gravity acceleration factor (980 cm/sec/sec). The flow across the valve is equal to the cardiac output (ml/min) divided by the product of the heart rate (beats/min) and the systolic ejection period or diastolic filling period (sec/beat). In 1972, Cohen and Gorlin revised the original formula and suggested the use of 0.85 for the mitral valve (instead of 0.7) as the discharge coefficient.2Because the original formula is cumbersome and time-consuming, it is rarely used by cardiologists who are not involved with hemodynamic measurements. We have simplified this formula, and our results by both the original and the simplified formulas in 100 patients with either aortic stenosis or mitral stenosis are the subject of this report. of the ejection to the dicrotic notch. The diastolic filling period was measured between the crossover points of the pulmonary artery wedge and the left ventricular pressure tracings. The heart rate was calculated at the time of cardiac output measurement by counting the RR cycles over a 60-second interval. The peak aortic gradient was measured as a simple peak-topeak gradient. The peaks were not necessarily at the exact time during systole. The mean pressure difference across the aortic or mitral valve was measured by planimetry. We used the same cardiac output in both the original Gorlin and the simplified formulas.The aortic or mitral valve area (cm2) was measured by the simplified formula as the cardiac output (1/min) divided by the square root of the pressure differences across the valve. For the aortic valve, we used either the peak or the mean pressure difference across the valve in the simplified formula, but for the mitral valve, we used only the mean pressure difference.We performed the statistical correlation by means of Pearson product moment correlation and the t test.

Seven patients with myocardial bridging of the left anterior descending coronary artery were evaluated by mens of thallium-201 exercise scintigraphy. The degree of systolic narrowing was 60-70% in five patients and 75-80% in two patients. All patients had presented with chest pain. The resting electrocardiogram was normal in six patients; there were ST segment and T-wave abnormalities in one patient. No patient complained of chest pain during exercise. The exercise electrocardiogram was negative in six patients and inconclusive in one patient. Exercise myocardial scans were negative in all seven patients. We conclude that no evidence of ischemia was demonstrated in patients with myocardial bridging of the left anterior descending coronary artery as determined by exercise electrocardiography and stress thallium-201 scintigraphy.