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

The effects of alterations in the diastolic filling pressure of the right ventricle on left ventricular (LV) geometry and filling pressure were studied in six isolated, supported canine hearts. This experimental preparation permitted graded increments in right ventricular (RV) end-diastolic pressure while LV cardiac output, heart rate, and mean aortic pressure were held constant. Endocardial radiopaque markers were placed in the ventricular septum, the anterior wall, the posterior wall, and the free wall in a plane perpendicular to the aortoapical axis. LV end-diastolic dimensions were recorded by x-ray cinematography at 60 frames/sec. The effects of varied RV end-diastolic pressure (0-16 mm Hg) on LV end-diastolic pressure and dimensions were studied at several LV cardiac outputs (780-2880 ml/min) and at several initial LV end-diastolic pressures (1-18 mm Hg). Increments of 5 mm Hg in RV end-diastolic pressure increased LV end-diastolic pressure 2.3 mm Hg. The septum-to-free wall distance decreased by 4.5% from the control distance, but the anterior-to-posterior dimension increased by 4.4%.Thus, LV end-diastolic pressure and LV end-diastolic dimensions were significantly related to RV end-diastolic pressure; LV end-diastolic geometry was increasingly distorted at elevated RV end-diastolic pressure. These data suggest that the high RV filling pressures that characterize certain diseases can secondarily alter LV filling pressures and geometry.

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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.