SUMMARY We studied the inferior vena cava (IVC) as an index of right-heart function in 111 patients. A two-dimensional echocardiographic sector was used to visualize the IVC, and its M-mode cursor was used to generate a time-motion record of the IVC size and pulsation. Normal subjects had a small presystolic A wave (less than 125% of the end-diastolic IVC dimension), a small systolic V wave (less than 140% of the enddiastolic IVC dimension), and a 50% inspiratory decrease in IVC dimension. GRAY-SCALE B-SCAN ULTRASONOGRAPHY is useful for diagnosing masses invading or compressing the inferior vena cava (IVC).'-8 Furthermore, realtime two-dimensional echocardiographic detection of IVC microcavitations after peripheral contrast injection is valuable for diagnosing tricuspid insufficiency.9Ill The purpose of this report is to describe the normal and abnormal time-motion echocardiographic characteristics of IVC size and pulsation and to identify the physiologic and pathophysiologic determinants of the IVC echogram. Materials and MethodsThe time-motion IVC ultrasonographic data in 1 1 1 patients who also had hemodynamic, contrast right ventricular angiographic, radionuclide right ventricular angiographic or pathologic study form the basis of this report. Ten patients were normal. Sixty-seven patients had mitral stenosis, mitral insufficiency or mitral valve prosthesis. Nine patients had an atrial septal defect. One patient had a patent ductus arteriosus, one anomalous pulmonary venous drainage, one primary tricuspid insufficiency, five patients had coronary artery disease, 13 hypertrophic or congestive cardiomyopathy, three constrictive pericarditis, and one patient had recurrent pulmonary emboli with pulmonary hypertension. Eighteen of these patients required maintenance hemodialysis for chronic renal failure. IVC echographic studies were performed using a Varian V-3000 or V-3400 phased-array ultrasonoscope. The transducer was placed in a subxiphoid or right subcostal position and rotated so that the twodimensional sector was parallel to the IVC. In this manner, the course of the IVC behind the liver, extending through the diaphragm, and anastomosing with the right atrium12 was imaged ( fig. 1). The transducer was rocked slightly medially and laterally to record the maximum IVC size. The M-mode cursor of the two-dimensional sector was used to generate a time-motion recording of the IVC. The cursor was positioned inferior to the junction of the hepatic veins with the IVC. Care was taken not to measure the IVC where it dilates at the junction of the right atrium. A time-motion study of the IVC was recorded through several respiratory cycles. All measurements were normalized for body surface area and a mean of two respiratory cycles during normal quiet breathing was calculated. The end-diastolic IVC dimension was measured as the minimum IVC size at or after the R wave of the ECG; this was usually, but not always, the smallest IVC diameter during the entire cardiac cycle. A presystolic (A wave) pulsation was recorded in p...

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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.

BACKGROUND Myocardial perfusion imaging during adenosine-induced hyperemia with dipyridamole or adenosine is an accepted method to diagnose coronary artery disease (CAD) and risk assessment. The mechanism of perfusion abnormality may be caused by disparate flow responses or coronary steal. This study examined the relation between 201Tl perfusion pattern and hemodynamic/angiographic changes during intravenous adenosine infusion. METHODS AND RESULTS Patients with suspected CAD underwent sequential hemodynamic, coronary arteriographic, and left ventriculographic studies simultaneously with 201Tl imaging during adenosine infusion (140 micrograms.kg-1.min-1 for 6 minutes). There were 33 patients with CAD and 12 patients without CAD. The 201Tl images (using single-photon emission computed tomography) were abnormal in 31 patients with CAD (sensitivity, 94%) and normal in the patients without CAD (specificity, 100%). In patients with and without CAD, there were significant increases in heart rate and cardiac output (p less than 0.0001) and decreases in systemic vascular resistance and blood pressure (p less than 0.0001). There was a 77 +/- 38% increase in pulmonary capillary wedge pressure in normal subjects and a 125 +/- 83% increase in patients with CAD (p = 0.02). ST segment depression was observed in 11 patients with CAD (33%). In CAD patients, there was no change in percent diameter or area stenosis measured quantitatively during adenosine infusion. In 15 patients, contrast left ventriculography was repeated during adenosine infusion. In these patients, 201Tl perfusion defects were seen in 31 of 75 segments (41%) whereas only six of 75 segments (8%) developed regional wall motion abnormality (p less than 0.001); the remaining segments showed either no change or improved function. The left ventricular ejection fraction did not change significantly (73% versus 75%). CONCLUSIONS There is a disparity between the effects of adenosine on left ventricular perfusion and function; most patients with CAD have perfusion defects whereas the global and regional systolic function remains unchanged or improves. Diastolic left ventricular dysfunction is a probable mechanism of the increase in pulmonary capillary wedge pressure.