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A mosaic pattern of lung attenuation at CT is a sign of variable regional perfusion and may suggest chronic pulmonary thromboembolism as a cause for pulmonary hypertension.

To compare radionuclide end-diastolic (EDV) and end-systolic (ESV) volumes with angiographic volume, we studied 52 patients with equilibrium radionuclide angiography using 99mTc-human serum albumin within 48 hours of contrast angiography. Each RR interval was divided into 20--28 equally timed frames and a time-activity curve generated. End-diastolic counts were taken at the early peak of the curve and end-systolic counts at its nadir. Counts were divided by the total number of processed heart beats and normalized for: 1) dose per body surface area; 2) plasma volume; and 3) counts/ml of plasma. A cardiac phantom was developed and serial volumes were studied using a normalization factor. Radionuclide values were expressed as dimensionless units and compared with either biplane angiographic volumes (in the patient studies) or known phantom volumes. Good correlations were obtained with methods 1 and 2 in 35 patients (r greater than 0.84), but the best correlation was obtained in 17 patients when normalization for counts/ml of plasma was used (r = 0.98; y = 0.255 x -0.121). The standard error of the estimate (SEE) was +/- 11.5 ml for EDV and +/- 7.3 ml for ESV. The phantom study also showed an excellent correlation (r = 0.99), with a SEE of +/- 6.5 ml. We conclude that a radionuclide method independent of geometric assumptions can be used to estimate left ventricular volume in man.

Preliminary studies have suggested that QRS-amplitude changes due to exercise-induced alterations in ventricular volume and function can improve the diagnostic value of the exercise test. To evaluate this, electrocardiographic data and equilibrium radionuclide angiographic images were recorded simultaneously in 18 normal subjects and 60 coronary artery disease patients at rest and during supine bicycle exercise. In 24 of the 60 coronary artery disease patients, left ventricular volumes were also calculated. The measured QRS amplitudes were the R waves in V, X, Y and Z, the Q wave in Z and the sum of amplitudes of R waves in X and Y and the Q wave in Z (2iR). The mean left ventricular ejection fraction increased significantly from rest to peak exercise in the normal subjects; however, the mean left ventricular ejection fraction and mean volumes did not change significantly in the coronary patients. There was no significant difference in the mean QRS-amplitude changes during exercise between the coronary artery disease patients and the normal subjects in any of the measured leads. The sensitivity and specificity of exercise-induced QRS-amplitude changes for coronary disease were lower than ST-segment changes. For ST-segment changes, the sensitivity was 57% and specificity was 100%; the best sensitivity and specificity for QRS amplitude occurred in RZ, 48% and 67%, respectively. When ejection fraction was related to 2R at rest and peak exercise for both normal subjects and coronary patients the correlations were fair (0.50, 0.51 respectively); however, the correlation between the magnitude of 2R and ejection fraction change from rest to peak exercise was poor and did not improve with any other measured QRS amplitudes or by separating normal subjects from coronary patients with and without previous myocardial infarction. There were also poor correlations between end-diastolic and endsystolic volumes to QRS amplitudes at rest, peak exercise and their magnitude of change from rest to peak exercise. Thus, R-wave amplitude changes during exercise testing have little diagnostic value and are not related to exercise-induced changes in left ventricular function or volumes.