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incorrectly interpreted to be irreversible if only stress-reinjection images were acquired. Dr. Freedman's finding of low differential uptake in 11% of their patients after reinjection appears to confirm our results. We agree with Dr. Freedman that similar information might be obtained if an analysis of thallium activity after a resting injection of 20`T1 were used. Preliminary data in our laboratory suggest a high concordance between the results of stress-redistribution-reinjection imaging and rest-redistribution imaging.5 We caution that a resting image alone may be insufficient and that a subsequent redistribution image after the injection at rest is often necessary. Bonow RO: Regional thallium uptake in irreversible defects: Magnitude of change in thallium activity after reinjection distinguishes viable from nonviable myocardium. viable myocardium in patients with chronic coronary artery disease and left ventricular dysfunction: Comparison of thallium scintigra-phy with reinjection and PET imaging with '8F-fluorodeoxyglucose. Enhanced detection of ischemic but viable myocardium by the rein-jection of thallium after stress-redistribution imaging. N Engl J Med 1990;323:141-146 4. Dilsizian V, Bonow RO: Differential uptake and apparent 2OITI washout after thallium reinjection: Options regarding early redistribution imaging before reinjection or late redistribution imaging after reinjection. RO: Concordance and discordance between rest-redistribution thallium imaging and thallium reinjection after stress-redistribution imaging for assessing viable myocardium: Comparison with metabolic activity by PET. Letter To the Editor Beuckelmann et al recently published a report in Circulation' showing that peak systolic intracellular calcium measured by fura-2 was diminished in single ventricular cells from patients with heart failure. Although the experimental findings were interesting, the suggestion by the authors that the major defect in contractile failure is a diminished intracellular calcium concentration was distressing. The authors propose that diminished calcium availability might explain impaired contractile performance in human heart failure because calcium concentration is intimately related to force production; it is important to note, however, that this conclusion is weakened by the fact that Beuckelmann et al did not measure force or cell shortening during excitation in their cells. These results are in contrast to those obtained by other investigators who used different experimental techniques and reported similar systolic calcium concentrations in myopathic and control human myocardium.2-6 More importantly, we and others have found similar force production in control and myopathic hearts, and it has been clearly demonstrated that in failing human myocardium, there is a significant increase in resting intracellular calcium concentration. The clinical extrapolation of the data proposed by the …

Intracellular [Ca2+] in normal and diseased human myocardium.