[Usefulness of lung and right ventricular thallium-201 uptake during single photon emission computed tomography in exercise testing of patients with coronary artery disease].

OBJECTIVES: Increased pulmonary or right ventricular 201Tl uptake during the exercise test has been used as a marker of multivessel coronary artery disease. The most useful method for assessing the severity of coronary artery disease was evaluated among conventional evaluation of single photon emission computed tomography (SPECT), measurement of lung to heart uptake ratio (L/H), and right ventricular to left ventricular uptake ratio (RV/LV) on 201Tl images during exercise testing. METHODS: Regions-of-interest (4 X 4 pixels) were placed at the lung and the heart, and L/H was defined as mean lung uptake/mean heart uptake. Correspondingly, regions-of-interest (4 X 4 pixels) were placed at the RV and the LV, and RV/LV was defined as maximum RV uptake /maximum LV uptake. L/H and RV/LV on the initial image were analyzed in 216 patients(angiographically normal coronary arteries: 89, single-vessel disease: 82, multivessel disease: 45). The diagnostic value was evaluated using the receiver operating characteristic curve. RESULTS: All methods showed significantly higher values in patients with multivessel disease than in patients with no coronary artery disease or single-vessel disease. L/H was significantly higher in patients with prior myocardial infarction and RV/LV was significantly higher in patients without infarction. The sensitivity of only conventional SPECT evaluation for multivessel coronary artery disease was low (sensitivity 53%, specificity 94%). However, addition of evaluation of L/H and RV/LV to SPECT improved the sensitivity for multivessel coronary artery disease (sensitivity 93%, specificity 49%). CONCLUSIONS: The diagnostic sensitivity for multivessel coronary artery disease was improved by adding L/H and RV/LV to conventional evaluation of exercise 201Tl SPECT. L/H and RV/LV during exercise 201Tl imaging may provide additional information regarding the severity of coronary artery disease.

CaMKII-dependent reactivation of SR Ca(2+) uptake and contractile recovery during intracellular acidosis.

In hearts, intracellular acidosis disturbs contractile performance by decreasing myofibrillar Ca(2+) response, but contraction recovers at prolonged acidosis. We examined the mechanism and physiological implication of the contractile recovery during acidosis in rat ventricular myocytes. During the initial 4 min of acidosis, the twitch cell shortening decreased from 2.3 +/- 0.3% of diastolic length to 0.2 +/- 0.1% (means +/- SE, P < 0.05, n = 14), but in nine of these cells, contractile function spontaneously recovered to 1.5 +/- 0.3% at 10 min (P < 0.05 vs. that at 4 min). During the depression phase, both the diastolic intracellular Ca(2+) concentration ([Ca(2+)](i)) and Ca(2+) transient (CaT) amplitude increased, and the twitch [Ca(2+)](i) decline prolonged significantly (P < 0.05). In the cells that recovered, a further increase in CaT amplitude and a reacceleration of twitch [Ca(2+)](i) decline were observed. The increase in diastolic [Ca(2+)](i) was less extensive than the increase in the cells that did not recover (n = 5). Blockade of sarcoplasmic reticulum (SR) function by ryanodine (10 microM) and thapsigargin (1 microM) or a selective inhibitor of Ca(2+)-calmodulin kinase II, 2-[N- (2-hydroxyethyl)-N-(4-methoxybenzenesulfonyl)] amino-N-(4-chlorocinnamyl)-N-methyl benzylamine (1 microM) completely abolished the reacceleration of twitch [Ca(2+)](i) decline and almost eliminated the contractile recovery. We concluded that during prolonged acidosis, Ca(2+)-calmodulin kinase II-dependent reactivation of SR Ca(2+) uptake could increase SR Ca(2+) content and CaT amplitude. This recovery can compensate for the decreased myofibrillar Ca(2+) response, but may also cause Ca(2+) overload after returning to physiological pH(i).