These results indicate that psoriatic skin after monochromatic excimer light therapy is associated with significant T-cell depletion and alterations of apoptosis-related molecules accompanied by a decreased proliferation index and clinical remission.

The warm-up phenomenon, described in patients with coronary artery disease, refers to the improved performance following a first exercise test. The aim of this study was to investigate the causes of the warm-up phenomenon. Fifteen patients with coronary artery disease and positive exercise test were enrolled. Patients were off treatment throughout the study. They underwent two consecutive treadmill exercise tests according to the Bruce protocol, with a recovery period of 10 min to re-establish baseline conditions. A third exercise test was then performed 2 h later. Before the onset of ischaemia, the rate-pressure product for a similar degree of workload was similar during the first and second exercise test, while it was lower during the third test (P < 0.05). Time to 1.5 mm ST-segment depression during the second and third exercise test was greater than during the first test (454 +/- 133 and 410 +/- 161 vs 354 +/- 127 s, P < 0.01, respectively). Similarly, the time to anginal pain onset was increased during the second and third exercise tests, compared to the first test (356 +/- 208 and 310 +/- 203 vs 257 +/- 204 s, P < 0.01, respectively). In contrast, rate-pressure product at 1.5 mm ST-segment depression during the second test was higher than that during the first test (232 +/- 47 vs 210 +/- 39 beats.min-1.mmHg.10(2), P < 0.01), while in the third test it was similar to that during the first (209 +/- 43 beats.min-1.mmHg.10(2), P = ns). The warm-up phenomenon observed a few minutes after exercise is characterized by an increase of both time to ischaemia and ischaemic threshold; this adaptation to ischaemia may be due to an improvement of myocardial perfusion or to preconditioning. Conversely, the warm-up phenomenon observed a few hours after repeated exercise is characterized by an increase of time to ischaemia but not of ischaemic threshold and is caused by a slower increase of cardiac workload. Thus, the mechanisms of the warm-up phenomenon may be different, time dependent and related to previous training.

DES and BMS thromboses have different clinical features, but a similar poor outcome. Indeed, PCI for ST is associated with a low rate of reperfusion and to a high rate of death and MACCE, calling for action in order to prevent its occurrence and to improve its management.

AimsThe increased tolerance to myocardial ischaemia observed during the second of two sequential exercise tests, i.e. the warm-up phenomenon, has been proposed as a clinical model of ischaemic preconditioning. As ATPsensitive K + channels appear to be a mediator of ischaemic preconditioning in both experimental and clinical studies, the aim of this study was to investigate the role of K ATP channels in the warm-up phenomenon. Methods and ResultsTwenty-six patients with coronary artery disease were randomized to receive 10 mg oral glibenclamide, a selective ATP-sensitive K + channel blocker, or placebo. Sixty minutes after glibenclamide or placebo administration, patients were given an infusion of 10% dextrose (8 ml . min 1 ) to correct glucose plasma levels or, respectively, an infusion of saline at the same infusion rate. Thirty minutes after the beginning of the infusions, both patient groups underwent two consecutive treadmill exercise tests, with a recovery period of 15 min to re-establish baseline conditions. Before exercise tests, blood glucose levels were similar in placebo and glibenclamide groups (96 10 vs 105 22 mg . 100 ml 1 , P=ns). After placebo administration, rate-pressure product at 1·5 mm STsegment depression significantly increased during the second exercise test compared to the first (220 41 vs 186 29 beats . min 1 . mmHg . 10 2 , P<0·01), but it did not change after glibenclamide (191 34 vs 187 42 beats . min 1 . mmHg . 10 2 , P=ns), with a significant drugtest interaction (P=0·0091, at two-way ANOVA).Conclusions Glibenclamide, at a dose previously shown to abolish ischaemic preconditioning during coronary angioplasty, prevents the increase of ischaemic threshold observed during the second of two sequential exercise tests. These findings confirm that ischaemic preconditioning plays a key role in the warm-up phenomenon and that in this setting is, at least partially, mediated by activation of ATP-sensitive K + channels.

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