Search

We investigated myocardial perfusion in acute patients with slow coronary flow (SCF) at angiography. Whether impaired myocardial perfusion occurs in acute patients with SCF is unknown.We enrolled 28 consecutive patients with SCF in the epicardial coronary arteries with no evidence of significant stenosis. SCF affected a single coronary artery in 14 patients (group A) and all three coronary vessels in 14 others (group B). Coronary angiography was repeated after dipyridamole infusion and single photon emission computed tomography was performed using dipyridamole as the stress agent. The Thrombolysis in Myocardial Infarction frame count was measured in SCF vessels at baseline and after dipyridamole infusion.Mean Thrombolysis in Myocardial Infarction frame count significantly decreased after dipyridamole in both groups. At baseline, mean values of the single photon emission computed tomography score were 31.5 +/- 1.6 and 25.1 +/- 2.1 in groups A and B, respectively. After dipyridamole, they increased from 31.5 +/- 1.6 to 37.8 +/- 1.4 (P0.001) in group A, whereas a further decrease to 15.0 +/- 1.2 (P0.005) was observed in group B.An opposite behavior of myocardial perfusion was observed after dipyridamole infusion: a normal response in patients with SCF affecting one single coronary artery versus an ischemic-like response in those with CSF affecting all three coronary arteries.

This study concerns the family of a girl affected by type 2 Crigler-Najjar syndrome; a brother and a sister died of kernicterus a few months after birth. The father and two living siblings had moderate unconjugated hyperbilirubinemia. The patient's liver uridine-diphospho-glucuronyl-transferase activity (UDPGT) was markedly reduced. All the family members underwent nicotinic acid (NA) load to test hepatic uptake capacity. This test, and NA half-life were normal in the patient and in her mother, and altered in the other relatives. The extent of the hyperbilirubinemic response to NA load, and of the NA half-life, together with physical examination over a one-year period were in good agreement with the diagnosis of Gilbert's syndrome in the patient's father and siblings. Our conclusion is that different impairments of hepatic handling of organic anions may be present in members of families with non-hemolytic bilirubinemia.