Limited role of aortic size in the genesis of acute type A aortic dissection

Objective: Increased dimension of the aortic root and proximal aorta is considered a significant risk factor for catastrophic events that involve the ascending aorta. The objective of this study was to determine the possible correlation between pre-dissection aortic diameter and the occurrence of Stanford type A aortic dissection. Methods: Samples of dissected ascending aortas were obtained from 220 patients at the time of their operation. Two groups were identified: patients with connective tissue disorders (Group 1, n = 94) and those without (Group 2, n = 126). Measurements of the true (intimal) lumen were conducted and extrapolated as reliable approximation of pre-dissection aortic diameter. The possible association of intimal diameter with anthropometric and demographic data was analyzed. Results: Median aortic diameter was, respectively, 41.8 and 41.3 mm for patients with and without connective tissue disorders (41.4 mm for the entire cohort). Data analysis indicated that 57% of patients had aortic diameter above 40 mm, while patients with frank aneurysm accounted only for 10%; this proportion was higher in Group 1 compared to Group 2 (17.2% vs 4.7%). Poor or no correlation was demonstrated between aortic size and any of the anthropometric or demographic variables essayed. Significant subgroup differences were found among patients with a history of cigarette smoking, hypertension, diabetes, chronic renal insufficiency, and bicuspid aortic valve. Conclusion: Although aortic diameter remains a strong indication for preventive surgery in patients with inherited connective tissue disorders, acute aortic dissection occurs rarely in the setting of true ascending aortic aneurysms, and despite normal or near-normal aortic size in more than one-third of subjects. Dissection superimposing on small aortic diameters can be regarded as an expression of substantial functional tissue susceptibility to aortic catastrophic events.     

Homocysteine-Lowering Therapy and Early Progression of Transplant Vasculopathy: A Prospective, Randomized, IVUS-Based Study

Although observational studies suggest that hyperhomocysteinemia may be a risk factor for coronary allograft vasculopathy (CAV), prospective data on homocysteine-lowering interventions and CAV development are lacking. We, therefore, randomized 44 de novo heart transplant (HT) recipients to 15 mg/day of 5-methyl-tetrahydrofolate (n=22), or standard therapy (control group, n=22) to investigate the effect of homocysteine lowering on the change in coronary intimal hyperplasia during the first 12 months after transplant, as detected by intra-vascular ultrasound (IVUS). Although 12 months after HT, homocysteinemia was lower in folate-treated patients (p<0.001), coronary intimal area increased similarly in the two groups (p>0.4). Conversely, hypercholesterolemia and cytomegalovirus infection were both associated with increased intimal hyperplasia (p<0.04), independently from folate intake. Sub-group analysis revealed that folate therapy reduced intimal hyperplasia in patients with hyperhomocysteinemia before randomization (n=19; p=0.02), but increased intimal hyperplasia in patients with normal homocysteine plasma concentrations (p=0.02). This bimodal effect of folate therapy persisted significantly after adjusting for cytomegalovirus infection and hypercholesterolemia. Despite effective in prevent hyperhomocysteinemia after heart transplantation, folate therapy does not seem to affect early CAV onset. However, sub-group analysis suggests that folate therapy may delay CAV development only in patients with baseline hyperhomocysteinemia, while may favor CAV progression in recipients with normal baseline homocysteinemia.     

Changes in hepatic folylpolyglutamate pattern in phenobarbitone-treated rats

Folate deficiency is a common unpleasant secondary effect of anticonvulsant therapy. In order to contribute to the knowledge of biochemical mechanisms leading to this condition, the effects of two i.p. high doses of phenobarbitone administered to the rat (acute treatment) on the distribution of hepatic folate derivatives have been studied. A significant decrease of unsubstituted tetrahydro- and dihydropteroylpentaglutamates and 5,10-methylenetetrahydropentaglutamates was observed. The hypothesis that a lower availability of NADPH, which is utilized for hydroxylation reactions in phenobarbitone metabolism, may limit folate reduction is proposed.     

Pseudo-angiomatous hyperplasia of mammary stroma: a case with gigantomastia

Pseudo-angiomatous hyperplasia of mammary stroma (PASH) is a histopathological entity which is a microscopic fortuitous finding in mammary biopsies performed for different reasons. It may be symptomatic and appears then as a palpable lump. The term pseudo-angiomatous emphasizes the characteristic aspect of the stroma simulating a vascular tumor. We report a case of PASH in a 71 year-old woman who presented a recurring breast mass with rapid swelling of the mammary gland (70 x 60 x 20 cm) treated by mastectomy. PASH must be distinguished from a well-differentiated angiosarcoma. It is ruled out by immunohistochemistry.     

Comparison of enzyme-linked immunosorbent assay (ELISA) and complement fixation test for detection of Mycoplasma pneumoniae antibodies.

An enzyme-linked immunosorbent assay (ELISA) for the detection of IgG and IgM antibodies against Mycoplasma pneumoniae, performed with commercial antigen and reagents, is compared with the complement fixation test (CF) in a serological study of 209 human sera. Concordant results were usually obtained by CF test and by IgG ELISA in sera from patients with recent M pneumoniae infection. In contrast, when used for an immunological survey of a general population, approximately 27% of the sera negative in the CF test were positive for IgG by the ELISA, and sera with low CF titres were found to have a broad range of IgG titre by the ELISA. This may be due to the greater sensitivity of the ELISA technique and/or to different types of antibody measured by both tests. IgM was detected by ELISA in sera from all patients with recent M pneumoniae infection diagnosed on the basis of clinical findings and by CF assay. Occasionally false-positive IgM antibodies were due to rheumatoid factor (RF); this potential interference necessitates routine testing of IgM antibody positive sera for RF.