Effect of type D personality on smoking status and their combined impact on outcome after acute myocardial infarction

Background

Smoking cessation is correlated with several psychological, social, biological, and pharmacological aspects. The combined tendency to experience negative emotions and to inhibit the expression of these emotions is indicated as “type D personality,” an independent risk marker for clinical outcome in cardiac disease. Despite this effect of type D personality on cardiovascular disease, it is still unclear whether this personality trait may influence smoking cessation after a myocardial infarction.

Hypothesis

we hypothesized that there is a relationship between type D personality and smoking persistence in acute coronary syndrome patients, and this association may predict a worse long‐term prognosis.

Methods

The study enrolled 231 patients with ST‐segment elevation myocardial infarction, treated with primary percutaneous coronary intervention. Type D scale 14 (ds 14) was administered upon admission to the hospital.

Results

After controlling for demographic and clinical confounders, non–type D patients reported statistically significant higher frequencies of smoking cessation when compared with the type D group. In addition, the presence of this psychological factor anticipates significantly the onset of smoking during adolescence. Furthermore, current type D smokers had a higher incidence of cardiovascular events during long‐term follow‐up.

Conclusions

Type D personality and smoking status increase the risk of cardiac events. An emotionally stressed personality and persistence of smoking after the first cardiac event, and mostly their mutual influence, indicate a population at high cardiovascular risk.     

The significance of the hemoglobin A2 value in screening for hemoglobinopathies

Background and objective

The inherited hemoglobinopathies are a large group of disorders that include thalassemias and hemoglobin variants. Accurate determination of the carrier phenotype is essential for detecting couples at risk for producing offspring with hemoglobinopathy. Heterozygous β-thalassemia is usually silent at the clinical level. His phenotype is characterized by microcytosis and hypochromia with increased hemoglobin A₂ (HbA₂) value. Therefore, HbA₂ determination plays a key role in screening programs for hemoglobinopathy. The aim of this review is to address and suggest an approach for reducing or abolishing hemoglobinopathy screening mistakes.

Design and methods

Quantitative methods for HbA₂ value determination, comment on the accuracy of the test and on the interpretation of data were discussed. The most probable diagnostic conclusion based on the HbA₂ level, hemoglobin pattern, hematological parameters and iron markers was suggested in this review.

Results

Hemoglobinopathies are the only genetic disease where it is possible to detect carriers using hematological findings rather than DNA analysis. However, hematological diagnosis is sometimes presumptive, and in these cases, DNA analysis becomes necessary. Complete screening is based on the detection of red cell indices, HbA₂, HbF and hemoglobin variant values. In particular, HbA₂ determination plays a key role in screening programs for β-thalassemia because a small increase in this fraction is one of the most important markers of β-thalassemia heterozygous carriers.

Conclusion

Genetic factors both related and unrelated to the β- and α-globin gene clusters, iron metabolism, endocrinological disorders, and some types of anemia, together with intra- and inter-laboratory variations in HbA₂ determination, may cause difficulties in evaluating this measurement in screening programs for hemoglobinopathies. Therefore, knowledge of all these issues is important for reducing or eliminating the risk of mistakes in screening programs for hemoglobinopathies.     

Lymphomagenic properties of a HIV p17 variant derived from a splenic marginal zone lymphoma occurred in a HIV‐infected patient

Despite antiretroviral therapy, HIV+ individuals still have increased risk to develop lymphomas, including marginal zone lymphomas, suggesting that factors other than HIV‐related immunosuppression are probably acting as lymphomagenic factors in the HIV setting. The possible pathogenic involvement of HIV p17 protein variants was investigated in a particularly informative case of HIV‐related splenic marginal zone lymphoma, which was negative for oncogenic virus infections, thus allowing us to assess the possible direct contribution of these HIV‐encoded proteins to lymphomagenesis. The presence of p17 protein was analyzed by immunohistochemistry in lymphoma tissue. Recombinant p17 protein derived from the dominant sequence detected in plasma and lymphoma biopsy was characterized for B‐cell proliferation, clonogenicity in soft agar, in vitro tube formation and wound healing. Intracellular signaling was investigated by immunoblotting. HIV p17 protein was detected in reactive lymphoid follicles but not within lymphoma cells. An identical dominant variant p17 sequence, p17‐Lyrm, carrying a 117 to 118 Ala‐Ala insertion was detected in both plasma and lymphoma tissue. Recombinant p17‐Lyrm enhanced B‐cell proliferation and clonogenicity promoted the formation of capillary‐like structures and enhanced endothelial cell migration. Unlike reference p17, the p17‐Lyrm variant enhanced the activation of Akt and ERK, critical kinases in lymphomagenesis. p17‐Lyrm clonogenic activity was dependent on the activation of Akt but not of ERK1/2. These results indicated that HIV p17 variants with distinct molecular signatures and functional properties may accumulate in lymphoid tissues of HIV‐infected individuals where they may act as a local stimulus promoting the development of lymphomas.