Right coronary artery aneurysm with fistula to left ventricle: multislice CT appearance

A 34-year-old male presented with prior radiographic evidence of enlargement of the right side of the heart. ECG-gated enhanced multislice CT was performed. Axial source images revealed a diffuse, hugely enlarged right coronary artery (RCA) aneurysm. The distal portion of the RCA flowed directly into the left ventricle (LV), suggesting an RCA to LV fistula. 3D volume rendered images clearly revealed a huge, enlarged RCA aneurysm from the proximal, mid, and distal portions of the RCA. The distal portion of the RCA aneurysm disappeared abruptly without showing distal branching, also suggesting an RCA to LV fistula.     

Different coronary blood flow increase in left ventricular hypertrophy due to hypertension compared to hypertrophic cardiomyopathy at elevated heart rate.

Coronary vasodilator reserve (CVR) is reduced in patients with left ventricular hypertrophy (LVH). However, it is not clear whether there is any difference between the coronary blood flow increase in LVH caused by hypertension (HTH) and that caused by hypertrophic cardiomyopathy (HCM) when the heart rate increases. In this study, 16 subjects with HTH, 10 subjects with HCM, and 10 subjects with normotension (NT) were investigated. Average peak velocities at rest, at pacing, and at dilatation were measured using a Doppler catheter placed at the left descending coronary artery to calculate coronary blood flow (CBF) and CVR. CVR at rest was identical in the HTH and HCM groups, and in both cases was lower than the resting CVR in NT subjects. There were significant differences in the CVR values at a pacing rate of 120 beats/min among the groups. These values were lowest in HCM, highest in NT, and intermediary in HTH subjects. And the percent increase in CBF in HCM at that pacing rate was higher than that in HTH (p < 0.05) or NT (p < 0.05). There was no difference in the percent increase in CBF at this pacing rate between the HTH and NT groups. The effects of elevated heart rate on the percent increase in CBF were different between the HTH and HCM groups. We conclude that cardiac hypertrophy has qualitatively different effects on coronary circulation depending on whether patients have HTH or HCM.     

Integrins play a critical role in mechanical stress-induced p38 MAPK activation

Mechanical stress activates various hypertrophic responses, including activation of mitogen-activated protein kinases (MAPKs) in cardiac myocytes. Stretch activated extracellular signal-regulated kinases partly through secreted humoral growth factors, including angiotensin II, whereas stretch-induced activation of c-Jun NH(2)-terminal kinases and p38 MAPK was independent of angiotensin II. In this study, we examined the role of integrin signaling in stretch-induced activation of p38 MAPK in cardiomyocytes of neonatal rats. Overexpression of the tumor suppressor PTEN, which inhibits outside-in integrin signaling, strongly suppressed stretch-induced activation of p38 MAPK. Overexpression of focal adhesion kinase (FAK) antagonized the effects of PTEN, and both tyrosine residues at 397 and 925 of FAK were necessary for its effects. Stretch induced tyrosine phosphorylation and activation of FAK and Src. Stretch-induced activation of p38 MAPK was abolished by overexpression of FAT and CSK, which are inhibitors of the FAK and Src families, respectively, and was suppressed by overexpression of a dominant-negative mutant of Ras. Mechanical stretch-induced increase in protein synthesis was suppressed by SB202190, a p38 MAPK inhibitor. These results suggest that mechanical stress activates p38 MAPK and induces cardiac hypertrophy through the integrin-FAK-Src-Ras pathway in cardiac myocytes.     

Acute acalculous cholecystitis with a decrease in CD4/CD8 ratio

Acute acalculous cholecystitis (AAC) usually occurs in the elderly and in those with severe preexisting pathological conditions. However, there have recently been reports of AAC in relatively young immunosuppressed patients, such as those with acquired immunodeficiency syndrome (AIDS). We report here a 27-year-old woman with AAC who received an emergent cholecystectomy. Although anti-human immunodeficiency virus antibody (anti-HIV) was not detected, a decrease in the CD4/CD8 ratio in sera was found. This rare case of AAC in a patient with decreased CD4/CD8 ratio who showed no other related diseases suggests that surgeons should keep in mind the possible presence of immunosuppression in this condition.     

Prognostic impact of left ventricular noncompaction in patients with Duchenne/Becker muscular dystrophy — Prospective multicenter cohort study

Background

The reported prevalence of left ventricular noncompaction (LVNC) varies widely and its prognostic impact remains controversial. We sought to clarify the prevalence and prognostic impact of LVNC in patients with Duchenne/Becker muscular dystrophy (DMD/BMD).

Methods

We evaluated the presence of LNVC in patients with DMD/BMD aged 4–64 years old at the study entry (from July 2007 to December 2008) and prospectively followed-up their subsequent courses (n = 186). The study endpoint was all-cause death and the presence of LVNC was blinded until the end of the study (median follow-up: 46 months; interquartile range: 41–48 months).

Results

There were no significant differences in baseline characteristics between patients with LVNC (n = 35) and control patients without LVNC (n = 151), with the exception of LV function. Patients with LVNC showed, in comparison with patients without LVNC, a significant negative correlation between age and LVEF (R = − 0.7 vs. R = − 0.4) at baseline; and showed a significantly greater decrease in absolute LVEF (− 8.6 ± 4.6 vs. − 4.3 ± 4.5, p < 0.001) during the follow-up. A worse prognosis was observed in patients with LVNC (13/35 died) than in patients without LVNC (22/151 died, Log-rank p < 0.001). Multivariate Cox analysis revealed that LVNC is an independent prognostic factor (relative hazard 2.67 [95% CI: 1.19–5.96]).

Conclusion

LVNC was prevalent in patients with DMD/BMD. The presence of LVNC is significantly associated with a rapid deterioration in LV function and higher mortality. Neurologists and cardiologists should pay more careful attention to the presence of LVNC.     

Human T-Lymphotropic Virus Type II in Japan

Serum specimens were assayed for human T-lymphotropic virus type II (HTLV-II) infection in 1,500 individuals known to be seropositive for HTLV-I and 30,000 blood donors in Japan. All HTLV-I-positive individuals were negative for HTLV-II. However, one of the blood donors was clearly seropositive for HTLV-II. Further, the donor was shown to be positive for HTLV-IIb. Here we report at least one case with HTLV-II in Japan and discuss the origin of the infection.     

Synergistic T-T cell interaction present in alloreactivity: determination of 'MLR helper' T cell subsets

CD4 and CD8 T cell subsets involved in primary allo-MLR responses were re-evaluated in the present study. The slope analysis of B6 allo-MLR responses to MHC class I-disparate bm1 and class II-disparate bm12 revealed the presence of a T-T cell interaction between CD4 and CD8 T cell subsets. The allo-MLR response of B6 CD4 T cells to bm12 was completely blocked by anti-L3T4, indicating that the function of CD4 T cells is required for allo-MLR responses to bm12. It was further demonstrated that the function of CD8 T cells in class II-disparate allo-MLR is to augment the proliferative response of CD4 T cells. On the other hand, CD8 T cells primarily responded to class I-disparate allo-MLR, and CD4 T cells function to augment the proliferative response of CD8 T cells. It was further indicated that CD4 and CD8 T cells recognize both class I and class II MHC. The CD4 T cell recognition of allo-class I and CD8 T cell recognition of allo-class II induces insufficient signals for proliferation of these T cells. Thus, the class I-reactive CD4 and class II-reactive CD8 T cell subsets function as helper cells ('MLR helper' T cells) for proliferating T cells in MLR responses.