Selective induction of matrix metalloproteinases and tissue inhibitor of metalloproteinases in atrial and ventricular myocardium in patients with atrial fibrillation

Atrial fibrillation (AF) produces changes in atrial structure and extracellular matrix composition, which is regulated by matrix metalloproteinases (MMPs). Moreover, AF often occurs in the setting of congestive heart failure (CHF), which also affects MMPs. Whether changes in MMPs or the tissue inhibitors of metalloproteinases (TIMPs) within atrial and ventricular myocardium are differentially regulated with AF remains unclear. Myocardium from the walls of the right atrium, right ventricle, left atrium, and left ventricle was obtained from the explanted hearts of 43 patients with end-stage CHF. AF was present in 23 patients (duration 1 to 84 months). The remaining 20 patients served as non-AF controls. The groups were well matched clinically, but left atrial (LA) size was increased in the AF cohort (5.5 +/- 0.8 vs 4.9 +/- 0.7 cm, p <0.05). Myocardial collagen content and levels of MMP-1, -2, -8, -9, -13, and -14, and TIMP-1, -2, -3, and TIMP-4 were determined. With AF, collagen content was greater within the atrial myocardium but less in the ventricular myocardium. There were chamber-specific differences in MMPs and TIMPs with AF. For example, MMP-1 in the right atrium and MMP-9 in the left atrium were greater with AF. TIMP-3 levels were greater in the right ventricle, left atrium, and left ventricle. Although total LA collagen was positively correlated with AF duration (r = 0.49, p <0.03), there was an inverse relation between soluble collagen I and AF duration (n = 6, r = -0.84, p <0.04). In conclusion, AF is associated with chamber-specific alterations in myocardial collagen content and MMP and TIMP levels, indicative of differential remodeling and altered collagen metabolism. Differences in MMP and TIMP profiles may provide diagnostic and mechanistic insights into the pathogenesis of AF with CHF.     

Proposal of a new classification for optimising outcome assessment following partial cricotracheal resections in severe pediatric subglottic stenosis

Objective

Creation of a patent subglottic airway after partial cricotracheal resection (PCTR) may not always result in successful decannulation due to associated parameters such as co-morbidity and/or glottic involvement. We classified patients after incorporating these additional parameters into the original Myer-Cotton classification to assess whether this could better predict the outcome measures after PCTR.

Methods

One hundred children with Myer-Cotton grade III or IV subglottic stenosis who underwent PCTR between 1978 and 2008 were identified from a prospectively collected database. The patients were classified into four groups based on the association of co-morbidity and/or glottic involvement. Delay in decannulation, revision open surgery and rates of decannulation were the outcome measures compared between the groups.

Results

There were 68 children with Myer-Cotton grade III and 32 children with grade IV stenosis. Based on the new classification, there were 36 children with isolated SGS, 31 with associated co-morbidity, 19 with associated glottic involvement and 14 children with both co-morbidity and glottic involvement. A trend towards less optimal results was noticed with the association of co-morbidity and/or glottic involvement. Statistical significance was reached for maximum decannulation failure in the group with both co-morbidity and glottic involvement. Delayed decannulation significantly correlated in the group with associated glottic involvement.

Conclusion

This new classification is relatively simple and aimed at providing more accurate and uniform prognostic information to both patients and surgeons when dealing with the whole spectrum of severe SGS.     

Hidden VIM-1 metallo-beta-lactamase phenotypes among Acinetobacter baumannii clinical isolates

A total of 87 Acinetobacter baumannii nonrepetitive consecutive clinical isolates were tested for the presence of metallo-β-lactamases (MBLs). Results of phenotypic assays (MBL Etest, imipenem/imipenem-EDTA combined-disk test, and imipenem/EDTA double-disk synergy test) were negative in all cases, but molecular testing revealed the presence of two bla_VIM-1-carrying isolates. One isolate had bla_VIM-1 preceded by a weak P1 promoter, and both had inactivated P2 promoters and reduced bla_VIM-1 expression, partially justifying the results revealing hidden MBL phenotypes.     

Severity of Alopecia Predicts Coronary Changes and Arterial Stiffness in Untreated Hypertensive Men

An association between androgenic alopecia (AGA), coronary artery disease, and hypertension has been reported in previous epidemiological studies. The authors evaluated the relationship of target organ damage caused by hypertension with AGA in 101 newly diagnosed and untreated hypertension men with mild to moderate AGA (AGA_m), severe AGA (AGA_s), and non‐AGA. Pulse wave velocity (PWV), office and 24‐hour pulse pressure (PP), carotid intima‐media thickness (IMT), left ventricular hypertrophy (LVH), coronary flow reserve (CFRd ), and AGA severity by Hamilton‐Norwood scale were estimated. CFRd was significantly impaired in AGA_s patients compared with AGA_m (P=.007) and non‐AGA patients (P=.02). No differences were found within groups regarding PWV, PP, IMT, and LVH. AGA severity was related to CFRd (independently) and PP while AGA duration and age of onset were related to CFRd and PP, respectively. The authors conclude that impaired coronary microcirculation and aortic stiffness might precede the appearance of significant stenotic coronary lesions in hypertensive patients with severe AGA. In addition, hypertensive patients with severe and early AGA onset seem to be exposed to an augmented cardiovascular risk.     

Arterial stiffness and Chlamydia pneumoniae infection in coronary artery disease. Is there a link?

BACKGROUND: We investigated the possible association between antichlamydial antibodies and pulse wave analysis (PWA) parameters in a cohort of patients with coronary artery disease (CAD). METHODS: The augmentation index (AI), the reflection time index (RTI) and the time to the beginning of the reflected wave (CT-1) were estimated (Sphygmocor ATCOR Medical). IgA titers >or= 40 and IgG >or=80 were considered as positive (microimmunofluorescence test). Patients also underwent coronary angiography, ultrasound carotid measurements and 24 h ambulatory blood pressure (BP) measurements. RESULTS: No differences existed in the traditional risk factors for CAD between the seronegative and seropositive IgA/ IgG groups. IgA seropositive subjects had higher values of AI (p < 0.01) comparing to seronegatives whilst the levels of CT-1 and RTI were lower (p < 0.011 and p < 0.02 respectively). No differences in AI, CT-1 and RTI values were found between IgG seropositive/ seronegatives patients. CONCLUSIONS: An association was indicated between IgA antichlamydial titers and PWA parameters in patients with CAD, supporting that the connecting link between arterial stiffness and CAD might include this microorganism.