Does therapeutic intervention achieve slowing of progression or bona fide regression of atherosclerotic lesions?

-This review focuses on the regression of atherosclerosis in humans and experimental animals. It highlights the difficulties to determine unequivocally whether with a given therapeutic intervention, such as diet, drugs, or apheresis, the progression of lesions was curtailed or bona fide regression of atherosclerotic lesions was achieved. It seems appropriate to mention that 2 very different ways to measure regression were used in experimental animals and in humans. Regression in animals was determined mainly in the aorta or coronary arteries isolated at post mortem, and the criteria used were degree of sudanophilia and/or aortic wall thickness and cellular composition or cholesterol content. In humans, the evaluation of regression relied mainly on quantitative coronary angiography. The literature of the past decade is reviewed selectively but not exhaustively, and in some instances, a brief historical overview is given.     

From scleredema to AL amyloidosis: disease progression or coincidence? Review of the literature

Scleredema (also called scleredema of Buschke) is a fibromucinous connective tissue disorder of unknown cause that belongs to a group of scleroderma-like disorders. We report the case of a 64-year-old lady with long-standing scleredema, associated with a paraprotein, and progressing to multiple myeloma and AL amyloidosis. The relationship of scleredema with paraprotein and multiple myeloma is well established, but only two cases of scleredema associated with amyloidosis have been reported to date. We suggest that amyloidosis may be underdiagnosed in patients with scleredema and paraproteinaemia. Features attributed to extracutaneous manifestations of scleredema could represent systemic amyloidosis. We review published reports of scleredema associated with paraprotein and discuss the difficulties in the differential diagnosis of scleroderma-like disorders. We discuss the diagnosis of plasma cell dyscrasias and amyloidosis and their relevance in rheumatology practice.     

Are calcifying matrix vesicles in atherosclerotic lesions of cellular origin?

Over recent years, the role of matrix vesicles in the initial stages of arterial calcification has been recognized. Matrix calcifying vesicles have been isolated from atherosclerotic arteries and the biochemical composition of calcified vesicles has been studied. No studies have yet been carried out to examine the fine structure of matrix vesicles in order to visualize the features of the consequent stages of their calcification in arteries. In the present work, a high resolution ultrastructural analysis has been employed and the study revealed that matrix vesicles in human atherosclerotic lesions are heterogeneous with two main types which we classified. Type I calcified vesicles were presented by vesicles surrounded by two electron-dense layers and these vesicles were found to be resistant to the calcification process in atherosclerotic lesions in situ. Type II matrix vesicles were presented by vesicles surrounded by several electron-dense layers and these vesicles were found to represent calcifying vesicles in atherosclerotic lesions.To test the hypothesis that calcification of matrix vesicles surrounded by multilayer sheets may occur simply as a physicochemical process, independently from the cell regulation, we produced multilamellar liposomes and induced their calcification in vitro in a manner similar to that occurring in matrix vesicles in atherosclerotic lesions in situ.     

Does regular blood transfusion prevent progression of cerebrovascular lesions in children with sickle cell disease?

A retrospective study was conducted to assess changes in cerebrovascular lesions, as assessed by magnetic resonance (MR) imaging and angiography in 18 children with sickle cell disease (SCD) receiving optimised chronic transfusions for primary stroke prevention (abnormal transcranial Doppler flow, nine patients, median follow-up 14.3 months (range, 7.9–48.9)) or secondary stroke prevention (nine patients, median follow-up 59.6 months (range, 11.0–127.9)). An experienced neuroradiologist blinded to patient data reviewed the 41 MR scans (median/patient, three (2–4)). Standard scores were used to evaluate parenchymal and vascular abnormalities at baseline and last follow-up. Within-patient score changes evaluated using Wilcoxon’s paired rank test indicated lesion progression in the secondary-prevention group (p = 0.027). Optimised transfusion therapy does not prevent progression of cerebral vasculopathy in SCD children with a history of stroke. Financial support: No financial assistance was received in support of this study.     

Cell-derived microparticles in the pathogenesis of cardiovascular disease: friend or foe?

Microparticles are ascribed important roles in coagulation, inflammation, and endothelial function. These processes are mandatory to safeguard the integrity of the organism, and their derangements contribute to the development of atherosclerosis and cardiovascular disease. More recently, the presumed solely harmful role of microparticles has been challenged because microparticles may also be involved in the maintenance and preservation of cellular homeostasis and in promoting defense mechanisms. Here, we summarize recent studies revealing these 2 faces of microparticles in cardiovascular disease.     

Aortic stenosis: an atherosclerotic disease?

Aortic stenosis is a common disorder, which affects an increasing number of elderly patients, and is responsible for considerable morbidity. Although some associations for this disorder have been described, factors driving its progression remain obscure. This review proposes the hypothesis that aortic stenosis is another manifestation of atherosclerotic disease, and that its progression can be explained by classical cardiovascular risk factors.     

Drug-coated balloon in the treatment of coronary bifurcation lesions: A hope or hype?

When compared to non-bifurcation lesions, percutaneous coronary intervention in coronary bifurcation lesions is technically demanding and has historically been limited by lower procedural success rates and inferior clinical results. Following the development of drug-eluting stents, dramatically better results have been demonstrated. In most of the bifurcation lesions, the provisional technique of implanting a single stent in the main branch (MB) remains the default approach. However, some cases require more complex two-stent techniques which carry the risk of side branch (SB) restenosis. The concept of leaving no permanent implant behind is appealing because of the complexity of bifurcation anatomy with significant size mismatch between proximal and distal MB which may drive rates of in-stent restenosis and the potential impact of MB stenting affecting SB coronary flow dynamics. With the perspective of leaving lower metallic burden, a drug-coated balloon (DCB) has been utilized to treat bifurcations in both the MB and SB. The author gives an overview of the existing state of knowledge and prospects for the future for using DCB to treat bifurcation lesions.     

An ultrasound-based comparative study on carotid plaques in HIV-positive patients vs. atherosclerotic and arteritis patients: atherosclerotic or inflammatory lesions?

BACKGROUND: We have previously described two cases of HIV-1-positive patients undergoing surgery for stenosis of the internal carotid arteries. Histology revealed an extensive inflammatory infiltration of the vascular wall and no evidence of atheromasic plaque. This unexpected pattern of carotid damage prompted us to perform a more accurate investigation of the characteristics of carotid plaques in a group of HIV-positive patients. The results were compared with those obtained from young patients affected by atherosclerosis of the epi-aortic vessels and patients with arteritis. METHODS: The patients underwent ultrasonography of the epi-aortic vessels using one of the latest generation power color-Doppler with 7.5 MHz probes. RESULTS: The study population included 61 HIV-positive patients and 47 HIV-negative patients (37 atherosclerotic and 10 with arteritis). Compared with HIV-negative atherosclerotic patients, there were significantly higher proportions of HIV-positive patients with iso-hypoechogenic lesions (81.8 vs. 29%) that were homogeneous both in their parietal and endoluminal portions (96.7 vs. 21.6% and 88.5 vs. 54.0%, respectively), with a smooth or slightly irregular surface (99.0 vs. 56.7%) (P=0.001 for all differences). No statistically significant differences were seen between HIV-positive and arteritis patients. CONCLUSION: Our study evidenced that the ultrasonographic structure of the epi-aortic lesions in HIV-positive patients substantially differ from those of the plaques in atherosclerotic patients, although they share similar characteristics with patients affected by arteritis. Further investigations are warranted to better define the structure and the mechanism of onset of these lesions.