Background-Growth of atherosclerotic plaques is accompanied by neovascularization from vasa vasorum microvessels extending through the tunica media into the base of the plaque and by lumen-derived microvessels through the fibrous cap. Microvessels are associated with plaque hemorrhage and may play a role in plaque rupture. Accordingly, we tested this hypothesis by investigating whether microvessels in the tunica media, the base of the plaque, and the fibrous cap are increased in ruptured atherosclerotic plaques in human aorta. Methods and Results-Microvessels, defined as CD34-positive tubuloluminal capillaries recognized in cross-sectional and longitudinal profiles, were quantified in 269 advanced human plaques by bicolor immunohistochemistry. Macrophages/T lymphocytes and smooth muscle cells were defined as CD68/CD3-positive and ␣-actin-positive cells. Total microvessel density was increased in ruptured plaques when compared with nonruptured plaques (Pϭ0.0001). Furthermore, microvessel density was increased in lesions with severe macrophage infiltration at the fibrous cap (Pϭ0.0001) and at the shoulders of the plaque (Pϭ0.0001). In addition, microvessel density was also increased in lesions with intraplaque hemorrhage (Pϭ0.04) and in thin-cap fibroatheromas (Pϭ0.038). Logistic regression analysis identified plaque base microvessel density (Pϭ0.003) as an independent correlate to plaque rupture. Conclusions-Thus, neovascularization as manifested by the localized appearance of microvessels is increased in ruptured plaques in the human aorta. Furthermore, microvessel density is increased in lesions with inflammation, with intraplaque hemorrhage, and in thin-cap fibroatheromas. Microvessels at the base of the plaque are independently correlated with plaque rupture, suggesting a contributory role for neovascularization in the process of plaque rupture. (Circulation.

The lens of the eye is one of the most radiosensitive tissues in the body, and exposure of the lens to ionizing radiation can cause cataract. Cumulative X-ray doses to the lenses of interventional cardiologists and associated staff can be high. The International Commission on Radiological Protection recently noted considerable uncertainty concerning radiation risk to the lens. This study evaluated risk of radiation cataract after occupational exposure in interventional cardiology personnel. Comprehensive dilated slit-lamp examinations were performed in interventional cardiologists, associated workers and controls. Radiation exposures were estimated using experimental data from catheterization laboratories and answers to detailed questionnaires. A total of 116 exposed and 93 similarly aged nonexposed individuals were examined. The relative risk of posterior subcapsular opacities in interventional cardiologists compared to unexposed controls was 3.2 (38% compared to 12%; P < 0.005). A total of 21% of nurses and technicians had radiation-associated posterior lens changes typically associated with ionizing radiation exposure. Cumulative median values of lens doses were estimated at 6.0 Sv for cardiologists and 1.5 Sv for associated medical personnel. A significantly elevated incidence of radiation-associated lens changes in interventional cardiology workers indicates there is an urgent need to educate these professionals in radiation protection to reduce the likelihood of cataract.

Caffeine is the most widely consumed stimulating substance in the world. It is found in coffee, tea, soft drinks, chocolate, and many medications. Caffeine is a xanthine with various effects and mechanisms of action in vascular tissue. In endothelial cells, it increases intracellular calcium stimulating the production of nitric oxide through the expression of the endothelial nitric oxide synthase enzyme. Nitric oxide is diffused to the vascular smooth muscle cell to produce vasodilation. In vascular smooth muscle cells its effect is predominantly a competitive inhibition of phosphodiesterase, producing an accumulation of cAMP and vasodilation. In addition, it blocks the adenosine receptors present in the vascular tissue to produce vasoconstriction. In this paper the main mechanisms of action of caffeine on the vascular tissue are described, in which it is shown that caffeine has some cardiovascular properties and effects which could be considered beneficial.

Prevalence of diabetes mellitus has increased drastically over time, especially in more populous countries such as the United States, India, and China. Patients with diabetes have an increased risk of major cardiovascular events such as acute myocardial infarction, cerebrovascular disease, and peripheral vascular disease. Arterial stiffness is a process related to aging and vascular, metabolic, cellular and physiological deterioration. In recent years, it has been described as an independent predictor of cardiovascular mortality and coronary artery disease. Additionally, it plays an important role in the measurement of chronic disease progression. Recent studies have suggested a strong relationship between diabetes mellitus and arterial stiffness since they share a similar pathophysiology involving endothelial dysfunction. The literature has shown that microvascular and macrovascular complications in diabetic patients could be screened and measured with arterial stiffness. Additionally, new evidence proposes that there is a relationship between blood glucose levels, microalbuminuria, and arterial stiffness. Moreover, arterial stiffness predicts cardiovascular risk and is independently associated with mortality in diabetic patients. Abnormal arterial stiffness values in diabetic patients should alert the clinician to the presence of vascular disease, which merits early study and treatment. We await more studies to determine if arterial stiffness could be considered a routine useful non-invasive tool in the evaluation of diabetic patients. There is enough evidence to conclude that arterial stiffness is related to the progression of diabetes mellitus.

Nitroglycerin, milrinone, and levosimendan completely reversed the contraction of the IMA segments induced by U46619 and norepinephrine. Levosimendan produced a potent, concentration-dependent preventive effect on the norepinephrine-induced contraction of IMA. The responses to levosimendan were similar in preparations with or without endothelium.

Currently, traditional and non-traditional risk factors for cardiovascular disease have been established. The first group includes age, which constitutes one of the most important factors in the development of chronic diseases. The second group includes inflammation, the pathophysiology of which contributes to an accelerated process of vascular remodelling and atherogenesis in autoimmune diseases. Indeed, the term inflammaging has been used to refer to the inflammatory origin of ageing, explicitly due to the chronic inflammatory process associated with age (in healthy individuals). Taking this into account, it can be inferred that people with autoimmune diseases are likely to have an early acceleration of vascular ageing (vascular stiffness) as evidenced in the alteration of non-invasive cardiovascular tests such as pulse wave velocity. Thus, an association is created between autoimmunity and high morbidity and mortality rates caused by cardiovascular disease in this population group. The beneficial impact of the treatments for rheumatoid arthritis at the cardiovascular level has been reported, opening new opportunities for pharmacotherapy.

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Stents farmacológicos e stents não-farmacológicos (SNF) são utilizados no tratamento de placas ateroscleróticas instáveis e podem levar à estabilização dos fibroateromas de capa fina (FACF). Este estudo foi desenhado para avaliar os efeitos estabilizadores dos SNF e dos stents farmacológicos em modelo experimental de FACF. Método: O estudo avaliou 16 coelhos hipercolesterolêmicos da raça Nova Zelândia, acompanhados por quatro anos, dos quais 6 receberam SNF, 5 receberam stents com liberação de everolimus (SLE) e 5, stents com liberação de 17-b estradiol (SLB) (Guidant-Santa Clara, Califórnia, Estados Unidos). Um stent com polímero também foi implantado em cada animal. Análises histológicas aos 28 dias dos FACF não tratados vs. FACF com implante de SLE, SLB e SNF foram realizadas. Resultados: Os FACF tratados com SNF, SLE e SLB mostraram redução da área lipídica de 62%, 67% e 61% e aumento da espessura da capa de 188%, 98% e 140%, respectivamente (p < 0,0001 para todos). Ruptura dos FACF induzida pela haste foi encontrada em 63% das seções histológicas que continham o stent, associada a espessamento da neoíntima nos SNF (p = 0,03), mas não nos SLE ou nos SLB (p = ns). Conclusões: O tratamento dos FACF com SNF, SLE e SLB reduz o acúmulo de lípides e aumenta a espessura da capa fibrosa. A ruptura da capa fibrosa SUMMARY Plaque Stabilization by Bare Metal and Drug-Eluting Stents in an Experimental Rabbit Model of Thin Cap Fibroatheroma Background: Bare metal stents (BMS) and drug-eluting stents (DES) are used to treat unstable plaques and may stabilize thin cap fibroatheromas (TCFA). This study was designed to evaluate stabilizing effects of bare compared to Everolimus (EES) and Beta-Estradiol (BES) eluting stents in a chronic atherosclerotic experimental animal model of TCFA. Methods: Sixteen New Zealand hypercholesterolemic rabbits followed for 4 years were studied. Six animals received BMS, 5 EES and 5 BES (Guidant-Santa Clara, CA, USA). One polymer stent per animal was also implanted. Histologic analysis at 28 days of de-novo vs. BMS, EES, and BES stented TCFA were performed. Results: BMS, EES, and BES stented TCFA showed reductions in lipid area by 62%, 67%, and 61%, and increases in cap thickness by 188%, 98%, and 140% respectively (p < 0.0001 for all). Strut-induced ruptured TCFA was found in 63% of stented sections and was associated with increased neointima in BMS (p = 0.03) but not in EES or BES (p = ns). Conclusions: Stenting thin cap fibroatheroma with BMS, EES and BES reduces lipid accumulation and increases cap thickness. Strut-induced fibrous cap rupture was frequently found