Evolving Management Paradigm for Stable Ischemic Heart Disease Patients: JACC Review Topic of the Week.

Management of stable coronary artery disease (CAD) has been based on the assumption that flow-limiting atherosclerotic obstructions are the proximate cause of angina and myocardial ischemia in most patients and represent an important target for revascularization. However, the role of revascularization in reducing long-term cardiac events in these patients has been limited mainly to those with left main disease, 3-vessel disease with diabetes, or decreased ejection fraction. Mounting evidence indicates that nonepicardial coronary causes of angina and ischemia, including coronary microvascular dysfunction, vasospastic disorders, and derangements of myocardial metabolism, are more prevalent than flow-limiting stenoses, raising concerns that many important causes other than epicardial CAD are neither considered nor probed diagnostically. There is a need for a more inclusive management paradigm that uncouples the singular association between epicardial CAD and revascularization and better aligns diagnostic approaches that tailor treatment to the underlying mechanisms and precipitants of angina and ischemia in contemporary clinical practice.

A Review of Laser Therapies for the Treatment of Scarring and Vascular Anomalies.

Significance: Laser use has become part of the gold standard of treatment as an effective adjuvant in multimodal therapy for pathologic scarring caused by burns, trauma, acne, and surgery, as well as vascular anomalies. Understanding indications and applications for laser therapy is essential for physicians to improve patient outcomes. Recent Advances: Since the 1980s, the medical use of lasers has continuously evolved with improvements in technology. Novel lasers and fractionated technologies are currently being studied in the hopes to improve treatment efficacy, while reducing complications. Recent advancements include acne treatment with novel picosecond lasers, new hypertrophic scar therapies with simultaneous laser and intense pulsed light use, and novel systems such as lasers with intralesional optical fiber delivery devices. In addition, optimizing the timing of laser therapy and its use in multimodal treatments continue to advance the field of photothermolysis. Critical Issues: Selecting the correct laser for a given indication is the fundamental decision when choosing a laser balancing effective treatment with minimal complications. This article covers the principles of laser therapy, the preferred lasers used for the treatment of scarring and vascular anomalies, and discusses the current evidence behind these laser choices. Future Directions: To optimize laser therapy, larger randomized control trials and split scar studies are needed. Continued advancement through better randomized controlled studies will help to improve patient outcomes on a broader scale.

Associations of vascular and bone status in arthritis patients.

Cardiovascular (CV) disease and osteoporosis (OP) have been associated with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Bone and vascular biomarkers and parameters along with the effect of 1-year anti-TNF therapy on these markers were assessed in order to determine correlations between vascular pathophysiology and bone metabolism in RA and AS. Thirty-six patients treated with etanercept or certolizumab pegol and 17 AS patients treated with ETN were included in a 12-month follow-up study. Bone and vascular markers were previously assessed by ELISA. Bone density was measured by DXA and quantitative CT (QCT). Flow-mediated vasodilation (FMD), common carotid intima-media thickness (IMT) and pulse-wave velocity (PWV) were assessed by ultrasound. Multiple correlation analyses indicated associations between bone and vascular markers. Osteoprotegerin, sclerostin and cathepsin K were significantly associated with FMD, IMT and PWV, respectively (p < 0.05). Moreover, total and trabecular BMD determined by QCT inversely correlated with IMT (p < 0.05). On the other hand, among vascular parameters, platelet-derived growth factor BB and IMT correlated with DXA femoral and QCT total BMD, respectively (p < 0.05). In the RM-ANOVA analysis, anti-TNF treatment together with baseline osteocalcin, procollagen 1 N-terminal propeptide (P1NP) or vitamin D3 levels determined one-year changes in IMT (p < 0.05). In the MANOVA analysis, baseline disease activity indices (DAS28, BASDAI), the one-year changes in these indices, as well as CRP exerted effects on multiple correlations between bone and vascular markers (p < 0.05). As the pattern of interactions between bone and vascular biomarkers differed between baseline and after 12 months, anti-TNF therapy influenced these associations. We found a great number of correlations in our RA and AS patients undergoing anti-TNF therapy. Some of the bone markers have been associated with vascular pathophysiology, while some vascular markers correlated with bone status. In arthritis, systemic inflammation and disease activity may drive both vascular and bone disease.

Long-term Audiometric Outcomes in Unilateral Sudden Sensorineural Hearing Loss without Recurrence.

OBJECTIVES: The recurrence rate of sudden sensorineural hearing loss (SSNHL) varies from 0.8% to 40%. However, to the best of our knowledge, no data on long-term hearing variations are present in the literature. The aim of this observational study was to analyze long-term variations of the hearing threshold in unilateral SSNHL without recurrence. MATERIALS AND METHODS: A total of 50 patients affected by unilateral SSNHL were evaluated. Patients underwent a treatment consisting of intravenous corticosteroids. Clinical and audiometric features were recorded. Patients underwent pure tone audiometry at a mean follow-up of 5.26±2.28 years. Differences between the affected and unaffected ear were analyzed. RESULTS: Comparing the post-treatment and follow-up audiograms, there was a worsening of hearing in the unaffected ear. On the contrary, no significant difference over time was found for the affected ear. 54% of patients showed no changes over time, 26% showed worsening, and 20% showed an improvement in hearing. The variation correlated with alcohol consumption and the presence of vasculopathies. An average improvement of hearing over time was observed at low frequencies. CONCLUSION: The time evolution in SSNHL is not predictable on the basis of the clinical and audiometric data. The majority the patients shows no changes in hearing loss in the affected ear. Patients who consume alcohol or have vasculopathies also have a higher risk of worsening of hearing. Further prospective studies are mandatory to better assess variations over time and their relationship with the effect of aging on hearing.

Phenotypic heterogeneity of obesity-related brain vulnerability: one-size interventions will not fit all.

Intact memory and problem solving are key to functional independence and quality of life in older age. Considering the unprecedented demographic shift toward a greater number of older adults than children in the United States in the next few decades, it is critically important for older adults to maintain work productivity and functional independence for as long as possible. Implementing early interventions focused on modifiable risk factors for cognitive decline at midlife is a strategy with the highest chance of success at present, bearing in mind the current lack of dementia cures. We present a selective, narrative review of evidence linking nutrition, body composition, vascular health, and brain function in midlife to highlight the phenotypic heterogeneity of obesity-related brain vulnerability and to endorse the development of individually tailored lifestyle modification plans for primary prevention of cognitive decline.

Metabolic/inflammatory/vascular comorbidity in psychiatric disorders; soluble epoxide hydrolase (sEH) as a possible new target.

The common and severe psychiatric disorders, including major depressive disorder (MDD) and bipolar disorder (BD), are associated with inflammation, oxidative stress and changes in peripheral and brain lipid metabolism. Those pathways are implicated in the premature development of vascular and metabolic comorbidities, which account for considerable morbidity and mortality, including increased dementia risk. During endoplasmic reticulum stress, the soluble epoxide hydrolase (sEH) enzyme converts anti-inflammatory fatty acid epoxides generated by cytochrome p450 enzymes into their corresponding and generally less anti-inflammatory, or even pro-inflammatory, diols, slowing the resolution of inflammation. The sEH enzyme and its oxylipin products are elevated post-mortem in MDD, BD and schizophrenia. Preliminary clinical data suggest that oxylipins increase with symptoms in seasonal MDD and anorexia nervosa, requiring confirmation in larger studies and other cohorts. In rats, a soluble sEH inhibitor mitigated the development of depressive-like behaviors. We discuss sEH inhibitors under development for cardiovascular diseases, post-ischemic brain injury, neuropathic pain and diabetes, suggesting new possibilities to address the mood and cognitive symptoms of psychiatric disorders, and their most common comorbidities.

Vitamin C, Aging and Alzheimer's Disease.

Accumulating evidence in mice models of accelerated senescence indicates a rescuing role of ascorbic acid in premature aging. Supplementation of ascorbic acid appeared to halt cell growth, oxidative stress, telomere attrition, disorganization of chromatin, and excessive secretion of inflammatory factors, and extend lifespan. Interestingly, ascorbic acid (AA) was also found to positively modulate inflamm-aging and immunosenescence, two hallmarks of biological aging. Moreover, ascorbic acid has been shown to epigenetically regulate genome integrity and stability, indicating a key role of targeted nutrition in healthy aging. Growing in vivo evidence supports the role of ascorbic acid in ameliorating factors linked to Alzheimer's disease (AD) pathogenesis, although evidence in humans yielded equivocal results. The neuroprotective role of ascorbic acid not only relies on the general free radical trapping, but also on the suppression of pro-inflammatory genes, mitigating neuroinflammation, on the chelation of iron, copper, and zinc, and on the suppression of amyloid-beta peptide (Aß) fibrillogenesis. Epidemiological evidence linking diet, one of the most important modifiable lifestyle factors, and risk of Alzheimer's disease is rapidly increasing. Thus, dietary interventions, as a way to epigenetically modulate the human genome, may play a role in the prevention of AD. The present review is aimed at providing an up to date overview of the main biological mechanisms that are associated with ascorbic acid supplementation/bioavailability in the process of aging and Alzheimer's disease. In addition, we will address new fields of research and future directions.

Role of folic acid in nitric oxide bioavailability and vascular endothelial function.

Folic acid is a member of the B-vitamin family and is essential for amino acid metabolism. Adequate intake of folic acid is vital for metabolism, cellular homeostasis, and DNA synthesis. Since the initial discovery of folic acid in the 1940s, folate deficiency has been implicated in numerous disease states, primarily those associated with neural tube defects in utero and neurological degeneration later in life. However, in the past decade, epidemiological studies have identified an inverse relation between both folic acid intake and blood folate concentration and cardiovascular health. This association inspired a number of clinical studies that suggested that folic acid supplementation could reverse endothelial dysfunction in patients with cardiovascular disease (CVD). Recently, in vitro and in vivo studies have begun to elucidate the mechanism(s) through which folic acid improves vascular endothelial function. These studies, which are the focus of this review, suggest that folic acid and its active metabolite 5-methyl tetrahydrofolate improve nitric oxide (NO) bioavailability by increasing endothelial NO synthase coupling and NO production as well as by directly scavenging superoxide radicals. By improving NO bioavailability, folic acid may protect or improve endothelial function, thereby preventing or reversing the progression of CVD in those with overt disease or elevated CVD risk.

Role of Vitamin D in Vascular Complications and Vascular Access Outcome in Patients with Chronic Kidney Disease.

Vitamin D has been known for a long time as a major factor involved in the calcium- phosphate balance and homeostasis, along with parathyroid hormone (PTH). While vitamin D effects on calcium and phosphate are fully known, recent studies attempted to link vitamin D status and cardiovascular diseases. The involvement of vitamin D on vascular remodeling is mediated by several mechanisms such as activation of renin-angiotensin-aldosterone system (RAAS), cell proliferation and anti-apoptotic cell pathways. This correlation is highlighted by the fact that the activated form of vitamin D (1,25 (OH)2 D3) can be synthesized by the same endothelial cells, due to the constitutive presence of endothelial 1α-hydroxylase. Vitamin D reduces the expression of angiotensin 2 receptor (AT2R) on the endothelial cell surface (AT2R), leading to a cascade of events that result in the synthesis of vasodilators, such as nitric oxide. The activation of vitamin D receptors (VDRs) on endothelial cells induces changes in the metabolic activity of the endothelium and is responsible for cell survival, proliferation and neoangiogenesis. Moreover, altered signaling of VDR due to gene polymorphisms has been demonstrated in patients with cardiac disorders and chronic kidney disease (CKD). Recently, vascular access outcome has been associated with vitamin D status. Future studies will help to better define the need of vitamin D supplementation for a better cardiovascular as well as vascular access outcome in patients with CKD.

Fibrinolytic effects of peroneal nerve stimulation in patients with lower limb vascular disease.

Patients with lower limb vascular disease are at an increased risk of thrombotic events. Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) are important components of the fibrinolytic system, responsible for clot lysis. This study aimed to establish whether peroneal nerve stimulation (PNS) could promote fibrinolysis within a cohort of vascular patients. Ethical approval was obtained for this prospective case-controlled study. Patients were randomly assigned to active stimulation or control groups. Arterial flow measurements and venous blood samples were taken bilaterally at baseline and following 45 min of PNS. ELISA analysis for plasma t-PA and PAI-1 was performed utilizing commercially available kits. Statistical analysis evaluated the changes in t-PA and PAI-1 levels from baseline for the active (device active), passive (contralateral limb) and control limbs (inactive device applied).Seventy-seven participants were recruited: 30 claudicants (25 active and five controls), 25 patients postoperative infra-inguinal bypass grafts (19 active and six controls) and 22 patients with varicose veins (17 active and five controls). t-PA levels reduced significantly in all groups; however, intergroup analysis demonstrated no statistically significant difference when comparing the active, passive and control limbs (P = 0.079). PAI-1 levels decreased by 16.2% (34.0 ng/ml, SD 52.2) in the active limbs but only 3.6% (11.4 ng/ml, SD 47.4) and 2.6% (2.7 ng/ml, SD 21.3) in the passive and control limbs, respectively (intergroup analysis P < 0.001). No relationship between changes in flow and plasma of t-PA and PAI-1 were demonstrated. Peroneal nerve stimulation may augment fibrinolysis by decreasing plasma levels of PAI-1 levels in patients with lower limb arterial and venous disease.

Contemporary results of carotid endarterectomy in "normal-risk" patients from the Society for Vascular Surgery Vascular Registry.

OBJECTIVE: Acceptable complication rates after carotid endarterectomy (CEA) are drawn from decades-old data. The recent Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) demonstrated improved stroke and mortality outcomes after CEA compared with carotid artery stenting, with 30-day periprocedural CEA stroke rates of 3.2% and 1.4% for symptomatic (SX) and asymptomatic (ASX) patients, respectively. It is unclear whether these target rates can be attained in "normal-risk" (NR) patients experienced outside of the trial. This study was done to determine the contemporary results of CEA from a broader selection of NR patients. METHODS: The Society for Vascular Surgery (SVS) Vascular Registry was examined to determine in-hospital and 30-day event rates for NR, SX, and ASX patients undergoing CEA. NR was defined as patients without anatomic or physiologic risk factors as defined by SVS Carotid Practice Guidelines. Raw data and risk-adjusted rates of death, stroke, and myocardial infarction (MI) were compared between the ASX and SX cohorts. RESULTS: There were 3977 patients (1456 SX, 2521 ASX) available for comparison. The SX group consisted of more men (61.7% vs 57.0%; P = .0045) but reflected a lower proportion of white patients (91.3% vs 94.4%; P = .0002), with lower prevalence of coronary artery disease (P < .0001), prior MI (P < .0001), peripheral vascular disease (P = .0017), and hypertension (P = .029), although New York Heart Association grade >3 congestive heart failure was equally present in both groups (P = .30). Baseline stenosis >80% on duplex imaging was less prevalent among SX patients (54.2% vs 67.8%; P < .0001). Perioperative stroke rates were higher for SX patients in the hospital (2.8% vs 0.8%; P < .0001) and at 30 days (3.4% vs 1.0%; P < .0001), which contributed to the higher composite death, stroke, and MI rates in the hospital (3.6% vs 1.8; P = .0003) and at 30 days (4.5% vs 2.2%; P < .0001) observed in SX patients. After risk adjustment, the rate of stroke/death was greater among SX patients in the hospital (odds ratio, 2.05; 95% confidence interval, 1.18-3.58) although not at 30 days (odds ratio, 1.36; 95% confidence interval, 0.85-2.17). No in-hospital or 30-day differences were observed for death or MI by symptom status. CONCLUSIONS: The SVS Vascular Registry results for CEA in NR patients are similar by symptom status to those reported for CREST and may serve as a benchmark for comparing results of alternative therapies for treatment of carotid stenosis in NR patients outside of monitored clinical trials. The contemporary perioperative risk of stroke after CEA in NR patients continues to be higher for SX than for ASX patients.

Prevention of vascular damage with Lisosan G wheat extract: the in vitro basis for a clinical investigation.

Vascular damage and impairment play a crucial role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Nutraceutical supplements might have a role in reducing vascular damage, provided that their efficacy is proven by controlled studies and is supported by a mechanistic rationale. Therefore, the use of nutraceutical supplements can have some effects also in the prevention of NFLD. Epidemiological evidence correlates the intake of whole grain and whole-grain products with a reduced occurrence of vascular disease. Lisosan G is a powder obtained from Triticum Sativum (wheat), which is registered with the Italian Ministry of Health as a nutritional supplement. In vivo, Lisosan G has been shown to protect against cisplatin induced toxicity, and the use of this compound in the prevention of cirrhosis and steatosis has been recently been proposed thanks to its marked anti-oxidant activity. We discuss here the rationale for further investigation on this compound in the prevention of NAFLD.

Reversible cerebral vasoconstriction syndrome (RCVS) in antiphospholipid antibody syndrome (APLA): the role of centrally acting vasodilators. Case series and review of literature.

Reversible cerebral vasoconstriction syndrome (RCVS) is Raynaud's phenomenon of the brain. Changes in neurological function are dependent upon which areas of the brain are deprived of normal blood flow. Antiphospholipid antibody syndrome (APLA) is a common cause of Raynaud's phenomenon that can occur anywhere in the body, including the brain. Management of CNS vasospasm generally involves the use of centrally acting calcium channel blockers, which have been shown to relieve the associated headaches and transient neurological symptoms associated with it. Three patients with APLA and RCVS from our clinics are illustrated. It is demonstrated that the use of centrally acting calcium channel-blocking drugs, such as nimodipine, which prevent and reverse CNS vasospasm, led to clinical improvement in our patients over the course of 5-9 years. All of them had MRIs done at the initiation of therapy and 5-9 years after being on therapy. MRI measures of T2 lesion volumes (LVs) and number were obtained. All three patients had a good response in controlling clinical symptoms related to CNS vasospasm, Raynaud's phenomenon, visual disturbances, confusion, headaches, and hearing loss. There was also a resolution in the MRI findings of these patients. This case series of three patients shows a clinical improvement and decrease in T2 LV and number in patients with APLA and Raynaud's syndrome on centrally acting calcium channel blockers. RCVS is much more common than that currently appreciated. APLA is the common cause of RCVS. Further studies are needed to determine the optimal methods to diagnose RCVS and optimal therapies to treat it.

Vascular dysfunction in a mouse model of Rett syndrome and effects of curcumin treatment.

Mutations in the coding sequence of the X-linked gene MeCP2 (Methyl CpG-binding protein) are present in around 80% of patients with Rett Syndrome, a common cause of intellectual disability in female and to date without any effective pharmacological treatment. A relevant, and so far unexplored feature of RTT patients, is a marked reduction in peripheral circulation. To investigate the relationship between loss of MeCP2 and this clinical aspect, we used the MeCP2 null mouse model B6.129SF1-MeCP2tm1Jae for functional and pharmacological studies. Functional experiments were performed on isolated resistance mesenteric vessels, mounted on a pressurized myograph. Vessels from female MeCP2(+/-) mice show a reduced endothelium-dependent relaxation, due to a reduced Nitric Oxide (NO) availability secondary to an increased Reactive Oxygen Species (ROS) generation. Such functional aspects are associated with an intravascular increase in superoxide anion production, and a decreased vascular eNOS expression. These alterations are reversed by curcumin administration (5% (w/w) dietary curcumin for 21 days), which restores endothelial NO availability, decreases intravascular ROS production and normalizes vascular eNOS gene expression. In conclusion our findings highlight alterations in the vascular/endothelial system in the absence of a correct function of MeCP2, and uncover related cellular/molecular mechanisms that are rescued by an anti-oxidant treatment.

Rice bran enzymatic extract restores endothelial function and vascular contractility in obese rats by reducing vascular inflammation and oxidative stress.

BACKGROUND: Rice bran enzymatic extract (RBEE) used in this study has shown beneficial activities against dyslipidemia, hyperinsulinemia and hypertension. Our aim was to investigate the effects of a diet supplemented with RBEE in vascular impairment developed in obese Zucker rats and to evaluate the main mechanisms mediating this action. METHODS AND RESULTS: Obese Zucker rats were fed a 1% and 5% RBEE-supplemented diet (O1% and O5%). Obese and their lean littermates fed a standard diet were used as controls (OC and LC, respectively). Vascular function was evaluated in aortic rings in organ baths. The role of nitric oxide (NO) was investigated by using NO synthase (NOS) inhibitors. Aortic expression of endothelial NOS (eNOS), inducible NOS (iNOS), tumor necrosis factor (TNF)-α and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunits and superoxide production in arterial wall were determined. Endothelial dysfunction and vascular hyperreactivity to phenylephrine in obese rats were ameliorated by RBEE treatment, particularly with 1% RBEE. Up-regulation of eNOS protein expression in RBEE-treated aortas should contribute to this activity. RBEE attenuated vascular inflammation by reducing aortic iNOS and TNF-α expression. Aortas from RBEE-treated groups showed a significant decrease of superoxide production and down-regulation of NADPH oxidase subunits. CONCLUSION: RBEE treatment restored endothelial function and vascular contractility in obese Zucker rats through a reduction of vascular inflammation and oxidative stress. These results show the nutraceutical potential of RBEE to prevent obesity-related vascular complications.

Magnetic resonance imaging signatures of vascular pathology in multiple sclerosis.

Venous vascular contributing factors to multiple sclerosis (MS) have been known for some time. Only recently has the scope of their potential role become more apparent with the theory of chronic cerebrospinal venous insufficiency (CCSVI). As research expands to further explore the role of vascular pathology in the MS population, it is expedient to review the evidence from an imaging perspective. In this paper, we review the current state-of-the-art methods using magnetic resonance imaging (MRI) as applied to imaging MS patients and CCSVI. This includes evaluating imaging signatures of vascular structure and flow as well as brain iron content. Upon review of the literature, we find that extracranial venous anomalies including stenosis, venous malformations, and collateralization of flow in the major veins of the neck have been observed to be prevalent in the MS population. Abnormal flow has been reported in MS patients both in major vessels using phase-contrast flow quantification and in the brain using perfusion-weighted imaging. We discuss the role of quantitative flow imaging and its potential in assessing possible biomarkers for abnormal flow. Finally, it has been suggested that the presence of high iron content may indirectly indicate progression of existing vascular pathology. To that end, we review the use of susceptibility-weighted imaging in monitoring iron in the thalamus, basal ganglia, and MS lesions.

Vertebral artery dominance, brainstem auditory evoked potential, and vertigo of vascular origin.

OBJECTIVE: Vertebral artery dominance (VAD) is defined when there is a significant difference between the diameters of the vertebral arteries (VAs). VAD may be a risk factor for vertigo of vascular origin. The objectives of this study were: (1) to investigate changes of brainstem auditory evoked potential (BAEP) in patients with vertigo caused by VAD through magnetic resonance; and (2) to understand the possible mechanism(s) by which VAD triggers vertigo of vascular origin. METHODS: This prospective study involved 64 patients with vertigo, including 35 patients with VAD (VAD group) and 29 without VAD (non-VAD group) as detected by head magnetic resonance angiography. Age, sex, and other clinical histories were comparable in both groups. The degree of vertigo was graded and BAEP examination was performed in each patient. BAEP changes as well as their correlations of BAEP with the dominant VA and basilar artery (BA) were analyzed in both groups. RESULTS: The rate of abnormal BA shapes was 60% in the VAD group compared with 34.5% in the non-VAD group (Chi-square = 4.135, P<0.05). The median BA curvature was higher in the VAD group than that in the non-VAD group, 3.67 and 1.73 mm, respectively (P<0.01). Peak latencies (I, III, and V) in the VAD group were longer than those in the non-VAD group (P<0.01), but the difference in the III did not reach statistical significance (t = 1.916, P>0.05). Interpeak latencies (III-V and I-V) were longer in the VAD group than those in the non-VAD group (P<0.05); there was no significant difference in the interpeak latencies of I-III (P>0.05). The III-V/I-III ratios were higher in the VAD group than those in the non-VAD group. The vertigo severity level was significantly higher in the VAD group than that in the non-VAD group (3.2 ± 1.0 versus 2.2 ± 0.7). The vertigo severity level correlated with VAD and every major anomaly index of BAEP; its correlations with III-V/I-III were remarkably significant (r = 0.617, P = 0.013). CONCLUSION: The incidence of abnormal BA shapes and abnormal BAEP, and the vertigo severity level were higher in VAD patients. Moreover, VAD was found to correlate with abnormal BAEP, suggesting that VAD contributed to vertigo of vascular origin.

[Advances in the prevention, diagnosis and therapy of vascular diseases]. / Újabb ismeretek a különbözo vascularis kórképek megelozésében, diagnosztikájában és terápiájában.

Atherosclerosis is a systemic disease affecting the coronary, carotid, intracerebral, renal and peripherial arteries. The early morphological and functional impairments could be detected in the second or third decades of life and their progression depend on the number and severity of risk factors and individual susceptility. Although the vascular risk factors (smoking, overweight, age, unhealthy diet, lack of physical exercise, hypertension, diabetes mellitus, chronic kidney disease and dyslipidemia) are the same and common in the different vascular diseases, the present clinical routine artificially classifies the diagnosis and therapy of different vascular diseases into different subfields of medicine with the negative impact of possible polypragmasia. Recently, worldwide health surveys (e.g. REACH registry) have proven the usefulness of a holistic approach in the diagnosis and therapy of multiorgan-affected vascular patients. This review summarizes the multidisciplinary advances and future perspective of vascular diseases.