Metabolic syndrome showed significant relationship with carotid atherosclerosis

Kawada, Tomoyuki; Andou, Takeshi; Fukumitsu, Masayuki

doi:10.1007/s00380-015-0668-y

Cited by 19 publications

(16 citation statements)

References 52 publications

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“…Some studies show that since they are related to multiple risk factors for cardiovascular diseases, particularly visceral fat, irrespective of the level of dyslipidemia, people with elevated CRP are at high risk of acute myocardial infarction. 6,29,30 In conclusion, it can be inferred that CRP levels are associated with cardiovascular morbidity and are strongly related to a number of components of the MS; but there is a stronger correlation with adiposity than with insulin sensitivity or glycemic control. Notwithstanding, certain limitations should be taken into account, since serum CRP levels can increase transitorily for 2 to 3 weeks after severe infections, traumas or acute ischemic events.…”

Section: -28mentioning

confidence: 99%

“…Notwithstanding, certain limitations should be taken into account, since serum CRP levels can increase transitorily for 2 to 3 weeks after severe infections, traumas or acute ischemic events. 6,20,22,23,31 Testing CRP can even be important for adults with Low Density Lipoprotein (LDL-c) results that are not a cause for concern and the result is predictive of whether or not statins should be prescribed. This indication is based on the recommendations of the JUPITER study (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin), which demonstrated possible beneficial effects of these drugs in apparently healthy people who have LDL-c < 130mg/dL and CRP levels over 2 mg/dL.…”

Section: -28mentioning

confidence: 99%

“…There is also evidence in the literature of a positive correlation between elevated CRP-us levels and hyperglycemia, hypertension, smoking and presence of MS or abnormal plasma lipid levels. 6,15,[23][24][25] Hyperglycemia is related to inflammation because of formation of advanced glycation end products (AGEs), which can lead to synthesis of IL-6, to activation of macrophages and to oxidative stress, which culminates in production of CRP, contributing to inflammation. Advanced glycation end products are derived from non-enzymatic reaction of glucose (in addition to oxidation of glucose) with proteins, lipids and nucleic acids, leading to oxidative stress and subsequent development of inflammatory and thrombotic processes.…”

Section: Inflammation: Can It Be Measured?mentioning

confidence: 99%

“…According to the International Diabetes Federation -IDF (2005), one quarter of the global adult population has the syndrome. [5][6][7] The MS was originally named Metabolic Syndrome X and there are a large number of criteria for its diagnosis, including the EGIR -European Group for the These criteria for diagnosis include glycemia disorders related to insulin resistance (IR); elevated BMI; elevated triglycerides and low HDL-c (high density lipoprotein); and high blood pressure. 5,[8][9][10] There is consensus in the recent literature that there are at least six criteria that define the presence of MS: obesity, waist circumference (> 102 cm in males or > 88 cm in females), IR (fasting glycemia greater than 100mg/dL), elevated triglycerides (> 150 mg/dL) and low HDL-c (< 40 mg/dL no male sex or < 50 mg/dL in female sex), arterial hypertension (BP > 130⁄85 mm Hg) and a proinflammatory and pro-thrombotic state.…”

Section: The Metabolic Syndromementioning

confidence: 99%

“…C-reactive protein also acts to regulate production of nitric oxide in vascular endothelium and coordinates production and secretion of many proinflammatory cytokines by adipocytes. 6,20,31,35,52 Published data show that increases in the levels of fibrinogen, fibrin and products of fibrinogen degradation are related to formation and development of atheromatous plaques. Fibrinogen plays a fundamental role in formation and growth of atheromatous plaques and is also a precursor of mural thrombi.…”

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confidence: 99%

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Síndrome metabólica, aterosclerose e inflamação: tríade indissociável?

et al. 2015

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Populations all over the world are increasingly inactive and are consuming increasing quantities of fats and sugars, which is generally linked to industrially processed foods. The consequences have rapidly manifest as an increase in overweight/obesity and in physiological and metabolic changes, such as the Metabolic Syndrome, which is a series of changes in glycemia, lipids and blood pressure. There is evidence of a close relationship between these changes and inflammatory processes, which can also be linked to oxidative stress. These conditions lead to the pathogenesis of vascular abnormalities or intensify metabolic processes that accompany the metabolic syndrome. The objective of this review is to compare the large number of bibliographic references that show correlations between components of the Metabolic Syndrome and increases in the mediators of inflammation. The publications reviewed were located using the Pubmed, Scopus, Lilacs and Scielo databases and the majority of the articles selected were published within the last 5 years.Keywords: metabolic syndrome ; arteriosclerosis; inflammation. ResumoObserva-se, nas populações mundiais, aumento do sedentarismo e aumento do consumo de gorduras e açúcares, sendo estes vinculados normalmente aos alimentos industrializados. A consequência disso rapidamente se manifestou no aumento do sobrepeso/obesidade e na instalação de alterações fisiológicas e metabólicas, como a Síndrome Metabólica, que é representada por alterações na glicemia, nos lipídeos e na pressão arterial. Há evidências de ligação estreita entre estas alterações e os processos inflamatórios, que também podem estar associados ao estresse oxidativo. Estas condições levam à patogênese das alterações vasculares ou intensificam os processos metabólicos que acompanham a Síndrome Metabólica. O objetivo desta revisão foi comparar as inúmeras referências literárias que mostram correlação entre os componentes da Síndrome Metabólica e o aumento dos mediadores de inflamação. Para isso, utilizou-se Pubmed, Scopus, Lilacs e Scielo como base de dados, sendo que os artigos selecionados dataram principalmente dos últimos cinco anos.Palavras-chave: síndrome metabólica; arteriosclerose; inflamação.

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Section: -28mentioning

confidence: 99%

Section: -28mentioning

confidence: 99%

Section: Inflammation: Can It Be Measured?mentioning

confidence: 99%

Section: The Metabolic Syndromementioning

confidence: 99%

mentioning

confidence: 99%

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Síndrome metabólica, aterosclerose e inflamação: tríade indissociável?

et al. 2015

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Long-term effects of L- and N-type calcium channel blocker on uric acid levels and left atrial volume in hypertensive patients

et al. 2016

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Left ventricular (LV) diastolic dysfunction is associated with hypertension and hyperuricemia. However, it is not clear whether the L- and N-type calcium channel blocker will improve LV diastolic dysfunction through the reduction of uric acid. The aim of this study was to investigate the effects of anti-hypertensive therapy, the L- and N-type calcium channel blocker, cilnidipine or the L-type calcium channel blocker, amlodipine, on left atrial reverse remodeling and uric acid in hypertensive patients. We studied 62 patients with untreated hypertension, randomly assigned to cilnidipine or amlodipine for 48 weeks. LV diastolic function was assessed with the left atrial volume index (LAVI), mitral early diastolic wave (E), tissue Doppler early diastolic velocity (E') and the ratio (E/E'). Serum uric acid levels were measured before and after treatment. After treatment, systolic and diastolic blood pressures equally dropped in both groups. LAVI, E/E', heart rate and uric acid levels decreased at 48 weeks in the cilnidipine group but not in the amlodipine group. The % change from baseline to 48 weeks in LAVI, E wave, E/E' and uric acid levels were significantly lower in the cilnidipine group than in the amlodipine group. Larger %-drop in uric acid levels were associated with larger %-reduction of LAVI (p < 0.01). L- and N-type calcium channel blocker but not L-type calcium channel blocker may improve LV diastolic function in hypertensive patients, at least partially through the decrease in uric acid levels.

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