Glucose intolerance, insulin resistance and metabolic syndrome in patients with stable angina pectoris. Obesity predicts coronary atherosclerosis and dysglycemia

2008 ◽  
Vol 118 (12) ◽  
pp. 719-726
Author(s):  
Aleksander Włodarczyk ◽  
Krzysztof Strojek
Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Atsushi Hirohata ◽  
Hirosuke Yamaji ◽  
Masaaki Murakami ◽  
Eiki Hirose ◽  
Keisuke Ohkawa ◽  
...  

Prior intravascular ultrasound (IVUS) trials suggest slowing of coronary plaque progression with some medicines but have not shown convincing evidence of regression using angiotension-II receptor blocking agents (ARB). A prospective, double-blind, randomized, multicenter trial (Impact of OLmesartan on progression of coronary atherosclerosis; evaluation by IntraVascular UltraSound [OLIVUS]) was performed in 247 stable angina pectoris patients with native coronary artery lesions. When these patients underwent percutaneous coronary intervention for culprit lesions, IVUS was performed in their non-culprit vessels (without angiographically documented coronary stenosis [<50%]). Patients were randomly assigned to receive 20 mg of Olmesartan or control, and treated with a combination of β-blockers, calcium channel blockers, diuretics, nitrates, glycemic control agents and/or statins per physician’s guidance. Patients already on ACE inhibitors or other ARBs were excluded. Serial IVUS examinations (baseline and 14-months follow-up) were performed to assess coronary plaque volume. Volumetric IVUS analyses (mean measured length:41.2 ± 8.7mm) included lumen (LV), plaque (PV), vessel volume (VV), percent plaque volume (% PV), percent change in total PV (PCPV) and percent change in % PV (PC%PV). At baseline, patient characteristics and all IVUS parameters were identical between the two groups. However, follow-up IVUS showed significantly decreased PCPV and PC%PV in the Olmesartan group, despite similar blood pressure (table ). In addition, multivariate analysis identified Olmesartan administration as one of the factors that decreased plaque volume (β-coefficient −0.29 (95%CI, −0.7 to 0.4), p<0.01). These observations suggest a positive role in potential plaque regression through the administration of Olmesartan, an angiotension-II receptor blocking agent, for patients with stable angina pectoris.


2015 ◽  
pp. 49-54
Author(s):  
E. P. Naumenko

The article deals with the evaluation of comprehensive and segmental systolic deformation of the myocardium by the method of speckle tracking echocardiography in patients with the stable angina pectoris of II and III functional class accompanied by diabetes mellitus type 2 and in patients with isolated stable angina pectoris and isolated diabetes mellitus type 2. This study resulted in the evaluation of the comprehensive and segmental systolic myocardium deformation indicators diagnostic utility, the indication of threshold levels for the diagnosis of comprehensive and segmental systolic deformation of myocardium caused by coronary atherosclerosis in patients.


2011 ◽  
Vol 107 (8) ◽  
pp. 121A
Author(s):  
Min Goo Lee ◽  
Myung Ho Jeong ◽  
Keun Ho Park ◽  
Doo Sun Sim ◽  
Young Joon Hong ◽  
...  

2018 ◽  
Vol 4 (2) ◽  
pp. 95
Author(s):  
Pramon Aditya Sudjana ◽  
Chaerul Achmad ◽  
Achmad Fauzi Yahya ◽  
Januar W. Martha ◽  
M. Rizki Akbar

Background: Triglycerides (TG) as a risk factor for coronary artery disease (CAD) is still a matter of controversy but when used as a single ratio with high density lipoprotein (HDL) the predictive value for CAD is better. The TG/HDL ratio is also associated with the presence of small dense LDL (sdLDL) in the body. SdLDL is a more atherogenic LDL subfraction and has been proven to be associated with CAD progression.Aims: This study aims to find the correlation between the TG/HDL ratio and the degree of coronary lesion severity based on the Gensini score in stable non diabetic angina pectoris patients.Methods: This study was a cross sectional study conducted at Dr. Hasan Sadikin Hospital and Hasna Medika Palimanan Hospital. Subjects were non diabetic stable angina pectoris patients ≥18 years old who underwent elective coronary angiography. Blood collection for TG and HDL examination was performed after coronary angiography. Gensini scoring system was used to assess the severity of coronary lesions. The relationship between the TG/HDL ratio and the Gensini score was analyzed using multiple linear regression tests against confounding variables.Results: This study involved 60 patients with stable angina pectoris with a mean age of 60±8 years. The mean TG/HDL ratio is 2.56 ± 1.04. The average Gensini score was 51 ± 36. The TG/HDL ratio was significantly associated with the Gensini score (R = 0.637; p <0.001). Analysis of confounding variables showed age, hypertension, and metabolic syndrome had a weak correlation with Gensini score (r values of 0.321, 0.270, and 0.333, p <0.05, respectively), while those correlating with TG/HDL ratios were men, hypertension, and metabolic syndrome (r values of 0.290, 0.287, and 0.362, p <0.05, respectively).Conclusion: TG/HDL ratio was significantly positively correlated significantly with the severity of coronary lesions based on Gensini score in non diabetic stable angina pectoris patients.


2013 ◽  
Vol 17 (2 (66)) ◽  
pp. 83-85
Author(s):  
I. V. Malyshevs’ka

The paper presents the results of an analysis of the influence of the presence of the metabolic syndrome (MS) on the myocardial dysfunction. More marked signs of a remodelling of the left ventricle (LV) have been established in patients with a combination of stable angina (SA) and MS, irrespective of the state of the global contractility of the LV. We haven’t detected a correlation between the indices of the intracardiac hemodynamics and the markers of the atherosclerotic process, namely, the level of total cholesterol (TCS) and C-reactive protein (CRP).


1996 ◽  
Vol 76 (02) ◽  
pp. 166-170 ◽  
Author(s):  
Moniek P M de Maat ◽  
Alf E R Arnold ◽  
Stef van Buuren ◽  
J H Paul Wilson ◽  
Cornells Kluft

SummaryElevated plasma fibrinogen levels are associated with an increased risk for cardiac events. Ticlopidine is a drug that inhibits the ADP-induced aggregation of blood platelets and it also has been described that ticlopidine can decrease the plasma fibrinogen level in patients with vascular diseases. The mechanism of this decrease has not yet been elucidated and therefore mechanisms that are known to affect fibrinogen levels were studied, viz. the acute phase reaction, total fibrin plus fibrinogen degradation (TDP) levels and the polymorphisms of the fibrinogen β-gene.The fibrinogen lowering effect of ticlopidine was studied in 26 healthy volunteers, selected on genotype of the BclI polymorphism of the fibrinogen β-gene, and in 26 patients with stable angina pectoris in a double blind, randomized cross-over study. Functional plasma fibrinogen levels were measured with the Clauss assay. Fibrinogen antigen, C-reactive protein (CRP) and TDP levels were measured using an enzyme immuno assay (EIA).In the healthy volunteers the functional fibrinogen levels had decreased by 0.20 g/l (9%, p = 0.005 using the paired Student t-test) after 4 weeks of 250 mg bid ticlopidine administration, whereas fibrinogen antigen, CRP and TDP levels were not significantly changed. In the stable angina pectoris patients the pre-treatment fibrinogen, CRP and TDP levels were significantly higher than in the volunteer group. After four weeks 250 mg bid ticlopidine administration the functional fibrinogen levels had decreased by 0.38 g/l (11%, p < 0.005), whereas the fibrinogen antigen, CRP and TDP levels were not significantly changed. The levels of functional and antigen fibrinogen, CRP and TDP did not change significantly during the placebo period in the volunteers or the patients. Neither in the volunteers nor in the patients was the effect of ticlopidine on the fibrinogen levels associated with the fibrinogen β-gene polymorphisms.Therefore, the fibrinogen lowering effect of ticlopidine is likely to be a modulation of the functionality of the molecule and unlikely to be modulated by the acute phase reaction, TDP-levels or the fibrinogen β-gene polymorphisms.


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