Severity Of Vascular Stenosis Research Articles

Correlation Between Risk Factors, Degree of Vascular Restenosis, and Inflammatory Factors After Interventional Treatment for Stroke: A Two-Center Retrospective Study.

To study the correlation between risk factors, degree of vascular restenosis, and inflammatory factors after interventional treatment for stroke. The clinical data of 96 stroke patients who received interventional therapy in our hospital from April 2020 to June 2021 were selected for retrospective study, and the postoperative follow-up was 1 year. Univariate and multivariate regression were used to analyze identified factors associated with interventional stroke efficacy. At the same time, the value of inflammatory factor levels in predicting vascular restenosis after interventional stroke was analyzed. According to our findings, several risk factors, including body mass index ≥ 25.51kg/m 2 , smoking, drinking, hypertension, and diabetes, were identified as contributors to poor postoperative efficacy following stroke intervention ( P <0.05). Furthermore, a notable association was observed between the severity of vascular stenosis ( P <0.001) and the levels of interleukin 6, interleukin 2, TNF-α, and C-reactive protein. The combined assessment of these serum inflammatory factors exhibited excellent predictive capability for postoperative vascular restenosis and stenosis severity, yielding a sensitivity of 84.30%, a specificity of 81.20%, and an area under the curve of 0.882. Obesity, smoking, alcohol consumption, hypertension, and diabetes have been found to be associated with suboptimal outcomes following interventional treatment for stroke. The assessment of preoperative levels of inflammatory factors holds promise in predicting the likelihood of postoperative restenosis to a certain degree.

White matter hyperintensities had a correlation with the cerebral perfusion level, but no correlation with the severity of large vessel stenosis in the anterior circulation.

The contribution of large vessel stenosis to the development of white matter hyperintensities (WMHs) has not been fully elucidated. This study aims to explore the correlation between ipsilateral white matter hyperintensities (WMHs) and the severity of large vessel stenosis in the anterior circulation and cerebral perfusion level, as well as analyze the factors influencing WMHs. A cross-sectional study of 150 patients with unilateral anterior circulation large vessel stenosis of ≥50% was conducted. The severity of ipsilateral WMHs was assessed by Fazekas scale on T2-weighted image and/or fluid-attenuated inversion recovery MR imaging, vascular stenosis severity was evaluated on computed tomography angiography images, and the level of cerebral perfusion was rated according to a staging system for abnormal cerebral perfusion based on CTP results. The relationships between the stenosis severity, cerebral perfusion level and ipsilateral WMHs severity were analyzed. A multivariate logistic regression analysis was performed to determine the factors independently influencing WMHs. Among 150 patients (mean age, 63.12±10.55 years), there was a statistically significant positive correlation between cerebral perfusion level and the severity of DWMHs and PWMHs (Gamma=0.561, p<.001; Gamma=0.600, p<.001), and a positive correlation between cerebral perfusion level and the severity of vascular stenosis (Gamma=0.495, p<.001).While, there was no statistically significant correlation between the severity of vascular stenosis and the severity of DWMHs and PWMHs (Gamma=0.188, p=.08; Gamma=0.196, p=.06). The multivariate logistic regression analysis results demonstrated that age (OR=1.047, 95% CI 1.003-1.093; p=.035), stroke/TIA history (OR=2.880, 95% CI 1.154-7.190; p=.023) and stage II of cerebral perfusion (OR=2.880, 95% CI 1.154-7.190; p=.023) were independent influencing factors on ipsilateral DWMHs. Age (OR=1.051, 95% CI 1.009-1.094; p=.018), and stage II of cerebral perfusion (OR=12.871, 95% CI 3.576-46.322; p<.001) were factors independently influencing ipsilateral PWMHs. White matter hyperintensities may be attributed to cerebral hypoperfusion secondary to vascular stenosis but not directly to the severity of stenosis in the large vessels of anterior circulation. Moreover, longitudinal studies with sequential imaging exams may further reveal the impact of cerebral perfusion secondary to vascular stenosis on the development and progression of WMHs.

Lower-extremity muscle wasting in patients with peripheral arterial disease: quantitative measurement and evaluation with CT.

Lower-extremity peripheral arterial disease (PAD) results in limb ischemia and is strongly associated with sarcopenia. This study aimed to retrospectively evaluate the association between the quantity of muscle mass in the lower extremities and the severity of vascular stenosis in PAD patients. Between January 2018 and August 2021, 128 patients with PAD and 53 individuals without PAD, diagnosed by computed tomography, were enrolled. The severity of stenosis of lower-extremity arteries was measured using a grading system. The muscle and fat mass areas were calculated in the abdomen at the L3 or L4 level, mid-thigh, and lower leg. Multivariable logistic regression was conducted to clarify the risk associated with low muscle mass. The difference in muscle mass between PAD and non-PAD patients was evaluated by using propensity score matching. A strong positive correlation between the abdomen muscle area and leg muscle area was observed. The muscle area and muscle index of the leg were lower in PAD patients. These changes occurred earlier than in the abdomen muscle area. The group with more severe artery stenosis had more muscle wasting in the lower extremities. Greater age, female, lower BMI, and PAD were associated with low muscle mass. After propensity score matching, the leg muscle area was still lower in PAD patients. There is a direct association between PAD and regional muscle wasting. This occurs earlier regionally in the lower extremities than in central muscles. Early diagnosis of PAD might prevent progressive muscle loss, improving disease outcome and quality of life. • Peripheral arterial disease is strongly associated with sarcopenia. • Muscle wasting in the lower extremities is earlier and more prominent than that in the abdomen. • More severe arterial stenoses are associated with higher muscle wasting in the lower extremities.

Evaluation of the relationship between haptoglobin polymorphisms with antioxidant enzymes activity in patients with coronary heart disease

BackgroundAtherosclerosis, the most common pathologic process underlying cardiovascular disease, defines a state of intensified oxidative stress and impaired antioxidative capacity. Haptoglobin (Hp) polymorphisms include three distinct human genotypes (Hp1-1, Hp2-1, and Hp2-2), managing functional differences related to the risk of developing cardiovascular diseases. The present study proposed to examine Haptoglobin polymorphisms concerning antioxidative enzyme activity in patients with coronary artery disease. MethodsThis case-control inquiry was managed through 398 samples consisting of 225 men and 173 women aged 30–80 who were suspect of CAD. Patients were classified as CAD cases (255) and controls (143). Hp genotyping was conducted using a polymerase chain reaction (PCR). Total antioxidant capacity (TAC) was examined using the Ferric Reducing Ability of Plasma (FRAP) method, and Erythrocyte CAT and GPx activity were measured as antioxidant enzymes. ResultsThe TG, Chol/HDL, diabetes, GPx enzyme, and FRAP results demonstrate a meaningful variation in patients than controls (p > 0.005). The frequency of haptoglobin polymorphisms was significantly different between patients compared to controls. The frequency of Hp genotypes had a significant association with the severity of vascular stenosis so that the Hp2 allele increased the probability of vascular stenosis (P = 0.03).GPx enzyme activity presented a significant difference in Hp2-2 compared to Hp2-1 and Hp1-1 patients. However, there were no notable variations between the Hp genotypes and the amount of catalase and total antioxidant capacity (p > 0.005). ConclusionThis examination confirms that antioxidative enzyme activities are Hp-phenotype-dependent in coronary artery disease. Impaired GPx enzyme activities were prominent among coronary artery disease patients with Hp2-2. Besides, diabetic and high BMI patients with Hp2-2 genotype possess a higher prevalence of coronary artery disease. This study proves the HP2 allele as a genetic determinant in controlling oxidative stress in CAD patients.

PERCUTANEOUS CORONARY INTERVENTIONS: INTRAVASCULAR IMAGING AND ASSESSMENT OF INTRACORONARY HAEMODYNAMICS

Conventional coronary angiography does not provide thorough information about the structure of atherosclerotic lesions and severity of vascular stenosis. Since their introduction in past decades, optical coherence tomography and intravascular ultrasound have demonstrated high diagnostic yield in patients with coronary heart disease, translated into improved clinical outcomes. The fractional flow reserve and instantaneous wave-free ratio have emerged as reliable criteria for assessment of hemodynamically significant lesions, and allowed a more tailored approach to myocardial revascularization. In the current paper, we aimed to review the main aspects of clinical utilization of invasive studies complementing coronary angiography and percutaneous coronary intervention.

Tissue hypoxia, inflammation, and loss of glomerular filtration rate in human atherosclerotic renovascular disease

The relationships between renal blood flow (RBF), tissue oxygenation, and inflammatory injury in atherosclerotic renovascular disease (ARVD) are poorly understood. We sought to correlate RBF and tissue hypoxia with glomerular filtration rate (GFR) in 48 kidneys from patients with ARVD stratified by single kidney iothalamate GFR (sGFR). Oxygenation was assessed by blood oxygenation level dependent magnetic resonance imaging (BOLD MRI), which provides an index for the levels of deoxyhemoglobin within a defined volume of tissue (R2*). sGFR correlated with RBF and with the severity of vascular stenosis as estimated by duplex velocities. Higher cortical R2* and fractional hypoxia and higher levels of renal vein neutrophil-gelatinase-associated-lipocalin (NGAL) and monocyte-chemoattractant protein-1 (MCP-1) were observed at lower GFR, with an abrupt inflection below 20 ml/min. Renal vein MCP-1 levels correlated with cortical R2* and with fractional hypoxia. Correlations between cortical R2* and RBF in the highest sGFR stratum (mean sGFR 51 ± 12 ml/min; R= -0.8) were degraded in the lowest sGFR stratum (mean sGFR 8 ± 3 ml/min; R= -0.1). Changes in fractional hypoxia after furosemide were also absent in the lowest sGFR stratum. These data demonstrate relative stability of renal oxygenation with moderate reductions in RBF and GFR but identify a transition to overt hypoxia and inflammatory cytokine release with severely reduced GFR. Tissue oxygenation and RBF were less correlated in the setting of reduced sGFR, consistent with variable oxygen consumption or a shift to alternative mechanisms of tissue injury. Identifying transitions in tissue oxygenation may facilitate targeted therapy in ARVD.

Correlation of C-Reactive Protein and Cardiac Enzymes with Angiographic Severity of Coronary Artery Disease in Pakistani Patients with Acute Coronary Syndrome.

To determine the correlation of C-reactive protein (CRP) levels with the severity of coronary stenosis on angiography and the association of cardiac enzymes with the degree of stenosis in acute coronary syndrome (ACS) patients. Secondly, to compare association of angiographic severity of vascular stenosis with CRP in patients with ST segment elevation myocardial infarction (STEMI) and non-STEMI / Unstable angina (UA). Prospective, descriptive study. Khan Research Laboratories (KRL) Hospital, from October 2014 to March 2015. CRP was measured on diagnosis of ACS in 70 patients. Cardiac enzymes were measured 6 hours after the onset of chest pain. Angiographic scoring for degree of stenosis and number of culprit vessels was done. Two groups consisting of patients with STEMI (group 1) and with NSTEMI/UA (group 2) were made. No correlation was found between CRP levels and angiographic stenosis in patients with ACS (r=0.162, p>0.05). No association was found between eosinophil count and severity of stenosis (p=0.88). Rise of cardiac enzymes and degree of coronary stenosis showed a positive correlation (p <0.001). There was significant difference in the means of coronary artery stenosis scores between the two groups (Gensini score of groups 1 and 2: 35.9 ±4 and 14 ±8, respectively) p<0.001, but there was no significant difference in CRP levels. CRP is a marker of inflammation in ACS rather than a risk factor for determining the severity of vascular stenosis. Rise in cardiac enzymes still grade high in predicting severity of vascular stenosis than eosinophil count or CRP levels.

Non-invasive imaging of atherosclerosis.

Atherosclerosis is an inflammatory disease that causes most myocardial infarctions, strokes, and acute coronary syndromes. Despite the identification of multiple risk factors and widespread use of drug therapies, it still remains a global health concern with associated costs. It is well known that the risks of atherosclerotic plaque rupture are not well correlated with stenosis severity. Lumenography has a central place for defining the site and severity of vascular stenosis as a prelude to intervention for relief of symptoms due to blood flow limitation. Atherosclerosis develops within the arterial wall; this is not imaged by lumenography and hence it provides no information regarding underlying processes that may lead to plaque rupture. For this, we must rely on other imaging modalities such as ultrasound, computed tomography, magnetic resonance imaging, and nuclear imaging methods. These are capable of reporting on the underlying pathology, in particular the presence of inflammation, calcification, neovascularization, and intraplaque haemorrhage. Additionally, non-invasive imaging can now be used to track the effect of anti-atherosclerosis therapy. Each modality alone has positives and negatives and this review will highlight these, as well as speculating on future developments in this area.

Clinical Value of MRA Analysis of the Vertebrobasilar System in Vertiginous Patients

Vertebrobasilar haemodynamics correlate closely with syndromal vertigo. The aim of this study is to examine the clinical value of MRA for evaluation of vertebrobasilar haemodynamics in vertiginous patients. We examined 40 individuals (20 with vertebrobasilar insufficiency and 20 diagnosed with other vestibular disorders). MRA results were quantified on the basis of the severity of vascular stenosis in the major arteries of the vertebrobasilar system and we analysed the relationship of these results with otoneurological diagnoses, eye-tracking tests (ETT) and optokinetic nystagmus (OKN). MRA results correlated well with otoneurological diagnoses and ETT results. Consequently, MRA can be used as a screening examination to evaluate vertebrobasilar haemodynamics and ETT may be a sensitive functional parameter of vertebrobasilar insufficiency.

Methoxyisobutylisonitrile (MIBI) Tc 99m SPECT to establish a correlate to coronary flow reserve, the perfusion reserve, from global and regional myocardial uptake after exercise and rest

With 99mTc-MIBI SPECT and a 4 h exercise (E: 150 MBq iv) and rest (R; 800 MBq iv) protocol, global and regional left ventricular (LV) myocardial uptake was determined in 70 patients with angiographically confirmed coronary heart disease (CHD) and in 10 controls. The aim was to establish an E/R ratio as a correlate to coronary vascular reserve, representing perfusion reserve (PR). E/R ratios, obtained from total LV myocardium or from normal or impaired regions, were greater than 1.19 under all conditions, indicating the presence of higher flow during exercise than at rest (even in areas of low flow). Global PR separated (P less than 0.01) controls (1.63 +/- 0.21; mean +/- SD) from severely diseased patients (1.29 +/- 0.14 in 2- or 3-vessel disease) only. Improved differential diagnosis was gained from calibrating the regional E/R ratio to regional differences (E minus R) of uptake. For the left ventricle regional PRs (RPR) for 25 ROIs of the target, framing the myocardium, were determined. RPR at the regional maximum of 99mTc-MIBI uptake was similar in both controls (1.66) and patients (1.63), indicating a high probability of meeting some areas with functionally normal perfusion in patients with CHD. RPR allowed sufficient separation (P less than 0.025) concerning the degree of coronary artery stenosis (RPR in occlusion, 0.26; stenosis greater than 75%, 0.39; less than 75%, 0.56). In controls, the overall value for RPR was 1.14 +/- 0.28 (P less than 0.001). LV global PR and RPR were useful in separating patients with CHD vs controls and in classifying the severity of vascular stenosis.