Vascular Health and Risk Management最新文献

Purpose: Peripheral arterial disease (PAD) is a common disease with multiple risk factors and affects patients worldwide. Several international studies have established correlations between anatomical topography/distribution of atherosclerosis and comorbidities in patients with PAD. In this cohort study, we aimed to analyze the patterns of atherosclerosis (site, distribution, and degree) in patients who underwent lower limb computed tomography angiography and arterial angiography by identifying the atherosclerotic plaque(s) that were possibly responsible for thrombi. Additionally, we aimed to determine any relationship between comorbidities and identified patterns.

Patients and methods: Between January 2015 and January 2021, we retrospectively recruited 140 patients at King Fahd Hospital of the University of Saudi Arabia. Data collected included patient characteristics, risk factors, and metabolic disorders, such as hypertension (HTN), diabetes mellitus (DM), dyslipidemia, and chronic kidney disease. Patients with incomplete records or unavailable radiological images were excluded.

Results: The infrapopliteal territory was the most common segment that was affected. HTN, DM, and dyslipidemia were found in 81.4%, 77.9%, and 62.9% of patients, respectively. Correlation analyses revealed that DM was the only independent metabolic disorder associated with a PAD distribution pattern in the femoropopliteal segment (p=0.039), thus denoting distal involvement. No significant association was found between PAD distribution and the severity of stenosis.

Conclusion: Segmental involvement in PAD varies with the risk factors and metabolic comorbidities present in patients. DM is an independent predictor of the anatomical distribution of PAD. The identification of such an anatomical distribution is paramount for screening procedures, early detection of disease, and prevention of complications, particularly limb amputation.

Objective: Since 2011, the Department of Vascular Surgery at Oslo University Hospital has offered screening for abdominal aortic aneurysm (AAA) to 65-year-old men living in Oslo, Norway. The aim of this study was to evaluate the effect of the screening project on AAA-related mortality and rupture and repair rates in the screened population.

Methods: This cohort study included men that participated in AAA screening at the Department of Vascular Surgery at Oslo University Hospital in the period May 2011 to September 2019. All men with screen-detected AAA (aortic diameter ≥30 mm) and subaneurysmal aortic dilatation (aortic diameter 25-29 mm) were included. A stratified (1:1 with the subaneurysm group), randomized selection of men with normal aortic diameter (<25 mm) upon screening was also included. The follow-up data on events (ruptures, repairs, and deaths) after screening were collected retrospectively from patient electronic medical records at Oslo University Hospital, the National Population Register and the Norwegian Cause of Death Registry (CoDR).

Results: In total, 2048 men were included, with a median follow-up time of 7.1 years (IQR 3.8). Among men with screen-detected AAA, 0.6% died of AAA-related causes (0.9 AAA-related deaths per 1000 person-years). The rupture rate was 0.3% among men with screen-detected AAA or subaneurysmal aortic dilatation, giving an incidence of 0.5 ruptures per 1000 person-years. The overall repair rate in the AAA group was 20.6% (36.1 repairs per 1000 person-years) and 0.6% (0.9 repairs per 1000 person-years) in the subaneurysm group.

Conclusion: In a population screened for AAA, the incidence of rupture and the AAA-related mortality was very low. Almost one-fifth of the participants with screen-detected AAA underwent elective repair, representing a group that might have presented with rupture if untreated. These results indicate that screening is valuable in preventing AAA rupture and AAA-related mortality.

Background: The prognostic role of the soluble circulating suppression of tumorigenicity 2 marker (sST2) in different cardiovascular diseases (CVD) is still under investigation. This research aimed to assess the serum levels of sST2 in the blood of individuals with ischemic heart disease and its relation to disease severity, also to examine any changes in sST2 levels following a successful percutaneous coronary intervention (PCI) in those patients.

Methods: A total of 33 ischemic patients and 30 non-ischemic controls were included. The plasma level of sST2 was measured using commercially available ELISA assay kit, at baseline and 24-48 h after the intervention in the ischemic group.

Results: On admission, there was a significant difference between the group of acute/chronic coronary syndrome cases and controls regarding the sST2 plasma level (p < 0.001). There was an insignificant difference between the three ischemic subgroups at the baseline sST2 level (p = 0.38). The plasma sST2 level decreased significantly after PCI (from 20.70 ± 1.71 to 16.51 ± 2.43, p = 0.006). There was a modestly just significant positive correlation between the acute change in post-PCI sST2 level and the severity of ischemia as measured by the Modified Gensini Score (MGS) (r = 0.45, p = 0.05). In spite of the highly significant improvement in the coronary TIMI flow of ischemic group after PCI, there was insignificant negative correlation between the post- PCI delta change in the sST2 level and the post-PCI TIMI coronary flow grade.

Conclusion: A significantly high plasma level of sST2 in patients with myocardial ischemia and controlled cardiovascular risk factors showed an immediate reduction after successful revascularization. The high baseline level of the sST2 marker and the acute post-PCI reduction was mainly related to the severity of ischemia rather than left ventricular function.

Backgrounds and aims: The role of Lipoprotein(a) (Lp(a)) in increasing the risk of cardiovascular diseases is reported in several populations. The aim of this study is to investigate the correlation of high Lp(a) levels with the degree of coronary artery stenosis.

Methods: Two hundred and sixty-eight patients were enrolled for this study. Patients who underwent coronary artery angiography and who had Lp(a) measurements available were included in this study. Binomial logistic regressions were applied to investigate the association between Lp(a) and stenosis in the four major coronary arteries. The effect of LDL and HDL Cholesterol on modulating the association of Lp(a) with coronary artery disease (CAD) was also evaluated. Multinomial regression analysis was applied to assess the association of Lp(a) with the different degrees of stenosis in the four major coronary arteries.

Results: Our analyses showed that Lp(a) is a risk factor for CAD and this risk is significantly apparent in patients with HDL-cholesterol ≥35 mg/dL and in non-obese patients. A large proportion of the study patients with elevated Lp(a) levels had CAD even when exhibiting high HDL serum levels. Increased HDL with low Lp(a) serum levels were the least correlated with stenosis. A significantly higher levels of Lp(a) were found in patients with >50% stenosis in at least two major coronary vessels arguing for pronounced and multiple stenotic lesions. Finally, the derived variant (rs1084651) of the LPA gene was significantly associated with CAD.

Conclusion: Our study highlights the importance of Lp(a) levels as an independent biological marker of severe and multiple coronary artery stenosis.

Aim: To compare incidence of first-ever acute cerebral infarction, etiology and traditional risk factors in young adults 15-49 years in 1988-1997 and 2008-2017 in Hordaland County, Norway.

Methods: Case-finding of young adults with acute cerebral infarction in 1988-1997 was done retrospectively by computer research from hospital registries in Hordaland County. Young adults with acute cerebral infarction living in the Bergen region in 2008-2017 were prospectively included in a database at Haukeland University Hospital. Traditional risk factors, etiology and modified Rankin scale score on discharge were registered.

Results: Crude average incidence of acute cerebral infarction was 11.4 per 100.000 per year in 1988-1997 and 13.2 per 100.000 per year in 2008-2017 (P=0.04). The prevalence of prior myocardial infarction, angina pectoris, and dyslipidemia were lower in the 2008-2017 cohort (all P<0.05). Atherosclerosis was less common in the 2008-2017 cohort (P<0.001).

Conclusion: The observed incidence of acute cerebral infarction in young adults increased from 1988-1997 to 2008-2017 in Hordaland County. Atherosclerosis was less common in the 2008-2017 cohort.

Background: A little is known about the risk factors and predictors of pulmonary embolism (PE) in Coronavirus disease 2019 (Covid-19) infected patients. Therefore, we directed this study to investigate the predictors of PE in patients infected with Covid - 19 in Upper Egypt.

Methods: We conducted a retrospective cohort study on 297 patients infected with COVID-19, aged ≥ 18 years old. Suspicion of COVID-19 infection was based on the World Health Organization (WHO) criteria and confirmed by nasal and pharyngeal swab for real-time reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. The patient was also determined to have COVID-19 when CT results that were thought to be typical for COVID-19 and clinical data that were compatible were present.

Results: PE was diagnosed in 18.2% of patients. We found that the incidence of PE was significantly higher in older patients, females, those with higher BMI, hypertensive patients, diabetics, and patients with co-morbidities. Also, PE was significantly higher in patients presented with dyspnea, chest pain, longer duration of symptoms at hospital admission, and lower oxygen concentration. The mean serum Hb level, platelet count, TLC and absolute lymphocytic count were markedly reduced in those who had PE. All the patients who developed PE had a CO-RADS scale five on their CT chest scan. Age > 65, BMI > 25, DM, and associated co-morbidities were the independent patients' characteristics associated with the development of PE after the multivariate regression analysis.

Conclusion: PE is a common complication of Covid 19 infection. PE is associated with a variety of clinical and laboratory parameters in univariate analysis, but age > 65, BMI > 25, DM, and associated co-morbidities were the independent patients' characteristics associated with the development of PE in those infected with Covid-19.

Pulmonary hypertension may develop as a disease process specific to pulmonary arteries with no identifiable cause or may occur in relation to other cardiopulmonary and systemic illnesses. The World Health Organization (WHO) classifies pulmonary hypertensive diseases on the basis of primary mechanisms causing increased pulmonary vascular resistance. Effective management of pulmonary hypertension begins with accurately diagnosing and classifying the disease in order to determine appropriate treatment. Pulmonary arterial hypertension (PAH) is a particularly challenging form of pulmonary hypertension as it involves a progressive, hyperproliferative arterial process that leads to right heart failure and death if untreated. Over the last two decades, our understanding of the pathobiology and genetics behind PAH has evolved and led to the development of several targeted disease modifiers that ameliorate hemodynamics and quality of life. Effective risk management strategies and more aggressive treatment protocols have also allowed better outcomes for patients with PAH. For those patients who experience progressive PAH with medical therapy, lung transplantation remains a life-saving option. More recent work has been directed at developing effective treatment strategies for other forms of pulmonary hypertension, such as chronic thromboembolic pulmonary hypertension (CTEPH) and pulmonary hypertension due to other lung or heart diseases. The discovery of new disease pathways and modifiers affecting the pulmonary circulation is an ongoing area of intense investigation.

Background: The coronary artery calcium (CAC) score can be used to increase (CAC score > 0) or decrease (CAC score = 0) the likelihood of coronary artery disease (CAD). We compared the CAC score with the pre-test probability (PTP) for CAD (low, intermediate, and high). Furthermore, we compared the CAC score with exercise electrocardiography (ECG) and compared both tests with coronary angiography.

Methods and results: We retrospectively identified patients with angina and/or dyspnea for whom CAC score was used to increase or decrease the likelihood of CAD. Of 882 patients, majority had low (45%) or intermediate (44%) PTP. Patients with higher PTP had significantly higher CAC scores (Cramer's V = 0.29, p < 0.0001). Most patients (57%) had a CAC score of zero, especially those with low (73%) and intermediate (49%) PTP. However, 20% of patients with high PTP had CAC score of zero. Higher CAC scores were observed in patients with abnormal exercise ECG, but association was weak and not significant (Cramer's V = 0.13, p = 0.08). Moreover, more than 40% of patients with an abnormal exercise ECG had CAC score of zero. Higher CAC scores were associated with more severe abnormalities on coronary angiography (Cramer's V = 0.43, p < 0.0001), whereas there was no association between results of exercise ECG and coronary angiography (Cramer's V = 0.11, p = 0.91).

Conclusion: CAC score can be used in addition to PTP to increase or decrease the likelihood of CAD, and it might be more useful than exercise ECG in the diagnostic work-up of chest pain.

Introduction: Cardiovascular disorders are one of the commonly recognized occupational diseases in the developed world. Individuals chronically exposed to noise at workplaces had a higher risk of developing elevated arterial blood pressure. There are limited studies in Ethiopia regarding this topic and thus this study determined the prevalence and determinant factors of occupational noise-induced pre-hypertension among metal manufacturing workers in Gondar city administration, Northwest Ethiopia.

Methods: An institution-based cross-sectional study design was carried out. In this study, 300 study participants were recruited by census sampling method. A sound level meter was used to measure the working area noise level. A semi-structured pre-tested interviewer-administered questionnaire was used to collect sociodemographic and clinical data. Blood pressure was measured in a quiet room in the morning using a mercurial sphygmomanometer. Both bivariable and multi-variable binary logistic regressions were used to identify factors associated with noise-induced prehypertension. Adjusted odds ratio with 95% confidence interval was reported, and variables with p < 0.05 were considered as statistically associated factors with pre-hypertension.

Results: The prevalence of noise-induced pre-hypertension was 27.7% (95% CI: 22.7-32.7). In multivariable logistic regression, working area noise level (AOR = 3.8, 95% CI: 6.8-8.9), 45-65 years' age (AOR = 9.8, 95% CI: 5.4-12.9), years of work experience ((6-10 years (AOR = 2.8, 95% CI: 1.98-5.90 and >10 years (AOR = 4.8, 95% CI: 7.8-9.75)), being a cigarette smoker (AOR = 3.6, 95% CI: 1.36-9.77), and alcohol consumption (AOR = 2.4, 95% CI: 1.06-1.04) were significantly associated with noise-induced prehypertension.

Conclusion: Workers in metal manufactures who were exposed to noise levels >85 dB developed elevated blood pressure. The odds of having prehypertension were increased by years of work experience, advanced age, smoking, and alcohol consumption. Our findings recommended that the real-world preventive strategies should be taken to lower the risk of noise-induced pre-hypertension hastened by occupational noise exposure.

Purpose: On-pump coronary artery bypass graft (CABG) causes myocardial ischemia, through the cardiopulmonary bypass (CPB) and aortic cross-clamping (AoX). Glutamine supplementation protects cardiac cells during cardiac ischemia. This study analysed the correlation between cardiac index (CI), plasma troponin I, myocardial histopathology, CPB and AoX duration in low ejection fraction patients receiving glutamine and no glutamine undergoing elective on-pump CABG.

Material and methods: This was a secondary analysis of a double-blind, randomised controlled trial of 60 patients, split into control and intervention (glutamine) groups. Glutamine was administered at a dose of 0.5 g/kg/24 hours. There were 29 patients in each respective groups after a total of two patients dropped out.

Results: A negative correlation (p = 0.037) was observed between CPB duration and CI at 6 hours after CPB in the glutamine group. A positive correlation (p = 0.002) was also observed between AoX duration and plasma troponin I at 6 hours after CPB in the control group. However, no correlation was observed between myocardial histopathology and plasma troponin I level at 5 minutes after CPB.

Conclusion: Significant negative correlation between CPB duration and CI at 6 hours after CPB in the glutamine group, along with significant positive correlation between AoX duration and plasma troponin I level at 6 hours after CPB in the control group demonstrated the myocardial protection qualities of intravenous glutamine administration in patients with low ejection fraction undergoing elective on-pump CABG surgeries.