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Background For parents at high risk for cardiovascular events, presence of cardiovascular disease or risk factors in their offspring may be an indicator of their genetic load or exposure to (unknown) risk factors and might be related to the development of new or recurrent vascular events. Methods In 4,267 patients with vascular disease, hypertension, diabetes, or hypercholesterolemia enrolled in the SMART cohort, the presence of cardiovascular risk factors (hypertension, diabetes, hypercholesterolemia, smoking, or overweight) and cardiovascular disease (coronary artery disease, cerebrovascular disease, peripheral artery disease, or abdominal aortic aneurysm) was assessed in their 10,564 children. The relation between presence of cardiovascular disease or cardiovascular risk factors in their offspring and new or recurrent vascular events was determined by Cox proportional hazard analyses. Results Of the patients, 506 (12%) had offspring with cardiovascular disease, hypertension, hypercholesterolemia, or diabetes. Smoking in offspring was present in 1,972 patients (46%), and overweight in 845 patients (20%). During a median follow-up of 7.0 years (interquartile range 3.7-10.4), the composite outcome of myocardial infarction (MI), stroke, or vascular mortality occurred in 251 patients. Patients with offspring with cardiovascular disease, hypertension, hypercholesterolemia, or diabetes had an increased risk of vascular mortality (hazard ratio [HR] 2.9, 95% CI 1.2-7.1), MI (HR 1.6, 95% CI 1.1-2.5), and the composite outcome (HR 1.5, 95% CI 1.1-2.2). Diabetes in offspring was related to an increased risk of the composite outcome (HR 2.7, 95% CI 1.5-5.0), MI (HR 3.3, 95% CI 1.7-6.6), and vascular mortality (HR 3.4, 95% CI 0.8-14.8). Smoking and overweight in offspring were not related to increased vascular risk in parents. Conclusions Presence of cardiovascular disease, hypertension, hypercholesterolemia, and diabetes in offspring, with diabetes mellitus being the most contributing cardiovascular risk factor, is related to an increased risk of developing new or subsequent vascular events in patients already at high vascular risk

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OBJECTIVE Our aim is to compare the effect of type 2 diabetes on recurrent major cardiovascular events (MCVE) for patients with symptomatic vascular disease at different locations. RESEARCH DESIGN AND METHODS A total of 6,841 patients from the single-center, prospective Second Manifestations of ARTerial disease (SMART) cohort study from Utrecht, the Netherlands, with clinically manifest vascular disease with (n = 1,155) and without (n = 5,686) type 2 diabetes were monitored between 1996 and 2013. The effect of type 2 diabetes on recurrent MCVE was analyzed with Cox proportional hazards models, stratified for disease location (cerebrovascular disease, peripheral artery disease, abdominal aortic aneurysm, coronary artery disease, or polyvascular disease, defined as >= 2 vascular locations). RESULTS Five-year risks for recurrent MCVE were 9% in cerebrovascular disease, 9% in peripheral artery disease, 20% in those with an abdominal aortic aneurysm, 7% in coronary artery disease, and 21% in polyvascular disease. Type 2 diabetes increased the risk of recurrent MCVE in coronary artery disease (hazard ratio [HR] 1.67; 95% CI 1.25-2.21) and seemed to increase the risk in cerebrovascular disease (HR 1.36; 95% CI 0.90-2.07), while being no risk factor in polyvascular disease (HR 1.12; 95% CI 0.83-1.50). Results for patients with peripheral artery disease (HR 1.42; 95% CI 0.79-2.56) or an abdominal aortic aneurysm (HR 0.93; 95% CI 0.23-3.68) were inconclusive. CONCLUSIONS Type 2 diabetes increased the risk of recurrent MCVE in patients with coronary artery disease, but there is no convincing evidence that it is a major risk factor for subsequent MCVE in all patients with symptomatic vascular disease

Організаційно-економічні передумови та особливості формування сфери фінансових послуг в економічній системі

Glucocorticoids (GCs) are widely used anti-inflammatory drugs well known to cause many adverse effects. Still, there is a dearth of data on the long-term cardiovascular effects of GCs in patients with established cardiovascular disease and the effect on atherosclerotic plaque composition. A total of 1894 patients who underwent carotid endarterectomy (CEA), of whom 40 patients received systemic GCs, were included in the Athero-Express Biobank. Atherosclerotic plaque samples and peripheral blood samples were obtained during CEA. Cardiovascular events during 3 years of follow-up were investigated using Cox regression modeling to adjust for possible confounding. Atherosclerotic plaque composition was examined using immunohistochemical staining. Use of GCs at inclusion was associated with markedly increased incidences of ischemic stroke (15.2% vs. 5.9%), composite events (48.5% vs. 26.9%), and cardiovascular death (21.2% vs. 5.7%), as well as an increased risk of cardiovascular death (hazards ratio 2.7, 95% confidence interval, 1.1-6.7) and all-cause death (hazards ratio 2.3, 95% confidence interval, 1.1-4.8) after 2.6 years of follow-up. None of the histological features of atherosclerotic plaques were significantly different in patients using GCs. After CEA, the use of systemic GCs is independently associated with an increased incidence of cardiovascular events and an increased risk of cardiovascular and all-cause death, but not atherosclerotic plaque compositio

Timing of Thoracic Outlet Decompression after Thrombolysis for Primary Upper Extremity Deep Venous Thrombosis: A Systematic Review

Background: The optimal timing of decompression surgery after thrombolysis in patients with primary upper extremity deep vein thrombosis (UEDVT) is still a matter of debate. This systematic review compares the safety and efficacy of early intervention versus postponed intervention in patients with primary UEDVT. Methods: A structured PUBMED, EMBASE, and COCHRANE search was performed for studies reporting on the timing of surgical intervention for primary UEDVT. Studies reporting on timing of decompression surgery in combination with recurrent thrombosis, bleeding complications, and symptom-free survival were included. Two treatment groups were defined; group A received surgical decompression within two weeks after thrombolysis and group B after two weeks or more. All end points were assessed in accordance with the reported outcomes in the included articles. Mean percentages were calculated using descriptive statistics. Results: Six articles (126 patients) were included: 87 patients in group A versus 39 in group B. In group A, bleeding complications occurred in 7% of patients versus 5% in group B. Two-third of the bleeding complications in group A occurred in patients receiving surgical decompression within 24 hr after thrombolysis while kept on intravenous heparin both preoperatively and postoperatively. Reported preoperative recurrent thrombosis was 7% in group A versus 11% in group B, another 13% had postoperative recurrent thrombosis versus 21% in group B. The effectiveness of both treatment strategies was comparable with a total of 89% of patients in group A with minimal or no symptoms at final follow-up compared with 90% in group B. The mean follow-up in group A was 35 months (1–168 months) and 28 months (1–168 months) in group B. Conclusions: Based on the limited available data presented in this review, early decompression surgery within two weeks after catheter-directed thrombolysis seems as safe and effective as postponed surgical intervention in patients with primary UEDVT

Atherosclerotic Plaque Biomarkers: Beyond the Horizon of the Vulnerable Plaque

Cardiovascular disease (CVD) is the number one cause of death globally, and the majority of CVD is caused by atherosclerosis. Atherosclerosis is a systemic inflammatory disease that leads to myocardial infarction, stroke and lower limb ischemia. Pathological studies have given insight to development of atherosclerosis and the importance of local plaque vulnerability, leading to thrombus formation and cardiovascular events. Due to the burden of cardiovascular disease, identification of patients at risk for cardiovascular events and treatment stratification is needed. The predictive power of classical risk factors is limited, especially in patients with manifest atherosclerosis. Imaging modalities have focused on the characteristics of the vulnerable plaque. However, it has become evident that not all so-called vulnerable plaques lead to rupture and subsequent thrombosis. The latter obviously limits the positive predictive value for imaging assessment of plaques and patients at risk. Serum biomarkers have also been studied extensively, but have very limited application in a clinical setting for risk stratification. In line with the important relation between vulnerable plaques and cardiovascular events, plaque biomarker studies have been initiated. These longitudinal studies are based on the concept, that a vulnerable plaque contains predictive information for future cardiovascular events, also in other territories of the vascular tree. Results look promising and plaque markers can be used to develop imaging modalities to identify patients at risk, or to monitor treatment effect. Plaque biomarker studies do not challenge the definition of the vulnerable plaque, but use its concept in favor of prediction improvement for vascular patients

Myocardial injury after noncardiac surgery and its association with short-term mortality

Background: To identify patients at risk for postoperative myocardial injury and death, measuring cardiac troponin routinely after noncardiac surgery has been suggested. Such monitoring was implemented in our hospital. The aim of this study was to determine the predictive value of postoperative myocardial injury, as measured by troponin elevation, on 30-day mortality after noncardiac surgery. Methods and Results: This observational, single-center cohort study included 2232 consecutive intermediate- to highrisk noncardiac surgery patients aged ≥60 years who underwent surgery in 2011. Troponin was measured on the first 3 postoperative days. Log binomial regression analysis was used to estimate the association between postoperative myocardial injury (troponin I level &gt;0.06 μg/L) and all-cause 30-day mortality. Myocardial injury was found in 315 of 1627 patients in whom troponin I was measured (19%). All-cause death occurred in 56 patients (3%). The relative risk of a minor increase in troponin (0.07-0.59 μg/L) was 2.4 (95% confidence interval, 1.3-4.2; P&lt;0.01), and the relative risk of a 10- to 100-fold increase in troponin (≥0.60 μg/L) was 4.2 (95% confidence interval, 2.1-8.6; P&lt;0.01). A myocardial infarction according to the universal definition was diagnosed in 10 patients (0.6%), of whom 1 (0.06%) had ST-segment elevation myocardial infarction. Conclusions: Postoperative myocardial injury is an independent predictor of 30-day mortality after noncardiac surgery. Implementation of postoperative troponin monitoring as standard of care is feasible and may be helpful in improving the prognosis of patients undergoing noncardiac surgery.</p

Patch angioplasty during carotid endarterectomy using different materials has similar clinical outcomes

OBJECTIVE: Patch angioplasty during carotid endarterectomy is commonly used to treat carotid artery stenosis. However, the choice of which patch to use is still a matter of debate. Autologous venous material has disadvantages such as wound-related problems at the harvest site and a prolonged intervention time. These limitations can be bypassed when synthetic or biological patches are used. Both materials have been associated with divergent advantages and disadvantages. Therefore, the aim of our study was to compare the long-term follow-up outcomes in patients who received carotid endarterectomy and closure with either bovine pericardial patch or polyester patch. METHODS: A retrospective cohort study was conducted, including all patients who underwent primary carotid endarterectomy and closure with bovine pericardial patch or polyester patch between January 2010 and December 2020 at our tertiary referral center. In 2015, bovine pericardial patch was introduced as an alternative for polyester. The primary outcome was the occurrence of transient ischemic attack or cerebrovascular accident during follow-up and secondary outcomes included restenosis, reintervention, all-cause mortality, and patch infection. Cox proportional hazard models were utilized and hazard ratios with 95%-confidence interval were used to predict the above-mentioned outcomes. RESULTS: 417 carotid endarterectomy patients were included. 254 (61%) patients received bovine pericardial patch and 163 received (39%) polyester. The mean age was 70.2 ± 8.7 and 67% were male. The median follow-up time was 15 (12-27) months for bovine pericardial patch and 42 (16-60) months for polyester (p<0.001). Postoperative hematoma (≤30 days) was significantly lower in the bovine pericardial patch cohort (2% bovine pericardial patch vs 6% polyester; p=0.047). No other significant differences on short-term outcomes were found. Univariable cox regression analyses showed no significant differences between the effect estimates of polyester and bovine pericardial patch on transient ischemic attack or cerebrovascular accident (p=0.106), restenosis (p=0.211), reintervention (p=0.549), and all-cause mortality (p=0.158). No significant differences were found after adjusting for confounders in the multivariable analyses: transient ischemic attack or cerebrovascular accident, (p=0.939), restenosis (p=0.057), reintervention (p=0.193) and all-cause mortality (p=0.742). Three patients with a polyester patch had patch infection compared to none of the patients in the group who received a bovine pericardial patch. CONCLUSION: This large retrospective study showed comparable safety and durability of both bovine pericardial patch and polyester suggesting that both patch types can be safely applied for carotid endarterectomy with patch angioplasty. Patch infection was rare while absent in the bovine pericardial patch group

Myocardial injury after noncardiac surgery and its association with short-term mortality

Background: To identify patients at risk for postoperative myocardial injury and death, measuring cardiac troponin routinely after noncardiac surgery has been suggested. Such monitoring was implemented in our hospital. The aim of this study was to determine the predictive value of postoperative myocardial injury, as measured by troponin elevation, on 30-day mortality after noncardiac surgery. Methods and Results: This observational, single-center cohort study included 2232 consecutive intermediate- to highrisk noncardiac surgery patients aged ≥60 years who underwent surgery in 2011. Troponin was measured on the first 3 postoperative days. Log binomial regression analysis was used to estimate the association between postoperative myocardial injury (troponin I level &gt;0.06 μg/L) and all-cause 30-day mortality. Myocardial injury was found in 315 of 1627 patients in whom troponin I was measured (19%). All-cause death occurred in 56 patients (3%). The relative risk of a minor increase in troponin (0.07-0.59 μg/L) was 2.4 (95% confidence interval, 1.3-4.2; P&lt;0.01), and the relative risk of a 10- to 100-fold increase in troponin (≥0.60 μg/L) was 4.2 (95% confidence interval, 2.1-8.6; P&lt;0.01). A myocardial infarction according to the universal definition was diagnosed in 10 patients (0.6%), of whom 1 (0.06%) had ST-segment elevation myocardial infarction. Conclusions: Postoperative myocardial injury is an independent predictor of 30-day mortality after noncardiac surgery. Implementation of postoperative troponin monitoring as standard of care is feasible and may be helpful in improving the prognosis of patients undergoing noncardiac surgery.</p