Enfermedad arterial periférica en pacientes en hemodiálisis 10 años después

Background and objectivePatients with chronic kidney disease on hemodialysis present high cardiovascular comorbidity. Peripheral arterial disease (PAD) is associated with higher mortality and the interest in its early detection and treatment is increasing. The objective of this study is to determine the frequency and severity of symptomatic PAD, and to establish its relationship with mortality in hemodialysis patients that have received treated early and compare them with a cohort of our center already reported.Material and methodsRetrospective study on a cohort of incident patients since 2014 and followed up until December 2019. Demographic data, cardiovascular risk, the presence of symptomatic PAD at baseline and during follow-up were collected. Trophic lesions were graded using the Rutherford scale.ResultsInitially, there were 91 patients and 7 cases that were not included in the study were lost to follow-up. Age 64 ± 16 years, men 51.6% (47/91). The percentage of baseline PAD was 10.7% (9/84). During a median follow-up of 35 months (20–57), the diagnosis of PAD increased to 25% (21/84). Half of the patients with PAD (52.38% [11/21]) obtained a score greater than 3 in the Rutherford Clinical Classification, which corresponds to severe disease. 13/21 patients required reoperation due to recurrence of symptoms (61.9% of cases with PAD).The development of PAD was significantly associated with the presence of an elevated index of Charlson (3.9 ± 2.1 vs 7.7 ± 3.5; P = .001) with being male (19 vs 2; P = .001), diabetic (no: 7; yes: 15; P = .001) and with a history of chronic ischemic heart disease (no: 13; yes: 8; P = .001), so that 38.1% (8/21) had ischemic heart disease in patients who developed PAD, while in the absence of PAD the presence of ischemic heart disease was 9.5% (6/63). Furthermore, more than half (66.7% [14/21]) of those who developed PAD were diabetic.Univariate analysis showed that age, C reactive protein, albumin, and number of surgical interventions, but not PAD, were associated with mortality. In the multivariate analysis adjusted for other factors, only C reactive protein was related to overall survival Exp β: 2.17; P = .011; CI (1.19–3.97). Regarding cardiovascular mortality, in the multivariate Cox analysis, only PAD was related to mortality of cardiovascular origin Exp β: 1.73; P = .006; CI (1.17–2.56).ConclusionsA significant number of patients on hemodialysis develop PAD requiring peripheral vascular surgery. PAD was not associated with overall mortality in our cohort, but it did show an association with cardiovascular mortality. Prospective studies with a larger sample size are necessary. New surgical treatments and follow-up by vascular surgeons could improve the severity of PAD and the long-term prognosis.     

Low ankle-brachial index predicts early risk of recurrent stroke in patients with acute cerebral ischemia

ObjectiveLow Ankle-Brachial Blood Pressure Index (ABI) identifies patients with symptomatic and asymptomatic peripheral arterial disease (PAD). We sought to investigate the association of low ABI with early risk of stroke recurrence in patients with acute cerebral ischemia (ACI) and without history of symptomatic PAD.MethodsConsecutive patients with acute ischemic stroke (AIS) or transient ischemic attack (TIA) and no previous history of PAD were prospectively evaluated with ABI measurements. Demographic characteristics, vascular risk factors and secondary prevention therapies were documented. An ABI ≤0.90 in either leg was considered as evidence of asymptomatic PAD, and an ABI >0.90 was considered as normal. Patients with elevated ABI (>1.30) were excluded. The outcome of interest was recurrent stroke during 30-day follow-up.ResultsA total of 176 patients with acute cerebral ischemia (mean age 64 ± 14 years, 59.1% men, 76.7% AIS) were evaluated. Asymptomatic PAD was detected in 14.8% (95%CI: 10.2–20.8%) of the studied population. The following factors were independently associated with low ABI on multivariate logistic regression models, after adjustment for potential confounders: coronary artery disease (p = 0.008), diabetes mellitus (p = 0.017) and increasing age (p = 0.042). The cumulative 30-day recurrence rate was higher in patients with low ABI (19.2%; 95%CI: 4.1–34.3) compared to the rest (3.3%; 95%CI: 0.4–6.2%; p = 0.001). Atherothrombotic stroke (ASCO grade I; p < 0.001), increasing age (p = 0.002) and low ABI (p = 0.004) were independent predictors of stroke recurrence on multivariate Cox regression models adjusting for confounders.ConclusionsLow ABI appears to be associated with a higher risk of early recurrent stroke in patients with ACI and no history of symptomatic PAD.     

Variation in PCSK9, low LDL cholesterol, and risk of peripheral arterial disease

BackgroundWe hypothesized that variants in PCSK9 that lower LDL cholesterol levels are associated with reduced prevalence and incidence of peripheral artery disease (PAD).MethodsThe Atherosclerosis Risk in Communities (ARIC) Study assessed risk factors and PCSK9 variants Y142X and C679X (relevant to blacks) and R46L (relevant to whites) in a cohort of 45–64-year olds in 1987–1989 (n = 13,634). Prevalent PAD (n = 619 cases) was defined by an ankle-brachial index <0.9 or a history of leg claudication. Incident PAD (n = 895) was identified from 1987 to 1998 by the same PAD criteria or a PAD hospitalization.ResultsAs expected, greater LDL cholesterol was a risk factor for prevalent and incident PAD. 2.4% of blacks and 3.1% of whites were carriers of one of the race-specific PCSK9 variants. Carriers had lower prevalence of PAD compared with non-carriers (2.3% vs. 4.6%). The corresponding age- and sex-adjusted odds ratio of PAD was 0.47 (95% confidence interval, 0.24–0.92). In contrast with the cross-sectional findings, there was no association between PCSK9 variants and incident PAD (age- and sex-adjusted hazard ratio, 1.09 (95% confidence interval, 0.76–1.57)).ConclusionsOur study provides mixed evidence that variation in PCSK9 may contribute to genetic risk of PAD.     

Diferencias en mortalidad intrahospitalaria tras IAMCEST frente a IAMSEST por sexo. Tendencia durante once años en el Sistema Nacional de Salud

Introduction and objectivesConflicting results have been reported on the possible existence of sex differences in mortality after myocardial infarction (MI). There is also a scarcity of data on the impact of sex on outcomes after ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI). The aim of this study was to analyze sex difference trends in sex-related differences in mortality for STEMI and NSTEMI.MethodsA retrospective analysis of 445 145 episodes of MI (2005-2015) was carried out using information from the Spanish National Health System. The incidence rates were expressed as events per 10 000 person-years. The denominators (age-specific groups) were obtained from the nationwide census. We calculated crude and adjusted (multilevel logistic regression) mortality. Poisson regression analysis was used to study temporal trends for in-hospital mortality.ResultsA total of 69.8% episodes occurred in men. The mean age in men was 66.1 ± 13.3 years, which was significantly younger than in women, 74.9 ± 12.1 (P < .001). A total of 272 407 (61.2%) episodes were STEMI, and 172 738 (38.8%) were NSTEMI. Women accounted for 28.8% of STEMI and 33.9% of NSTEMI episodes (P < .001). The effect of female sex on risk-adjusted models for in-hospital mortality was the opposite in STEMI (OR for women, 1.18; 95%CI, 1.14-1.22; P < .001) and NSTEMI (OR for women, 0.85; 95%CI, 0.81-0.89; P < .001). MI hospitalization rates were higher in men than in women for all age groups [20 vs 7.7 per 10 000 individuals aged 35-94 years (P < .001)], with a trend to diminish in both sexes.ConclusionsWomen had a slight but significantly increased risk of in-hospital mortality after MI, but the effect of sex depended on MI type, with women exhibiting higher mortality for STEMI and lower mortality for NSTEMI     

Percutaneous Implantation of an Intraventricular Device for the Treatment of Heart Failure: Experimental Results and Proof of Concept

BackgroundA percutaneous system to implant a ventricular partitioning device (VPD) has been developed to partition the left ventricular (LV) cavity for treating regional wall motion abnormalities associated with post-left anterior descending (LAD) infarction, dilated left ventricle, and systolic dysfunction. The hemodynamic effects of this novel approach were evaluated in an ovine model with an anteroapical infarction created by a coil placed in the LAD.Methods and ResultsLV anteroapical infarction (MI) was induced in 10 animals. The VPD device was implanted at 6 weeks after MI in 5 animals. The hemodynamic status of each animal was evaluated at 30 weeks post-MI in treated (“VPD + MI” group, n = 5) and nontreated (“MI” group, n = 5). The comparison of end-point hemodynamic variables shows a significantly smaller end-systolic LV volume in the animals receiving the implant (70.1 ± 9.0 mL in “VPD + MI” group vs. 102.9 ± 10.3 mL in “MI” group, P < .02), improved ejection fraction (46.9 ± 5.2% in “VPD + MI” group vs. 34.7 ± 6.8% in “MI” group, P < .04) and preserved cardiac output (5.2 ± 0.7 L/min in “VPD + MI” group vs. 5.0 ± 1.8 L/min in “MI” group, P = NS), suggesting more efficient mechanical performance of the LV with the implanted VPD.ConclusionsA significant reduction in LV volumes and corresponding improvement in LV function occurred after device implantation indicating a potential beneficial effect of this new device in treatment of post MI LV dilation.     

Knowledge of cardiovascular risk factors and awareness of non-pharmacological approach for risk prevention in young survivors of acute myocardial infarction. The cardiovascular risk prevention project "Help Your Heart Stay Young"

Background and aimsKnowledge of cardiovascular disease (CVD) risk factors in young patients who experienced myocardial infarction (MI) is poorly described.Methods and resultsKnowledge of traditional CVD risk factors, non-fatal cardiovascular events and of non-pharmacological factors able to reduce CVD risk and education level were evaluated by questionnaires in subjects who visited their family doctors. Sixty-one participants with history of MI in age <50 years (MI+) were compared with 3749 subjects with age <50 years, from the same population source, but without history of MI (MI−). MI+ were more frequently men (p < 0.01), did not have significantly higher prevalences of family history of CVD, diabetes and hypertension. MI+ individuals reported previous non-fatal stroke (13% vs. 0.5%, p < 0.001), overweight, diabetes, and hypercholesterolemia (all p < 0.001) more frequently than controls, whereas prevalence of arterial hypertension, smoking habit and physical inactivity did not differ between the two groups; MI+ and MI− individuals did not differ in terms of the proportion of those who were unaware of being hypertensive, diabetic or hypercholesterolemic. MI+ participants reported more frequently lower education level than controls (p < 0.05). Knowledge of non-pharmacological approach for CVD risk reduction was similar in MI+ and MI−. In a logistic multivariate analysis, male gender (adjusted odds ratio = 5.8) and high cholesterol level (adjusted odds ratio 2.8, both p < 0.01) were independent correlates of MI+. CVD risk factors distribution was similar between participants with juvenile MI+ and MI in age ≥50 years (n = 167) extracted from the same population source; however, stroke was reported more frequently in juvenile MI+ than in those who had MI at age ≥50 years/old (13% vs. 4%, p < 0.01).ConclusionsJuvenile non-fatal MI was associated with metabolic CVD risk factors, with higher cerebrovascular co-morbidity and lower education level.     

Associations of symptomatic or asymptomatic peripheral arterial disease with all-cause mortality and cardiovascular mortality

BackgroundTo investigate the rate of all cause and cardiovascular mortality in patients with symptomatic or asymptomatic peripheral arterial disease (PAD) compared to those without PAD.Methods and resultsAll the subjects were inpatients at high risk of atherosclerosis and enrolled from February to November, 2006. A total of 320 were followed up until an end-point (death) was reached or until February 2010. The mean follow-up time was 37.7 ± 1.5 months. Compared with non-PAD, PAD patients had significantly higher rates of hypertension, diabetes mellitus, and smoking (P < 0.01). Those with symptomatic and asymptomatic PAD had a much higher all cause (37.5% and 23.0% vs. 12.1%) and cardiovascular mortality (18.8% and 13.8% vs. 6.7%) compared to those without PAD (P < 0.001). The symptomatic PAD patients were 1.831 times (95% CI: 1.222–2.741) as likely to die as those without PAD, and 1.646 times (95% CI: 1.301–2.083) in asymptomatic PAD patients after adjusting for other factors. Those with symptomatic or asymptomatic PAD were more than twice as likely to die of CVD as those without PAD (RR: 2.248, 95% CI: 1.366–3.698 and RR: 2.105, 95% CI: 1.566–2.831, respectively).ConclusionsPAD was associated with a higher all cause and cardiovascular mortality whether or not PAD is symptomatic.     

Glycated apolipoprotein B and myocardial infarction

AimsTo evaluate the association of serum concentrations of glycated apolipoprotein B (ApoBg) with the incidence of myocardial infarction (MI) in subjects with and without diabetes.MethodsThe design is a nested case-control study. The cohort included 5632 subjects over 50 years of age attending the clinical laboratories of a small geographic area in southern Italy. After five years, 4563 subjects were traced and 103 had developed MI. We sampled from the cohort two controls for each incident case of MI, frequency matched for sex and diabetes. ApoBg was measured using a monoclonal antibody. Logistic regression was used for statistical analysis of the data.ResultsApoBg at baseline was higher in subjects who developed myocardial infarction than in controls in both non-diabetic and diabetic subjects (t test, P = 0.009 and P = 0.05 respectively). MI odds ratio in the third tertile of ApoBg was 2.01 (95 % CI 0.93–4.33) in non-diabetic and 2.88 (0.85–9.68) in diabetic subjects (chi-square test for trend; non-diabetics P = 0.03, diabetics P = 0.06). Serum triglycerides, cholesterol, HDL and LDL cholesterol, glucose and insulin were not associated with MI (P > 0.10).ConclusionApoBg at baseline is directly associated with the development of MI in the following five years in both diabetic and non-diabetic individuals.     

Long-term outcomes after medical and interventional therapy of critical limb ischemia

BackgroundRecommendations of clinical guidelines for the treatment of critical limb ischemia (CLI) are based on randomized controlled trials. Recent data from clinical practice are however lacking. Therefore a prospective observational study in patients with critical limb ischemia (CLI) in 3 hospitals with a specialized vascular medicine department was conducted to document the clinical course and outcome of patients with critical limb ischemia (CLI) in clinical practice.Methods155 patients were stratified: 56 received endovascular intervention, 82 prostanoids and 17 antibiotic treatment. Patients with surgical revascularisation and primary amputation were excluded. All patients received structured wound treatment, analgesia and vascular risk factor treatment during hospital stay.ResultsAge 72.0 ± 12.7 years, hospitalisation 23.2 ± 20.3 days. 56.1% had Diabetes, 9.7% multiresistant staphylococcus aureus infection. 40% patients had rest pain, 60% ischemic tissue loss. At discharge 40.0% had no ulcers, 48.4% ongoing trophic alterations, 10.3% received major amputation and 4.5% had stable necrosis. After 18 month rate of major amputation was 6.3% (prostanoids), 14.5% (endovascular treatment; p = n.s. vs. prostanoids) and 26.7% (antibiotics; p = 0.0323 vs. prostanoids). Major amputations were not different in logistic regression analyses adjusting for baseline characteristics. Wound healing and mortality rate was not different between groups (26.8, 25.0 and 23.5%).ConclusionStructured therapy at specialized vascular centres in combination with interventional or conservative treatment is beneficial in patients with critical limb ischemia. Survival without amputation is higher than expected over 18 months.     

Toe Amputation: A predictor of future limb loss?

BackgroundDigital toe amputation is a relatively minor surgical procedure but there is a historical view that it is the “first stage in a predictable clinical course” leading to eventual limb loss. There is a paucity of contemporaneous data on the long-term outcomes of patients undergoing toe amputation. We aim to study the experience from our institution, focussing on the risk factors for progression to future limb loss, by conducting a retrospective review of our practice.MethodsSixty-three patients undergoing toe amputation within our institution were identified and the clinical notes retrospectively reviewed. A database of vascular risk factors and co-morbidity was constructed and correlation with future limb loss was analysed with Chi-squared testing and a logistic regression model.ResultsSixty-three patients with a mean age of 69 (IQR 62–76.5) years were identified. Thirty-five (55.6%) of these patients went on to have a further surgical amputation; 22 major amputations (16 below-knee and 6 above-knee amputations) and 23 minor amputations were performed in total. Forty three (68.3%) patients had diabetes and 31 (49.2%) patients had one or more revascularisation procedures undertaken. There was a significant correlation between patients who did not have diabetes and future limb loss (Chi-squared = 4.31, p = 0.038), however no other identified risk factor predicted the need for major amputation.ConclusionToe amputation is a significant predictor of future limb loss. Our study identified that patients with diabetes are significantly less likely to progress to further limb loss than those with the disease. We hypothesise that this difference is due to the more intensive, multi-disciplinary foot care follow-up that diabetic patients receive. These results highlight the significance of toe amputation and contribute to the evidence for a more intensive out-patient service for these high risk patients.     

YKL-40 is elevated in patients with peripheral arterial disease and diabetes or pre-diabetes

ObjectiveYKL-40 is secreted by macrophages in atherosclerotic lesions and involved in plaque rupture. YKL-40 is elevated in coronary artery disease, and predicts cardiovascular mortality. Experimental in vivo and in vitro data suggest a role of YKL-40 in tissue remodeling. A disease modulating potency of YKL-40 was not investigated in peripheral arterial disease (PAD).MethodsWe measured YKL-40 in 460 subjects: 316 PAD: 71 normal glucose metabolism (PAD-NGM), 90 pre-diabetes (PAD-PREDM) and 155 diabetes (PAD-DM); 20 diabetes with atherosclerosis but without PAD (AS-DM); 85 diabetes without macro-vascular complications (DM) and 39 healthy controls (CO).ResultsYKL-40 is higher in PAD vs. CO (median [25–75 percentile]: 103 [69–159] vs. 43 [30–80] ng/ml; p < 0.001). In addition, YKL-40 is elevated in DM (p < 0.001), PAD-NGM (p = 0.001), PAD-PREDM (p < 0.001), PAD-DM (p < 0.001) and AS-DM (p = 0.002) compared to CO. Among PAD, YKL-40 is increased in PAD-PREDM (p = 0.001) and PAD-DM (p = 0.01) vs. PAD-NGM. By multivariate regression YKL-40 is significantly associated with age (beta = 0.272), triglycerides (beta = 0.216), aspartate-amino-transferase (beta = 0.177) and c-reactive-protein (beta = 0.178). Underpinning its role YKL-40 was found to be associated with micro-/macroalbuminuria (p = 0.014/p = 008) – a strong remodeling inducer. In addition, YKL-40 was elevated in existence of mediasclerosis (p = 0.008), a remodeling process.ConclusionWe are first to show that YKL-40 is higher in subjects with peripheral arterial disease. YKL-40 was higher in PAD patients with pre-/diabetes. In addition, YKL-40 was associated with the “severity” of generalized atherosclerosis estimated by affected vascular beds. All our findings point towards a role of YKL-40 in the progression/prognosis of patients with PAD and concomitant diabetes.     

Interventions to increase osteoporosis treatment in patients with 'incidentally' detected vertebral fractures

BackgroundMost vertebral compression fractures are not recognized or treated. We conducted a controlled trial in older patients with vertebral fractures incidentally reported on chest radiographs, comparing usual care with osteoporosis interventions directed at physicians (opinion-leader-endorsed evidence summaries and reminders) or physicians+patients (adding activation with leaflets and telephone counseling).MethodsPatients aged >60 years who were discharged home from emergency departments and who had vertebral fractures reported but were not treated for osteoporosis were allocated to usual care (control) or physician intervention using alternate-week time series. After 3 months, untreated controls were re-allocated to physician+patient intervention. Allocation was concealed, outcomes ascertainment blinded, and analyses intent-to-treat. Primary outcome was starting osteoporosis treatment within 3 months.ResultsThere were 1315 consecutive patients screened, and 240 allocated to control (n = 123) or physician intervention (n = 117). Groups were similar at baseline (average age 74 years, 45% female, 58% previous fractures). Compared with controls, physician interventions significantly (all P <.001) increased osteoporosis treatment (20 [17%] vs 2 [2%]), bone mineral density testing (51 [44%] vs 5 [4%]), and bone mineral density testing or treatment (57 [49%] vs 7 [6%]). Three months after controls were re-allocated to physician+patient interventions, 22% had started treatment and 65% had bone mineral density testing or treatment (P <.001 vs controls). Physician+patient interventions increased bone mineral density testing or treatment an additional 16% compared with physician interventions (P = .01).ConclusionsAn opinion-leader-based intervention targeting physicians substantially improved rates of bone mineral density testing and osteoporosis treatment in patients with incidental vertebral fractures, compared with usual care. Even better osteoporosis management was achieved by adding patient activation to physician interventions [NCT00388908].     

Triple nutrient supplementation improves survival, infarct size and cardiac function following myocardial infarction in rats

Background and aimWe evaluated the impact of triple nutrient supplementation (TNS: carnitine, taurine and coenzyme Q₁₀) vs. carnitine alone (CARN) or placebo on survival, infarct size, cardiac function and metabolic gene expression using a model of myocardial infarction (MI) in rats.Methods and resultsMale Wistar rats were randomized to three groups divided in two independent studies prior to ligation of the left anterior descending coronary artery (LAD): TNS vs. Placebo and TNS vs. CARN. Nutrient supplementation [l-carnitine (300 mg/day), coenzyme Q₁₀ (15 mg/kg body weight/day) and taurine (0.1 M)] was administered daily for four weeks prior to and for 10 days after MI. At that time, cardiac function and infarct size were measured. Metabolic gene (mRNA) expression in the peri-infarct tissue of left ventricle from TNS, placebo or corresponding time-control rats (TNS or placebo without LAD ligation) was measured 10 days after MI.When compared to placebo, TNS significantly improved survival (60% vs. 34%, p < 0.02), cardiac function, and reduced infarct size (30 ± 7% vs. 42 ± 9%, p < 0.001). Although CARN improved survival like TNS (45% vs. 50%, not significant), it did not reduce infarct size (32 ± 14% vs. 19 ± 10%, p < 0.05) or delay myocardial remodeling. In the placebo group, MI was associated with a significantly altered pattern of metabolic gene expression (glucose transporter 1, liver carnitine palmitoyl transferase 1, medium-chain acyl-CoA dehydrogenase; p < 0.01 for all three) in the left ventricle peri-infarct tissue. In contrast, gene expression was normalized in the group receiving TNS.ConclusionsOur results support the potential cardioprotective impact of TNS during myocardial ischemia. In contrast to carnitine supplementation alone, TNS improved survival as well as cardiac function, gene expression and delayed remodeling.     

Homocysteine is a determinant of ApoA-I and both are associated with ankle brachial index, in an ambulatory elderly population

ObjectiveThe ankle brachial index (ABI) is an indicator of lower extremity peripheral arterial disease (PAD) and a predictor of atherothrombosis. ApoA-I and HDL are associated with PAD, in humans. Homocysteine influences the liver expression of ApoA-I and decreases its blood level and HDL in genetic mice models. We aimed therefore to evaluate whether homocysteine and its nutritional determinants, folate and vitamin B12 are associated with ABI by influencing HDL metabolism, in an ambulatory elderly population.Methods667 elderly volunteers from rural Sicily were assessed for ABI, homocysteine and its determinants, lipid markers and other predictors of PAD. HDL size was assessed in 15 sera in upper and lower quartiles of Hcy distribution.ResultsIn multivariate analysis, ApoA-I and homocysteine were two predictors of ABI (β-coefficient = 2.86, P < 0.004 and β-coefficient = ?3.41, P < 0.001, respectively). Homocysteine correlated negatively with ApoA-I (R = ?0.147, P < 0.001) and with HDL-Cholesterol (R = ?0.113, P = 0.003). The associations of homocysteine, vitamin B12 and methylmalonic acid with ApoA-I and HDL2a particles and that of homocysteine with increased small size HDL3c suggested mechanisms related with impaired synthesis of ApoA-I and HDL and abnormal maturation of HDL particles.ConclusionThe influence of homocysteine on ApoA-I and HDL metabolism provides new insights on its role on vascular diseases, at a cross-point between atherosclerosis and atherothrombosis.     

The association of tooth scaling and decreased cardiovascular disease: a nationwide population-based study

ObjectivePoor oral hygiene has been associated with an increased risk for cardiovascular disease. However, the association between preventive dentistry and cardiovascular risk reduction has remained undetermined. The aim of this study is to investigate the association between tooth scaling and the risk of cardiovascular events by using a nationwide, population-based study and a prospective cohort design.MethodsOur analyses were conducted using information from a random sample of 1 million persons enrolled in the nationally representative Taiwan National Health Insurance Research Database. Exposed individuals consisted of all subjects who were aged ≥ 50 years and who received at least 1 tooth scaling in 2000. The comparison group of non-exposed persons consisted of persons who did not undergo tooth scaling and were matched to exposed individuals using propensity score matching by the time of enrollment, age, gender, history of coronary artery disease, diabetes, hypertension, and hyperlipidemia.ResultsDuring an average follow-up period of 7 years, 10,887 subjects who had ever received tooth scaling (exposed group) and 10,989 age-, gender-, and comorbidity-matched subjects who had not received tooth scaling (non-exposed group) were enrolled. The exposed group had a lower incidence of acute myocardial infarction (1.6% vs 2.2%, P < .001), stroke (8.9% vs 10%, P = .03), and total cardiovascular events (10% vs 11.6%, P < .001) when compared with the non-exposed group. After multivariate analysis, tooth scaling was an independent factor associated with less risk of developing future myocardial infarction (hazard ratio [HR], 0.69; 95% confidence interval [CI], 0.57-0.85), stroke (HR, 0.85; 95% CI, 0.78-0.93), and total cardiovascular events (HR, 0.84; 95% CI, 0.77-0.91). Furthermore, when compared with the non-exposed group, increasing frequency of tooth scaling correlated with a higher risk reduction of acute myocardial infarction, stroke, and total cardiovascular events (P for trend < .001).ConclusionTooth scaling was associated with a decreased risk for future cardiovascular events.     

Dietary fatty acids and peripheral artery disease in adults

BackgroundPeripheral artery disease (PAD) is a debilitating condition involving atherosclerosis. Although saturated, monounsaturated and polyunsaturated fatty acids have strong associations with atherosclerosis, it is unclear if diets high in these fatty acids affect PAD.MethodsWe studied 6352 adults aged 40 years and older who participated in the U.S. National Health and Nutrition Examination Survey between 1999 and 2004. Ankle brachial index (ABI) was assessed by standardized blood pressure measurements, and we defined PAD as an ABI < 0.9. Fatty acid intake was assessed by validated 24-h dietary recall. We used multivariable linear and logistic regression to estimate associations between intakes of dietary saturated fatty acids (SFAs), monounsaturated fatty acids (MFAs), marine omega-3 fatty acids (N-3), linolenic acid (LNA), and omega-6 fatty acids (N-6) and ABI/PAD.ResultsThe prevalence and 95% confidence interval (CI) of PAD was 5.2% (95% CI 4.6–5.8).There were no associations between ABI and intakes of marine N-3 (p = 0.83) or N-6 (p = 0.19) in adjusted models. In contrast, LNA was associated with higher ABI (p = 0.04) and SFA tended to be associated with lower ABI (p = 0.06) in adjusted models. In addition, higher SFA was associated with a higher prevalence of PAD: adjusted odds ratio 1.30 (95% CI 1.01–1.67; p = 0.04) and a trend toward slower gait speed (p = 0.08).ConclusionIn this nationally representative sample, higher dietary intakes of LNA and SFAs were associated with higher and lower ABI, respectively. Prospective studies are needed to confirm the potential protective effects of dietary LNA and detrimental effects of dietary SFAs on PAD.     

Serum albumin as a determinant of cortisol release in patients with acute ischemic stroke

ObjectiveAnimal studies demonstrated that protein malnutrition increases pituitary-adrenorcortical activity and leads to excessive cortisol release. The aim of our study was to determine the association between serum albumin and cortisol level in patients with acute ischemic stroke.MethodsFifty-nine patients with first-ever ischemic stroke were included. Serum albumin level was measured within 36 h after stroke symptoms onset. Serum cortisol was measured between 36 and 72 h after stroke onset at 6 a.m., 10 a.m., 6 p.m. and 10 p.m.ResultsThe patients in upper tertile of serum albumin had significantly lower cortisol level measured at 6 a.m. (median with interquartiles: 549.0 [430.4–667.7] nmol/L vs 590.4 [482.8–918.7] nmol/L, P = 0.047) and 10 a.m. (402.8 [344.9–510.4] nmol/L vs 634.6 [482.8–827.7] nmol/L, P < 0.01) than patients in lower and middle tertiles. On logistic regression analysis adjusted for age and stroke severity, patients in lower and middle tertile of serum albumin had about 7-times higher risk of hypercortisolemia than patients in upper tertile (P < 0.01).ConclusionsLow serum albumin level in patients with ischemic stroke is associated with higher serum cortisol level and predisposes to hypercortisolemia.     

Altered monocyte CD44 expression in peripheral arterial disease is corrected by fish oil supplementation

Background and aimsCD44 and its splice variants can be expressed on all leukocytes, conferring adhesive properties and enhancing cellular recruitment to the endothelium during inflammation. CD44 expression is increased in inflammatory conditions such as rheumatoid arthritis and CD44 variant 3 (CD44v3) expression may be associated with inflammation. We have examined CD44 and CD44v3 expression on peripheral blood monocytes from patients with peripheral arterial disease (PAD) and healthy controls. We have also examined the effect of fish oil supplementation on these markers.Methods and resultsCD44 and CD44v3 were assessed at baseline and following dietary supplementation with fish oil for 12 weeks in both PAD and control groups. Monocytes from PAD patients had higher CD44 expression than those from controls (median intensity fluorescence (MIF): 480 ± 278 vs 336 ± 251 (mean ± SD); p < 0.001). Following 12 weeks dietary supplementation with fish oil, CD44 expression was reduced in PAD patients (MIF: 480 ± 278 vs 427 ± 262; p = 0.05) but not in controls (336 ± 251 vs 355 ± 280; ns). Monocyte CD44v3 expression was lower in cultured monocytes from PAD patients compared to those from controls (0.15 ± 0.15 vs 0.22 ± 0.14 OD units; p < 0.02). This was increased in the PAD group following fish oil supplementation (0.15 ± 0.14 to 0.27 ± 0.23 OD units; p < 0.001).ConclusionMonocyte CD44 and CD44v3 expression are altered in arterial disease but are returned towards levels seen in control subjects by dietary fish oil supplementation.     

Facteurs prédictifs d’amputation après angioplastie de l’artère iliaque chez les patients avec artériopathie sévère

IntroductionDespite the success of angioplasty of the iliac artery, this technique remains associated with significant amputation rates. The purpose of this study was to identify predictive factors for lower limb amputation after iliac angioplasty in patients with critical ischemia.MethodsWe reported a retrospective study including patients who successfully underwent angioplasty of the iliac artery between 2014 and 2018. The primary endpoint was limb salvage at 1 month. The variables were studied in univariate and multivariate analysis.ResultsOur study included 86 patients. The median age was 57 ± 10 and the sex ratio was 4.7. Cardiovascular risk factors were represented by smoking in 14 cases (16.3%), diabetes in 25 cases (29.1%), arterial hypertension in 2 cases (2.3%) and dyslipidemia in 2 cases (2.3%). Seventy patients (81.3%) were classified as stage 4 according to the Leriche and Fontaine classification and 16 patients (18.7%) were classified as stage 3. The lesions were stenosing in 48 cases (55.8%) and occlusive in 38 cases (44.2%). These lesions were classified according to the TASC classification “Trans-Atlantic-Society-Consensus” in TASC A-B in 61 cases (70.9%) and TASC C-D in 35 cases (29.1%). Distal arteritis was found in 8 cases (9.3%). Balloon angioplasty was performed in 36 cases (41.8%) and angioplasty stenting in 50 cases (58.2%). At 1 month, the amputation rate was 9.3%. Univariate analysis showed that diabetes and smoking were the most important factors associated with amputation (respectively P = 0.007, OR = 9.31, 95% CI = [1.73–50.07] and P = 0.022; OR = 6.8; 95% CI = [1.46 to 31.61]). Multivariate analysis showed that diabetes and distal arteritis were the predictive factors for amputation (respectively P = 0.034, OR = 21.06, 95% CI = [1.25 to 354.46] and P = 0.008, OR = 11,61, 95% CI = [1.88 to 71.69]).ConclusionDiabetes and distal arteritis are the predictive factors for lower limb amputation after iliac angioplasty.     

Simplified contrast ultrasound accurately reveals muscle perfusion deficits and reflects collateralization in PAD

BackgroundSimplified contrast-enhanced ultrasound (CEUS) can be used to evaluate muscle perfusion in peripheral arterial disease (PAD). Here, we report its diagnostic accuracy for detecting symptomatic PAD. Additionally, we hypothesize that the extent of collateral formation is reflected by CEUS.MethodsUltrasound contrast agent was injected into an antecubital vein of 58 control subjects and 52 symptomatic PAD patients and its appearance in the calf muscle was evaluated. Interreader variability was tested using 118 raw data films. Arterial collateralization of PAD patients was assessed by angiographic imaging.ResultsPAD patients showed a significantly longer median time to peak intensity (TTP, 36.9 s) than control subjects (19.4 s, p < 0.001) with longer TTPs in advanced PAD stages. The area under the receiver operating characteristic curve was 0.942 and the mean TTP difference between two blinded readers was 0.28 s. A TTP cut off at 30.5 s was associated with 91% positive predictive value. PAD patients with good collateralization showed a significantly shorter TTP (34.1 s) than patients with poor collateralization (44.0 s, p = 0.008) but not a higher ankle–brachial index (ABI).ConclusionsCEUS accurately displays perfusion deficits of the calf muscle in symptomatic PAD patients. The degree of arterial collateralization is reflected by CEUS and not by ABI.