Kaido Paapstel

Association Between Fibulin-1 and Aortic Augmentation Index in Male Patients with Peripheral Arterial Disease

BACKGROUND Fibulin-1 (FBLN-1), a newly identified biomarker for vascular stiffness in type 2 diabetes, may participate in the pathophysiological processes leading to progression of arterial stiffness in atherosclerosis. In the present study, the relationship between FBLN-1 and arterial stiffness was examined in patients with atherosclerosis and in healthy subjects. METHODS Thirty-eight patients with peripheral arterial disease (PAD) (age 62.4 ± 9.0 years), 38 patients with coronary artery disease (CAD) (age 64.0 ± 9.5 years), and 30 apparently healthy controls (age 61.1 ± 6.4 years) were studied. Serum FBLN-1, oxidized low density lipoprotein (oxLDL), resistin and plasminogen activator inhibitor-1 (PAI-1) levels were measured using the enzyme linked immunosorbent assay method. The technique of applanation tonometry was used for non-invasive pulse wave analysis and pulse wave velocity assessments. RESULTS The levels of FBLN-1 (PAD = 9.4 [4.9-17.8] vs. CAD = 7.1 [4.8-11.8] vs. controls = 5.6 [4.1-8.4] μg/mL; p = .005), carotid-femoral pulse wave velocity (cf-PWV) (9.8 ± 2.2 vs. 9.5 ± 2.2 vs. 8.3 ± 2.2 m/s; p = .023) and the heart rate corrected augmentation index (AIx@75) (29.4 ± 7.2 vs. 19.2 ± 7.2 vs. 15.4 ± 7.1%; p < .001), differed among the three groups. A correlation between FBLN-1 and AIx@75 was observed only in patients with PAD (rho = 0.37, p = .021). The relationship retained statistical significance in a multiple regression model after adjustment for potential confounders. CONCLUSIONS An independent association was demonstrated between serum FBLN-1 and AIx@75 in the PAD group. Thus, the findings suggest that FBLN-1 may play a role in arterial stiffening in patients with atherosclerosis.

Metabolic factors and oxidative stress in osteoarthritis: a case–control study

Abstract Previous studies suggest that metabolic disturbances might be involved in the development of osteoarthritis (OA). Associations have been found between the individual components of metabolic syndrome (MetS) and OA. MetS has been associated with increased oxidative stress (OxS). The study aimed to clarify the role of MetS components in OA and to evaluate the levels of OxS in OA patients and in age-matched controls. Fifty-five patients with end-stage OA (age 63 ± 7 years) prior to hip or knee joint replacement surgery and 55 age-, gender- and body mass index matched controls (61 ± 8 years) were enrolled in the study. Serum levels of glucose, insulin, c-peptide, cholesterols and OxS markers were recorded. Homeostasis model assessment for insulin resistance was used as the proxy measure of insulin resistance. Radiographic severity was assessed using the Kellgren–Lawrence score. The OA patients had higher total peroxide concentration and oxidative stress index [488 (250–612) μmol/L vs. 326 (168–442) μmol/L, p = .011 and 34 (17–51) vs. 20 (11–28), p = .002, respectively] and decreased total antioxidant capacity (1.49 ± 0.27 vs. 1.66 ± 0.27 mmol trolox equivalent/L, p= .008) compared with the controls. In addition, OA group had significantly higher level of C-peptide compared with the controls [1.8 (0.94–2.47) vs. 1.3 (0.46–1.42) ng/mL, p < .001, respectively]. Furthermore, OA radiographic severity was independently associated with LDL-cholesterol (p = .007) and oxidized LDL (p = .022). This study demonstrates that end-stage OA patients have increased levels of OxS and decreased antioxidant capacity. OA is associated with impaired lipid metabolism and dysglycemia. Our results underline the importance OxS and metabolic disturbances in the pathogenesis of OA.

The acute effects of passive heat exposure on arterial stiffness, oxidative stress, and inflammation.

BACKGROUND AND OBJECTIVE The aim of the study was to determine the acute effect of passive heat exposure (PHE) on arterial stiffness, oxidative stress (OxS) and inflammatory parameters. MATERIALS AND METHODS Subjects were studied in thermoneutral conditions before and after PHE in a climatic chamber. Pulse wave analysis was used for assessment of central hemodynamic and arterial stiffness parameters. Venous blood samples were obtained to measure OxS and inflammatory parameters. RESULTS Rectal temperature increased after PHE exposure compared to baseline: 37.01°C±0.19°C and 36.4°C±0.31°C, respectively (P<0.001). There was a 17% (P<0.05) decrease in large artery elasticity index (from 24.68±5.53 to 20.42±2.65mL/mmHg*10), which was predicted upon normothermic value (r=-0.878, P<0.01). However, no significant changes were found in others arterial stiffness parameters. A 30% (P<0.05) increase occurred in blood IL-6 concentration (from 0.43±0.15 to 0.56±0.23pg/mL), but OxS parameters remained significantly unchanged. CONCLUSIONS This study describes for the first time acute PHE effects on arterial stiffness, inflammation and OxS. PHE significantly decreases large artery elasticity index and increases inflammatory IL-6 level. However, further larger investigations are needed for clarifying acute PHE effects on arterial function and biomarkers.

Mortality After Elective and Ruptured Abdominal Aortic Aneurysm Surgical Repair: 12-Year Single-Center Experience of Estonia

Background and Aims: Abdominal aortic aneurysm is a degenerative vascular pathology with high mortality due to its rupture, which is why timely treatment is crucial. The current single-center retrospective study was undertaken to analyze short- and long-term all-cause mortality after operative treatment of abdominal aortic aneurysm and to examine the factors that influence outcome. Material and Methods: The data of all abdominal aortic aneurysm patients treated with open repair or endovascular aneurysm repair in 2004–2015 were retrospectively retrieved from the clinical database of Tartu University Hospital. The primary endpoint was 30-day, 90-day, and 5-year all-cause mortality. The secondary endpoint was determination of the risk factors for mortality. Results and Conclusion: Elective abdominal aortic aneurysm repair was performed on 228 patients (mean age 71.8 years), of whom 178 (78%) were treated with open repair and 50 (22%) with endovascular aneurysm repair. A total of 48 patients with ruptured abdominal aortic aneurysm were treated with open repair (mean age 73.8 years) at the Department of Vascular Surgery, Tartu University Hospital, Estonia. Mean follow-up period was 4.2 ± 3.3 years. In patients with elective abdominal aortic aneurysm, 30-day, 90-day, and 5-year all-cause mortality rates were 0.9%, 2.6%, and 32%, respectively. In multivariate analysis, the main predictors for 5-year mortality were preoperative creatinine value and age (p < 0.05). In patients with ruptured abdominal aortic aneurysm, 30-day, 90-day, and 5-year all-cause mortality rates were 22.9%, 33.3%, and 55.1%, respectively. In multivariate analysis, the risk factors for 30-day mortality in ruptured abdominal aortic aneurysm were perioperative hemoglobin and lactate levels (p < 0.05). According to this study, the all-cause mortality rates of elective abdominal aortic aneurysm and ruptured abdominal aortic aneurysm at our hospital were comparable to those at other centers worldwide. Even though some variables were identified as potential predictors of survival, the mortality rates after ruptured abdominal aortic aneurysm remain high. Early diagnosis, timely treatment, and detection of the risk factors for abdominal aortic aneurysm progression would improve survival in patients with abdominal aortic aneurysm.

Heart rate reduction decreases central blood pressure in sick sinus syndrome patients with a permanent cardiac pacemaker

Increased resting heart rate (HR) contributes to higher cardiovascular mortality and morbidity in the healthy as well as in people with cardiovascular diseases, possibly due to elevated blood pressure (BP) among other mechanisms. Data on the relationship between HR and central (aortic) BP remains controversial, however, and concerning β-blockers, it has been proposed that pharmacological HR lowering is associated with augmentation of central BP. We aimed to study the role of pharmacologically unaffected HR on central BP indices in sick sinus syndrome patients with a permanent cardiac pacemaker in the HR range from 40 to 90 bpm. We included 27 subjects (mean age 65.8 ± 9.5 years, 12 men) with a dual-chamber pacemaker implanted due to sick sinus syndrome. We determined central hemodynamic indices noninvasively during an atrial pacing mode at low (40 bpm), middle (60 bpm), and high (90 bpm) HR levels with an oscillometric cuff-based device (Sphygmocor XCEL). There was no difference in central systolic BP at the middle versus the high HR level (mean 121.2 ± 13.0 and 121.2 ± 12.1 mmHg, respectively, P = 0.9), but at the low HR level, it was significantly lower than at the middle HR level (mean 117.2 ± 13.1 and 121.2 ± 13.0 mmHg, P < 0.01). Our acute study provides evidence to suggest that at a HR of <60 bpm, sick sinus syndrome patients may have a lower central BP than at a higher HR, despite the proposed augmenting effects of low HR on central BP.