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Background and Aims: Interarm blood pressure difference (IABPD) was associated with increased cardiovascular and all-cause mortality in various cohorts previously. In this study, we planned to explore the association between the IABPD obtained with simultaneous measurements in both arms and the risk of mortality over a 2-year follow-up of patients with acute coronary syndrome (ACS)., Methods: Simultaneous blood pressure (BP) measurements were performed during initial admission in patients with ACS. Systolic ≥10 mmHg and diastolic ≥5 mmHg absolute IABPD was defined as cutoff values in this study. The relationship of IABPD and all-cause mortality was assessed using Kaplan-Meier curves and Cox analysis., Results: A total of 532 patients with ACS were included in the study. Mean age of the study participants was 60.1 ± 12.6. Patients included in the study were followed for 23.2 ± 7.2 months (median 25.3, min: 0, max: 28.7 months). Survival was assessed using Kaplan-Meier curves. Patients with systolic IABPD ≥ 10 mmHg and systolic IABPD < 10 mmHg had an average survival time of 25.94 ± 0.84 and 25.92 ± 0.38 months (P = 0.925), respectively. Survival times of diastolic IABPD ≥5 mmHg and diastolic IABPD <5 mmHg were 26.44 ± 0.62 and 25.71 ± 0.41 (P = 0.251) months, respectively., Conclusions: In the current study, we did not find a significant association between IABPD and all-cause mortality in patients with ACS in 2-years follow-up. Future studies may be required for further evaluation of the prognostic importance of IABPD in patients with ACS., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

: The mechanism of restenosis in bioresorbable vascular scaffold (BVS) may be different from that of metallic stents and it is still poorly investigated. Intravascular imaging techniques are useful tools for corroborating or excluding possible mechanisms of intra-scaffold restenosis. In these novel devices intravascular imaging should be systematically used for a better comprehension of the in-scaffold restenosis mechanism.

The clinical effect of intracoronary thrombus aspiration during percutaneous coronary intervention in patients with unstable angina pectoris is unknown. In this study, we aimed to assess how thrombus aspiration during percutaneous coronary intervention affects in-hospital and 30-month mortality and complications in patients with unstable angina pectoris.We undertook an observational cohort study of 645 consecutive unstable angina pectoris patients who had performed percutaneous coronary intervention from February 2011 to March 2013. Before intervention, 159 patients who had culprit lesion with thrombus were randomly assigned to group 1 (thrombus aspiration group) and group 2 (stand-alone percutaneous coronary intervention group). All patients were followed-up 30 months until August 2015.Thrombus aspiration was performed in 64 patients (46%) whose cardiac markers (ie, creatinine kinase [CK-MB] mass and troponin T) were significantly lower after percutaneous coronary intervention than in those of group 2 (CK-MB mass: 3.80 ± 1.11 vs 4.23 ± 0.89, P = 0.012; troponin T: 0.012 ± 0.014 vs 0.018 ± 0.008, P = 0.002). Left ventricular ejection fraction at 6, 12, and 24 months postintervention was significantly higher in the group 1. During a mean follow-up period of 28.87 ± 6.28 months, mortality rates were 6.3% in the group 1 versus 12.9% in the group 2. Thrombus aspiration was also associated with significantly less long-term mortality in unstable angina pectoris patients (adjusted HR: 4.61, 95% CI: 1.16-18.21, P = 0.029).Thrombus aspiration in the context of unstable angina pectoris is associated with a limited elevation in cardiac enzymes during intervention that minimises microembolization and significantly improves both of epicardial flow and myocardial perfusion, as shown by angiographic TIMI flow grade and frame count. Thrombus aspiration during percutaneous coronary intervention in unstable angina pectoris patients has better survival over a 30-month follow-up period.

The aim of this study is to investigate the presence of limitations in the shoulder range of motion (ROM) or the loss of upper extremity function on the affected side in patients with cardiac implantable electronic devices (CIEDs) with respect to the implantation time. Forty-nine patients (30 men and 19 women), mean age 64.84±11.18 years, who had been living with a CIED for less than 3 months were included in the short-term recipient (STR) group and 127 patients (85 men and 42 women), mean age 64.91±14.70 years, and with the device for longer than 3 months were included in the long-term recipients group. Shoulder ROMs were measured using a digital goniometer. The other arm was used as the control. The Constant-Murler Score, Shoulder Pain Disability Index, and Shoulder Disability Questionnaire were used to assess the functional status. Limitations of ROM for flexion, abduction, and internal rotation were found to be significantly lower in the arm on the side of CIED compared with the control arm. Significant differences in shoulder flexion, abduction, and external rotation in STRs were found compared with long-term recipient (P<0.05). However, the functional comparison of groups by the Constant-Murler Score was not significant. A low to moderate amount of shoulder disability measured by Shoulder Pain Disability Index and Shoulder Disability Questionnaire was found in patients with CIEDs, which was more prominent in STRs (P<0.05). Pain, association of CIED with pectoral muscles, a possible subtle ongoing capsular pathology, and avoidance behaviors of patients to minimize the risk of lead dislodgement might be related to restriction of motion and function in the shoulder joint in patients with CIEDs.

Background: Although disturbed flow is thought to play a central role in the development of advanced coronary atherosclerotic plaques, no causal relationship has been established. We evaluated whether inducing disturbed flow would cause the development of advanced coronary plaques, including thin cap fibroatheroma., Methods and Results: D374Y-PCSK9 hypercholesterolemic minipigs (n=5) were instrumented with an intracoronary shear-modifying stent (SMS). Frequency-domain optical coherence tomography was obtained at baseline, immediately poststent, 19 weeks, and 34 weeks, and used to compute shear stress metrics of disturbed flow. At 34 weeks, plaque type was assessed within serially collected histological sections and coregistered to the distribution of each shear metric. The SMS caused a flow-limiting stenosis, and blood flow exiting the SMS caused regions of increased shear stress on the outer curvature and large regions of low and multidirectional shear stress on the inner curvature of the vessel. As a result, plaque burden was ≈3-fold higher downstream of the SMS than both upstream of the SMS and in the control artery (P<0.001). Advanced plaques were also primarily observed downstream of the SMS, in locations initially exposed to both low (P<0.002) and multidirectional (P<0.002) shear stress. Thin cap fibroatheroma regions demonstrated significantly lower shear stress that persisted over the duration of the study in comparison with other plaque types (P<0.005)., Conclusions: These data support a causal role for lowered and multidirectional shear stress in the initiation of advanced coronary atherosclerotic plaques. Persistently lowered shear stress appears to be the principal flow disturbance needed for the formation of thin cap fibroatheroma., (© 2015 American Heart Association, Inc.)

The aim of this study was to evaluate and compare systolic blood pressure recovery and heart rate recovery (HRR) values obtained at various time intervals after maximal graded exercise treadmill testing between patients with metabolic syndrome (MS) and the controls without MS. To our knowledge, this is the first study indicating systolic blood pressure recovery (SBPR) impairment and its relations to HRR and other variables in this group of patients. The study population included 110 patients with MS (67 men, 43 women; mean age: 46 ± 9 years) and 110 control subjects who did not meet the criteria for MS (58 men, 52 women; mean age: 44 ± 10 years). All patients were selected from nonobese, apparently healthy sedentary individuals who had the ability to perform maximum exercise testing. SBPR was assessed by calculating the ratio of systolic blood pressure (SBP) obtained in the third minute of the recovery period to either the peak-exercise SBP or the SBP in the first minute of the recovery period after graded exercise testing. HRR values were calculated by subtracting the HR at the first, second, third, fourth, and fifth minutes of the recovery period from the HR reached at peak exercise. There was no significant difference found between the 2 groups with respect to age and sex distribution. As expected, patients with MS had higher waist circumference, fasting plasma glucose and serum triglyceride, and lower high-density lipoprotein cholesterol compared with control subjects. All HRR values calculated in the first, second, third, fourth, and fifth minutes were significantly detected lower in the MS group compared with the control group (HRR 1st: 32 ± 10 vs 36 ± 11; P = 0.009; HRR 2nd: 47 ± 10 vs 51 ± 11; P = 0.02; HRR 3rd: 53 ± 11 vs 58 ± 12; P = 0.001; HRR 4th: 57 ± 11 vs 64 ± 12; P < 0.001; HRR 5th: 60 ± 16 vs 69 ± 15; P < 0.001). In addition, calculated mean values for SBPR1 and SBPR2 were >1 in patients with MS (1.01 ± 0.2 vs 0.91 ± 0.1 and 1.01 ± 0.1 vs 0.94 ± 0.1) and these were statistically significant compared with the control group (P < 0.001 and P = 0.002, respectively). The existence of MS was found to be the only parameter that was independently and positively related to SBPR values in the study population. Our findings suggest that only the existence of MS itself, not the presence of any MS components, is independently associated with SBPRs. We are of the opinion that significantly impaired SBPR values, in addition to the decreased HRR values observed in this group of patients, such as those with MS, may especially help identify patients with potentially increased cardiovascular risk despite normal exercise stress testing findings.