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Background: Transcatheter aortic valve replacement (TAVR) is associated with procedural-related neurological events and acute cognitive decline. However, data on the effect of TAVR on mid-term cognitive outcome are scarce. Therefore, we aimed to assess the impact of TAVR on mid-term cognitive outcome using different neurocognitive test batteries.Methods: Patients with severe aortic valve stenosis scheduled for TAVR were enrolled. Cognitive assessment was performed at baseline and 4 months post-TAVR using an eight-word verbal-learning test ("Immediate Recall Memory Test" [IRMT], "Delayed Recall Memory Test" [DRMT], "Recognition of Verbal Information Test" [RVIT]), global cognitive function ("Mini Mental State Examination" [MMSE]), and executive function ("Trail Making Test" [TMT], "Clock-Drawing Test" [CDT]).Results: A total of 30 patients (age: 81±6years, logistic EuroSCORE: 19±10%) completed the follow-up cognitive assessments. Postoperatively, 17% (n=5) developed delirium, 13% (n=4) received permanent pacemaker, and there were no cerebrovascular events. Mean hospital duration time was 5±2 days. Patients (n=22) who did not complete the follow-up cognitive assessments had comparable baseline, procedural and hospital outcome. At follow-up there was a significant improvement in IRMT (27±5 vs. 30±4, p=0.016), with a trend toward improved DRMT (4±2 vs. 5±2, p=0.079). Moreover, patients with lower baseline MMSE and IRMT improved significantly during the follow-up.Conclusions: Transcatheter aortic valve replacement was associated with an improved IRMT during follow-up. Both MMSE and IRMT were significantly improved among those with lower baseline scores. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate the incidence of in‐hospital postoperative delirium (IHPOD) after transcatheter aortic valve replacement (TAVR). Design: Systematic review and meta‐analysis. Setting: Elective procedures Participants: Individuals undergoing TAVR. Measurements: A literature search was conducted in PubMed, Embase, BioMedCentral, Google Scholar, and the Cochrane Central Register of Controlled Trials (up to December 2017). All observational studies reporting the incidence of IHPOD after TAVR (sample size > 25) were included in our meta‐analysis. The reported incidence rates were weighted to obtain a pooled estimate rate with 95% confidence interval (CI). Results: Of 96 potentially relevant articles, 31 with a total of 32,389 individuals who underwent TAVR were included in the meta‐analysis. The crude incidence of IHPOD after TAVR ranged from 0% to 44.6% in included studies, with a pooled estimate rate of 8.1% (95% CI=6.7–9.4%); heterogeneity was high (Q = 449; I = 93%; pheterogeneity < .001). The pooled estimate rate of IHPOD was 7.2% (95% CI=5.4–9.1%) after transfemoral (TF) TAVR and 21.4% (95% CI=10.3–32.5%) after non‐TF TAVR. Conclusion: Delirium occurs frequently after TAVR and is more common after non‐TF than TF procedures. Recommendations are made with the aim of standardizing future research to reduce heterogeneity between studies on this important healthcare problem. J Am Geriatr Soc 66:2417–2424, 2018. [ABSTRACT FROM AUTHOR]

Background Previous reports suggest that biventricular pacing (BiVp) fused with intrinsic conduction (BiVp-fusion, triple wavefront fusion) is associated with improved resynchronization compared to pure-BiVp in cardiac resynchronization therapy (CRT). This study aimed to assess the association between acute hemodynamic benefit of CRT and signs of BiVp-fusion by using a novel electrogram (EGM)-based method. Methods In 17 patients undergoing CRT implantation, 28 combinations of atrioventricular (AV) and interventricular (VV) delays were applied while invasively measuring acute hemodynamic response based on maximum rate of left ventricular (LV) pressure rise (LV dP/dtmax) to assess optimal BiVp settings. BiVp-fusion was noted if farfield signal (caused by first intrinsic ventricular depolarization) was seen prior to right ventricular (RV) pacing (RVp) artifact on integrated bipolar RV EGM, or QRS morphology changed compared to pure-BiVp (short AV-delay) as seen on electrocardiogram (ECG). Results Mean optimal RVp timing was at 98 ± 17% of intrinsic right atrial (RA)-RVfarfield (interval from right atrial pace or sense to RV farfield signal) interval, while preactivating the LV at 50 ± 11% of RA-RVsense (interval from right atrial pace or sense to RV sense interval) interval. BiVp-fusion was noted in 16 of 17 (94%) patients on ECG during optimal BiVp. Eight of these patients showed intrinsic farfield signal prior to RVp artifact on RV EGM. In the remaining eight, the RVp was paced just within the RA-RVfarfield interval with a mean of 25 ± 14 ms prior to the onset; therefore, the intrinsic farfield was masked. Conclusion Optimal hemodynamic BiVp facilitates triple wavefront fusion, by pacing the RV around the onset of intrinsic farfield signal on RV EGM, while preactivating the LV. Aiming at BiVp-fusion could be a target for noninvasive EGM-based CRT device setting optimization. [ABSTRACT FROM AUTHOR]

Cardiac cell therapy suffers from limitations related to poor engraftment and significant cell death after transplantation. In this regard, ex vivo tissue engineering is a tool that has been demonstrated to increase cell retention and survival. The aim of our study was to evaluate the therapeutic potential of a 3D-printed patch composed of human cardiac-derived progenitor cells (hCMPCs) in a hyaluronic acid/gelatin (HA/gel) based matrix. hCMPCs were printed in the HA/gel matrix (30 × 10 6 cells/ml) to form a biocomplex made of six perpendicularly printed layers with a surface of 2 × 2 cm and thickness of 400 μm, in which they retained their viability, proliferation and differentiation capability. The printed biocomplex was transplanted in a mouse model of myocardial infarction (MI). The application of the patch led to a significant reduction in adverse remodeling and preservation of cardiac performance as was shown by both MRI and histology. Furthermore, the matrix supported the long-term in vivo survival and engraftment of hCMPCs, which exhibited a temporal increase in cardiac and vascular differentiation markers over the course of the 4 week follow-up period. Overall, we developed an effective and translational approach to enhance hCMPC delivery and action in the heart. [ABSTRACT FROM AUTHOR]

Obesity is related to left ventricular hypertrophy (LVH). Whether LVH on electrocardiography (ECG-LVH) is a result of increased cardiac electrical activity or due to increased left ventricular mass (LVM) remains to be determined. The aims of the present study were to investigate the relation between obesity and ECG-LVH and LVM by magnetic resonance imaging (MRI-LVM) in patients with hypertension and to investigate the relation of insulin resistance (IR) and LVH. Patients with hypertension (n = 421) were evaluated using Sokolow-Lyon voltage, Cornell voltage, and cardiac magnetic resonance imaging. Waist circumference was used as a measure of abdominal obesity. Linear regression analysis revealed an inverse relation (adjusted β = −0.02, 95% confidence interval −0.02 to −0.01) between waist circumference and Sokolow-Lyon voltage, indicating a decrease of 0.02 mV per 1-cm increase in waist circumference. There was a positive relation between waist circumference and MRI-LVM (β = 0.49, 95% confidence interval 0.32 to 0.67). Patients in the highest quartile of LVM had a worse metabolic profile than patients with the Sokolow-Lyon voltage criterion. The relations of IR with ECG-LVH and MRI-LVM were similar to those of waist circumference in relation to ECG-LVH and MRI-LVM. In conclusion, there is an inverse relation between waist circumference and ECG-LVH and a positive relation between waist circumference and MRI-LVM. This study indicates that obesity has a different relation to voltage criteria for LVH compared to anatomic criteria for LVH, supporting the hypothesis that IR decreases electrocardiographic voltages, despite an increase in MRI-LVM. The clinical implication is that especially in patients with IR, Sokolow-Lyon voltage is low in contrast to high MRI-LVM. [ABSTRACT FROM AUTHOR]

Variation in the NOS3 gene has been related to the development of restenosis. The Glu298Asp polymorphism has previously been investigated for its effect on NO levels and the development of restenosis. However, the variability of findings gave rise to the hypothesis that the functional significance of this polymorphism may only become manifest under conditions of endothelial dysfunction. Since patients with the metabolic syndrome are known to have endothelial dysfunction, we aimed to investigate if the significance of NOS3 polymorphisms may depend on the presence of the metabolic syndrome. We examined the impact of the -949 A/G, the -716 C/T and the Glu298Asp polymorphisms in the NOS3 gene on the risk of clinical restenosis in a previously described subpopulation of the GENDER-study, a multicenter prospective study design that enrolled consecutive patients after successful PCI. This subpopulation consisted of 901 patients of whom sufficient data were available to establish absence or presence of the metabolic syndrome. Of these patients, 448 had the metabolic syndrome. Clinical restenosis, defined as target vessel revascularization (TVR), was the primary endpoint. We demonstrated that the minor -949G, -716T and 298Asp alleles were associated with a significantly increased risk of TVR in patients with the metabolic syndrome (HR: 1.58 [95%CI: 1.04–2.40], HR: 1.95 [95%CI: 1.02–3.70] and HR: 1.67 [95%CI: 1.09–2.54], respectively). In the group without the metabolic syndrome we observed no association between the three polymorphisms and TVR. [ABSTRACT FROM AUTHOR]

There is evidence that coronary collaterals improve the prognosis in patients with acute myocardial infarction (MI). However, there is limited clinical information on the protective role of collaterals in patients with stable coronary artery disease. This information may help risk stratification and the development of novel therapies, such as arteriogenesis and angiogenesis. The relation between collaterals and cardiac death or MI at 1 year after coronary revascularization was studied in 561 patients who were enrolled in a randomized study that compared stent implantation with bypass grafting. Collaterals were assessed on an angiogram using Rentrop’s classification and considered present with a Rentrop grade >1. Unadjusted and adjusted odds ratios for cardiac death or MI at 1 year were calculated using univariate and multivariate regression analyses. In addition, determinants of collaterals were assessed using univariate and multivariate analyses. Collaterals were present in 176 patients (31%). The adjusted odds ratio of cardiac death or infarction was 0.18 (95% confidence interval 0.04 to 0.78) in the presence of collaterals. Independent determinants of collaterals were age (odds ratio 0.97, 95% confidence interval 0.95 to 0.99), multivessel disease (odds ratio 1.60, 95% confidence interval 1.02 to 2.51), impaired ventricular function (odds ratio 1.85, 95% confidence interval 1.04 to 3.29), type C lesion (odds ratio 3.72, 95% confidence interval 2.33 to 5.95), and stenosis severity >90% (odds ratio 9.08, 95% confidence interval 4.65 to 17.73). In conclusion, in patients with a low risk profile, the presence of collaterals protects against cardiac death and MI at 1 year after coronary revascularization. Variables that reflect the duration and severity of the atherosclerotic and ischemic burden determine their presence. [Copyright &y& Elsevier]

The renin-angiotensin system (RAS) is thought to play a major role in the pathophysiology of de-novo restenotic lesions and in-stent restenosis after percutaneous coronary intervention (PCI). Heme oxygenase-1 (HO-1), is thought to beneficially influence these processes. We examined the effect of pharmacologic as well as genetic RAS interactions on restenosis in a large population of consecutive patients undergoing PCI, and evaluated possible gene-gene interactions in both systems.The GENDER project is a multicenter prospective follow-up study, including 3146 patients after successful PCI. Genotyping in these patients was performed for the ACE gene insertion/deletion, the angiotensinogen 235Met/Thr, T174M and A(-6)G, the angiotensin-II type 1 receptor (AT1R) 1166A/C and T810A, the angiotensin-II type 2 receptor (AT2R) 1675G/A and 3123A polymorphisms and the length polymorphism in the HO-1 promoter region.A total of 3104 patients were followed for 10 months. In 2975 patients at least one of the nine genotypes could be determined. The AT1R 1166 CC genotype showed a significant association with TVR; the other polymorphisms did not. RAS-inhibitory drugs were not associated with the incidence of TVR, nor did they interact with any of the investigated polymorphisms. Patients with the ACE I/I polymorphism showed a trend towards a better outcome if they had a short number of repeats in the HO-1 promoter. This relationship was inversely present in carriers of the ACE D/D polymorphism.We could only establish a role for the AT1R 1166A/C polymorphism in restenosis after PCI. However, significant gene-gene interaction was suggested for the ACE gene and the HO-1 promotor. The RAS and HO-1 relation in restenosis merits further investigation. [ABSTRACT FROM AUTHOR]

The management of a department of cardiology has to plan the capacity of both elective and non-elective patients. Heart failure (HF) patients are admitted to the hospital in a non-elective way. The precision with which the capacity needed for non-elective patients can be predicted determines the degree of flexibility in planning the admission of elective patients. In this study we want to determine how accurately we can predict the bed occupancy of HF patients using a simulation model. Data of the year 2000 were used to obtain the necessary probability distribution functions. Data from the year 2001 were used for determining the prediction accuracy. The results show that the arrival of new HF patients can be adequately predicted. However, the bed occupancy by new and especially current patients is predicted less accurately. Still in 70% (90%) of the days of a 5-day-prediction interval the error is at most one (two) bed(s). The results may improve if the cardiologist is asked to predict the length of stay of the current patients. [Copyright &y& Elsevier]