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  • 1
    Online Resource
    Online Resource
    Frequent Mutation in the ABCC6 Gene (R1141X) Is Associated With a Strong Increase in the Prevalence of Coronary Artery Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Circulation Vol. 106, No. 7 ( 2002-08-13), p. 773-775
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 106, No. 7 ( 2002-08-13), p. 773-775
    Abstract: Background— Pseudoxanthoma elasticum (PXE) is an inborn disorder of the connective tissue with specific skin, ocular, and cardiovascular disease (CVD) manifestations. Recently, we and others have identified mutations in the gene coding for the ABCC6 transporter in PXE patients with ocular and skin involvement. In the Netherlands, as in the rest of Europe, a particular premature truncation variant ABCC6 (R1141X) was found in a large cohort of PXE patients. Given the association between CVD and PXE, we hypothesized that heterozygosity of this ABCC6 mutation could also confer an increased risk for CVD. Methods and Results— To assess the relationship between the frequent R1141X mutation in the ABCC6 gene and the prevalence of premature coronary artery disease (CAD), we conducted a case-control study of 441 patients under the age of 50 years who had definite CAD and 1057 age- and sex-matched population-based controls who were free of coronary disease. Strikingly, the prevalence of the R1141X mutation was 4.2 times higher among patients than among controls (3.2% versus 0.8%; P 〈 0.001). Consequently, among subjects with the R1141X mutation, the odds ratio for a coronary event was 4.23 (95% CI: 1.76 to 10.20, P = 0.001). Conclusion— The presence of the R1141X mutation in the ABCC6 gene is associated with a sharply increased risk of premature CAD.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000028420.27813.C0
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 1466401-X
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  • 2
    Online Resource
    Online Resource
    Implantable Cardioverter Defibrillator Therapy in Adults With Congenital Heart Disease : Who Is at Risk of Shocks?
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation: Arrhythmia and Electrophysiology Vol. 5, No. 1 ( 2012-02), p. 101-110
    Details
    In: Circulation: Arrhythmia and Electrophysiology, Ovid Technologies (Wolters Kluwer Health), Vol. 5, No. 1 ( 2012-02), p. 101-110
    Abstract: The value of implantable cardioverter defibrillators (ICDs) in adults with congenital heart disease (CHD) is unknown. We investigated the long-term outcome after ICD implantation and developed a simple risk stratification score for ICD therapy. Methods and Results— A total of 136 adults with CHD and ICD (mean age±SD, 41±13 years; 67% male) were identified from 10 tertiary referral centers in the Netherlands and Belgium. The indication for ICD implantation was primary prevention in 50% of patients. Diagnoses included tetralogy of Fallot (51%), septal defects (20%), (congenitally corrected) transposition of the great arteries (13%), and other (16%). Thirty-nine patients (29%) received appropriate ICD shocks during a median follow-up of 4.6 years. Secondary prevention indication (hazard ratio [HR], 3.6; 95% CI, 1.3–9.5; P= 0.009), coronary artery disease (HR, 2.7; 95% CI, 1.0–7.2; P= 0.042), and symptomatic nonsustained ventricular tachycardia (NSVT; HR, 9.1; 95% CI, 2.8–29.2; P= 0.001) were associated with appropriate ICD shocks. A risk score was developed to evaluate the likelihood of appropriate ICD shocks. The 8-year survival curve to first appropriate shocks was 94%, 57%, and 26% for low-, intermediate-, and high-risk patients, respectively. In primary prevention, symptomatic NSVTs (HR, 8.0; 95% CI, 2.3–27.1; P= 0.001) and subpulmonary ventricular dysfunction (HR, 3.0; 95% CI, 1.2–12.6; P =0.02) were associated with appropriate shocks in univariable analysis. Inappropriate shocks occurred in 41 patients (30%). In addition, 40 patients (29%) experienced 45 implantation-related complications. Conclusions— Adults with CHD and ICDs receive high rates of appropriate and effective shocks. Patients with secondary prevention indication, coronary artery disease, and symptomatic NSVT are at highest risk of receiving appropriate ICD shocks. ICD implantation is accompanied by considerable morbidity, including inappropriate shocks and procedure- related complications.
    Type of Medium: Online Resource
    ISSN: 1941-3149 , 1941-3084
    URL: Article
    DOI: 10.1161/CIRCEP.111.966754
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2425487-3
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  • 3
    Online Resource
    Online Resource
    Neurogenic Regulation of Coronary Blood Flow: Evidence for a Central Nervous System Pathway
    Ovid Technologies (Wolters Kluwer Health) ; 1987
    In:  Circulation Research Vol. 61, No. 5_supplement ( 1987-11)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 61, No. 5_supplement ( 1987-11)
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.61.5_supplement.ii-42
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1987
    detail.hit.zdb_id: 1467838-X
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  • 4
    Online Resource
    Online Resource
    Age of First Arrhythmic Event in Brugada Syndrome : Data From the SABRUS (Survey on Arrhythmic Events in Brugada Syndrome) in 678 Patients
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Circulation: Arrhythmia and Electrophysiology Vol. 10, No. 12 ( 2017-12)
    Details
    In: Circulation: Arrhythmia and Electrophysiology, Ovid Technologies (Wolters Kluwer Health), Vol. 10, No. 12 ( 2017-12)
    Abstract: Data on the age at first arrhythmic event (AE) in Brugada syndrome are from limited patient cohorts. The aim of this study is 2-fold: (1) to define the age at first AE in a large cohort of patients with Brugada syndrome, and (2) to assess the influence of the mode of AE documentation, sex, and ethnicity on the age at first AE. Methods and Results A survey of 23 centers from 10 Western and 4 Asian countries gathered data from 678 patients with Brugada syndrome (91.3% men) with first AE documented at time of aborted cardiac arrest (group A, n=426) or after prophylactic implantable cardioverter–defibrillator implantation (group B, n=252). The vast majority (94.2%) of the patients were 16 to 70 years old at the time of AE, whereas pediatric ( 〈 16 years) and elderly patients ( 〉 70 years) comprised 4.3% and 1.5%, respectively. Peak AE rate occurred between 38 and 48 years (mean, 41.9±14.8; range, 0.27–84 years). Group A patients were younger than in Group B by a mean of 6.7 years (46.1±13.2 versus 39.4±15.0 years; P 〈 0.001). In adult patients (≥16 years), women experienced AE 6.5 years later than men ( P =0.003). Whites and Asians exhibited their AE at the same median age (43 years). Conclusions SABRUS (Survey on Arrhythmic Events in Brugada Syndrome) presents the first analysis on the age distribution of AE in Brugada syndrome, suggesting 2 age cutoffs (16 and 70 years) that might be important for decision-making. It also allows gaining insights on the influence of mode of arrhythmia documentation, patient sex, and ethnic origin on the age at AE.
    Type of Medium: Online Resource
    ISSN: 1941-3149 , 1941-3084
    URL: Article
    DOI: 10.1161/CIRCEP.117.005222
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2425487-3
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  • 5
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    Online Resource
    Macrophage p53 Deficiency Leads to Enhanced Atherosclerosis in APOE*3-Leiden Transgenic Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Circulation Research Vol. 88, No. 8 ( 2001-04-27), p. 780-786
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 88, No. 8 ( 2001-04-27), p. 780-786
    Abstract: Abstract —Cell proliferation and cell death (either necrosis or apoptosis) are key processes in the progression of atherosclerosis. The tumor suppressor gene p53 is an essential gene in cell proliferation and cell death and is upregulated in human atherosclerotic plaques, both in smooth muscle cells and in macrophages. In the present study, we investigated the importance of macrophage p53 in the progression of atherosclerosis using bone marrow transplantation in APOE*3-Leiden transgenic mice, an animal model for human-like atherosclerosis. APOE*3-Leiden mice were lethally irradiated and reconstituted with bone marrow derived from either p53-deficient ( p53 −/− ) or control ( p53 +/+ ) donor mice. Reconstitution of mice with p53 −/− bone marrow did not result in any hemopoietic abnormalities as compared with p53 +/+ transplanted mice. After 12 weeks on an atherogenic diet, APOE*3-Leiden mice reconstituted with p53 −/− bone marrow showed a significant ( P =0.006) 2.3-fold increase in total atherosclerotic lesion area as compared with mice reconstituted with p53 +/+ bone marrow. Although likely a secondary effect of the increased lesion area, p53 −/− transplanted mice also showed significantly more lesion necrosis (necrotic index, 1.1±1.3 versus 0.2±0.7; P =0.04) and lesion macrophages (macrophage area, 79.9±40.0 versus 39.7±27.3×10 3 μm 2 per section; P =0.02). These observations coincided with a tendency toward decreased apoptosis (terminal deoxynucleotidyl transferase end-labeling [TUNEL]–positive nuclei going from 0.42±0.39 to 0.14±0.15%, P =0.071), whereas the number of proliferating cells (5′-bromo-2′-deoxyuridine–positive nuclei) was not affected (3.75±0.98 versus 4.77±2.30%; P =0.59). These studies indicate that macrophage p53 is important in suppressing the progression of atherosclerosis and identify a novel therapeutic target for regulating plaque stability.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/hh0801.089261
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 1467838-X
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  • 6
    Online Resource
    Online Resource
    Reactive Oxygen Species–Induced Stimulation of 5′AMP-Activated Protein Kinase Mediates Sevoflurane-Induced Cardioprotection
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Circulation Vol. 120, No. 11_suppl_1 ( 2009-09-15)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 120, No. 11_suppl_1 ( 2009-09-15)
    Abstract: Background— 5′AMP-activated protein kinase (AMPK), a well-known regulator of cellular energy status, is also implicated in ischemic preconditioning leading to cardioprotection. We hypothesized that AMPK is involved in anesthetic-induced cardioprotection and that this activation is mediated by reactive oxygen species (ROS). Methods and Results— Isolated Langendorff-perfused rat hearts were subjected to 35 minutes of global ischemia (I) followed by 120 minutes of reperfusion (I/R). Hearts were assigned to a control group (Con) or a sevoflurane (Sevo) group receiving 3 times 5-minute episodes of sevoflurane (2.5vol%) before I/R. Phosphorylation of both AMPK and endothelial nitric oxide synthase (eNOS) were determined by Western blot analysis. Cardioprotection was assessed after I/R from recovery of left ventricular pressure and from infarct size (triphenyltetrazolium chloride staining). In the control group, ischemia resulted in a 2-fold increase in phosphorylation levels of AMPK (Con 0.13±0.01 versus Con-I 0.28±0.05, P 〈 0.05), which was sustained after 120 minutes of reperfusion (Con-I/R 0.26±0.02, P 〈 0.05). Sevoflurane preconditioning had no affect on AMPK phosphorylation before ischemia (Sevo 0.12±0.03, P 〉 0.05), but almost doubled the increase in AMPK phosphorylation relative to control after ischemia (Sevo-I 0.48±0.09, P 〈 0.05), an effect that was sustained after reperfusion (Sevo-I/R 0.49±0.12, P 〈 0.05). The AMPK-inhibitor compound C (10 μmol/L) reduced the sevoflurane-mediated increase in phosphorylation of AMPK and its target eNOS and abolished cardioprotection. The ROS-scavenger n-(2-mercaptopropionyl)-glycine (1 mmol/L) blunted the sevoflurane-mediated increase in AMPK and eNOS phosphorylation and prevented cardioprotection. Conclusions— Sevoflurane-induced AMPK activation protects the heart against ischemia and reperfusion injury and relies on upstream production of ROS.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.108.828426
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 1466401-X
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  • 7
    Online Resource
    Online Resource
    Characterization of Ascending Aortic Flow in Patients With Degenerative Aneurysms : A 4D Flow Magnetic Resonance Study
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Investigative Radiology Vol. 56, No. 8 ( 2021-8), p. 494-500
    Details
    In: Investigative Radiology, Ovid Technologies (Wolters Kluwer Health), Vol. 56, No. 8 ( 2021-8), p. 494-500
    Abstract: Degenerative thoracic aortic aneurysm (TAA) patients are known to be at risk of life-threatening acute aortic events. Guidelines recommend preemptive surgery at diameters of greater than 55 mm, although many patients with small aneurysms show only mild growth rates and more than half of complications occur in aneurysms below this threshold. Thus, assessment of hemodynamics using 4-dimensional flow magnetic resonance has been of interest to obtain more insights in aneurysm development. Nonetheless, the role of aberrant flow patterns in TAA patients is not yet fully understood. Materials and Methods A total of 25 TAA patients and 22 controls underwent time-resolved 3-dimensional phase contrast magnetic resonance imaging with 3-directional velocity encoding (ie, 4-dimensional flow magnetic resonance imaging). Hemodynamic parameters such as vorticity, helicity, and wall shear stress (WSS) were calculated from velocity data in 3 anatomical segments of the ascending aorta (root, proximal, and distal). Regional WSS distribution was assessed for the full cardiac cycle. Results Flow vorticity and helicity were significantly lower for TAA patients in all segments. The proximal ascending aorta showed a significant increase in peak WSS in the outer curvature in TAA patients, whereas WSS values at the inner curvature were significantly lower as compared with controls. Furthermore, positive WSS gradients from sinotubular junction to midascending aorta were most prominent in the outer curvature, whereas from midascending aorta to brachiocephalic trunk, the outer curvature showed negative WSS gradients in the TAA group. Controls solely showed a positive gradient at the inner curvature for both segments. Conclusions Degenerative TAA patients show a decrease in flow vorticity and helicity, which is likely to cause perturbations in physiological flow patterns. The subsequent differing distribution of WSS might be a contributor to vessel wall remodeling and aneurysm formation.
    Type of Medium: Online Resource
    ISSN: 1536-0210 , 0020-9996
    URL: Article
    DOI: 10.1097/RLI.0000000000000768
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2041543-6
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  • 8
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    Online Resource
    Beneficial Outcome of Losartan Therapy Depends on Type of FBN1 Mutation in Marfan Syndrome
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Circulation: Cardiovascular Genetics Vol. 8, No. 2 ( 2015-04), p. 383-388
    Details
    In: Circulation: Cardiovascular Genetics, Ovid Technologies (Wolters Kluwer Health), Vol. 8, No. 2 ( 2015-04), p. 383-388
    Abstract: It has been shown that losartan reduces aortic dilatation in patients with Marfan syndrome. However, treatment response is highly variable. This study investigates losartan effectiveness in genetically classified subgroups. Methods and Results— In this predefined substudy of COMPARE, Marfan patients were randomized to daily receive losartan 100 mg or no losartan. Aortic root dimensions were measured by MRI at baseline and after 3 years. FBN1 mutations were classified based on fibrillin-1 protein effect into (1) haploinsufficiency, decreased amount of normal fibrillin-1, or (2) dominant negative, normal fibrillin-1 abundance with mutant fibrillin-1 incorporated in the matrix. A pathogenic FBN1 mutation was found in 117 patients, of whom 79 patients were positive for a dominant negative mutation (67.5%) and 38 for a mutation causing haploinsufficiency (32.5%). Baseline characteristics between treatment groups were similar. Overall, losartan significantly reduced aortic root dilatation rate (no losartan, 1.3±1.5 mm/3 years, n=59 versus losartan, 0.8±1.4 mm/3 years, n=58; P =0.009). However, losartan reduced only aortic root dilatation rate in haploinsufficient patients (no losartan, 1.8±1.5 mm/3 years, n=21 versus losartan 0.5±0.8 mm/3 years, n=17; P =0.001) and not in dominant negative patients (no losartan, 1.2±1.7 mm/3 years, n=38 versus losartan 0.8±1.3 mm/3 years, n=41; P =0.197). Conclusions— Marfan patients with haploinsufficient FBN1 mutations seem to be more responsive to losartan therapy for inhibition of aortic root dilatation rate compared with dominant negative patients. Additional treatment strategies are needed in Marfan patients with dominant negative FBN1 mutations. Clinical Trial Registration— http://www.trialregister.nl/trialreg/index.asp ; Unique Identifier: NTR1423.
    Type of Medium: Online Resource
    ISSN: 1942-325X , 1942-3268
    URL: Article
    DOI: 10.1161/CIRCGENETICS.114.000950
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2927603-2
    detail.hit.zdb_id: 2457085-0
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  • 9
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    Online Resource
    Response to Letter Regarding Article, “Reactive Oxygen Species–Induced Stimulation of 5′AMP-Activated Protein Kinase Mediates Sevoflurane-Induced Cardioprotection”
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Circulation Vol. 121, No. 18 ( 2010-05-11)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 121, No. 18 ( 2010-05-11)
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIR.0b013e3181df9220
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 1466401-X
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