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  • 1
    Online Resource
    Online Resource
    Cardiovascular and metabolic effects of 48-h glucagon-like peptide-1 infusion in compensated chronic patients with heart failure
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 298, No. 3 ( 2010-03), p. H1096-H1102
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 298, No. 3 ( 2010-03), p. H1096-H1102
    Abstract: The incretin hormone glucagon-like peptide-1 (GLP-1) and its analogs are currently emerging as antidiabetic medications. GLP-1 improves left ventricular ejection fraction (LVEF) in dogs with heart failure (HF) and in patients with acute myocardial infarction. We studied metabolic and cardiovascular effects of 48-h GLP-1 infusions in patients with congestive HF. In a randomized, double-blind crossover design, 20 patients without diabetes and with HF with ischemic heart disease, EF of 30 ± 2%, New York Heart Association II and III ( n = 14 and 6) received 48-h GLP-1 (0.7 pmol·kg −1 ·min −1 ) and placebo infusion. At 0 and 48 h, LVEF, diastolic function, tissue Doppler regional myocardial function, exercise testing, noninvasive cardiac output, and brain natriuretic peptide (BNP) were measured. Blood pressure, heart rate, and metabolic parameters were recorded. Fifteen patients completed the protocol. GLP-1 increased insulin (90 ± 17 pmol/l vs. 69 ± 12 pmol/l; P = 0.025) and lowered glucose levels (5.2 ± 0.1 mmol/l vs. 5.6 ± 0.1 mmol/l; P 〈 0.01). Heart rate (67 ± 2 beats/min vs. 65 ± 2 beats/min; P = 0.016) and diastolic blood pressure (71 ± 2 mmHg vs. 68 ± 2 mmHg; P = 0.008) increased during GLP-1 treatment. Cardiac index (1.5 ± 0.1 l·min −1 ·m −2 vs. 1.7 ± 0.2 l·min −1 ·m −2 ; P = 0.54) and LVEF (30 ± 2% vs. 30 ± 2%; P = 0.93), tissue Doppler indexes, body weight, and BNP remained unchanged. Hypoglycemic events related to GLP-1 treatment were observed in eight patients. GLP-1 infusion increased circulating insulin levels and reduced plasma glucose concentration but had no major cardiovascular effects in patients without diabetes but with compensated HF. The impact of minor increases in heart rate and diastolic blood pressure during GLP-1 infusion requires further studies. Hypoglycemia was frequent and calls for caution in patients without diabetes but with HF.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00930.2009
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Influence of insulin and free fatty acids on contractile function in patients with chronically stunned and hibernating myocardium
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 289, No. 2 ( 2005-08), p. H938-H946
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 289, No. 2 ( 2005-08), p. H938-H946
    Abstract: It is unknown whether short-term modulation of substrate supply affects cardiac performance in heart failure patients with chronic ischemic myocardium. The aim of this study was to determine whether modulation of myocardial substrate metabolism with insulin and free fatty acids (FFAs) affects contractile function of chronically stunned (CST) and hibernating (HIB) myocardium at rest and after maximal exercise. We studied eight nondiabetic patients with ejection fraction (EF) 30 ± 4% (SE) and CST/HIB in 49 ± 6% of the left ventricle: 36 ± 6% CST and 13 ± 2% HIB as determined by 99m Technetium-Sestamibi single photon emission computed tomography (SPECT) and [ 18 F]fluorodeoxyglucose (FDG) positron emission tomography (PET). Each patient was subjected to a 3-h infusion of 1) saline, 2) insulin-glucose (i.e., euglycemic insulin clamp; high insulin, suppressed FFA), and 3) somatostatin-heparin (suppressed insulin, high FFA). Echocardiographic endpoints were global EF and regional contractile function [maximum velocity ( V max ) and strain rate (ε max )] as determined by tissue Doppler imaging at steady state and after maximal exercise. EF was similar at baseline and steady state and increased after exercise to 36 ± 5% ( P 〈 0.05). Baseline regional V max and ε max were highest in control, intermediate in CST and HIB, and lowest in infarct regions ( P 〈 0.05). Steady-state EF, V max , and ε max were not affected by metabolic modulation in any region. After maximal exercise, contractile function increased in control, CST, and HIB ( P 〈 0.05), but not in infarct, regions. Exercise-induced contractile increments were unaffected by metabolic modulation. Metabolic modulation does not influence contractile function in CST and HIB regions. Chronic ischemic myocardium has preserved ability to adapt to extreme, short-term changes in substrate supply at rest and after maximal exercise.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00150.2005
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Suppression of circulating free fatty acids with acipimox in chronic heart failure patients changes whole body metabolism but does not affect cardiac function
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 299, No. 4 ( 2010-10), p. H1220-H1225
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 299, No. 4 ( 2010-10), p. H1220-H1225
    Abstract: Circulating free fatty acids (FFAs) may worsen heart failure (HF) due to myocardial lipotoxicity and impaired energy generation. We studied cardiac and whole body effects of 28 days of suppression of circulating FFAs with acipimox in patients with chronic HF. In a randomized double-blind crossover design, 24 HF patients with ischemic heart disease [left ventricular ejection fraction: 26 ± 2%; New York Heart Association classes II ( n = 13) and III ( n = 5)] received 28 days of acipimox treatment (250 mg, 4 times/day) and placebo. Left ventricular ejection fraction, diastolic function, tissue-Doppler regional myocardial function, exercise capacity, noninvasive cardiac index, NH 2 -terminal pro-brain natriuretic peptide (NT-pro-BNP), and whole body metabolic parameters were measured. Eighteen patients were included for analysis. FFAs were reduced by 27% in the acipimox-treated group [acipimox vs. placebo ( day 28 − day 0): −0.10 ± 0.03 vs. +0.01 ± 0.03 mmol/l, P 〈 0.01]. Glucose and insulin levels did not change. Acipimox tended to increase glucose and decrease lipid utilization rates at the whole body level and significantly changed the effect of insulin on substrate utilization. The hyperinsulinemic euglycemic clamp M value did not differ. Global and regional myocardial function did not differ. Exercise capacity, cardiac index, systemic vascular resistance, and NT-pro-BNP were not affected by treatment. In conclusion, acipimox caused minor changes in whole body metabolism and decreased the FFA supply, but a long-term reduction in circulating FFAs with acipimox did not change systolic or diastolic cardiac function or exercise capacity in patients with HF.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00475.2010
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 4
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    Online Resource
    Hidden burden of arrhythmias in patients with small atrial septal defects: a nationwide study
    BMJ ; 2019
    In:  Open Heart Vol. 6, No. 1 ( 2019-06), p. e001056-
    Details
    In: Open Heart, BMJ, Vol. 6, No. 1 ( 2019-06), p. e001056-
    Abstract: In recent Danish nationwide register-based study, adults with small, unrepaired atrial septal defects (ASD) have increased risk of pneumonia, atrial fibrillation (AF) and stroke. Moreover, they revealed higher mortality than the background population. Objective In this nationwide study, we evaluate the hidden burden of atrial and ventricular arrhythmias in adult patients with a small, unrepaired ASD without a previous diagnosis of AF. Methods All Danish patients, aged 18–65, diagnosed between 1953 and 2011 with an unrepaired ASD and no documented AF were invited for 7 days Holter-recording, echocardiography and 6 min walk test. The first 48 hours Holter-recording was completely analysed, while only AF was screened for throughout all 7 days. Furthermore, the entire patient group were characterised using the unique Danish registries. Results A total of 151 patients (mean age 32 years) were included. Approximately 80% of the patients had spontaneous closure of their defect. Despite this, occult arrhythmias were frequent. The most common arrhythmia was supraventricular tachycardia (n=24, 16%) with non-sustained atrial arrhythmias in 21 patients and AF in two patients. A considerable number of patients had non-sustained ventricular tachycardia (n=12, 8%). Patients with ASD and tachyarrhythmias had increased right ventricular to left ventricular diastolic area in echocardiography and higher age when compared with ASD patients without arrhythmias. Conclusion Adult patients with small, unrepaired ASD have a hidden burden of both atrial and ventricular tachyarrhythmias. The mechanism likely relates to the residua of previous right-heart volume overload and incomplete reverse remodelling. Our results support guidelines recommending continued follow-up of patients with small, unrepaired ASD.
    Type of Medium: Online Resource
    ISSN: 2053-3624
    URL: Article
    DOI: 10.1136/openhrt-2019-001056
    Language: English
    Publisher: BMJ
    Publication Date: 2019
    detail.hit.zdb_id: 2747269-3
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  • 5
    Online Resource
    Online Resource
    Effects of phosphodiesterase-5 inhibition by sildenafil in the pressure overloaded right heart
    Wiley ; 2008
    In:  European Journal of Heart Failure Vol. 10, No. 12 ( 2008-12), p. 1158-1165
    Details
    In: European Journal of Heart Failure, Wiley, Vol. 10, No. 12 ( 2008-12), p. 1158-1165
    Type of Medium: Online Resource
    ISSN: 1388-9842
    URL: Article
    DOI: 10.1016/j.ejheart.2008.09.016
    Language: English
    Publisher: Wiley
    Publication Date: 2008
    detail.hit.zdb_id: 1500332-2
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  • 6
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    Online Resource
    Transcatheter Intervention for Coarctation of the Aorta
    Elsevier BV ; 2023
    In:  JACC: Cardiovascular Interventions Vol. 16, No. 4 ( 2023-02), p. 444-453
    Details
    In: JACC: Cardiovascular Interventions, Elsevier BV, Vol. 16, No. 4 ( 2023-02), p. 444-453
    Type of Medium: Online Resource
    ISSN: 1936-8798
    URL: Article
    DOI: 10.1016/j.jcin.2022.11.007
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 2452163-2
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  • 7
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    Online Resource
    5-Aminoimidazole-4-carboxamide-1-β-d-ribofuranoside Increases Myocardial Glucose Uptake during Reperfusion and Induces Late Pre-conditioning: Potential Role of AMP-Activated Protein Kinase
    Wiley ; 2009
    In:  Basic & Clinical Pharmacology & Toxicology Vol. 105, No. 1 ( 2009-07), p. 10-16
    Details
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 105, No. 1 ( 2009-07), p. 10-16
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    URL: Article
    DOI: 10.1111/pto.2009.105.issue-1
    DOI: 10.1111/j.1742-7843.2009.00402.x
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 2151592-X
    SSG: 15,3
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  • 8
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    Effects of KATP Channel Modulation on Myocardial Glycogen Content, Lactate, and Amino Acids in Nonischemic and Ischemic Rat Hearts
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Journal of Cardiovascular Pharmacology Vol. 45, No. 5 ( 2005-05), p. 456-461
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 45, No. 5 ( 2005-05), p. 456-461
    Abstract: ATP-sensitive potassium (K ATP ) channels are involved in the mechanisms underlying ischemic preconditioning. K ATP channels open during ischemia, presumably secondary to intracellular metabolic alterations. The direct effects of K ATP channel modulation on myocardial metabolism have not been studied. The aim of the present study was to investigate whether a K ATP opener (diazoxide) and blocker (glibenclamide) modulates myocardial glycogen, lactate, and amino acid content before, during, and after ischemia. In isolated perfused rat hearts, we investigated the effect of diazoxide (30 μM) and glibenclamide (10 μM) administered 15 minutes before ischemia on myocardial glycogen, lactate, and amino acid content before, during, and after ischemia. Diazoxide increased left-ventricular developed pressure during reperfusion ( P 〈 0.05) and decreased myocardial glycogen depletion ( P 〈 0.05) and lactate accumulation ( P 〈 0.05) during ischemia compared with the control group. Glibenclamide decreased myocardial glycogen content ( P 〈 0.05) and increased myocardial lactate ( P 〈 0.05) and alanine ( P 〈 0.05) content before ischemia and reduced myocardial glycogen content after ischemia ( P 〈 0.05) compared with control. K ATP channel activation by diazoxide modulates myocardial metabolism. These findings suggest that activation of K ATP channels protects against ischemia-reperfusion injury by a mechanism that involves decreased energy depletion.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/01.fjc.0000159045.35241.95
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 9
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    Online Resource
    Remote preconditioning reduces ischemic injury in the explanted heart by a K ATP channel-dependent mechanism
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 288, No. 3 ( 2005-03), p. H1252-H1256
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 288, No. 3 ( 2005-03), p. H1252-H1256
    Abstract: Local and remote ischemic preconditioning (IPC) reduce ischemia-reperfusion (I/R) injury and preserve cardiac function. In this study, we tested the hypothesis that remote preconditioning is memorized by the explanted heart and yields protection from subsequent I/R injury and that the underlying mechanism involves sarcolemmal and mitochondrial ATP-sensitive K + (K ATP ) channels. Male Wistar rats (300–350 g) were randomized to a control ( n = 10), a remote IPC ( n = 10), and a local IPC group ( n = 10). Remote IPC was induced by four cycles of 5 min of limb ischemia, followed by 5 min of reperfusion. Local IPC was induced by four cycles of 2 min of regional myocardial ischemia, followed by 3 min of reperfusion. The heart was excised within 5 min after the final cycle of preconditioning, mounted in a perfused Langendorff preparation for 40 min of stabilization, and subjected to 45 min of sustained ischemia by occluding the left coronary artery and 120 min of reperfusion. I/R injury was assessed as infarct size by triphenyltetrazolium staining. The influence of sarcolemmal and mitochondrial K ATP channels on remote preconditioning was assessed by the addition of glibenclamide (10 μM, a nonselective K ATP blocker), 5-hydroxydecanoic acid (5-HD; 100 μM, a mitochondrial K ATP blocker), and HMR-1098 (30 μM, a sarcolemmal K ATP blocker) to the Langendorff preparation before I/R. The role of mitochondrial K ATP channels as an effector mechanism for memorizing remote preconditioning was further studied by the effect of the specific mitochondrial K ATP activator diaxozide (10 mg/kg) on myocardial infarct size. Remote preconditioning reduced I/R injury in the explanted heart (0.17 ± 0.03 vs. 0.39 ± 0.05, P 〈 0.05) and improved left ventricular function during reperfusion compared with control ( P 〈 0.05). Similar effects were obtained with diazoxide. Remote preconditioning was abolished by the addition of 5-HD and glibenclamide but not by HMR-1098. In conclusion, the protective effect of remote preconditioning is memorized in the explanted heart by a mechanism that involves mitochondrial K ATP channels.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00207.2004
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 10
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    Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of Cardiovascular Pharmacology Vol. 69, No. 1 ( 2017-01), p. 1-12
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 69, No. 1 ( 2017-01), p. 1-12
    Abstract: Prostacyclin mimetics are vasodilatory agents used in the treatment of pulmonary arterial hypertension. The direct effects of prostanoids on right-ventricular (RV) function are unknown. We aimed to investigate the direct effects of prostacyclin mimetics on RV function in hearts with and without RV hypertrophy and failure. Methods: Wistar rats were subjected to pulmonary trunk banding to induce compensated RV hypertrophy (n = 32) or manifest RV failure (n = 32). Rats without banding served as healthy controls (n = 30). The hearts were excised and perfused in a Langendorff system and subjected to iloprost, treprostinil, epoprostenol, or MRE-269 in increasing concentrations. The effect on RV function was evaluated using a balloon-tipped catheter inserted into the right ventricle. Results: In control hearts, iloprost, treprostinil, and MRE-269 improved RV function. The effect was, however, absent in hearts with RV hypertrophy and failure. Treprostinil and MRE-269 even impaired RV function in hearts with manifest RV failure. Conclusions: Iloprost, treprostinil, and MRE-269 improved RV function in the healthy rat heart. RV hypertrophy abolished the positive inotropic effect, and in the failing right ventricle, MRE-269 and treprostinil impaired RV function. This may be related to changes in prostanoid receptor expression and reduced coronary flow reserve in the hypertrophic and failing right ventricle.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000000435
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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