A high adrenergic strain during reperfusion after ischemia impedes functional recovery. Conversely, adrenergic blockade may be beneficial during reperfusion. This study was undertaken to find out if early postoperative high-dose infusion of the selective beta 1-blocking agent metoprolol tartrate has additional effects on metabolic variables related to myocardial energy supply/demand balance compared with those obtained with a late preoperative oral dose. The study included 21 male patients undergoing coronary bypass grafting. All patients received an oral dose of metoprolol before the operation. After the operation, patients were randomized to a control group or a group receiving intravenous infusion of metoprolol. Myocardial uptake of oxygen and substrates was determined before and during atrial pacing. Metoprolol reduced arterial concentrations of free fatty acids, reduced myocardial uptake of free fatty acids, and enhanced myocardial uptake of lactate. During paced tachycardia, the metoprolol concentration correlated negatively with myocardial uptake of free fatty acids (r = -0.80; p < 0.001) and positively with myocardial uptake of lactate (r = 0.53; p < 0.05). It is concluded that postoperative infusion of metoprolol induces myocardial metabolic changes compatible with an improved energy supply/demand balance.
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Eur J Nucl Med Mol Imaging
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Nuclear Medicine and Clinical Molecular Imaging, University Hospital Tuebingen, Otfried-Mueller-Str. 14, 72076, Tuebingen, Germany.
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Cardiology Department, Coimbra Hospital and University Center, 3004-561 Coimbra, Portugal.
Hypertrophic cardiomyopathy (HCM) is a heterogeneous cardiac disease and one of its major challenges is the limited accuracy in stratifying the risk of sudden cardiac death (SCD). Positron emission tomography (PET), through the evaluation of myocardial blood flow (MBF) and metabolism using fluorodeoxyglucose (FDG) uptake, can reveal microvascular dysfunction, ischemia, and increased metabolic demands in the hypertrophied myocardium. These abnormalities are linked to several factors influencing disease progression, including arrhythmia development, ventricular dilation, and myocardial fibrosis.
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January 2025
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Faculty of Medicine, Institute of Anatomy, University of Belgrade, 11000 Belgrade, Serbia.
Two billion people worldwide suffer from anemia, which can lead to the onset of cardiac disorders; nevertheless, the precise mechanisms remain unclear. There are at least three distinct mechanisms by which iron deficiency (ID) contributes to the development of cardiac disorders. First, ID increases concentrations of intact fibroblast growth factor-23 (iFGF-23), which promotes left ventricular hypertrophy.
View Article and Find Full Text PDFJ Cardiovasc Med (Hagerstown)
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Center for Diagnosis and Treatment of Cardiomyopathies, Cardiovascular Department, Azienda Sanitaria Universitaria Giuliano-Isontina (ASUGI), University of Trieste.
Diagnosing cardiac amyloidosis (CA) is challenging because of its phenotypic heterogeneity, multiorgan involvement requiring interaction among experts in different specialties and subspecialties, lack of a single noninvasive diagnostic tool, and still limited awareness in the medical community. Missing or delaying the diagnosis of CA may profoundly impact on patients' outcomes, as potentially life-saving treatments may be omitted or delayed. The suspicion of CA should arise when "red flags" for this condition are present, together with increased left ventricular wall thickness.
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