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Diabetic cardiomyopathy: ongoing controversies in 2012

Diabetische Kardiomyopathie: aktuelle Kontroversen 2012

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Abstract

Diabetic cardiomyopathy is a controversial clinical entity that in its initial state is usually characterized by left ventricular diastolic dysfunction in patients with diabetes mellitus that cannot be explained by coronary artery disease, hypertension, or any other known cardiac disease. It was reported in up to 52–60% of well-controlled type-II diabetic subjects, but more recent studies, using standardized tissue Doppler criteria and more strict patient selection, revealed a much lower prevalence. The pathological substrate is myocardial damage, left ventricular hypertrophy, interstitial fibrosis, structural and functional changes of the small coronary vessels, metabolic disturbance, and autonomic cardiac neuropathy. Hyperglycemia causes myocardial necrosis and fibrosis, as well as the increase of myocardial free radicals and oxidants, which decrease nitric oxide levels, worsen the endothelial function, and induce myocardial inflammation. Insulin resistance with hyperinsulinemia and decreased insulin sensitivity may also contribute to the left ventricular hypertrophy. Clinical manifestations of diabetic cardiomyopathy may include dyspnea, arrhythmias, atypical chest pain, and dizziness. Currently, there is no specific treatment of diabetic cardiomyopathy that targets its pathophysiological substrate, but various therapeutic options are discussed that include improving diabetic control with both diet and drugs (metformin and thiazolidinediones), the use of ACE inhibitors, beta blockers, and calcium channel blockers. Daily physical activity and a reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles.

Zusammenfassung

Die diabetische Kardiomyopathie stellt eine umstrittene klinische Entität dar, deren Anfangsstadium meist durch eine linksventrikuläre diastolische Dysfunktion bei Patienten mit Diabetes mellitus charakterisiert ist. Diese Funktionsstörung lässt sich nicht durch eine koronare Herzkrankheit (KHK), Bluthochdruck oder eine andere kardiale Ursache erklären. Ihr Vorkommen wurde bei 52–60% der Patienten mit einem gut eingestellten Typ-2-Diabetes angegeben, aber aktuellere Studien, in denen standardisierte Gewebedopplerkriterien verwendet wurden und eine strengere Patientenauswahl erfolgte, ergaben eine deutlich niedrigere Prävalenz. Das pathologische Substrat besteht aus degenerativen Veränderungen, einer linksventrikulären Hypertrophie und interstitiellen Fibrose, strukturellen und funktionellen Veränderungen kleiner Koronargefäße, metabolischen Veränderungen und einer autonomen kardialen Neuropathie. Die Hyperglykämie kann Myozytenuntergang, interstitielle Fibrose, die vermehrte Bildung von freien Radikalen und Oxidanzien verursachen, die die Stickoxid(NO)-Spiegel erniedrigen, die Endothelfunktion verschlechtern und eine Entzündung im Myokard begünstigen. Insulinresistenz mit Hyperinsulinämie und verminderter Insulinansprechbarkeit dürften zur Ausbildung einer Hypertrophie beitragen. – Das klinische Erscheinungsbild der diabetischen Kardiomyopathie umfasst Dyspnoe, Arrhythmien, atypische Herzschmerzen und Schwindelgefühl. Gegenwärtig gibt es keine Behandlung, die spezifisch das pathophysiologische Substrat einer diabetischen Kardiomyopathie anzugreifen vermag. Zu den gegenwärtig diskutierten therapeutischen Optionen gehören die diätetische und medikamentöse Optimierung des Diabetes durch Metformin und Thiazolidin sowie der Einsatz von ACE-Hemmern, Betablockern und Kalziumantagonisten. Tägliche körperliche Aktivität und, falls erforderlich, eine Gewichtsreduktion dürften die Glukosehomöostase durch Senkung der Glukose-Insulin-Ratio und die Erhöhung der Glukoseoxidation in Skelett- und Herzmuskel sowie der Insulinsensitivität verbessern.

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Seferović, P., Milinković, I., Ristić, A. et al. Diabetic cardiomyopathy: ongoing controversies in 2012. Herz 37, 880–886 (2012). https://doi.org/10.1007/s00059-012-3720-z

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