PURPOSE: To study myocardial perfusion reserve and myocellular metabolic alterations indicated by triglyceride content as possible causes of diastolic dysfunction in patients with type 2 diabetes mellitus, preserved systolic function, and without clinically evident coronary artery disease. MATERIALS AND METHODS: Patients with type 2 diabetes mellitus (n = 42) underwent cardiac magnetic resonance (CMR) for quantification of 1) myocardial contractility by strain-encoded MR (SENC); 2) myocardial triglyceride content by proton magnetic resonance spectroscopy ((1) H-MRS); and 3) myocardial perfusion reserve during pharmacologic hyperemia. Age-matched healthy volunteers (n = 16) also underwent CMR to acquire normal values for myocardial strain and perfusion reserve. RESULTS: Stress CMR procedures were successfully performed in all subjects, and no regional inducible perfusion defects were observed in type 2 diabetes mellitus patients. Diastolic strain rate and myocardial perfusion reserve were significantly impaired in patients with type 2 diabetes mellitus compared to control subjects (P < 0.001 for both). Interestingly, impaired diastolic function in type 2 diabetes mellitus was not associated with impaired myocardial perfusion reserve (r = 0.12, P = NS). Conversely a significant association was observed between diastolic dysfunction and myocardial triglyceride content (r = -0.71, P < 0.001), which proved to be independent of age, gender, diabetes duration, blood pressure, and fasting blood glucose. CONCLUSION: Myocardial steatosis may represent an early marker of diabetic heart disease, triggering subclinical myocardial dysfunction irrespective of myocardial perfusion reserve.
PURPOSE: To study myocardial perfusion reserve and myocellular metabolic alterations indicated by triglyceride content as possible causes of diastolic dysfunction in patients with type 2 diabetes mellitus, preserved systolic function, and without clinically evident coronary artery disease. MATERIALS AND METHODS:Patients with type 2 diabetes mellitus (n = 42) underwent cardiac magnetic resonance (CMR) for quantification of 1) myocardial contractility by strain-encoded MR (SENC); 2) myocardial triglyceride content by proton magnetic resonance spectroscopy ((1) H-MRS); and 3) myocardial perfusion reserve during pharmacologic hyperemia. Age-matched healthy volunteers (n = 16) also underwent CMR to acquire normal values for myocardial strain and perfusion reserve. RESULTS: Stress CMR procedures were successfully performed in all subjects, and no regional inducible perfusion defects were observed in type 2 diabetes mellituspatients. Diastolic strain rate and myocardial perfusion reserve were significantly impaired in patients with type 2 diabetes mellitus compared to control subjects (P < 0.001 for both). Interestingly, impaired diastolic function in type 2 diabetes mellitus was not associated with impaired myocardial perfusion reserve (r = 0.12, P = NS). Conversely a significant association was observed between diastolic dysfunction and myocardial triglyceride content (r = -0.71, P < 0.001), which proved to be independent of age, gender, diabetes duration, blood pressure, and fasting blood glucose. CONCLUSION:Myocardial steatosis may represent an early marker of diabetic heart disease, triggering subclinical myocardial dysfunction irrespective of myocardial perfusion reserve.
Authors: Janet Wei; Michael D Nelson; Edward W Szczepaniak; Laura Smith; Puja K Mehta; Louise E J Thomson; Daniel S Berman; Debiao Li; C Noel Bairey Merz; Lidia S Szczepaniak Journal: Am J Physiol Heart Circ Physiol Date: 2015-10-30 Impact factor: 4.733
Authors: Majd AlGhatrif; Vabren L Watts; Xiaolin Niu; Marc Halushka; Karen L Miller; Konrad Vandegaer; Djahida Bedja; Karen Fox-Talbot; Alicja Bielawska; Kathleen L Gabrielson; Lili A Barouch Journal: J Cardiovasc Transl Res Date: 2013-03-02 Impact factor: 4.132
Authors: Petra C Kienesberger; Thomas Pulinilkunnil; Jeevan Nagendran; Martin E Young; Juliane G Bogner-Strauss; Hubert Hackl; Rammy Khadour; Emma Heydari; Guenter Haemmerle; Rudolf Zechner; Erin E Kershaw; Jason R B Dyck Journal: Cardiovasc Res Date: 2013-05-25 Impact factor: 10.787