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Drake-Holland, Angela J.; Vusse, Ger J.; Roemen, Theo H.M.; Hynd, J.; Mansaray, M; Wright, Zoe; Noble, Mark I. M.

doi:10.1023/a:1011114627288

Cited by 18 publications

(2 citation statements)

References 21 publications

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“…A prevalent cardiac sympathetic activity with subsequent abnormal norepinephrine signaling and metabolism, increased mitochondrial oxidative stress [31], and calcium-dependent apoptosis [32] may contribute to myocardial injury [31, 33] and explain the high cardiovascular risk in these patients. The sympathetic imbalance associated with CAN may also critically influence myocardial substrate utilization [34] and contribute to mitochondrial uncoupling [35], regional ventricular motion abnormalities, functional deficits, and cardiomyopathy [36]. Sympathetic toxicity induces insulin resistance and may compromise regional glucose utilization [37].…”

Section: Discussionmentioning

confidence: 99%

What Do We Know and We Do Not Know About Cardiovascular Autonomic Neuropathy in Diabetes

Pop‐Busui

2012

J. of Cardiovasc. Trans. Res.

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Cardiovascular autonomic neuropathy (CAN) in diabetes is generally overlooked in practice, although awareness of its serious consequences is emerging. Challenges in understanding the complex, dynamic changes in the modulation of the sympathetic/parasympathetic systems’ tone and their interactions with physiologic mechanisms regulating the control of heart rate, blood pressure, and other cardiovascular functions in the presence of acute hyper-or-hypoglycemic stress, other stressors or medication, and challenges with sensitive evaluations have contributed to lower CAN visibility compared with other diabetes complications. Yet, CAN is a significant cause of morbidity and mortality, due to a high-risk of cardiac arrhythmias, silent myocardial ischemia and sudden death. While striving for aggressive risk factor control in diabetes practice seemed intuitive, recent reports of major clinical trials undermine established thinking concerning glycemic control and cardiovascular risk. This review covers current understanding and gaps in that understanding of the clinical implications of CAN and prevention and treatment of CAN.

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Section: Discussionmentioning

confidence: 99%

What Do We Know and We Do Not Know About Cardiovascular Autonomic Neuropathy in Diabetes

Pop‐Busui

2012

J. of Cardiovasc. Trans. Res.

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“…1–3 Changes in both systolic and diastolic LV function have been demonstrated in otherwise healthy T1DM subjects, preceding the development of other clinically recognizable diabetic complications. 4–6 One proposed mechanism mediating these changes is the presence of cardiovascular autonomic neuropathy (CAN), and associated sympathetic/parasympathetic imbalance, which may promote earlier changes in LV function by critically influencing myocardial substrate utilization, 7 impairing oxidative metabolism, and altering LV efficiency. The pathophysiology of diabetic cardiomyopathy, which includes increased myocardial fibrosis as well as accelerated apoptosis, may be partially related to these changes in myocardial substrate utilization and increased oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Left ventricular metabolism, function, and sympathetic innervation in men and women with type 1 diabetes

Duvernoy

Raffel

Swanson

et al. 2016

Journal of Nuclear Cardiology

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Background In type I diabetes (T1DM), alterations in LV function may occur due to changes in innervation, metabolism, and efficiency. Objectives We evaluated the association between sympathetic nerve function, oxidative metabolism, resting blood flow, LV efficiency and function in healthy diabetics, and assessed gender differences. Methods Cross-sectional study of 45 subjects with T1DM, 60% females, age 34 ± 13 years, and 10 age-matched controls. Positron emission tomography (PET) imaging with [11C]acetate and [11C]meta-hydroxyephedrine was performed, in addition to cardiac magnetic resonance imaging. Results There were no significant differences in LV function, innervation, or oxidative metabolism between T1DM and controls. Cardiac oxidative metabolism was positively associated with higher levels of sympathetic activation, particularly in women. Diabetic women had significantly lower efficiency compared with diabetic men. Resting flow was significantly higher in diabetic women compared with diabetic men, and tended to be higher in female controls as well. Conclusions Measures of myocardial function, metabolism, blood flow, and sympathetic activation were preserved in young, otherwise healthy, T1DM patients. However, T1DM women presented with greater myocardial oxidative metabolism requirements than men. Ongoing studies are evaluating changes over time.

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