Diabetic Cardiovascular Autonomic Neuropathy

Vinik, Aaron I.; Ziegler, Dan

doi:10.1161/circulationaha.106.634949

Cited by 1,031 publications

(1,098 citation statements)

References 110 publications

(99 reference statements)

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“…In the VADT [8], 43% of the patients had diabetic neuropathy at study entry. Although not specified, such a high prevalence probably includes patients with autonomic neuropathy, a condition associated, in an independent manner, with a greater rate of CV mortality [27].…”

Section: Hypoglycaemia: a Trigger For CV Events?mentioning

confidence: 99%

Megatrials in type 2 diabetes. From excitement to frustration?

Prato

2009

Diabetologia

118

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Whether glycaemic control may result in a reduction of cardiovascular (CV) risk has been a matter of continuous discussion and investigation. Epidemiological analyses have extensively suggested a relationship between glycaemic control and CV events; however, the results of intervention trials have been less conclusive. The UKPDS reported a 16% reduction in the risk of myocardial infarction, but this reduction was not statistically significant. The results of the Kumamoto and PROactive studies could not allow any firm conclusions to be drawn either, because of limited size and the defined primary endpoint, respectively. The results of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) and Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE) trials and the Veteran Administration Diabetes Trial (VADT) were published in rapid succession over the second half of 2008 and at the beginning of 2009. A total number of almost 25,000 type 2 diabetic patients were recruited in these three trials, which assessed the effect of intensive glycaemic control vs conventional treatment on well-defined CV endpoints. In spite of the achievement and maintenance of strict glycaemic control (HbA 1c <7.0%), no beneficial effect of intensive therapy was apparent in any of the studies. At the same time these results were presented, the results of an analysis of the 10 year follow-up of the UKPDS also became available and provided a more optimistic view of the potential benefit of achieving good glycaemic control. The relative risk reductions for myocardial infarction and all-cause mortality were significantly lower in the patients who initially received the intensive treatment compared with those in the conventional treatment arm. Moreover, the initial benefit in terms of microvascular complications observed at the end of the intervention trial remained unaltered at follow-up. Once again the debate on the importance of glycaemic control in preventing macrovascular complications remains unsettled. These results, however, require some reconciliation, and the objective of this commentary is to analyse a series of elements, including the changes in the treatment approach to CV risk factors in type 2 diabetes, the effect of glucoselowering agents, and the characteristics of the patients included in the different trials, that should be taken into account when interpreting the results of intervention trials in type 2 diabetes.

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Section: Hypoglycaemia: a Trigger For CV Events?mentioning

confidence: 99%

Megatrials in type 2 diabetes. From excitement to frustration?

Prato

2009

Diabetologia

118

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“…A number of studies have reported that diabetes mellitus (DM) leads to autonomic neuropathic dysfunctions, including impairment of the baroreflex control of heart rate (HR) in both diabetic patients and chemically induced diabetic rats [2,3] . Impairment of the baroreflex sensitivity (BRS) underlying the diabetic state was closely related to lifethreatening arrhythmias, heart failure and sudden death [4,5] .…”

Section: Introductionmentioning

confidence: 99%

Influence of fluvastatin on cardiac function and baroreflex sensitivity in diabetic rats

Xie

Sun

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate whether fluvastatin is able to ameliorate the impaired cardiac function or baroreflex sensitivity (BRS) in rats with type 1 diabetes. Methods: Type 1 diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ) and then administered fluvastatin (1.5, 3.0, and 6.0 mg·kg -1 ·d -1 ) for 30 d. Food and drink intake was recorded every day. Fasting blood glucose (FBG) level, blood lipid level, cardiac function and BRS were measured in diabetic rats after fluvastatin treatment for 30 d. Results: The polydipsia, polyphagia and abnormal biochemical indexes of blood were significantly ameliorated by the the 3.0-and 6.0-mg doses of fluvastatin in STZ-induced diabetic rats. FBG was decreased in diabetic rats after fluvastatin treatment for 30 d. The left ventricular systolic pressure (LVSP) and the maximum rate of change of left ventricular pressure in the isovolumic contraction and relaxation period (±dp/dt max ) were elevated, and left ventricular diastolic pressure (LVEDP) was decreased by fluvastatin. The attenuated heart rate responses to arterial blood pressure (ABP) increase induced by phenylephrine (PE) and ABP decrease induced by sodium nitroprusside (SNP) were reversed by the 3.0-mg dose of fluvastatin. Conclusion: Fluvastatin regulates blood lipid levels and decreases the FBG level in diabetic rats. These responses can protect the diabetic heart from complications by improving cardiac function and BRS.

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“…Several studies have shown that as compared with those free of diabetes, diabetic patients with cardiac or peripheral autonomic neuropathy related to poor glycemic control and sedentary status have lower baroreflex sensitivity [32,33]. The impaired short-term cardiovascular control in diabetes mellitus may be caused by the functional or structural impairment of nerve fibers of the autonomic nervous system innervating the heart and blood vessels [34]. de MouraTonello et al [35] further concluded that the presence of diabetic neuropathies may account for the additional impairment of the sympathetic control to the blood vessels, possibly leading to the reduction of large-scale MSE, while the vagal impairment is a primary result of type 1 or 2 diabetes which is associated with the reduced small-scale MSE [36].…”

Section: Discussionmentioning

confidence: 99%

Glycemic Control, Hand Activity, and Complexity of Biological Signals in Diabetes Mellitus

Lin

Haryadi

et al. 2017

Complexity

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Both glycemic control and handgrip strength affect microvascular function. Multiscale entropy (MSE) of photoplethysmographic (PPG) pulse amplitudes may differ by diabetes status and hand activity. Of a middle-to-old aged and right-handed cohort without clinical cardiovascular disease, we controlled age, sex, and weight to select the unaffected (no type 2 diabetes, = 36), the wellcontrolled diabetes (HbA1c < 8%, = 22), and the poorly controlled diabetes (HbA1c ≥ 8%, = 22) groups. MSEs were calculated from consecutive 1,500 PPG pulse amplitudes of bilateral index fingertips. The small-, medium-, and large-scale MSEs were defined as the average of scale 1 (MSE 1 ), scales 2-4 (MSE 2-4 ), and scales 5-10 (MSE 5-10 ), respectively. Intra-and intergroups were compared by one-and two-sample -tests, respectively. The dominant hand MSE 5-10 was lower in the poorly controlled diabetes group than the well-controlled diabetes and the unaffected (1.28 versus 1.52 and 1.56, = 0.019 and 0.001, resp.) groups, whereas the nondominant hand MSE 5-10 was lower in the well-and poorly controlled diabetes groups than the unaffected group (1.35 and 1.29 versus 1.58, = 0.008 and 0.005, resp.). The MSE 1 of dominant hand was higher than that of nondominant hand in the well-controlled diabetes (1.35 versus 1.10, = 0.048). In conclusion, diabetes status and hand dominance may affect the MSE of PPG pulse amplitudes.

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Diabetic Cardiovascular Autonomic Neuropathy

Cited by 1,031 publications

References 110 publications

Megatrials in type 2 diabetes. From excitement to frustration?

Megatrials in type 2 diabetes. From excitement to frustration?

Influence of fluvastatin on cardiac function and baroreflex sensitivity in diabetic rats

Glycemic Control, Hand Activity, and Complexity of Biological Signals in Diabetes Mellitus

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