Autonomic influence on cardiovascular performance in diabetic subjects

Roy, Thomas M.; Peterson, Hugh R.; Snider, Harvy L.; Cyrus, Jahangir; Broadstone, Vasti L.; Fell, R. D.; Rothchild, Armand H.; Samols, Ellis; Pfeifer, Michael

doi:10.1016/0002-9343(89)90648-7

Cited by 22 publications

(29 citation statements)

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“…Catecholamine levels were similar at rest and during exercise between the two groups studied. There have been varied reports of increased (11,40), normal (12), and decreased (41) catecholamine levels in diabetic patients that may be related to the duration of diabetes and the presence of autonomic neuropathy (40). There were no significant differences in FFA, glycerol, or hydroxybutyrate levels in this study Increased levels have been reported in poorly controlled diabetic patients with ketosis (39), but the diabetic patients in this study were all stable.…”

Section: Conclusion-this Study Hascontrasting

confidence: 51%

“…Abnormalities of systolic (7)(8)(9) and diastolic (10) cardiac function, including impaired cardiac output responses to exercise (11,12), have been reported in the absence of coronary artery disease, and the existence of a specific cardiac disease, diabetic cardiomyopathy, has been postulated (13)(14)(15)(16). However, a recent study (17) using first-pass radionuclide angiography to assess left ventricular ejection fraction (EF) at peak exercise failed to identify abnormal cardiac function in young patients with IDDM.…”

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confidence: 99%

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Exercise Responses in Patients With IDDM

et al. 1997

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Section: Conclusion-this Study Hascontrasting

confidence: 51%

mentioning

confidence: 99%

Exercise Responses in Patients With IDDM

et al. 1997

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“…The present study also shows an inverse correlation between neuropathy and longitudinal myocardial diastolic function. The sympathetic overactivity [27] and increase in resting work product in these patients [28] may be directly related to functional compensation. Possibly, the change in autonomic function and myocardial innervation is responsible for compensated increased radial function in diabetic patients with preserved global ejection fraction.…”

Section: Changes In Longitudinal and Radial Functionmentioning

confidence: 93%

Relationship between longitudinal and radial contractility in subclinical diabetic heart disease

2004

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Subclinical left ventricular (LV) dysfunction may be identified by reduced longitudinal contraction. We sought to define the effects of subclinical LV dysfunction on radial contractility in 53 patients with diabetes mellitus with no LV hypertrophy, normal ejection fraction and no ischaemia as assessed by dobutamine echocardiography, in comparison with age-matched controls. Radial peak myocardial systolic velocity (Sm) and early diastolic velocity (Em), strain and strain rate were measured in the mid-posterior and mid-anteroseptal walls in parasternal views and each variable was averaged for individual patients (radial contractility). These variables were also measured in the mid-posterior and mid-anteroseptal walls in the apical long-axis view and each variable was averaged for individual patients (longitudinal contractility). Mean radial Sm, strain and strain rate were significantly increased in diabetic patients (2.9 +/- 0.6 cm/s, 28 +/- 5% and 1.8 +/- 0.4 s(-1) respectively) compared with controls (2.4 +/- 0.7 cm/s, 23 +/- 4% and 1.6 +/- 0.3 s(-1) respectively; all P<0.001), but there was no difference in Em (3.3 +/- 1.2 compared with 3.1 +/- 1.1 cm/s, P=not significant). In contrast, longitudinal Sm, Em, strain and strain rate were significantly lower in diabetic patients (3.6 +/- 1.1 cm/s, 4.3 +/- 1.6 cm/s, 21 +/- 4% and 1.6 +/- 0.3 s(-1) respectively) than in controls (4.3 +/- 1.0 cm/s, 5.7 +/- 2.3 cm/s, 26 +/- 4% and 1.9 +/- 0.3 s(-1) respectively; all P< or =0.001). Thus radial contractility appears to compensate for reduced longitudinal contractility in subclinical LV dysfunction occurring in the absence of ischaemia or LV hypertrophy.

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“…Attenuated oxygen uptake (V o 2 ) in response to incremental exercise and slower V o 2 kinetics compared with control subjects have been observed [1][2][3]. Abnormalities related to cardiac output, arteriovenous oxygen difference, and skeletal muscle metabolism have been associated with these altered exercise responses in patients with diabetes [4,5]. However, the underlying pathophysiologic process responsible for these limitations is unknown.…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, hyperglycemia is deleterious on several levels: it is associated with (1) endothelial dysfunction [6], (2) increased formation of advanced glycation end products altering the structure and function of molecules in several biologic systems [6][7][8][9][10], (3) altered cardiomyocyte bioenergetics [8], (4) abnormalities in pulmonary function [11], and (4) cardiovascular autonomic neuropathy [12]. However, results of studies evaluating whether glycemic control affects exercise tolerance in patients with type 2 diabetes mellitus are conflicting [2,[13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%