Dipyridamole myocardial SPECT with low heart rate response indicates cardiac autonomic dysfunction in patients with diabetes

2001 ◽  
Vol 8 (2) ◽  
pp. 129-135 ◽  
Author(s):  
K Lee
1989 ◽  
Vol 76 (6) ◽  
pp. 567-572 ◽  
Author(s):  
Marco ROSSI ◽  
Giuliano Marti ◽  
Luigi Ricordi ◽  
Gabriele Fornasari ◽  
Giorgio Finardi ◽  
...  

1. The prevalence of cardiac autonomic alterations was evaluated in 23 obese subjects with body mass index 37.2 ± 3.03 kg/m2 (mean ± sd), compared with 78 controls with body mass index 22.5 ± 2.6 kg/m2 (P < 0.001). 2. Cardiac autonomic function was assessed by four standard tests (heart rate response to deep breathing and to the Valsalva manoeuvre, systolic blood pressure fall after standing and diastolic pressure rise during handgrip) and by the cross-correlation test, a new method of computerized analysis of respiratory sinus arrhythmia based on spectral analysis of electrocardiographic and respiratory signals. 3. Considering tests indicative of parasympathetic function, only the heart rate response to the deep breathing and the cross-correlation test were significantly lower in the obese than in the control group [deep breathing = 13.95 ± 8.65 beats/min (mean ± sd) vs 24.5 ± 7.65, P < 0.001; cross-correlation 4.28 ± 0.74 units vs 5.14 ± 0.63, P < 0.001]. Deep breathing and/or cross-correlation were abnormal in 10 (43.5%) obese subjects (deep breathing: seven subjects, cross-correlation: eight subjects). No significant difference between groups was found for the response to the Valsalva manoeuvre: the Valsalva ratio was 1.69 ± 0.45 in obese subjects and 1.88 ± 0.33 in controls (P = NS). The Valsalva ratio was abnormal in three obese subjects. 4. No significant differences were found between groups for tests indicative of sympathetic function. The rise in diastolic blood pressure after handgrip was 12.6 ± 6.2 mmHg (1.67 ± 0.82 kPa) in obese subjects and 18.2 ± 4.9 mmHg (2.42 ± 0.65 kPa) in controls (P = NS), and the fall in systolic blood pressure after standing was −6.8 ± 8.6 mmHg (−0.90 ± 1.14 kPa) in obese subjects and −6.9 ± 10.4 mmHg (−0.91 ± 1.38 kPa) in controls (P = NS). The handgrip test was abnormal in four obese subjects, while no obese subject had an abnormal blood pressure response to standing. 5. Our findings suggest a high incidence of cardiac autonomic dysfunction in obese subjects. Since cardiac autonomic alterations have been shown to be involved in the mechanisms of cardiac sudden death, our data suggest a possible role of autonomic dysfunction in the increased risk for sudden death in obesity.


2016 ◽  
Vol 46 (3) ◽  
pp. 338-343 ◽  
Author(s):  
Magda M. Maia ◽  
Bruno Gualano ◽  
Ana L. Sá-Pinto ◽  
Adriana M.E. Sallum ◽  
Rosa M.R. Pereira ◽  
...  

1985 ◽  
Vol 68 (5) ◽  
pp. 545-552 ◽  
Author(s):  
André Grimaldi ◽  
Wojciech Pruszczynski ◽  
Francis Thervet ◽  
Raymond Ardaillou

1. Thirty-three insulin-dependent diabetic patients were separated into two groups from the results of three different tests for cardiac vagal neuropathy: heart rate response to deep breathing, Valsalva manoeuvre and heart rate response to postural change. Seventeen patients were considered as without ('intact’ patients) and 16 as with ('denervated’ patients) cardiac autonomic dysfunction. One patient with a transplanted heart was also studied. 2. Plasma antidiuretic hormone (ADH), plasma aldosterone and plasma renin activity (PRA) were measured immediately before and 60 min after intravenous administration of frusemide and passage from lying to standing. The kinetics of hormonal responses were analysed more precisely (five blood collections) in six patients of each group who were studied again. Heart rate and blood pressure were recorded before each blood collection. 3. Volume depletion estimated from the rise in plasma protein (+ 11.9 and + 12.2% in ‘denervated’ and ‘intact’ patients respectively) and heart rate response (+ 10.6 and + 14.7%) were similar in both groups. Mean blood pressure was unchanged in the ‘intact’ patients whereas it fell in the ‘denervated’ patients (−13.5%). PRA (+ 161.5 and + 231.2% in ‘denervated’ and ‘intact’ patients respectively) and plasma aldosterone (+ 318.2 and 279%) increased in both groups whereas plasma ADH was stimulated only in ‘intact’ patients (+ 55.3%). The failure of ADH to respond significantly to the volume stimulus in ‘denervated’ patients was confirmed by the results of the time-course study. Plasma ADH remained at the same levels in ‘denervated’ patients whereas it increased significantly (+ 82.4%) in ‘intact’ patients. There was no ADH response in the transplanted patient. 4. These results suggest that, in humans, cardiac receptors and vagal pathways play a role in ADH response to volume depletion.


Author(s):  
Masahiko Hashizume ◽  
Saori Kinami ◽  
Keiichi Sakurai ◽  
Kazuhiro Izawa ◽  
Hideyuki Shiotani

Background Few reports have evaluated the relationship between changes in postprandial blood pressure and the severity of autonomic dysfunction in patients with type 2 diabetes. This was a cross-sectional study designed to investigate postprandial blood pressure changes in individuals without type 2 diabetes and patients with type 2 diabetes and mild or severe cardiac autonomic dysfunction. Methods Forty patients with type 2 diabetes mellitus and 20 individuals without type 2 diabetes participated in this study. Fifty-two participants underwent a meal tolerance test. Blood pressure (brachial systolic blood pressure (bSBP) and central systolic blood pressure (cSBP)), electrocardiogram recordings, and blood samples were assessed before and after meal ingestion. Patients with diabetes were divided into two groups based on their coefficient of variation of R–R intervals (CVRR): a normal or mildly dysfunctional group (mild group, CVRR ≥ 2%; n = 20) and a severely dysfunctional group (severe group, CVRR < 2%; n = 15). Results In the control group, bSBP and cSBP did not significantly change after meal ingestion, whereas both decreased significantly at 60 min after meal ingestion in the mild and severe groups. While blood pressure recovered at 120 min after meal ingestion in the mild group, a significant decrease in blood pressure persisted at 120 min after meal ingestion in the severe group. Conclusions Based on these results, adequate clinical attention should be paid to the risk of serious events related to postprandial decreases in blood pressure, particularly in patients with diabetes and severe cardiac autonomic dysfunction.


2010 ◽  
Vol 141 (3) ◽  
pp. 322-325 ◽  
Author(s):  
Piotr Bienias ◽  
Michał Ciurzyński ◽  
Dariusz Korczak ◽  
Krzysztof Jankowski ◽  
Maria Glińska-Wielochowska ◽  
...  

2015 ◽  
pp. 459-466 ◽  
Author(s):  
M. CHASWAL ◽  
S. DAS ◽  
J. PRASAD ◽  
A. KATYAL ◽  
M. FAHIM

Nitric oxide (NO) plays a crucial role not only in regulation of blood pressure but also in maintenance of cardiac autonomic tone and its deficiency induced hypertension is accompanied by cardiac autonomic dysfunction. However, underlying mechanisms are not clearly defined. We hypothesized that sympathetic activation mediates hemodynamic and cardiac autonomic changes consequent to deficient NO synthesis. We used chemical sympathectomy by 6-hydroxydopamine to examine the influence of sympathetic innervation on baroreflex sensitivity (BRS) and heart rate variability (HRV) of chronic NG-nitro-L-arginine methyl ester (L-NAME) treated adult Wistar rats. BRS was determined from heart rate responses to changes in systolic arterial pressure achieved by intravenous administration of phenylephrine and sodium nitroprusside. Time and frequency domain measures of HRV were calculated from 5-min electrocardiogram recordings. Chronic L-NAME administration (50 mg/kg per day for 7 days orally through gavage) in control rats produced significant elevation of blood pressure, tachycardia, attenuation of BRS for bradycardia and tachycardia reflex and fall in time as well as frequency domain parameters of HRV. Sympathectomy completely abolished the pressor as well as tachycardic effect of chronic L-NAME. In addition, BRS and HRV improved after removal of sympathetic influence in chronic L-NAME treated rats. These results support the concept that an exaggerated sympathetic activity is the principal mechanism of chronic L NAME hypertension and associated autonomic dysfunction.


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