Diabetes and cardiac autonomic neuropathy: Clinical manifestations, cardiovascular consequences, diagnosis and treatment

Cardiac autonomic neuropathy (CAN) is a frequent chronic complication of diabetes mellitus with potentially life-threatening outcomes. CAN is caused by the impairment of the autonomic nerve fibers regulating heart rate, cardiac output, myocardial contractility, cardiac electrophysiology and blood vessel constriction and dilatation. It causes a wide range of cardiac disorders, including resting tachycardia, arrhythmias, intraoperative cardiovascular instability, asymptomatic myocardial ischemia and infarction and increased rate of mortality after myocardial infarction. Etiological factors associated with autonomic neuropathy include insufficient glycemic control, a longer period since the onset of diabetes, increased age, female sex and greater body mass index. The most commonly used methods for the diagnosis of CAN are based upon the assessment of heart rate variability (the physiological variation in the time interval between heartbeats), as it is one of the first findings in both clinically asymptomatic and symptomatic patients. Clinical symptoms associated with CAN generally occur late in the disease process and include early fatigue and exhaustion during exercise, orthostatic hypotension, dizziness, presyncope and syncope. Treatment is based on early diagnosis, life style changes, optimization of glycemic control and management of cardiovascular risk factors. Medical therapies, including aldose reductase inhibitors, angiotensin-converting enzyme inhibitors, prostoglandin analogs and alpha-lipoic acid, have been found to be effective in randomized controlled trials. The following article includes the epidemiology, clinical findings and cardiovascular consequences, diagnosis, and approaches to prevention and treatment of CAN

Effects of Three Month Nasal Continuous Positive Airway Pressure Treatment on Electrocardiographic, Echocardiographic and Overnight Polysomnographic Parameters in Newly Diagnosed Moderate/Severe Obstructive Sleep Apnea Patients

The objective of the study was to determine the effects of nasal continuous positive airway pressure (nCPAP) therapy on left ventricular (LV) function and electrocardiographic parameters in newly diagnosed moderate/severe obstructive sleep apnea (USA) patients without cardiovascular comorbidities and medical treatments. We examined 44 patients who underwent overnight polysomnography together with 24-hour Ho lter electrocardiography, cardiopulmonary exercise testing including heart rate recovery at 1 minute (HRR-1), echocardiography, surface electrocardiography, and those who were diagnosed with moderate/severe USA apnea-hypopnea index >= 15. After 3 months of nCPAP treatment, the above-mentioned examinations were repeated. Forty-four patients completed the treatment period. Twelve weeks on effective nCPAP induced a significant increase in the mitral E/A ratio (P = 0.001), as well as reductions in isovolumic relaxation time (P = 0.001) and mitral deceleration time (DT) (P = 0.002). There were no significant differences in LV ejection fraction, LV mass index, and pulsed wave Doppler parameters. Mean heart rate was 79.2 +/- 12.5 pulses/minute, maximum P-wave duration 117.5 +/- 8.6 msec, P-wave dispersion (PWd) 54.6 +/- 10.2 msec, corrected QT interval (QTc) 436.5 +/- 40.5 msec, and QT dispersion (QTd) 46.3 +/- 7.1 msec, which significantly decreased to 70.4 +/- 9.6 pulses/minute (P <0.001), 111.5 +/- 8.7 msec (P <0.001), 51.6 +/- 8.9 msec (P <0.001), 418.4 +/- 31.2 msec (P <0.001), and 33.8 +/- 3.4 msec (P < 0.001), respectively. Exercise capacity at baseline determined as 10.5 +/- 2.2 metabolic equivalents (METS) and HRR-1 (20.6 +/- 11.7 bpm) significantly increased (12.1 +/- 1.5 METS and 27.4 +/- 8.6 bpm). There was no significant difference in aortic root parameters. Three-month nCPAP therapy significantly increased LV shortening fraction, with no effect on systolic function or aortic root diameters and a positive effect on heart rate, PWd, HRR-1, QTc and QTd time following nCPAP therapy

The effect of epicardial adipose tissue thickness with irritable bowel syndrome

Durakoglugil, Emre/0000-0001-5268-4262; duman, hakan/0000-0002-1441-7320; Erdogan, Turan/0000-0003-2986-5457WOS: 000446564700008PubMed: 30317341Objective: To investigate the association of epicardial adipose tissue thickness with irritable bowel syndrome. Methods: This case-control and observational study was conducted in Recep Tayyip Erdogan University between January and December 2014, and comprised patients of irritable bowel syndrome and healthy controls who underwent a complete transthoracic echocardiographic examination as well as measurements of epicardial adipose tissue. They were screened for psychiatric or organic bowel diseases for the sake of precise diagnosis. Epicardial fat thickness was measured perpendicularly in front of the right ventricular free wall at end-diastole.SPSS 15 was used to analyse the data. Results: of the 75 subjects, 44(59%) were patients and 31(41%) were controls. There was no statistically significant difference between the groups except epicardial adipose tissue thickness, which was significantly elevated in patients (p<0.001). C-reactive protein was significantly higher in patients (p=0.002). Epicardial adipose tissue (p<0.001) and haematocrit (p<0.05) were independent predictors of irritable bowel syndrome. Conclusion: Increased epicardial adipose tissue thickness, and accompanying low-grade inflammation appeared to be involved in irritable bowel syndrome pathogenesis

Cardiac autonomic nervous dysfunction detected by both heart rate variability and heart rate turbulence in prediabetic patients with isolated impaired fasting glucose

Objective: Cardiac autonomic nervous dysfunction (CAND), a severe complication of diabetes, has also been shown to affect prediabetic patients. The role of isolated impaired fasting plasma glucose (IFG), a subtype of prediabetes, is not clear in the pathogenesis of CAND. The aim of this study was to examine the relationship between isolated IFG and cardiac autonomic function using heart rate variability (HRV) and heart rate turbulence (HRT) indices derived from 24-h Holter-electrocardiogram recordings. Methods: This observational, prospective, cross-sectional study examined 400 consecutive subjects divided into three groups according to oral glucose tolerance test results: the control group [Group I, fasting plasma glucose (FPG) = 100 and <126 mg/dL, n=134), and the isolated impaired glucose tolerance (IGT), both IFG and IGT, or newly diagnosed diabetes' group (Group III, n=73). Patients with non-sinus rhythm, known diabetes mellitus, coronary artery disease, heart failure, severe valvular disease, or receiving medical therapy that may affect HRV and HRT indices were excluded. Time domain HRV parameters, turbulence onset (TO), turbulence slope (TS), and HRT category were examined. Chi-square, one-way analysis of variance, Kruskal-Wallis H, and Mann-Whitney U tests were used to compare variables where appropriate. The correlation between Holter data and FPG levels was analyzed using the Spearman's test. Multiple linear regression analysis was performed to identify independent predictors of the HRV and HRT parameters. Results: Median (interquartile range 25-75) FPG levels in Groups I, II, and III were 89 (83/93) mg/dL, 109 (104/116) mg/dL, and 174 (150.5/197) mg/dL, respectively. There were significant differences in HRV and HRT parameters between and among all groups. While HRV parameters and TS decreased from Group I to Group III, TO and HRT category gradually increased. Additionally, FPG level was significantly correlated with SDNN, r=-0.220; SDNN index, r=-0.192; SDANN, r=-0.207; RMSSD, r=-0.228; pNN50, r=-0.226; TO, r=0.354; and TS, r=-0.331 (all p<0.001). Conclusion: CAND, as detected by both HRV and HRT, appear to be present in the isolated IFG subtype of prediabetes