Akif Serhat Balcıoğlu

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 (OSA) patients without cardiovascular comorbidities and medical treatments. We examined 44 patients who underwent overnight polysomnography together with 24-hour Holter electrocardiography, cardiopulmonary exercise testing including heart rate recovery at 1 minute (HRR-1), echocardiography, surface electrocardiography, and those who were diagnosed with moderate/severe OSA 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.

Which is responsible for cardiac autonomic dysfunction in non-diabetic patients with metabolic syndrome: Prediabetes or the syndrome itself?

AIMS Cardiac autonomic dysfunction (CAD) is associated with both prediabetes and metabolic syndrome (MS). Heart rate variability (HRV) and heart rate turbulence (HRT) are reliable 24-h Holter-ECG findings of cardiac autonomic function. This study aimed to investigate the relation between MS and its components and CAD using HRV and HRT. MATERIALS AND METHODS The study included 80 non-diabetic patients with MS and 70 control subjects. All study population and the patients with MS were further analyzed for each diagnostic component of MS to investigate which criteria impaired HRV and HRT. RESULTS HRV and HRT parameters were disturbed in patients in the MS group. While impairment in HRV and HRT was significantly related to the presence of the fasting plasma glucose (FPG) criterion, there were no differences between groups in terms of the other 4 MS criteria. Moreover, FPG level was significantly correlated with SDNN (r=-0.352, p<0.001), SDNN index (r=-0.423, p<0.001), SDANN (r=-0.301, p<0.001), RMSSD (r=-0.237, p<0.001), pNN50 (r=-0.237, p<0.001), turbulence onset (TO) (r=0.365, p<0.001) and turbulence slope (TS) (r=-0.365, p<0.001). Among the MS diagnostic criteria, only FPG level was an independent determinant of all HRV and HRT parameters. CONCLUSIONS This study confirms the relation between MS and CAD. Increased FPG alone appears to be responsible for the mentioned findings among the 5 diagnostic criteria. Accordingly, CAD may be the result of prediabetes, not MS in patients with MS.

The relationship between epicardial adipose tissue and P wave and QT dispersions.

OBJECTIVE Epicardial adipose tissue (EAT) secretes various pro-inflammatory and atherogenic mediators that have several endocrine and paracrine effects on heart. This study investigated the influence of EAT on QT and P wave dispersions (QTd, PWd), as simple, non-invasive tools of proarrhythmia on surface ECG. METHODS This was a cross-sectional study and included 70 patients with normal coronary arteries who underwent 12-derivation electrocardiography, echocardiography and biochemical examinations in order for QTd, PWd, and EAT thickness to be measured. RESULTS Median EAT thickness was 4.1 mm. Correlation analyses revealed that EAT was significantly associated with age (r=0.412, p<0.001), weight (r=0.262, p=0.028), body mass index (r=0.396, p<0.001), left atrium diameter (r=0.518, p<0.001), fasting plasma glucose (r=0.245, p=0.041), maximum P wave duration (r=0.343, p=0.004), minimum P wave duration (r=0.275, p=0.021) and PWd (r=0.265, p=0.026). No relation was found between study parameters and QTd. However, P wave dispersion was significantly related to EAT thickness (r=0.265, p=0.026), left atrium diameter (r=0.483, p<0.001), and the triglyceride levels (r=0.267, p=0.028). Multiple linear regression analyses revealed left atrial diameter as the only independent predictor of PWd. CONCLUSION A significant association between EAT and PWd was demonstrated in the study. While EAT is related to both increased PWd and left atrial size, left atrial diameter seems to be more important than EAT for prediction of atrial fibrillation (AF) in patients with normal coronary arteries.