Diabetes mellitus is an important coronary artery disease risk factor. The presence of microalbuminuria, which indicates renal involvement in diabetic patients, is associated with an increased cardiovascular risk. There are suggestions that diabetic patients with microalbuminuria have more adverse risk profile such as higher ambulatory blood pressure and total cholesterol levels to account for the increased cardiovascular morbidity and mortality. QT dispersion is increasingly being recognized as a prognostic factor for coronary artery disease and sudden death. Some studies have suggested that QT dispersion is an important predictor of mortality in Type II diabetic patients. Our cross sectional study was to compare the QT dispersion and 24 hour ambulatory blood pressure monitoring between diabetic patients with microalbuminuria and those without microalbuminuria. Diabetic patients with overt coronary artery disease were excluded from the study. A total of 108 patients were recruited of which 57 patients had microalbuminuria and 51 were without microalbuminuria. The mean value of QT dispersion was significantly higher in patients with microalbuminuria than in patients without microalbuminuria (58.9 +/- 27.9 ms vs. 47.1 +/- 25.0 ms, p < 0.05). The mean 24 hour systolic and diastolic blood pressures were significantly higher in patients with microalbuminuria than in patients without microalbuminuria (129.5 +/- 12.3 mm Hg vs 122.3 +/- 10.2 mm Hg, p < 0.05 and 78.4 +/- 6.9 mm Hg vs 75.3 +/- 6.8 mm Hg, p < 0.05, respectively). Our study suggests that QT dispersion prolongation, related perhaps to some autonomic dysfunction, is an early manifestation of cardiovascular aberration in diabetic patients with microalbuminuria. The higher blood pressure levels recorded during a 24-hour period min diabetics with microalbuminuria could also possibly account for the worse cardiovascular outcome in this group of patients.
There is evidence for impairment in both central nervous system (CNS) and autonomic nervous system (ANS) function with prolonged alcohol use. While these impairments persist into abstinence, partial recovery of function has been demonstrated in both systems during sleep. To investigate potential ANS dysfunction associated with cortical CNS responses (impairment in CNS-ANS coupling), we assessed phasic heart rate (HR) fluctuation associated with tones that did and those that did not elicit a K-complex (KC) during stable N2 non-rapid eye movement (NREM) sleep in a group of 16 recently abstinent alcohol use disorder (AUD) patients (41.6 ± 8.5 years) and a group of 13 sex- and age-matched control participants (46.6 ± 9.3 years). Electroencephalogram (EEG) and electrocardiogram (ECG) data were recorded throughout the night. Alcohol consumption questionnaires were also administered to the AUD patients. AUD patients had elevated HR compared to controls at baseline prior to tone presentation. The HR fluctuation associated with KCs elicited by tone presentation was significantly smaller in amplitude, and tended to be delayed in time, in the AUD group compared with the control group, and the subsequent deceleration was also smaller in AUD patients. In both groups, the increase in HR was larger and occurred earlier when KCs were produced than when they were not, and there was no difference in the magnitude of the KC effect between groups. Phasic HR changes associated with KCs elicited by tones are impaired in AUD participants, reflecting ANS dysfunction possibly caused by an alteration of cardiac vagal trafficking. However, only the timing of the HR response was found to relate to estimated lifetime alcohol consumption in AUD. The clinical meaning and implications of these novel findings need to be determined.
Epilepsy is a debilitating disorder of uncontrollable recurrent seizures that occurs as a result of imbalances in the brain excitatory and inhibitory neuronal signals, that could stem from a range of functional and structural neuronal impairments. Globally, nearly 70 million people are negatively impacted by epilepsy and its comorbidities. One such comorbidity is the effect epilepsy has on the autonomic nervous system (ANS), which plays a role in the control of blood circulation, respiration and gastrointestinal function. These epilepsy-induced impairments in the circulatory and respiratory systems may contribute toward sudden unexpected death in epilepsy (SUDEP). Although, various hypotheses have been proposed regarding the role of epilepsy on ANS, the linking pathological mechanism still remains unclear. Channelopathies and seizure-induced damages in ANS-control brain structures were some of the causal/pathological candidates of cardiorespiratory comorbidities in epilepsy patients, especially in those who were drug resistant. However, emerging preclinical research suggest that neurotransmitter/receptor dysfunction and synaptic changes in the ANS may also contribute to the epilepsy-related autonomic disorders. Thus, pathological mechanisms of cardiorespiratory dysfunction should be elucidated by considering the modifications in anatomy and physiology of the autonomic system caused by seizures. In this regard, we present a comprehensive review of the current literature, both clinical and preclinical animal studies, on the cardiorespiratory findings in epilepsy and elucidate the possible pathological mechanisms of these findings, in hopes to prevent SUDEP especially in patients who are drug resistant.