Sudden death: Neurogenic causes, prediction and prevention

Abstract

Sudden death is a major health problem all over the world. The most common causes of sudden death are cardiac but there are also other causes such as neurological conditions (stroke, epileptic attacks and brain trauma), drugs, catecholamine toxicity, etc. A common feature of all these diverse pathologies underlying sudden death is the imbalance of the autonomic nervous system control of the cardiovascular system. This paper reviews different pathologies underlying sudden death with emphasis on the autonomic nervous system contribution, possibilities of early diagnosis and prognosis of sudden death using various clinical markers including autonomic markers (heart rate variability and baroreflex sensitivity), present possibilities of management and promising prevention by electrical neuromodulation.

Keywords: Sudden death; baroreflex sensitivity; heart rate variability; parasympathetic; sympathetic.

Figure 1.

Alpha subunit of the voltage operated K⁺ channel. The voltage operated K⁺ channel is a symmetric tetramer of four alpha subunits around a pore. Each α subunit encoded by the human ether-to-go-go gene (hERG) has six transmembrane helices.

Figure 2.

Isoprenaline-induced cardiac dysfunction. (a) Parasternal long axis image at end-systole showing typical akinesia of left ventricular septal wall in one male Wistar rat two hours after 50 mg/kg isoprenaline injection. (b) M mode of long axis view. Dotted circle and arrows indicate akinetic parts of myocardium Source: reproduced with permission of M. Vasić.

Figure 3.

Spectrograms of heart rate variability (HRV) in cardiomyopathy induced by doxorubicin (right). Note the reduction of HRV in lower frequencies (marked in red) by toxic doses of doxorubicin three days before fatal outcome. Source: reproduced with permission of D. Bajić.

Figure 4.

Poincaré plots and the corresponding contour density plots of the heart rate (HR) in one rat before and after treatment with doxorubicin. Note the comet-shaped plot before treatment and the change of the shape after treatment due to a reduction of HR variability three days before fatal outcome. Source: reproduced with permission of D. Bajić.