Cardiac autonomic neuropathy: Risk factors, diagnosis and treatment

Cardiac autonomic neuropathy(CAN)is a serious complication of diabetes mellitus(DM)that is strongly associated with approximately five-fold increased risk of cardiovascular mortality.CAN manifests in a spectrum of things,ranging from resting tachycardia and fixed heart rate(HR)to development of"silent"myocardial infarction.Clinical correlates or risk markers for CAN are age,DM duration,glycemic control,hypertension,and dyslipidemia(DLP),development of other microvascular complications.Established risk factors for CAN are poor glycemic control in type 1 DM and a combination of hypertension,DLP,obesity,and unsatisfactory glycemic control in type 2DM.Symptomatic manifestations of CAN include sinus tachycardia,exercise intolerance,orthostatic hypotension(OH),abnormal blood pressure(BP)regulation,dizziness,presyncope and syncope,intraoperative cardiovascular instability,asymptomatic myocardial ischemia and infarction.Methods of CAN assessment in clinical practice include assessment of symptoms and signs,cardiovascular reflex tests based on HR and BP,short-term electrocardiography(ECG),QT interval prolongation,HR variability(24 h,classic24 h Holter ECG),ambulatory BP monitoring,HR turbulence,baroreflex sensitivity,muscle sympathetic nerve activity,catecholamine assessment and cardiovascular sympathetic tests,heart sympathetic imaging.Although it is common complication,the significance of CAN has not been fully appreciated and there are no unified treatment algorithms for today.Treatment is based on early diagnosis,life style changes,optimization of glycemic control and management of cardiovascular risk factors.Pathogenetic treatment of CAN includes:Balanced diet and physical activity;optimization of glycemic control;treatment of DLP;antioxidants,first of allα-lipoic acid(ALA),aldose reductase inhibitors,acetylL-carnitine;vitamins,first of all fat-soluble vitamin B1;correction of vascular endothelial dysfunction;prevention and treatment of thrombosis;in severe cases-treatment of OH.The promising methods include prescription of prostacyclin analogues,thromboxane A2 blockers and drugs that contribute into strengthening and/or normalization of Na^+,K^+-ATPase(phosphodiesterase inhibitor),ALA,dihomo-γ-linolenic acid(DGLA),ω-3 polyunsaturated fatty acids(ω-3 PUFAs),and the simultaneous prescription of ALA,ω-3 PUFAs and DGLA,but the future investigations are needed.Development of OH is associated with severe or advanced CAN and prescription of nonpharmacological and pharmacological,in the foreground midodrine and fludrocortisone acetate,treatment methods are necessary.

Diabetic cardiac autonomic neuropathy: Do we have any treatment perspectives?

Cardiac autonomic neuropathy(CAN) is a serious and common complication of diabetes mellitus(DM). Despite its relationship to an increased risk of cardiovascular mortality and its association with multiple symptoms and impairments, the significance of CAN has not been fully appreciated. CAN among DM patients is characterized review the latest evidence and own data regarding the treatment and the treatment perspectives for diabetic CAN. Lifestyle modification, intensive glycemic control might prevent development or progression of CAN. Pathogenetic treatment of CAN includes: balanced diet and physical activity; optimization of glycemic control; treatment of dyslipoproteinemia; correction of metabolic abnormalities in myocardium; prevention and treatment of thrombosis; use of aldose reductase inhibitors; dihomo-γ-linolenic acid(DGLA), acetyl-Lcarnitine, antioxidants, first of all α-lipoic acid(α-LA), use of long-chain ω-3 and ω-6 polyunsaturated fatty acids(ω-3 and ω-6 PUFAs), vasodilators, fat-soluble vitamin B1, aminoguanidine; substitutive therapy of growth factors, in severe cases-treatment of orthostatic hypotension. The promising methods include research and use of tools that increase blood flow through the vasa vasorum, including prostacyclin analogues, thromboxane A_2 blockers and drugs that contribute into strengthening and/or normalization of Na^+, K^+-ATPase(phosphodiesterase inhibitor), α-LA, DGLA, ω-3 PUFAs, and the simultaneous prescription of α-LA, ω-3 PUFA and DGLA.