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Promoting excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
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To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Prof. Guido Grassi
The sympathetic nervous system is overactive in congestive heart failure, acute myocardial infarction, ischemic stroke, hypertension and renal failure. Sympathetic deactivation should be an important goal of pharmacologic treatment in these diseases. Diuretic and direct vasodilatory agents almost invariably worsen the sympathetic dysfunction, while beta-blocking agents and drugs acting on the renin-angiotensin system (ACE-inhibitors and angiotensin II receptors blockers) have sympathoinibithory effects. Calcium channel blockers appear to be sympathetically neutral, while the results obtained so far with the use of a new class of central sympathicolitic agents acting on central Imidazoline receptor are promising.
The Sympathetic nervous system plays a fundamental role in the homeostatic control of the cardiovascular function by regulating both in the short-term and in the long-term period a number of haemodynamic variables, such as heart rate, cardiac output and peripheral vascular resistance, on which systolic and diastolic blood pressure values respectively depend. The relevance of the sympathetic function is not limited, however, only to physiologic states. Evidence has been indeed provided that in a variety of diseases which directly (e.g congestive heart failure, acute myocardial infarction, ischemic stroke and hypertension) and/or indirectly (renal failure, diabetes) affect cardiovascular function, sympathetic overactivity carries major prognostic implications. This may imply that sympathetic deactivation should be an important goal of pharmacologic treatment in the above mentioned disease.
A number of direct and indirect approaches have been extensively employed through the years to investigate sympathetic cardiovascular influences in humans (1). These include, for example, the assessment of plasma norepinephrine and epinephrine in peripheral venous blood as wall as the assay of 24 hours urinary catecholamines and their metabolites. These biomedical workers, although of large use particularly in the diagnosis of phoeochromocytoma, have been criticised in cardiovascular research due to a number of technical limitations which frequently reduce the sensitivity and specificity of these variables as faithful workers of adrenergic drive (1). A similar conclusion can also be drawn in regard to the use of heart rate as an adrenergic marker, given the evidence that tachycardia does not invariably reflect a state of sympathetic overdrive (2). In the past few years sophisticated approaches to assess adrenergic function have been developed. These include
1) spectral analysis of heart rate variability in bands that are reported as specific for sympathetic modulation of the sinus node, 2) microneurographic recording of efferent postganglionic sympathetic nerve traffic in peroneal or brachial nerves, 3) norepinephrine spillover technique, which allows to quantify the amount of the adrenergic neurotransmitter secreted in different vascular district and 4) neuroimaging techniques which allow to directly visualise cardiac sympathetic activation.
Several of the above mentioned techniques to assess sympathetic function have allowed to document an increase in the sympathetic cardiovascular drive in the heart failure syndrome (3-5). In the initial stages of the disease the adrenergic overdrive is a compensatory mechanism which preserves homeostasis by 1) increasing heart rate, myocardial contractility and thus cardiac output, 2) reducing arteriolar vasoconstriction and 3) determining sodium and water retention. In the more advanced clinical stages of the disease, however, the sympathetic activation exerts a wide range of adverse effects which include 1) increased cardiac output, 2) reduced coronary perfusion, 3) increased cardiac preload, 4) fluid retention and circulatory congestion and 5) direct necrotic effects on myocardial tissue (3). These effects are the pathophysiologic rationale for the evidence that in heart failure patients, plasma norepinephrine values are inversely related to patient’s survival, their prognostic importance being greater than that of haemodynamic variables (3-5). Interestingly, the prognostic value of sympathetic activation in heart failure patients is closely linked to the occurrence of life-threatening cardiac arrhythmias and sudden death, a finding that once again underlines the clinical relevance of neurogenic mechanisms in the development and progression of cardiac arrhythmic events. Similar findings have been reported in the early phases of an acute myocardial infarction, in which the degree of the sympathetic overdrive also appears to be related to arrhythmic episodes, ventricular fibrillation and sudden death (6). Other neurogenic abnormalities typical of heart failure and myocardial infarction disease deserve to be briefly mentioned. These include for example the finding that in both these conditions, vagal drive to the heart is reduced and that the sympathetic / parasympathetic imbalance appears to be associated with (and probably caused by) a dysfunction of the reflex control mechanisms (arterial baroreflexes, cardiopolmonary reflexes, chemoreflexes) involved in homeostatic cardiovascular control (1).
In acute post-stroke phases, in vasospastic angina, and in end-stage renal failure evidence has been provided that an increase in plasma norepinephrine values and a depressed heart rate variability pattern are frequently linked to poor clinical outcome and to the occurrence of life-threatening complications (7-8). This also appears to be the case in diabetic patients, in whom cardiovascular complications are more easily predictable by the autonomic dysfunction (sympathetic/parasympathetic imbalance) rather than by metabolic abnormalities (9).
In contrast, no data are available on the prognostic significance of the sympathetic activation charactering essential hypertension, although evidence has been provided that the phenomenon is involved in the patophysiology of hypertension-related end-organ damage and that its detection may predict the development of left ventricular hypertrophy (10).
Given the adverse effects of sympathetic activation on patients' prognosis and the development of complications, the conclusion can be drawn that sympathetic deactivation should represent a primary goal of non-pharmacological as well as of pharmacological therapeutic strategies (11). Among pharmacological interventions, some differences between various drug classes should be highlighted. Diuretic and direct vasodilatory agents, for example, almost invariably worsen the sympathetic dysfunction, while beta-blocking agents and drugs acting on the renin-angiotensin system (ACE-inhibitors and angiotensin II receptors blockers) exert clearcut sympathoinibithory effects. Calcium channel blockers appear to be sympathetically neutral, while the results obtained so far with the use of a new class of central sympathicolitic agents acting on central Imidazoline receptor are promising. On the whole, the early available data indicate that sympathomodulation represents a major goal of cardiovascular treatment aimed at improving cardioprotection and thus at prolonging patients’ survival.
The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.
1. Grassi G, Esler M. How to assess sympathetic activity in humans .J Hypertens 1999;17:719-734. Link 2. Grassi G, Vailati S, Bertinieri G, Seravalle G, Stella ML, Dell'Oro R, Mancia G. Heart rate as marker of sympathetic activity. J Hypertens 1998;16:1635-1639. Link 3. Cohn JN, Levine TB, Olivari MT, Garberg V, Lura D, Francis GS, Simon AB, Rector T. Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med 1984;311:819-823. Link 4. Kaye DM, Lefkovits J, Jennings GL, Bergin P, Broughton A, Esler MD. Adverse consequences of high sympathetic nervous activity in the failing human heart. J Am Coll Cardiol 1995;26:1257-1263. Link 5. Brunner-La Rocca HP, Esler MD, Jennings GL, Kaye DM. Effect of cardiac sympathetic nervous activity on mode of death in congestive heart failure. Eur Heart J. 2001;22:1136-1143. Link 6. Copie X, Hnatkova K, Staunton A, Fei L, Camm AJ, Malik M. Predictive power of increased heart rate versus depressed left ventricular jection fraction and heart rate variability for risk stratification after myocardial infarction. Results of a two-year follow-up study. J Am Coll Cardiol 1996;27:270-276. Link 7. Sander D, Winbeck K, Klingelhofer J, Etgen T, Conrad B. Prognostic relevance of pathological sympathetic activation after acute thromboembolic stroke. Neurology 2001;57:833-838. Link 8. Zoccali C, Mallamaci F, Parlongo S, Cutrupi S, Benedetto FA, Tripepi G, Bonanno G, Rapisarda F, Fatuzzo P, Seminara G, Cataliotti A, Stancanelli B, Malatino LS. Plasma norepinephrine predicts survival and incident cardiovascular events in patients with end-stage renal disease. Circulation 2002;105:1354-1359. Link 9. Endo A, Kinugawa T, Ogino K, Kato M, Hamada T, Osaki S, Igawa O, Hisatome I. Cardiac and plasma catecholamine responses to exercise in patients with type 2 diabetes: prognostic implications for cardiac-cerebrovascular events. Am J Med Sci.2000;320:24-30. Link 10. Grassi G. Sympathetic overdrive as an independent predictor of left ventricular hypertrophy: prospective evidence. J Hypertens 2006;24:815-817. Link 11. Grassi G. Sympathetic deactivation as a goal of nonpharmacologic and pharmacologic antihypertensive treatment: rationale and options. Curr Hypertens Rep 2003;5:277-280. Link
Prof. Guido Grassi Milan, Italy Chairman ESC working Group “Hypertension and the Heart".