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Chronic heart failure (CHF) is a complex syndrome characterized by impaired left ventricle function and increased activation of the sympathetic nervous system. The mortality rate is approximately 10% in the first month after onset and increases after 5 years up to 54% in men and 40% in women. 1 Although beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers and diuretics have improved the prognosis of these patients, the outcome remains unfavorable. 2-4, 4 Even when treated according to the latest guidelines, most studies report annual mortality rates between 8 and 10 %. The majority of the mortality can be attributed to progression of heart failure, ventricular arrhythmias or sudden cardiac death. The use of devices like cardiac resynchronization therapy (CRT) and implantable cardioverter-defibrillators (ICD) have further improved the prognosis of CHF, but these devices have their disadvantages like high costs, operative complication and device malfunction. 5,6 . Although there is a plethora of parameters associated with fatal arrhythmias, cardiac death and long-term prognosis in patients with CHF, it remains a challenge to identify those patients who are at the highest risk of death and who are most likely to benefit from currently available therapies. In this setting the parameters most reported on in patients with CHF are amongst others decreased left ventricular systolic function, renal dysfunction, broadening of the QRS complex, lower blood pressure, lower functional capacity (i.e. higher NYHA functional class) and higher plasma concentration of brain natriuretic peptide (BNP). In addition to these patient driven issues, there are socio-economic considerations with respect to the ever increasing costs of healthcare and the inevitable subsequent constrains on healthcare budget, especially with the use of expensive devices. Taken these issues together there is pressing call to improve risk stratification for CHF patients, with a special focus on identification of patients likely to benefit from more aggressive and device driven therapies.

Sympathetic hyperactivity in chronic heart failure; the role of123I-MIBG for the assessment of appropriate device allocation