Over the past decade the number of patients presenting with heart failure has increased exponentially.¹ It has been estimated that 4.7 million patients in the USA have chronic heart failure, with 400 000 new cases per year, resulting in one million hospitalisations.¹ The diagnostic and therapeutic costs involved with heart failure are estimated to be more than $11 billion per year.¹ Gheorghiade and Bonow emphasised that the aetiology of heart failure may be coronary artery disease in > 70% of patients.²

Currently, three routine courses of action are available: medical treatment, heart transplantation, and revascularisation. Newer therapeutic modalities include laser therapy, advanced surgery, assist devices, artificial hearts,³ and transplantation of different (progenitor) cells.⁴ These options should currently be considered experimental but may offer alternative treatments in the future. Medical treatment has improved substantially over the past years, with the introduction of angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, and spironolactone. Four recent trials have demonstrated the value of β adrenergic blocking agents in the treatment of patients with heart failure.⁵ Finally, amiodarone has been demonstrated to reduce sudden death in patients with heart failure.⁶ Despite all of these new drugs, mortality of patients with severe heart failure remains high; Cowie and colleagues⁷ reported 12 month mortality to be 38% and extrapolation of these results demonstrated five year mortality to be > 70%.

The second option, heart transplantation, has fairly good long term prognosis but the limited number of donor hearts is largely exceeded by demand.⁸ In addition, many patients with heart failure have significant co-morbidities, excluding them as candidates for heart transplantation.

Revascularisation is the third option in patients with heart failure. The major drawback to performing revascularisation in these patients is the high periprocedural morbidity and mortality. …