Comparison of four alternative national universal anterior cruciate ligament injury prevention programme implementation strategies to reduce secondary future medical costs.

BACKGROUND/AIM: Anterior cruciate ligament (ACL) injury is a common and devastating sporting injury. With or without ACL reconstruction, the risk of knee osteoarthritis (OA) and permanent disability later in life is markedly increased. While neuromuscular training programmes can prevent 50-80% of ACL injuries, no national implementation strategies exist in Australia. The aim of this study was to compare the ability of four alternative national universal ACL injury prevention programme implementation strategies to reduce future medical costs secondary to ACL injury. METHODS: A Markov economic decision model was constructed to estimate the value in lifetime future medical costs prevented by implementing a national ACL prevention programme among four hypothetical cohorts: high-risk sport participants (HR) aged 12-25 years; HR 18-25 years; HR 12-17 years; all youths (ALL) 12-17 years. RESULTS: Of the four programmes examined, the HR 12-25 programme provided the greatest value, averting US$693 of direct healthcare costs per person per lifetime or US$221 870 880 in total. Without training, 9.4% of this cohort will rupture their ACL and 16.8% will develop knee OA. Training prevents 3764 lifetime ACL ruptures per 100 000 individuals, a 40% reduction in ACL injuries. 842 lifetime cases of OA per 100 000 individuals and 584 TKRs per 100 000 are subsequently averted. Numbers needed to treat ranged from 27 for the HR 12-25 to 190 for the ALL 12-17. CONCLUSIONS: The HR 12-25 programme was the most effective implementation strategy. Estimation of the break-even cost of health expenditure savings will enable optimal future programme design, implementation and expenditure.

Fibrosis as a therapeutic target post-myocardial infarction.

The extracellular matrix (ECM) is a dynamic microenvironment and a major contributor to the adverse ventricular remodelling that follows myocardial infarction (MI), via activation of both direct pro-fibrotic pathways and matrix metalloproteinases (MMPs) that enhance collagenase activity. Reactive fibrosis, i.e. deposition of ECM materials remote from the region of the MI is clearly detrimental to ventricular function and contributory to adverse outcomes post-MI. Therefore, reversal of this process represents an important therapeutic target in post-MI management and treatment of established heart failure. A number of existing agents exert their beneficial effects in part via reductions in ECM deposition. Furthermore, specific anti-fibrotic drugs have been developed and are currently being explored for these and other cardiac conditions where pathological ECM deposition is felt to be contributory to disease progression.