Lessons from the 'legitimate' misuse of Medicare Benefits Schedule Item 45503.

This Perspective begins with a case study that raises two important questions: who is responsible for the existence of non-compliant Medicare billing, and who is responsible for eliminating it? In the discussion that follows, I argue, first, that the problem has been created by individual clinicians and by Medicare itself (i.e. the organisational structure that administers Medicare). Second, and more importantly, I argue that the ethical obligation to eliminate the problem extends more broadly to include both the government and the medical profession.

Private health insurance incentives and passive adverse selection: is Lifetime Health Cover responsible for the excess ageing of Australia's hospital cover risk pool?

Objective Lifetime Health Cover (LHC) was introduced in mid-2000 to increase participation in private health insurance that includes hospital cover (PHI-HC) and improve the risk profile of PHI-HC participants. It initially achieved both objectives, but since 2001 the PHI-HC population has aged faster than the general population. The aim of this study was to determine if the excess ageing of the PHI-HC risk pool has been due to passive age-based adverse selection, an inherent risk of LHC. This study has potential implications for the retention of LHC. Methods A descriptive population-level analysis of publicly available administrative datasets was performed. Data relating to PHI-HC were obtained from the Australian Prudential Regulatory Authority. National population data were obtained from the Australian Bureau of Statistics. Trends in demography, PHI-HC participation rates and LHC loading payments were analysed. Results By 2021, age-based adverse selection had returned to the pre-LHC level. Based on the available data, this was due to passive age-based adverse selection not active age-based adverse selection. Specifically, it reflected the combination of an avoidable unintended consequence of the introduction of LHC (the over-representation, in 2001, of individuals aged 45-59) and one of LHC's intended effects (incentivisation of insured individuals to retain PHI-HC). Conclusions This study supports the retention of LHC. Nonetheless, it highlights the risk of passive age-based adverse selection created by incentivising insured individuals to retain PHI-HC in the presence of distortions in the age distribution of the PHI-HC risk pool. Early targeted interventions are required when such distortions arise.

Enhanced cardioprotection of the rat heart during hypothermic storage with combined Na+ - H+ exchange inhibition and ATP-dependent potassium channel activation.

BACKGROUND: We investigated the ability of mitochondrial adenosine triphosphate-dependent potassium-channel activation to augment the protection of Na(+)-H(+) exchanger inhibition in isolated working rat hearts after 6 hours of hypothermic storage in an extracellular-based cardioplegic solution. METHODS: We treated hearts with the potassium-channel openers diazoxide (100 micromol/liter) or BMS-180448 (10 micromol/liter) or with the Na(+)-H(+) exchanger inhibitor cariporide (10 micromol/liter). Cariporide also was administered in combination with either diazoxide or BMS-180448 in 2 other treatment groups. All hearts were arrested and stored at 2 to 3 degrees C. After storage, we reperfused hearts for 10 minutes before performing work for a further 15 minutes, and then we measured and assessed cardiac function using a 2-way analysis of variance model. RESULTS: Neither diazoxide nor BMS-180448 significantly improved recovery of cardiac output. Cariporide therapy significantly improved cardiac output compared with control. However, we obtained the greatest recovery of cardiac output when we combined cariporide with either diazoxide or BMS-180448. CONCLUSIONS: Cariporide is more cardioprotective than the potassium-channel openers diazoxide and BMS-180448 after prolonged hypothermic storage. Co-administration of diazoxide or BMS-180448 with cariporide results in additive cardioprotection, with significantly improved cardiac function when compared with either treatment given alone. Such a combination could be used to improve the functional recovery of hearts stored for cardiac transplantation.

Cardioprotection by cariporide after prolonged hypothermic storage of the isolated working rat heart.

BACKGROUND: Inhibition of the sodium-hydrogen (Na(+)-H(+)) exchanger decreases the extent of ischemia-reperfusion injury in the myocardium. Inhibition may also improve preservation of hearts stored for transplantation. Our aim was to characterize the dose response and to determine optimal timing for administering cariporide, an Na(+)-H(+) exchange inhibitor, during prolonged hypothermic storage. METHODS: We used the rat isolated working-heart model to measure cardiac function. To determine the optimal dose of cariporide, hearts received either no treatment (control) or incremental doses of cariporide (1, 3.2, 10, or 30 micromol/liter) before storage and during reperfusion. Hearts were arrested with and stored in an extracellular-based cardioplegic solution at 2 to 3 degrees C for 6 hours. To determine optimal timing, we arrested a group of hearts with and stored them in a cariporide-supplemented (10 micromol/liter) cardioplegic solution but did not pre-treat them with cariporide. Finally, we treated a separate group of hearts with 10 micromol/liter cariporide before, during, and after storage. RESULTS: Recovery of cardiac function in control hearts was poor. The cardioprotective effect of cariporide was dose dependent, with maximal protection observed at a concentration of 10 micromol/liter. Storing hearts in a cariporide-supplemented cardioplegic solution did not result in better recovery of cardiac function compared with cariporide given before storage and during reperfusion. Moreover, recovery of cardiac function was significantly worse in hearts that had not been pre-treated with cariporide. CONCLUSIONS: Sodium-hydrogen-exchange inhibition with cariporide significantly protects the hypothermic ischemic rat heart, increasing cardiac function after reperfusion. The timing of cariporide administration is an important determinant of this cardioprotection.