Medical Devices at the Limits – a glimpse of the future
Dr William Wijns
Cardiology and Diabetes at the Limits, Cape Town, Feb 2011.
An explosion in the development of medical devices has occurred over the past 2 decades with increasingly rapid cycles of evolution as technological pace has accelerated. Often the next generation of device is ready for market as the RCT’s for the previous generation are being published. This may be a limit to the development of future devices in an age of evidence based practice.
Disease substitution is also a potential problem. As one disease is resolved by devices, another may replace the original as a consequence of the device itself. An example would be coronary artery stents, which overcome stenotic lesions but cause stent thrombosis. Disease substitution leads inevitably to a need to evolve the technology (eg. drug eluting stents) thus leading to escalating cycles of cost for next generation devices and also a need for renewed RCT’s to prove the latest development. There is a limit to the costs that any health economy will bear for devices, thus it follows that there is a natural life cycle for any device in which repeated development cycles to overcome substitute diseases will eventually price it out of the market.
In essence it appears that the pace of technology change may be an increasing challenge as the speed of development outweighs the ability of RCT’s to keep pace, and the costs of technological solutions increase. In addition as the risks posed by diseases are systematically reduced through newer technologies, the cost effectiveness of any further improvements in outcomes becomes harder to establish – for instance a device which achieves 100% reduction in risk of death in a common disease will be easier for payers to justify than a next generation solution which treats a substitute disease to achieve a further smaller overall benefit.
Thus the limit to medical devices may be the speed and success of technological development itself.
Tuesday, March 1, 2011
The future of intervention for acute coronary syndromes – have we reached the limits?
The future of intervention for acute coronary syndromes – have we reached the limits?
Prof Keith Fox
Cardiology and Diabetes at the Limits, Cape Town, Feb 2011.
Tunsdall-Pedo defined Scotland and in particular Glasgow as the heart disease capital of the world in 1994, and quoted 50% immediate mortality rates. 16 years later the pattern is different, and acute STEMI is a relatively rare event compared to 1994. However acute coronary syndrome (ACS) has replaced STEMI as the condition that commonly faces acute services. Death rates from ACS have declined dramatically over the past 2 decades as treatments have developed and evolved. This makes it ever harder for further improvement to be achieved. It thus becomes increasingly important that patients with the greatest remaining risk due to ACS are identified and treatment targeted accordingly.
The GRACE programme uses factors such as previous angina, hypertension, hyperlipidaemia and diabetes to qualitatively stratify risk due to ACS. This appears to be better than physicians assessing risk where the evidence suggests that those at lowest risk may be the ones most likely to undergo coronary intervention. Thus there is a demonstrable risk assessment paradox when objective assessment with for example the GRACE programme is compared to clinical judgement by physicians. In recent work the GRACE C index has been shown to have high predictive value for those who will die after ACS, whereas physician assessment seems to be a poor predictor.
Evidence is emerging that more people have plaque rupture than actually present with syndromes caused by this pathology. Work published by Davies and Falk suggests that nearly 10% of asymptomatic RTA autopsy subjects had incidental plaque rupture with this figure being 16% if diabetes or hypertension were present. Thus plaque rupture not leading to ACS appears to be common, implying that the balance between inflammation and repair in plaques may offer new avenues for therapeutic development. The identification of 9q21 – a gene present in 45-50% of people which significantly increases risk in CHD also offers a possible glimpse of the future. Recent evidence has shown that this gene is involved in control of Interferon gamma and Stat-1 and thus linking genetics to biology in ACS.
Searching for the benefits of treatments for ACS should not be limited to the short term. Recent evidence shows that there is a latent benefit from PCI in ACS as well. Fox et al in J Am Coll Cardiol 2010 showed that 5 years after PCI for ACS there is an 11% reduction in risk for death or myocardial infarction in those at highest risk. This compared with only a 3% reduction in those at intermediate risk and 2% in those at low risk. Thus the selection of patients at high risk after ACS has significant benefits years after the event, and emphasises the importance of appropriate case selection through objective assessment using tools such as GRACE. The MINAP (Myocardial Ischaemia National Audit Programme) Report 2010 showed that the UK has achieved a reduction in risk of death during STEMI/NSTEMI from around 12-13 to 7-8% by 2010, and at 6 months after NSTEMI from 18% to 13%. The limit to achieving even greater reductions may be how acute services identify patients who will derive the most long term benefit.
Prof Keith Fox
Cardiology and Diabetes at the Limits, Cape Town, Feb 2011.
Tunsdall-Pedo defined Scotland and in particular Glasgow as the heart disease capital of the world in 1994, and quoted 50% immediate mortality rates. 16 years later the pattern is different, and acute STEMI is a relatively rare event compared to 1994. However acute coronary syndrome (ACS) has replaced STEMI as the condition that commonly faces acute services. Death rates from ACS have declined dramatically over the past 2 decades as treatments have developed and evolved. This makes it ever harder for further improvement to be achieved. It thus becomes increasingly important that patients with the greatest remaining risk due to ACS are identified and treatment targeted accordingly.
The GRACE programme uses factors such as previous angina, hypertension, hyperlipidaemia and diabetes to qualitatively stratify risk due to ACS. This appears to be better than physicians assessing risk where the evidence suggests that those at lowest risk may be the ones most likely to undergo coronary intervention. Thus there is a demonstrable risk assessment paradox when objective assessment with for example the GRACE programme is compared to clinical judgement by physicians. In recent work the GRACE C index has been shown to have high predictive value for those who will die after ACS, whereas physician assessment seems to be a poor predictor.
Evidence is emerging that more people have plaque rupture than actually present with syndromes caused by this pathology. Work published by Davies and Falk suggests that nearly 10% of asymptomatic RTA autopsy subjects had incidental plaque rupture with this figure being 16% if diabetes or hypertension were present. Thus plaque rupture not leading to ACS appears to be common, implying that the balance between inflammation and repair in plaques may offer new avenues for therapeutic development. The identification of 9q21 – a gene present in 45-50% of people which significantly increases risk in CHD also offers a possible glimpse of the future. Recent evidence has shown that this gene is involved in control of Interferon gamma and Stat-1 and thus linking genetics to biology in ACS.
Searching for the benefits of treatments for ACS should not be limited to the short term. Recent evidence shows that there is a latent benefit from PCI in ACS as well. Fox et al in J Am Coll Cardiol 2010 showed that 5 years after PCI for ACS there is an 11% reduction in risk for death or myocardial infarction in those at highest risk. This compared with only a 3% reduction in those at intermediate risk and 2% in those at low risk. Thus the selection of patients at high risk after ACS has significant benefits years after the event, and emphasises the importance of appropriate case selection through objective assessment using tools such as GRACE. The MINAP (Myocardial Ischaemia National Audit Programme) Report 2010 showed that the UK has achieved a reduction in risk of death during STEMI/NSTEMI from around 12-13 to 7-8% by 2010, and at 6 months after NSTEMI from 18% to 13%. The limit to achieving even greater reductions may be how acute services identify patients who will derive the most long term benefit.
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