20 years ago today two pivotal papers were published in the New England Journal of Medicine. The BENESTENT and the Stent Restenosis Study compared balloon angioplasty to coronary stenting in people with stable angina. What people remember is that stents were superior to balloons and the rest as they say is history. But the story is more complex than that as the trials show. Stents had been around since the late 1980's and they were effective in treating acute vessel closure due to balloon-induced dissection. This complication was the Achilles heel of interventional cardiology and led patients to emergency bypass grafting when their coronary artery closed off during or shortly after the procedure. Unfortunately Achilles had two heels and the other one was restenosis. Some people thought that stents might be useful to reduce the rate of restenosis but there was a problem. Stents were metal which required use of combinations of aspirin, dipyridamole, heparin and then for three months warfarin. This therapy exposed the patient to a risk of major bleeding and vascular complications prolonging hospital stay. In those days vascular access was via the femoral artery and the sheaths were about 3mm wide. Read today the results of the trials are interesting. Take the BENESTENT trial, the rate of in-hospital events was similar in both groups (6.2% in the balloon vs. 6.9% in the stent group). There was no difference in the incidence of myocardial infarction or in the need for urgent or elective cardiac surgery or second angioplasty during the hospital stay. Stent thrombosis occurred in 3.5% and subacute vessel closure after balloon angioplasty in 2.7%. The incidence of bleeding and vascular complications was 4 times higher at 13.5% after stent implantation than after balloon angioplasty. Hospital stay was 8.5 days after a stent and 3.1 days after a balloon. Now reading this is I am surprised. Stents were not so much better than plain old balloon angioplasty. Acute vessel occlusion was swapped for stent thrombosis and because of the anticoagulation patients had more complications and stayed much longer in hospital. There was no early gain. 20 years on an a coronary stent is a day case procedure done through a tube less than 2mm wide via the wrist and with a complication rate less than 1% and re-stenosis rates almost as low. The requirement for on site surgery is a thing of the past. The speciality of interventional cardiology is now mature. Where will it be in another 20 years?
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It seemed so simple. If there is a coronary artery narrowing then dilate it with a balloon and insert a stent. The narrowing goes away and the patient is improved. If the artery is the proximal LAD and the narrowing is 90% then surely this must be of benefit, after all, isn't a 90% proximal LAD lesion know as a widow-maker lesion? The problem is that despite the intuitive simplicity of this approach cardiologists have struggled to find the evidence to prove that angioplasty does anything beyond reduce symptoms in stable angina. Only last week a commentary in JAMA Internal Medicine called for better patient information about stenting procedures arguing that many patients consented to these procedures thinking they would not only improve their angina but also reduce risk of death and heart attack. Most recent discussions regarding angioplasty have been reached on the basis of the COURAGE trial. When the COURAGE trial is critiqued you often hear that interventional practice is different and if the trial were done using modern stents then the outcomes would almost certainly be different. These comments are often made by cardiologists keen on promoting angioplasty. However the point is critical since there are major differences between the bare metal stents used in COURAGE and the second generation drug eluting stents used today. No one would argue that the current stents are not vastly superior to bare metal and first generation stents in terms of rates of restenosis and acute stent thrombosis. Earlier this week the BMJ published an important meta-analysis of trials of revascularisation in stable angina. Credit should go to the authors for pulling together and analysing the results of a 100 clinical trials and reviewing the information shown in the Web accessible supplement shows how much work goes into pulling these reviews together. The results are fascinating and at provide evidence to support the argument that judging contemporary practice using historical trials may be misleading. The results showed that when comparing coronary artery bypass grafting (CABG) to medication there was a 20% reduction in death. Angioplasty but importantly only with new generation (everolimus or zotarolimus) stents reduced deaths by 25-35%. All other interventional procedures had no effect. CABG reduced myocardial infarction by 21% compared to medical treatment and all angioplasty procedures except bare metal stents and paclitaxel eluting stents also showed evidence for possible reduction. Compared with medical treatment, revascularisation with CABG reduce subsequent revascularisation by 84% and stents reduced revascularisation by 66-73% depending on the type of stent used. So for t the moment it reasonable to conclude that in stable coronary disease CABG reduces the risk of death, MI and the need for revascularisation compared with medical treatment. Stent procedures reduce the need for revascularisation but also improve survival when new generation drug eluting stents are used. So at last there is a glimmer of hope that coronary stents do more than just treat angina in stable coronary disease. This will be music to the ears of many interventional cardiologists but whether this glimmer of hope will turn into a bright beacon or a fizzle out will be largely dependent on the results of the ISCHAEMIA trial. In 1958 Mason Sones famously, and apparently accidentally, performed the first coronary angiogram at the Cleveland Clinic. From then on much of the clinical care of patients with ischaemic heart disease was based on research that relied heavily on the visual interpretation of the coronary angiogram. However it wasn't long before papers stared to appear which questioned the accuracy and reproducibility of these visual estimates. One paper from 1976 reported than nearly half the time a group of experienced cardiologists could not agree on the presence of significant coronary artery disease. Other studies followed alleging to to demonstrate the benefits of performing quantitative coronary angiography using computers to assist in the measurement of the degree of narrowing. These methods were more reproducible than eyeballing the angiogram but still there was disagreement and the methodology was time consuming. Take for example this angiogram on shown below. Do you think the this LAD stenosis is flow limiting? Why not vote here and see what others think? By early 1990's the literature on the accuracy of angiogram went quiet. Cardiologists had other things on their mind - namely coronary angioplasty and stenting. Angiography was the test which fuelled the fire of angioplasty and so the problems with assessment of flow limiting lesions and lesion significance drifted into the background. The occulo-stenostic reflex was strong. Cardiologists needed their angiograms too much to call into question the ability of the test to diagnose and classify the severity of the coronary lesions. This was the era of eminence-based medicine when expert opinion trumped anything else. The poor reproducibility and difficulty in assessment of lesion was forgotten.
When you learn angiography you quickly realise that the interpretation is difficult. When you work for a number of bosses you start to see a difference in their practice. Some always see a moderate lesion as severe, or a severe lesion as critical. The phrase "the angiogram often underestimates the severity of disease" is often be heard in the catheter lab control room as the guide catheter is being opened ready for angioplasty. Whilst there is usually agreement about the mild (<30%) and severe (>80%) lesions it is the moderate ones which are most difficult and unfortunately most common. As I teach my fellows the percent stenosis is the wrong way to think about lesions, rather we should say whether we believe a lesion to be flow limiting or not. Flow limitation is dependent on the stenosis but also on the reference vessel size, the lesion length, the size of the territory supplied by the vessel and the presence or absence of collaterals. The issue of interpretation is vital to the individual patient since it determines what treatment is recommended, You don't want a cardiologist to put in a stent or offer bypass surgery if your coronary artery lesion is not flow limiting. Recent studies have revealed what we knew all along namely that when coronary artery disease is moderate it is not possible to accurately know by visual assessment whether the lesion(s) are flow limiting or not. We need better methods not based on anatomy but rather on physiology. I have previously written about the RIPCORD trial but recently a large French registry has published its results which support the idea that the angiogram is difficult to interpret and that use of a pressure wire to measure fractional flow reserve (FFR) alters the cardiologists decision making. The R3F study looked at 1000 people having a diagnostic angiogram. The vessels were assessed and significant lesions documented. The patients symptoms and the results of any non-invasive investigations were considered and a recommendation made as to whether the patient should have medical therapy, angioplasty or bypass surgery. After this the cardiologists performed a pressure wire measurement (FFR) of any stenosis. The results were then used to determine whether the stenosis was flow limiting and with this information in hand the treatment recommendation adjusted. So for example if a patient had a 40% stenosis on the angiogram with medical therapy recommended initially but then the pressure wire was significant (e.g. FFR 0.74) the recommended treatment would be to offer an angioplasty. Using the pressure wire data the overall number of people recommended for medical therapy, angioplasty or bypass did not change but the decision for an individual patient changed 43% of the time. Overall the decision changed in 33% of patients initially recommended to have medical therapy and 50% of patients recommended to have angioplasty or bypass surgery. These results are very important for individual patients since the treatment recommendation means the difference between just taking tablets versus having a procedure or an operation. We don't know yet whether a pressure wire guided approach makes a difference to clinical endpoints such as survival, mortality, rates of heart attacks and a large trial is needed to answer this question. For the moment when a moderate stenosis is diagnosed the patient should be asking their cardiologist what is the FFR? How good are cardiologists at assessing the significance of a coronary narrowing on an angiogram. If your cardiologist tells you that your artery is 95% narrowed is that really true? A 3mm vessel narrowed by 95% means the lumen size is only 0.15mm wide. That's very small - smaller in fact than a standard angioplasty guide-wire (0.36mm) and so the wire should occlude the artery when it crosses the lesion - this rarely happens. Precise assessments of severity of coronary stenosis by angiography are unreliable. But how unreliable? Patients and cardiologists are fixated on the degree of coronary stenosis. Tell a patient his artery is 50% narrow he is worried, tell him it's 90% narrowed his is beside himself - it could block off at any time he thinks. Is a patient with a 60% stenosis in less trouble than someone with an 80% one? Rather than becoming fixated about the percentage stenosis of an artery I prefer to grade lesions as significant or non-significant. Significant lesions cause limitation of blood flow during exercise or stress, non-significant ones don't. Patients with significant lesions may have improved quality of life/symptoms improved by local lesion treatment with a stent or coronary bypass. Patients with non-significant lesions are better off with medical therapy and should avoid stents or bypass as they are unlikely to be beneficial. The discussions of significance require cardiologists to transform anatomical data derived from an angiogram into functional data which is dependent on length of lesion, severity of stenosis, presence of collaterals etc. When lesions are very severe or very mild cardiologists will agree when asked to grade the severity. When arteries are moderately diseased the agreement turns to disagreement. What we need is a functional assessment of lesion significance. This can be provided by pre-angiography investigation with tests such as nuclear perfusion imaging and stress echocardiography giving information about regional ischaemia. But NICE says we should move to angiography when the risk of underlying coronary artery disease is more than 60% and so often patients find themselves having an invasive angiogram as the first line investigation in the absence of any information about coronary ischaemia. This week sees the publication of the RIPCORD trial which is a UK based study which looked at the role of pressure wire assessment to guide therapy of coronary artery disease. The group took 200 patients with angina and performed coronary angiography. A cardiologist formulated a management plan of either medical therapy, angioplasty, bypass surgery or unable to make a decision with further information required. At that point a second cardiologist came in an performed an FFR measurement with a pressure wire. After this the results were shared with the first cardiologist to see whether this altered the management plan for the patient. The good news is that 74% of the time the management plan didn't change after the FFR measurement. In 72 patients medical treatment was recommended. In 9 patients revascularization was recommended after the FFR test (6 PCI, 3 CABG). In contrast, 25 patients who had been recommended for revascularization after angiogram (24 PCI, 1 CABG) were switched to medical therapy after the FFR data became available. In the total group of 200 cases after an angiogram 90 were led to the recommendation of PCI to ≥1 vessel, but in 24 (26.7%) there was no physiologically significant stenosis detected by FFR. So a quarter of patients recommended for an angioplasty did not have evidence of flow limiting disease and therefore the procedure would have been potentially worthless. So what does all this mean. First cardiologists can predict lesion significance from an angiogram in about 75% of cases. In fact that is not bad an it would be very interesting to see in this study if some cardiologists were better than others at making this prediction. My guess is there would be. Second it means that we are recommending some patients to have medical therapy when they would be benefit from revascularisation and we are subjecting some patients to invasive or surgical treatments without any reliable evidence that their coronary arteries are significantly narrowed. An approach to use the FFR measurement more widely gets the right treatment for the right patient. But this comes at a cost of about £450 extra per case because the pressure wire adds an expense to the angiogram. Second the complication rate from an FFR procedure is higher than that of diagnostic angiography and some patients with non-flow limiting lesions may sustain a complication such as coronary dissection which requires emergency surgery or stenting. Overall we should move to a more accurate way of diagnosing coronary artery disease and being able to assess lesions in detail at the time of angiography is likely to gain momentum. Cardiologists need to stop kidding themselves and their patients that they can assess the significance of a coronary stenosis accurately every time. When discussing revascularisation procedures (coronary artery bypass grafting (CABG) or stents), patients often ask: How long will my bypass/stent last? There is no easy answer to this question. I have patients with stents implanted 20 years ago which are still working perfectly and also known people who had a CABG in the 1980’s where all the grafts are in excellent condition. Conversely patients may return rapidly after surgery with graft failure or develop critical in-stent restenosis within months of angioplasty. Results from randomised clinical trials of stents versus surgery such as the SOS and SYNTAX favour CABG as superior treatment compared to stenting. CABG appears to be associated with a lower likelihood of repeat revascularisation. But there is a problem with these trials. Inherent clinician bias usually favours repeating angiograms in patients treated with stents who develop symptoms after the procedure compared to those patients who have received treatment with CABG. Since the clinician and the patients are not blinded to the original treatment this belief that surgery is a more robust and reliable method of revascularisation is likely to increases the rate of repeat angiography which leads to a high rate of repeat revascularisation. So what is the rate of CABG vein graft occlusion? A recent paper looked at this question in 1829 patients who had a coronary angiogram within 12-18 months after CABG and were then followed for a further 3 years. Within 18 months after CABG 43% of patients (770/1829) had at least one vein graft occlusion. The identification of this occlusion was associated with a 5-fold increase in repeat revascularisations procedures although it did not lead to a higher number of heart attacks or deaths compared to patients whose grafts were all patent. There rate of revascularization procedures within 14 days of angiography demonstrating a vein graft occlusion shows the power of the occlulostenotic reflex as discussed before in an earlier blog. Since the angiography was protocol, and not symptom, driven the identification of the stenosis on an angiogram was enough to result in a repeat revascularisation procedure with a stent. What is the reason for the graft occlusion? Surgical technique, quality of the vein graft and target vessels or is it perhaps that the stenosis didn’t need bypassing in the first place. The FAME study using pressure wire showed that 20% of coronary arteries with significant stenosis (70-90%) on an angiogram were not associated with ischemia and in such cases vein graft failure could easily ay occur without clinical consequence or symptoms. So when answering the question about the longevity of a bypass graft we should say that nearly half of patients will lose at least one graft within 18 months of surgery but the chance that it will cause harm to the patient is low unless someone discovers that it is occluded. In the Summer of 2012 David Brailsford presided over Team GB’s incredible haul of cycling medals in the Olympic games. What was the secret of this team’s success? The simple answer was there wasn’t one secret but as Dave Brailsford said it was the aggregation of marginal gains. Performing a coronary angioplasty can take as little as 15 minutes but even with the simplest procedure there are many different choices which the operator needs to make and each of these influences the outcome of the procedure and the risk of complications. Close attention to detail, wise choices and the sum of the marginal gains makes the difference between getting a bronze and achieving gold. Here is an example. The patient is a 75 year old obese man with diabetes and hypertension. He has a stenosis in the mid right coronary artery. The artery is mildly calcified and a somewhat tortuous. Dr Groin is a default femoral operator. With a 6F sheath, a right Judkin’s guide catheter and a hydrophilic guide wire most cases can be done. Groin access takes but a moment and the coronary artery is easily intubated, the wire glides through the vessel with its usual speed and hydrophilic coating. Within moments the lesion is pre-dilated with a balloon. Then comes the stent but there is a problem, the tortuousity and the calcification makes the stent difficult to track through the vessel. The JR4 catheter does not give any support and the stent cannot be manoeuvred into the correct place. A buddy wire is passed but still the stent won’t track to the lesion. Further ballooning is performed in the vessel which results in a small dissection and without the ability to deliver a drug coated stent they try a bare metal stent which is finally deployed with a reasonable result. The procedure takes 75 minutes and there is 300ml contrast used. An angioseal vascular closure device is deployed but does not quite seal the artery completely and the patient develops a haematoma. The patient eventually leaves the hospital 4 days later. His procedure was a success, the vessel was stented but was this as good as it could possibly be. Dr Wrist usually takes the radial approach. A 5Fglideliner sheath and a 6F AL1 guide catheter are used because the vessel is calcified and somewhat tortuous and he thinks that extra support may be needed. The lesion is crossed with a supportive angioplasty wire, the wire is harder to manipulate than the hydrophilic coated wires but once in the distal vessel it gives excellent support and remains very stable. The vessel is tortuous but the AL-1 gives a really good back up support and the lesion is ballooned with a 2.5x12 balloon and then a 3.5x15 drug eluting stent is deployed with a good result. Because the lesion was calcified a further 3.5x12 non-compliant balloon inflation is made to high pressure with a very good angiographic result. The procedure takes 27 minutes and there is 60ml contrast used. A TR band is placed on the wrist with patent haemostasis and the patient is discharged from the hospital 6h later. His procedure was a success, the vessel was stented. Both patients had a successful PCI on paper but Dr Wrist’s procedure was more successful for the patient. The sum of the small parts – access site, catheter choice, wire choice and ability to deliver devices. All of these single decisions feed into the outcome of the procedure for the patient. Alone each one of these things may contribute only a fraction of a percent to a difference in outcome but when they are all put together they can add up and the sum of marginal gains leads to safer and more effective practice. So how do we achieve these marginal gains in practice: Set audacious goals, work with others who share your vision. Focus, Focus, Focus. Collect high quality procedure data, outcomes data and learn from it. Be disciplined to capture every gain. This is the angiogram of a 48 year old man who exercises regularly and has no cardiac symptoms. His story is not uncommon. He has a medical up every 2 years including an exercise stress test. He completes 9 minutes of exercise without symptoms but there are some ECG changes and cardiology referral is recommended. The cardiologist agrees the exercise ECG is abnormal and requires further investigation. In the absence of symptoms or risk factors for coronary artery disease a CT coronary angiogram was recommended. This surprisingly to the patient indicated a stenosis in the proximal LAD which was then confirmed with an invasive angiogram. Now the cardiologist and patient are faced with a decision: What to do next? There are few things cardiologists agree on but I reckon if you showed 10 interventional cardiologist this angiogram they would all say that something must be done. There might be a discussion about the long term pros and cons of drug eluting stents versus surgical revascularisation but most would agree that medical therapy alone in the absence of revascularisation would represent a sub-standard level of care. Most would agree that a 3.5x23mm drug eluting stent could be placed efficiently with very small risk of complication and an excellent result. There would be complete relief of vessel obstruction and at the same time a reduction in patient and physician anxiety. When it comes to the decision to place a stent are we too strongly influenced by our heart rather than our head. Is it a case of emotion trumping science! The COURAGE study compared optimal medical therapy with stenting in patients with significant coronary disease. After 7 years of follow up in COURAGE study was there was no significant difference between stent treatment and medication. But what of patients with 90% stenosis in the proximal LAD the so called "widow-maker" lesion. Surely patients with this pattern of coronary disease benefit from revascularisation? A recent paper from the COURAGE study looked at just this group of patients and found that there was no significant difference between the patient treated with stents or optimal medical therapy. The figure on the left shows the that the group of patients with >90% stenosis in the proximal LAD did not fair well over the 7 years. The surprising thing is that those treated with angioplasty and bare metal stenting (lowest solid green line) appeared if anything to fair less well than those treated with optimal medical therapy (second lowest green dotted line). The presence of proximal LAD disease as a rationale for favouring stenting was therefore not proven. This finding is provocative and instructive. If you ask interventional cardiologists (and this has been done in focus groups) they will acknowledge that stenting offers no reduction in the risk of death or heart attack in patients with stable coronary artery disease but despite this they generally believe that stenting does benefit such patients. One senior cardiologist said to me that he preferred to treat the cause of coronary artery disease with a stent rather than merely manage the symptoms with tablets. Reasons for performing stenting include belief in the benefits of treating ischaemia, the open artery hypothesis, potential regret for not intervening if a cardiac event could be averted, alleviation of patient anxiety and medico-legal concerns. If asked, most cardiologists believe that the oculo-stenotic reflex prevails and all significant and amenable stenosis should receive intervention even in asymptomatic patients. When cardiologists are challenged about the lack of evidence of adding stenting to optimal medical therapy in preventing future coronary events most still feel that any patient with significant coronary disease should get a stent even whilst acknowledging the evidence. This disconnect between knowledge and behaviour reflects the discordance between cardiologists’ clinical knowledge and their beliefs about the benefits of angioplasty and that non-clinical factors have substantial influence on cardiologists' decision making. So what happened to this patient? I will leave you to decide and to post your thoughts and comments. When a patient has a coronary angiogram the cardiologist will report the results in terms of the degree of narrowing of the arteries. For example a 60% stenosis in the LAD, a 40% stenosis in the circumflex. But what does that really mean? Is the stenosis flow limiting? Is it responsible for the patients symptoms? Is the lesion prognostically significant? Should a stent be place? Is a bypass indicated? Many questions but the fundamental one is: "Would this patient's outcome be better with or without revascularisation or is medical therapy more appropriate?" When there is mild or critical coronary artery disease then the decision making is straightforward. However in many cases there are moderate areas of coronary narrowing. Showing the angiogram to several cardiologists will usually result in differing opinions about whether a lesion is flow limiting or not. For some cardiologists the "Oculostenotic reflex" is already potentiated leading to "iatrogenosis fulminans." In 1995 Steve Nissen and Eric Topol wrote about cardiologists preoccupation with luminography and eloquently showed how lesion assessment with angiography performed very poorly compared to intravascular ultrasound. They also wrote of the dissociation between the angiogram and clinical outcome and called for a shift in our with luminology towards measures that improve survival, freedom from myocardial infarction and symptoms of angina. Whether a coronary lesion is flow limiting is not just dependent on the degree of arterial stenosis but also on the amount of cardiac muscle supplied, the presence of collateral vessels, the length of the lesion and the function of the endothelium. Some of these factors can be assessed subjectively by angiography but others cannot. What is required is a more functional or physiological assessment. Cardiologists have fooled themselves for too long that they are able to determine the functional significance of a moderate coronary stenosis from the angiogram alone. Recent data using the pressure wire has challenged some of this thinking although there are still some sceptics. The FAME studies showed that use of the pressure wire to measure fractional flow reserve (FFR) could be useful to help in selecting the appropriate therapy and guiding coronary revascularization in patients referred for a percutaneous coronary intervention (PCI) procedure. Very recently a real world study has been published using FFR in patients referred for diagnostic angiography and looking at its impact on the decisions involved in revascularization. In this study patients referred for diagnostic angiography had a treatment plan for intermediate lesions (35-65% by eye) made on the basis of the angiography alone. 55% of patients were recommended to receive medical therapy and 45% revascularization (PCI, 38%; CABG, 7%). FFR measurement was then performed with the pressure wire and after this 58% of patients were recommended for medical therapy and 42% for revascularization (PCI, 32%; CABG, 10%). The results were not so different overall but in individual patients the FFR strategy changed the recommended treatment in 43% of cases. Reclassification was observed in 33% medical patients, 56% of PCI patients and 51% of CABG patients. These results are hugely important since they indicate that even experienced cardiologists are unable to judge the flow limiting nature of moderate lesions. In the initial medical treatment group one third of patients met FFR criteria for revascularisation. In the PCI group, half of patients were due to receive inappropriate or a less optimal type of revascularisation. In the surgical group over half of patients could have avoided an operation. What this study is telling us is that using the eyeball technique to judge the severity of coronary disease is not the best way to decide on a management plan for cardiac patients. If the practice of using a pressure wire became standard in diagnostic coronary angiograms it would lead to more patients receiving medical therapy, less receiving angioplasty and more patients having CABG. The effects on the economics of management of coronary disease are complex. Assuming everyone gets medical therapy then the cost of the increased CABG although a more expensive procedure is offset by the reduction in expenditure on angioplasty. The repeat revascularisation costs are likely to be lower since this has been shown routinely in most of the CABG versus PCI studies. There is of course the cost of the pressure wire for every case. Overall the most improtant thing is that the patient receives the most appropriate treatment and not at the mercy of the oculostenotic reflex. The first coronary stent was implanted in 1986 by Dr Ulrich Sigwart. Stents are metal scaffolds which have revolutionised coronary angioplasty. Prior to stents, coronary dissection, caused by balloon angioplasty, usually resulted in an emergency coronary bypass operation or at best a 90% stenosis was reduced to a 40% one. Stents solved these problems but led to different ones. First there was stent thrombosis. Patients were initially treated with aspirin and warfarin to inhibit the clotting pathways but the bleeding problems were terrible. Then we then realised that aspirin could be combined with ticlopidine and subsequently clopidogrel to provide a safe treatment to reduce stent thrombosis but without the bleeding. Then there was the problem of restenosis (re-narrowing) at the site of the coronary stent implant. This led to spot stenting to keep the length of stent as short as possible. After that and thanks to Antonio Colombo and the use of intra-vascular ultrasound we realised that stents needed to be implanted at high to reduce restenosis. However problems with restenosis still existed and cardiologists developed complex treatments such as brachytherapy (intra-arterial radiotherapy) which now have all but disappeared. In the early 2000's we were introduced to the drug eluting stent. First Cypher, then Taxus and then the second generation stents such as Xience, Promus and Integrity Resolute. No longer did interventional cardiologists have to worry about the length of stent they were implanting. Treat from normal vessel to normal vessel became the mantra. But the downside was stent thrombosis, originally thought to just be a short term problem it is clear that it could occur years after stent implantation. Also in some high risk patients such as those with diabetes the restenosis problem has not been completely solved. There are some patients with in-stent, in-stent re-stenosis for which the treatment options are limited. The holy grail of stenting has been seen as the biodegradable or resorbable stent. Implant the stent when it is needed for the first few months and then when it has done its job, like a self absorbing suture, it dissolves away. This sounds an attractive prospect and in 2012 the world of stenting was revolutionised by the entry of the first commercially available biodegradable stent called ABSORB. In the early phase after implantation the ABSORB revascularises like a drug eluting stent. It releases the anti-proliferative drug everolimus to minimise neo-intimal growth and restenosis. During the restoration the scaffold benignly resorbs and the stent gradually ceases to provide luminal support resulting in a discontinuous structure embedded within the coronary artery. As the scaffold degrades, the polymer is converted into lactic acid which is metabolised and is ultimately converted into benign by-products of carbon dioxide and water. Several studies support this concept and indicate that there is no clinical benefit of a permanent stent over time. The ABSORB eliminates the permanent mechanical restraint on the vessel and should allow for more normal blood vessel function. Three-year results from 101 patients in the second stage of the ABSORB trial have shown that the rate of major adverse cardiovascular events was 10% at three years, similar to a comparative set of data with a best-in-class drug eluting stent at the same follow-up period. In a subset of 45 patients, intravascular imaging techniques showed improvements in vessel movement and a 7.2% increase in late lumen gain (an increase in the area within the blood vessel) from measurements taken at one and three years. These findings are unique to the absorbable stent and are not typically observed with metallic stents that cage the vessel. The ABSORB stent is now available and patients interested in receiving it should discuss with their cardiologist to see if they are suitable for the device. References: ABSORB II Trial ABSORB-Extend Trial
The data on angioplasty in the UK is out this week on the BCIS website and it appears that all 557 cardiologists whose data is reported have a MACCE (major adverse cardiac and cerebrovascular event) rate within that expected. MACCE is a measure of the number of patients who died, had a stroke or needed an emergency bypass operation after an angioplasty procedure. BCIS estimate the MACCE rate for each patient based on parameters which are reported in a study from data obtained some 10 years ago called NWQIP. This model predicts, apparently, with 70% accuracy according to the patient's age, sex, emergent PCI, urgency of treatment, cardiogenic shock and whether a bypass graft or the left main stem was intervened on. From this BCIS estimate the 95% confidence intervals (CI) of the predicted MACCE and provided the cardiologists actual MACCE rate is lower than the upper CI then everything is apparently fine. So statistically if there were 1000 cardiologists you would expect that by chance alone then 25 of them would be above the upper 95% confidence interval and 25 would lie below the lower confidence interval. So what is the chance that not one of the 557 cardiologists in the BCIS report would be outside the top 95% confidence interval? Well its a very small number (actually p=0.000000751). So currently this is an exam which a cardiologist has a 1 in 100 million chance of failing. Now as BCIS say you can't directly compared different operators but what you can do is look at people who have a similar practice. If you pool data from cardiologists who do more than 75 angioplasty procedures per year (the BCIS recommended minimum) and who do more than 10 primary PCI procedures (treating patients with acute heart attacks who are the sickest patients) then the average MACCE rate is 2.2%. This is much lower than 8.2% MACCE rate which is predicted by the BCIS model. Although we might like to regard interventional cardiologists are superhuman creatures what this data really tells us is that the model BCIS has used to predict risk vastly over predicts the actual MACCE making this truly an exam which cannot be failed. To be fair BCIS do acknowledge the limitations of the data but there is an urgent need for more contemporary risk prediction models going forward. |
Dr Richard BogleThe opinions expressed in this blog are strictly those of the author and should not be construed as the opinion or policy of my employers nor recommendations for your care or anyone else's. Always seek professional guidance instead. Archives
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