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.
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.
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.
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