Pondering on Paradigms from Across the Pond

Currently, coronary investigation (in the UK) is based on the paradigm of hemodynamics, in which a large coronary plaque causes significant luminal obstruction, symptoms and hypoperfusion of the myocardium. This paradigm has been the cornerstone of our therapeutic approaches to chronic stable angina, acute coronary syndromes and acute myocardial infarction for the last 40 years. Unfortunately, in the majority of cases, this diagnosis comes after a plaque has become significant or ruptured and the patient has been exposed to the risk and ultimately an inferior outcome. Surely, to improve cardiovascular risk prediction, outcomes and prevention we must change our investigational strategy? Why do we wait till symptoms come, risk builds and bad prognostic events happen before trying to patch things up in the cath lab?

We already know that disruption of a non-obstructive atherosclerotic plaque is the culprit event in at least two-thirds of acute coronary events. The histopathology of these ruptured plaques demonstrates a large, positively remodeled, plaque volume with a necrotic core covered by a thin fibrous cap (TCFA), where the thickness of the fibrous cap is 65 µm or less. Therefore, while severe anatomic stenoses can lead to symptoms of ischemia, plaque composition of non-obstructive lesions may identify lesions “at-risk” for future cardiovascular events. This introduces the alternative plaque composition paradigm. It would appear logically more important to prevent silent or clinical atherothromboses (and the subsequent mortality risk; than to wait till unrecognized lesion(s) become hemodynamically significant. In order to take this new plaque composition paradigm forward in the future, we must embrace better technologies now during screening (CT, IVUS, OCT, FFR)

The ultimate goal of future studies must be to try and prove that earlier intervention (medical or invasive), based on the results, can alter subsequent MACE. Looking to the future, I say we stop time-wasting, scrap the exercise test and scrap plain old angiography. We should decide as a community the definition of a “vulnerable patient” and screen these people with CT. If they have significant plaque, we should scrutinize it with some combination of angiography, IVUS, OCT and FFR.

Screw the credit crunch! Screw quality-adjusted life years and cost effectiveness! I know what I would want done if it was my plaque! Nothing is more important than finding and preventing the plaques that could pop.

Dr Scott Murray is a Specialist Registrar in Cardiology and a Clinical Research Fellow at Liverpool Heart and Chest Hospital, U.K He does not expect you to agree with him, but hopes you can post discussion points that will improve on his ideas.

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  Anonymoussays:
  October 20.2010 at 22:56 pm
  
Er,...


So whom do you suggest screening? Those with angina hopefully, as there are plenty of (indirect) data to suggest that ischaemia correlates with risk, and reducing ischaemia improves outcome (Hachamovitch, Courage Nuclear, etc, etc)


There's no evidence sticking in foreign metallic bodies (or bio-absorbables, or 'vascular shields') is anything other than a bad idea unless the lesion is flow-limiting (think FAME, etc). Results from pending SECRIT trial (Serruys et al) will help (but I bet negative)


I'd guess the money is in true primary prevention. So, you find a vulnerable plaque in an asymptommatic 'patient'(and they don't stroke doing the procedure). Apart from scaring them into taking a statin not sure what you'd do. I'd rather do it the old-fashioned way than glow (CT+angio+IVUS/OCT) in the dark for no reason just 'cos I've a family history. Take the pills and ban the fags.


Like the blogs BTW.


D Kelly

Int. fellow, NZ

  

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