Rescue angioplasty as a concept in PCI is advocated for the past two decades. Rescue angioplasty continues to enjoy the controversy over the years. A procedure which fails to shrug off the controversy for so long inspite of multiple studies , would indicate there is something seriously wrong in the procedure or in the conceptualization.
The fundamental question that is often and not answered properly is :
What is being rescued in R angioplasty ?
Is it the
Patient’s life ?
Rescues ischemic myocytes
Infarct related artery ?
*Or it simply rescues physician from the legal issue arising out of labeling his patient as failed thrombolysis
The term rescue generally implies tackling an impending crisis .The threat is either to the patient’s life or to the myocardium or both.
In STEMI when the initial reperfusion strategy fails (Usually thrombolysis) R -angioplasty is considered. Here the aim is to rapidly rescue and salvage myocardium . The problem here is , contrary to our expectation the population of failed thrombolysis is not a homogenous one .In one end of the spectrum , is a patient with persistent ST elevation , totally comfortable and pain free and hemodynamically stable.The other end is , deteriorating blood pressure , tachycardia , progressive angina and impending cardiogenic shock. Considering the above situations it is very simple to guess who will require the rescue and who will benefit more. In fact, R -angioplasty in patients with asymptomatic failed thrombolysis without ongoing ischemia defies logic and conveys no meaning ! .This is especially true if the patient has crossed 12 hours of time since the first symptom.
In deteriorating patients R- PCI has a role where one can potentially arrest the progression of cardiogenic shock or even reverse it.
A third group among failed thrombolysis have predominate angina with hemodynamic stabilty. This group will benefit from R angioplasty irrespective of time window , as the pain is often due to a critical non IRA lesion .Technically again we can’t call this PCI as rescue as nothing is done to salvage the myocardium . (Of course one wish to call it so , as the patient is rescued from angina !)
A tricky issue is to know where does the pain come from in a post MI patient ?
It should be realised a post MI patient can have variety of source of chest pain. There has been instances where a persistent pericardial pain has resulted in emergency R-PCI !
The critical question that has not been answered by cardiologists is
How long a STEMI pain last and when doespost infarct angina begin in a susceptible patient .
In other words how do differentiate present(Index event) infarct angina from post infarct angina ?
Studies on pain signal transmission (medullated type c) would suggest a dull aching retrosternal pain may occur in a substantial number of patients following STEMI .These pain signals come from necrosed cells and not from ischemic cells. This pain ceases after complete ischemic destruction of nerve endings . The threshold , duration and central perception of this pain is highly variable.
One can imagine the importance of the above issue , as there is a potential to misdiagnose recurrent post MI angina for the relatively benign infarct related pain. Though experience have suggested a 12 hour cut off to define post MI angina , it is too empirical .
Rescue angioplasty remains as a disputed entity in vast majority of post MI population .
It is most useful when it is done in impending cardiogenic shock .Note the word. Impending not established cardiogenic shock. (After prompt recognition of failed thrombolyis within overall time window <6h ideally , but may be done to up to 12h)
There is no role for routine rescue in all failed thrombolysis patients , for the simple reason there may not be any clinical or live myocardial targets for rescue.