Archive for April, 2022

William Heberden first introduced the term angina to the medical community in 1772. His descriptions became immortal. Still, no one would ever know what was the angina-related artery, Heberden was alluding to.

Now, some jobless cardiologist is asking this question after 200 years. How is angina from the LAD system differ from the RCA  system? or let me put it another way, How does angina of anterior circulation (LAD) differ from posterior circulation (RCA/LCX)? Though there is distinct hemodynamic profiling of RCAvs LAD ACS, surprisingly, cardiology literature does not answer the chest pain aspect of it. One rare study, done  4 decades ago throws some light

Here is a curious little study, with a simple & crisp conclusion.

chest pain and IRA localisation angina LAD angian RCA

It concludes, that LAD angina rarely radiates to JAW or epigastrium. While RCA angina relay radiates to the left shoulder.

So, why does this happen?

What I could guess is the ubiquitous vagal fibers that travel in the posterior aspect of the heart, and carries pain signal directly up to the jaw whenever these areas become ischemia. LAD is less likely to irritate the vagus. Of course, there can be a definite overlap.

OMG, give me some time to keep in touch with  basic science 

Now, fellows of cardiology, please take a  pause from your regular aggressive cardiac cath lab workouts and get a break at least once in a while. How does the ischemia of myocardial tissue generate pain? Why it is severe in some, trivial in others, and even dead silent in some, 

The chest pain genesis is initiated by sensory electrical neural action potential, that captures the epicardial neural plexus first, switching over from somatic to the visceral pathway and trespassing the para ganglionic plexus and traveling further to the spinal cord. Where it may collide with other incoming sensory signals ascends in specific myelinated and non-myelinated neural cables, reaching the brainstem, interacting with local nuclei, and finally reflecting on subcortical and cortical pain matching centers.  We haven’t yet located the exact center for anginal pain. (Perithalmic and amygdala could be closer to real centers) 

So, it is a really complex sensory world yet to be understood fully. Mind you, I haven’t touched upon the neurophysics of referred pain, linked or clandestine angina.

  • What is the effect of cardiac denervation, autonomic neuropathy, or on the perception of chest pain(Does a quadriplegic feel angina ? or post-transplant heart immune to angina ? (Gallego Page JC,Rev Esp Cardiol. 2001) 
  • Is it biochemical or neural, can substance P in blood cause pain hitting the amygdala? 
  • Will hypoglycemia and anemia cause angina due to lack of glucose and oxygen?
  • Finally, how is Infarct pain is different from ischemic pain (Ischemic)

Where do get the answer to these questions?

This paper from Dr. Robert Formean(Ref 2) university of Oklahoma is just the best source I think, to explore and understand the topic. (Reading time 60 minutes: Let me tell you, it is worth more than a time spent on an insignificant angioplasty of painless PDA lesions)

Final message 

So, what have you learned from this post? Does this question about angina matter at all? Surely not. in this space-age cardiac care where we are right inside the coronary even before we listen to the patient’s complaint properly. We are always at liberty to do what we want( or love) to do. But, the urge to understand the foundations of clinical science is the last remaining hope, that will keep the specialty of cardiology enchanting. 

A comprehensive reference for the genesis and signal processing  of chest pain 

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This graph is a rare treasure in CAD therapeutics (fished out from a huge, often conflicting chronic CAD literature) that elegantly shows us the complexities involved in the revascularization of ischemic hearts with risks and benefits criss-cross each other. Our job is to identify, that critical point in a given patient’s CAD timeline for optimal management. To make things difficult, this point is a moving target and makes this delicate clinical exercise truly complicated.

It conveys a simple message in strong terms. It says the inflection point is around 10-15%. When the total ischemic areas are beyond this the benefits increase and when it is less there is sure shot harm.

Now comes the tough part. How best we can identify and quantify the true area of ischemia?

There is no such thing called coronary mathematics. Even if we try to make out one, vascular biology will giggle at us. Still, we have no other option but to go for sophisticated imaging modalities. Stress Echo, Nuclear Imaging, Scar imaging, MRI, PET, quantify total ischemic burden, plot it with corresponding coronary anatomical zones for a potential correction.

What this curve does not convey is the complex interplay between Ischemia vs symptoms. Ischemic myocytes have so many invisible tricks to adopt themselves. Should I go after the burden of Ischemia (Often Imaginary) or the burden of symptoms? Despite the lack of benefit in most trials on CTO in hard endpoints, it is yet to rectify the thinking patterns of many elite evidence-based cardiologists.

Final message

However, It will be an unpardonable act of omission if we miss or fail to offer the benefit of opening a critical LAD disease that has troublesome symptoms.

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