Dr.S.Venkatesan MD

The term Ischemic heart disease (IHD) was once very popular, but many abandoned it as it became an academic cliche.  CAD & CAHD are the other terms that are equally popular and prevalent. Stable IHD was in vogue till recently, which was again replaced by “chronic coronary syndrome’ now. Honestly, I feel the original term IHD to be restored however outdated it may look. it encompasses the entire spectrum of clinical cardiac disorders.

Manifestation of Ischemia heart disease 

1. Angina
2. Infarction
3. Cardiac failure
4. Arrhythmias 
5. Silent ischemia
6. Sudden cardiac death

 The purpose of this post is to share some thoughts on the link between Ischemia and cardiac arrhythmia. 

What is the relation between  Ischemia and cardiac arrhythmia (especially VT)

A.Strong relation

B.Weak relation 

C.No relation 

D. Recurrent ischemia protects against arrhythmia.

The fact that. acute Ischemia triggers primary VT and VF and is the leading cause of electrical death is sufficient to fix the answer without any doubt. But, the  truth is, the link between Ischemia and cardiac arrhythmia is more complex  

If we could agree ischemia is a powerful trigger of ventricular arrhythmia, will every patient with chronic stable angina be at risk of  VT after walking a certain distance?  

So, where does cardiac arrhythmia fall in the Ischemic cascade of events? the fact that chronic ischemia on exertion rarely precipitates an arrhythmia conveys a strong hidden message. 

Coming back to, STEMI where the arrhythmic risk is powerful, still, if the same acute ischemia, presents as UA/NSTEMI, with severe compromise of resting blood flow, it doesn’t trigger a VT usually. This fact should baffle us and question why even acute ischemia carries low arrhythmic risk except when it happens with STEMI.

The potential mechanisms of lack of VT in UA* (No evidence /Class C evidence) 

• In UA, ischemia is primarily subendocardial, and the neuronal innervation which is more in the epicardial plexus fails to get stimulated. This is in contrast to what happens in STEMI. Here It is transmural ischemia and the sub-epicardial is always involved.
• In this context, the high prevalence of VT in Prinzmeal angina where there is subepicardial injury is a point to be noted. In young NSTEMI/STEMI crossover entities like Wallens and De-winters, there is a high adrenergic drive, which triggers the VT rather than ischemia per-se.
• Finally, even in STEMI, only a minority of 15-20 % of myocardium become arrhythmogenic and face fatal complications. What protects the rest of the 75 %? is genetics, epigenetics, or fate.? 

The practical implication of this question

1. The VT in ischemic cardiomyopathy is related more, to the scar burden, strategically placed islands of dead and live tissues, and the overall severity of LV dysfunction. This makes the Ischemic VT, as a term,  could be a misnomer.  In fact, it is the viable ischemic tissue that is a powerful trigger.
2. If baseline chronic ischemia is less likely to trigger any VT, revascularisation in chronic CAD (PCI/CABG) is unlikely to give relief from it as well.

Anti-arrhythmic adaptation in chronic Ischemia 

We know about ischemic preconditioning and angina relief. It may apply to arrhythmic preconditions as well. Recurrent ischemia, while we expect to elevate the arrhythmic risk, it is a curious and exciting possibility it might work as an “anti-arrhythmia vaccination” at the molecular level. 

Final message 

So, what is the true relation between ischemia and cardiac arrhythmia?  

It is not as strong as one would believe it to be( Except in the early hours of STEMI and a very small subset of NSTEMI.

Curiously, in certain lucky beings, recurrent baseline ischemia may protect against future arrhythmias.

Reference 

1.A V Ghuran, A J Camm, Ischaemic heart disease presenting as arrhythmias, British Medical Bulletin, Volume 59, Issue 1, October 2001, Pages 193–210, https://doi.org/10.1093/bmb/59.1.193

2.Janse MJ, Wit AL. Electrophysiological mechanisms of ventricular arrhythmias resulting from myocardial ischemia and infarction. Physiol Rev 1989:  69 ; 1049 –169

Few more questions worth pondering 

Why do certain VTs struggle to become sustained?

Will discuss this later (Will need to talk about the diameter of the primary Rotor, the Curvature of rotors and source-sink mismatch, etc. )

How often  Ischemia triggers AF?

I haven’t heard of Ischemic SVT, or ischemic AF much. Trying to accumulate more Info on this.