Dr.S.Venkatesan MD

Anginal equivalents are distinct  (often vague  ) symptoms that occur in response to myocardial Ischemia , instead of angina. Dyspnea or shortness of breath  is the commonest anginal equivalent . The incidence and exact mechanism  is not clear. Both angina and dyspnea are sensory  events . Both are  perceived  at the level of cortex. Angina occurs when ischemic  muscle  triggers pain signals from the   nerve  twigs engulfing the myocytes membranes  and the vasavasorum.

Dyspnea during myocardial  ischemia  is multi-factorial

1. Signalling error .( Mismatch between respiratory /Cardiac  receptors  neural traffic)
2. Cortical perception disorder.
3. Autonomic neuropathy (Blocks pain signals  but still may carry  myocardial stretch response)
4. Coronary sinus lactate –  Biochemical /Chemo receptor stimulation
5. Isolated  Ischemic LV relaxation defects  , and resultant elevation of LVEDP
6. Ischemic systolic stunning  and secondary  diastolic dysfunction  (elevated PCWP  pulmonary stretch receptors stimulation )
7. Ischemic MR . Eccentric MR jets and regional and segmental elevation of pulmonary venous pressure has been reported. (Unilateral and segmental pulmonary edema)
8. It is possible  ,  Ischemic wall motion defect per-se  can induce myocardial stretch and create a feeling of dyspnea.

Out of the above eight factors  which is  most important  ?

The most popular and easy to comprehend   mechanism   is number 5 : Ischemic diastolic dysfunction .

(Fellows will be appreciated if they  know this !   )