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
- Signalling error .( Mismatch between respiratory /Cardiac receptors neural traffic)
- Cortical perception disorder.
- Autonomic neuropathy (Blocks pain signals but still may carry myocardial stretch response)
- Coronary sinus lactate – Biochemical /Chemo receptor stimulation
- Isolated Ischemic LV relaxation defects , and resultant elevation of LVEDP
- Ischemic systolic stunning and secondary diastolic dysfunction (elevated PCWP pulmonary stretch receptors stimulation )
- Ischemic MR . Eccentric MR jets and regional and segmental elevation of pulmonary venous pressure has been reported. (Unilateral and segmental pulmonary edema)
- 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 ! )