Q. Describe Coronary Spasm?

Usually spasm develops at the site of subcritical or critical stenoses, but it may also occur in angiographically normal coronary arteries, the so called variant form of angina. Occlusive spasm causes transmural ischaemia with ST-segment elevation, but when spasm is subocclusive, it may cause subendocardial ischaemia and ST-segment depression.

Coronary Collateral Circulation

1) The drop in poststenotic pressure caused by flow-limiting stenoses stimulates the development of collateral circulation from other coronary artery beds. The supply of collateral blood flow increases poststenotic pressure, thus improving coronary flow reserve and raising the ischaemic threshold.

2) Collateral vessels develop from the progressive enlargement of preexisting intercoronary arterial anastomoses.

3) Blood flow through these anastomeses begins as a consequence of the flow-limiting stenosis when a pressure gradient develops between their origin and termination.

4) In unanesthetized dogs, a pressure gradient of about 10mm Hg, caused by a lumen reduction of 70 to 80 per cent has been shown to elicit the development of collateral flow.

5) Preexisiting anastomoses progressively transform to vessels with a final diameter of 20 to 200 um.

6) Blood flow through collaterals is determined by the driving pressure and by their resistance, which is influenced by neural and humoral stimuli and by local vasoactive autacoids.

7) In patients, heparin and fibroblastic growth factor 1 (FGF-1) have been suggested to promote collateral growth.