Pathophysiology
The coronary resistance consists of 3 components:
It is formed in the epicardial conduction vessels (Classen 2009) and depends on the lumen width of the epicardial coronary artery.
It depends on the resistance of the intramyocardial arterioles (Herold 2019) and is mainly locally metabolically regulated. The coronary blood flow can increase 4 to 5 times by dilatation of the intramyocardial resistance vessels (Classen 2009).
The extravasal component depends on the systolic vessel compression as a consequence of the intramyocardial pressure increase (Herold 2019).
Increased left ventricular pressure results in increased extravasation resistance. This resistance exists from the subendocardium to the subbepicardium as a transmural resistance gradient.
As a result, the coronary reserve in the subendocardium is exhausted earlier than in the subbicardium. This explains why myocardial ischemia always occurs first in the subendocardium (Classen 2009).
Increase in coronary resistance
An increase in coronary resistance can be caused by:
- vasal factors such as
- Macroangiopathy (e.g. CHD)
- Microangiopathy (small vessel disease)
- Coronary spasms (can be triggered by cocaine, among other things)
- Anomalies of the coronaries
- arteriovenous fistulas
- congenital myocardial bridges
- Arrhythmias
- arterial hypertension
(Herald 2019)
- Hypercapnia (Kretz 1989)
- Various drugs (such as Atenolol etc. [Schlegel 1980])
Reduction of coronary resistance
- Tachycardia (Lüderitz 1983)
- various drugs (such as calcium antagonists [Wappler 2006], nitrates [Rietbrock 1986]) etc.