Reservoir/excess pressure analysis of coronary haemodynamics

Much of our work in wave intensity analysis has been in the coronary arteries. This is for two reasons: the coronaries are the most clinically significant arteries and flow in the coronaries is one of the greatest challenges in haemodynamics. The first reason is factual; coronary artery disease is one of the major causes of mortality and morbidity in the world. A small improvement in the diagnosis, treatment or prevention of coronary artery disease could mean a significant improvement in world health. The second reason arises because the contraction and relaxation of the myocardium affects not only the lumenal pressure in the coronaries but also the extravascular pressure of the intramyocardial vessels giving rise to very complicated haemodynamics.

As an illustration, the following two figures show the pressure and velocity measured in a typical systemic artery and in one of the coronary arteries. The pressures are similar, but the flows are profoundly different. Understanding why is the challenge.

pressure and flow measured in the distal aorta

pressure and flow measured in the LAD coronary artery

Note that the pressure is very similar in the aorta and the coronary artery. There is a slight delay in the distal aortic pressure that is expected because of the time it takes for the wave to travel there from the aortic root. There is also a slight decrease in the diastolic pressure and a slight increase in the pulse pressure; both of which are expected in pressure waveforms measured more distally.

The velocity waveform is, however, very different. Whereas the flow is almost completely confined to systole in the aorta with virtually no flow measured during diastole, the flow in the coronary is larger in diastole than it is in systole in the coronary artery. This is a feature of flow in all of the coronary arteries and it means that coronary perfusion occurs primarily in diastole.

There are several theories to account for the details of this process but the physical reasons are fairly clear: The compression of the the myocardium during systole results in a higher pressure in the interstium surrounding the intramyodardial blood vessels and impedes flow through them during systole. When the myocardium decompresses during late systole, this interstitial pressure is removed from the intramyocardial blood vessels and flow resumes, driven by the diastolic aortic pressure.

Understanding the details of coronary flow is very important clinically and much of our effort recently has been to apply wave intensity analysis to coronary flow to see if we can elucidate the basic haemodynamics. The application of the reservoir-wave hypothesis is part of this research programme. So far the results have been encouraging but is not conclusive. We will discuss some of the findings here.

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