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1 Department of Pediatrics, Cardiovascular Research Institute, University of California, San Francisco, California 94143; and 2 Department of Physiology, Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
CORONARY PRESSURE-FLOW RELATIONS have long
interested physiologists but are so complex that even today they have
still not been completely unraveled. Early investigators like Rebatel
in 1872 (Ref. 33; cited by van der Meer), Anrep and von Saalfeld in
1933 (1), Gregg and Green in 1940 (17), and
Wiggers in 1954 (39) observed that, when aortic pressures
were high in systole, coronary flow was low; conversely, when aortic
pressures were low in diastole, coronary flows increased. They
attributed this inverse relationship to the impediment to myocardial
flow occurring during systole, although there were differences in their detailed views on the mechanisms. All of these studies were done with
relatively crude instruments, and the more modern studies of coronary
pressure-flow relations can be regarded as beginning in 1965 with the
use of electromagnetic flowmeters [by Gregg and colleagues
(18)]. Not only were high-frequency recordings of coronary flow and pressure obtained, often in conscious chronically instrumented dogs, but also the careful attention to detail together with simple manipulations of cardiac function allowed these
investigators to make inferences from minor changes in the complex flow
signals from the left and right coronary arteries.
At this point, the belief was that, because of assumed differences in
intramyocardial pressure across the wall of the left ventricle, the
systolic coronary flow perfused the outer or subepicardial muscle, but
the deeper or subendocardial muscle could be perfused only in diastole.
These inferences were based on mathematical models of the myocardium by
bioengineers (27, 28) and on the results of direct
measurements of intramyocardial pressures (4, 5, 16, 24,
44). Unfortunately, these different studies often disagreed,
sometimes markedly, about the exact pressures in different regions of
the ventricle. Some of the disagreement stemmed from unrealistic
assumptions and lack of computational power for the models and from
artifacts caused by introducing finite-sized probes into the dense
myocardium (32). With time, many of these difficulties
were overcome, and, eventually, models and experiments began to agree
closely (6, 7, 25, 26, 32, 38). There was general
agreement that, in systole, intramyocardial pressures were close to
cavity pressures beneath the endocardium of the left ventricle and
decreased almost linearly to near atmospheric beneath the epicardium.
To this extent, the inferences of Gregg et al. (18) seemed
to have been correct.
A change in thought was required when investigators began to take the
capacitance of the extramural coronary arteries into account. Douglas
and Greenfield (13) concluded that all of the systolic
flow into the origins of the canine left coronary artery could be
stored in the extramural arteries so that there might be no systolic
perfusion of the subepicardial muscle. This argument was reinforced
when Chilian and Marcus (9) showed that, in the absence of
any capacitance in the extramural coronary arteries (septal artery,
distal branch just before myocardial penetration), there was reverse
systolic coronary flow. In addition, retrograde flow in the extramural
coronary arteries was also demonstrated by Kajiya et al.
(20).
None of the above-mentioned studies measured regional flows, which
could be studied by diffusible indicators (11, 19, 26, 30)
or radioactive microspheres (12). These methods soon
brought out the importance of subendocardial underperfusion in various
models of heart disease (4, 19, 29). It took many years,
however, before the likely mechanism for this selective regional
underperfusion was elucidated (14, 15).
While these studies were in progress, newer microscopic techniques were
used to evaluate regional vascular reactivity (2, 3, 5-8,
10, 16, 21, 31, 40, 41). These studies confirmed the narrowing
of the subendocardial arterioles during systole and also showed
variations in vascular reactivity in arterioles of different sizes and
different locations. Others explored the role of the intramyocardial
blood volume in regulating regional flows in systole and diastole
(34-37); eventually, the elastance concept was
applied to the coronary vascular bed (22-25).
Many of these studies were done with at least two artificial
constraints. The coronary arteries were usually cannulated so that
their pressure could be controlled independent of left ventricular pressure and work. In addition, because most of the techniques used required a steady state, many of the studies were done with maximally vasodilated coronary vessels. Although these studies revealed
many things about the coronary circulation, it was difficult to predict
what results would have been obtained without these constraints. Some
investigators used beat-by-beat analysis (38), but this
required cannulation and some interpretation of the data.
The new approach introduced by wave-intensity analysis helps to
overcome some of the existing problems. It does not require coronary
arterial cannulation and obtains results beat by beat, thus not
requiring a long steady state. So far, however, it has not produced new
insights into the coronary circulation because it has only begun to be
applied, but it promises to be a powerful new tool. One caveat is
needed: methods such as this yield global information and so far are
not capable of exploring regional differences. This caveat is also a
criticism of the elastance concept of coronary flow, treating as it
does the intramyocardial circulation as a single entity with all its
components responding in the same way. One of the future challenges
will be to adapt this method to investigate regional relationships.
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