(Circulation. 1995;92:2790-2793.)
© 1995 American Heart Association, Inc.
Articles |
There May Be More to Myocardial Viability Than Meets the Eye!
From the Cardiovascular Division, University of Virginia School of Medicine, Charlottesville.
Correspondence to Sanjiv Kaul, MD, Cardiovascular Division, University of Virginia Medical Center, Box 158, Charlottesville, VA 22908.
Key Words: myocardium • contractility • Editorials
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Introduction |
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 Top Introduction References |
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According to the Oxford English Dictionary, "viable" means "capable of living."1 Incorrectly, the terms viable and capable of contracting in the presence of adequate blood flow have been used interchangeably for the myocardium. Consequently, it has been suggested that viable myocardium is only that which demonstrates improved thickening after restoration of blood flow.2
This definition of viability is inaccurate because it ignores a
fundamental physiological principle: that at rest,
most left ventricular wall thickening occurs as a result of
endocardial thickening; the middle layer of the myocardium
contributes only modestly to thickening; and the contribution of the
epicardium is negligible (Fig 1
).3 4
Thus,
if the endocardium is necrosed, wall thickening will be significantly
diminished at rest even if blood flow is restored to the middle and
outer thirds of the ventricular wall.5 When
infarction involves <20% of the wall thickness, hypokinesia is noted.
When it involves 
20% of the wall thickness, akinesia or dyskinesia
is seen.6
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Defining viability as recovery in regional function after revascularization also presupposes that revascularization successfully restores resting nutrient blood flow to normal levels. It ignores the all too frequent occurrence of inadequate revascularization for technical reasons, poor distal runoff, or the presence of abnormal microvasculature within the revascularized bed.7
Thus, defining viability as recovery of regional function after a
revascularization procedure is inaccurate, albeit
expedient. Ideally, the definition of viability should be as simple as
that in the Oxford English Dictionary. It should also be
independent of the result of an intervention, be it
percutaneous or surgical. The ideal imaging method for
assessing viability should be able to delineate infarcted from
noninfarcted tissue with the same resolution as shown in Fig 2,
in which infarction represents nonviable
tissue and the rest of the heart represents viable
myocardium.
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There may be several benefits to nonischemic viable
myocardium even if it does not demonstrate systolic
thickening at rest. Although the middle and outer layers of the
myocardium thicken little at rest, they thicken more with
catecholamine stimulation8 and may thus
contribute to overall wall thickening and an increase in global left
ventricular systolic performance during
exercise and other forms of stress. The presence of viable
myocardium in the outer layers of the
ventricular wall may also contribute to maintenance
of left ventricular shape and size by preventing infarct
expansion (Fig 2
) and subsequent heart failure and thus reduce
late
mortality after acute myocardial
infarction.5 9 10 11
In the assessment of viability, one should separate postinfarction patients from those who have left ventricular systolic dysfunction on the basis of chronic coronary artery disease. In the former, the two questions to be asked are: Is there any viable myocardium? Is that myocardium susceptible to ischemia? Since tissue has to be viable to become ischemic, any imaging method that can detect ischemia will answer the second question. A patient with a moderate to large amount of ischemic myocardium is a candidate for a revascularization procedure.
The benefit of uncovering viability in postinfarction patients who do not have ischemia is unknown. If most of the myocardium in an infarct zone is viable and not susceptible to ischemia, then recovery of resting function in that zone will occur spontaneously within weeks.5 12 13 14 If the endocardium is necrosed, however, spontaneous recovery in resting function will not occur. Although it is not proven, knowledge of whether there is substantial nonischemic viable myocardium in the middle and outer layers of the left ventricular wall may provide prognostic information and may also be valuable in selecting patients most likely to benefit from angiotensin-converting enzyme inhibitors.
In patients with chronic coronary artery disease and reduced global left ventricular systolic function, the most difficult question usually is whether the global dysfunction is due to ischemia or other causes. Many such patients have comorbidity, such as hypertension, that can also result in a reduction in global function. Even in patients with reduced function associated with chronic coronary artery disease, it may be important to assess viability in the different myocardial layers. For instance, many patients with remote infarction and partial-thickness scarring will not show recovery in regional function after revascularization, whereas those with viable myocardium throughout the entire wall may show immediate recovery in function.
Another important clinical issue relates to assessing the benefits of revascularization in patients with chronic ischemic heart disease and global left ventricular systolic dysfunction. Assessment of resting global systolic function alone may underestimate the level of benefit received. Even in the absence of improved resting global function, patients may feel better and have a reduction in their cardiac size and filling pressures, and their exercise capacity may improve. They may also no longer be susceptible to exercise-induced ischemia and pulmonary edema. Consequently, the assessment of cardiac volumes, anaerobic threshold, and left ventricular systolic function during exercise may provide a better assessment of the benefit from revascularization than the measurement of resting systolic function alone.
In the postinfarction reperfused myocardium, the degree of
contractile reserve provides an excellent assessment of the quantum of
viable myocardium if there is no residual
stenosis limiting hyperemic flow.8 A
number of catecholamines have been used to evaluate
contractile reserve. If blood flow does not increase commensurate with
the increase in myocardial oxygen consumption caused by these agents,
ischemia will result and wall thickening will decrease.
Consequently, the degree of residual infarct-related artery
stenosis will determine the contractile response for a given
amount of viable myocardium. A mild stenosis
(<50% luminal diameter narrowing) will not attenuate the contractile
reserve, whereas a critical stenosis (>85%) will completely
attenuate it. In many instances, the residual stenosis after
reperfusion is not critical (
85%), and thus variable degrees of
attenuation of the contractile responses will be seen at various doses
of dobutamine. As a result, the contractile response may be
maximal at doses of 5 to 10
µg · kg-1 · min-1 of
dobutamine and may diminish at higher doses (the
so-called "biphasic response").15
Thus, although the presence of viability may be detected when there is a residual stenosis, the amount of viability in the infarct zone cannot be quantified on the basis of the magnitude of thickening elicited during dobutamine.16 It is obvious, however, that if the myocardium responds to a low dose of dobutamine, the infarct is probably small and located in the endocardium. Not surprisingly, therefore, the response of the myocardium to a low dose of dobutamine is highly predictive of spontaneous recovery in regional function,15 since patients with small endocardial infarcts are the subset that shows recovery in resting regional function after reperfusion.5 12 13 14
One of the intriguing findings reported by deFilippi et
al17 in this issue of Circulation and by
these18 and other authors in other recent
publications19 20 is the presence of contractile
reserve
in patients with chronic coronary artery disease and reduced
regional function. It has heretofore been believed that regional
dysfunction seen in hibernation is due to reduction in resting blood
flow to the myocardium. Thus, flow and function are coupled
in a parallel manner to that noted in acute ischemia, in which
reduction in flow results in a commensurate reduction in function (Fig
3).21 22 23 If the
situation were identical to
acute ischemia, catecholamine stimulation would
result in increased myocardial oxygen consumption, which in the absence
of a concomitant increase in blood flow would cause worsening
dysfunction. Downregulation of metabolism in the presence
of slowly developing ischemia,24 however, may
result in a rightward shift of the flow-function relation such that
the reduction in function may be more than the reduction in flow (Fig
3). In this situation, low-dose dobutamine may result
in an improvement in function, with further increase in the dose of
dobutamine causing ischemia-mediated worsening
of function (the biphasic response).
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The hibernating myocardium may not be entirely described by this one relation, however. For example, patients who either have a small infarction or do not infarct during coronary occlusion because of good collateral flow may have normal or near-normal resting flow25 26 but may experience repeated episodes of ischemia during routine daily activities, and the myocardium may demonstrate dysfunction simply because it never recovers from repetitive stunning. A similar situation may exist when the coronary artery supplying the myocardium has a severe but subcritical stenosis. In this setting, although resting myocardial flow may be normal, repeated episodes of ischemia may result from even modest levels of exertion, causing the myocardium to appear perpetually "stunned." In these settings, the degree of vascular reserve and the amount of viable myocardium will influence the response to catecholamines. If there is a significant amount of viability and some vascular reserve, improvement in function will be observed at low doses of dobutamine. By contrast, if the endocardium is necrosed and vascular reserve is good, then increased thickening will be noted only at moderate to high doses of dobutamine. The heterogeneity in the myocardial response to dobutamine seen by deFilippi and others17 18 19 20 may therefore potentially provide insights into the underlying pathophysiology of myocardial dysfunction in individual patients and in specific myocardial segments.
The assessment of microvascular integrity within the myocardium is also gaining credence as a method of assessing myocardial viability. Normal microvasculature and normal microvascular reserve are present in regions of viable myocardium, whereas regions of necrosis have either abnormal microvasculature or abnormal microvascular reserve.27 28 29 Myocardial contrast echocardiography has the spatial resolution to examine the different myocardial layers of the left ventricular wall for microvascular function. The assessment of viability by use of this technique has been demonstrated previously in postinfarction patients by several investigators.30 31 32 33 The report of deFilippi and colleagues17 in this issue of Circulation is the first description of this technique in patients with chronic coronary artery disease. It is too early to tell which of these two aspects of viability (contractile or microvascular reserve) is more accurate in this subset of patients. Since our understanding of viability is rudimentary at present, more than one method, as implied by deFilippi and colleagues,17 may be necessary at times to make the correct management decisions in complex cases.
There may be much more to myocardial viability than meets the eye. Although recovery in function spontaneously or after successful revascularization is the best possible outcome, there may be other advantages of viable myocardium. We are at the dawn of an exciting era in our further understanding of coronary pathophysiology in humans, and it will be years before we fully understand the multiple mechanisms responsible for regional and global dysfunction in patients with coronary artery disease and the prognostic and therapeutic implications of these mechanisms. Although clinical studies are vital for this understanding, we should be careful to interpret clinical findings in the context of defined pathophysiological principles. Medicine without physiology is merely phenomenology. We have too much of that already.
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Acknowledgments |
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Supported in part by a grant (R01-HL-48890) from the National Institutes of Health, Bethesda, Md, and an Established Investigator Award from the National Center of the American Heart Association, Dallas, Tex. The author acknowledges the helpful critique of the manuscript by Ian J. Sarembock, MD, and Jonathan R. Lindner, MD.
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