CORRESPONDENCE
Does flow reserve match contractility?
Giuseppe Barletta, MD, FESCa
a Viale Morgagni 85, Careggi Hospital, Florence, 50134 Italy
g.barletta{at}dfc.unifi.it
I have read with great interest the report by Barillà et al. (1). The data reported are intriguing because, to the best of my knowledge, this is the first report indicating that the restoration of regional contractility during low dose dobutamine administration may occur despite different perfusion patterns, depending on the presence or absence of collateral filling.
Let me raise an issue not addressed in the Discussion of Barillà’s article. I definitely agree with Bonow (2) that the increase in flow in patients with collateral filling is expected, because the drop of pressure beyond the fixed obstruction can increase the flow, despite the coronary driving pressure’s being unchanged. The no-measurable-flow response in patients without collateral channels can also be expected. In fact, why should the flow increase through a stenosis or an occlusion? Irrespective of flow regimen, the authors (1) noted an amelioration in contractility of dysfunctional myocardium—one that was still present at 2-methoxy-isobutyl-isonitrile (MIBI) administration and during the time allowed for it to distribute to the myocardium (i.e., up to 8 min), I presume, because no mention was ever made to subsequent deterioration of wall motion. This is an astonishingly long time, which would more appropriately define the response to low dose dobutamine of stunned myocardium (but this was not the case, as indicated by the low sestamibi uptake). It seems inconceivable that such a prolonged increase in contractility may occur in the absence of an adequate increase in blood flow, the situation being absolutely different from the postextrasystolic potentiation of contractility, when myocytes burn their energy stores all in one go. By contrast, the increase in contractility of ischemic but viable myocardium at low dose dobutamine is a short-lived phenomenon: it may begin at very low dosage (as low as 2.5 µg/kg body weight per min, in our experience) and usually fades away at 10 µg/kg per min, seldom at 20 µg/kg per min. In patients with very severe coronary stenosis or coronary occlusion without collateral blood filling, a biphasic response to dobutamine should be expected at a dosage even lower than that at which the authors injected technetium-99m sestamibi. Given this, as well as the notion of the ischemic cascade (3,4), I make the point that Barillà et al. (1) described an intermediate phase of the biphasic response phenomenon—that is, the time when the flow reserve is exhausted, but wall contractility has not yet deteriorated in response to forthcoming or ongoing ischemia, or both. I suggest that this possibility is whispered to the reader.
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References
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1. Barillà F, De Vincentis G, Mangieri E, et al. Recovery of contractility of viable myocardium during inotropic stimulation is not dependent on an increase of myocardial blood flow in the absence of collateral filling. J Am Coll Cardiol. 1999;33:697–704[Abstract/Free Full Text]
2. Bonow RO. Contractile reserve and coronary blood flow reserve in collateral-dependent myocardium. J Am Coll Cardiol. 1999;33:705–707[Free Full Text]
3. Nesto RW, Kowalchunck GJ. The ischemic cascade: temporal response of hemodynamic, electrocardiographic and symptomatic response of ischemia. Am J Cardiol. 1987;59:23C–30C[CrossRef][Medline]
4. Hauser AM, Gangadharan V, Ramos G, Gordon S, Timmis GC, et al. Sequence of mechanical, electrocardiographic and clinical effects of repeated coronary artery occlusion in human beings: echocardiographic observations during coronary angioplasty. J Am Coll Cardiol. 1985;5:193–197[Abstract]
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