Coronary collateral vessels in cyanotic congenital heart disease

LETTERS CORONARY COLLATERAL VESSELS IN CYANOTIC CONGENITAL HEART DISEASE In his interesting report on collateral vessels between the coronary and bronchial arteries in patients with cyanotic congenital heart disease, Zureikatl discusses the fact that these patients did not have hypoxemic episodes; a comparable group of cyanotic patients without such collateral vessels often presented anoxic spells. It is not very likely that coronary collateral vessels increase pulmonary blood flow to a great extent, but they could well be, as the author suggests, part of a more extensive collateral network connecting systemic to pulmonary arteries. In that case the absence of hypoxemic spells is not surprising. In a study of patients with cyanotic congenital heart disease who underwent rapid atria1 pacing during routine catheterization, we2 were able to differentiate two types of response: either (1) a reduction in arterial oxygen saturation with pacing, accompanied by signs of myocardial anoxia (lactate production), or (2) no change in arterial oxygen saturation, with no myocardial metabolic changes. The first group comprised patients with typical tetralogy and “reactive” infundibular stenosis and few collateral arteries; cyanotic spells occurred in over one half of these children. The second group contained patients with either predominantly valvular stenosis or pulmonary atresia with extensive aortopulmonary collateral channels; none of these had a history of anoxic spells. Thus, in classic tetralogy, the stress of atria1 pacing, of exercise and, of course, of anoxic spells decreases pulmonary blood flow acutely resulting in severe hypoxemia and its metabolic changes. If large collateral vessels are present, such a reduction in pulmonary blood flow is presented. Beat Friedli, MD Clinique Universitaire Geneva, Switzerland

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Lionel H. Opie, MD Groote Schuur Hospital Cape Town, South Africa References 1. Zurelkai HC. Collateral vessels between the coronary and bronchial arteries in patients with cyanotic congenital heart disease. Am J Cardiol 1990:45:599. 2. Frledli B, Haennl 6, Morel P, Opie LH. Myocardial metabolism I” cyanotic congenital heart disease at rest and during atrial pacing. Circulation 1977:55:647-52

REPLY I agree that the flow through the coronary bronchial collateral channels is not enough to explain the absence of hypoxemic episodes in some patients with cyanotic congenital heart disease. These collateral channels, however, can provide a significant increment to pulmonary blood flow; by comparing the size of the collateral vessels with that of the catheter, it is obvious that the flow through these vessels must be significant indeed. The presence of coronary bronchial collateral vessels reflects the extent of collateral circulation between the bronchial (systemic) and the pulmonary arteries. Collateral vessels between the coronary and bronchial arteries do not become functional unless there is a significant pressure gradient between the two circulations, as is the case when there is extensive collateral flow from the bronchial arteries to the pulmonary arteries leading to a decrease of pressure in the bronchial arteries. Harran Y. Zureikat, MD Amman, Jordan

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EJECTION FRACTION AND ATRIAL PACING Ricci and co-workers’ concluded that an increase in heart rate produced by right atria1 pacing results in a significant decrease in ejection fraction in human beings. Of the 17 patients studied, 10 were recipients of cardiac allografts; the other 7 had had aortocoronary bypass surgery. The results of atria1 pacing in this unique group of patients cannot serve, in our opinion, as a standard for behavior of normal human beings. We studied 18 patients with right atria1 pacing and multigated radionuclide angiography; 7 patients had angiographically normal coronary arteries and left ventricular function and 11 had advanced coronary artery disease.2 In none of the 7 normal subjects was a decrease in ejection fraction observed during atria1 pacing, but in 9 of the 11 patients with coronary disease, a decrease in ejection fraction was noticed. Our conclusions are therefore contrary to those of Ricci and coworkers; that is, in normal persons ejection fraction remains unchanged, but in patients with coronary disease ejection fraction decreases during atria1 pacing. Dan Tzivoni, MD Avraham T. Weiss, MD Mervyn S. Gotsman, MD Henry Atlan, MD, PhD Department of Cardiology and Medical Biophysics Hadassah University Hospital Jerusalem, Israel References 1

Rlccl DR, Orllck AE, Alderman EL, lngles NB Jr, Daughters GT, Stlnsons EB. Influence of heart rate on left ventricular ejection fraction in human beings. Am J Cardiol 1979: 441447. 2. Tzlvonl D, W&s AT, Saksl A, et al. Multiple gated blood pool cardiac scan during right atrial pacing: a sensitive method to detect myocardial ischemia (abstr). Am J Cardiol 1980:45:408.

REPLY Our patients were either cardiac allograft recipients or patients with coronary artery disease who had undergone complete coronary revascularization. It is possible that the progressive reduction in ejection fraction seen in our patients was due to slightly reduced ventricular compliance rather than to some abnormality of systolic function. Our observations on ejection fraction are supported by several studies (quoted in our Table I), and the results of Tzivoni are supported by a similar number of studies (summarized by Slutskyl). We believe that, while some controversy continues regarding the change in ejection fraction during atria1 pacing in patients with normal and diseased coronary arteries, this technique should not be used to identify patients with coronary artery disease. Furthermore, particularly when there may be some abnormalities of left ventricular compliance, as in the postoperative stage, we believe that heart rate does indeed influence ejection fraction and therefore must be taken into account when serially measuring left ventricular function. Donald R. Ricci, MD Division of Cardiology The University of British Columbia Vancouver, British Columbia, Canada Reference 1. Slulsky Ft. afterload

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Response of the left ventricle to stress: effects stress and drugs. Am .I Cardiol 1981;47:357-364.

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atrial pacing,