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Coronary artery spasm can occur during coronary angiography in pediatric heart transplant recipients. The angiographic appearance can suggest allograft vasculopathy. We report coronary artery spasm in a pediatric heart transplant recipient in whom intracoronary nitroglycerin administration prevented a repetition of spasm upon subsequent diagnostic coronary angiography. Additional studies of dose response, particularly in cardiac transplant recipients, may help determine whether lower doses of intracoronary nitrates, such as that administered to our patient, can be effective in preventing coronary artery vasospasm in pediatric heart transplant recipients.
Coronary artery spasm has been reported to occur in 4.9% of adult heart transplant recipients during subsequent coronary angiography,1 but its frequency in children during coronary angiography after heart transplantation is unreported. Because coronary artery spasm can produce generalized luminal narrowing, such spasm can be difficult to distinguish angiographically from cardiac allograft vasculopathy, although this last is morphologically different and at times distinguishable from coronary spasm.2
We describe a case wherein coronary spasm resulted from coronary angiography and produced temporary cardiac compromise, leading to a provisional diagnosis of graft vascular disease. Subsequent angiography, preceded by the intracoronary administration of nitroglycerin, showed the affected vessels to be closer to normal in appearance and had no adverse effects, which suggested that transient vasospasm had been responsible for the angiographic appearance of diffuse luminal narrowing.
In January 2005, a 9-year-old boy who had undergone heart transplantation as an infant presented for surveillance biopsy and coronary angiography. Prior surveillance coronary angiography had shown no evidence of vasculopathy. At the time of the procedure, the patient had no cardiac symptoms, and echocardiography immediately before the procedure had shown normal graft function.
The patient weighed 39.8 kg. After sedation, right femoral arterial access was obtained and a 5F sheath placed. The left main coronary artery was cannulated with a 5F 2.5 Judkins left coronary catheter. Approximately 3 cc of undiluted contrast agent was injected by hand. Thereupon, the left main coronary artery appeared normal, but the left anterior descending and circumflex coronary arteries were diffusely narrow and the transit time was prolonged (Fig. 1). Marked ST-segment elevation occurred, and the patient became hypotensive. He developed ventricular tachycardia and further reduction in systolic pressure as measured via the arterial sheath. Cardiopulmonary resuscitation was initiated immediately, and lidocaine infusion and cardioversion enabled the resumption of sinus rhythm, accompanied by the normalization of ST segments and blood pressure. An echocardiogram obtained immediately thereafter showed normal graft systolic function. The patient recovered uneventfully and was discharged from the hospital on the following day.
Review of the angiograms led us to consider whether the patient had graft vascular disease or had experienced coronary artery vasospasm. We decided to perform another coronary angiographic procedure, preceded by the intracoronary administration of nitroglycerin.
Therefore, approximately 1 month after the original procedure, the patient underwent repeat coronary angiography. After sedation, a 5F sheath was placed in the right femoral artery. A 5F 2.5 Judkins catheter was placed in the orifice of the left coronary artery. We injected 50 μg of nitroglycerin and flushed it with 2 cc of normal saline. We injected 3 cc of contrast agent by hand. There were no changes in ST segments, cardiac rhythm, or blood pressure. The caliber of the left main coronary artery again appeared normal. The left anterior descending and circumflex coronary arteries appeared to have improved (Fig. 2). The patient recovered uneventfully and was discharged from the hospital later the same day. After 5 years and subsequent coronary angiography (preceded in each instance by intracoronary nitroglycerin administration), he remained well and free of angiographically apparent graft vasculopathy.
Although other diagnostic methods are widely reported, coronary angiography remains an important tool in the diagnosis of graft vasculopathy.3,4 Coronary spasm can occur in patients without vasculopathy or can be superimposed on organic disease. Distinguishing this complication from organic disease is therefore vitally important,1 as is preventing its occurrence.
The angiographic appearance of coronary vasculopathy has been described. It may take the form of multiple discrete stenoses (type A lesion), distal concentric narrowing (type B1 lesion), proximal concentric narrowing with distal extension (type B2 lesion), or abrupt distal branch termination (type C lesion).2 Other reported patterns include proximal narrowing of the coronary artery just distal to the catheter and a more generalized narrowing that affects the length of the artery and its branches.1,5 This last pattern is similar to that of the type B2 lesion.
Coronary spasm has been reported to lead to the erroneous diagnosis of organic disease. In adult patients, the routine use of intracoronary nitrates during angiography is recommended by some clinicians to prevent coronary spasm. Such use can eliminate diagnostic confusion, improve angiographic visualization, and prevent the adverse effects of coronary spasm.6
The injection of intracoronary nitrates can prevent or reverse coronary spasm associated with coronary angiography. The recommended dose for adult patients is based on dose-response studies that show maximal vasodilation with a dose of 150 μg. A standard reference text lists a dose of 200 μg.7 In a study of coronary vasodilation capacity in 6 control subjects and in 19 pediatric patients after the arterial switch operation, a dose of 3 μg/kg was administered, on the basis of extrapolation from a 200-μg adult dose. This produced vasodilation in the control group and a 10% to 15% reduction in blood pressure, with less than a 10% increase in heart rate, in both groups.8 The dose used in our patient was 1.25 μg/kg, which is lower than the previously reported pediatric dose. It produced no significant hemodynamic or ST-segment changes, and coronary spasm did not recur. Additional studies of dose response, particularly in cardiac transplant recipients, may help determine whether lower doses of intracoronary nitrates, such as that administered to our patient, can be effective in preventing coronary artery vasospasm in pediatric heart transplant recipients.
Address for reprints: F. Bennett Pearce, MD, University of Alabama School of Medicine, NHB 320, 619 19th St. South, Birmingham, AL 35249–6852