Because the true size of coronary arteries is unknown, it is common practice in many labs to give NTG before every angiogram. Enhanced vasomotor tone is often evident during angioplasty and can be clearly seen when IC NTG is used to produce maximal vasodilation. The NTG permits better assessment of stenosis severity, eliminates false narrowings (i.e., spasm) and produces the best measurement of absolute vessel size for device selection.
Catheter-induced vasospasm is produced by mechanical stimulation of a vessel by contact with a catheter. Poking and prodding of these muscular arteries might occur during engagement of any catheter into a coronary artery or into any muscular artery. Catheter-induced vasospasm is fortunately uncommon and unpredictable. It is rarely of clinical importance, except that it must be distinguished from true organic narrowings of a vessel. It is interesting that catheter spasm is as rare as it is, given the manipulations we perform during coronary angiography. Beginning angiographers learn about catheter spasm early in their experience in the lab. One of the first observations made by the beginning coronary angiographer is that of an ostial coronary narrowing which is related to engagement of the right coronary Judkins catheter. One clue to ostial narrowing is also the associated and often dramatic change in the arterial pressure wave which is flattened, rounded or ventricularized. These pressure damping patterns, which can occur with any ostial narrowing, whether spasm or organic, indicate obstruction at the catheter tip. The left main coronary artery segment may also be involved in either spontaneous or catheter-induced spasm.1
Coronary ostial stenosis may be produced by a number of conditions, the most reversible of which is catheter-induced spasm. Soo et al2 described isolated left main coronary ostial stenosis in a patient having what appeared to be catheter-induced spasm. The many potential causes of coronary ostial stenosis are listed in Table 1.
Coronary ostial stenosis may easily be missed because of subselective angiography and engagement of the catheter in the deep position. This is especially true with the smallest of catheters, 4-5 French. The lack of catheter dampening may obscure presence of significance of left main narrowing. Coronary spasm may produce an identical picture and angiography should be repeated after giving sublingual or intracoronary nitroglycerin. Two findings should alert the angiographer to the presence of true ostial stenosis: 1) pressure dampening identified by the large systolic and diastolic differences in the waveform, sometimes characterized as ventricularized pressure, and 2) failure of contrast to reflux into the coronary sinus to Valsalva on vigorous injection. Both findings can be associated with coronary catheter-induced ostial narrowing from catheter spasm.
The major concern for the angiographer is whether the narrowing with or without pressure damping is due to a true organic stenosis or catheter-induced spasm. Catheter-induced spasm may also occur at some distance from the catheter tip, but this response is also rare. One uncommon and surprising finding is a narrowing found at the initial angiogram, which is completely relieved by NTG when imaged again prior to proceeding with coronary intervention.3
To differentiate vasospasm from an organic ostial narrowing, it is necessary to perform a series of catheter maneuvers after giving NTG (either IC [1-3 doses of 200mcg] or sublingual [1-2 tabs of 0.4mg]). One of the first maneuvers is a cusp flush. The operator performs a cusp injection with the catheter positioned just below the coronary ostia. Because the sinus of Valsalva is partly spherical, the cusp may fill with contrast and obscure the ostial narrowing depending on the angle of the ostial take-off (Figure 1). Another maneuver is a pullback injection. The operator performs a continuous injection of contrast while withdrawing the catheter to see the difference in the ostial narrowing without the catheter in place. It is helpful to re-inject IC NTG, remove the catheter, wait a minute or two and repeat the first two maneuvers. If, after all of these maneuvers, the ostial narrowing persists, the narrowing must be considered to be genuine. However, if ostial imaging is still in question as to its severity, fractional flow reserve (FFR) or intravascular ultrasound (IVUS) may be required to provide the definite physiologic importance of the narrowing.
When this problem involves the left main (LM), the correct interpretation and clinical decision-making is even more critical. In this issue of Cath Lab Digest, Chen presents a case of LM coronary spasm presenting as a critical narrowing, highlighting the dilemma faced by angiographers. Factors predictive of LM spasm included increased catheter:LM diameter ratio, catheter-to-LM wall contact, vessel bulging, and acute catheter-to-LM angle.
Finally, it is also important that angiographers recognize that spontaneous coronary vasospasm elsewhere in the coronary tree that may masquerade as luminal narrowings which can be mistaken for true stenoses. We reported just such an example of multivessel spasm being mistaken for multiple lesion coronary artery disease. Before deploying a stent in the worst lesion, IC NTG resulted in resolution of all stenoses, obviating the need for stents.3,4 We learned that we should consider and certainly exclude coronary spasm before stent insertion, but such is the confounding nature of coronary spasm. Don't be fooled in your lab.
1. Deligonul U, Kern MJ, Caralis D. Left main and right catheter-induced coronary artery spasm in a patient with vasospastic angina. Cathet Cardiovasc Diagn 1989;17:39-44.
2. Soo CS et al. Isolated Left Main Coronary Ostial Stenosis versus Catheter Tip Left Main Coronary Spasm. Journal of Hong Kong College of Cardiology 1995;3:34.
3. Parham WA, Kern MJ. The Disappearing Coronary Stenosis: Reemphasizing the importance of excluding coronary vasospasm before coronary intervention. Cathet Cardiovasc Interven 2002; 57:224-228.
4. Kern MJ, Miller JT. Coronary spasm, steal and stenosis. Implications for therapy of ischemic heart disease. Curr Prob Cardiol 1985;11(1):1-67.