Iatrogenic Left Main Coronary Lesion? Don't Rush to Operate
- Posted on: 6/19/08
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A 3.5 x 15 mm Driver (Medtronic, Inc., Minneapolis, MN) stent was directly deployed in the circumflex artery without difficulty (Figure 2). On the third day, the patient developed chest pain with new electrocardiographic infero-lateral T-wave inversions (Figure 3). Due to availability issues, another physician performed urgent cardiac catheterization and found the circumflex stent to be widely patent. However, the left main (LM) lumen was significantly narrowed, hugging the catheter. There was accompanying dampening of the pressure waveform. Given the recent intervention, the catheterizing physician diagnosed a new iatrogenic LM lesion, possibly due to traumatic guide catheter dissection (Figure 4). Cardiac surgical consultation was obtained and the patient was scheduled for semi-urgent coronary bypass surgery the next day.
We subsequently reviewed the second catheterization and questioned the diagnosis, especially given the deep catheter engagement of the LM. The next day, the patient was pain-free and the T-waves inversions had normalized (Figure 5). Repeat catheterization was performed to confirm the need for surgery and subsequently revealed a normal LM segment and patent circumflex stent (Figure 6). Coronary surgery was cancelled. Extended-release diltiazem as well as nitrate therapy were prescribed as anti-spasmodic therapy, in addition to the previous standard post-infarct medical regimen of aspirin, simvastatin, clopidogrel, and atenolol. Beta-blockade was continued because the benefits on post-infarct secondary prevention were felt to outweigh its potential adverse effects on vasospasm, especially in the presence of concomitant nitrate and calcium antagonist therapy. Angiotensin-converting-enzyme inhibitor was withheld and welbutrin was added for relative hypotension and smoking cessation, respectively. A myocardial perfusion scan revealed only lateral wall scar without ischemia. The patient was discharged 2 days later and has remained angina-free for over a year.
Coronary spasm can occur spontaneously or secondary to catheter manipulation. Prinzmetal first described variant angina secondary to spontaneous coronary spasm in 1959.1 Approximately 60% of spontaneous coronary spasm occurs in segments of stenoses or thrombi.2 Vasoactive substances such as Neuropeptide-Y, acetylcholine, ergonovine, histamine, dopamine, and serotonin may potentially trigger spasm.3 Additionally, vascular injury may further heighten sensitivity to these compounds as well as inhibit release of vasodilatory factors such as endothelium-derived relaxing factor and nitrous oxide.4 Both sympathetic and parasympathetic activation have been reported to aggravate this process.3 Other predisposing factors include hyperthyroidism as well as tobacco and cocaine abuse.5 The atypical chest pain syndrome associated with mitral valve prolapse has also been attributed to spontaneous coronary spasm.6 As opposed to patients with fixed coronary stenoses, variant angina patients frequently present with angina at rest, although exertional pain has also been described.2
Morita et al found elevated morning LM vascular tone in patients with vasospastic angina. Using this observation, they were able to echocardiographically identify patients with this condition by a 15% LM diameter increase in response to sublingual nitroglycerine administration during morning hours.7 Bertrand and co-investigators were able to provoke spasm in 134 of 1,089 consecutive catheterized patients with intracoronary administration of 0.4 mg of methergine.2 It is postulated that such a positive test result is predictive of spontaneous spasm. The right coronary artery appears more prone to spasm, likely owing to an ostial muscular band.4 Less frequently, the LM can also undergo spontaneous spasm, as in 2 cases reported by Hattori and others.8
Catheter-induced spasm is usually related to mechanical irritation. Chang and colleagues found 30 cases of LM coronary spasm in 7,295 reviewed cases. In their study, factors predictive of LM spasm included increased catheter: LM diameter ratio, catheter-to-LM wall contact, vessel bulging, and acute catheter-to-LM angle.9 Separate cases of simultaneous LM/right coronary5 as well as LM/saphenous vein graft4 spasm have been reported. Clearly, a global pro-spasmodic milieu can exist, even involving a denervated venous conduit in the latter case. Moreover, extra-cardiac extension of this global spasmodic state was observed by Myers and coauthors in a woman with acute anterior wall infarction after cocaine abuse. She presented with severe LM and femoral artery spasm. Fortunately, both were relieved by nitroglycerine and diltiazem.10 One interesting report described severe, sustained spasm of the left anterior descending artery during percutaneous intervention of the left circumflex artery. This resulted in prolonged cardiac arrest and subsequent LM thrombus, which was dislodged and subsequently dissolved.11 Alvarez and coworkers reported severe, diffuse accordion-like spasm of an angulated LM during percutaneous intervention of the left anterior descending artery using a stiff guidewire.12
Jain and co-presenters described a case of severe LM spasm, refractory to 600 mcg of intracoronary nitroglycerine. The patient was initially diagnosed with a fixed LM stenosis on catheterization but refused bypass surgery. Several days later, he was referred for percutaneous intervention but found to have a normal LM lumen.13 As in our case, the delay to surgery and subsequent re-imaging of the LM segment proved prudent.
In our patient, the diagnosis of new LM dissection or stenosis from the second angiogram was suspect for 3 reasons. First of all, the catheter tip was deeply engaged into the LM, almost reaching the bifurcation. Overly aggressive catheter manipulation has been described as a trigger of coronary spasm. Next, review of the initial interventional case revealed no evidence of post-stent LM dissection, trauma, or flow limitation. Additionally, the patient's clinical status as well as electrocardiographic abnormalities normalized after the second catheterization. This presentation would be atypical following an iatrogenically-induced LM lesion. Furthermore, the patient had been hemodynamically stable throughout the hospitalization and received no vasospastic agents. Clearly, in addition to catheter-induced LM spasm, our patient also exhibited Prinzmetal's angina or spontaneous spasm, as manifested by her post-stent angina and accompanying dynamic electrocardiographic changes at rest. Perhaps the spontaneous spasm was further aggravated by the deep catheter engagement. Although speculative, an association likely exists between the propensities for spontaneous and catheter-induced spasm, as illustrated in our presentation.
Treatment of coronary spasm is overwhelmingly medical. Calcium antagonist and nitrate therapy should be maximized to tolerability. Overall, these patients have excellent long-term prognoses. The role of stenting for this condition is unknown. In rare, refractory cases, coronary bypass surgery has been performed with variable results. The intermittently preserved inter-spasm native coronary flow can lead to graft occlusion.14 Complete denervation by plexectomy has also been described for severe cases of variant angina.15
Thus, in cases of isolated LM luminal stenosis, with or without patent stents elsewhere, we recommend intracoronary nitroglycerine administration for confirmation. Moreover, deep catheter engagement can not only induce LM spasm, mimicking a stenotic lesion; but also potentially cause iatrogenic dissection as its own complication. In this case, with catheter disengagement, a cusp shot may well have demonstrated a widely patent LM segment. Either or both of these maneuvers could possibly have clarified the erroneous diagnosis. While intravascular ultrasound can be considered in these situations, differentiation from true stenosis may be difficult. Additionally, introduction of this relatively large profile device into a true severe stenosis, or even a segment of refractory spasm, may lead to vessel trauma, further spasm, or other clinical sequelae. Unfortunately, without demonstration of spasm resolution, definitive diagnosis may not always be possible. Meticulous scrutiny in these situations is crucial to avoid unnecessary bypass surgeries, most of which would likely result in premature graft thrombosis from competitive flow.
Dr. Chen can be contacted at chenjackapollo (at) yahoo.com
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