Percutaneous coronary intervention (PCI) in patients with depressed left ventricular function requires patience, technical skills and, at times, even a counterintuitive approach. In this high-risk group, standard PCI methods, mainly balloon angioplasty and stenting, are incapable of adequate reduction of target plaque burden, frequently resulting in suboptimal outcomes. The extent of atherosclerotic disease, complex plaque morphology, diminished myocardial reserve for tolerance of ischemia during intervention and associated comorbidities, render PCI a considerable challenge.
Useful debulking devices for these patients are applied insufficiently in most catheterization laboratories nowadays, to a large extent due to a prevailing erroneous belief that balloons and stents “can do it all”. When not in use, debulking devices fall out of favor. Currently, only a few academic training programs offer adequate training in application of rotational atherectomy. This is unfortunate because its success in debulking diffuse disease and in calcifications in particular, is well documented.¹ Furthermore, a cautionary approach on the part of a manufacturer may restrict the use of a device to only patients with preserved ventricular function. Unfortunately, such is the case with the useful Rotablator^® device (Boston Scientific Corp., Natick, Massachusetts). Admittedly, early experience raised concerns regarding adverse effects on platelets. Then there were observations of a “no-reflow” phenomenon which was attributed to device-induced microembolizations. However, with adjunct glycoprotein IIb/IIIa antagonists, and with refinements in rotational atherectomy techniques such as maintenance of proper burr speed (approximately 160,000 rpm), utilization of gentle “peck-and-retreat” debulking rather than aggressive ablation (“drilling” the lesion), and incorporation of the efficient Rotaglide^™ (Boston Scientific) lubricant infusion into the controller — most device-related problems were resolved. Consequently, it can be used successfully in long, diffuse and calcified plaques, ostial stenoses, in-stent restenosis and in lesions not amenable to crossing or dilatation with standard balloons. However, as mentioned, depressed left ventricular function remains a lingering limitation, as the manufacturer does not recommend rotational ablation in patients with a left ventricular ejection fraction (LVEF) of less than 30%.
With an aging population, the number of ischemic patients with severe left ventricular dysfunction whose only revascularization option is PCI, continues to increase. They frequently exhibit lesion morphology favoring rotational debulking. Hence, the paper by Ramana and colleagues² in this issue of the journal successfully breaks old barriers, as it describes the safety and efficacy of rotational atherectomy in a series of 23 patients with severe left ventricular dysfunction (mean LVEF = 21%). The patients’ clinical profile is typical: the LAD was the most frequent target vessel, with a majority (87%) having multivessel coronary artery disease and severely stenosed, calcified target lesions. The frequency of bifurcation lesions in this series also attests to the challenge. The results achieved by Ramana et al are excellent, yet realistic: 100% angiographic success, 0% in-hospital target vessel revascularization (TVR) and a 17% in-hospital combined major adverse cardiac event (MACE) rate, albeit, troponin levels were checked in only 43% of patients. The authors demonstrated that rotational atherectomy can be performed without the “no-reflow”, abrupt closure, dissections or perforations seen in the early 1990s.
Interestingly, the results can be corroborated by comparison with experience gained with other debulking modalities in such high-risk procedures. Using a mid-infrared holmium YAG laser, we performed angioplasty in 22 patients with severely depressed LVEF (mean 25%) and recorded a 100% success rate, 0% emergency coronary artery bypass graft surgeries (CABG) and no deaths or perforations. Comparing these patients to a group with preserved LVEF (mean 58%), no significant difference was found in safety or efficacy of the laser debulking.³ More recently, we compared the effectiveness of ultraviolet excimer laser in patients with acute coronary syndromes and depressed LVEF (25 patients; mean LVEF = 28%) versus those with preserved ventricular function (75 patients; mean LVEF = 53%). There was a high device success rate (87% vs. 93%, respectively; p = ns) and procedural success (93% vs. 98%, respectively; p = ns) in both groups. There were no deaths, emergency CABG procedures, strokes or acute vessel closure in either group. Notably, thrombus did not adversely affect device or procedural success in both groups.⁴
Whether administration of a direct thrombin inhibitor instead of a glycoprotein IIb/IIIa antagonist and prophylactic intra-aortic balloon pump placement can further reduce rotational atherectomy-related MACE is unknown and remains at the discretion of operators. In selected patients with depressed ventricular function, a Swan-Ganz catheter could be beneficial, because ischemia and hemodynamic instability are readily detected, a crucial element for a successful intervention in these difficult cases.
It is clear that outdated axioms such as the elimination of rotational atherectomy in depressed ventricular function should be reassessed. To put the issue in perspective, we note that not too long ago, stents were not recommended in depressed ventricular dysfunction.⁵ The experience of Ramana et al with rotational atherectomy is encouraging, as it offers improved management options for patients with depressed ventricular function.