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J Am Coll Cardiol, 2004; 43:328-336, doi:10.1016/j.jacc.2003.09.032
© 2004 by the American College of Cardiology Foundation
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VIEWPOINT

Myocardial perfusion imaging following percutaneous coronary intervention

the importance of restenosis, disease progression, and directed reintervention

Kenneth N. Giedd, MD, FACC*,* and Steven R. Bergmann, MD, PhD, FACC*

* Division of Cardiology, Department of Medicine, College of Physicians and Surgeons of Columbia University, New York, New York, USA

Manuscript received April 25, 2003; revised manuscript received August 25, 2003, accepted September 9, 2003.

* Reprint requests and correspondence: Dr. Kenneth N. Giedd, Division of Cardiology, College of Physicians and Surgeons of Columbia University, 630 West 168th Street, New York, New York 10032, USA.
kng1{at}columbia.edu


   Abstract
Top
 Abstract
Restenosis and disease...
 Use of noninvasive testing
 Impact of reintervention on...
 Conclusions and recommendations
 References
 
Percutaneous coronary intervention (PCI) has become a mainstay in the treatment of patients with coronary artery disease. Currently, more than one million coronary angioplasty and stent implantation procedures are performed annually. Although increasingly complex lesions and higher risk patients are being successfully treated percutaneously, restenosis and disease progression continue to cause significant morbidity. Restenosis occurs in approximately one-third of patients, one-half of who remain asymptomatic, while disease progression occurs at rates approaching 7% per year. Despite technological advances, unadjusted mortality rates have actually increased since the mid-1980s, and the current annual risk of a major adverse cardiac event following PCI is 5% to 7%. Although randomized clinical trials are needed to more definitively show a benefit, when performed six or more months following PCI, myocardial perfusion imaging reliably identifies patients most at risk of a poor long-term outcome. Directed reintervention can have a salutary impact on the prognosis of these patients. In view of recent data showing a positive impact of imaging and reintervention in patients after PCI, current guidelines should be reassessed.

Abbreviations and Acronyms
  CABG = coronary artery bypass grafting
  CAD = coronary artery disease
  ECG = electrocardiography
  ISR = in-stent restenosis
  MI = myocardial infarction
  MPI = myocardial perfusion imaging
  PCI = percutaneous coronary intervention
  PTCA = percutaneous transluminal coronary angioplasty
  SPECT = single-photon emission computed tomography

Cardiovascular disease is the leading cause of morbidity and mortality in industrialized nations, and caused 39.4% of all deaths in the U.S. in 2000 (1). Coronary artery disease (CAD) is the most prevalent form of cardiovascular disease, affecting 12.9 million Americans. The impact of CAD on the health of individuals in the developed world has declined over the past three decades as a result of the identification of modifiable risk factors and the introduction of new primary and secondary prevention strategies. Nonetheless, CAD continues to be a major public health problem.

Percutaneous treatment of CAD began in 1977, when Grüntzig et al. (2) introduced percutaneous transluminal coronary angioplasty (PTCA). In the mid 1990s, publication of two multicenter trials (3,4) demonstrating improved outcomes led to widespread use of stents, while development of new antiplatelet agents (5) resulted in even fewer complications following percutaneous coronary intervention (PCI). As a result, the use of, and indications for, PCI have greatly expanded, such that transcatheter revascularization is now routinely performed in patients with acute myocardial infarction (MI) and unstable coronary syndromes, and is increasingly employed to treat complex lesions, small-diameter vessels, chronic total occlusions, and diseased bypass conduits. For many patients with multivessel disease, PCI is an alternative to coronary artery bypass grafting (CABG) (6). More than one million PCI procedures were performed in the U.S. in 2000 (1). In contemporary practice, approximately 70% of PCI procedures involve placement of a stent (7). The number of transcatheter interventions is likely to increase further as the population ages and as increasingly complex lesions and more cases of multivessel disease are treated with PCI rather than surgery.

Although long-term outcome following PCI is good (6,8,9), a comparison of the 1997 to 1998 Dynamic Registry and the 1985 to 1986 National Heart, Lung, and Blood Institute Registry (10) of patients undergoing an initial PCI procedure revealed that, despite higher procedural success rates, one-year crude mortality was higher for patients in the Dynamic Registry (5.4% vs. 3.6%; p < 0.05), particularly among women (7.6% vs. 4.4%; p < 0.05). Increased mortality resulted from inclusion of more patients >65 years of age, more patients with diabetes and congestive heart failure, treatment of more total occlusions and vein graft lesions, and other "circumstances of the procedure." There was no difference in outcome between patients who received stents and those who did not.

In the multicenter Lescol Intervention Prevention Study (11), the annual risk of a major adverse cardiac event, defined as cardiac death, nonfatal MI, or a reintervention procedure (CABG, repeat PCI, or PCI for a new lesion) approached 7%, whereas the annual risk of a hard event (cardiovascular death or nonfatal MI) was 2% in the placebo group over 3.9 years of follow-up. Although statin therapy improved outcome, the annual adverse event rate remained >5% whereas the hard event rate remained >1% in treated patients.

Hachamovitch et al. (12) showed that among patients with normal myocardial perfusion imaging (MPI), those with a history of CAD have a higher annual hard event rate (cardiac death or nonfatal MI) than patients without such a history (1.4% vs. 0.4%; p < 0.001). Furthermore, the risk of a hard event increases with time for patients with CAD, whereas the risk is uniform for those without CAD.


   Restenosis and disease progression
Top
 Abstract
 Restenosis and disease...
Use of noninvasive testing
 Impact of reintervention on...
 Conclusions and recommendations
 References
 
Restenosis has been defined in numerous ways, making comparisons between restenosis rates problematic. Nonetheless, restenosis remains the Achilles heel of PCI (4,13–22) and, however defined, remains a major clinical problem (Table 1). In addition, progression of disease at untreated sites occurs at rates approaching 7% per year (23,24). When restenosis does occur, it usually happens within three to nine months (14,25,26). Patients with symptomatic restenosis generally develop angina within four to five months of PCI (13). Angina developing after nine months is usually due to progression of disease at another site (23,27). Approximately 50% of patients remain asymptomatic when restenosis occurs (Table 1). Conversely, up to 45% of patients developing chest pain after PCI do not have angiographic restenosis (13).


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  		Table 1 Restenosis Following Percutaneous Coronary Intervention

 
Most of the factors associated with restenosis (8,13,16,22,26,28–31) are listed in Table 2. Although stents decrease restenosis (3,4,17,18,22), deployment of stents in high-risk lesions has led to in-stent restenosis (ISR) rates as high as 58% (8,9,18,31). In 1999, approximately 150,000 patients in the U.S. developed ISR (31). Although drug-eluting stents and intracoronary brachytherapy may prevent or treat ISR, the long-term efficacy of these technologies is unproven (9,31–33).


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  		Table 2 Factors Associated With Restenosis

 
Asymptomatic restenosis.   Several investigators (13–16,22,34) have shown that chest pain following PCI is a poor indicator of restenosis (Table 3). Asymptomatic restenosis occurs in 18% to 59% of patients following PTCA and in 30% to 58% of patients after stenting (Table 1). Angiographic factors associated with asymptomatic restenosis include severe or totally occlusive target lesions (35), presence of collateral vessels (35,36), left anterior descending artery lesions (37), single-vessel disease (16,36), more complete revascularization (16,37), and larger reference vessel diameter (22).


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  		Table 3 Chest Pain as a Marker of Restenosis Following Percutaneous Coronary Intervention

 
Several investigators (16,22) found that symptomatic status is related to the severity of the recurrent lesion. Others (35–37) observed no such correlation. Minimal lumen diameter rather than stenosis severity may be more predictive of angina (34). Some have found that neither angina status before PCI (22,37,38) nor diabetes mellitus (16,22,34,37,38) is correlated with symptomatic status. The converse was noted by others (9). Both the presence (22) and absence (16) of unstable angina at presentation, and both younger (36) and older age (15) have been associated with asymptomatic restenosis. Because no meta-analysis of the interaction among clinical and angiographic factors and symptomatic status has been performed, there is no reliable method of predicting which patients are most at risk of developing asymptomatic restenosis and silent ischemia following PCI. Using a logistic regression model, Zellweger et al. (38) found that the only independent predictor of silent ischemia after coronary stenting was a less extensive and severe ischemic defect on MPI performed six months after revascularization.

However, of those factors that have been associated with asymptomatic restenosis, diabetes mellitus, unstable angina, and severe or totally occlusive target lesions were more prevalent in patients in the 1997 to 1998 Dynamic Registry than in patients in the 1985 to 1986 registry (10). Thus, in contemporary practice, more patients are likely to remain asymptomatic when restenosis occurs.

The prognostic significance of silent ischemia following PCI is unclear. Although some studies (16,35) demonstrated a favorable prognosis for patients with asymptomatic restenosis, more recent studies (36,38,39) found such patients to be at increased risk for adverse events.

Hernández et al. (16) followed 839 PTCA patients who underwent electrocardiography (ECG) stress testing and angiography at six to nine months. Of the 277 patients with restenosis, 48% were asymptomatic. During the 17 months of follow-up, there were 81 repeat PTCAs, 11 CABGs, and 6 deaths in the symptomatic cohort. There were no CABGs or deaths in asymptomatic patients. However, of the 77 patients with asymptomatic restenosis who had a positive or nondiagnostic stress test, 24 underwent reintervention. In all, 18% of asymptomatic patients underwent repeat PCI, which undoubtedly favorably influenced the outcome of this group. The authors concluded that "asymptomatic restenosis is a frequent phenomenon with a good prognosis mainly in patients with a negative exercise test result."

Cottin et al. (39) followed 152 coronary stent patients. Single-photon emission computed tomography (SPECT) performed five months after stenting showed reversible perfusion defects in 47 patients; ischemia was silent in 70%. Adverse events (MI or death) occurred in 28% of patients with ischemia, including death in 15%, but in only 3% of patients without ischemia. Angina was not an independent predictor of adverse events.

Zellweger et al. (38) prospectively followed 356 patients who underwent coronary stenting and routine SPECT imaging six months thereafter for four years. Eighty-one patients had target vessel ischemia, which was silent in 62%. Sixteen patients with target vessel ischemia who underwent MPI-driven repeat revascularization within 60 days of imaging were excluded from the "prognostic patient" group; the extent and severity of ischemia in these 16 patients were greater than in the 65 patients with ischemia included in the prognostic group. Among patients in the prognostic group, the composite end point (death, nonfatal MI, and late revascularization) occurred more frequently in patients with ischemia than in those without ischemia (cumulative event rate = 38% vs. 17%; p = 0.001), although this difference was driven mainly by repeat revascularization. The extent and severity of ischemia determined by MPI, not symptom status, were the best predictors of outcome. Patients with silent target-vessel ischemia tended to have less extensive and severe ischemia than symptomatic patients, and although they also tended to have better event-free survival (event rate = 32% vs. 52%; p = NS), patients with silent target vessel ischemia fared worse than patients with no ischemia (32% vs. 17%; p < 0.01). An additional 32 patients with ischemia in an untreated vascular territory, 59% of who were asymptomatic, were also excluded from the prognostic patient group. The event rate in these patients (cumulative event rate = 28%) was similar to that in patients with target-vessel ischemia included in the prognostic patient group (overall cumulative event rate = 38%).

Disease progression.   Following PCI, progression of disease in untreated vessel segments occurs at rates approaching 7% per year in both symptomatic and asymptomatic patients (23,24). More than one-half of patients presenting with chest pain more than one year after PCI have a new obstructive lesion or significant worsening of a previously nonobstructive stenosis (27). During late follow-up, outcomes are more strongly correlated with disease progression than disease recurrence (40).

Kober et al. (24) performed angiography on 87 patients more than two years after PTCA. Significant disease at an untreated site was evident in 44%. Importantly, 45% of asymptomatic patients had obstructive lesions. In an angiographic study of patients presenting with angina or acute MI more than one year after PCI (25), significant disease progression was found in 57%.


   Use of noninvasive testing
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 Abstract
 Restenosis and disease...
 Use of noninvasive testing
Impact of reintervention on...
 Conclusions and recommendations
 References
 
Appropriate use of noninvasive testing following PCI has never been systematically investigated. Thus, it is not surprising that physicians' practice patterns vary widely (41). While acknowledging that myocardial ischemia, whether painful or silent, worsens prognosis, current guidelines (29,42,43) and several authors (44,45) recommend against routine testing of asymptomatic patients. Others (36,46) argue that all patients should undergo MPI following PCI, citing data demonstrating adverse outcomes in asymptomatic patients with ischemia.

Although there have been case reports of acute occlusion following coronary angioplasty and stenting, occurring in association with stress testing (47), multiple investigators have shown that stress testing early after PCI is safe (48–53). Exercise ECG has repeatedly been demonstrated to be inaccurate in detecting restenosis following revascularization (13,15,16,34,36,37,54). In contrast, the sensitivity and specificity of MPI, performed at varying times after PCI, range from 39% to 100% and 46% to 100%, respectively (15,26,37,45,54–59), improving with time since revascularization (Table 4).


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  		Table 4 Accuracy of Myocardial SPECT Imaging Following Percutaneous Coronary Intervention

 
Myocardial perfusion imaging early after PCI.   A decrease in specificity has been observed when MPI is performed within two months of PCI. This phenomenon was initially noted following PTCA in the early days of PCI (49,50,53,60), and has been observed more recently in studies using MPI shortly after coronary stenting (48,51,52,61). Reversible perfusion defects were seen in 18% to 45% of asymptomatic patients using planar MPI 1 day to 7 weeks after coronary angioplasty (49,60) and in 35% of patients undergoing dipyridamole SPECT within 19 days of coronary angioplasty (53). Rodés-Cabau et al. (48) detected reversible defects in 17% of patients who underwent exercise stress SPECT within one week of stenting. Nagaoka et al. (51) observed reversible defects in 36% of patients four days after stenting using adenosine SPECT, which persisted in 50% of patients who underwent repeat imaging at 1.5 months.

The incidence of restenosis is 52% to 75% in patients with reversible defects on early imaging, compared with an incidence of 12% to 17% in those with normal perfusion (48,49). This observation prompted some (49,60,62) to contend that MPI performed early after PCI can "predict" future restenosis. Others (63) argue that "stress testing probably does not predict which patients are at risk of developing restenosis, but rather identifies those in whom restenosis has already occurred at the time of stress testing."

Bachmann et al. (61) observed reversible perfusion defects in the treated vascular territory within 48 h of angiographically successful PCI in 54% of patients following PTCA or atherectomy, and in 43% of patients after coronary stenting (p = NS). Using intracoronary ultrasound, they found that although such defects were associated with greater residual stenoses and higher plaque burdens, there was significant overlap of residual stenosis values between patients with and those without perfusion defects. Thus, they concluded that there are "additional mechanisms capable of impairing myocardial blood flow" and cite endothelial dysfunction as a possible cause of perfusion defects following PCI.

The ability of stress MPI to detect epicardial coronary disease depends upon regional differences in tracer uptake occurring as a consequence of impaired relative coronary flow reserve, the ratio of maximal blood flow in stenotic arteries to maximal flow in patent arteries. However, myocardial perfusion, and thus MPI, also depends upon microvascular function. Regional hypoperfusion can occur in the absence of coronary obstruction if absolute myocardial flow reserve, the ratio of blood flow during maximal vasodilation to blood flow under resting conditions, is impaired. Early after PCI, absolute coronary flow reserve is diminished (62,64,65). Thus, even in the presence of a patent artery, regional perfusion can be impaired by endothelial dysfunction and medial injury at the treated site and/or abnormal microvascular and resistive vessel function distal to the site (64,65).

Myocardial perfusion imaging late after PCI.   Eight studies involving 640 patients, in which stress SPECT and coronary angiography were performed within 2 to 48 months of PCI, are listed in Table 4. The overall sensitivity and specificity of SPECT for detecting myocardial ischemia two or more months after PCI are both 79%, and are roughly equivalent in all three vascular territories (15,54).

Manyari et al. (50) performed a longitudinal study, assessing patients with planar MPI nine days, three months, and seven months following PTCA. Forty percent of defects observed early after PCI improved two to nine months later. At seven-month angiographic follow-up, no patient had restenosis. In another serial imaging study, Versaci et al. (52) performed stress planar imaging within 24 h of PCI. Reversible defects were observed in 100% of PTCA patients and in 44% of stented patients. At six-month follow-up, 60% of PTCA patients without angiographic restenosis had persistent defects; no patients in the stent cohort had restenosis or a perfusion defect.

Among patients without known CAD, but with low-to-intermediate likelihood of disease, the rate of cardiac death or MI is 0.6% per year for those with normal SPECT, 1.4% for those with one or two abnormal segments, and 2.1% per year for those with three or more abnormal segments (66). Less is known about the prognostic value of MPI following PCI. In the Angioplasty Compared to Medicine Study (67), 328 patients were randomized to PTCA or medical therapy. At six months, 270 patients underwent stress MPI and were followed for a minimum of five years thereafter. Mortality in the PTCA cohort was 20% for those with a reversible defect versus 7% for those without such a defect (p = 0.03). By multivariate analysis, the strongest predictors of mortality were diabetes, smoking, and a reversible perfusion defect.

Alazraki et al. (68) assessed the prognostic value of SPECT among 165 patients who underwent PCI for multivessel disease as part of the Emory Angioplasty Versus Surgery Trial. At least 43% of the 76 PCI patients with evidence of ischemia one year after revascularization were asymptomatic and, after three years, 29% had an MI and/or died. In contrast, only 14% of PCI patients without ischemia had a cardiac event at three years.


   Impact of reintervention on prognosis
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 Abstract
 Restenosis and disease...
 Use of noninvasive testing
 Impact of reintervention on...
Conclusions and recommendations
 References
 
Data addressing the effects of reintervention on the prognosis of patients with restenosis are scarce. In the study of Hernández et al. (16), none of the 18 patients with asymptomatic restenosis and a positive or nondiagnostic stress test who underwent "elective" reintervention had a cardiac event over the ensuing 17 months. In contrast, of the 29 asymptomatic patients with positive stress tests who were treated medically, 21% developed recurrent angina.

Pfisterer et al. (36) studied 109 patients with angiographic restenosis and ischemia on MPI six months following PTCA. At two-year follow-up there was a trend toward a lower event rate (cardiac death, MI, revascularization, or hospital admission) in patients who underwent reintervention compared with those who did not (5% vs. 15%; p = NS), despite the presence of more ominous prognostic indicators in patients undergoing reintervention. Among patients with silent ischemia, the event rate was significantly lower in those who underwent reintervention than in those who did not (14% vs. 44%; p < 0.05). The event rate was also lower in a parallel asymptomatic cohort without ischemia than in patients with silent ischemia who did not undergo reintervention (27% vs. 44%; p < 0.02).

In the study of Zellweger et al. (38), 16 patients with target vessel ischemia underwent early MPI-driven repeat revascularization. These patients tended to have more severe and extensive ischemia than those patients with ischemia included in the "prognostic patient" group. Nonetheless, they had a favorable outcome. Although the numbers of patients were too small to permit statistical comparison, the four-year cumulative event rate was 29% for the 17 patients who underwent MPI-driven revascularization (16 with target vessel ischemia and 1 with no ischemia), whereas the overall event rate was 38% for patients with target-vessel ischemia included in the prognostic patient group, with event rates of 29% and 69%, respectively, for those with mild and moderate-to-severe ischemia.


   Conclusions and recommendations
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 Abstract
 Restenosis and disease...
 Use of noninvasive testing
 Impact of reintervention on...
 Conclusions and recommendations
References
 
Coronary atherosclerosis is a chronic disease. Despite excellent short-term benefits, PCI does not confer long-term immunity from adverse cardiac events. Whereas chest pain is a poor indicator of ischemia and does not risk-stratify patients following revascularization, MPI does. Current guidelines (29,42,43) recognize that myocardial ischemia worsens prognosis, whether manifest or asymptomatic. However, routine testing of patients after PCI is not recommended because "the prognostic benefit of controlling silent ischemia needs to be proved" (42) and because there is "a lack of data that outcomes are affected by this approach" (43).

Clearly what is needed is a prospective randomized study assessing the efficacy of routine noninvasive testing and directed reintervention to optimize management of the increasing number of patients undergoing PCI. In the interim, we believe that the preponderance of the evidence currently available demonstrates a benefit to routine screening with MPI and directed reintervention, when appropriate.

Given the high false-positive rate, there is little role for MPI early (<3 months) after PCI. To most efficaciously manage patients who develop chest pain within three months of revascularization, angiography should be performed (Fig. 1). Between three and six months, patients with typical angina, ECG changes, or elevated cardiac enzymes should also undergo angiography. Patients with atypical symptoms having characteristics associated with an increased likelihood of restenosis (Table 2) should undergo angiography as well. Patients lacking such characteristics who develop atypical symptoms should undergo MPI. Although the specificity of MPI three to six months following PCI is diminished, normal perfusion reliably excludes restenosis. If perfusion is abnormal, angiography should be performed.



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  		Figure 1 Treatment algorithm following percutaneous coronary intervention (PCI). If patients undergo repeat PCI, they are treated as though it was their first intervention. If repeat coronary angiography shows no evidence of restenosis or progression of disease elsewhere, patients should have clinical follow-up and undergo single-photon emission computed tomography myocardial perfusion imaging (SPECT MPI) in two years. If patients develop chest pain, they should undergo SPECT MPI if unstable angina is not present and coronary angiography if pain is accompanied by electrocardiographic changes or release of cardiac enzymes. *Increased risk of restenosis (see Table 2); {dagger}no factors listed in Table 2 present. CABG = coronary artery bypass grafting.

 
The accuracy of MPI performed six or more months following PCI is excellent (Table 4). We believe that following PCI, asymptomatic patients should initially be followed clinically and undergo MPI at six to nine months. Patients with normal, low-risk, or intermediate-risk scans (small or medium-sized defects of mild-to-moderate severity) can be managed medically. Patients with high-risk scans (medium-sized severe defects, large defects of any severity, or scans showing stress-induced left ventricular failure) should undergo angiography.

Thereafter, asymptomatic PCI patients should undergo MPI every one to three years. This recommendation is based on the study of Hachamovitch et al. (12), who determined that the time to a 1.5% predicted risk of cardiac death or nonfatal MI in most patients with known CAD and a normal index MPI ranges from 0.9 to 2.5 years. If symptoms develop, MPI should be performed sooner. Most patients presenting with acute coronary syndromes should be managed invasively.

Developments in the percutaneous treatment of CAD made over the past two decades should be paralleled by similar advances in the ongoing care of patients after revascularization. The benefits obtained through PCI should be complemented by a sound follow-up strategy. This includes implementation of lifestyle modifications, such as smoking cessation, appropriate dietary changes, weight loss, and regular exercise; optimal control of blood pressure and serum glucose; and use of angiotensin-converting enzyme inhibitors, antiplatelet agents, beta-blockers, and lipid-lowering agents when indicated. In addition, MPI can accurately identify patients at greatest risk of adverse cardiac events following PCI. Together with other standard-of-care secondary prevention strategies, routine MPI and directed reintervention will likely have an incremental benefit on the long-term outcome of patients after percutaneous revascularization.


   References
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 Abstract
 Restenosis and disease...
 Use of noninvasive testing
 Impact of reintervention on...
 Conclusions and recommendations
 References
 

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