Volume 146, Issue 1 , Pages 68-72, 7 January 2011
12-month follow-up results of high dose rosuvastatin loading before percutaneous coronary intervention in patients with acute coronary syndrome
Article Outline
- Abstract
- 1. Introduction
- 2. Materials and methods
- 3. Results
- 4. Discussion
- Acknowledgements
- References
- Copyright
Abstract
Background
Statin pretreatment before percutaneous coronary intervention (PCI) is associated with a reduced incidence of short-term adverse events and periprocedural myocardial infarction (MI). However, the long-term effects of statin pretreatment have not been evaluated.
Methods
Consecutive 445 patients with acute coronary syndrome (ACS) who underwent PCI were randomly assigned to receive no statin treatment before PCI (control group, n
=220) or to receive 40mg rosuvastatin loading before PCI (rosuvastatin group, n=225). The incidence of major adverse cardiac events (MACE), including cardiac death, non-fatal MI, non-fatal stroke, and any ischemia-driven revascularization, was assessed after 12months.
Results
During 11±3months of follow-up, MACE occurred in 20.5% of patients in the control group and 9.8% of patients in the rosuvastatin group (p=0.002). The Kaplan–Meier curves showed that the incidence of death and non-fatal MI was significantly greater in the control group than in the rosuvastatin group (hazard ratio, 3.71; p=0.021). High-sensitivity C-reactive protein levels were less elevated in the rosuvastatin group than in the control group at 24h after PCI. Multivariate analysis revealed that rosuvastatin loading was an independent predictor of a reduction in the risk of MACE at 12months (odds ratio, 0.5; p=0.006).
Conclusions
High dose rosuvastatin loading before PCI significantly improved 12-month clinical outcomes in patients with ACS who underwent an early invasive strategy.
Keywords: Statins, Angioplasty, Acute coronary syndrome, Stents, Complications
1. Introduction
There are increasing evidence that early and aggressive statin therapy in patients with acute coronary syndrome (ACS) can decrease periprocedural myocardial infarction (MI) and adverse cardiovascular events [1], [2], [3]. Recently, the effects of statin loading therapy before percutaneous coronary intervention (PCI) on clinical outcomes were evaluated. The Atorvastatin for Reduction of MYocardial Damage during Angioplasty-Acute Coronary Syndrome (ARMYDA-ACS) trial showed that pretreatment with 80mg atorvastatin before PCI was associated with an 88% reduction in the risk of 30-day major adverse cardiac events (MACE) [1]. Furthermore, we have reported that 40mg rosuvastatin loading therapy before PCI significantly reduced the incidence of periprocedural MI and 30-day MACE in patients with non-ST-segment elevation ACS [4].
However, the long-term effects of statin loading therapy on patients with ACS have not been evaluated. Therefore, we conducted a 12-month clinical follow-up study in patients with ACS to investigate whether a single high dose statin loading before PCI has beneficial effects on the long-term clinical outcomes.
2. Materials and methods
2.1. Study population and design
The patients included in this study participated in our previous statin study [4]. In brief, from March 2005 to December 2007, 677 consecutive patients with non-ST-segment elevation ACS who underwent diagnostic coronary angiography were screened. A total of 107 patients were excluded because of previous or current treatment with statins, 41 patients were excluded because they had to undergo emergency angiography due to cardiogenic shock or ongoing pain, and 19 patients were excluded because of renal insufficiency (serum creatinine >2.0mg/dl) or hepatic disease (a history of liver cirrhosis or alanine aminotransferase >2.5 times the upper normal limit). Eligible patients were randomly assigned to receive no statins (control group) or to receive 40mg rosuvastatin loading treatment before PCI (rosuvastatin group). After coronary angiography, 65 patients who did not receive PCI were excluded from the study; thus, 445 patients with significant coronary artery disease who underwent PCI were enrolled in the current study. The study design is represented in Fig. 1.
Fig. 1
Study design. ACS: acute coronary syndrome; PCI: percutaneous coronary intervention; CABG: coronary artery bypass graft.
PCI was performed immediately after diagnostic angiography according to current clinical practices at the physician's discretion. Intervention was performed within 48h after admission. Angiographic success of PCI was defined as thrombolysis in myocardial infarction (TIMI) III flow with residual stenosis below 20%. Aspirin (300mg/day) and clopidogrel (300mg/day) were administered to all patients before the procedure; patients in the rosuvastatin group also received 40mg rosuvastatin. Platelet glycoprotein IIb/IIIa inhibitors were administered at the operator's discretion. The occurrence of angiographic complications during PCI, including failed PCI such as wire or balloon passage failure, side branch occlusion, slow or no reflow, major dissection, and distal embolization, was recorded.
Aspirin (200mg/day), clopidogrel (75mg/day), and rosuvastatin (10mg/day) were prescribed to all patients after the procedure. CK-MB and troponin T levels were measured before (at admission, mean 20±4h before PCI), and at 6 and 24h after PCI. Additional samples were obtained if the patients showed signs or symptoms of myocardial ischemia. Low density lipoprotein (LDL)-cholesterol and high-sensitivity C-reactive protein (hsCRP) levels were also assessed before PCI, and at 24h, 1month, and 6months thereafter.
Patients were followed up for 12months at 3-month intervals, through direct contact or by telephonic investigation. Seven patients did not complete the 12-month follow-up, but their data were included in the statistical analysis until loss of follow-up. All patients gave written informed consent according to the protocol approved by the Institutional Review Board of the hospital.
2.2. End points
Periprocedural MI was defined as a post-procedural increase of CK-MB over 2 times higher the normal upper limit in patients with a normal baseline enzyme level [5]. In patients with elevated baseline CK-MB levels, MI was defined as a subsequent increase of more than two-fold in CK-MB from the baseline value and an additional increase in the second sample [6]. The primary end point was the occurrence of MACE, including cardiac death, non-fatal MI, non-fatal stroke, and any ischemia-driven revascularization. Non-fatal MI was defined as the elevation of troponin T (≥0.01ng/ml) with at least one of following: (1) symptoms of ischemia, (2) electrocardiogram (ECG) changes indicative of new ischemia, (3) development of new Q waves, and (4) imaging evidence of new loss of viable myocardium at any post interventional visit [7]. In this study, we did not consider the elevation of the post-procedural biomarker without symptoms or ECG changes as indicative of non-fatal MI. Target vessel revascularization included bypass surgery or ischemia-driven repeated PCI. Secondary end points included the change in LDL-cholesterol and hsCRP levels 24h after PCI, and at 1 and 6months thereafter.
2.3. Statistical analyses
In our previous study, the sample size was selected to demonstrate a reduction in the primary end point from 12% in the control group to 6% in the statin group [8]. Minimal sample size of 390 randomized patients would provide 80% power with a two-sided alpha of 0.05. Because we had previously demonstrated that the 30-day incidence of MACE was 15.9% in the control group and 6.7% in the rosuvastatin loading group, we did not require additional patient enrollment [4].
All measurements are represented as the mean±standard deviation. Continuous variables between two groups were compared by independent t-tests and chi-square tests, which were conducted using SPSS 12.0 for Windows (SPSS Inc., Chicago, IL). Proportions were compared by Fisher's exact test when the expected frequency was less than 5, and the chi-square test was applied otherwise. Odds ratios (OR) and 95% confidence intervals (CI) assessing the risk of the primary end point according to potential confounding variables were determined by logistic regression analysis. A multivariable logistic regression model was constructed using the following variables, selected according to the corresponding significant univariate analysis; rosuvastatin loading, complex lesion, periprocedural MI, baseline troponin and peak troponin levels. For continuous variables, the median value was used as a cut-off point to define the two subgroups in logistic regression analysis. Event-free survival analysis was performed using the Kaplan–Meier method with log-rank test group comparison. Statistical significance was set at p<0.05 (2-tailed).
3. Results
3.1. Baseline characteristics
Baseline clinical and procedural characteristics of all randomized patients are shown in Table 1. There were no significant differences between the two groups. Rosuvastatin loading was performed for 16±5h (range 7–25h) prior to the index procedure. We used drug-eluting stents in most cases (96.2%), and over 32% of the patients underwent multi-vessel stenting. Procedural success was achieved in all patients. Angiographic complications during the procedure occurred in 28 patients (12.7%) in the control group and 24 patients (10.7%) in the rosuvastatin group (p=0.499). Periprocedural MI was observed in 11.4% and 5.8% of patients in the control and rosuvastatin groups, respectively (p=0.035).
Table 1. Baseline clinical and procedural characteristics.
| Control group (n =220) | Rosuvastatin group (n =225) | p value | |
|---|---|---|---|
| Age (years) | 63±11 | 64±10 | 0.635 |
| Male (%) | 137 (62.3) | 136 (60.4) | 0.692 |
| Hypertension (%) | 121 (55.0) | 123 (54.7) | 0.944 |
| Diabetes (%) | 65 (29.5) | 75 (33.3) | 0.390 |
| Current smoker (%) | 80 (36.4) | 83 (36.9) | 0.908 |
| Left ventricular EF (%) | 60±10 | 61±11 | 0.328 |
| Creatinine (mg/dl) | 1.1±0.5 | 1.0±0.3 | 0.121 |
| Total cholesterol (mg/dl) | 202±49 | 196±44 | 0.165 |
| Triglyceride (mg/dl) | 174±129 | 175±119 | 0.943 |
| HDL-cholesterol (mg/dl) | 45±12 | 44±10 | 0.575 |
| LDL-cholesterol (mg/dl) | 124±40 | 122±38 | 0.497 |
| Troponin T (ng/ml) | 0.2±0.6 | 0.2±0.7 | 0.982 |
| Multi-vessel disease (%) | 118 (53.6) | 126 (56.0) | 0.616 |
| ACC/AHA B2/C lesion (%) | 165 (75.0) | 169 (75.1) | 0.978 |
| Drug-eluting stent (%) | 212 (96.4) | 216 (96.0) | 0.841 |
| Stent diameter (mm) | 3.2±0.4 | 3.2±0.4 | 0.060 |
| Stent length (mm) | 46±29 | 45±24 | 0.707 |
| Stent number | 1.7±1.0 | 1.7±0.8 | 0.858 |
| Maximal pressure (atm) | 17±4 | 17±3 | 0.331 |
| Multi-vessel stenting (%) | 70 (31.8) | 80 (35.6) | 0.404 |
| Use of GPI (%) | 18 (8.2) | 14 (6.2) | 0.424 |
| Procedural complications (%) | 28 (12.7) | 24 (10.7) | 0.499 |
| Periprocedural MI (%) | 25 (11.4) | 13 (5.8) | 0.035 |
Medication use was similar between treatment groups at the time of the intervention and during the 12-month follow-up (Table 2). Most of the patients (86.1%) continued rosuvastatin 10mg after PCI. Mean dose of statin was similar between two groups (10.7±4.0mg vs. 10.7±3.4mg, p=0.894). Only 1.1% of the patients discontinued statin treatment during the follow-up period.
Table 2. Pre- and post-procedural medication use.
| Control group (n =220) | Rosuvastatin group (n =225) | p value | |
|---|---|---|---|
| Pre-PCI medication (%) | |||
| ACEI | 83 (38) | 87 (39) | 0.838 |
| ARB | 22 (10) | 25 (11) | 0.703 |
| Beta blocker | 83 (38) | 96 (43) | 0.288 |
| Calcium antagonist | 23 (11) | 28 (12) | 0.510 |
| Post-PCI medication (%) | |||
| Aspirin | 217 (98.6) | 222 (98.2) | 1.000 |
| Clopidogrel | 220 (100) | 225 (100) | 1.000 |
| ACEI or ARB | 198 (90.0) | 204 (90.7) | 0.812 |
| Beta blocker | 168 (76.4) | 162 (72.0) | 0.293 |
| Calcium antagonist | 80 (36.4) | 82 (36.4) | 0.986 |
| Statin therapy (%) | 0.499 | ||
| Continued rosuvastatin 10mg | 191 (86.8) | 192 (85.3) | |
| Discontinued | 4 (1.8) | 1 (0.4) | |
| Dose reduction to 5mg | 2 (0.9) | 1 (0.4) | |
| Dose elevation to 20mg | 2 (0.9) | 2 (0.9) | |
| Changed to other statin | 21 (9.5) | 29 (12.9) |
3.2. Primary end point
MACE occurred in 15.1% of all patients during the 11±3months of the follow-up period (Table 3). The composite primary end point of death, non-fatal MI, non-fatal stroke, and revascularization occurred in 20.5% and 9.8% of the patients in the control and rosuvastatin groups, respectively (p=0.002). The incidence of MACE at 1month and between 1 and 12months was significantly greater in the control group compared with the rosuvastatin group (Table 3). This difference resulted mainly from a higher incidence of revascularization in the control group, but hard end points (death, MI) were also more developed in the control group than in the rosuvastatin group.
Table 3. Clinical outcomes during the 12-month follow-up.
| Control group | Rosuvastatin group | p value | |
|---|---|---|---|
| 0–1-month clinical events (%) | n=220 | n=225 | |
| Death | 3 (1.4) | 0 (0.0) | 0.120 |
| Non-fatal MI | 5 (2.3) | 2 (0.9) | 0.280 |
| Non-fatal stroke | 2 (0.9) | 1 (0.4) | 0.620 |
| Revascularization | 3 (1.4) | 0 (0.0) | 0.120 |
| Any of the above | 13 (5.9) | 3 (1.3) | 0.010 |
| 1–12-month clinical events (%)a | n=206 | n=222 | |
| Death | 5 (2.4) | 2 (0.9) | 0.269 |
| Non-fatal MI | 1 (0.5) | 0 (0.0) | 0.481 |
| Non-fatal stroke | 4 (1.9) | 3 (1.4) | 0.715 |
| Revascularization | 22 (10.7) | 14 (6.3) | 0.103 |
| Any of the above | 32 (15.5) | 19 (8.6) | 0.026 |
| Total clinical events (%) | n=220 | n=225 | |
| Death | 8 (3.6) | 2 (0.9) | 0.060 |
| Non-fatal MI | 6 (2.7) | 2 (0.9) | 0.171 |
| Non-fatal stroke | 6 (2.7) | 4 (1.8) | 0.540 |
| Revascularization | 25 (11.4) | 14 (6.2) | 0.055 |
| Any of the above | 45 (20.5) | 22 (9.8) | 0.002 |
aPatients with adverse events or loss of follow-up within 1 |
The Kaplan–Meier curves showed that the incidence of death and non-fatal MI was significantly greater in the control group than in the rosuvastatin group (hazard ratio, 3.71; p=0.021) (Fig. 2). In terms of the combined MACE, a significantly better event-free survival at 12months was observed in the rosuvastatin group (hazard ratio, 2.23; p=0.002).
Fig. 2
The incidence of (A) death or non-fatal myocardial infarction (MI); and (B) death, non-fatal MI, stroke, or revascularization in patients with acute coronary syndrome who received no rosuvastatin treatment (control group) or high dose rosuvastatin loading (rosuvastatin group) before percutaneous coronary intervention. HR: hazard ratio.
3.3. Secondary end points
Mean LDL-cholesterol levels were similar at baseline but were significantly more reduced at 24h after PCI in the rosuvastatin group than in the control group (p<0.001; Fig. 3). 54.3% of the rosuvastatin group and 56.0% of the control group reached LDL-cholesterol <70mg/dl at 1month (p=0.410), 60.0% of the rosuvastatin group and 60.5% of the control group reached LDL goal at 6months (p=0.509). Triglyceride and non-HDL-cholesterol goal achievement rate of both groups was similar at 1 and 6months. After 40mg rosuvastatin loading, hsCRP levels were less elevated in the rosuvastatin group, with a level change from 4.6±8.7mg/l to 9.2±12.5mg/l at 24h after PCI (Fig. 4), compared to patients without rosuvastatin loading, with a level change from 4.9±8.7 to 15.9±27.7mg/l (p<0.001 compared to the rosuvastatin group). However, the 1-month and 6-month levels of LDL-cholesterol and hsCRP were not different between the two groups.
Fig. 3
The change in low density lipoprotein-cholesterol level over time in patients with acute coronary syndrome who received no rosuvastatin treatment (control group) or high dose (40
mg) rosuvastatin loading (rosuvastatin group) before percutaneous coronary intervention (PCI).
Fig. 4
The change in high-sensitivity C-reactive protein level over time in patients with acute coronary syndrome who received no rosuvastatin treatment (control group) or high dose (40
mg) rosuvastatin loading (rosuvastatin group) before percutaneous coronary intervention (PCI).
3.4. Multivariate analysis
Multivariate analysis revealed that rosuvastatin loading (OR=0.5; 95% CI=0.3–0.8, p=0.006) was the independent predictor for decreased risk of 12-month MACE (Table 4). Periprocedural MI was a predictor for MACE (OR=2.5; 95% CI=1.1–5.6, p=0.025).
Table 4. Univariate and multivariate analysis for the prediction of 12-month adverse clinical outcomes.
| Univariate analysis | Multivariate analysis | |||||
|---|---|---|---|---|---|---|
| OR | 95% CI | p | OR | 95% CI | p | |
| Rosuvastatin loading | 0.4 | 0.2–0.7 | 0.002 | 0.5 | 0.3–0.8 | 0.006 |
| Age ≥65years | 1.1 | 0.7–1.9 | 0.628 | |||
| Multi-vessel disease | 1.6 | 0.9–2.8 | 0.077 | |||
| ACC/AHA B2/C lesion | 2.1 | 1.0–4.3 | 0.037 | 1.6 | 0.8–3.3 | 0.192 |
| Periprocedural MI | 3.3 | 1.6–6.9 | 0.001 | 2.5 | 1.1–5.6 | 0.025 |
| Serum creatininea | 1.1 | 0.6–1.8 | 0.777 | |||
| LDL-cholesterola | 1.1 | 0.7–1.8 | 0.641 | |||
| Baseline hsCRPa | 1.0 | 0.6–1.7 | 1.000 | |||
| Post-procedural hsCRPa | 1.5 | 0.9–2.6 | 0.110 | |||
| Baseline troponin Ta | 1.9 | 1.1–3.2 | 0.017 | 1.8 | 0.9–3.1 | 0.106 |
| Peak troponin Ta | 2.4 | 1.4–4.1 | 0.002 | 1.5 | 0.8–3.0 | 0.206 |
| Diabetes mellitus | 1.1 | 0.6–1.8 | 0.863 | |||
aFor continuous variables, the median value was used as a cut-off point. |
4. Discussion
In this study, we have demonstrated that high dose rosuvastatin loading therapy before PCI reduced the incidence of MACE in patients with ACS, and slowed the post-PCI inflammatory response.
Previous studies have shown that statin therapy improves the prognosis of patients with ACS. The Pravastatin or Atorvastatin Evaluation and Infection Therapy (PROVE-IT) study reported that intensive statin therapy with 80mg atorvastatin within 10days after ACS results in 28% and 6% risk reductions at 30days and 2years, respectively [3]. The Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study reported that 80mg atorvastatin within 24–96h after admission reduced the risk of the composite primary end point of death, MI, cardiac arrest and recurrent ischemia by 16% compared with that seen with the placebo [2]. These studies indicate that early and high doses of statin therapy significantly improve the prognosis of patients with ACS. However, there is a limitation on data about the clinical benefits of pretreatment with statins in patients undergoing PCI.
A meta-analysis of six trials in patients with stable angina showed that statin pretreatment resulted in a 59.3% reduction of relative risk of procedural MI and a 20.5% overall reduction in MACE [9]. However, this result cannot be applied to patients with ACS requiring early invasive strategy. Thus, studies to assess the benefits of acute loading with high dose statins in this patient population were performed. The ARMYDA-ACS trial was the first randomized study to assess the efficacy of high dose statin loading therapy before PCI in patients with ACS [1]. The results of this trial indicated that 80mg atorvastatin loading at 12h before PCI reduced post-procedural biomarker elevation and 30-day MACE. We previously performed a similar randomized study, using rosuvastatin 40mg, in which statin loading approximately 16h before PCI resulted in a 53% reduction in the risk of periprocedural MI and a 63% reduction in the risk of 30-day MACE, compared to no statin pretreatment [4]. Moreover, in the current study, we have established the long-term benefits of high dose statin loading in patients with ACS undergoing PCI by demonstrating significant improvements in the 12-month prognosis of such patients.
The benefits of statins in cardiovascular diseases can be explained not only by their lipid-lowering potential but also by non-lipid-related mechanisms, so called pleiotropic effects [10]. Pleiotropic effects encompass non-lipid mechanisms that modify endothelial function, inflammatory responses, plaque stability and thrombus formation [11], [12], [13]. These effects may potentially improve clinical outcomes after PCI. In our current study, the hsCRP peak after stenting was significantly lower in the rosuvastatin group than in the control group, supporting the hypothesis that the anti-inflammatory effects of statins reduce the risk of periprocedural MI and improve clinical outcomes. Several studies have reported the association between the inflammatory response after PCI and prognosis [14], [15], [16], [17]. Gach et al. reported that hsCRP increases induced by PCI from baseline were more predictive of MACE than hsCRP levels before or after PCI separately [14]. Gaspardone et al. showed that, in 81 patients with stable angina pectoris, a lack of normalization of plasma CRP concentration after PCI with stent implantation was associated with a greater incidence of MACE [15]. Saleh et al. reported that the CRP measurement on the day after PCI was a predictor of adverse outcomes in patients with unstable angina, as well as those with stable angina [16]. Therefore, the benefits of statin pretreatment on clinical outcomes are dependent on periprocedural inflammatory status. In addition, in our study, patients receiving high dose rosuvastatin loading had lower LDL-cholesterol levels 24h after PCI, which is possibly accounted for by some benefit of the high dose statin therapy.
Although we have demonstrated the benefits of high dose statin loading in patients with ACS undergoing PCI, our study has several limitations. The study was not blinded, and the sample size to assess the outcomes was small. Furthermore, the optimal dose of loading and time of onset before stent implantation were not identified. Use of platelet GP IIb/IIIa inhibitors was not controlled, but it had little influence on the results because only 7.2% of the patients received platelet GP IIb/IIIa inhibitors. The purpose of our original study was not to assess the long-term benefits of high dose statin loading therapy. However, we found a significant difference in 12-month MACE between the two study groups. Further study is needed to confirm our results.
In conclusion, high dose rosuvastatin loading therapy before PCI significantly improved long-term clinical outcomes in patients with unstable angina and non-ST-segment elevation MI, possibly via inhibition of the periprocedural inflammatory response. These results support the use of high dose statin loading therapy before PCI in patients with ACS.
Acknowledgements
This study was supported by grants from Wonkwang University in 2009. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [18].
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PII: S0167-5273(10)00283-4
doi:10.1016/j.ijcard.2010.04.052
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Volume 146, Issue 1 , Pages 68-72, 7 January 2011
