2016 Volume 80 Issue 1 Pages 93-100
Background: Since the introduction of PCI in 1977, it has evolved along with advances in the technology, improvement in operator technique and establishment of medical therapy. However, little is known of the improvement in clinical outcome following PCI.
Methods and Results: Data from the Juntendo PCI Registry during 1984–2010 were analyzed. The patients were divided into 3 groups according to date of index PCI: POBA era, January 1984–December 1997; BMS era, January 1998–July 2004; and DES era, August 2004–February 2010. The primary endpoint was a composite of MACE including all-cause mortality, non-fatal MI, non-fatal stroke and revascularization. A total of 3,831 patients were examined (POBA era, n=1,147; BMS era, n=1,180; DES era, n=1,504). Mean age was highest in the DES era. The prevalence of diabetes and hypertension was higher in the DES and BMS eras than in the POBA era. Unadjusted cumulative event-free survival rate for 2-year MACE was significantly different across the 3 eras. Adjusted relative risk reduction for 2-year MACE was 56% in the DES era and 34% in the BMS era, both compared with the POBA era. Age, ACS, and LVEF were associated with the incidence of MACE.
Conclusions: Clinical outcome of PCI improved across the 26-year study period, despite the higher patient risk profile in the recent era. (Circ J 2016; 80: 93–100)
Since the introduction of plain old balloon angioplasty (POBA) for coronary artery disease (CAD) in 1977,1 percutaneous coronary intervention (PCI) has evolved, along with advances in the technology, improvement in operator technique and establishment of medical therapy for secondary prevention.2–5 In Japan, bare metal stents (BMS) have been available since 1993, and the use of drug-eluting stents (DES) began in 2004. The advent of DES has significantly reduced the occurrence of target lesion revascularization from 20–30% in the BMS era to <10%.6,7 DES, however, are associated with a safety concern regarding stent thrombosis, which could result in a high mortality rate.8–10 Moreover, age and the prevalence of comorbid diseases in patients who undergo PCI have become increasingly higher with the aging of society. Thus, comparison of clinical outcome across generations is of great interest. A previous study in the USA reported that the incidence of major adverse cardiovascular events (MACE) was reduced during the follow-up period of 25 years.11 Similar results were reported from other studies on temporal trends in clinical outcome following PCI in older patients,12 but little is known of the temporal trends in clinical outcome after PCI in daily clinical practice in Japan. We hypothesized that the considerable improvements in PCI would yield a net benefit in clinical outcome. We compared long-term clinical outcomes after PCI across the 3 generations (POBA era, BMS era and DES era) in Japanese clinical practice.
We analyzed the data from the Juntendo PCI Registry database, in which information on patients who underwent PCI at Juntendo University Hospital (Tokyo, Japan) between January 1984 and February 2010, was recorded. The study groups were divided according to the date of the index PCI: POBA era, January 1984–December 1997; BMS era, January 1998–July 2004; and DES era, August 2004–February 2010). Information on clinical outcome was collected during clinical visit, via telephone interview or from the referring physician. The institutional review board approved the protocol of this study, which was performed in accordance with the principles established in the Declaration of Helsinki and the institutional ethics policy.
Clinical OutcomeThe endpoints were MACE and a composite of all-cause death and acute coronary syndrome (ACS) that occurred within 2 years after the index PCI. MACE were defined as ≥1 of the following: (1) all-cause death; (2) non-fatal myocardial infarction (MI); (3) non-fatal stroke; and (4) repeat revascularization.
DefinitionsMyocardial infarction was diagnosed on 2 of the following 3 criteria: (1) typical chest pain for at least 20 min; (2) increased serum creatine kinase ≥2-fold the upper normal range; and (3) new Q wave on electrocardiography. ACS included ST-elevation MI (STEMI) and non-ST-elevation ACS (NSTE-ACS). The procedural success of PCI was defined as decrease in the residual luminal diameter stenosis to <50% or achievement of Thrombolysis in Myocardial Infarction (TIMI) grade 3, in the final angiogram of the procedure. Diabetes was defined as presence of glycated hemoglobin A1c (HbA1c) with National Glycohemoglobin Standardization Program (NGSP) ≥6.5% or treatment with anti-diabetic agents or insulin. HbA1c (Japan Diabetes Society [JDS]) was converted to HbA1c (NGSP) units using the following equation: NGSP(%)=1.02×JDS(%)+0.25%.13 Hypertension was defined as systolic blood pressure ≥140 mmHg and diastolic blood pressure ≥90 mmHg or treatment with anti-hypertensive medication. Dyslipidemia was defined as triglyceride ≥150 mg/dl, low-density lipoprotein cholesterol (LDL-C) ≥140 mg/dl, and high-density lipoprotein cholesterol (HDL-C) <40 mg/dl or treatment for dyslipidemia. Current smokers were defined as individuals who smoked at the time of admission or had quit within 1 year before the study period. Renal dysfunction was defined as estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2 calculated using the modification of diet in renal disease equation modified with a Japanese coefficient using baseline serum creatinine.14 Left ventricular ejection fraction (LVEF) was assessed on echocardiography using the Teichholz method or left ventriculography. LVEF was measured at the time of discharge. In patients with ACS, LVEF was measured after the index PCI, while it was assessed at the time of diagnostic angiography in patients with non-ACS.
Statistical AnalysisContinuous variables are expressed as mean±SD. Categorical data are expressed as count and percentage. The continuous variables were compared using 1-way analysis of variance followed by post-hoc analysis with Dunnett’s test for multiple comparisons. The POBA era served as a control group in the post-hoc analysis. The categorical variables were analyzed using chi-squared test or Fisher’s exact probability test. Intergroup comparison with the POBA era for the categorical variables was done using Bonferroni correction. In the analysis, P<0.025 was considered significant. The unadjusted cumulative event rate for 3-year MACE was estimated using the Kaplan-Meier method and compared on log-rank test across the 3 groups. To identify predictors of outcome, univariate Cox regression analysis was performed that included age, gender, body mass index (BMI), diabetes mellitus, hypertension, dyslipidemia, current smoking, family history of CAD, aspirin use, β-blocker use, calcium-channel blocker use, statin use, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB) use, LDL-C, HDL-C, triglycerides, total cholesterol, eGFR, Hb, HbA1c, LVEF, ACS, multivessel disease (MVD) and the PCI eras (with the POBA era as the reference) as the independent variables. Hazard ratio (HR) and 95% confidence interval (CI) were also calculated. The variables with P<0.1 in the analysis were then entered in multivariate Cox regression analysis. P<0.05 was considered statistically significant. All data were analyzed using JMP version 10.0 for Windows (SAS Institute, Cary, NC, USA).
A total of 3,831 patients were analyzed (POBA era, n=1,147; BMS era, n=1,180; and DES era, n=1,504). Data on medication use were available for 1,001 of the 1,147 patients (87.2%) in the POBA era, 1,135 of the 1,180 patients (96.2%) in the BMS era and 1,497 of the 1,504 patients (99.5%) in the DES era. DES use was limited to first-generation DES. Baseline subject characteristics are listed in Table 1. Mean age was highest in the DES era, and BMI was higher in the DES and BMS eras than in the POBA era. A higher prevalence of diabetes and hypertension was observed in the DES and BMS eras than in the POBA era, whereas the percentage of current smoking was highest in the POBA era. Lipid profile was favorable in the DES and BMS eras, and the success rate of PCI was higher in the DES and BMS eras than in the POBA era. Hb and LVEF were lower in the DES and BMS eras than in the POBA era. The patients in the DES and BMS eras had a higher prevalence of ACS at the time of the initial procedure. The lesion characteristics are also listed in Table 1. The presence of diseased vessels differed between the groups, and a higher prevalence of MVD was observed in the DES and BMS eras than in the POBA era. The use of evidence-based medical therapy (ie, aspirin, statins, β-blockers and ACEI/ARB) for the secondary prevention of cardiovascular events significantly increased over time (Table 2).
| POBA era (n=1,147) |
BMS era (n=1,180) |
DES era (n=1,504) |
P-value | |
|---|---|---|---|---|
| Age (years) | 59.9±10.2 | 63.9±10.3* | 66.1±10.6* | <0.0001 |
| Male | 969 (84.5) | 964 (81.8) | 1,225 (81.5) | 0.1 |
| BMI (kg/m2) | 23.7±4.2 | 24.1±3.7 | 24.2±3.4* | 0.003 |
| Diabetes mellitus | 414 (36.1) | 494 (41.9)† | 676 (45.0)† | 0.002 |
| Hypertension | 692 (60.6) | 761 (64.5) | 1,098 (73.0)† | <0.0001 |
| Dyslipidemia | 706 (68.7) | 754 (64.4) | 1,084 (72.1) | <0.0001 |
| Current smoking | 559 (49.6) | 280 (23.8)† | 403 (26.8)† | <0.0001 |
| Family history | 340 (30.2) | 333 (28.6) | 424 (28.2) | 0.3 |
| LDL-C (mg/dl) | 127.0±41.3 | 117.1±32.0* | 113.7±33.6* | <0.0001 |
| HDL-C (mg/dl) | 41.7±12.7 | 44.3±14.2* | 44.6±12.6* | <0.0001 |
| TC (mg/dl) | 197.7±46.3 | 187.8±36.9* | 186.0±38.6* | <0.0001 |
| TG (mg/dl) | 144.9±75.5 | 133.0±75.3* | 136.4±75.3* | 0.0005 |
| HbA1c (NGSP) (%) | 6.8±2.9 | 6.3±1.3* | 6.4±1.3* | <0.0001 |
| Hb (g/dl) | 13.6±4.1 | 13.0±1.8* | 13.1±1.9* | 0.0009 |
| LVEF (%) | 65.6±12.7 | 63.4±13.1* | 60.3±12.2* | <0.0001 |
| eGFR (ml/min/1.73 m2) | 63.6±25.7 | 66.7±22.3* | 65.0±23.4 | 0.01 |
| ACS | 199 (17.4) | 409 (34.7)† | 466 (31.0)† | 0.02 |
| STEMI | 127 (63.8) | 235 (57.5) | 270 (58.0) | 0.3 |
| NSTE-ACS | 72 (36.2) | 174 (42.5) | 196 (42.0) | |
| Success rate | 1,010 (88.1) | 1,132 (95.9)† | 1,433 (95.3)† | <0.0001 |
| Type of procedure | <0.0001 | |||
| POBA | 1,099 (95.8) | 240 (20.5) | 86 (5.9) | |
| BMS | 48 (4.2) | 930 (79.5) | 543 (37.1) | |
| DES | 0 (0) | 0 (0) | 1,463 (57.0) | |
| Diseased vessel | <0.0001 | |||
| LAD | 599 (52.2) | 577 (48.9) | 694 (46.1) | |
| LCX | 172 (15.0) | 205 (17.4) | 280 (18.6) | |
| RCA | 289 (25.2) | 344 (29.15) | 463 (30.8) | |
| LMT | 11 (1.0) | 10 (0.85) | 44 (2.9) | |
| Others | 76 (6.6) | 44 (3.7) | 23 (1.5) | |
| MVD | 435 (39.5) | 674 (48.7)† | 879 (59.1)† | <0.0001 |
| QCA | ||||
| Reference diameter (mm) | 2.97±0.70 | 3.06±0.54* | 2.80±0.50* | <0.0001 |
| MLD before | 0.53±0.38 | 0.46±0.41* | 0.38±0.34* | <0.0001 |
| MLD after | 2.08±0.67 | 2.61±0.74* | 2.66±0.58* | <0.0001 |
| Stent diameter (mm) | 3.18±0.41 | 2.96±0.42 | <0.0001 | |
| Stent length (mm) | 16.8±4.07 | 19.8±5.90 | <0.0001 | |
Data given as mean±SD or n (%). The continuous variables with statistical significance are marked with * (the POBA-era as a control group). The categorical variables with statistical significance are marked with † (the POBA-era as a control group). ACS, acute coronary syndrome; BMI, body mass index; BMS, bare metal stent; DES, drug-eluting stent; eGFR, estimated glomerular filtration rate; Hb, hemoglobin; HbA1c (NGSP), hemoglobin A1c of National Glycohemoglobin Standardization Program; HDL-C, high density lipoprotein-cholesterol; LAD, left anterior descending artery; LCX, left circumflex; LDL-C, low density lipoprotein-cholesterol; LMT, left main trunk; LVEF, left ventricular ejection fraction; MLD, minimum lumen diameter; MVD, multivessel coronary disease; NSTE, non-ST-elevation; POBA, plain old balloon angioplasty; QCA, quantitative coronary angiography; RCA, right coronary artery; STEMI, ST-elevation myocardial infarction; TC, total cholesterol; TG, triglyceride.
| POBA era (n=1,101) |
BMS era (n=1,135) |
DES era (n=1,497) |
P-value | |
|---|---|---|---|---|
| Aspirin | 738 (64.3) | 1,045 (92.0)† | 1,421 (94.9)† | <0.0001 |
| Statin | 177 (15.4) | 463 (40.4)† | 933 (62.3)† | <0.0001 |
| ACEI/ARB | 133 (13.3) | 558 (49.1)† | 804 (53.7)† | <0.0001 |
| β-blocker | 269 (26.9) | 477 (42.0)† | 813 (54.3)† | <0.0001 |
| Calcium channel blocker | 502 (50.2) | 424 (37.4)† | 570 (38.1)† | <0.0001 |
Data given as n (%). The categorical variables with statistical significance are marked with † (the POBA-era as a control group). ACEI/ARB, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker. Other abbreviations as in Table 1.
The unadjusted cumulative event-free survival rate for 2-year MACE was significantly different between the eras (Figure 1). Two-year all-cause death and incidence of ACS were significantly different between the groups (Figure 2A). No statistically significant difference was observed in the 2-year rate of stroke, while there was a significant difference in the event-free survival rate for 2-year repeat revascularization between the eras (Figures 2B,C). Adjusted relative risk reduction for 2-year MACE was 56% in the DES era compared with the POBA era, and 34% in the BMS era compared with the POBA era. Additionally, high age, presentation with ACS, and reduced LVEF were associated with the 2-year incidence of MACE (Table 3). No significant difference was observed in 2-year all-cause death and incidence of ACS between the 3 eras. After controlling for the variables, only higher age was associated with increase in 2-year all-cause death and incidence of ACS (HR, 1.03; 95% CI: 1.005–1.05, P=0.017; Table 4). On univariate Cox regression analysis for 2-year MACE specifically in patients with ACS or stable CAD, both the BMS era and the DES era were associated with reduction in 2-year MACE compared with the POBA era (Table 5). The effect of advances in the PCI era on reduction in 2-year MACE was emphasized in patients with stable CAD compared with ACS patients (P for interaction<0.001).
Kaplan-Meier curves for 2-year major adverse cardiovascular events (MACE) across the plain old balloon angioplasty (POBA), bare metal stent (BMS) and drug-eluting stent (DES) eras, showing significant difference across the 3 eras.
Kaplan-Meier curves for (A) 2-year all-cause death and incidence of acute coronary syndrome (ACS), (B) 2-year stroke and (C) 2-year repeat revascularization across the 3 percutaneous coronary intervention eras. (A) Clinical outcome was higher in the BMS era than in the other eras. (B) No statistically significant difference was observed in the rate of 2-year stroke, while (C) there was a significant difference in the event-free survival rate for 2-year repeat revascularization between the eras. BMS, bare metal stent; DES, drug-eluting stent; POBA, plain old balloon angioplasty.
| Univariate | Multivariate | |||||
|---|---|---|---|---|---|---|
| HR | 95% CI | P-value | HR | 95% CI | P-value | |
| Age (years) | 1.01 | 1.001–1.012 | 0.014 | 1.02 | 1.01–1.03 | <0.0001 |
| BMI (kg/m2) | 0.98 | 0.97–0.998 | 0.03 | 0.98 | 0.96–1.004 | 0.1 |
| Dyslipidemia | 0.83 | 0.73–0.95 | 0.006 | 0.95 | 0.80–1.13 | 0.5 |
| Smoking | 1.20 | 1.06–1.36 | 0.005 | 1.17 | 0.98–1.39 | 0.08 |
| ACS | 1.26 | 1.11–1.44 | 0.0005 | 1.31 | 1.10–1.55 | 0.0025 |
| HbA1c | 1.02 | 0.997–1.04 | 0.08 | 1.05 | 0.99–1.11 | 0.1 |
| eGFR | 0.997 | 0.994–0.9996 | 0.03 | 0.998 | 0.994–1.001 | 0.2 |
| LVEF (%) | 0.99 | 0.98–0.996 | 0.0006 | 0.99 | 0.98–0.996 | 0.001 |
| β-blocker | 0.86 | 0.76–0.98 | 0.02 | 1.06 | 0.91–1.24 | 0.5 |
| Ca blocker | 0.83 | 0.72–0.95 | 0.007 | 0.96 | 0.81–1.14 | 0.7 |
| Statin | 0.70 | 0.61–0.80 | <0.0001 | 0.87 | 0.74–1.04 | 0.1 |
| Aspirin | 0.62 | 0.53–0.74 | <0.0001 | 0.81 | 0.63–1.07 | 0.1 |
| BMS era (POBA era as reference) | 0.64 | 0.55–0.74 | <0.0001 | 0.66 | 0.53–0.83 | 0.0004 |
| DES era (POBA era as reference) | 0.44 | 0.38–0.51 | <0.0001 | 0.44 | 0.35–0.57 | <0.0001 |
CI, confidence interval; HbA1c, glycated hemoglobin; HR, hazard ratio; MACE, major adverse cardiovascular events. Other abbreviations as in Table 1.
| Univariate | Multivariate | |||||
|---|---|---|---|---|---|---|
| HR | 95% CI | P-value | HR | 95% CI | P-value | |
| Age (years) | 1.05 | 1.04–1.06 | <0.0001 | 1.03 | 1.005–1.05 | 0.017 |
| Male gender | 0.72 | 0.56–0.92 | 0.009 | 0.76 | 0.45–1.32 | 0.3 |
| BMI (kg/m2) | 0.94 | 0.91–0.96 | <0.0001 | 1.02 | 0.95–1.09 | 0.3 |
| Dyslipidemia | 0.60 | 0.48–0.74 | <0.0001 | 1.16 | 0.75–1.83 | 0.5 |
| ACS | 2.57 | 2.09–3.15 | <0.0001 | 1.51 | 0.96–2.38 | 0.07 |
| MVD | 1.48 | 1.21–1.83 | 0.0002 | 0.85 | 0.57–1.26 | 0.4 |
| TC | 0.995 | 0.992–0.997 | <0.0001 | 1.01 | 0.99–1.02 | 0.5 |
| TG | 0.996 | 0.994–0.998 | <0.0001 | 0.997 | 0.993–1.001 | 0.1 |
| LDL-C | 0.996 | 0.993–0.999 | 0.004 | 0.995 | 0.98–1.01 | 0.6 |
| eGFR | 0.986 | 0.981–0.99 | <0.0001 | 1.001 | 0.99–1.01 | 0.9 |
| Hb (g/dl) | 0.80 | 0.75–0.85 | <0.0001 | 1.04 | 0.94–1.16 | 0.5 |
| LVEF (%) | 0.97 | 0.96–0.98 | <0.0001 | 0.996 | 0.98–1.01 | 0.6 |
| ACEI/ARB | 0.76 | 0.61–0.95 | 0.015 | 1.02 | 0.66–1.58 | 0.9 |
| Statin | 0.53 | 0.42–0.67 | <0.0001 | 1.12 | 0.72–1.71 | 0.6 |
| Aspirin | 0.68 | 0.52–0.92 | 0.01 | 0.67 | 0.38–1.24 | 0.2 |
| BMS era (POBA era as reference) | 1.71 | 1.31–2.24 | <0.0001 | 0.66 | 0.41–1.07 | 0.09 |
| DES era (POBA era as reference) | 1.23 | 0.95–1.63 | 0.1 | 0.59 | 0.29–1.19 | 0.1 |
Abbreviations as in Tables 1–3.
| ACS | Stable CAD | |||||
|---|---|---|---|---|---|---|
| HR | 95% CI | P-value | HR | 95% CI | P-value | |
| POBA era | 1.0 | 1.0 | ||||
| BMS era | 0.72 | 0.54–0.96 | 0.03 | 0.59 | 0.49–0.70 | <0.001 |
| DES era | 0.69 | 0.53–0.92 | 0.01 | 0.33 | 0.27–0.40 | <0.001 |
CAD, coronary artery disease. Other abbreviations as in Tables 1,3.
Short-term clinical outcomes (30-day all-cause death and 30-day ACS) were examined and percentage of each outcome according to PCI era is shown in Figure 3. Improvement in 30-day all-cause death was not observed in patients with both ACS and stable CAD. No difference was observed in the incidence of 30-day ACS in both ACS and stable CAD patients.
Percentage of 30-day all-cause death and incidence of acute coronary syndrome (ACS) according to percutaneous coronary intervention (PCI) era. BMS, bare metal stent; CAD, coronary artery disease; DES, drug-eluting stent; POBA, plain old balloon angioplasty.
The main findings of this study are the following: (1) the baseline characteristics have become unfavorable over the 26-year period in terms of higher age and higher prevalence of comorbid disease (diabetes mellitus, hypertension, dyslipidemia and MVD); (2) the success rate of PCI and the use of evidence-based medical therapy for secondary prevention have improved over time; and (3) despite the higher patient risk profile, no significant difference was observed in 2-year all-cause mortality or incidence of ACS on multivariate Cox regression analysis. The incidence of 2-year MACE has significantly decreased with PCI era. This indicates that the improvement in PCI devices and the increased use of evidence-based medical therapy for secondary prevention have offset the higher patient risk profile in the recent era. With regard to short-term clinical outcome, no improvement was observed across the 3 eras in the incidence of 30-day all-cause death and incidence of ACS in patients with both ACS and stable CAD. In a previous report on death after PCI between 1991 and 2008, the rate of in-hospital death decreased over the time period in patients with stable CAD but not in those with ACS,15 which is different to the present results. This difference might have been due to the different patient backgrounds between the studies and to the small size of the present study group.
Prior studies conducted in the USA have produced results similar to the present ones. Singh et al reported that long-term MACE significantly decreased over 25 years in a single center.11 Age and prevalence of comorbid disease increased, and a higher PCI success rate was observed over the time period, which is similar to the present results. Rao et al examined a temporal trend in the clinical outcome after PCI from 1991 to 2006 in a large cohort of Medicare beneficiaries.12 In that study, a significant decrease in long-term clinical outcomes including death, MI and repeat revascularization was found. Patient background was unfavorable in the recent era of that study period, which was observed in the present study as well. The improvement in clinical outcomes over the present 26-year study period could be explained by advances in PCI technology, including the advent of DES, the high rate of PCI success and the introduction of evidence-based therapy for secondary prevention including aspirin, statins, β-blockers and ACEI/ARB as well as smoking cessation. The Global Registry of Acute Coronary Events (GRACE) registry has previously shown that adherence to guideline-recommended medical therapy for secondary prevention yielded favorable clinical outcome after acute coronary events.16 The positive effect of guideline-recommended medical therapy on clinical outcome was also demonstrated in the Prevention of AtherothrombotiC Incidents Following Ischemic Coronary attack (PACIFIC) registry, a multicenter, prospective observational study of Japanese ACS patients.17
To the best of our knowledge, this study is the first to elucidate the positive effects of the evolution of PCI on clinical outcome of PCI over a 26-year period in Japanese clinical practice. The results have demonstrated the importance of the advances in PCI technology, medical therapy for secondary prevention and smoking cessation in reducing cardiovascular events following PCI.
Future PerspectivesThis study, in conjunction with previous reports, emphasizes the importance of evidence-based medical therapy for secondary prevention and, further, illustrates the ongoing need for establishment of measures to reduce fatal cardiovascular and non-cardiovascular events. Additionally, considering that increased physical activity and nutrition therapy have positive effects on lowering the rate of cardiovascular events,18,19 future studies are advised to consider non-pharmacological treatment when investigating the factors associated with clinical outcome in CAD patients.
Study LimitationsThe present study had several limitations. First, this study was conducted in a single institution, which could limit the generalization of the results. The data are of importance, however, because PCI was introduced at Juntendo University Hospital at the beginning of the advent of PCI in Japan. Second, the data collection rate (87%) regarding medication use in the POBA era patients might have affected the results. Third, because of the long-term follow-up period across the 3 PCI eras, undetermined factors that were not assessed in this analysis might have had an effect on the incidence of clinical outcomes. Fourth, although the present results suggest that improvement in PCI might offset the higher patient risk profile in the recent eras, this was not demonstrated on statistical analysis. Further studies focusing on the effect of the improvement of PCI on clinical outcome in patients undergoing PCI are needed.
Clinical outcome of PCI at Juntendo University Hospital improved across the study period of 26 years (1984–2010), despite the higher patient risk profile in the recent era.
We gratefully acknowledge the contributions made by Ms Yumi Nozawa and Ms Ayako Onodera in data collection and management.
H.D. has received speakers’ Bureau/Honoraria from MSD, AstraZeneca, Kowa Pharmaceutical, Sanofi-Aventis, GlaxoSmithKline, Shionogi, Daiichi-Sankyo, Takeda Pharmaceutical, Mitsubishi Tanabe Pharma, Pfizer, and Astellas Pharma and research funds from Takeda Pharmaceutical, Bristol-Myers Squibb, Nippon Boehringer Ingelheim, Astellas Pharma, Novartis Pharma, MSD, Sanofi-Aventis, Otsuka Pharmaceutical, Dainippon Sumitomo Pharma, Pfizer, Kowa Pharmaceutical, Shionogi, AstraZeneca, Teijin, and Morinaga Milk Industry. K.M. has received speakers’ Bureau/Honoraria from MSD, AstraZeneca, Kowa Pharmaceutical, Sanofi-Aventis, Shionogi, Daiichi-Sankyo, Takeda Pharmaceutical, Pfizer, Astellas Pharma, and Novartis Pharma. The other authors report no conflicts of interest.
This study was supported by a grant for scientific research from the Ministry of Health, Labour and Welfare (23591063).
