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. 2020 Mar 19;59(12):1489–1495. doi: 10.2169/internalmedicine.4016-19

Determinants of Insufficient Optimal Medical Therapy after Acute Myocardial Infarction

Yumiko Haraguchi 1, Kenichi Sakakura 1, Kei Yamamoto 1, Yousuke Taniguchi 1, Takunori Tsukui 1, Masaru Seguchi 1, Hiroshi Wada 1, Shin-ichi Momomura 1, Hideo Fujita 1
PMCID: PMC7364243  PMID: 32188806

Abstract

Objective

Although the importance of evidence-based optimal medical therapy (OMT) after acute myocardial infarction (AMI) has been recognized, the prescription rate of OMT is not sufficiently high in real-word clinical settings. The purpose of this study was to identify the clinical characteristics of AMI patients who did not receive OMT.

Methods

The present study was a retrospective study. OMT was defined as the combination of antiplatelet therapy, angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARBs), beta-blockers, and statins at the time of hospital discharge. Non-OMT was defined as the lack of either antiplatelet therapy, ACE inhibitors/ARBs, beta-blockers, or statins.

Results

A total of 457 AMI patients were included as the final study population, and 98 patients (22.4%) lacked at least 1 OMT medication. The prescription rates of antiplatelet therapy, ACE inhibitors/ARBs, beta-blockers, and statins were 98.7%, 87.5%, 90.4%, and 96.7%, respectively. In the multivariate logistic regression analysis, age [per 1-year increase: odds ratio (OR) 1.033, 95% confidence interval (CI) 1.007-1.059, p=0.014], hemodialysis (vs. no hemodialysis: OR 2.707, 95% CI 1.082-6.774, p=0.033), estimated glomerular filtration rate <30 mL/min/1.73 m2 without hemodialysis (OR 4.585, 95% CI 1.975-10.644, p<0.001), AMI caused by vasospastic angina (VSA) (vs. no VSA: OR 13.198, 95% CI 1.809-96.260, p=0.011), and asthma (vs. no asthma: OR 7.241, 95% CI 1.716-30.559, p=0.007) were significantly associated with non-OMT, whereas heart rate on admission (per 1-bpm increase: 0.987, 95% CI 0.975-0.999, p=0.033), any PCI (vs. no PCI: OR 0.156, 95% CI 0.066-0.373, p<0.001), and ST-elevation myocardial infarction (STEMI) (vs. NSTEMI: OR 0.384, 95% CI 0.218-0.675, p=0.001) were inversely associated with non-OMT.

Conclusion

An advanced age, VSA, bradycardia, asthma, impaired renal function, non-PCI revascularization, and non-ST-elevation myocardial infarction were significantly associated with non-OMT.

Keywords: optimal medical therapy, acute myocardial infarction, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-blockers

Introduction

Evidence-based optimal medical therapy (OMT) after acute myocardial infarction (AMI) consists of antiplatelet therapy, angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARBs), beta-blockers, and statins (1, 2). Since non-adherence to OMT after AMI has been shown to be associated with poor clinical outcomes (3, 4), the importance of OMT is emphasized in contemporary clinical guidelines (5, 6). Nevertheless, the prescription rate of OMT is not sufficiently high in real-word clinical settings. The Tokyo CCU network cohort including 4,329 AMI patients reported that approximately 60% and 40% of AMI patients received ACE inhibitors/ARBs and beta-blockers, respectively (7). However, why OMT is not prescribed has not been fully discussed.

The present study explored the clinical characteristics of AMI patients who did not receive OMT at the time of hospital discharge.

Materials and Methods

Study patients

The present study was a retrospective and single-center study. From our medical records, we included AMI patients who were treated at our institution between January 2015 and December 2016. The diagnosis of AMI required the following criteria: symptoms consistent with AMI, elevated cardiac enzymes including Troponin I and/or creatinine kinase (at least a two-fold increase from the normal upper limit), and ST-segment elevation or depression in electrocardiograms compatible with AMI (8, 9). Furthermore, diagnostic ST-segment elevation was defined as new ST elevation at the J point in at least 2 contiguous leads of 2 mm (0.2 mV); all others were defined as not having ST-segment elevation (10, 11). The exclusion criteria were no coronary angiography, in-hospital death, and second or beyond AMI during the study period. OMT was defined as the combination of antiplatelet therapy (at least single), ACE inhibitors/ARBs, beta-blockers, and statins at the time of hospital discharge. Non-OMT was defined as the lack of either antiplatelet therapy, ACE inhibitors/ARBs, beta-blockers, or statins at the time of hospital discharge. We divided the study patients into OMT and non-OMT groups.

This study was approved by the institutional review board and written informed consent was waived because of the retrospective study design. This study was conducted in accordance with the principles of the Declaration of Helsinki.

Definition

Hypertension was defined as systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or medical treatment for hypertension (9). Dyslipidemia was defined as a total cholesterol level ≥220 mg/dL or a low-density lipoprotein cholesterol level ≥140 mg/dL or medical treatment for dyslipidemia (9). Diabetes mellitus was defined as a hemoglobin A1c level ≥6.5% (as NGSP value) or medical treatment for diabetes mellitus (12). We also calculated the estimated glomerular filtration rate (eGFR) from the serum creatinine levels, age, weight, and gender using the following formula: eGFR=194×Cr−1.094×age−0.287 (male), eGFR=194×Cr−1.094×age−0.287×0.739 (female) (13). An impaired renal function was defined as an eGFR <60 mL/min/1.73 m2 (12). Shock was defined as systolic blood pressure ≤90 mmHg, need for vasopressors to maintain blood pressure, need for percutaneous mechanical support, or attempted cardiopulmonary resuscitation.

Statistical analyses

Data are shown as the mean±standard deviation or percentage. Categorical variables are presented as numbers (percentages) and compared using Pearson's χ2 test. The Kolmogorov-Smirnov test was performed to determine if the continuous variables were normally distributed. Normally distributed continuous variables were compared between the groups using the unpaired Student's t-test. Otherwise, continuous variables were compared using the Mann-Whitney U test. Multivariate logistic regression analyses were performed to identify the determinants of non-OMT. In this model, the non-OMT group was used as the dependent variable. The multivariate logistic regression model included covariates found to have significant differences between the OMT and non-OMT groups (defined as p<0.05). The odds ratios (ORs) and 95% confidence intervals (CIs) were also calculated. A p value <0.05 was considered statistically significant. We analyzed all data using the SPSS software program, ver. 24, for Windows (SPSS, Chicago, USA).

Results

During the study period, a total of 504 AMI patients were treated at our institution. Of those, 457 AMI patients were included as the final study population and divided into the OMT group (n=359) and non-OMT group (n=98) (Figure). Table 1 shows the comparison of the background characteristics between the two groups. The mean age was significantly older in the non-OMT group (74±12 years old) than in the OMT group (68±12 years old) (p<0.001). The eGFR was significantly lower in the non-OMT group (52.3±31.7 mL/min/1.73 m2) than in the OMT group (65.9±26.5 mL/min/1.73 m2) (p<0.001). The heart rate on admission was significantly lower in the non-OMT group (72±24 bpm) than in the OMT group (80±23 bpm) (p=0.001). The prevalence of ST-elevation myocardial infarction (STEMI) was significantly lower in the non-OMT group (40.8%) than in the OMT group (65.5%) (p<0.001). The prevalence of AMI caused by vasospastic angina (VSA) was significantly greater in the non-OMT group (12.2%) than in the OMT group (0.6%) (p<0.001). Hemoglobin levels on admission was significantly lower in the non-OMT group (12.4±2.2 g/dL) than in the OMT group (13.5±1.9 g/dL) (p<0.001). The prevalence of a history of malignancy was significantly greater in the non-OMT group (21.4%) than in the OMT group (13.4%) (p=0.048). Blood transfusion during admission was more frequently performed in the non-OMT group (34.7%) than in the OMT group (8.9%) (p<0.001).

Figure.

Figure.

Patient flowchart.

Table 1.

Comparison of Patient Characteristics between the OMT and Non-OMT Groups.

Patient characteristics All
(n=457)
OMT group
(n=359)
Non-OMT group
(n=98)
p value
Age, years 70±12 68±12 74±12 <0.001
Male sex, n (%) 343 (75.1) 269 (74.9) 74 (75.5) 0.906
Hypertension, n (%) 385 (84.2) 307 (85.5) 78 (79.6) 0.154
Hyperlipidemia, n (%) 318 (69.6) 254 (70.8) 64 (65.3) 0.299
Diabetes mellitus, n (%) 203 (44.4) 161 (44.8) 42 (42.9) 0.725
Chronic obstructive pulmonary disease, n (%) 14 (3.1) 11 (3.1) 3 (3.1) 1.000
Asthma, n (%) 12 (2.6) 5 (1.4) 7 (7.1) 0.005
Chronic kidney disease, n (%) 197 (43.1) 139 (38.7) 58 (59.2) <0.001
Serum creatinine, mg/dL 1.6±4.4 1.5±4.8 2.1±2.6 <0.001
eGFR, mL/min/1.73 m2 62.9±28.2 65.9±26.5 52.3±31.7 <0.001
Hemodialysis, n (%) 30 (6.6) 17 (4.7) 13 (13.3) 0.003
Hemoglobin levels on admission, g/dL 13.3±2.0 13.5±1.9 12.4±2.2 <0.001
Potassium levels (mEq/L) 4.2±0.6 4.2±0.5 4.3±0.6 0.095
Atrial fibrillation, n (%) 67 (14.7) 47 (13.1) 20 (20.4) 0.070
Current smoking, n (%) 144 (31.5) 120 (33.4) 24 (24.5) 0.091
History of malignancy, n (%) 69 (15.1) 48 (13.4) 21 (21.4) 0.048
Previous PCI, n (%) 90 (19.7) 64 (17.8) 26 (26.5) 0.055
Previous CABG, n (%) 17 (3.7) 10 (2.8) 7 (7.1) 0.065
Previous myocardial infarction, n (%) 75 (16.4) 55 (15.3) 20 (20.4) 0.228
STEMI, n (%) 275 (60.2) 235 (65.5) 40 (40.8) <0.001
NSTEMI, n (%) 182 (39.8) 124 (34.5) 58 (59.2) <0.001
AMI caused by vasospastic angina, n (%) 14 (3.1) 2 (0.6) 12 (12.2) <0.001
Killip 1 or 2, n (%) 369 (80.7) 294 (81.9) 75 (76.5) 0.233
Systolic blood pressure on admission, mmHg 138±33 140±33 130±35 0.021
Diastolic blood pressure on admission, mmHg 79±21 80±21 72±22 0.001
Heart rate on admission, bpm 79±23 80±23 72±24 0.001
Shock status, n (%) 62 (13.6) 45 (12.5) 17 (17.3) 0.218
Cardio-pulmonary arrest, n (%) 21 (4.6) 15 (4.2) 6 (6.1) 0.417
Catecholamine use before coronary angiography, n (%) 44 (9.6) 30 (8.4) 14 (14.3) 0.078
Use of intra-aortic balloon pumping, n (%) 61 (13.3) 44 (12.3) 17 (17.3) 0.189
Use of veno-arterial extra-corporeal membrane oxygenation, n (%) 11 (2.4) 6 (1.7) 5 (5.1) 0.063
Blood transfusion during hospitalization, n (%) 66 (14.4) 32 (8.9) 34 (34.7) <0.001

Categorical variables were compared using the Pearson χ2 test. Normally distributed continuous variables were compared using the unpaired Student’s t test. Non-normally distributed continuous variables were compared using the Mann-Whitney U test.

OMT: optimal medical therapy, eGFR: estimate glomerular filtration rate, PCI: percutaneous coronary intervention, CABG: coronary artery bypass graft surgery, STEMI: ST-segment elevation myocardial infarction, NSTEMI: non-ST-segment elevation myocardial infarction, AMI: acute myocardial infarction

Table 2 shows the comparison of the lesion and therapeutic characteristics between the OMT and non-OMT groups. Percutaneous coronary intervention (PCI) was more frequently selected in the OMT group (95.5%) than in the non-OMT group (71.4%). Peak creatinine kinase (CK) and creatinine kinase-myocardial band (CK-MB) levels were significantly greater in the OMT group than in the non-OMT group. In the overall study population, the prescription rates of antiplatelet therapy, ACE inhibitors/ARBs, beta-blockers, and statins were 98.7%, 87.5%, 90.4%, and 96.7%, respectively. In addition, we compared the clinical characteristics between patients who did and did not receive antiplatelet therapy (Supplementary material 1), between patients who did and did not receive ACE inhibitors/ARBs (Supplementary material 2), between patients who did and did not receive beta-blockers (Supplementary material 3), and between patients who did and did not receive statins (Supplementary material 4).

Table 2.

Comparison of Lesion and Therapeutic Characteristics between the OMT and Non-OMT Groups.

All (n=457) OMT group
(n=359)
Non-OMT group
(n=98)
p value
Infarct related artery 0.876
Left main-left anterior descending artery, n (%) 237 (51.9) 188 (52.4) 49 (50.0)
Left circumflex artery, n (%) 58 (12.7) 47 (13.1) 11 (11.2)
Right coronary artery, n (%) 158 (34.6) 121 (33.7) 37 (37.8)
Bypass graft vessel, n (%) 4 (0.9) 3 (0.8) 1 (1.0)
Number of narrowed coronary arteries 0.445
1 246 (53.9) 190 (53.1) 56 (57.1)
2 135 (29.6) 111 (31.0) 24 (24.5)
3 75 (16.4) 57 (15.9) 18 (18.4)
Type of revascularization <0.001
PCI only, n (%) 411 (89.9) 343 (95.5) 68 (69.4)
CABG, n (%) 17 (3.7) 6 (1.7) 11 (11.2)
PCI and CABG, n (%) 2 (0.4) 0 (0.0) 2 (2.0)
Medication and others, n (%) 27 (5.9) 10 (2.8) 17 (17.3)
Any PCI, n (%) 413 (90.4) 343 (95.5) 70 (71.4) <0.001
Type of PCI (n=413) 0.053
Drug-eluting stent use, n (%) 369 (89.3) 312 (91.0) 57 (81.4)
Bare metal stent use, n (%) 18 (4.4) 12 (3.5) 6 (8.6)
Others, n (%) 26 (6.3) 19 (5.5) 7 (10.0)
Final TIMI-3 flow, n (%) 424 (92.8) 333 (92.8) 91 (92.9) 0.973
Outcomes
Peak creatinine kinase level, mU/mL 1,468±2,336 1,622±2,536 902±1,226 0.001
Peak creatinine kinase-myocardial band level, mU/mL 128±175 144±186 67±110 <0.001
Left ventricular ejection fraction, (%) 55.0±13.8 55.5±13.4 53.0±13.2 0.077
Length of hospital stay, days 11±11 10±8 16±16 0.002
Medication at discharge
Antiplatelet therapy (at least single) 451 (98.7) 359 (100) 92 (93.9) -
ACE inhibitors/ARBs 400 (87.5) 359 (100) 41 (41.8) -
Beta-blockers 413 (90.4) 359 (100) 54 (55.1) -
Statins 442 (96.7) 359 (100) 83 (84.7) -

Categorical variables were compared using the Pearson χ2 test. Normally distributed continuous variables were compared using the unpaired Student’s t test. Non-normally distributed continuous variables were compared using the Mann-Whitney U test. OMT: optimal medical therapy, TIMI: thrombolysis in myocardial infarction, ACE: angiotensin converting enzyme, ARBs: angiotensin II receptor blockers

Table 3 shows the results of a multivariate logistic regression analysis to identify the determinants of non-OMT group. Age (per 1-year increase: OR 1.033, 95% CI 1.007-1.059, p=0.014), hemodialysis (vs. no hemodialysis: OR 2.707, 95% CI 1.082-6.774, p=0.033), eGFR<30 mL/min/1.73 m2 without hemodialysis (OR 4.585, 95% CI 1.975-10.644, p<0.001), AMI caused by VSA (vs. no VSA: OR 13.198, 95% CI 1.809-96.260, p=0.011), and asthma (vs. no asthma: OR 7.241, 95% CI 1.716-30.559, p=0.007) were significantly associated with non-OMT, whereas heart rate on admission (per 1-bpm increase: 0.987, 95% CI 0.975-0.999, p=0.033), any PCI (vs. no PCI: OR 0.156, 95% CI 0.066-0.373, p<0.001), and STEMI (vs. NSTEMI: OR 0.384, 95% CI 0.218-0.675, p=0.001) were inversely associated with non-OMT.

Table 3.

Multivariate Logistic Regression Analysis to Identify the Determinants of Non-OMT Group.

Variables Multivariate logistic regression analysis
Odds ratio 95% confidence interval p value
Age (per 1 year increase) 1.033 1.007-1.059 0.014
Systolic blood pressure on admission (per 1 mmHg increase) 0.994 0.986-1.003 0.202
Heart rate on admission (per 1 bpm increase) 0.987 0.975-0.999 0.033
Hemoglobin levels on admission (per 1 g/dL increase) 0.885 0.756-1.036 0.129
Hemodialysis (vs. non-hemodialysis) 2.707 1.082-6.774 0.033
eGFR<30 mL/min/1.73 m2 without hemodialysis 4.585 1.975-10.644 <0.001
Any PCI (vs. no PCI) 0.156 0.066-0.373 <0.001
AMI caused by Vasospastic angina (vs. no vasospastic angina) 13.198 1.809-96.260 0.011
STEMI (vs. NSTEMI) 0.384 0.218-0.675 0.001
Asthma (vs. no asthma) 7.241 1.716-30.559 0.007
History of malignancy (vs. no malignancy) 1.684 0.843-3.362 0.140

OMT: optimal medical therapy, PCI: percutaneous coronary intervention, eGFR: estimate glomerular filtration rate, AMI: acute myocardial infarction, STEMI: ST-segment elevation myocardial infarction, NSTEMI: non-ST-segment elevation myocardial infarction

Discussion

A total of 457 AMI patients were included in the present study and divided into 359 patients (78.6%) who had sufficient OMT and 98 (22.4%) who did not have sufficient OMT at the time of hospital discharge. While the prescription rate of each OMT medication was reasonably high (87.5-98.7%), more than 20% of study patients lacked at least 1 OMT medication. Aging, AMI caused by VSA, asthma, and an impaired renal function were significantly associated with non-OMT, whereas heart rate, any PCI, and STEMI were inversely associated with non-OMT. It may be important to recognize the above factors as risk factors for insufficient OMT.

In the present study, aging was associated with non-OMT. Since we prescribe OMT for better clinical outcomes in AMI patients, we might hesitate to prescribe OMT for the very elderly. Yan et al. also reported that advanced age was a negative independent predictor of OMT (14). The association between AMI caused by VSA and non-OMT may be explained by the association between VSA and beta-blockers. Although no studies have proven a cause-and-effect relationship between beta-blockers and VSA, several case reports suggest that beta-blockers may provoke coronary spasm (15, 16). The administration of beta-blockers alone for VSA was reported to be class III in clinical guidelines (17). Therefore, we tended to avoid administering beta-blockers to patients with AMI caused by VSA without coronary artery stenosis, especially when the left ventricular function was preserved. We might also avoid introducing antiplatelet therapy to patients with AMI caused by VSA without coronary artery stenosis. The association between asthma and non-OMT may be explained by the association between asthma and beta-blockers, as beta-blockers are generally contraindicated in patients with asthma.

The association between the heart rate and non-OMT may be explained by the non-administration of beta-blockers. Generally, we did not administer beta-blockers to patients with bradycardia (<50 bpm). In fact, a recent Japanese multicenter registry reported that the introduction of beta-blockers was associated with poor clinical outcomes in AMI patients whose admission heart rate was <50 bpm (18). The association between an impaired renal function and non-OMT may be explained by the non-administration of ACE inhibitors/ARBs. While we understand the importance of administering ACE inhibitors/ARBs to patients with an impaired renal function (19), we might hesitate to administer ACE inhibitors/ARBs to patients with an impaired renal function, as the use of ACE inhibitors/ARBs during coronary angiography may increase the incidence of contrast-induced acute kidney injury (20). Furthermore, patients with hemodialysis might have hypotension during hemodialysis.

PCI for revascularization was inversely associated with non-OMT, suggesting that AMI patients who underwent CABG for revascularization might not receive OMT. In fact, CABG during hospitalization is reported to be a risk factor for non-OMT (14). One possible explanation for this is that AMI patients who underwent CABG were managed by cardiovascular surgeons during hospitalization. Unlike cardiovascular physicians, cardiovascular surgeons might not administer OMT to patients who underwent CABG. Furthermore, STEMI was inversely associated with non-OMT, indicating that NSTEMI was associated with non-OMT. Because NSTEMI patients included those whose troponin I levels were significantly elevated while their CK levels were normal, the left ventricular systolic function was preserved in some NSTEMI patients. While the clinical guidelines strongly recommend administering ACE inhibitors to NSTEMI patients with a left ventricular ejection fraction <40% (21), the significance of ACE inhibitors for NSTEMI patients with a normal left ventricular ejection fraction has not been established. Therefore, we might not administer ACE inhibitors/ARBs to NSTEMI patients without a reduced ejection fraction.

The clinical implications of the present study should be noted. As we discussed above, some reasons for non-OMT might be unavoidable, especially for patients with AMI caused by VSA. However, there is likely room for improvement, especially for patients with an advanced age. Since Japan is becoming a super-aged society (22), secondary prevention for elderly patients should be prioritized, not only for achieving better clinical outcomes but also for reducing medical expenses. However, whether or not OMT is equally effective for the frail elderly, especially for the bedridden elderly, is unclear. A comprehensive discussion regarding OMT for the elderly is warranted, as healthcare resources will be considerably limited in a super-aged society (22).

Study limitations

Several limitations associated with the present study warrant mention. Because this study was a single-center retrospective observational study, there was a risk of selection bias. Our prescription rates of ACE inhibitors/ARBs (87.5%) and beta blockers (90.4%) were considerably higher than the prescription rates of ACE inhibitors/ARBs (60%) and beta blockers (40%) in contemporary Japanese AMI registries (7), partly because we introduced a novel acute myocardial infarction risk stratification system (nARS) in April 2015 (23, 24). In the nARS, the early introduction of ACE inhibitors/ARBs was strongly encouraged by our daily conference (23). Therefore, the reasons for non-OMT in our study may be different from those in contemporary Japanese AMI registries. The present study focused on the OMT at the time of hospital discharge. We were unable to conduct monitoring to see whether or not OMT was maintained after hospital discharge. Finally, because we did not routinely check the low-density lipoprotein cholesterol levels following statin administration during hospitalization, the statin dose might not have been titrated at the time of hospital discharge.

Conclusion

Although the prescription rate of each OMT medication was reasonably high (87.5-98.7%), 22.4% of AMI patients lacked at least 1 OMT medication. An advanced age, VSA, bradycardia, asthma, impaired renal function, non-PCI revascularization, and NSTEMI were significantly associated with non-OMT.

Author's disclosure of potential Conflicts of Interest (COI).

Kenichi Sakakura: Honoraria, Abbott Vascular, Boston Scientific, Medtronic Cardiovascular, Terumo, OrbusNeich, Japan Lifeline and NIPRO. Hideo Fujita: Honoraria, Mehergen Group Holdings.

Supplementary Materials

Supplemental table 1.

Comparison of clinical characteristics between patients who had antiplatelet therapy and patients who did not have antiplatelet therapy

Supplemental table 2

Comparison of clinical characteristics between patients who had ACE inhibitors/ARBs and patients who did not have ACE inhibitors/ARBs

Supplemental table 3

Comparison of clinical characteristics between patients who had beta-blockers and patients who did not have beta-blockers

Supplemental table 4.

Comparison of clinical characteristics between patients who had statins and patients who did not have statins

Acknowledgement

The authors thank all staff in the catheter laboratory, ICU/CCU, and cardiology ward in Saitama Medical Center, Jichi Medical University, for their technical support in this study.

References

  • 1. Bramlage P, Messer C, Bitterlich N, et al. The effect of optimal medical therapy on 1-year mortality after acute myocardial infarction. Heart 96: 604-609, 2010. [DOI] [PubMed] [Google Scholar]
  • 2. Lee JH, Yang DH, Park HS, et al. Suboptimal use of evidence-based medical therapy in patients with acute myocardial infarction from the Korea Acute Myocardial Infarction Registry: prescription rate, predictors, and prognostic value. Am Heart J 159: 1012-1019, 2010. [DOI] [PubMed] [Google Scholar]
  • 3. Ho PM, Spertus JA, Masoudi FA, et al. Impact of medication therapy discontinuation on mortality after myocardial infarction. Arch Intern Med 166: 1842-1847, 2006. [DOI] [PubMed] [Google Scholar]
  • 4. Setoguchi S, Glynn RJ, Avorn J, Mittleman MA, Levin R, Winkelmayer WC. Improvements in long-term mortality after myocardial infarction and increased use of cardiovascular drugs after discharge: a 10-year trend analysis. J Am Coll Cardiol 51: 1247-1254, 2008. [DOI] [PubMed] [Google Scholar]
  • 5. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 61: e78-e140, 2013. [DOI] [PubMed] [Google Scholar]
  • 6. Drozda JP Jr, Ferguson TB Jr, Jneid H, et al. 2015 ACC/AHA focused update of secondary prevention lipid performance measures: a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures. Circ Cardiovasc Qual Outcomes 9: 68-95, 2016. [DOI] [PubMed] [Google Scholar]
  • 7. Miyachi H, Takagi A, Miyauchi K, et al. Current characteristics and management of ST elevation and non-ST elevation myocardial infarction in the Tokyo metropolitan area: from the Tokyo CCU network registered cohort. Heart Vessels 31: 1740-1751, 2016. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8. Yamamoto K, Sakakura K, Akashi N, et al. Comparison of clinical outcomes between the ostial versus non-ostial culprit in proximal left anterior descending artery acute myocardial infarction. Int Heart J 60: 37-44, 2019. [DOI] [PubMed] [Google Scholar]
  • 9. Otani A, Sakakura K, Yamamoto K, et al. Comparison of mid-term clinical outcomes after acute myocardial infarction in diabetic men between living alone and living together. Heart Vessels 34: 1288-1296, 2019. [DOI] [PubMed] [Google Scholar]
  • 10. Tsukui T, Sakakura K, Taniguchi Y, et al. Determinants of short and long door-to-balloon time in current primary percutaneous coronary interventions. Heart Vessels 33: 498-506, 2018. [DOI] [PubMed] [Google Scholar]
  • 11. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. Circulation 126: 2020-2035, 2012. [DOI] [PubMed] [Google Scholar]
  • 12. Watanabe Y, Sakakura K, Taniguchi Y, et al. Determinants of slow flow in percutaneous coronary intervention to the culprit lesion of non-ST elevation myocardial infarction. Int Heart J 59: 1237-1245, 2018. [DOI] [PubMed] [Google Scholar]
  • 13. Matsuo S, Imai E, Horio M, et al. Revised equations for estimated GFR from serum creatinine in Japan. Am J Kidney Dis 53: 982-992, 2009. [DOI] [PubMed] [Google Scholar]
  • 14. Yan AT, Yan RT, Tan M, et al. Optimal medical therapy at discharge in patients with acute coronary syndromes: temporal changes, characteristics, and 1-year outcome. Am Heart J 154: 1108-1115, 2007. [DOI] [PubMed] [Google Scholar]
  • 15. Nanas JN, Sutton RB, Alazraki N, Tsagaris TJ. Acute myocardial infarction in post infarct patient possibly through beta blocker-induced coronary artery spasm. Am Heart J 113: 388-391, 1987. [DOI] [PubMed] [Google Scholar]
  • 16. Kurabayashi M, Suzuki H, Shimura T, Yamauchi Y, Okishige K. Ventricular fibrillation in a patient with multi-vessel coronary spasm four days after the initiation of an oral beta-blocker. Eur J Case Rep Intern Med 3: 000439, 2016. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 17. JCS Joint Working Group. Guidelines for diagnosis and treatment of patients with vasospastic angina (Coronary Spastic Angina) (JCS 2013). Circ J 78: 2779-2801, 2014. [DOI] [PubMed] [Google Scholar]
  • 18. Okuno T, Aoki J, Tanabe K, et al. Admission heart rate is a determinant of effectiveness of beta-blockers in acute myocardial infarction patients. Circ J 83: 1054-1063, 2019. [DOI] [PubMed] [Google Scholar]
  • 19. Jafar TH, Schmid CH, Landa M, et al. Angiotensin-converting enzyme inhibitors and progression of nondiabetic renal disease. A meta-analysis of patient-level data. Ann Intern Med 135: 73-87, 2001. [DOI] [PubMed] [Google Scholar]
  • 20. Rim MY, Ro H, Kang WC, et al. The effect of renin-angiotensin-aldosterone system blockade on contrast-induced acute kidney injury: a propensity-matched study. Am J Kidney Dis 60: 576-582, 2012. [DOI] [PubMed] [Google Scholar]
  • 21. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 64: e139-e228, 2014. [DOI] [PubMed] [Google Scholar]
  • 22. Karako K, Chen Y, Song P, Tang W. Super-aged society: Constructing an integrated information platform of self-recording lifelogs and medical records to support health care in Japan. Biosci Trends 13: 276-278, 2019. [DOI] [PubMed] [Google Scholar]
  • 23. Yamamoto K, Sakakura K, Akashi N, et al. Clinical outcomes after acute myocardial infarction according to a novel stratification system linked to a rehabilitation program. J Cardiol 72: 227-233, 2018. [DOI] [PubMed] [Google Scholar]
  • 24. Yamamoto K, Sakakura K, Akashi N, et al. Novel acute myocardial infarction risk stratification (nARS) system reduces the length of hospitalization for acute myocardial infarction. Circ J 83: 1039-1046, 2019. [DOI] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Supplemental table 1.

Comparison of clinical characteristics between patients who had antiplatelet therapy and patients who did not have antiplatelet therapy

Supplemental table 2

Comparison of clinical characteristics between patients who had ACE inhibitors/ARBs and patients who did not have ACE inhibitors/ARBs

Supplemental table 3

Comparison of clinical characteristics between patients who had beta-blockers and patients who did not have beta-blockers

Supplemental table 4.

Comparison of clinical characteristics between patients who had statins and patients who did not have statins


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