PLoS ONE
Home Factors associated with temporary pacing insertion in patients with inferior ST-segment elevation myocardial infarction
Factors associated with temporary pacing insertion in patients with inferior ST-segment elevation myocardial infarction
Factors associated with temporary pacing insertion in patients with inferior ST-segment elevation myocardial infarction

Competing Interests: I have read the journal’s policy and the authors of this manuscript have the following competing interests: Dr. Sakakura has received speaking honoraria from Abbott Vascular, Boston Scientific, Medtronic Cardiovascular, Terumo, OrbusNeich, Japan Lifeline, Kaneka, and NIPRO; he has served as a proctor for Rotablator for Boston Scientific, and he has served as a consultant for Abbott Vascular and Boston Scientific. Prof. Fujita has served as a consultant for Mehergen Group Holdings, Inc. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

Article Type: Research Article Article History
Abstract

Background

High-degree atrioventricular block (HAVB) is a prognostic factor for survival in patients with inferior ST-segment elevation myocardial infarction (STEMI). However, there is little information about factors associated with temporary pacing (TP). The aim of this study was to find factors associated with TP in patients with inferior STEMI.

Methods

We included 232 inferior STEMI patients, and divided those into the TP group (n = 46) and the non-TP group (n = 186). Factors associated with TP were retrospectively investigated using multivariate logistic regression model.

Results

The incidence of right ventricular (RV) infarction was significantly higher in the TP group (19.6%) than in the non-TP group (7.5%) (p = 0.024), but the incidence of in-hospital death was similar between the 2 groups (4.3% vs. 4.8%, p = 1.000). Long-term major adverse cardiovascular events (MACE), which were defined as a composite of all-cause death, non-fatal myocardial infarction (MI), target vessel revascularization (TVR) and readmission for heart failure, were not different between the 2 groups (p = 0.100). In the multivariate logistic regression analysis, statin at admission [odds ratio (OR) 0.230, 95% confidence interval (CI) 0.062–0.860, p = 0.029], HAVB at admission (OR 9.950, 95% CI 4.099–24.152, p<0.001), and TIMI-thrombus grade ≥3 (OR 10.762, 95% CI 1.385–83.635, p = 0.023) were significantly associated with TP.

Conclusion

Statin at admission, HAVB at admission, and TIMI-thrombus grade ≥3 were associated with TP in patients with inferior STEMI. Although the patients with TP had the higher incidence of RV infarction, the incidence of in-hospital death and long-term MACE was not different between patients with TP and those without.

Yanase,Sakakura,Jinnouchi,Taniguchi,Yamamoto,Tsukui,Seguchi,Wada,Fujita,and den Uil: Factors associated with temporary pacing insertion in patients with inferior ST-segment elevation myocardial infarction

Introduction

Ischemic heart disease (IHD) remains the number 1 cause of death globally, although the complications and mortality rates of acute myocardial infarction (AMI) have declined over the past 20 years owing to the progress of coronary intervention and optimal medical therapy [1, 2]. In order to improve clinical outcomes in patients with AMI, it is essential to collect more specific data about each complication of AMI. High-degree atrioventricular block (HAVB) is a common complication following ST-segment elevation myocardial infarction (STEMI), the incidence of which is reported to be 2.7 to 19.6% [37]. Each complication of AMI depends on the size and anatomic location of the infarction, and HAVB is more common in inferior STEMI [3, 4].

Temporary pacing (TP), which is indicated for symptomatic or hemodynamically significant bradycardia, is indispensable for some patients with bradycardia due to inferior STEMI [8]. Insertion of a transvenous TP is a time-consuming procedure, and has its own complications including bleeding, thrombosis, infection, delirium, arrhythmia and cardiac perforation [911]. When a patient with inferior STEMI comes to a catheter laboratory, an interventional cardiologist has to decide whether to insert a TP within a short time period. Several groups reported factors associated with HAVB in patients with inferior STEMI, but there is little information regarding factors associated with TP in patients with inferior STEMI [12]. HAVB does not necessarily require TP, whereas bradycardia without HAVB may require TP in certain situations. In the present study, we aimed (1) to find factors associated with TP in patients with inferior STEMI, and (2) to compare clinical outcomes between those who received TP and those who did not.

Methods

Study design

This was a retrospective, single center study. We reviewed consecutive AMI patients from hospital records in our medical center from January 2015 to December 2019. The inclusion criteria were (1) AMI due to right coronary artery (RCA) and (2) STEMI. The exclusion criteria were (1) in-hospital onset, (2) no revascularization, (3) underwent coronary artery bypass graft surgery to the culprit lesion of AMI, (4) second or more than second AMI during the same study period, (5) had undergone permanent pacing implantation before the AMI, and (6) TP was not activated, because pacing was inserted for prophylactic purpose. Final study population was divided into a TP group and a non-TP group according to the insertion of TP. Clinical characteristics were compared between the TP and non-TP groups. Our primary interest was to find factors associated with TP using multivariate logistic regression model. We also examined major adverse cardiovascular events (MACE) until September 30th 2020. MACE were a composite of all-cause death, non-fatal myocardial infarction (MI), target vessel revascularization (TVR) and readmission for heart failure. We defined the admission day as the index day in this follow-up analysis. This study was approved by the institutional review board of Saitama Medical Center, Jichi Medical University (S20-132), and written informed consent was waived because of the retrospective study design.

Definitions

AMI was defined according to the universal definition [3, 13]. Diagnostic ST elevation was defined as new ST elevation at the J point in at least two contiguous leads of 2 mm (0.2 mV), and the AMI patients with ST elevation were diagnosed as STEMI [14]. HAVB was defined as the presence of either Mobitz II second-degree AV block or third-degree AV block [15]. Sick sinus syndrome (SSS) was defined as sinus bradycardia, sinoatrial pause of 3 seconds or more, sinoatrial exit block, or sinus arrest [16]. Bradycardia was defined as a rate below 60 beats per minute [17]. Hypertension was defined as systolic blood pressure (SBP) >140 mmHg, diastolic blood pressure >90 mmHg, or medical treatment for hypertension [18, 19]. Diabetes mellitus was defined as hemoglobin A1c (HbA1c) ≥6.5% or treatment for diabetes mellitus [19, 20]. Dyslipidemia was defined as total cholesterol ≥220 mg/dL, low-density lipoprotein cholesterol ≥140 mg/dL, or treatment for dyslipidemia [19, 20]. We also calculated estimated glomerular filtration rate (eGFR) using serum creatinine (Cr), age, weight, and gender according to the following formula: eGFR = 194×Cr−1.094×age−0.287 (male), or eGFR = 194×Cr−1.094×age−0.287×0.739 (female) [21]. Shock was defined as SBP <90 mmHg, vasopressors required to maintain blood pressure, or attempted cardiopulmonary resuscitation [19, 20]. Left ventricular ejection fraction (LVEF) was measured using a modified Simpson method. Echocardiography was evaluated during the index hospitalization. Right ventricular (RV) infarction was defined as ST-segment elevation in V4R (1mm) or abnormal RV wall motion on echocardiography, accompanying clinical symptoms such as hypotension [20].

Quantitative coronary angiography parameters were measured using a cardiovascular angiography analysis system (QAngio XA 7.3, MEDIS Imaging Systems, Leiden, Netherlands). The lesion length and reference diameter were measured. Intracoronary thrombus was angiographically identified by the thrombolysis in myocardial infarction (TIMI) thrombus grade, and was scored in 5 grades as previous studies reported [22]. G0, no thrombus present; G1, possible thrombus present, with angiographic characteristics suggestive of thrombus but not diagnostic of thrombus (i.e., reduced contrast density, haziness, irregular lesion contour or a smooth convex meniscus at the site of total occlusion); G2, definite thrombus present, with greatest dimensions ≤0.5 the vessel diameter; G3, definite thrombus present, with greatest linear dimension >0.5 but <2 vessel diameters; G4, definite thrombus present, with the largest dimension ≥2 vessel diameters; G5, total occlusion, the size of thrombus cannot be assessed [22]. Dominant RCA was defined when RCA supplied circulation to both the inferior portion of the interventricular septum via the right posterior descending artery and the atrioventricular node via the right postero-lateral branch [23, 24]. Balanced RCA was defined when RCA supplied circulation to only the right posterior descending artery [23]. In addition, we counted the number of atrioventricular node branch (#4AV) to evaluate the size of RCA. We defined a #4AV artery as an artery branched from atrioventricular groove with ≥1 mm diameter.

Statistical analysis

Data are presented as a percentage for categorical variables and the mean ± SD for continuous variables. Categorical variables were compared using Pearson’s χ2 test or Fisher’s exact test. The Shapiro-Wilk test was conducted to determine whether 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. Kaplan-Meier survival analysis was performed with respect to MACE, and the difference between the two survival curves was compared by the log rank test. Furthermore, we performed multivariate logistic regression analysis to investigate factors associated with TP. Univariate logistic regression analysis was performed to identify variables that had marginal association with TP, and all variables that had marginal association (P < 0.20) in univariate analysis were adopted as independent variables in multivariate logistic regression analysis. Moreover, when there are ≥2 similar variables, only one variable was entered into the multivariable logistic model to avoid multi-collinearity. Odds ratio (OR) and 95% confidence interval (CI) were calculated. All reported P-values were determined by two-sided analysis, and P-values <0.05 were considered significant. All analyses were performed with IBM SPSS statistics version 25 (Chicago, IL, USA).

Results

Among 1402 patients admitted to our medical center from January 2015 to December 2019, a total of 232 patients were included as the final study population, and were divided into the TP group (n = 46) and the non-TP group (n = 188) (Fig 1).

Study flow chart.
Fig 1

Study flow chart.

AMI indicates acute myocardial infarction.

The details of the TP group are shown in Table 1. Of 46 patients with TP, 43 patients (93.5%) received TP before the revascularization, and 38 patients (82.6%) removed TP just after the revascularization. The reasons for TP were HAVB (69.6%), SSS (23.9%), atrial fibrillation with bradycardia (4.3%), and bradycardia (details unknown) (2.2%). The more detail regarding the catecholamine and mechanical circulatory support use by each bradyarrhythmias is shown in S1 Table.

Table 1
Details of the temporary pacing group.
TP group (n = 46)
Placement of temporary pacing
    Before CAG, n (%)21 (45.7)
    After CAG and before PCI, n (%)22 (47.8)
    During PCI, n (%)3 (6.5)
Removal of temporary pacing
    After PCI, n (%)38 (82.6)
    The next day, n (%)2 (4.3)
    3rd hospital day, n (%)2 (4.3)
    4th hospital day, n (%)1 (2.2)
    7th hospital day, n (%)1 (2.2)
    9th hospital day, n (%)1 (2.2)
    13th hospital day, n (%)1 (2.2)
Reason for temporary pacing
    High-degree atrioventricular block, n (%)32 (69.6)
    Sick sinus syndrome, n (%)11 (23.9)
    Atrial fibrillation with bradycardia, n (%)2 (4.3)
    Bradycardia (details unknown)1 (2.2)

Abbreviations: CAG coronary angiography, PCI percutaneous coronary intervention.

Table 2 shows the comparison of patients’ characteristics between the 2 groups. The patients who had statin at admission were significantly less in the TP group (6.5%) than in the non-TP group (26.0%) (p = 0.004). The incidence of shock at admission was greater in the TP group (32.6%) than in the non-TP group (12.9%) (p = 0.001). The frequency of HAVB at admission was significantly higher in the TP group (50.0%) than in the non-TP group (5.9%) (p<0.001). In the non-TP group, eleven patients presented with HAVB were not treated with TP, because junctional escape rhythm was observed in 2 patients, and HAVB was transient in 9 patients.

Table 2
The comparison of patient’s clinical characteristic between the temporary pacing group and the non-temporary pacing group.
All (n = 232)TP group (n = 46)Non-TP group (n = 186)P value
Age, year69.8 ± 13.969.4 ± 15.169.9 ± 13.60.948
Male, n (%)176 (75.9)36 (78.3)140 (75.3)0.671
Height, cm161.8 ± 9.9 (226/232)161.8 ± 9.3161.8 ± 10.1 (180/1867)0.935
Weight, kg63.1 ± 14.0 (230/232)63.1 ± 17.263.1 ± 13.2 (184/186)0.996
Current smoker, n (%)91/227 (40.1)19 (41.3)72/181 (39.8)0.850
Hypertension, n (%)164/230 (71.3)32 (69.6)132/184 (71.7)0.771
Diabetes mellitus, n (%)93/230 (40.4)16 (34.8)77/184 (41.8)0.382
HbA1c, %6.7 ± 1.6 (221/232)6.7 ± 1.5 (45/47)6.7 ± 1.6 (176/186)0.883
Dyslipidemia, n (%)119/227 (52.4)17/45 (37.8)102/182 (56.0)0.028
Serum creatinine, mg/dl1.3 ± 1.81.5 ± 1.61.3 ± 1.80.016
eGFR, mL/min/1.73m264.1 ± 35.754.9 ± 25.766.5 ± 37.40.037
eGFR <60, n (%)111 (47.8)26 (56.5)85 (45.7)0.188
Chronic renal failure on hemodialysis, n (%)12 (5.2)2 (4.3)10 (5.4)1.000
Hemoglobin, g/dL13.2 ± 2.012.8 ±2.113.3 ± 2.00.198
C-reactive protein, mg/L1.7 ± 4.0 (229/232)1.8 ± 3.6 (45/46)1.7 ± 4.0 (184/186)0.460
Brain natriuretic peptide, pg/ml254.2 ± 454.4 (219/232)307.4 ± 490.0 (45/46)240.4 ± 445.2 (174/186)0.885
History of previous myocardial infarction, n (%)25 (10.8)2 (4.3)23 (12.4)0.181
History of previous CABG, n (%)1 (0.4)0 (0.0)1 (0.5)1.000
History of previous PCI, n (%)31 (13.4)3 (6.5)28 (15.1)0.128
Killip classification0.508
    1 or 2, n (%)193 (83.2)36 (78.3)157 (84.4)
    3, n (%)6 (2.6)1 (2.2)5 (2.7)
    4, n (%)33 (14.2)9 (19.6)24 (12.9)
Cardiac arrest at out of hospital, n (%)10 (4.3)1 (2.2)9 (4.8)0.691
Shock at admission, n (%)39 (16.8)15 (32.6)24 (12.9)0.001
Pre-hospital syncope, n (%)28 (12.1)11 (23.9)17 (9.1)0.006
High-degree atrioventricular block at admission, n (%)34 (14.7)23 (50.0)11 (5.9)< 0.001
Atrial fibrillation, n (%)9 (3.9)3 (6.5)6 (3.2)0.386
Systolic blood pressure at admission, mmHg127.2 ± 31.1 (228/232)114.0 ± 27.9 (45/46)130.5 ± 31.1 (183/186)0.002
Diastolic blood pressure at admission, mmHg74.4 ± 20.4 (227/232)65.0 ± 21.6 (45/46)76.7 ± 19.5 (182/186)< 0.001
Heart rate at admission, bpm69.9 ± 21.6 (231/232)51.9 ± 15.674.3 ± 20.6 (185/186)< 0.001
Admission route0.024
    Referred from another hospital, n (%)89 (38.4)12 (26.1)77 (41.4)
    Walk in, n (%)10 (4.3)0 (0.0)10 (5.4)
    Ambulance transport, n (%)133 (57.3)34 (73.9)99 (53.2)
From the onset0.886
    Within 24 hours, n (%)201 (86.6)39 (84.8)162 (87.1)
    Over 24 hours, n (%)19 (8.2)4 (8.7)15 (8.1)
    Undetermined, n (%)12 (5.2)3 (6.7)9 (4.8)
Medical therapy at admission
    Aspirin, n (%)33/229 (14.4)3 (6.5)30/183 (16.4)0.088
    Thienopyridine, n (%)18/228 (7.9)1 (2.2)17/182 (9.3)0.133
    Chronic statin therapy, n (%)50/227 (22.0)3 (6.5)47/181 (26.0)0.004
    Calcium channel blocker, n (%)79/227 (34.8)18 (39.1)61/181 (33.7)0.490
    ACE inhibitors or ARBs, n (%)75/227 (33.0)15 (32.6)60/181 (33.1)0.945
    Beta-blockers, n (%)21/227 (9.3)3 (6.5)18/181 (9.9)0.581
    Diuretics, n (%)19/228 (8.3)4 (8.7)15/182 (8.2)1.000
    Oral antidiabetic, n (%)47/229 (20.5)9 (19.6)38/183 (20.8)0.857
    Insulin, n (%)15/230 (6.5)5 (10.9)10/184 (5.4)0.188
    Warfarin, n (%)4/226 (1.8)1 (2.2)3/180 (1.7)1.000
DOAC, n (%)2/226 (0.9)1 (2.2)1/180 (0.6)0.366

Data were expressed as mean ± SD or numbers (percentages). A Student’s t test was used for normally distributed continuous variables, and Mann–Whitney U test was used for abnormally distributed continuous variables. A Chi-square test was used for categorical variables.

Abbreviations: ACE inhibitors angiotensin-converting enzyme inhibitor, ARB angiotensin receptor blockers, CABG coronary artery bypass grafting, CK creatine kinase, CK-MB creatine kinase MB, DAPT dual antiplatelet therapy, eGFR estimated glomerular filtration rate, HDL high-density lipoprotein, LDL low-density lipoprotein, PCI percutaneous coronary intervention, DOAC direct oral anticoagulants.

Table 3 shows the comparison of angiographic lesion and procedural characteristics between the TP and non-TP groups. There were significant differences between the 2 groups in the initial TIMI flow grade (p = 0.024) and TIMI thrombus grade (p = 0.001). The prevalence of patients who underwent thrombectomy was higher in the TP group (58.7%) than in the non-TP group (26.3%) (p<0.001). There were no significant differences in RCA dominance (p = 0.351), and the number of #4AV (p = 0.167) between the 2 groups.

Table 3
The comparison of lesion and procedural characteristic between the temporary pacing group and the non-temporary pacing group.
All (n = 232)TP group (n = 46)Non-TP group (n = 186)P value
Number of narrowed coronary arteries0.875
    1, n (%)88 (37.9)18 (39.1)70 (37.6)
    2, n (%)83 (35.8)15 (32.6)68 (36.6)
    3, n (%)61 (26.3)13 (28.3)48 (25.8)
Left main trunk stenosis > 50%, n (%)19 (8.2)2 (4.3)17 (9.1)0.380
Chronic total occlusion in other vessels, n (%)16 (6.9)4 (8.7)12 (6.5)0.530
Intra-aortic balloon pump, n (%)9 (3.9)2 (4.3)7 (3.8)0.854
Veno-arterial extracorporeal membrane oxygenation, n (%)7 (3.0)1 (2.2)6 (3.2)1.000
Atropine, n (%)68 (29.3)15 (32.6)53 (28.5)0.583
Norepinephrine before revascularization, n (%)60 (25.9)17 (37.0)43 (23.1)0.055
Dopamine before revascularization, n (%)6 (2.6)3 (6.5)3 (1.6)0.094
Dobutamine before revascularization, n (%)4 (1.7)4 (8.7)0 (0.0)0.001
Culprit lesion0.341
    1, n (%)60 (25.9)16 (34.8)44 (23.7)
    2, n (%)84 (36.2)17 (37.0)67 (36.0)
    3, n (%)63 (27.2)11 (23.9)52 (28.0)
    4AV, n (%)19 (8.2)2 (4.3)17 (9.1)
    4PD, n (%)6 (2.6)0 (0.0)6 (3.2)
Initial TIMI flow grade0.024
    0, n (%)156 (67.2)39 (84.8)117 (62.9)
    1, n (%)18 (7.8)3 (6.5)15 (8.1)
    2, n (%)27 (11.6)3 (6.5)24 (12.9)
    3, n (%)31 (13.4)1 (2.2)30 (16.1)
Final TIMI flow grade0.331
    0, n (%)2 (0.9)0 (0.0)2 (1.1)
    1, n (%)3 (1.3)1 (2.2)2 (1.1)
    2, n (%)10 (4.3)0 (0.0)10 (5.4)
    3, n (%)217 (93.5)45 (97.8)172 (92.5)
TIMI Thrombus grade0.001
    1, n (%)36 (15.5)0 (0.0)36 (19.4)
    2, n (%)16 (6.9)1 (2.2)15 (8.1)
    3, n (%)16 (6.9)2 (4.3)14 (7.5)
    4, n (%)8 (3.4)4 (8.7)4 (2.2)
    5, n (%)156 (67.2)39 (84.8)117 (62.9)
Approach site< 0.001
    Radial, n (%)148 (63.8)18 (39.1)130 (69.9)
    Brachial, n (%)3 (1.3)0 (0.0)3 (1.6)
    Femoral, n (%)81 (34.9)28 (60.9)53 (28.5)
Size of guide catheter0.043
    6 Fr, n (%)174 (75.0)30 (65.2)144 (77.4)
    7 Fr, n (%)57 (24.6)15 (32.6)42 (22.6)
    8 Fr, n (%)1 (0.4)1 (2.2)0 (0.0)
Thrombectomy, n (%)76 (32.8)27 (58.7)49 (26.3)< 0.001
Final PCI procedures0.291
    POBA, n (%)13 (5.6)0 (0.0)13 (7.0)
    Thrombectomy, n (%)6 (2.6)1 (2.2)5 (2.7)
    Thrombectomy and POBA, n (%)4 (1.7)0 (0.0)4 (2.1)
    Drug-coated balloon, n (%)2 (0.9)0 (0.0)2 (1.1)
    Drug-eluting stent implantation, n (%)194 (83.6)41 (89.1)153 (82.3)
    Bare-metal stent implantation, n (%)11 (4.7)4 (8.7)7 (3.8)
    Bougie only, n (%)2 (0.9)0 (0.0)2 (1.1)
Right coronary artery0.351
    Dominance, n (%)225 (97.0)46 (100.0)179 (96.2)
    Balanced dominance, n (%)7 (3.0)0 (0.0)7 (3.8)
Number of #4AV0.167
    0, n (%)8 (3.4)0 (0.0)8 (4.3)
    1, n (%)72 (31.0)17 (37.0)55 (29.6)
    2, n (%)69 (29.7)10 (21.7)59 (31.7)
    3, n (%)63 (27.2)17 (37.0)46 (24.7)
    4, n (%)16 (6.9)1 (2.2)15 (8.1)
    5, n (%)4 (1.7)1 (2.2)3 (1.6)
QCA lesion length, mm15.5 ± 9.1 (230/232)16.6 ± 9.415.3 ± 9.0 (184/186)0.380
QCA reference diameter, mm2.9 ± 0.7 (230/232)2.9 ± 0.62.9 ± 0.7 (184/186)0.814
Stent length, mm26.6 ± 12.6 (207/207)28.4 ± 12.3 (45/45)26.1 ± 12.7 (162/162)0.248
Stent diameter, mm2.9 ± 0.4 (207/207)3.0 ± 0.3 (45/45)2.9 ± 0.4 (162/162)0.126
Door to balloon time, min76.2 ± 36.7 (217/233)79.7 ± 42.0 (44/46)75.2 ± 35.3 (173/186)0.798
Fluoroscopy time, min25.3 ± 16.9 (225/232)28.9 ± 20.5 (44/46)24.5 ± 15.9 (181/186)0.033
Amount of contrast agent, mL113.1 ± 37.8 (227/232)112.1 ± 36.9 (45/46)113.3 ± 38.1 (182/186)0.582
Revascularization strategy to multi-vessel disease0.594
    Single vessel disease, n (%)88 (37.9)18 (39.1)70 (37.6)
    Complete revascularization for multi-vessel disease during the index hospitalization, n (%)70 (30.2)13 (28.3)57 (30.6)
    Complete revascularization for multi-vessel disease after discharge of the index hospitalization, n (%)36 (15.5)5 (10.9)31 (16.7)
    Incomplete revascularization for multi-vessel disease, n (%)38 (16.4)10 (21.7)28 (15.1)

Data were expressed as mean ± SD or numbers (percentages). A Student’s t test was used for normally distributed continuous variables, and Mann–Whitney U test was used for abnormally distributed continuous variables. A Chi-square test was used for categorical variables.

Abbreviations: BMS bare metal stent, CABG coronary artery bypass grafting, DCB drug-coated balloon, DES drug eluting stent, PCI percutaneous coronary intervention, POBA Percutaneous old balloon angioplasty, TIMI thrombolysis in myocardial infarction.

The comparisons of clinical outcomes between the TP and non-TP groups are shown in Table 4. The frequency of right ventricular infarction was significantly higher in the TP group (19.6%) than in the non-TP group (7.5%) (p = 0.024). The incidence of in-hospital death was similar between the 2 groups (p = 1.000). The length of hospital and CCU stay were longer in the TP group (11.0 ± 7.8 and 3.7 ± 2.5) than in the non-TP group (9.6 ± 9.1 and 3.4 ± 3.6) (p = 0.014 and 0.015, respectively). Median follow-up duration was 316.5 days (Q1: 196.25 days—Q3: 876.25 days). The Kaplan-Meier curves for MACE are shown in Fig 2. MACE were not different between the 2 groups (P = 0.100).

Kaplan–Meier curves for MACE.
Fig 2

Kaplan–Meier curves for MACE.

MACE were not different between the 2 groups (P = 0.100). Abbreviations: MACE = major adverse cardiovascular events.

Table 4
The comparison of clinical outcomes between the temporary pacing group and the non-temporary pacing group.
All (n = 232)TP group (n = 46)Non-TP group (n = 186)P value
In-hospital outcomes
    Right ventricular infarction23 (9.9)9 (19.6)14 (7.5)0.024
    Peak CK, mg/dL1963.3 ± 1995.72384.4 ± 2633.31859.1 ± 1797.60.302
    Peak CK-MB, mg/dL180.1 ± 186.7185.7 ± 183.5178.7 ± 188.00.782
    Left ventricular ejection fraction, %53.1 ± 10.7 (173/232)54.0 ± 8.8 (30/46)52.9 ± 11.0 (143/186)0.805
    In-hospital death, n (%)11 (4.7)2 (4.3)9 (4.8)1.000
    Length of hospital stay, days9.9 ± 8.911.0 ± 7.89.6 ± 9.10.014
    Length of CCU stay, days3.5 ± 3.43.7 ± 2.53.4 ± 3.60.015
    Permanent pacemaker implantation during the admission, n (%)1 (0.4)0 (0.0)1 (0.5)1.000
Long-term clinical outcomes
    Follow-up duration543.6 ± 512.8505.1 ± 475.9553.1 ± 522.20.654
    MACE, n (%)73 (31.5)10 (21.7)63 (33.9)0.113
    All cause death, n (%)21 (9.1)4 (8.7)17 (9.1)1.000
    Re-admission for heart failure, n (%)11 (4.7)4 (8.7)7 (3.8)0.235
    No fatal MI, n (%)13 (5.6)2 (4.3)11 (5.9)1.000
    TVR, n (%)43 (18.5)2 (4.3)41 (22.0)0.006

MACE indicates major adverse cardiovascular events: composite of all cause death, no fatal MI, TVR and re-admission for heart failure.

Data were expressed as mean ± SD or numbers (percentages). A Student’s t test was used for normally distributed continuous variables, and Mann–Whitney U test was used for abnormally distributed continuous variables. A Chi-square test was used for categorical variables.

Abbreviations: CCU coronary care unit, CK creatine kinase, CK-MB creatine kinase MB, MACE major adverse cardiovascular events, MI myocardial infarction, TVR target vessel revascularization.

We performed univariate and multivariate logistic regression analysis to find factors associated with TP (Table 5). Statin use at admission (OR 0.230, 95% CI 0.062–0.860, p = 0.029), HAVB at admission (OR 9.950, 95% CI 4.099–24.152, p<0.001), and TIMI-thrombus grade ≥3 (OR 10.762, 95% CI 1.385–83.635, p = 0.023) were significantly associated with TP.

Table 5
Determinants of temporary pacing: Univariate and multivariate logistic regression analysis.
Dependent variable: temporary pacing
Univariate logistic regression analysisMultivariate logistic regression analysis
OR95% CIP valueOR95% CIP value
Independent variables
    Age (10 year increase)0.9860.784–1.2400.903
    Male (vs. female)1.1830.545–2.5690.671
    Hypertension0.9000.445–1.8230.771
    Diabetes mellitus0.7410.378–1.4540.383
    Dyslipidemia0.4760.244–0.9310.030
    Aspirin0.3560.104–1.2220.101
    Thienopyridine0.2160.028–1.6650.141
    Statin at admission0.1990.059–0.6710.0090.2300.062–0.8600.029
    History of previous myocardial infarction0.3220.073–1.4190.134
    High-degree atrioventricular block at admission15.9096.870–36.843< 0.0019.9504.099–24.152< 0.001
    Shock at admission3.2661.541–6.9200.0022.0990.833–5.2930.116
    Systolic blood pressure at admission (10 mmHg)0.8350.745–0.9370.002
    Diastolic blood pressure at admission (10 mmHg)0.7290.607–0.8750.001
    Heart rate at admission (5 bpm)0.6800.598–0.774< 0.001
    Atropine, n (%)1.2140.607–2.4300.583
    QCA lesion length (5 mm increase)1.0640.902–1.2560.459
    QCA reference diameter (0.5 mm)1.0030.804–1.2500.982
    Right coronary artery dominant*---
    TIMI-thrombus grade ≥317.0002.283–126.5770.00610.7621.385–83.6350.023
    Thrombectomy3.9732.030–7.776<0.001

Univariate logistic regression analysis was performed to identify variables that had marginal association with temporary pacing. All variables that had marginal association in univariate analysis were adopted as independent variables in multivariate logistic regression analysis.

*Univariate and multivariate logistic regression analysis cannot be conducted in “Right coronary artery dominant” because all of the patient in the TP group have dominant right coronary artery.

Abbreviations: eGFR estimated glomerular filtration rate, PCI percutaneous coronary intervention.

Discussion

The present study included 232 inferior STEMI patients, and divided those into 46 patients (19.8%) who required TP and 186 patients (80.2%) who did not. The TP group showed a higher incidence of RV infarction, and a longer period of hospital stay compared to the non-TP group, but the incidence of in-hospital death and long-term MACE was not different between the 2 groups. We found that statin use at admission, HAVB at admission, and TIMI-thrombus grade ≥3 were significantly associated with TP. It may be important for interventional cardiologists to recognize those factors to prepare TP in emergent situations.

The earlier studies in the thrombolytic era reported that HAVB in inferior AMI was associated with older age, larger infarct size, female predominance, and higher mortality [2527]. Since primary PCI has replaced thrombolysis in the treatment of STEMI in most developed countries, the incidence of HAVB has been decreasing and the mortality rate has been significantly improved. However, the presence of HAVB was still a significant prognostic factor for a lower chance of survival [3, 4, 28]. Indeed, the TP group showed a higher rate of RV infarction and a longer period of hospital compared to the non-TP group in the present study, but those reported factors including age, infarct size, sex, and mortality were not different between the 2 groups in the present study.

We should discuss why TIMI-thrombus grade was closely associated with TP in inferior STEMI. Tanboga et al. [29] reported high thrombus burden in patients with STEMI was associated with distal embolization and impaired post-procedural epicardial and myocardial perfusion. Thus, in patients with high thrombus burden, the incidence of distal embolization to the territory of cardiac conduction system might be high, which lead to bradycardia requiring TP. However, most patients with TP underwent the insertion of TP before revascularization in the present study, which suggests that the distal embolization caused by PCI might not be associated with insertion of TP. High thrombus burden itself might be the cause of bradycardia requiring TP. Another possibility was that high thrombus burden was not the cause of bradycardia, but the effect of bradycardia. Bradycardia might provoke the stagnation of coronary flow, which results in thrombus formation. Our retrospective study could not provide an answer whether high thrombus burden was either a cause or an effect of bradycardia.

In our study, statin use at admission was inversely associated with insertion of TP in patients with inferior STEMI. Early statin administration in patients with AMI is known to reduce the prevalence of positive vascular remodeling and to alter plaque components such as the amount of necrotic core and fibro-fatty plaque. Furthermore, chronic statin treatment is reported to reduce positive remodeling in the culprit lesions of patients with ACS [3033]. In this way, statin before admission might stabilize the plaque of the culprit lesions, and could consequently reduce the thrombus burden.

Clinical implications of the present study should be noted. In general, if a patient with inferior STEMI comes to an emergency room with shock caused by HAVB, we would not hesitate to insert TP. However, since insertion of TP is a time-consuming and invasive procedure, the decision to insert TP is sometimes difficult for interventional cardiologists. When we cannot make a quick decision whether to insert TP for patients with inferior STEMI, information regarding statin treatment before admission or TIMI-thrombus grade from initial coronary angiography may be helpful. Specific techniques such as distal protection devices may be considered to prevent distal embolization and subsequent bradycardia for patients with high thrombus burden [34]. Moreover, when a patient with inferior STEMI requires TP, we should be careful about the occurrence of RV infarction as a possible complication.

Study limitations

Our study has several limitations. First, since our study was designed as a single-center, retrospective observational study, there is a risk of selection bias. Second, since our study was conducted with a relatively small number of patients, especially only 46 patients in the TP group, there is a possibility of beta errors. Third, the decision whether or not to use TP finally depended on the interventional cardiologist’s discretion. Some interventional cardiologists might not insert TP for patients with HAVB, whereas other interventional cardiologists might insert TP in a preventive manner for patients without bradycardia. In order to minimize this limitation, we excluded the patients with TP whose TP was not activated. Although TP is class I recommendation in clinical guidelines for symptomatic bradyarrhythmias unresponsive to medical treatment in patients with STEMI [35], the literatures supporting TP for inferior STEMI are sparse. Since it may be ethically difficult to randomly allocate patients with symptomatic bradyarrhythmias into the non-TP group, further well-conducted retrospective studies including registry data are warranted to confirm our results.

Conclusions

Statin use at admission, HAVB at admission, and TIMI-thrombus grade ≥3 were closely associated with insertion of TP in patients with inferior STEMI. Patients with TP showed a higher incidence of RV infarction and a longer period of hospital stay than patients without, but the incidence of in-hospital death and long-term MACE was not different.

Acknowledgements

The authors acknowledge all staff in the catheter laboratory and cardiology units in Jichi Medical University, Saitama Medical Center for their technical support in this study.

References

MHanssen, YCottin, KKhalife, LHammer, PGoldstein, EPuymirat, et al. French Registry on Acute ST-elevation and non ST-elevation Myocardial Infarction 2010. FAST-MI 2010. Heart. 2012; 98: 699705. 10.1136/heartjnl-2012-301700 .

DMZhang, SChen. In-Stent Restenosis and a Drug-Coated Balloon: Insights from a Clinical Therapeutic Strategy on Coronary Artery Diseases. Cardiol Res Pract. 2020; 2020: 8104939. 10.1155/2020/8104939 .

HLNguyen, DLessard, FASpencer, JYarzebski, JCZevallos, JMGore, et al. Thirty-year trends (1975–2005) in the magnitude and hospital death rates associated with complete heart block in patients with acute myocardial infarction: a population-based perspective. Am Heart J. 2008; 156: 227233. 10.1016/j.ahj.2008.03.011 .

UJGang, AHvelplund, SPedersen, AIversen, CJøns, SZAbildstrøm, et al. High-degree atrioventricular block complicating ST-segment elevation myocardial infarction in the era of primary percutaneous coronary intervention. Europace. 2012; 14: 16391645. 10.1093/europace/eus161 .

SGómez-Talavera, DVivas, MJPerez-Vizcayno, RHernández-Antolín, AFernández-Ortíz, CBañuelos, et al. Prognostic implications of atrio-ventricular block in patients undergoing primary coronary angioplasty in the stent era. Acute Card Care. 2014; 16: 18. 10.3109/17482941.2013.869343 .

HLKim, SHKim, JBSeo, WYChung, JHZo, MAKim, et al. Influence of second- and third-degree heart block on 30-day outcome following acute myocardial infarction in the drug-eluting stent era. Am J Cardiol. 2014; 114: 16581662. 10.1016/j.amjcard.2014.08.038 .

SNLee, YMHwang, GHKim, JHKim, KDYoo, CMKim, et al. Primary percutaneous coronary intervention ameliorates complete atrioventricular block complicating acute inferior myocardial infarction. Clin Interv Aging. 2014; 9: 20272031. 10.2147/CIA.S74088 .

DJSlotwiner, MHRaitt, FDel-Carpio Munoz, SKMulpuru, NNasser, PNPeterson. Impact of Physiologic Pacing Versus Right Ventricular Pacing Among Patients With Left Ventricular Ejection Fraction Greater Than 35%: A Systematic Review for the 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2019; 74: 9881008. 10.1016/j.jacc.2018.10.045 .

JMerrer, BDe Jonghe, FGolliot, JYLefrant, BRaffy, EBarre, et al. Complications of femoral and subclavian venous catheterization in critically ill patients: a randomized controlled trial. Jama. 2001; 286: 700707. 10.1001/jama.286.6.700 .

10 

YMHwang, CMKim, KWMoon. Periprocedural temporary pacing in primary percutaneous coronary intervention for patients with acute inferior myocardial infarction. Clin Interv Aging. 2016; 11: 287292. 10.2147/CIA.S99698 .

11 

FVYTjong, UWde Ruijter, NEGBeurskens, REKnops. A comprehensive scoping review on transvenous temporary pacing therapy. Neth Heart J. 2019; 27: 462473. 10.1007/s12471-019-01307-x .

12 

YYaqub, APerez-Verdia, LAJenkins, SSehli, RLPaige, KMNugent. Temporary Transvenous Cardiac Pacing in Patients With Acute Myocardial Infarction Predicts Increased Mortality. Cardiol Res. 2012; 3: 17. 10.4021/cr111w .

13 

KThygesen, JSAlpert, ASJaffe, BRChaitman, JJBax, DAMorrow, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018; 72: 22312264. 10.1016/j.jacc.2018.08.1038 .

14 

TTsukui, KSakakura, YTaniguchi, KYamamoto, HWada, SIMomomura, et al. Determinants of short and long door-to-balloon time in current primary percutaneous coronary interventions. Heart Vessels. 2018; 33: 498506. 10.1007/s00380-017-1089-x .

15 

GRACE investigators. Rationale and design of the GRACE (Global Registry of Acute Coronary Events) Project: a multinational registry of patients hospitalized with acute coronary syndromes. Am Heart J. 2001; 141: 190199. 10.1067/mhj.2001.112404 .

16 

MSemelka, JGera, SUsman. Sick sinus syndrome: a review. Am Fam Physician. 2013; 87: 691696. .

17 

DHSpodick. Normal sinus heart rate: sinus tachycardia and sinus bradycardia redefined. Am Heart J. 1992; 124: 11191121. 10.1016/0002-8703(92)91012-p .

18 

KYamamoto, KSakakura, NAkashi, YWatanabe, MSeguchi, YTaniguchi, et al. Association of slow flow with clinical factors in intravascular ultrasound-guided percutaneous coronary intervention for patients with left main trunk-acute myocardial infarction. J Cardiol. 2020; 75: 5359. 10.1016/j.jjcc.2019.06.008 .

19 

MSeguchi, KSakakura, TTsukui, KYamamoto, YTaniguchi, HWada, et al. Determinants of In-Hospital Death Among the Very Elderly with Acute Myocardial Infarction. Int Heart J. 2020; 61: 879887. 10.1536/ihj.20-165 .

20 

MNoguchi, KSakakura, NAkashi, YAdachi, YWatanabe, YTaniguchi, et al. The Comparison of Clinical Outcomes Between Inferior ST-Elevation Myocardial Infarction with Right Ventricular Infarction Versus Without Right Ventricular Infarction. Int Heart J. 2019; 60: 560568. 10.1536/ihj.18-515 .

21 

SMatsuo, EImai, MHorio, YYasuda, KTomita, KNitta, et al. Revised equations for estimated GFR from serum creatinine in Japan. Am J Kidney Dis. 2009; 53: 982992. 10.1053/j.ajkd.2008.12.034 .

22 

CMGibson, JAde Lemos, SAMurphy, SJMarble, CHMcCabe, CPCannon, et al. Combination therapy with abciximab reduces angiographically evident thrombus in acute myocardial infarction: a TIMI 14 substudy. Circulation. 2001; 103: 25502554. 10.1161/01.cir.103.21.2550 .

23 

ZAKaimkhani, MMAli, AMFaruqi. Pattern of coronary arterial distribution and its relation to coronary artery diameter. J Ayub Med Coll Abbottabad. 2005; 17: 4043. .

24 

GFemia, AFaour, JAssad, LSharma, HIdris, OGibbs, et al. Comparing the clinical and prognostic impact of proximal versus nonproximal lesions in dominant right coronary artery ST-elevation myocardial infarction. Catheter Cardiovasc Interv. 2020. 10.1002/ccd.29245 .

25 

YBirnbaum, SSclarovsky, IHerz, BZlotikamien, AChetrit, LOlmer, et al. Admission clinical and electrocardiographic characteristics predicting in-hospital development of high-degree atrioventricular block in inferior wall acute myocardial infarction. Am J Cardiol. 1997; 80: 11341138. 10.1016/s0002-9149(97)00628-0 .

26 

SBehar, EZissman, MZion, UGoldbourt, HReicher-Reiss, YShalev, et al. Complete atrioventricular block complicating inferior acute wall myocardial infarction: short- and long-term prognosis. Am Heart J. 1993; 125: 16221627. 10.1016/0002-8703(93)90750-4 .

27 

MHJim, AOChan, HFTse, CPLau. Predictors of inhospital outcome after acute inferior wall myocardial infarction. Singapore Med J. 2009; 50: 956961. .

28 

VAuffret, ALoirat, GLeurent, RPMartins, EFilippi, ICoudert, et al. High-degree atrioventricular block complicating ST segment elevation myocardial infarction in the contemporary era. Heart. 2016; 102: 4049. 10.1136/heartjnl-2015-308260 .

29 

IHTanboga, STopcu, EAksakal, KKalkan, SSevimli, MAcikel. Determinants of angiographic thrombus burden in patients with ST-segment elevation myocardial infarction. Clin Appl Thromb Hemost. 2014; 20: 716722. 10.1177/1076029613483169 .

30 

THiro, TKimura, TMorimoto, KMiyauchi, YNakagawa, MYamagishi, et al. Effect of intensive statin therapy on regression of coronary atherosclerosis in patients with acute coronary syndrome: a multicenter randomized trial evaluated by volumetric intravascular ultrasound using pitavastatin versus atorvastatin (JAPAN-ACS [Japan assessment of pitavastatin and atorvastatin in acute coronary syndrome] study). J Am Coll Cardiol. 2009; 54: 293302. 10.1016/j.jacc.2009.04.033 .

31 

ITaguchi, KOda, SYoneda, MKageyama, TKanaya, SToyoda, et al. Evaluation of serial changes in tissue characteristics during statin-induced plaque regression using virtual histology-intravascular ultrasound studies. Am J Cardiol. 2013; 111: 12461252. 10.1016/j.amjcard.2013.01.265 .

32 

TToi, ITaguchi, SYoneda, MKageyama, AKikuchi, MTokura, et al. Early effect of lipid-lowering therapy with pitavastatin on regression of coronary atherosclerotic plaque. Comparison with atorvastatin. Circ J. 2009; 73: 14661472. 10.1253/circj.cj-08-1051 .

33 

HJinnouchi, KSakakura, HWada, KIshida, KArao, NKubo, et al. Effect of chronic statin treatment on vascular remodeling determined by intravascular ultrasound in patients with acute myocardial infarction. Am J Cardiol. 2014; 113: 924929. 10.1016/j.amjcard.2013.11.054 .

34 

KHibi, KKozuma, SSonoda, TEndo, HTanaka, HKyono, et al. A Randomized Study of Distal Filter Protection Versus Conventional Treatment During Percutaneous Coronary Intervention in Patients With Attenuated Plaque Identified by Intravascular Ultrasound. JACC Cardiovasc Interv. 2018; 11: 15451555. 10.1016/j.jcin.2018.03.021 .

35 

PTO’Gara, FGKushner, DDAscheim, DECaseyJr., MKChung, JAde Lemos, 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. Circulation. 2013; 127: e362425. 10.1161/CIR.0b013e3182742cf6 .