Second peak of myocardial markers predicts in-hospital adverse outcomes after primary PCI for ST-segment elevation myocardial infarction

doi:10.21203/rs.3.rs-4668201/v1

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Research Article

Second peak of myocardial markers predicts in-hospital adverse outcomes after primary PCI for ST-segment elevation myocardial infarction

https://doi.org/10.21203/rs.3.rs-4668201/v1

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Background

A second peak of high-sensitivity cardiac troponin T (hs-cTnT) after reperfusion therapy in acute myocardial infarction (AMI) patients was reported, while the causes and clinical meanings remain controversial.

Methods

In this retrospective study, we enrolled patients diagnosed with ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (PPCI). The association between second peak of myocardial markers, including creatine kinase-MB (CK-MB) and hs-cTnT and clinical outcomes, D-dimer (D-D), cardiac structure and function were analyzed. The main study outcome was in-hospital major adverse cardiovascular events (MACE), including cardiac death, non-fatal AMI, revascularization and stroke.

Results

A total of 264 patients were included in the study, with an average age of 63 ± 12 years. Of these, 220 were male. Second peak of cardiac markers including hs-cTnT and CK-MB of STEMI patients after PPCI was universal: The proportion of STEMI patients with secondary elevation of cardiac troponin T (cTnT) was 62.8%, while CK-MB 28.8%. Maximum D-D during hospitalization independently predicted second myocardial markers elevation. STEMI patients with second cardiac markers elevation after PPCI had a worse in-hospital composite endpoint.

Conclusions

D-D was an independent predictor of secondary cardiac markers elevation in STEMI patients after PPCI. Patients with second peak of cardiac markers had a worse outcome.

STEMI

cardiac markers

second peak

prognosis

Despite significant improvements in pharmacotherapy, reperfusion strategies, and mechanical interventions for ST-segment elevation myocardial infarction (STEMI) over the past two decades, morbidity and mortality remain high. Multiple factors including severe target lesion calcifications^[1], no reperfusion^[2] after percutaneous coronary intervention (PCI) and the extent of infarcted area^[3] had an influence on the prognosis.

As biomarkers of myocardial infarction, cardiac troponin (cTN) and creatine kinase-MB (CK-MB) have been widely used in clinical practice and play an important role in the diagnosis of acute myocardial infarction (AMI). Troponin is the gold standard myocardial marker of myocardial injury, with high sensitivity and specificity. CK-MB is less sensitive than cTN, but the two can be used in combination to diagnose acute coronary syndrome (ACS) more rapidly ^[4]. The level of cTN and CK-MB after PCI has been shown to predict the prognosis of AMI patients by previous studies ^[5–8]. Moreover, studies have found that CK-MB has a greater predictive value for prognosis than cardiac troponin T (cTnT) in patients with NSTEMI after PCI ^[9].

In recent years, a second peak of hs-cTnT after PCI of STEMI had been reported ^{[10, 11]} and its influence on prognosis remained controversial. A previous study found that a second peak was closely related to infarct size and microvascular obstruction^[12], while another study claimed that the secondary hs-cTnT elevation had no obvious association with poorer outcome in the 4 years’ follow-up^[13].

In this study, we found that both cTnT and CK-MB had secondary elevation after PPCI in STEMI patients, and it may be more objective to judge their clinical significance by combining the secondary elevation of both cTnT and CK-MB. Also, we aimed to find the possible factors influencing the secondary elevation of cTnT and CK-MB and evaluate the prognostic values in this research.

Study design and patient selection

As previously reported ^[14], we retrospectively screened consecutive STEMI patients who underwent primary PCI at Zhongshan Hospital Fudan University between January 2008 and December 2018. Diagnosis criteria for STEMI refered to the Fourth Universal Definition of Myocardial Infarction (2018) ^[15]. A total of 1355 patients were screened and 190 patients were excluded for the following reasons: aortic dissection (n = 3); history of coronary artery bypass graft surgery (CABG, n = 6); complications during procedure (1 death and 1 hemorrhagic stroke); medical therapy or CABG after angiography per patient’s choice (n = 63); only percutaneous transluminal coronary angioplasty (PTCA) without stent implantation due to small vessel or angiographically evident thrombus (AET) (n = 27); and myocardial infarction with no obstructive coronary atherosclerosis (MINOCA, n = 89). Finally, 1165 patients were identified and 264 patients between January 2018 and December 2018 with continuous myocardial biomarkers were analyzed. This study was approved by the Ethics Committee of Zhongshan Hospital Fudan university (B2022-246R) and adhered to the principles of Helsinki Declaration. All participants themselves or their legally authorized representatives signed the informed consent after admission.

Laboratory testing and echocardiography

Upon admission to the hospital, patients immediately underwent laboratory tests, including cTnT, CK-MB, Brain natriuretic peptide (BNP), D-dimer (D-D) and C-reactive protein (CRP). Subsequent follow-ups to retest these indicators were conducted daily or every other day based on the patient’s condition, until they decreased to an acceptable range. According to previous studies, a second increase of cTnT was defined as a rise of 15% after an initial decrease following primary PCI ^[13]. Since CK-MB is less sensitive than cTnT, the second increase of CK-MB was defined as any rise after an initial decrease. All the laboratory assays were performed by the central laboratory at our hospital. Echocardiography was performed within 24 hours of admission and left ventricular ejection fraction (LVEF) was determined.

Coronary angiography and PCI

All patients received a chewable loading dose of aspirin (300mg) and P2Y12 antagonist (300mg clopidogrel or 180mg ticagrelor) upon the diagnosis of STEMI, and the primary PCI procedures were performed by experienced cardiologists. A total of 2500IU heparin was administered after successful puncture, and a weight dependent dose (up to 100 IU/kg) was added for PCI. After angiography, blood flow in the infarct-related artery was graded according to the Thrombolysis in Myocardial Infarction (TIMI) classification ^[16], and no-reflow phenomenon was defined as a coronary TIMI grade flow < 3 after vessel reopening. If there was AET, defined as the presence of an angiographically apparent luminal filling defect as described previously^{[17, 18]}, thrombus aspiration was performed. All other procedures and decisions, including radial/femoral approach, use of glycoprotein IIb/IIIa inhibitors and interventional strategy were at operator’s discretion.

Study outcomes

The main study outcome was in-hospital major adverse cardiovascular events (MACE), including cardiac death, recurrent AMI, revascularization and stroke.

Data analysis

SPSS 27.0.0 software was used for data analysis. Baseline values were expressed as mean ± standard deviation (SD) for normally distributed data, while non-normally distributed data as median (interquartile range (IQR)). The categorical variables were described by quantity and percentage n (%). The independent t-test were used to compare continuous variables for normally distributed data, and non-parametric test for non-normally distributed data, while categorical variables were tested by chi-square test. We first used univariate logistic regression analysis to analyze the common factors that may affect the second increase of myocardial markers, and then multivariate regression analysis to identify the influence factors. Receiver operating characteristic (ROC) curve was used to evaluate the D-D value in predicting the secondary elevation of myocardial enzymes. P < 0.05 was considered statistically significant.

Baseline characteristics

As shown in Table1, the average age of selected patients was 63±12 years old, including 220 male patients, accounting for 85.6% of the total number. Among them, patients with hypertension accounted for 58.7%, diabetes for 32.2%, and smokers 36.4%. Secondary elevation of CK-MB occurred in 76 (28.8%) of these patients and secondary elevation of cTnT occurred in 103 (39.0%). And 43 (16.3%) patients had secondary elevation of both cTnT and CK-MB.

Table 1. Characteristics of the overall population.

Variables	N=264
Baseline characteristics
Age (years)	63±12
Male, n (%)	220 (85.6)
Risk factors
Hypertension, n (%)	155 (58.7)
Diabetes, n (%)	85 (32.2)
Smoker, n (%)	96 (36.4)
Laboratory examinations
CRP on admission (mg/L) (Median (IQR))	7 (1.65-28.5)
D-D on admission (mg/L) (Median (IQR))	0.48 (0.26-1.72)
Peak D-D (mg/L) (Median (IQR))	2.2 (0.76-6.9)
Peak CKMB (U/L) (Median (IQR))	72 (53-90)
Peak cTnT (ng/ml) (Median (IQR))	4.3 (1.4-7.1)
Peak BNP (pg/ml) (Median (IQR))	1535.0 (744.8-5145.5)
CKMB second peak, n (%)	76 (28.8)
cTnT second peak, n (%)	103 (39.0)
Both CKMB and cTnT second peak, n (%)	43 (16.3)
LVEF (%) (Median (IQR))	53 (49-57)
Coronary angiogram characteristics
Tirofiban before stent, n (%)	89 (33.7)
No-reflow phenomenon, n (%)	28 (10.6)
AET, n (%)	113 (42.8)
Tirofiban after stent, n (%)	201 (76.1)

Abbreviations: IQR, Interquartile Range; CRP, C-reactive protein; CK-MB, creatine Kinase MB; cTnT, cardiac troponin T; BNP, Brain natriuretic peptide; LVEF, left ventricular ejection fraction; AET, angiographically evident thrombus.

Characteristics of patients with secondary elevation of myocardial enzyme

The patients were grouped based on secondary increase of cTnT and CK-MB and the characteristics were shown in Table 2. In the cTnT-based grouping, the maximum cTnT in the second peak group was significantly lower than that in no-second peak group (1.7 [0.4-5.0] vs 2.8 [0.7-7.3], P=0.03), while no significant difference was found in other variables, including the MACE rate. In the CK-MB-based grouping, patients were more likely to be elder in second peak group. The D-D at admission in the second peak group (0.53 [0.26-1.47]) was significantly higher than that in no-second peak group (0.34 [0.21-0.53]) (P<0.001). In addition, the comparisons of maximum D-D, cTnT, BNP and LVEF showed similar results. The in-hospital stay in the second peak group was longer than no-second peak group (11.0 [8.0-16.0] vs 7.0 [6.0-8.0], P<0.001). The MACE rate was higher in the second peak group (9.2% vs 1.6%, p=0.011).

Table 2. Characteristics of the overall population by second peak of cTnT/CK-MB

*Parameters*	cTnT			CK-MB
*Parameters*	No second peak (N=161)	Second peak (N=103)	P value	No second peak (N=188)	Second peak (N=76)	P value
Age	62.9±11.2	63.9±12.4	0.468	62.0±11.0	66.4±12.7	0.006
Male, n (%)	136 (84.5)	84 (81.6)	0.532	158 (84.0)	62 (81.6)	0.627
Hypertension, n (%)	90 (55.9)	65 (63.1)	0.246	108 (57.4)	47 (61.8)	0.511
Diabetes, n (%)	52 (32.3)	33 (32.0)	0.965	56 (29.8)	29 (38.2)	0.188
Smoke, n (%)	89 (55.3)	56 (54.4)	0.885	104 (55.3)	41 (52.9)	0.839
CRP on admission (mg/L)	4.8 (1.5-20.0)	5.0 (1.5-12.6)	0.379	4.1 (1.43-13.4)	6.4 (1.85-28.7)	0.058
D-D on admission (mg/L)	0.37 (0.20-0.79)	0.35 (0.22-0.62)	0.806	0.34 (0.21-0.53)	0.53 (0.26-1.47)	<0.001
Peak D-D (mg/L)	0.69 (0.33-2.26)	0.92 (0.41-2.21)	0.517	0.60 (0.34-1.45)	2.04 (0.86-6.513)	<0.001
Peak BNP (pg/ml)	1123.0 (667.6-2994.5)	1146.0 (635.8-2957.0)	0.854	973.9 (618.0-2531.7)	2530.5 (889.6-5473.8)	0.000
Peak CKMB (U/L)	62.0 (47.0-83.5)	66.0 (53.0-87.0)	0.217	62.5 (49.3-84.8)	66 (46-87)	0.788
Peak cTnT (ng/ml)	2.800 (0.744-7.340)	1.740 (0.419-4.970)	0.030	2.15 (0.50-5.85)	3.70 (1.07-6.69)	0.026
LVEF (%)	53.0 (48.5-57.0)	52.5 (49.0-58.0)	0.964	54.0 (50.0-58.0)	52.5 (46.0-55.0)	0.040
No-reflow phenomenon, n (%)	21 (13.0)	7 (6.8)	0.108	17 (9.0)	11 (14.5)	0.194
AET, n (%)	74 (46.0)	39 (37.9)	0.195	78 (41.5)	35 (46.1)	0.497
Tirofiban before stent, n (%)	58 (36.0)	31 (30.1)	0.320	69 (36.7)	20 (26.3)	0.106
Tirofiban after stent, n (%)	123 (76.4)	78 (75.7)	0.901	149 (79.3)	52 (68.4)	0.061
In-hospital stay (days)	7.0 (6.0-9.5)	7.0 (6.0-10.0)	0.455	7.0 (6.0-8.0）	11.0 (8.0-16.0)	<0.001
MACE, n (%)	6 (3.7)	4 (3.9)	0.948	3 (1.6)	7 (9.2)	0.003

Abbreviations: CRP, C-reactive protein; D-D, D-dimer; BNP, Brain natriuretic peptide; CK-MB, creatine Kinase MB; cTnT, cardiac troponin T; LVEF, left ventricular ejection fraction; AET, angiographically evident thrombus; MACE, major adverse cardiovascular events.

Characteristics of patients with both cTnT and CK-MB secondary elevation group

Then we divided the patients into 2 groups according to whether they had secondary elevations of both cTnT (15% secondary rise) and CK-MB (any secondary rise). The characteristics of the two groups were listed in Table 3. We found no statistically significant differences in mean age, proportion of male, hypertension, diabetes, smoking patients, and CRP value at admission between the two groups, while D-D at admission was significantly higher in the second peak group. In addition, the peak cTnT was also significantly higher (P=0.018), although the peak CK-MB was with similar between 2 groups (P=0.136). In addition, the left ventricular ejection fraction was lower in the second peak group (P=0.042), implying poorer cardiac function. Longer in-hospital stay (P<0.01) and higher incidence of MACE (P=0.038) were observed in the second peak group. There was no significant difference regarding to coronary angiogram characteristics between the two groups (Table3).

Table 3. Characteristics of the overall population by both cTnT and CK-MB secondary peak

*Parameters*	No second peak (N=221)	Second Peak (N=43)	P value
Age	63.0±11.2	65.0±13.8	0.288
Male (n, %)	184 (83.3)	36 (83.7)	0.941
Hypertension (n, %)	132 (59.7)	23 (53.5)	0.447
Diabetes (n, %)	72 (32.6)	13 (30.2)	0.763
Smoker (n, %)	124 (56.1)	21 (48.8)	0.381
CRP on admission(mg/L)	4.4 (1.5-15.8)	7.0 (1.6-29.3)	0.227
D-D on admission(mg/L)	0.35 (0.21-0.58)	0.48 (0.25-1.73)	0.012
Peak D-D (mg/L)	0.69 (0.35-1.76)	2.16 (0.83-6.80)	<0.001
Peak BNP (pg/ml)	1123.0 (637.9-4702.0)	1535.0 (771.6-4674.0)	0.091
Peak CKMB (U/L)	62.0 (48.0-84.0)	72.0 (56.0-90.0)	0.136
Peak cTnT (ng/ml)	2.20 (0.50-5.84)	4.60 (1.70-7.43)	0.018
LVEF (%)	54.0 (50.0-58.0)	52.5 (44.0-54.0)	0.042
No-reflow phenomenon, n (%)	25 (11.3)	3 (7.0)	0.398
AET, n (%)	92 (41.6)	21 (48.8)	0.382
Tirofiban before stent, n (%)	76 (34.4)	13 (30.2)	0.598
Tirofiban after stent, n (%)	171 (77.4)	30 (69.8)	0.284
In-hospital stay (days)	7.0 (6.0-9.0)	11.0 (8.0-14.0)	<0.001
MACE, n (%)	6 (2.7)	4 (9.3)	0.038

Factors influencing the secondary elevation of both cTnT and CK-MB

Logistic regression was performed to investigate the factors influencing the secondary elevation of both CKMB and cTnT (Table 4). Univariate logistic regression analysis showed that peak D-D was a predictor of cardiac enzyme second increase, while intraoperative factors such as AET (OR=1.338; 95% CI: 0.695-2.577; P=0.383) and no-reflow phenomenon after PCI (OR=0.588; 95% CI: 0.169-2.042; P=0.403) had no significant difference in correlation with secondary elevation of myocardial markers. The multivariate analysis showed that independent factors were the third quartile peak D-D (OR=4.4; 95% CI: 1.6-12.3; P=0.005) and the fourth quartile (OR=12.3; 95% CI: 3.7-40.6; P<0.001).

Table 4. Logistic regression analysis of predictors of both CK-MB and cTnT secondary peak

*Parameters*	Univariate		Multivariate
*Parameters*	OR（95%Cl）	P value	OR（95%Cl）	P value
Age
<60	Reference		Reference
(60, 80]	1.752 (0.821-3.740)	0.147	1.378 (0.609-3.120)	0.442
(80, 100]	2.469 (0.812-7.506)	0.111	0.959 (0.261-3.517)	0.949
Male	1.034 (0.428-2.501)	0.941	1.321 (0.506-3.452)	0.569
Hypertension	0.775 (0.402-1.495)	0.448	1.072 (0.513-2.239)	0.853
Diabetes	0.897 (0.441-1.822)	0.763	0.704 (0.319-1.553)	0.385
Smoke	0.747 (0.388-1.437)	0.382	1.058 (0.52-2.154)	0.877
Peak D-D
(0, 0.76]	Reference		Reference
(0.76, 2.2]	2.786 (1.240-6.576)	0.013	2.400 (0.940-6.129)	0.067
(2.2, 6.9]	7.571 (2.796-20.498)	0.000	4.403 (1.582-12.251)	0.005
>6.9	7.800 (1.16-52.26)	0.034	12.251 (3.701-40.552)	<0.001
No-reflow phenomenon	0.588 (0.169-2.042)	0.403	0.556 (0.161-1.922)	0.354
AET	1.338 (0.695-2.577)	0.383	0.876 (0.401-1.915)	0.740
Tirofiban before stent	0.827 (0.407-1.677)	0.598	0.771 (0.321-1.851)	0.561
Tirofiban after stent	0.675 (0.327-1.391)	0.286	0.969 (0.396-2.376)	0.946

Abbreviations: D-D, D-dimer; AET, angiographically evident thrombus.

D-D to predict second peak of both cTnT and CK-MB

D-D at admission and maximum D-D were used to plot ROC curves to analyze their predictive value for secondary elevation of myocardial enzyme profiles. As shown in Figure 1, AUC of admission D-D is 0.621 (specificity=0.878, sensibility=0.395, best cutoff value=1.07), while AUC of peak D-D is 0.684 (specificity=0.633, sensibility=0.721, best cutoff value=1.13).

In this study, our demonstrations are as follows: (1) We find a high proportion of secondary elevation of cTnT and CK-MB in STEMI patients after PPCI. (2) A second peak of cardiac markers is associated with worse composite endpoints during hospitalization. (3) Intraoperative factors such as thrombotic load indicated by coronary angiography and no-reflow phenomenon after PCI had no significant correlation with secondary elevation. (4) Peak plasma D-dimer level independently predicts second peak of cardiac markers.

As early as 1991, a study by Hugo A. Katus marked the first documentation of cardiac troponin T (cTnT) dynamics in patients with acute myocardial infarction (AMI) who received thrombolytic therapy within 3.5 hours of chest pain onset. This study delineated that the initial peak of cTnT appeared approximately 14 hours post-onset, succeeded by a rapid clearance from the circulation, until a resurgence occurred, with a second peak appeared on the fourth day^[19]. In contrast, research conducted by Guillaume Laugaudin et al. observed that in ST-segment elevation myocardial infarction (STEMI) patients treated with percutaneous coronary intervention (PCI), creatine kinase (CK) and troponin I (TnI) levels exhibited a singular peak followed by a log-linear decline, without any secondary increase. Conversely, cTnT levels demonstrated a transient decrease post-initial peak, followed by a plateau and a second peak at around 77 h, thus presenting a diphasic wave^[10]. Another investigation reported a secondary elevation in cTnT levels in 57.8% of STEMI patients after an average of 4.48 days post-admission, while noting an absence of secondary elevation in CK-MB levels^[13], contrary to our findings, which indicated a secondary rise in both markers. Studies had shown that both intact cTnT and its fragments existed in AMI patients after reperfusion therapy, and intact cTnT was rapidly cleared in circulation in the early stage, while its fragments still existed for a long time, which might be the reason for the second peak value of cTnT^[20]. However, the direct mechanisms underlying the secondary rise in cardiac biomarkers are yet to be elucidated comprehensively.

Studies had shown that the secondary increase of troponin was strongly correlated with myocardial infarction size and microvascular occlusion^[12]. The secondary increase of troponin could predict microvascular occlusion（MVO）, and patients with MVO were more likely to have the secondary increase of cTnT^[21]. In Tau S. Hartikainen’s study, after 4 years of follow-up, the authors found no significant difference in all-cause mortality between the group with and without secondary cTnT elevation^[13]. Another previous study showed that elevated CK-MB after PCI is more predictive of prognosis than cTnT^[22]. Our study found that the secondary elevation of both cTnT and CK-MB was associated with compound events in hospital, suggesting that clinical attention should be paid to whether these two indicators were elevated simultaneously. In our study, we categorized patients based on whether there was a secondary increase in cTnT levels, and found no significant difference in clinical outcomes between the groups, consistent with previous research outcomes. However, when grouping was based on a secondary increase in CK-MB levels or on a secondary increase in both cTnT and CK-MB levels, significant differences in clinical outcomes were observed. This suggested that the secondary rise in cTnT might be attributed to its higher sensitivity. Hence, focusing solely on the rise in cTnT could lead to excessive diagnostics and treatment. Our findings indicated that further research is necessary, and the changes in cTnT levels alone should not be used as the sole predictor of prognosis. Incorporating changes in CK-MB appeared to be more meaningful.

According to findings from our previous research, elevated D-dimer levels were associated with adverse outcomes during hospitalization for patients who had experienced a myocardial infarction and subsequently undergone primary PCI^[14]. Existing literature also indicated that an increase in D-dimer levels might predict the occurrence of the no-reflow phenomenon following PCI in patients with ST-segment elevation myocardial infarction (STEMI)^{[23, 24]}, and it could independently predict MACE events^[24]. In our investigation, we found that the plasma D-D level was significantly associated with a secondary increase in myocardial markers. Patients with higher D-D were more likely to have a second peak of cardiac enzymes and correspondingly a poorer prognosis. Nonetheless, our research did not establish a significant correlation between the no-reflow phenomenon and secondary elevations in troponin T levels, suggesting that additional studies are warranted to further explore this relationship.

In conclusion, d-dimer is an independent predictor of second cardiac markers elevation in STEMI patients after reperfusion. Patients with second peak of cardiac markers have a worse outcome.

Study limitations

The present study has several limitations. First, this was a single center and retrospective study. Second, the study observation time was limited to in-hospital stay; therefore, analysis of long-term prognosis is warranted. Finally, factors such as total ischemic time, culprit lesion characteristics and procedural details were not analyzed because of insufficient data.

cTN: cardiac troponin

cTnT; cardiac troponin T

TnI: troponin I

AMI: acute myocardial infarction

STEMI: ST-segment elevation myocardial infarction

PPCI: primary percutaneous coronary intervention

CK-MB: creatine Kinase MB

D-D: D-dimer

MACE: major adverse cardiovascular events

PCI: percutaneous coronary intervention

ACS: acute coronary syndrome

CABG: coronary artery bypass graft surgery

PTCA: percutaneous transluminal coronary angioplasty

AET: angiographically evident thrombus

MINOCA: myocardial infarction with no obstructive coronary atherosclerosis

BNP: Brain natriuretic peptide

CRP: C-reactive protein

LVEF: left ventricular ejection fraction

TIMI: Thrombolysis in Myocardial Infarction

SD: standard deviation

IQR: interquartile range

ROC: Receiver operating characteristic

MVO: microvascular occlusion

Ethical approval and Consent to participate

The study protocol was approved by the Ethics Committee of Zhongshan Hospital Fudan university (B2022-246R) and adhered to the principles of Helsinki Declaration. All involved patients or their legally authorized representatives signed the consent to participate in this observational study.

Consent for publication

All authors have reviewed the manuscript and given their approval for publication.

Conflict of interest

The authors have no conflicts of interest to disclose.

Funding

This study was supported by the Natural Science Foundation of Shanghai, Grant 21ZR1412700.

Authors' contributions

Niu X, Ma Y and Cui X performed all the data analysis and wrote the main manuscript text. Xia Y, Wu S, Zhang M and Chen Y contributed to design figure 1 and table 1-4. Guan L and Wu H provided essential theoretical insights, revised the manuscript and conducted final approval of the manuscript submitted. All authors reviewed the manuscript.

Acknowledgements

Not applicable

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No competing interests reported.

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Editorial decision: Revision requested
26 Jul, 2024
Editor assigned by journal
23 Jul, 2024
Submission checks completed at journal
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01 Jul, 2024

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Second peak of myocardial markers predicts in-hospital adverse outcomes after primary PCI for ST-segment elevation myocardial infarction

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Abstract

Background

Methods

Results

Conclusions

Figures

Introduction

Materials and methods

Study design and patient selection

Laboratory testing and echocardiography

Coronary angiography and PCI

Study outcomes

Data analysis

Results

Discussion

Abbreviations

Declarations

References

Additional Declarations

Status:

Version 1