Background

Periprocedural myocardial injury is a predictor of cardiovascular morbidity and mortality after percutaneous coronary intervention.

Methods

The authors examined the effects of preprocedural lipid levels (low-density lipoprotein, high-density lipoprotein, and triglycerides) in 977 patients with coronary artery disease who underwent elective percutaneous coronary intervention.

Results

Elevated cardiac troponin I level (≥5× the upper limit of normal) was used to indicate periprocedural myocardial injury. Serum lipid samples were collected 12 hours preprocedurally. Cardiac troponin I was collected 1, 6, and 12 hours postprocedurally. Correlations between preprocedural lipid levels and postprocedural cardiac troponin I were studied. Low-density lipoprotein levels were less than 70 mg/dL in 70% of patients and greater than 100 mg/dL in only 7.4% of patients; 13% had triglyceride levels greater than or equal to 150 mg/dL, and 96% had high-density lipoprotein levels less than 40 mg/dL. Patients with elevated cardiac troponin I had significantly lower left ventricular ejection fraction than did those with cardiac troponin I levels less than 5× the upper limit of normal (P = .01). Double-and triple-vessel disease were more common in patients with elevated cardiac troponin I (P < .002). Multivariable logistic and linear regression analyses revealed no statistically significant associations between lipid levels and postprocedural cardiac troponin I elevation, possibly because such large proportions of included patients had low levels of low-density lipoprotein (70%) and a history of statin intake (86%).

Conclusion

The authors found no association between lipid profile and periprocedural myocardial injury.

Coronary artery disease (CAD) is a substantial global health problem and is considered the leading cause of death worldwide.1  Percutaneous coronary intervention (PCI) is the most common invasive cardiology treatment performed to treat CAD the world over.2 

The incidence of periprocedural myocardial injury (infarction) has not fallen substantially despite technological advances and effective medical treatment.3  Many clinical studies have shown that periprocedural myocardial injury is a predictor of adverse clinical outcomes after PCI. According to the Global Working Group on Myocardial Infarction (comprising members of the European Society of Cardiology and the American Heart Association), one of the criteria for defining periprocedural myocardial injury is an elevation in serum biomarkers (specifically, cardiac troponin).4  Cardiac troponins are sensitive, specific markers of myocardial necrosis, and troponin elevation portends an increase in long-term all-cause mortality and related adverse events that underlie periprocedural myocardial injury.57 

Dyslipidemia is an independent risk factor for CAD. Clinical trials have shown that elevated levels of serum low-density lipoprotein (LDL) cholesterol and low levels of serum high-density lipoprotein (HDL) cholesterol are linearly associated with CAD and that aggressive therapy to lower LDL levels reduces the frequency of adverse outcomes in patients with CAD.811  Previous debate about the role of elevated triglyceride (TG) levels in CAD has given way to new data showing that hypertriglyceridemia is indeed an independent risk factor for CAD.12,13  What remains unclear is whether aggressive treatment aiming to improve the lipid profile before intervention can further diminish periprocedural myocardial injury and enhance outcomes and prognosis in patients with stable CAD who are undergoing elective PCI.

In this study, the authors evaluated preprocedural LDL, HDL, and TG levels to determine their effect, if any, on periprocedural myocardial injury in patients undergoing elective PCI.

This prospective, single-center study recruited consecutive patients with a primary diagnosis of stable CAD who underwent percutaneous revascularization between March 1, 2019, and February 29, 2020, at Rajaie Cardiovascular Medical and Research Center, Tehran, Iran. Patients were eligible for inclusion if they exhibited stable angina with normal cardiac troponin I (cTnI) levels before the procedure. Patients with recent myocardial infarction or incomplete lipid profile data were excluded.

Experienced interventional cardiologists performed all PCI procedures in accordance with the latest guidelines from the American College of Cardiology and the American Heart Association, which recommend aspirin, clopidogrel, and moderate- to high-intensity statin therapy.14  Before the procedure, all patients received a loading dose of 300 mg of aspirin irrespective of whether they were already on daily aspirin therapy. The day before the procedure, patients on daily clopidogrel received a clopidogrel loading dose of 300 mg; patients not on daily clopidogrel received a 600-mg loading dose. At the beginning of angioplasty, a 100-U/kg bolus of intravenous unfractionated heparin was injected. Additional boluses of 2,000 to 3,000 U were given every hour if the procedure lasted for more than 1 hour, up to a maximum dose of 10,000 U. All participants underwent continuous electrocardiographic monitoring before, during, and after PCI to detect possible ischemic events.

Baseline samples for the serum lipid profile, including LDL, HDL, and TG, were collected before PCI after 12 to 14 hours of fasting. Lipid levels were measured using the electroluminescence method with a Hitachi 917 rack chemistry analyzer (Roche). Postprocedural samples for cTnI analysis were collected 1, 6, and 12 hours after PCI and were analyzed using the chemiluminescence immunoassay method with an Abbott ARCHITECT analyzer.

Diagnoses of procedure-related myocardial injury were based on either (1) the development of new pathological Q waves in at least 2 contiguous electrocardiogram leads or (2) cTnI elevation greater than or equal to 5× the upper limit of normal (ULN), according to the Fourth Universal Definition of Myocardial Infarction.6 

The study was performed in accordance with the ethical standards of the Declaration of Helsinki and approved by the Review Board and the Human Ethics Committee of Rajaie Cardiovascular Medical and Research Center. Informed consent was obtained from all participants.

Statistical Analysis

Results are presented as mean (SD) for numerical variables and absolute frequencies and percentages for categorical variables. The numerical variables were compared by using the independent 2-sample t test or 1-way analysis of variance between the 2 groups. Categorical variables were compared by using the χ2 test.

For analysis, patients were stratified into various comparator groups, both by preprocedural lipid type and level (LDL, <70, 70–99, or ≥100 mg/dL; HDL, <40 or ≥40 mg/dL; and TG, <150, 150–199, or ≥200 mg/dL) and by peak level of postprocedural cTnI (≥5× the ULN or <5× the ULN).

Multivariable logistic regression analyses were performed to determine the relationship between the baseline clinical parameters (LDL, HDL, and TG) and elevated postprocedural cTnI (≥5× the ULN). As a sensitivity analysis, the relationships between the clinical parameters and the postprocedural cTnI level (considered a continuous dependent variable rather than a dichotomized variable) were examined by using multivariable linear regression analyses.

In the multivariable regressions, adjustments were made according to clinical judgment and similar studies.15,16  Covariates used in the adjustment included age; sex; the number of diseased vessels subjected to PCI; fasting blood sugar level; creatinine level; left ventricular ejection fraction (LVEF); coronary angiography results; presence of diabetes mellitus, hypertension, bifurcation, chronic total occlusion, or in-stent restenosis; and use of predilation or postdilation. These confounding variables were regarded as preprocedural covariates independently associated with postprocedural cTnI levels.

All P values were considered 2-tailed, with statistical significance set at P < .05. The statistical software SPSS version 22.0 for Windows (SPSS, Inc) was used for the statistical analyses.

During the study period, 1,024 patients at Rajaie Cardiovascular Medical and Research Center had a primary diagnosis of stable CAD and underwent percutaneous revascularization. Of these, 20 patients were excluded because of an elevated baseline cTnI level (indicating previous myocardial infarction) and 27 were excluded because of incomplete lipid profile tests or missing laboratory data. The remaining 977 patients were enrolled, including 697 men (mean [SD] age, 59.8 [10.5] years) and 280 women (mean [SD] age, 62.4 [9.0] years).

Low-Density Lipoprotein

Table I depicts baseline patient characteristics and angiographic and lab data by LDL subgroup. In terms of distribution, LDL less than 70 mg/dL was reported in 681 patients (69.7%), LDL 70 to 99 mg/dL in 224 patients (22.9%), and LDL greater than or equal to 100 mg/dL in 72 patients (7.4%). A higher proportion of patients in all LDL categories were male, and patients in all 3 LDL categories tended to have hypertension (P = .048). Patients with LDL greater than or equal to 100 mg/dL were younger than those in the other groups (P = .01). Other clinical characteristics did not differ significantly by LDL group, nor were there any statistically significant differences in medical therapy by group.

TABLE I

Baseline Clinical and Procedural Characteristics by LDL Cholesterol

Baseline Clinical and Procedural Characteristics by LDL Cholesterol
Baseline Clinical and Procedural Characteristics by LDL Cholesterol

Angiography characteristics did not differ by LDL category, except for chronic total occlusion (P = .04). Preprocedural platelet and hemoglobin levels differed significantly by LDL group (P = .03 and P = .02, respectively). Although patients with LDL greater than 100 mg/dL had a higher platelet level, the level was within the normal range and the difference was not clinically meaningful.

High-Density Lipoprotein

Baseline clinical and procedural characteristics by HDL subgroup are detailed in Table II. In terms of distribution, HDL less than 40 mg/dL was reported in 933 patients (95.5%) and HDL greater than or equal to 40 mg/dL in 44 (4.5%). Patients in either group tended to be nonsmokers (P = .04). Patients with HDL less than 40 mg/dL were more likely to be younger (P = .03) and to be male than were patients with HDL greater than or equal to 40 mg/dL (P = .001). No other statistically significant differences were noted. No correlation was found between HDL and periprocedural myocardial injury in patients with LDL less than 70 mg/dL (β = .018; 95 CI, −.037 to .059; P = .64; R2 = −0.001).

TABLE II

Baseline Clinical and Procedural Characteristics by HDL Cholesterol Group

Baseline Clinical and Procedural Characteristics by HDL Cholesterol Group
Baseline Clinical and Procedural Characteristics by HDL Cholesterol Group

Triglycerides

Demographic, clinical, and angiographic characteristics by TG subgroup are shown in Table III. In terms of distribution, TG less than 150 mg/dL was reported in 855 patients (87.5%), TG 150 to 199 mg/dL in 71 (7.3%), and TG greater than or equal to 200 mg/dL in 51 (5.2%). Patients with TG greater than or equal to 200 mg/dL were more often younger (P < .001), had a higher mean fasting blood sugar level (P = .005), and had a higher frequency of diabetes mellitus (P = .04) than the other groups. Patients in the group with TG less than 150 mg/dL were more likely to be taking aspirin (P = .045). There were no substantial differences in angiography data among these subgroups. Remarkably, we found a positive correlation between TG and LDL levels (β = .311; 95% CI, .056–.090; P < .001; R2 = 0.095), despite the absence of an association between TG and cTnI elevation.

TABLE III

Baseline Clinical and Procedural Characteristics by TG Group

Baseline Clinical and Procedural Characteristics by TG Group
Baseline Clinical and Procedural Characteristics by TG Group

Postoperative Coronary Troponin I Elevation

Table IV compares the baseline clinical and procedural characteristics of the patients with and without elevated cTnI (≥5× the ULN) after the procedure. Most of the patients had a cTnI level less than 5× the ULN (n = 698 vs 279). The patients with elevated cTnI were less likely to have diabetes mellitus (P = .01) but more likely to have had a previous myocardial infarction (P = .002). The remaining clinical characteristics did not differ significantly between the 2 groups. Nevertheless, there were significant differences vis-à-vis coronary angiography results, the number of vessels subjected to PCI, and use of predilation. Patients with double- and triple-vessel disease were more likely to have elevated cTnI (P < .001). All but 1 patient underwent 1 intervention only. One patient exhibited acute symptoms and electrocardiogram changes 6 hours after PCI, at which time cTnI was 3× the ULN. The changes were attributed to acute stent thrombosis, and the patient underwent immediate angioplasty.

TABLE IV

Baseline Clinical and Procedural Characteristics by cTnI Elevation Group

Baseline Clinical and Procedural Characteristics by cTnI Elevation Group
Baseline Clinical and Procedural Characteristics by cTnI Elevation Group

Preoperatively, in-stent restenosis was reported in 61 patients and bifurcation in 156. Bifurcation PCI techniques included provisional stenting in 120/977 patients (12.3%), double-kissing crush in 4/977 (0.4%), mini-crush in 9/977 (1%), T-stenting in 2/977 (0.2%), and culotte in 3/977 (0.3%). Patients with elevated cTnI were more likely to have had predilation (P = .009) or bifurcation (P = .003) and had significantly lower LVEF (P = .01) and higher hemoglobin levels (P = .02). Still, mean hemoglobin levels were within the normal range for physiologic blood concentrations. No statistically significant differences were detected in the LDL, HDL, and TG categories by cTnI group (P = .98, .62, and .20, respectively).

Logistic Regression Analyses

Table V shows the logistic regression analysis results for LDL, HDL, and TG according to elevated post-PCI cTnI (cTnI ≥5× the ULN). Neither the unadjusted nor adjusted logistic regression models found an association between elevated postprocedural cTnI and the various LDL, HDL, and TG categories.

TABLE V

Logistic Regression Analysis of the Impact of Clinical Parameters on Elevated Postprocedural cTnI (≥5× ULN)

Logistic Regression Analysis of the Impact of Clinical Parameters on Elevated Postprocedural cTnI (≥5× ULN)
Logistic Regression Analysis of the Impact of Clinical Parameters on Elevated Postprocedural cTnI (≥5× ULN)

As a sensitivity analysis, the relationships between cTnI elevation in the 12 hours after PCI as a continuous variable (in contrast to a dichotomized variable) and the LDL, HDL, and TG categories were separately explored via multiple linear regression analyses (see Table VI). At 1 and 6 hours after PCI, similar results were obtained for the LDL, HDL, and TG categories, except for a difference in LDL and cTnI in patients without periprocedural myocardial injury at 1 hour post-PCI.

TABLE VI

Multiple Linear Regression Analysis of the Impact of Lipid Profile on Elevated cTnI (≥5× ULN) at the 12th Postprocedural Hour a

Multiple Linear Regression Analysis of the Impact of Lipid Profile on Elevated cTnI (≥5× ULN) at the 12th Postprocedural Hour a
Multiple Linear Regression Analysis of the Impact of Lipid Profile on Elevated cTnI (≥5× ULN) at the 12th Postprocedural Hour a

Periprocedural myocardial injury is a frequent complication during PCI and is strongly associated with postprocedural cardiovascular morbidity and death.17  Major risk factors for periprocedural myocardial injury after PCI can be categorized as patient related, lesion related, or procedure related, all of which contribute equally.18 

Lipid profile was classified as a patient-related factor. Elevated serum LDL is a major cause of CAD and is a key component of coronary plaque development and rupture.19,20  Nevertheless, the existing literature lacks data on the relationship between lipid levels and periprocedural myocardial injury, especially in the present era of statin use. In the present study, the value of the preprocedural lipid profile (LDL, HDL, and TG) in predicting the incidence of periprocedural myocardial injury (evidenced by elevated cTnI) was examined in patients with stable CAD who underwent PCI. This evaluation was performed in a population with a high prevalence of statin intake and better-controlled LDL. No meaningful association between periprocedural myocardial injury and preprocedural lipid levels were found.

Li et al16  investigated the association between preprocedural LDL and periprocedural myocardial injury in 2,529 patients with CAD who underwent elective PCI and found a log-linear relationship between LDL and cTnI levels. These authors concluded that a 1-SD increment in preprocedural LDL increased the risk of postprocedural cTnI elevation by 12% to 20%. Similarly, Buturak et al21  observed a direct connection between preprocedural LDL levels and periprocedural myocardial injury in 195 patients with stable angina pectoris who underwent elective PCI: In that study, elevated LDL or non-HDL levels were positively correlated with postprocedural cTnI levels. Another study found that non-HDL was more valuable than LDL in predicting periprocedural myocardial injury in patients with type 2 diabetes mellitus.22  In the present study, after adjusting for confounding factors in both the logistic and linear regression analyses, the authors found no association between LDL and postprocedural cTnI elevation.

The researchers also found no relationship between HDL and cTnI elevation, even after adjusting for confounding factors. Silbernagel et al23  concluded that HDL was inversely associated with cardiovascular mortality in individuals without CAD but not in patients with CAD. Li et al15  assessed 2,529 patients undergoing elective PCI and found that HDL level was not predictive of periprocedural myocardial injury. However, among patients with LDL less than 70 mg/dL, a 1-mg/dL increase in HDL was associated with a 3% reduction in risk of postprocedural cTnI greater than 3× the ULN. Li et al16  also reported that patients with LDL greater than or equal to 70 mg/dL had higher TG and C-reactive protein levels, which can lead to HDL dysfunction. Barter et al24  evaluated 2,661 participants with LDL less than 70 mg/dL and concluded that higher HDL levels were associated with a lower risk of major cardiovascular events. Moreover, recent data which investigated the atheroprotective potential of HDL particles elucidated that the large HDL particles are linked to a lower number of circulating LDL particles.25,26  The present analysis yielded no correlation between HDL and periprocedural myocardial injury in patients with LDL less than 70 mg/dL (β = .018; 95% CI, −.037 to .059; P = .64; R2 = −0.001).

Jiao et al27  found that plasma TG and HDL exerted a synergistic effect on the occurrence of CAD. When the plasma LDL concentration was less than 130 mg/dL, the risk of CAD was 10 times as high in a population with high TG levels (>263.93 mg/dL) and low HDL concentrations (<25.90 mg/dL) as it was in a population with low TG levels (<59.34 mg/dL) and high HDL concentrations (>64.19 mg/dL). Li et al16  found that HDL levels rose in tandem with a substantial fall in TG. Two other studies on the relationship between pre-procedural LDL and periprocedural myocardial injury reported substantially lower TG levels in a population with lower LDL.16,28  Likewise, the researchers found a positive correlation between TG and LDL (β = .311; 95% CI, .056–.090; P < .001; R2 = 0.095), despite the absence of an association between TG and cTnI elevation.

Evidence showing an association between lipid profile and periprocedural myocardial injury comes from studies on lipid-lowering therapy that compare the effects of different doses of statins on periprocedural myocardial injury. Of note, because many included patients adhered to their long-term statin therapy throughout the perioperative period, the authors studied the baseline lipid profile.

Takano et al29  found that high-dose rosuvastatin reduced the incidence of periprocedural myocardial injury more than low-dose rosuvastatin in statin-naive patients but not in patients who were already taking statins. Herrmann et al30  showed that the incidence of creatine kinase elevation greater than 3× the ULN was more than 90% lower in statin-treated patients (0.4% vs 6.0%) and that statin therapy was the only factor independently associated with a lower risk of creatine kinase elevation greater than 3× the ULN; no substantial differences between statin-treated patients and controls were found in terms of TG, LDL, HDL, total cholesterol, and lipoprotein(a). What remains unclear, however, is whether HDL alterations during statin therapy contribute to considerable cardiovascular risks. In the JUPITER trial, HDL and vascular events were inversely associated in patients on rosuvastatin (20 mg/d), whereas patients receiving placebo exhibited no such association.31  Moreover, in a meta-analysis of 8 statin trials, HDL increase during statin therapy was not associated with reduced risk of major cardiovascular events.32 

In the current study, no substantial interaction between statin therapy and cTnI was found, even after adjustments were made for confounders (Table V). More than 85% of included patients had statins in their medication history. Therefore, this study's findings can be explained by intensive and optimal medical treatment before the procedure, which might have eliminated the effects of lipids on periprocedural myocardial injury.

As for other patient-related factors, results showed a substantial difference pertaining to LVEF between patients with and without post-PCI cTnI elevation. Patients with cTnI greater than or equal to 5× the ULN had a markedly lower mean LVEF (43.3% [10.5%] vs 45.2% [9.7%]; P = .01). Previous research has indicated that patients with increased cTnI have substantially lower LVEF, higher clinical grading of heart failure, and higher mortality rates.33,34  Gili et al35  sought to determine the predictors of periprocedural myocardial injury after PCI and concluded that LVEF was a univariate predictor of major adverse cardiovascular events and death. Mancini et al36  found that despite optimal medical treatment and PCI, LVEF and disease burden at baseline were prognostic of residual risk of secondary ischemic events.

Among procedure-related risk factors, the researchers detected a significant association between cTnI elevation and PCI for bifurcation, one of the more complex PCI procedures. Bifurcation correlated with higher levels of postprocedural cTnI, whereas the authors found no significant association between in-stent restenosis and cTnI elevation. Zhang et al37  found that a true bifurcation lesion was a predictor of occlusion in a small side branch and that patients with small branch occlusions had a substantially higher incidence of periprocedural myocardial injury. Ojeda et al38  concluded that the presence of a bifurcation lesion in the context of chronic total occlusion was linked to a higher incidence of periprocedural myocardial injury. Multivessel PCI and predilation during the procedure also may prompt cTnI elevation and periprocedural myocardial injury: Qadir et al39  showed that elevated cTnI was correlated with the greater severity and larger extent of myocardial ischemic territory during non–ST-segment elevation myocardial infarction.

Study Limitations

The study had several limitations. First, the observational nature of the study might have incorporated bias into the results. Second, the lack of an association between lipid profile and elevated cTnI might have derived from the fact that approximately 70% of the studied population had LDL levels less than 70 mg/dL and only 7% had LDL levels greater than 100 mg/dL. Moreover, 88% of patients had TG levels less than 150 mg/dL, whereas only 5% had TG levels greater than 200 mg/dL. These factors could have lessened the sensitivity of this study.

Lipid levels were not associated with an increased incidence of periprocedural myocardial injury in a sample of patients undergoing elective PCI, possibly because these patients received extensive, optimal medical therapy before the procedure. However, angiographic factors such as a lower LVEF, previous myocardial infarction, and the number of vessels subjected to PCI were associated with cTnI elevation and thus with periprocedural myocardial injury.

Although these findings suggest that, in the current era of intervention with fully optimized medical therapy, lipid profile exerts no influence on periprocedural myocardial injury, this does not agree with the findings of previous investigations. It may be that complex vessel anatomy, procedures, and low LVEF may have more influence on postprocedural outcomes based on cTnI elevation. It is essential to evaluate these data in future multicenter studies with a wider range of patients and a wider distribution of lipid values in both elective and nonelective procedures.

The authors would like to thank the Catheterization Laboratory staff of Rajaie Cardiovascular Medical and Research Center and Maria Elena Vilar Alvarez for their contributions to this research.

Conflict of Interest Disclosures: None

Funding/Support: None

1.
GBD 2013 Mortality and Causes of Death Collaborators.
Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013
.
Lancet..
2015
;
385
(
9963
):
117
171
.
doi:
2.
Chin
CT,
Wong
ASL.
The appropriate use of percutaneous coronary intervention in contemporary clinical practice
.
Pro Singapore Healthc.
2015
;
24
(
1
):
29
34
.
doi:
3.
Zeng
RX,
Li
JJ,
Liao
PD,
Zhang
MZ.
Relationship of non-cardiac biomarkers with periprocedural myocardial injury in patients undergoing percutaneous coronary intervention
.
Int J Cardiol.
2016
;
221
:
726
733
.
doi:
4.
Thygesen
K,
Alpert
JS,
Jaffe
AS,
et al.
Fourth universal definition of myocardial infarction (2018)
.
J Am Coll Cardiol.
2018
;
72
(
18
):
2231
2264
.
doi:
5.
Eggers
KM,
Lindahl
B.
Application of cardiac troponin in cardiovascular diseases other than acute coronary syndrome
.
Clin Chem.
2017
;
63
(
1
):
223
235
.
doi:
6.
Feldman
DN,
Kim
L,
Rene
AG,
Minutello
RM,
Bergman
G,
Wong
SC.
Prognostic value of cardiac troponin-I or troponin-T elevation following nonemergent percutaneous coronary intervention: a meta-analysis
.
Catheter Cardiovasc Interv.
2011
;
77
(
7
):
1020
1030
.
doi:
7.
Garg
P,
Morris
P,
Fazlanie
AL,
et al.
Cardiac biomarkers of acute coronary syndrome: from history to high-sensitivity cardiac troponin
.
Intern Emerg Med.
2017
;
12
(
2
):
147
155
.
doi:
8.
Arsenault
BJ,
Rana
JS,
Stroes
ESG,
et al.
Beyond low-density lipoprotein cholesterol: respective contributions of non–high-density lipoprotein cholesterol levels, triglycerides, and the total cholesterol/high-density lipoprotein cholesterol ratio to coronary heart disease risk in apparently healthy men and women
.
J Am Coll Cardiol.
2009
;
55
(
1
):
35
41
.
doi:
9.
Hosseini
SK,
Tahvildari
M,
Ansari
MJA,
Nakhjavani
M,
Esteghamati
A,
Tokaldany
ML.
Clinical lipid control success rate before and after percutaneous coronary intervention in Iran; a single center study
.
Iran Red Crescent Med J.
2013
;
15
(
6
):
467
472
.
doi:
10.
Bandeali
S,
Farmer
J.
High-density lipoprotein and atherosclerosis: the role of antioxidant activity
.
Curr Atheroscler Rep.
2012
;
14
(
2
):
101
107
.
doi:
11.
Chang
TI,
Streja
E,
Moradi
H.
Could high-density lipoprotein cholesterol predict increased cardiovascular risk?
Curr Opin Endocrinol Diabetes Obes.
2017
;
24
(
2
):
140
147
.
doi:
12.
Bhatt
DL,
Steg
PG,
Miller
M,
et al;
REDUCE-IT Investigators
.
Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia
.
N Engl J Med.
2019
;
380
(
1
):
11
22
.
doi:
13.
Reiner
Ž.
Hypertriglyceridaemia and risk of coronary artery disease
.
Nat Rev Cardiol.
2017
;
14
(
7
):
401
411
.
doi:
14.
Lawton
JS,
Tamis-Holland
JE,
Bangalore
S,
et al.
2021 ACC/AHA/SCAI guideline for coronary artery vascularization: executive summary: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines
.
J Am Coll Cardiol.
2022
;
79
(
2
):
197
215
.
doi:
15.
Li
XL,
Guo
YL,
Zhu
CG,
et al.
Relationship of high-density lipoprotein cholesterol with periprocedural myocardial injury following elective percutaneous coronary intervention in patients with low-density lipoprotein cholesterol below 70 mg/dL
.
J Am Heart Assoc.
2015
;
4
(
1
):
e001412
.
doi:
16.
Li
XL,
Li
JJ,
Guo
YL,
et al.
Association of preprocedural low-density lipoprotein cholesterol levels with myocardial injury after elective percutaneous coronary intervention
.
J Clin Lipidol.
2014
;
8
(
4
):
423
432
.
doi:
17.
Cutlip
DE,
Kuntz
RE.
Does creatinine kinase-MB elevation after percutaneous coronary intervention predict outcomes in 2005? Cardiac enzyme elevation after successful percutaneous coronary intervention is not an independent predictor of adverse outcomes
.
Circulation.
2005
;
112
(
6
):
916
922
;
discussion 922. doi:10.1161/CIRCULATIONAHA.104.478347
18.
Huang
Z,
Shui
X,
Ling
Y,
et al.
Serum lipoprotein (a) and risk of periprocedural myocardial injury in patients undergoing percutaneous coronary intervention
.
Clin Cardiol.
2021
;
44
(
2
):
176
185
.
doi:
19.
National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report
.
Circulation.
2002
;
106
(
25
):
3143
3421
.
20.
Burke
AP,
Farb
A,
Malcom
GT,
Liang
YH,
Smialek
J,
Virmani
R.
Coronary risk factors and plaque morphology in men with coronary disease who died suddenly
.
N Engl J Med.
1997
;
336
(
18
):
1276
1282
.
doi:
21.
Buturak
A,
Degirmencioglu
A,
Erturk
M,
et al.
Impact of increased admission lipid levels on periprocedural myocardial injury following an elective percutaneous coronary intervention
.
Coron Artery Dis.
2015
;
26
(
4
):
333
340
.
doi:
22.
Zeng
RX,
Li
XL,
Zhang
MZ,
et al.
Non-HDL cholesterol is a better target for predicting periprocedural myocardial injury following percutaneous coronary intervention in type 2 diabetes
.
Atherosclerosis.
2014
;
237
(
2
):
536
543
.
doi:
23.
Silbernagel
G,
Schöttker
B,
Appelbaum
S,
et al.
High-density lipoprotein cholesterol, coronary artery disease, and cardiovascular mortality
.
Eur Heart J.
2013
;
34
(
46
):
3563
3571
.
doi:
24.
Barter
P,
Gotto
AM,
LaRosa
JC,
et al;
Treating to New Targets Investigators
.
HDL cholesterol, very low levels of LDL cholesterol, and cardiovascular events
.
N Engl J Med.
2007
;
357
(
13
):
1301
1310
.
doi:
25.
Parish
S,
Offer
A,
Clarke
R,
et al;
Heart Protection Study Collaborative Group
.
Lipids and lipoproteins and risk of different vascular events in the MRC/BHF Heart Protection Study
.
Circulation.
2012
;
125
(
40
):
2469
2478
.
doi:
26.
Kosmas
CE,
Christodoulidis
G,
Cheng
JW,
Vittorio
TJ,
Lerakis
S.
High-density lipoprotein functionality in coronary artery disease
.
Am J Med Sci.
2014
;
347
(
6
):
504
508
.
doi:
27.
Jiao
ZY,
Li
XT,
Li
YB,
et al.
Correlation of triglycerides with myocardial infarction and analysis of risk factors for myocardial infarction in patients with elevated triglyceride
.
J Thorac Dis.
2018
;
10
(
5
):
2551
2557
.
doi:
28.
Zhong
Z,
Liu
J,
Zhang
Q,
et al.
Relationship between preoperative low-density lipoprotein cholesterol and periprocedural myocardial injury In patients following elective percutaneous coronary intervention in southern China
.
Med Sci Monit.
2018
;
24
:
4154
4161
.
doi:
29.
Takano
H,
Ohba
T,
Yamamoto
E,
et al;
PRIMITIVE Study Investigators
.
Usefulness of rosuvastatin to prevent periprocedural myocardial injury in patients undergoing elective coronary intervention
.
Am J Cardiol.
2013
;
111
(
12
):
1688
1693
.
doi:
30.
Herrmann
J,
Lerman
A,
Baumgart
D,
et al.
Preprocedural statin medication reduces the extent of periprocedural non–Q-wave myocardial infarction
.
Circulation.
2002
;
106
(
17
):
2180
2183
.
doi:
31.
Ridker
PM,
Genest
J,
Boekholdt
SM,
et al;
JUPITER Trial Study Group
.
HDL cholesterol and residual risk of first cardiovascular events after treatment with potent statin therapy: an analysis from the JUPITER trial
.
Lancet.
2010
;
376
(
9738
):
333
339
.
doi:
32.
Boekholdt
SM,
Arsenault
BJ,
Hovingh
GK,
et al.
Levels and changes of HDL cholesterol and apolipoprotein A-I in relation to risk of cardiovascular events among statin-treated patients: a meta-analysis
.
Circulation.
2013
;
128
(
14
):
1504
1512
.
doi:
33.
La Vecchia
L,
Mezzena
G,
Zanolla
L,
et al.
Cardiac troponin I as diagnostic and prognostic marker in severe heart failure
.
J Heart Lung Transplant.
2000
;
19
(
7
):
644
652
.
doi:
34.
Korff
S,
Katus
HA,
Giannitsis
E.
Differential diagnosis of elevated troponins
.
Heart.
2006
;
92
(
7
):
987
993
.
doi:
35.
Gili
S,
D'Ascenzo
F,
Moretti
C,
et al.
Impact on prognosis of periprocedural myocardial infarction after percutaneous coronary intervention
.
J Interv Cardiol.
2014
;
27
(
5
):
482
490
.
doi:
36.
Mancini
GBJ,
Hartigan
PM,
Bates
ER,
et al.
Prognostic importance of coronary anatomy and left ventricular ejection fraction despite optimal therapy: assessment of residual risk in the Clinical Outcomes Utilizing Revascularization and Aggressive DruG Evaluation Trial
.
Am Heart J.
2013
;
166
(
3
):
481
487
.
doi:
37.
Zhang
D,
Xu
B,
Yin
D,
et al.
Predictors and periprocedural myocardial injury rate of small side branches occlusion in coronary bifurcation intervention
.
Medicine (Baltimore).
2015
;
94
(
25
):
e992
.
doi:
38.
Ojeda
S,
Pan
M,
Gutiérrez
A,
et al.
Bifurcation lesions involved in the recanalization process of coronary chronic total occlusions: incidence, treatment and clinical implications
.
Int J Cardiol.
2017
;
230
:
432
438
.
doi:
39.
Qadir
F,
Farooq
S,
Khan
M,
Hanif
B,
Lakhani
MS.
Correlation of cardiac troponin I levels (10 folds upper limit of normal) and extent of coronary artery disease in non-ST elevation myocardial infarction
.
J Pak Med Assoc.
2010
;
60
(
6
):
423
428
.