Research ArticleClinical Studies
Open Access

Impact of Triglyceride Levels on the Long-term Clinical Outcomes in Patients With Acute Myocardial Infarction

KAZUFUMI KATO, HIROAKI YOKOYAMA, TOSHIHIRO IWASAKI, YUKI KONNO, KEN YAMAZAKI, SHUN SHIKANAI, TOMO KATO, MICHIKO TSUSHIMA, MAIKO SENOO, NORITOMO NARITA, HIROAKI ICHIKAWA, SHUJI SHIBUTANI, KENJI HANADA and HIROFUMI TOMITA
In Vivo November 2024, 38 (6) 3078-3084; DOI: https://doi.org/10.21873/invivo.13792

Abstract

Background/Aim: Hypertriglyceridemia is a known cardiovascular risk factor. However, the relationship between serum triglyceride (TG) levels and the clinical outcomes in patients with acute myocardial infarction (AMI) is unclear. Patients and Methods: We conducted a single-center, retrospective observational study involving 538 consecutive patients with AMI who underwent emergent percutaneous coronary intervention within 12 hours of onset. Patients were categorized into three groups based on their serum TG levels at admission as follows: T1 group (TG <78 mg/dl, n=172), T2 group (78≤TG<141 mg/dl, n=177), and T3 group (141 mg/dl ≤TG, n=176). The primary endpoint was major adverse cardiovascular events (MACEs) defined as a composite of cardiovascular death, non-fatal MI, and non-fatal stroke. The median follow-up period was 2.4 (1.5-4.2) years. Results: Patients in the T1 group were older, had a higher proportion of females, and had fewer cardiovascular risk factors. However, they also had a higher prevalence of multi-vessel coronary artery disease and severely calcified culprit lesions. The T1 group had a significantly higher rate of MACEs (20.4% in T1, 12.4% in T2 and 8.5% in T3, p<0.05 by Log-rank test, respectively). Multivariate analysis revealed that T1 was an independent predictor of MACEs (hazard ratio=2.19, 95% confidence interval=1.16-4.14, p<0.05). Conclusion: Although patients with AMI with low TG levels at admission had fewer coronary risk factors, they had more severe calcified culprit lesions and worse clinical outcomes.

Key Words:

Dyslipidemia is one of the most common causes of systemic atherosclerosis and is an important issue worldwide. In the secondary prevention of acute myocardial infarction (AMI), guidelines recommend strictly managing LD-cholesterol levels to be as low as possible (1-3). While high triglyceride (TG) levels are also considered a risk factor for cardiovascular diseases, similar to LDL-cholesterol, the impact of interventions targeting TG levels in secondary prevention has not been well established. In a multinational, double-blind, randomized, controlled trial (the PROMINENT trial), the incidence of cardiovascular events did not differ between type 2 diabetic patients with high TG levels who received pemafibrate, a selective peroxisome proliferator-activated receptor α modulator, and those who received a placebo. Although pemafibrate lowered serum triglyceride levels more than the placebo, this did not translate into a reduction in cardiovascular events (4).

The impact of TG levels on clinical outcomes in patients with AMI is not well established. Therefore, we evaluated the relationship between TG levels at admission in patients with AMI and long-term clinical outcomes.

Patients and Methods

Patient selection. This single-center retrospective observational study evaluated 538 consecutive patients with AMI who underwent emergent percutaneous coronary intervention (PCI) within 12 hours from onset between December 2008 and March 2013 at Hirosaki University Hospital, Japan. AMI was diagnosed as per the universal definition (5, 6). Finally, we enrolled 525 patients with AMI after excluding the patients with stent thrombosis, and they were divided into the following three groups as per their TG levels at admission as follows: T1 group (TG <78 mg/dl, n=172), T2 group (78 mg/dl≤TG<141 mg/dl, n=177), T3 group (141 mg/dl ≤TG, n=176) (Figure 1). All patients gave their consent before the procedure. The present study complied with the 1975 Declaration of Helsinki and was approved by the ethical committee of the Hirosaki University Graduate School of Medicine (2020-070-2).

Figure 1.
Figure 1.

Patient selection flowchart.

Data collection and follow-up. Baseline patient data were collected from our institution’s medical records and database. Clinical events, including all-cause death, and major adverse cardiac events were collected from the medical records, inquiring primary care physicians, patients themselves, or family. The severity of calcification in the culprit lesion was evaluated using coronary angiography according to the criteria from a previous report (7), and this grading was performed by two physicians blinded to the outcomes of all patients in this study. Patients were divided into three groups according to the severity of calcification in the culprit lesion as follows: None/Mild, Moderate, and Severe. Moderate calcification was defined as radiopaque densities that were noted only during the cardiac cycle and that typically involved only one side of the vascular wall. Severe calcification was defined as radiopaque densities that were noted without cardiac motion prior to contrast injection and that were generally involved in both sides of the arterial wall.

Study endpoints. The primary endpoint of this study was major adverse cardiovascular events (MACEs) defined as a composite of cardiovascular death, non-fatal MI, and non-fatal stroke. The median follow-up period of this study was 2.4 (1.5-4.2) years.

Statistical analysis. Baseline continuous variables are presented as mean±standard deviation (SD) values or median and interquartile ranges. Categorical variables are presented as percentages. We used one-way analysis of variance to compare continuous variables, and the chi-squared test to compare categorical variables. Kaplan-Meier curves for a composite of clinical outcomes (cardiovascular death, non-fatal MI, and non-fatal stroke) were analyzed using the Log-rank test. Multivariate Cox proportional hazard models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (95%CIs) for the primary endpoint. Age, sex, hypertension, diabetes mellitus, history of smoking, max creatinine phosphokinase (CPK) per 100 IU/l, and time to admission were included in the models as confounding factors. We performed all statistical analyses using JMP®Pro version 16.0 (SAS Institute Inc., Cary, NC, USA) and considered p-value <0.05 as significant.

Results

Baseline characteristics of the patients. Baseline patient characteristics among three groups are shown in Table I. Patients in the T1 group were older than those in the T2 and T3 groups and had more female patients. With decreasing TG levels, body mass index (BMI) also decreased. The prevalences of coronary risk factors including dyslipidemia, diabetes mellitus, and current smoking were fewer in the T1 group compared to the other two groups. However, there were more patients with higher brain natriuretic peptide (BNP) and multi-vessel lesions in the T1 group. Moreover, higher tendency of Killip classification IV was observed in the T1 group compared to the other two groups, although there was no statistically significant difference. Left ventricular ejection fraction at acute phase and culprit vessel of AMI were comparable among the three groups. The time from AMI onset to admission in the T1 group tended to be longer than that in the other two groups, while the maximum CPK levels were equivalent among the three groups. Calcification severity in the culprit lesion was evaluated by coronary angiography according to a previous report (7). There were more patients with severe calcification of the culprit vessel in the T1 group compared to the other two groups (p<0.05) (Figure 2).

View this table:
Table I.

Patient profiles divided into three groups according to triglyceride levels at admission.

Figure 2.
Figure 2.

Severity of the calcification in the culprit lesion evaluated using coronary angiography according to triglyceride (TG) levels at admission, n (%). T1 group: TG <78 mg/dl, T2 group: 78 mg/dl≤TG<141 mg/dl, and T3 group: 141 mg/dl ≤TG.

Clinical outcomes. The Kaplan-Meier curves for MACEs of the three groups are presented in Figure 3 and the details of the clinical outcomes are shown in Table II. Patients in the T1 group had higher MACEs (20.4% in T1, 12.4% in T2, and 8.5% in T3, p<0.05 by Log-rank test, respectively). Higher cardiovascular death was observed in the T1 group, while the prevalences of non-fatal MI and non-fatal stroke were comparable among the three groups.

Figure 3.
Figure 3.

Kaplan-Meier curves for major adverse cardiovascular events (MACEs) according to triglyceride (TG) levels at admission. T1 group: TG<78 mg/dl, T2 group: 78 mg/dl≤TG<141 mg/dl, and T3 group: 141 mg/dl ≤TG.

View this table:
Table II.

Clinical outcomes of the study patients.

Predictors of the clinical outcomes. Multivariate analyses for MACEs were performed and showed that T1 group (HR=2.19, 95%CI=1.16-4.14), age (HR=1.06, 95%CI=1.04-1.19), diabetes mellitus (HR=2.01, 95%CI=1.24-3.26), and max CPK per 100 IU/l (HR=1.01, 95%CI=1.01-1.02) were independent predictors for MACEs (Table III).

View this table:
Table III.

Adjusted hazard ratios for major adverse cardiovascular events.

Discussion

We evaluated the impact of TG levels at admission on the long-term clinical outcomes of patients with AMI who underwent emergent PCI within 12 hours of onset. The main findings of this study were as follows: patients with AMI with low TG levels at admission had worse clinical outcomes even though they had fewer coronary risk factors, and low TG levels were an independent predictor for clinical outcomes. Furthermore, higher prevalences of severely calcified culprit lesion and multivessel disease were observed in patients with AMI with low TG levels at admission.

In our study, patients with AMI with low TG levels at admission were older, had low BMI, and had fewer coronary risk factors, consistent with the previous report according to the Japan Acute Myocardial Infarction Registry (JAMIR) (8). In this Japanese multi-center and prospective observational registry, patients with AMI with low BMI had lower TG levels at admission and had worse mortality compared with obese or normal-weight patients with high TG levels. The results suggested that poor nutritional status and the lower rate of optimal LDL-lowering therapy with statin for secondary prevention might be contributing factors for the poor clinical outcomes in patients with AMI with low BMI. Furthermore, it has been shown that underweight patients with AMI had lower TG levels and worse mortality compared with those with normal or high-weight patients (9), consistent with the results in this study.

Although the relationship between serum TG levels and the severity of the coronary artery calcification has not been fully evaluated, the present study showed a higher prevalence of severely calcified culprit lesions in patients with AMI with low TG levels at admission. Factors contributing to vascular calcification include genetic, environmental, and cellular biological factors (10). First, various genes involved in vascular calcification have been reported with mutations in histone deacetylase 9 (HDAC9), being relatively common among Asians. Second, environmental factors include coronary risk factors, such as diabetes, chronic kidney disease, hypertension, smoking, and obesity. Last, cellular biological factors encompass osteogenic transformation of vascular smooth muscle cells, cellular senescence, and calcium and phosphorus metabolism abnormalities. The prevalence of these environmental factors was lower in patients with AMI with low TG in this study, which does not explain the high prevalence of severely calcified coronary artery lesions. Hypertension, dyslipidemia, smoking, and diabetes contribute to more than half of AMIs, which are referred to as standard modifiable cardiovascular risk factors (SMuRFs) (11). The prognosis for patients with AMI without SMuRFs is known to be poor (12, 13), which was consistent with our results, and this has been suggested to be due to a lack of preconditioning against ischemia and the involvement of systemic diseases, such as active cancer and inflammatory diseases. Further investigation is needed to evaluate the relationship between serum low TG levels and the severity of the coronary artery calcification.

Additionally, the TG metabolism rate is considered a risk factor for cardiovascular and cancer mortality (14). TG metabolism is determined by the concentrations of plasma glycerol and β-hydroxybutyrate, and higher levels of these TG metabolites are associated with an increased incidence of cardiovascular and cancer deaths. This relationship has been reported to be independent of TG levels. The mechanisms contributing to increased cardiovascular mortality may include the harmful effects of free fatty acids on the vascular wall and their impact on insulin resistance. The higher cancer mortality may be due to the requirement of fatty acids for the proliferation and metastasis of cancer cells. The point that high TG levels do not contribute to mortality is noteworthy and challenges the conventional management of TG as a coronary risk factor.

It is widely known that an increase in fasting TG level, especially above 150 mg/dl, is associated with the risk of coronary artery disease (CAD), and that non-fasting TG level is also correlated with the development of CAD (15-18). Hence, many treatment guidelines recommend the treatment of hypertriglyceridemia. However, few studies have shown a beneficial impact of TG lowering therapy on the cardiovascular events. Moreover, the PROMINENT trial did not show the efficacy of the intensive TG lowering therapy (4) in diabetic patients. When LDL-cholesterol is strictly controlled, the additional effect of lowering TG levels on reducing cardiovascular events is unclear.

A recent study in China showed TG levels in the elderly were inversely correlated with frailty (19). They argued that high TG levels in the elderly are associated with a decreased risk of cognitive decline, weakened activity of daily living, and worsening frailty. Patients with AMI with low TG levels may have difficulty in recognizing ischemic symptoms because of a combination of various factors, including decreased activity and cognitive decline. In the current situation, where the effect of lowering TG levels on cardiovascular events has not been demonstrated, additional intervention for hypertriglyceridemia, especially in the elderly, may be a critical issue. While TG level is one of the cardiovascular risk factors, it may reflect frailty in the elderly and may be more useful as a predictor rather than a therapeutic target.

Study limitations. First, this was a single-center and retrospective observational study, and the number of patients was small to allow generalization of our results. Second, because data on medications before admission were not collected, the interventions for coronary risk factors before the onset of AMI were not assessed. Third, while data on TG levels were collected only at admission, the effect of the serial changes in TG levels on clinical outcomes was not discussed. Fourth, cognitive function and frailty were not assessed, and their impact on clinical outcomes is unclear.

Conclusion

Patients with AMI with low TG levels at admission had severely calcified culprit lesions and worse long-term clinical outcomes, despite having fewer coronary risk factors.

Footnotes

  • Authors’ Contributions

    Conception: Kazufumi Kato, and Hirofumi Tomita. Study design: Kazufumi Kato, Hiroaki Yokoyama, and Hirofumi Tomita. Data collection and processing: Kazufumi Kato, Hiroaki Yokoyama, Toshihiro Iwasaki, Yuki Konno, Ken Yamazaki, Shun Shikanai, Tomo Kato, Michiko Tsushima, Maiko Senoo, Noritomo Narita, Hiroaki Ichikawa, Shuji Shibutani, and Kenji Hanada. Article writing: Kazufumi Kato. Critical review: Hiroaki Yokoyama and Hirofumi Tomita.

  • Funding

    None.

  • Conflicts of Interest

    The Authors declare no conflicts of interest associated with this article.

  • Received August 22, 2024.
  • Revision received September 14, 2024.
  • Accepted September 16, 2024.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY-NC-ND) 4.0 international license (https://creativecommons.org/licenses/by-nc-nd/4.0).

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Impact of Triglyceride Levels on the Long-term Clinical Outcomes in Patients With Acute Myocardial Infarction
KAZUFUMI KATO, HIROAKI YOKOYAMA, TOSHIHIRO IWASAKI, YUKI KONNO, KEN YAMAZAKI, SHUN SHIKANAI, TOMO KATO, MICHIKO TSUSHIMA, MAIKO SENOO, NORITOMO NARITA, HIROAKI ICHIKAWA, SHUJI SHIBUTANI, KENJI HANADA, HIROFUMI TOMITA
In Vivo Nov 2024, 38 (6) 3078-3084; DOI: 10.21873/invivo.13792
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