The Effect of Coenzyme Q10 Supplementation on Global Longitudinal Strain Values in Acute ST Segment Elevation Myocardial Infarction Patients Treated With Primary Percutaneous Coronary Intervention
Phase: NA
Conditions: ST Segment Elevation Myocardial Infarction (STEMI), Coenzyme Q10
Sponsor: Universitas Diponegoro

1 
 
The Effect of Coenzyme Q10 Supplementation on Global Longitudinal Strain Values 
in Acute ST Segment Elevation Myocardial Infarction Patients Treated With Primary 
Percutaneous Coronary Intervention 
24th January 2024 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

2 
 
The Effect of Coenzyme Q10 Supplementation on Global Longitudinal Strain Values 
in Acute ST Segment Elevation Myocardial Infarction Patients Treated With Primary 
Percutaneous Coronary Intervention 
Carina Adriana*, Ilham Uddin*, Safir*, Mochamad Ali Sobirin*, 
Suhartono** 
*Departement of Cardiology and Vascular Medicine, Faculty of Medicine 
Diponegoro University, Semarang, Indonesia 
** Public Health Department, Faculty of Medicine Diponegoro University, 
Semarang, Indonesia 
 
1. Introduction 
Cardiovascular diseases, particularly coronary artery disease (CAD), remain 
one of the leading causes of morbidity and mortality worldwide.1,2 Acute Myocardial 
Infarction (AMI) is a life-threatening manifestation of acute CAD that can lead to 
sudden cardiac death.3 Subjects with ST-Elevation Myocardial Infarction (STEMI) 
have a worse long-term prognosis compared to those with Non-ST-Elevation 
Myocardial Infarction (NSTEMI).4 Revascularization and pharmacological therapy 
have successfully reduced mortality from Myocardial Infarction (MI), but subjects still 
experience progressive left ventricular dilation after MI, even after undergoing Primary 
Percutaneous Coronary Intervention (PPCI).5,6,7 Left ventricular remodeling after MI 
affects long term prognosis, with post-infarction adverse remodeling being a parameter 
for the risk of cardiovascular events such as ventricular arrhythmias, heart failure, and 
death in AMI subjects. This makes the identification of at-risk subjects crucial for 
important prognostic value and therapeutic implications.8,9 
The strain and strain rate techniques have been developed for echocardiographic 
examination to quantitatively assess and evaluate changes in left ventricular function 
both globally and regionally. Echocardiographic assessment of Global Longitudinal 
Strain (GLS) has been used to predict left ventricular remodeling after MI.10,11 Peksiene 
et al. reported that a GLS cutoff value of -12.5% can predict left ventricular remodeling 
in STEMI subjects after PPCI, with a sensitivity of 78% and specificity of 73%.12 
Lacalzada et al. reported that the optimal cutoff value for GLS as a predictor of left 
ventricular remodeling in STEMI subjects after PPCI is -12.46%.13 
Pharmacological management of cardiac remodeling, such as beta-receptor 
blockers, angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin II 
receptor blockers (ARBs), has been proven to reduce mortality and is considered 
standard therapy after myocardial infarction.14 Supplements can be beneficial as 
adjunctive therapy for managing cardiac remodeling, with Coenzyme Q10 (CoQ10) 
potentially offering significant cardiovascular protective effects.15,16,17 In the early 
1980s, Karl Folkers discovered the therapeutic potential of CoQ10 in cardiovascular 
diseases and used it in subjects with heart failure. Research on CoQ10 has since 
expanded to other cardiovascular conditions, including hypertension, ischemic heart 
disease, and myocardial infarction. Decreased levels of CoQ10 in myocardial tissue and 
serum are associated with disease severity and poorer clinical outcomes in subjects with 
cardiovascular disease.18,19 CoQ10 helps reduce oxidative stress, plays a role in ATP 
synthesis, alleviates the inflammatory response, restores intracellular calcium 
homeostasis, and reduces cellular apoptosis, thereby potentially decreasing cardiac 
remodeling after MI.15,16,17 Therefore, this study aims to determine the effect of CoQ10 

3 
 
supplementation post-MI on left ventricular remodeling, assessed through changes in 
GLS values. 
 
2. Materials and Methods 
Subjects population 
 
The study included acute STEMI subjects (less than 12 hours after symptom 
onset) who underwent PPCI from January 2024 to Apil 2024. Furthermore, a sequence 
of GLS measurements were collected within the first 24 hour after PPCI and 8 weeks 
after the intervention. Relevant clinical parameters (age, hypertension, diabetes, 
dyslipidemia, gender, body mass index, total ischemia time) along with thorax x-ray, 
laboratory tests, electrocardiography and echocardiography data were prospectively 
documented. 
 
Subjects with hemodynamic conditions of Killip class III-IV and NYHA class 
III-IV, those who received fibrinolytic therapy prior to admission, had a past history of 
coenzyme Q10 consumption, or were receiving warfarin therapy were excluded. 
Additionally, subjects with severe valvular heart disease, isolated right ventricular 
infarction, a history of Percutaneous Coronary Intervention (PCI), Coronary Artery 
Bypass Grafting (CABG), myocardial infarction, or abnormal heart rhytms detected 
through electrocardiogram were also excluded from the study. 
 
Coenzyme Q10 
 
Coenzyme Q10 was administered at a dose of 100 mg every 12 hours starting 
on the second day following primary PCI, after the baseline GLS examination. CoQ10 
was taken every morning and evening after meal for 8 weeks until participant 
underwent a repeat GLS examination. 
 
Coronary Angiography and PCI 
 
Coronary angiography was performed using the conventional Judkins method, 
along with computerized picture acquisition and storage. An individual proficient in 
invasive cardiology conducted the analysis offline without knowledge of the results 
from the other imaging investigations. In cases of single-vessel disease, the affected 
blood vessel was determined to be the primary factor. The primary responsible vessel 
in cases of multivessel disease was determined using a combination of 
electrocardiographic and angiographic markers. PCI was performed based on the 
operator’s judgment, with all subjects demonstrating TIMI 3 flow in the culprit arteries. 
 
Echocardiography and Global Longitudinal Srain Analysis 
 
Three sequential cardiac cycles of apical 4, 2, and 3 chamber view images were 
stored using optimal machine settings and frame rates of 50-70 frames per second for 
strain measurement using speckle tracking echocardiography. Two-dimentional 
speckle-tracking investigations were conducted using the Epiq 7C ultrasound machine 
manufactured by Philips Medical Systems. These studies utilized QLAB/automated 
cardiac motion quantification (ACMQ) version 10.85 and QLAB/LV auto-strain 
version 12.0, both developed by Philips Healthcare. The endocardial border was 
delineated either manually or automatically during the cardiac cycle using the highest 
quality image. If speckle visibility was insufficient, the region of interest was manually 

4 
 
adjusted. Tracking data that did not meet specified criteria or was affected by shadows 
or artifacts was excluded. The software subsequently generated time-domain Left 
Ventricle (LV) strain curve automatically for each segment. Data for calculating GLS 
were extracted from the 18 cardiac segments using standard methods of the American 
Society of Echocardiography. The strain value was obtained from automatic 
measurements based on the formula : strain (ε) = L– L0/L0, where L represents changes 
in the length of longitudinal myocardial fibers at the end of systole and L0 represents 
the initial myocardial fiber length at rest at end diastole. Each inspection was conducted 
by a single operator. With an intraclass coefficient reliability above 0.90 and minimal 
differences in GLS values across two operators (-12,94 ± 5.3% vs. -12,76 ± 5,8%), our 
lab demonstrated strong intraobserver and interobserver variability. The identity of the 
subject and other data were not disclosed to the operators during any of the offline 
analysis. 
 
Follow-Up Data and Assessment of Recovery 
 
Each participant in this randomized control trial was monitored for a period of 
8 weeks after PPCI. All subject received treatment consisting of beta blockers, ACEIs 
/ARBs, statins, nitrates, MRAs and dual antiplatelet agents (specifically aspirin in 
combination with clopidogrel or ticagrelor). The improvement in systolic function was 
measured by calculating the delta GLS, which represents the difference between GLS 
measurements taken within the first 24 hour after primary PCI and 8 weeks after the 
intervention. A lower (more negative) GLS signifies superior left ventricular function. 
Conversely, a higher value of delta GLS indicates a more effective recovery of function. 
 
Statistical Analysis 
 
The chi-square test was employed to assess disparities between groups. 
Descriptive discrete characteristics are presented as counts and percentages. 
Continuous variables that follow a normal distribution are presented as means and 
standard deviations (SD). The analysis focused on comparing measurements taken at 
baseline with those taken at follow-up using paired subjects. The Student’s t-test was 
used for normally distributed data, whereas the Wilcoxon test was used for data that 
were not normally distributed. The t-test or the Mann-Whitney U-test was employed to 
assess disparities in GLS between each group, depending on the data distribution. 
Statistically significant was defined as a p-value less than or equal to 0.05 in two-sided 
testing. Statistical analyses were conducted using SPSS version 26. 
 
Ethical Clearance and Informed Consent 
 
The Ethical Committee of the Faculty of Medicine, Diponegoro University, and 
the Ethical Committee of Kariadi Central General Hospital Semarang approved the 
study protocol, which followed the Second Declaration of Helsinki. This research 
complies with seven (7) WHO 2011 Standards in terms of ethics, referring to the 2016 
CIOMS Guidelines: 1) Social Values, 2) Scientific Values, 3) Equitable Assessment and 
Benefits, 4) Risks, 5) Persuasion and Exploitation, 6) Confidentiality and Privacy, and 
7) Informed Consent. The fact that each standard’s indicators are met (Ethical Approval 
No. 1648/EC/KEPK-RSDK/2023) indicates this. 
 

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3. Results 
The study comprised a total of forty-six subjects with acute onset STEMI, as 
shown in Table 1. Following the intervention, the participants were divided into two 
groups: Coenzyme Q10 (standard treatment+ CoQ10 100mg/12hours, comprising 23 
subjects) and Placebo (standard treatment+ placebo 1 chewable tablet/12hours, 
comprising 23 subjects). There were no statistically significant differences in 
demographic characteristics between the two groups regarding gender, age, and Body 
Mass Index (BMI). Subjects in both groups were predominantly male, with 14 subjects 
(60.9%) in the CoQ10 group and 19 subjects (82.6%) in the placebo group (p=0.190). 
The median age of the participants in the CoQ10 group was 55 (33-74) years, while in 
the placebo group it was 54 (41-71) years (p=0.768). The average BMI of subjects in 
both groups indicated overweight status (according to WHO Asia Pacific criteria), with 
25±2.5 kg/m² in the CoQ10 group and 24.6±2.3 kg/m² in the placebo group (p=0.604). 
Based on risk factors for CAD, smoking was the most common risk factor in both 
groups (47.8% and 65.2%), followed by hypertension, diabetes mellitus, and 
dyslipidemia. No significant differences were found between the two groups regarding 
CAD risk factors. 
In the clinical characteristics of STEMI, no significant differences were found in 
the location of the infarct between the two groups, with anterior infarction at 52.2% in 
the CoQ10 group and 47.8% in the placebo group (p=1.000). The average total ischemic 
time was 493.39±179.08 minutes in the CoQ10 group, while in the placebo group it 
was 510.87±179.36 minutes (p=0.742). Most subjects had Killip Class I (95.7% in the 
CoQ10 group and 82.6% in the placebo group). The average TIMI score was 3 for both 
the CoQ10 and placebo groups (p=0.973). Of the 23 subjects in the CoQ10 group, 6 
subjects (26.1%) underwent complete revascularization, while in the placebo group 8 
subjects (34.8%) received complete revascularization (p=0.749). In the CoQ10 group, 
43.5% had 2 vessel disease (2VD), while in the placebo group, 39.1% had 3 vessel 
disease (3VD) (p=0.464). 
During hospitalization, all subjects received standard STEMI therapy according 
to guidelines and adjusted to their clinical condition. All study subjects received dual 
antiplatelet therapy and statins. All subjects also received ACEIs or ARBs. The most 
commonly administered ACEIs during hospitalization was ramipril 2.5 mg/24 hours 
(43.5%) in both the CoQ10 and placebo groups, while the most common ARBs was 
candesartan 4 mg/24 hours (17.4%) in both groups (p=0.785). During the study, there 
was an increase in dosage for 10 subjects in the CoQ10 group and 8 subjects in the 
placebo group (p=0.602). The dosage increases included ramipril 10 mg/24 hours for 1 
subject in the CoQ10 group, perindopril 5 mg/24 hours for 5 subjects in the CoQ10 
group and 3 subjects in the placebo group, candesartan 8 mg/24 hours for 4 subjects in 
the CoQ10 group and 3 subjects in the placebo group, and valsartan 80 mg/24 hours for 
2 subjects in the placebo group. 
Nearly all subjects received beta-blockers, with 100% in the CoQ10 group and 
91.3% in the placebo group (p=0.489). The most commonly administered beta-blocker 
during hospitalization in both groups was bisoprolol 1.25 mg/24 hours (39.2% and 
34.8%), followed by bisoprolol 2.5 mg/24 hours, carvedilol 3.125 mg/12 hours, and 
carvedilol 6.25 mg/12 hours (p=0.994). During the study, there was an increase in 
dosage for 9 subjects in the CoQ10 group and 9 subjects in the placebo group (p=0.408). 
The dosage increases included bisoprolol 2.5 mg/24 hours for 2 subjects in the CoQ10 
group and 5 subjects in the placebo group, bisoprolol 5 mg/24 hours for 2 subjects in 
the CoQ10 group, carvedilol 6.25 mg/12 hours for 5 subjects in the CoQ10 group and 
4 subjects in the placebo group. 

6 
 
Most subjects also received mineralocorticoid receptor antagonists, with 19 
(82.6%) in the CoQ10 group and 18 (78.3%) in the placebo group (p=1.000). After the 
PPCI procedure, some subjects were still given additional anticoagulants. A total of 8 
(34.8%) subjects in the CoQ10 group and 11 (47.8%) subjects in the control group 
received anticoagulants, including unfractionated heparin, enoxaparin, or fondaparinux 
for 3-5 days (p=0.550). A total of 15 (65.2%) subjects in the CoQ10 group and 17 
(73.9%) subjects in the control group received nitrates, including isosorbide dinitrate 
or glyceryl trinitrate (p=0.749). Eight (34.8%) subjects in the CoQ10 group and 7 
(30.4%) subjects in the control group received insulin during hospitalization. The oral 
antihyperglycemic medications used during outsubject care included gliclazide at doses 
of 30 mg and 60 mg, as well as glimepiride 2 mg/24 hours (p=0.352). 
All study subjects underwent laboratory tests, including routine blood tests, blood 
glucose levels, lipid profiles, and kidney function. The average random blood glucose 
level for the CoQ10 group was 187.35±49.32 mg/dl, while for the placebo group it was 
184.3±67.99 mg/dl (p=0.333). The average total cholesterol level for the CoQ10 group 
was 184.30±36.5 mg/dl, while for the placebo group it was 192.04±48.2 mg/dl 
(p=0.860). The average LDL level for the CoQ10 group was 118.70±24.33 mg/dl, while 
for the placebo group it was 113.30±35.39 mg/dl (p=0.272). The average serum 
creatinine level for the CoQ10 group was 1.11±0.40 mg/dl, while for the placebo group 
it was 1.17±0.39 mg/dl (p=0.596). No significant differences were found between the 
two groups for the laboratory parameters. There was a significant improvement in 
LVEF values in the CoQ10 group, with an increase of 10.39 ± 8.93% (p < 0.001). The 
placebo group also showed a significant improvement in LVEF values, with an increase 
of 3.21 ± 5.74% (p = 0.014). The difference (Δ) in average LVEF values between the 
CoQ10 group and the placebo group was significantly higher in the CoQ10 group (Δ 
10.39 ± 8.93 vs. 3.21 ± 5.74, p = 0.007). 
The average baseline GLS value in the CoQ10 group was more negative 
compared to the placebo group, but there was no significant difference between the two 
groups (-10.13 ± 2.64% vs -9.94 ± 3.38%, p = 0.835). In the follow-up data, the average 
GLS value in the CoQ10 group was more negative than in the placebo group, and there 
was a significant difference between the two groups (-15.75 ± 2.52% vs -10.64 ± 2.97%, 
p < 0.001). There was a significant improvement in GLS values in the CoQ10 group of 
5.62 ± 2.16% (p < 0.001). The placebo group also showed a significant improvement 
in GLS values of 0.70 ± 1.56% (p = 0.043). The difference (Δ) in average GLS values 
between the CoQ10 group and the placebo group showed a significantly higher 
improvement in the CoQ10 group (Δ 5.62 ± 2.16 vs 0.70 ± 1.56, p < 0.001). Comparison 
of GLS values between Coenzyme Q10 and placebo group is shown in Figure 1. 
None of the subjects reported any toxicity related to CoQ10 consumption. 
Gastrointestinal complaints, such as diarrhea, were observed in 1 subject (4.3%) in the 
CoQ10 group and 1 subject (4.3%) in the placebo group (p=1.000). Nausea was 
reported in 2 subjects (8.7%) in the CoQ10 group and 3 subjects (13%) in the placebo 
group (p=1.000). Abdominal pain occurred in 1 subject in the placebo group (4.3%) but 
was not found in the CoQ10 group (p=1.000). No allergic reactions/itching or 
headaches related to CoQ10 use were reported. Statistically, no significant differences 
were found in safety profiles related to CoQ10 use in this study's subjects. 
 
 
4. Discussion 
 
Baseline demographic and clinical characteristics were comparable between the 
two groups. The majority of participants were male, reflecting the demographic trends 

7 
 
often seen in STEMI populations.13,20 Notably, smoking was the most prevalent risk 
factor for CAD in both groups, followed by hypertension, diabetes mellitus, and 
dyslipidemia. The uniformity in CAD risk factors suggests that the findings are 
representative of typical STEMI patients.20,21 In terms of clinical outcomes, both groups 
exhibited similar characteristics regarding infarct location, ischemic times, Killip class 
classifications, and the average Thrombolysis In Myocardial Infarction (TIMI) scores. 
The majority of subjects were classified as Killip Class I (89.1%), and had TIMI scores 
of ≤5, indicating that the patients in this study were of low-risk stratification. The 30-
day mortality rate for these patients is estimated to be 2-3% based on Killip class and 
≤12.4% based on TIMI score.22,23  
In this study, the average total ischemic time was notably long, at 502.13 ± 
177.44 minutes (8.36 ± 2.95 hours). The study by De Luca et al. indicated that a 
symptom onset to door-to-balloon time of more than 4 hours is an independent predictor 
of one-year mortality (p < 0.05). Additionally, every 30-minute delay in reperfusion is 
associated with a 7.5% increase in mortality at one-year follow-up.24 In this study, 
30.4% of patients achieved complete revascularization. Those with incomplete 
revascularization are at a higher risk for adverse remodeling compared to those with 
complete revascularization. Sohn et al. further stated that complete revascularization 
through PCI can decrease the rates of cardiovascular and cerebrovascular events, as 
well as mortality, in patients with multivessel coronary artery disease, when compared 
to incomplete revascularization.25 
The use of medications such as ACE inhibitors or ARBs and beta-blockers has 
been clinically proven to prevent remodeling and reduce mortality following AMI. The 
AIRE (Acute Infarction Ramipril Efficacy) study using ramipril reported a 27% 
reduction in mortality among post-myocardial infarction patients.26 The use of β-
blockers in patients with left ventricular dysfunction after myocardial infarction was 
demonstrated by the Carvedilol Post Infarct Survival Control in Left Ventricular 
Dysfunction (CAPRICORN) study, which found that treatment with carvedilol was 
associated with a 23% reduction in mortality and a 40% reduction in recurrent infarction 
after a 1.3-year follow-up. 27 The echocardiographic substudy of CAPRICORN 
assessed left ventricular remodeling and showed that in the carvedilol therapy group, 
there was a reduction in end-systolic LV volume of 9.2 ml (p=0.023) and an increase in 
LVEF of 3.9% (p=0.015) compared to the placebo group over 6 months. Thus, the use 
of carvedilol in conjunction with ACEIs has a protective effect against ventricular 
remodeling.28 
Several studies indicate that assessing GLS is a superior method compared to 
Left Ventricular Ejection Fraction (LVEF) for evaluating left ventricular injury and 
function following STEMI.29,30 GLS provides a more comprehensive view of 
myocardial function by measuring the deformation of the heart muscle during 
contraction. Subendocardial longitudinal fibers in the left ventricle are sensitive to 
ischemic conditions, making them useful for detecting early stages of myocardial 
dysfunction and possessing prognostic strength in patients at risk of developing heart 
failure. Global longitudinal strain as the primary outcome, revealed a greater 
improvement in the CoQ10 group post-intervention compared to the placebo group. 
The difference in GLS values (Δ 5.62 ± 2.16 vs 0.70 ± 1.56, p < 0.001) highlights the 
beneficial effect of CoQ10 supplementation on myocardial function following acute 

8 
 
STEMI. The significant enhancement in GLS values suggests improved myocardial 
contractility and function, which is crucial for recovery after ischemic events. 
Both groups showed improvements in LVEF and GLS, whether in the CoQ10 
group or the placebo group. These improvements in LVEF and GLS are likely due to 
the beneficial effects of revascularization procedures and the pharmacological 
management of STEMI patients, including ACE inhibitors/ARBs, beta-blockers, 
MRAs, and statins, which were administered to both groups and have clinically proven 
benefits in preventing remodeling and reducing mortality after myocardial infarction. 
The use of ACE inhibitors/ARBs, beta-blockers, and MRAs has a protective effect 
against ventricular remodeling by inhibiting the progression of remodeling. 
The more pronounced improvement in GLS in the CoQ10 group indicates its 
potential as an effective adjunct therapy in STEMI management. The mechanisms 
behind these improvements may involve CoQ10’s role in mitochondrial function and 
oxidative stress reduction, thereby enhancing myocardial energy metabolism and 
overall cardiac performance. The results of this study are consistent with theories and 
several studies suggesting that CoQ10 can help reduce oxidative stress and alleviate the 
inflammatory 
response 
by 
preventing 
neutrophil 
activation 
and 
matrix 
metalloproteinases, thus potentially reducing cardiac remodeling following myocardial 
infarction.31 Oxidative stress is a pathophysiological mediator of myocardial 
remodeling in heart failure. CoQ10 supplementation may be beneficial by intervening 
in the increased production of reactive oxygen species that contribute to post-ischemic 
injury and the progression to heart failure.32,33  However, this study did not measure 
serum levels of CoQ10 or inflammatory factors; both parameters could indicate the 
cardioprotective pathways of CoQ10. 
The effect of CoQ10 suplementation on GLS values in patients with STEMI 
underwent PPCI has not been previously studied, making this research the first clinical 
trial in humans to investigate this matter. Nonetheless, other research has explored the 
impact of CoQ10 on infarct size in both animal models and human subjects. Awad et 
al. reported that CoQ10 significantly reduced myocardial infarct size by 11.36% 
compared to the control group in an animal model experiencing ischemia-reperfusion 
injury.34 Mohseni et al. found that supplementation with CoQ10 at a dose of 200 mg 
per day for 12 weeks improved blood pressure, reduced inflammatory markers [serum 
levels of ICAM-1 (Intercellular Adhesion Molecule-1) and IL-6 (Interleukin-6)], and 
increased HDL-C (High-Density Lipoprotein Cholesterol) in patients with myocardial 
infarction.35 Singh et al. reported that the incidence of nonfatal recurrent infarction and 
cardiac-related death was significantly lower in the CoQ10 group receiving 120 mg per 
day compared to the placebo group (15.0% vs. 30.9%, p < 0.02) during a 28-day follow-
up.36  
From a safety profile perspective, this study found that subjects receiving 
CoQ10 did not experience any serious side effects. Gastrointestinal disturbances were 
observed, but these were not significantly different between the CoQ10 and placebo 
groups (p=1.000). These side effects generally occurred only during the initial treatment 
phase. All participants tolerated the side effects, with or without the addition of 
symptomatic medications, without needing to stop CoQ10 treatment. Thus, it can be 
concluded that CoQ10 at a dose of 100 mg every 12 hours for 8 weeks is safe for use 
in STEMI patients undergoing PCI. The results are consistent with previous studies that 

9 
 
have safely used higher doses of CoQ10 for longer durations.37,38 We acknowledge the 
limitations of this study, which include the lack of measurement of serum Coenzyme 
Q10 (ubiquinone) levels and inflammatory factors prior to the intervention, as well as 
the absence of a gold standard evaluation for cardiac remodeling, specifically cardiac 
magnetic resonance. 
 
5. Conclusions 
In conclusion, this study demonstrates that CoQ10 supplementation has a 
greater effect on the improvement of GLS values in patients with acute STEMI 
undergoing PPCI, with a favorable safety profile and no significant adverse effects. 
These findings support the potential of CoQ10 as an adjunct therapy in acute STEMI 
treatment, warranting further investigation into its long-term benefits and optimal 
dosing strategies. Future studies should aim to explore the underlying mechanisms of 
action and confirm these results in larger and diverse populations.. 
 
6. Acknowledgements 
There is no acknowledgement. 
 
7. Funding/Support 
This research received no specific grant from any funding agency in the public, 
commercial, or not-for-profit sectors. 
 
8. Financial Disclosure 
This authors have NO affiliations with or involvement in any organization or 
entity with any financial interest (such as honoraria, educational grants, membership, 
employment, consultancies, stock ownership, or other equity interests), or non-financial 
interest (such as personal or professional relationaships, affiliations, knowledge or 
beliefs) in the subject matter or materials discussed in this manuscript. 
 
9. Conflict of Interest 
The authors have no conflict of interest to declare. 
 
10. Availability of data and materials 
The datasets generated and/or analysed during the current study are not publicly 
available due to our local policy but are available from the corresponding author on 
reasonable request. 
Main Points 
• Global Longituinal Strain assessment using speckle-tracking echocardiography could 
be used as predictor of left ventricular recovery after myocardial infarction. 
• Coenzyme Q10 as a potential adjunctive therapy that may improve outcomes and  
provides benefits for myocardial recovery in acute STEMI underwent PPCI. 
 
 
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13 
 
Abbreviation List 
ACEIs 
ACMQ 
AIRE 
AMI 
ARBs 
BMI 
CABG 
CAD 
CAPRICORN 
CoQ10 
GLS 
LV 
LVEF 
MI 
NSTEMI 
NYHA 
PPCI 
SD 
STE 
STEMI 
TIMI 
: Angiotensin Converting Enzyme Inhibitors 
: Automated Cardiac Motion Quantification 
: Acute Infarction Ramipril Efficacy 
: Acute Myocardial Infarction 
: Angiotensin II Receptor Blockers 
: Body Mass Index 
: Coronary Artery Bypass Grafting 
: Coronary Artery Disease 
: Carvedilol Post Infarct Survival Control in Left Ventricular Dysfunction 
: Coenzyme Q10 
: Global Longitudinal Strain 
: Left Ventricle 
: Left Ventricle Ejection Fraction 
: Myocardial Infarction 
: Non ST-elevation Myocardial Infarction 
: New York Heart Association 
: Primary Percutaneus Coronary Intervention 
: Standard Deviation 
: Speckle Tracking Echocardiography 
: ST-elevation Myocardial Infarction 
: Thrombolysis in Myocardial Infarction  
 
Figures and Tables 
 
Figure 1. Comparison of GLS values before and after 8 weeks of intervention. 
Coenzyme Q10 group showed significantly greater improvement in GLS values. 
GLS, global longitudinal strain 
 
 
 

14 
 
Table 1. Baseline  characteristics of the study participants. 
Variable 
  
Group 
 p value 
Coenzyme Q10 
(n=23) 
Placebo 
(n=23) 
Age 
55,22 ± 8,43 
54,48 ± 8,44 
0,768§ 
Gender 
Male 
14 (60,9%) 
19 (82,6%) 
0,190¥ 
Female 
9 (39,1%) 
4 (17,4%) 
Body mass index (kg/m2) 
25,01 ± 2,55 
24,63 ± 2,38 
0,604§ 
CAD Risk factor 
Hipertension 
14 (60,9%) 
10 (43,5%) 
0,376¥ 
DM 
8 (34,8%) 
7 (30,4%) 
1,000¥ 
Smoker 
11 (47,8%) 
15 (65,2%) 
0,372¥ 
Dislipidemia 
5 (21,7%) 
6 (26,1%) 
1,000¥ 
Hipertension and DM 
5 (21,7%) 
3 (13,0%) 
0,699¥ 
STEMI detail 
Infarct location 
 
 
 
Anterior 
12 (52,2%) 
11 (47,8%) 
1,000¥ 
Non Anterior 
11 (47,8%) 
12 (52,2%) 
 
Killip class 
 
 
 
Killip I 
22 (95,7%) 
19 (82,6%) 
0,346¥ 
Killip II 
1 (4,3%) 
4 (17,4%) 
 
TIMI STEMI score 
3 (1-5) 
3 (1-5) 
0,973‡ 
Door to Balloon (minute) 
130,78±77,83 
131,30±52,32 
0,488‡ 
Total Ischemic Time 
(minute) 
493,39±179,08 
510,87±179,36 
0,742§ 
Complete revascularisation 
6 (26,1%) 
8 (34,8%) 
0,749¥ 
Vessel Disease 
 
 
 
1VD 
6 (26,1%) 
8 (34,8%) 
0,464¥ 
2VD 
10 (43,5%) 
6 ( 26,1%) 
 
3VD 
7 (30,4%) 
9 (39,1%) 
 
Culprit lesion 
 
 
 
LAD 
12 (52,2%) 
11 (47,8%) 
0,542¥ 
LCX 
1 (4,3%) 
0 (0%) 
 
RCA 
10 (43,5%) 
12 (52,2%) 
 
Laboratorium Parameter  
 
 
 
Ureum (mg/dl) 
26,3±7,83 
28,57±7.05 
0,309§ 
Creatinin (mg/dl) 
1,11±0.40 
1,17±0,38 
0,596‡ 
Glucose ad random (mg/dl) 
187,35 ± 49,32 
184,30 ± 67,98 
0,333‡ 
HbA1c (%) 
6,81 ± 1,99 
6,67 ± 1,87 
0,834‡ 
Lipid Profile 
 
 
 
Total Cholesterol (mg/dl) 
184,30 ± 36,52 
192,04 ± 48,24 
0,860‡ 
Trigliserid (mg/dl) 
149,87 ± 59,65 
158,26 ± 51,23 
 0,482‡ 
HDL (mg/dl) 
33,39 ± 8,82 
33,26 ± 7,60 
0,957§ 
LDL (mg/dl) 
118,70 ± 24,33 
113,30 ± 35,39 
0,272‡ 
§ Independent-t; ¥ Chi-Square; ‡ Mann-Whitney 
Abbreviations: CAD: coronary artery disease; DM: Diabetes Mellitus; STEMI: 
ST elevation myocardial infarction; VD: Vessel Disease; LDL: Low Density 
Lipoprotein; HDL: High Density Lipoprotein; LAD: Left Anterior Descending; 
LCX: Left Circumflex 

15 
 
Table 1. Baseline  characteristics of the study participants. 
Variable 
  
Group 
 p value 
Coenzyme Q10 
(n=23) 
Placebo 
(n=23) 
Medicamentosa 
 
 
 
Aspilet 
23 (100%) 
23 (100%) 
– 
Ticagrelor 
23 (100%) 
21 (91,3%) 
0,489¥ 
Clopidogrel 
0 (0%) 
2 (8,7%) 
0,489¥ 
ACE-i/ARB 
23 (100%) 
23 (100%) 
– 
In hospital 
 
 
 
Ramipril 2,5mg/24hour 
10 (43,5%) 
10 (43,5%) 
0,785¥ 
Ramipril 5mg/24hour 
2 (8,7%) 
1 (4,3%) 
 
Perindopril 2,5mg/24hour 
5 (21,7%) 
4 (17,4%) 
 
Perindopril 5mg/24hour 
2 (8,7%) 
2 (8,7%) 
 
Candesartan 4mg/24hour 
4 (17,4%) 
4 (17,4%) 
 
Valsartan 40mg/12hour 
0 (0%) 
2 (8,7%) 
 
Follow up 
 
 
 
Ramipril 2,5mg/24hour 
10 (43,5%) 
10 (43,5%) 
0,602¥ 
Ramipril 5mg/24hour 
1 (4,3%) 
1 (4,3%) 
 
Ramipril 10mg/24hour 
1 (4,3%) 
0 (0%) 
 
Perindopril 2,5mg/24hour 
0 (0%) 
1 (4,3%) 
 
Perindopril 5mg/24hour 
7 (30,4%) 
5 (21,7%) 
 
Candesartan 4mg/24hour 
0 (0%) 
1 (4,3%) 
 
Candesartan 8mg/24hour 
4 (17,4%) 
3 (13,0%) 
 
Valsartan 80mg/12hour 
0 (0%) 
2 (8,7%) 
 
Beta blocker 
23 (100%) 
21 (91,3%) 
0,489¥ 
In hospital 
 
 
 
Bisoprolol 1,25mg/24hour 
9 (39,2%) 
8 (34,8%) 
0,994¥ 
Bisoprolol 2,5mg/24hour 
8 (34,8%) 
8 (34,8%) 
 
Carvedilol 3,125mg/12hour 
5 (21,7%) 
4 (17,4%) 
 
Carvedilol 6,25mg/12hour 
1 (4,3%) 
1 (4,3%) 
 
Follow up 
 
 
 
Bisoprolol 1,25mg/24hour 
   5 (21,7%) 
3 (13,0%) 
0,408¥ 
Bisoprolol 2,5mg/24hour 
  10 (43,5%) 
13 (56,6%) 
 
Bisoprolol 5mg/24hour 
  2 (8,7%) 
0 (0%) 
 
Carvedilol 6,25mg/12hour 
6 (26,1%) 
5 (21,7%) 
 
Statin 
 
 
 
Atorvastatin 40mg/24hour 
23 (100%) 
23 (100%) 
– 
MRA 
 
 
 
Spironolacton 25mg/24hour 
19 (82,6%) 
18 (78,3%) 
1,000¥ 
Anticoagulant 
8 (34,8%) 
11 (47,8%) 
0,550¥ 
Fondaparinux 2,5mg/24hour 
6 (26,1%) 
7 (30,4%) 
0,734¥ 
Enoxaparin 0,6cc/12hour 
1 (4,3%) 
3 (13,0%) 
 
Heparine 500 U/hour 
1 (4,3%) 
1 (4,3%) 
 
Nitrat 
15 (65,2%) 
17 (73,9%) 
0,749¥ 
ISDN 5mg/8hour 
5 (21,7%) 
7 (30,4%) 
0,726¥ 
Nitrokaf R 2,5mg/12hour 
10 (43,5%) 
10 (43,5%) 
 
Insulin (in hospital) 
8 (34,8%) 
7 (30,4%) 
1,000¥ 
Glicazide 30mg/24hour 
1 (4,3%) 
3 (13,0%) 
0,352¥ 
Glicazide 60mg/24hour 
4 (17,4%) 
3 (13,0%) 
 
Glimepiride 2mg/24hour 
3 (13,0%) 
1 (4,3%) 
 
§ Independent-t; ¥ Chi-Square; ‡ Mann-Whitney; Abbreviations: ACEi: Angiotensin 
Converting Enzyme inhibitor; ARB: Angiotensin Receptor Blocker; MRA: 
Mineralocorticoid Receptor Antagonist; ISDN: Isosorbid Dinitrat  

16 
 
 
Table 2. Comparison of LVEF (Biplane) value before and before and after 8 weeks 
intervention in each group. 
LVEF (B) % 
Group 
p value 
Coenzyme Q10 
(n=23) 
Placebo 
(n=23) 
Pre 
52,42 ± 6,84 
49,77 ± 7,76 
0,226§ 
Post 
62,81 ± 8,91 
52,98 ± 6,82 
<0,001§* 
p 
<0,001†* 
0,014¶* 
 
Delta 
10,39 ± 8,93 
3,21 ± 5,74 
0,007‡* 
* Significant (p < 0,05) § Independent t; ‡ Mann-Whitney; † Wilcoxon; ¶ Paired t. GLS, 
global longitudinal strain. 
 
Table 3. Comparison of GLS value before and after 8 weeks intervention in each group.  
GLS 
Group 
p value  
Coenzyme Q10 
(n=23) 
Placebo 
(n=23) 
Pre test 
-10,13 ± 2,64 
-9,94 ± 3,38 
0,835§ 
Post test 
-15,75 ± 2,52 
-10,64 ± 2,97 
<0,001§* 
p value 
 
<0,001¶* 
0,043¶* 
Delta GLS 
5,62 ± 2,16 
0,70 ± 1,56 
<0,001§* 
* Significant (p < 0,05); § Independent t; ¶ Paired t. GLS, global longitudinal strain. 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

17 
 

18