GET THE APP

Impact of Hyperuricemia on the Prognosis in Patients with Acute Myocardial Infarction and Atrial Fibrillation
Internal Medicine: Open Access

Internal Medicine: Open Access
Open Access

ISSN: 2165-8048

Research - (2021)Volume 11, Issue 5

Impact of Hyperuricemia on the Prognosis in Patients with Acute Myocardial Infarction and Atrial Fibrillation

Xin-Yao Liu1, Shi-Dong Guo2, Zhen-Zhou Wang3, Peng Zhong4 and Ying Bai1*
 
*Correspondence: Ying Bai, Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China, Tel: +86-10-58268421, Email:

Author info »

Abstract

Background: Hyperuricemia (HUA) is associated with poor prognosis in patients with Acute Myocardial Infarction (AMI). However, its prognostic value in patients with AMI and coexisting Atrial Fibrillation (AF) is not clear.

Methods: We retrospectively studied patients admitted to three hospitals in Beijing, China with the diagnoses of both AMI and AF at discharge/death. HUA was defined as serum uric acid levels ≥ 6.8 mg/dl. The endpoint of the study was in-hospital all-cause mortality. The relationship between HUA and the endpoint was analyzed by multivariate logistic regression. Subgroup analyses were done in patients categorized by sex and in those who underwent Coronary Angio Graphy (CAG).

Results: After excluding those with missing data, a total of 651 patients were included in the study with the median age of 76 and 40.25% were women. Patients with HUA counted up to 40.40% of the study population and 15.51% of the patients died during hospitalization. HUA was shown to be an independent predictor of in-hospital mortality after adjusting for confounding factors (Adjusted Odds Ratio (OR) 2.09, 95% Confidence Interval (CI) 1.29-3.40, p=0.003). Subgroup analysis categorized by sex showed similar results for HUA in male patients (Adjusted OR 2.02, 95% CI 1.04-3.95, p=0.039) but not in female patients. HUA was also not included in the final adjusted model in patients who underwent CAG.

Conclusion: HUA was an independent predictor of in-hospital all-cause mortality in patients with AMI and coexisting AF. Similar conclusion could be drawn in male patients but not in female patients and patients who underwent CAG.

Keywords

Hyperuricemia; Acute myocardial infarction; Atrial fibrillation; Mortality

Introduction

Although treatment strategies keep improving, the mortality of Acute Myocardial Infarction (AMI) remains high [1]. As a result, searching for better predictive factors of adverse outcomes is an issue of interest. While some risk factors have been well identified, such as advanced age, Diabetes Mellitus (DM), prior Myocardial Infarction (MI) and renal insufficiency, there are still debates on the new emerging factor Uric Acid (UA) [2-8]. Some studies showed that adding UA to the prognosis predictive models improved their discriminatory power in patients with acute coronary syndrome including AMI [9-11]. While some other studies showed no association between UA and cardiovascular mortality [12,13].

Actually, patients suffering both AMI and Atrial Fibrillation (AF) are not rare in clinical practice [14]. Known as the most common sustained arrhythmia, AF increases rapidly and leads to severe complications such as stroke and heart failure [15]. Although associated with atrial thrombosis, it is unclear whether UA is of prognostic value for AF patients [16,17]. Furthermore, some studies have shown adverse impact of coexisting AF on the outcomes of AMI patients, which makes this population at even higher risk of death [18-20]. However, prognostic predictors of such patients have not been fully studied. UA was considered to be related to both AMI and AF, but less studied and with more debate than other well-established factors. Therefore, our study aimed to explore the role of UA in the mortality of patients with AMI and AF.

Methods

Study population and design

The study population was chosen from a database described elsewhere [21]. Briefly, the database consisted of hospitalization information of 1,204 adult patients admitted to three hospitals (Beijing Tongren Hospital, Capital Medical University, from September 2008 to December 2018; Beijing Friendship Hospital, Capital Medical University, from January 2013 to March 2018; China-Japan Friendship Hospital, from April 2011 to May 2018) in Beijing, China, who diagnosed with both AF and AMI at discharge or on death.

The diagnosis of AMI was made in accordance with the recent guideline, which required cardiac biomarkers elevation plus at least one of the following items: (i) Cardiac ischemic symptoms; (ii) Suggestive changes in the electrocardiograms (e.g. ST segment elevation or depression or pseudonormalization, newly appeared left or right bundle branch block or Q waves); (iii) Ventricular wall motion abnormalities detected by images with the exclusion of a previous MI of the same ventricular segment; (iv) Thrombi demonstrated by Coronary Angiography (CAG). Patients with either acute ST-segment Elevation MI (STEMI) or acute Non- STEMI (NSTEMI) were included [22].

AF was defined as the discharge/death diagnoses including at least one of the following diagnosis codes: I48xx01, I48xx02, I48xx03, I48xx04, I48xx05, I48xx06, I48xx07, I48xx08, I48xx09, I48xx10, I48xx11, I48xx12, I48xx13 and I48xx14 according to the International Classification of Disease - 10th edition (ICD-10) [23]. With these criteria, patients with different types of AF could be enrolled. They were further classified as Paroxysmal AF (PAF) and non-PAF, of which the latter including both persistent AF and permanent AF.

Among patients with re-admissions, only the first was studied. Patients’ demographics (e.g. age, sex, smoking status), comorbidities (e.g. history of hypertension, DM, Heart Failure (HF), stroke, previous MI), results of laboratory biochemical tests (e.g. Serum Uric Acid (SUA), Creatinine (Cr), low Density Lipoprotein- Cholesterol (LDL-C)) and discharge status (alive/dead) were collected from medical records. Only laboratory tests within one day before or after the admission were studied. UA was used both as a continuous variable (SUA, mg/dl) and a categorical variable (Hyperuricemia (HUA)) during analyses. HUA was defined as SUA ≥ 6.8 mg/dl according to the recent guideline [24]. Furthermore, data on ventricular arrhythmia, Killip classification and undergoing CAG or not were also collected. Ventricular arrhythmia was defined as sustained ventricular tachycardia required medical or electrical cardioversion, ventricular flutter or ventricular fibrillation occurring during hospitalization or emergency care prior to the admission. Device support referred to the use of circulation supporting devices, such as Intra-Aortic Balloon Pump (IABP) and Extra Corporeal Membrane Oxygenation (ECMO). Invasive or non-invasive treatment strategies were chosen according to the physicians’ opinions for each individual.

Endpoint of the study

The endpoint of the study was in-hospital all-cause mortality, which was defined as death due to any cause during hospitalization. The direct cause of death for each patient was extracted from the medical record.

Subgroup analyses

Subgroup analyses were done categorized by sex and in those who underwent CAG. As for the latter, further information of CAG and revascularization results were collected. Left Main (LM) coronary artery disease referred to ≥ 50% stenosis or less than grade 3 of the Thrombolysis In Myocardial Infarction (TIMI) blood flow of the vessel. Multivessel disease was defined as ≥ 50% stenosis or TIMI blood flow less than 3 in more than one coronary artery branch except LM (left anterior descending branch, left circumflex branch or right coronary artery). Those who accepted Percutaneous Coronary Intervention (PCI) treatment with all target vessels reaching TIMI 3 blood flow and with residual stenosis <20% with stent implanting or <50% with balloon dilation, or those who received Coronary Artery Bypass Grafting (CABG) were considered as with successful revascularizations.

Ethics statement

The study was conducted in accordance with the Declaration of Helsinki (as revised in 2013). The study was approved by clinical research ethics committee of our centers (NO.:TRECKY2020-097) and individual consent for this retrospective analysis was waived.

Statistical analysis

SPSS version 24.0 (SPSS Inc., Chicago, IL, USA) was used for statistical analyses. Whether continuous data was conformed to normal distribution was tested by one-sample Kolmogorov-Smirnov test. Continuous data were reported as median with interquartile (median (25th percentile-75th percentile)). Comparisons between groups were performed with student’s t tests for variables with normal distribution or Wilcoxon rank sum tests for variables not normally distributed. Categorical data were expressed as counts with percentages and comparisons between groups were performed with Pearson’s Chi-square test or Chi-square test with continuity correction when appropriate.

Univariate logistic regression was done for every variable including SUA/HUA to explore whether it was a risk factor of the endpoint and a backward stepwise multivariate logistic regression with HUA was done to adjust for the confounding factors.

The input cut-off p value was 0.05 and the output cut-off p value was 0.1 for multivariate logistic regressions. Other results were considered statistically significant with two-tailed p values <0.05.

Results

Patients’ characteristics

After excluding 444 patients without SUA results during the required period and another 109 for missing data of other studied variables, 651 patients were included in the study Figure 1, with the median age of 76 years old and 40.25% were women. According to the cut-off value described previously, 263 (40.40%) belonged to the HUA group. Patients’ characteristics at baseline were listed in Table 1. Patients with HUA were elder, more likely to have DM and previous MI, with higher Cr and LDL-C levels, more Killip class ≥ 2 and circulation supporting devices using but fewer receiving CAG. There also appeared to be more patients died in the HUA group (62 (23.57%) vs. 39 (10.05%), p<0.001).

internal-Myocardial

Figure 1: Flow chart summarizing the study population. AMI: Acute Myocardial Infarction; AF: Atrial Fibrillation; SUA: Serum Uric Acid.

Total patients With HUA Without HUA p
(n=651) (n=263) (n=388)
Age (years)* 76 (66-82) 77 (68-82) 75 (64-81) 0
Sex (female) 262 (40.25%) 95 (36.12%) 167 (43.04%) 0
HBP history 480 (73.73%) 199 (75.67%) 281 (72.42%) 0
DM history* 271 (41.63%) 122 (46.39%) 149 (38.40%) 0
HF history 257 (39.48%) 113 (42.97%) 144 (37.11%) 0
Previous MI* 101 (15.51%) 58 (22.05%) 43 (11.08%) <0.001
Stroke history 126 (19.35%) 54 (20.53%) 72 (18.56%) 1
Current smoker 176 (27.04%) 69 (26.24%) 107 (27.58%) 1
SUA (mg/dl)* 6.27 (4.88-7.69) 8.25 (7.39-9.76) 5.13 (4.24-5.85) <0.001
LDL-C (mmol/L)* 2.48 (1.88-3.09) 2.56 (2.00-3.14) 2.40 (1.80-3.03) 0
Cr (mg/dl)* 1.04 (0.83-1.43) 1.30 (1.00-1.90) 0.92 (0.77-1.14) <0.001
AF type (PAF) 460 (70.66%) 175 (66.54%) 285 (73.45%) 0
Ventricular arrhythmia 67 (10.29%) 28 (10.65%) 39 (10.05%) 1
Killip class ≥ 2* 417 (64.06%) 191 (72.62%) 226 (58.25%) <0.001
CAG* 394 (60.52%) 140 (53.23%) 254 (65.46%) 0
Device support* 57 (8.76%) 30 (11.41%) 27 (6.96%) 0
Died during hospitalization* 101 (15.51%) 62 (23.57%) 39 (10.05%) <0.001

Table 1: Baseline characteristics of patients with/without HUA.

In-hospital mortality

One hundred and one (15.51%) patients died during hospitalization. Among these patients, 68 died of cardiac causes, including lethal ventricular arrhythmia, heart failure, cardiac shock and heart rupture while 19 died of other causes, such as pneumonia and respiratory failure, and there were no clear records of the direct cause of death for the rest 14 patients.

The SUA level of survived patients was significantly lower than that of patients who died (6.03 (4.75-7.49) mg/dl vs. 7.18 (5.41-9.98) mg/dl, p<0.001). Univariate logistic regressions showed that SUA level (Odds Ratio (OR) 1.24, 95% Confidence Interval (CI) 1.15- 1.34, p<0.001) and HUA (OR 2.76, 95%CI 1.78-4.27, p<0.001) were both predictors of in-hospital all-cause mortality (Table 2). The crude ORs of other variates were also shown in Table 2.

Univariate Multivariate
  OR 95% CI p Adjusted OR 95% CI p
Age (years)* 1 1.03-1.08 <0.001 1 1.01-1.06 0
Sex (female) 1 0.73-1.72 1      
HBP history 1 0.67-1.79 1      
DM history* 2 1.32-3.12 0 2 1.21-3.35 0
HF history 1 0.80-1.88 0      
Previous MI 1 0.76-2.30 0      
Stroke history 1 0.83-2.27 0      
Current smoker 1 0.46-1.26 0      
SUA (mg/dl)* 1 1.15-1.34 <0.001 NA NA NA
HUA* 3 1.78-4.27 <0.001 2 1.29-3.40 0
LDL-C (mmol/L) 1 0.78-1.25 1      
Cr (mg/dl) 1 0.98-1.08 0      
AF type (PAF) 1 0.53-1.31 0      
Ventricular arrhythmia* 3 1.78-5.48 <0.001 5 2.24-9.49 <0.001
Killip class ≥ 2* 17 6.32-48.06 <0.001 7 2.28-18.85 <0.001
CAG* 0 0.13-0.33 <0.001 0 0.12-0.43 <0.001
Device support* 3 1.55-5.20 0 3 1.47-7.40 0

Table 2: Results of univariate and multivariate logistic regressions for in-hospital all-cause mortality.

HUA remained as an independent predictor of in-hospital all-cause mortality in the final model of the multivariate logistic regression after adjusting for age, sex, hypertension history, DM history, HF history, previous MI, stroke history, smoking status, LDL-C, Cr, AF type, ventricular arrhythmia, Killip classification, CAG and device support (Adjusted OR 2.09, 95% CI 1.29-3.40, p=0.003). Other independent predictors were elder age, history of DM, ventricular arrhythmia occurrence, Killip class ≥ 2, without CAG, and with IABP or ECMO support (Table 2).

Subgroup analysis

Subgroup analysis by sex: Subgroup analyses in male and female patients were performed. SUA level of male patients was significantly higher than that of female patients (6.48 (5.02-8.04) mg/dl vs. 5.95 (4.65-7.40) mg/dl, p=0.014). Baseline characteristics of male and female patients were shown in Table S1.

The result of the univariate logistic regression with HUA was similar to the whole population for both male and female patients (Male: OR 3.21, 95% CI 1.78-5.81, p<0.001; Female: OR 2.35, 95% CI 1.21-4.55, p=0.012) (Table S2 and Table S3). However, multivariate logistic regression results were different. When the same variates were adjusted as the whole population except for sex, HUA was still an independent predictor of in-hospital all-cause mortality in the final model for male patients (Adjusted OR 2.02, 95% CI 1.04- 3.95, p=0.039) Table S2, but not for female patients (Table S3).

Subgroup analysis in patients underwent CAG

As approximately only 60% patients received CAG, we performed the subgroup analysis in this population. The SUA level (6.08 (4.95-7.36) mg/dl vs. 6.66 (4.76-8.82) mg/dl, p=0.002) and HUA prevalence (35.53% vs. 47.86%, p=0.002) were lower in patients who underwent CAG compared to those who did not.

With univariate logistic regressions, significant associations were found between the in-hospital mortality and SUA (OR 1.45, 95% CI 1.23-1.72, p<0.001) or HUA (OR 2.39, 95% CI 1.12-5.13, p=0.025) (Table S4). As for the multivariate logistic regression, besides HUA and the covariates used for the whole population, LM disease, multivessel disease and successful or no need for revascularization were also added to the analysis. However, HUA was excluded from the final model which included age, DM history, ventricular arrhythmia, Killip classification and the use of circulation supporting devices (Table S4).

Discussion

The present study showed that HUA (SUA ≥ 6.8 mg/dl) was an independent predictor of in-hospital all-cause mortality in patients with AMI and AF. The results in male patients were mostly consistent with the whole population, but different in the female patients or those who underwent CAG. To our knowledge, this might be the first study specifically concerning the impact of UA on in-hospital mortality of such population.

The relationship between UA and AMI has long been investigated, but the role of UA in the prognosis is still controversial. In 2005, Japanese investigators found that the all-cause mortality of patients with AMI in the highest UA quartile was 3.7 fold of that in the lowest quartile [25,26]. Similar results were seen in some later studies involving patients with different MI types (STEMI only or STEMI and NSTEMI), using SUA or “HUA” defined by different cut-off values and with either short- or long-term follow-ups [4- 6,10,27-30]. A retrospective study involving 621 AMI patients demonstrated that higher SUA (every 10 μmol/L increase) was an independent predictor of in-hospital mortality after adjusting for con-founders (OR 1.016, 95% CI 1.001-1.031, p=0.043), which was similar to our study, but the population was younger and the death rate appeared lower [31]. Moreover, the association between UA and AMI outcomes was also supported by some meta-analyses [32-35]. Α recent meta-analysis which involved 29 studies and more than 950,000 participants showed that, for every 1 mg/dl increment in UA, the mortality of Coronary Heart Disease (CHD) would increase by 13% [36].

However, some studies showed different results [7,8,37]. In a cohort study of AMI patients with mild renal dysfunction, no significant difference was found in in-hospital and one-year mortality among patients in different SUA tertiles [38]. Besides, a recent study of elder AMI patients showed similar short-term death rate between those with lower and higher SUA levels [39]. The divergence of the results probably came from the difference of the study populations and “HUA” stratification values. The heterology in con-founders chosen might also contribute to the difference of the results.

It was still not clearly explained on the mechanism of the impact caused by UA on the prognosis of AMI patients. Impaired myocardial reperfusion was supposed to be one of the possible explanations [40]. However, conflicting results were seen in the protective effect of allopurinol on reperfusion injury [41]. Besides, UA was found to be an independent risk factor for new-onset AF in the setting of AMI, which was associated with worse outcomes [18-20,42]. Furthermore, UA was associated with many other wellestablished risk factors for adverse outcomes in AMI patients, such as age, obesity, serum Cr and cholesterol [43]. It was hard to confirm whether UA had direct impact on AMI outcomes or was just a marker for adverse prognosis by observational studies. However, as an easily obtained and widely tested biomarker, UA was still of importance in clinical practice.

Substantial data were available for the relationship between UA and AF. A recent meta-analysis found higher SUA levels in patients with AF than those without AF [44]. Several large scale cohort studies with long-term follow-ups consistently demonstrated the association between UA and AF incidence [45-48]. Their causal relationship was also supported by a recent Mendelian randomization study [49]. However, studies concerning the effect of UA on AF patients’ prognosis were rare. Some studies showed the association between higher UA levels and atria thrombosis [16,17]. As atrial thrombi were the major causes of stroke and other thromboembolism complications, it might be reasonable to assume an adverse impact of HUA on the outcomes of AF patients.

Subgroup analyses categorized by sex were performed because some previous researches reported different results between males and females in the effect of UA on the prognosis of AMI. In the multivariate logistic regression of 184 patients with STEMI, HUA was an independent predictor of in-hospital and 30-day mortality in men but not in women [50]. On the contrary, a recent study only showed significant association between UA and fatal MI in women yet not in men [51]. Results from a meta-analysis showed stronger association between HUA and CHD and all-cause mortality in women [52]. However, the definition of HUA varied among studies. Some took different cut-off values for males and females [5,6,27,50]. While others used the same standard for both sexes [7,26,28,39]. We chose the uniform cut-off value of 6.8 mg/dl based on the recent guideline [24]. With this cut-off value, results were similar for male patients and the whole population, but different for females. A higher SUA level was seen in the present study in male than in female patients, which was consistent with some epidemiological studies [53,54]. Although the effect of estrogen on UA metabolism was proven to be a cause of this phenomenon, it might be of less importance in the present population as most of the female patients might be menopause due to their age shown in the baseline characteristics [55]. Better renal function and more complications with DM might be some potential reasons [56]. The mechanism of sex difference in the prognostic role of HUA was unclear. In the study population, a possible explanation could be the higher prevalence of DM in female patients, which was a stronger risk factor for fatal ischemic heart disease especially for women, but further investigations were needed [57].

Some previous studies have shown the association of higher UA levels and poor prognosis in patients undergoing PCI [4,26,27,29]. However, in our study, HUA was not remained in the final adjusted multivariate model. The level of SUA and the proportion of HUA were significantly lower in patients who received CAG, but the prevalence of stronger risk factors for mortality were much higher, such as ventricular arrhythmia, Killip class and device support, which could weaken the value of HUA to some extent. However, further studies are required to confirm the hypothesis.

Conclusion and Limitations

In conclusion, Hyperuricemia (HUA) defined as Serum Uric Acid (SUA) ≥ 6.8 mg/dl was an independent predictor of in-hospital allcause mortality in patients with Acute Myocardial Infarction (AMI) and coexisting Atrial Fibrillation (AF), who were at high risk of death. Similar impacts were found in male patients, but not in the female patients or those who underwent Coronary Angio Graphy (CAG).

At last, some limitations of our study should be noticed. Firstly, as the study was retrospective, bias could not be avoided and the insufficiency in confounding factors adjusting might exist. Secondly, the number of patients was relatively small and long-term follow-up data was not available. The results, therefore, should be restricted in specific population and with conditions. Thirdly, due to the data deficit, we were unable to precisely identify whether the AF was new-onset or previously existed.

Funding

This study was supported by grants from National Natural Science Foundation of China (81800291), Beijing Municipal Administration of Hospitals’ Youth Programme (QML20180207).

Conflicts of Interest

None.

References

  1. Ibanez B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The task force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2018; 39 (2): 119-177.
  2. Castro-Dominguez Y, Dharmarajan K, McNamara RL. Predicting death after acute myocardial infarction. Trends Cardiovasc Med. 2018; 28 (2): 102-109.
  3. Kowalczyk J, Francuz P, Swoboda R, Lenarczyk R, Sredniawa B, Golda A, et al. Prognostic significance of hyperuricemia in patients with different types of renal dysfunction and acute myocardial infarction treated with percutaneous coronary intervention. Nephron Clin Pract. 2010; 116 (2): 114-122.
  4. Akgul O, Uyarel H, Pusuroglu H, Gul M, Isiksacan N, Turen S, et al. Predictive value of elevated uric acid in Turkish patients undergoing primary angioplasty for ST elevation myocardial infarction. Acta Cardiol Sin. 2014; 30 (2): 119-127.
  5. Mora-Ramírez M, Estevez-Garcia IO, Irigoyen-Camacho ME, Bojalil R, Gonzalez-Pacheco H, Amezcua-Guerra LM. Hyperuricemia on admission predicts short-term mortality due to myocardial infarction in a population with high prevalence of cardiovascular risk factors. Rev Invest Clin. 2017; 69 (5): 247-253.
  6. Guo W, Yang D, Wu D, Liu H, Chen S, Liu J, et al. Hyperuricemia and long-term mortality in patients with acute myocardial infarction undergoing percutaneous coronary intervention. Ann Transl Med. 2019; 7 (22): 636.
  7. Homayounfar S, Ansari M, Kashani KM. Evaluation of independent prognostic importance of hyperuricemia in hospital death after acute myocardial infarction. Saudi Med J. 2007; 28 (5): 759-761.
  8. Lazzeri C, Valente S, Chiostri M, Picariello C, Gensini GF. Uric acid in the early risk stratification of ST-elevation myocardial infarction. Intern Emerg Med. 2012; 7 (1): 33-39.
  9. Ndrepepa G, Braun S, Haase HU, Schulz S, Ranftl S, Hadamitzky M, et al. Prognostic value of uric acid in patients with acute coronary syndromes. Am J Cardiol. 2012; 109 (9): 1260-1265.
  10. Wildi K, Haaf P, Reichlin T, Acemoglu R, Schneider J, Balmelli C, et al. Uric acid for diagnosis and risk stratification in suspected myocardial infarction. Eur J Clin Invest. 2013; 43 (2): 174-182.
  11. Levantesi G, Marfisi RM, Franzosi MG, Maggioni AP, Nicolosi GL, Schweiger C, et al. Uric acid: A cardiovascular risk factor in patients with recent myocardial infarction. Int J Cardiol. 2013; 167 (1): 262-269.
  12. Culleton BF, Larson MG, Kannel WB, Levy D. Serum uric acid and risk for cardiovascular disease and death: The Framingham Heart Study. Ann Intern Med. 1999; 131 (1): 7-13.
  13. Cheong E, Ryu S, Lee JY, Lee SH, Sung JW, Cho DS, et al. Association between serum uric acid and cardiovascular mortality and all-cause mortality: A cohort study. J Hypertens. 2017; 35 (1): S3-9.
  14. Schmitt J, Duray G, Gersh BJ, Hohnloser SH. Atrial fibrillation in acute myocardial infarction: A systematic review of the incidence, clinical features and prognostic implications. Eur Heart J. 2009; 30 (9): 1038-1045.
  15. Kirchhof P, Benussi S, Kotecha D, Ahlsson A, Atar D, Casadei B, et al. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J. 2016; 74 (12): 1359-1469.
  16. Numa S, Hirai T, Nakagawa K, Ohara K, Fukuda N, Nozawa T, et al. Hyperuricemia and transesophageal echocardiographic thromboembolic risk in patients with atrial fibrillation at clinically low-intermediate risk. Circ J. 2014; 78 (7): 1600-1605.
  17. Ning W, Li Y, Ma C, Qiu L, Yu B. The refinement of risk stratification for atrial thrombus or spontaneous echo contrast in nonvalvular atrial fibrillation serum uric acid and left atrial diameter. Int Heart J. 2017; 58 (6): 885-893.
  18. Pedersen OD, Abildstrøm SZ, Ottesen MM, Rask-Madsen C, Bagger H, Køber L, et al. Increased risk of sudden and non-sudden cardiovascular death in patients with atrial fibrillation/flutter following acute myocardial infarction. Eur Heart J. 2006; 27 (3): 290-295.
  19. Consuegra-Sánchez L, Melgarejo-Moreno A, Galcerá-Tomás J, Alonso-Fernández N, Díaz-Pastor Á, Escudero-García G, et al. Short-and long-term prognosis of previous and new-onset atrial fibrillation in ST-segment elevation acute myocardial infarction. Rev Esp Cardiol. 2015; 68 (1): 31-38.
  20. Karataş MB, Çanga Y, İpek G, Özcan KS, Güngör B, Durmuş G, et al. Association of admission serum laboratory parameters with new-onset atrial fibrillation after a primary percutaneous coronary intervention. Coron Artery Dis. 2016; 27 (2): 128-134.
  21. Guo SD, Bai Y, Liu XY, Liu Y, Wang ZZ, Zhong P. Patients with acute myocardial infarction and atrial fibrillation: Association of anaemia with risk of in-hospital bleeding, stroke and other death causes. Biomarkers. 2021; 26 (2): 163-167.
  22. Levine GN, Bates ER, Bittl JA, Brindis RG, Fihn SD, Fleisher LA, et al. 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2016; 68 (10): 1082-1115.
  23. Bai Y, Yue QM, Sun H, Guo SD, Wang ZZ, Zhong P, et al. Prevalence and sex-and age-related risk of pulmonary embolism in in-hospital patients with atrial fibrillation: A multicenter retrospective study from China. Ann Transl Med. 2020; 8 (23): 1558.
  24. FitzGerald JD, Dalbeth N, Mikuls T, Brignardello‐Petersen R, Guyatt G, Abeles AM, et al. 2020 American College of Rheumatology guideline for the management of gout. Arthritis Rheumatol. 2020; 72 (6): 744-760.
  25. Kojima S, Sakamoto T, Ishihara M, Kimura K, Miyazaki S, Yamagishi M, et al. Prognostic usefulness of serum uric acid after acute myocardial infarction (the Japanese Acute Coronary Syndrome Study). Am J Cardiol. 2005; 96 (4): 489-495.
  26. Basar N, Sen N, Ozcan F, Erden G, Kanat S, Sokmen E, et al. Elevated serum uric acid predicts angiographic impaired reperfusion and 1-year mortality in ST-segment elevation myocardial infarction patients undergoing percutaneous coronary intervention. J Investig Med. 2011; 59 (6): 931-937.
  27. Kaya MG, Uyarel H, Akpek M, Kalay N, Ergelen M, Ayhan E, et al. Prognostic value of uric acid in patients with ST-elevated myocardial infarction undergoing primary coronary intervention. Am J Cardiol. 2012; 109 (4): 486-491.
  28. Lazzeri C, Valente S, Chiostri M, Sori A, Bernardo P, Gensini GF. Uric acid in the acute phase of ST elevation myocardial infarction submitted to primary PCI: Its prognostic role and relation with inflammatory markers: A single center experience. Int J Cardiol. 2010; 138 (2): 206-209.
  29. Akpek M, Kaya MG, Uyarel H, Yarlioglues M, Kalay N, Gunebakmaz O, et al. The association of serum uric acid levels on coronary flow in patients with STEMI undergoing primary PCI. Atherosclerosis. 2011; 219 (1): 334-341.
  30. Çanga Y, Emre A, Karataş MB, Çalık AN, Yelgeç NS, İnan D, et al. Prognostic value of serum uric acid levels in patients with non-STEMI undergoing percutaneous coronary intervention. Herz. 2020; 45 (4): 389-396.
  31. Car S, Trkulja V. Higher serum uric acid on admission is associated with higher short-term mortality and poorer long-term survival after myocardial infarction: Retrospective prognostic study. Croat Med J. 2009; 50 (6): 559-566.
  32. Trkulja V, Car S. On-admission serum uric acid predicts outcomes after acute myocardial infarction: Systematic review and metaanalysis of prognostic studies. Croat Med J. 2012; 53 (2): 162-172.
  33. Yan L, Liu Z, Zhang C. Uric acid as a predictor of in-hospital mortality in acute myocardial infarction: A meta-analysis. Cell Biochem Biophys. 2014; 70 (3): 1597-1601.
  34. Von Lueder TG, Girerd N, Atar D, Agewall S, Lamiral Z, Kanbay M, et al. High‐Risk Myocardial Infarction Database Initiative Investigators. Serum uric acid is associated with mortality and heart failure hospitalizations in patients with complicated myocardial infarction: Findings from the high‐risk myocardial infarction database initiative. Eur J Heart Fail. 2015; 17 (11): 1144-1151.
  35. Xu Q, Zhang M, Abeysekera IR, Wang X. High serum uric acid levels may increase mortality and major adverse cardiovascular events in patients with acute myocardial infarction. Saudi Med J. 2017; 38 (6): 577.
  36. Li M, Hu X, Fan Y, Li K, Zhang X, Hou W, et al. Hyperuricemia and the risk for coronary heart disease morbidity and mortality a systematic review and dose-response meta-analysis. Sci Rep. 2016; 6 (1): 1-1.
  37. Hajizadeh R, Ghaffari S, Salehi R, Mazani S, Aghavali S. Association of serum uric acid level with mortality and morbidity of patients with acute ST-elevation myocardial infarction. J Cardiovasc Thorac Res. 2016; 8 (2): 56-60.
  38. Lazzeri C, Valente S, Chiostri M, Spini V, Angelotti P, Gensini GF. Uric acid and mild renal impairment in patients with ST-elevation myocardial infarction. Scand Cardiovasc J. 2015; 49 (1): 14-19.
  39. Li L, Ma Y, Shang XM, Hong Y, Wang JH, Tan Z, et al. Hyperuricemia is associated with short-term outcomes in elderly patients with acute myocardial infarction. Aging Clin Exp Res. 2018; 30 (10): 1211-1215.
  40. Mandurino-Mirizzi A, Crimi G, Raineri C, Pica S, Ruffinazzi M, Gianni U, et al. Elevated serum uric acid affects myocardial reperfusion and infarct size in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. J Cardiovasc Med. 2018; 9 (5): 240-246.
  41. Pacher PA, Nivorozhkin A, Szabó C. Therapeutic effects of xanthine oxidase inhibitors: Renaissance half a century after the discovery of allopurinol. Pharmacol Rev. 2006; 58 (1): 87-114.
  42. Braga CG, Ramos V, Vieira C, Martins J, Ribeiro S, Gaspar A, et al. New-onset atrial fibrillation during acute coronary syndromes: Predictors and prognosis. Rev Port Cardiol. 2014; 33 (5): 281-287.
  43. Meisinger C, Koenig W, Baumert J, Döring A. Uric acid levels are associated with all-cause and cardiovascular disease mortality independent of systemic inflammation in men from the general population: The MONICA/KORA cohort study. Arterioscler Thromb Vasc Biol. 2008; 28 (6): 1186-92.
  44. Pak S, Yatsynovich Y, Valencia D, Chen T. Serum uric acid and atrial fibrillation: Meta-analysis. Crit Pathw Cardiol. 2018; 17 (3): 161-166.
  45. Tamariz L, Agarwal S, Soliman EZ, Chamberlain AM, Prineas R, Folsom AR, et al. Association of serum uric acid with incident atrial fibrillation (from the Atherosclerosis Risk in Communities [ARIC] study). Am J Cardiol. 2011; 108 (9): 1272-1276.
  46. Nyrnes A, Toft I, Njølstad I, Mathiesen EB, Wilsgaard T, Hansen JB, et al. Uric acid is associated with future atrial fibrillation: An 11-year follow-up of 6308 men and women-the Tromsø Study. Europace. 2014; 16 (3): 320-326.
  47. Kwon CH, Lee SH, Lee JY, Ryu S, Sung KC. Uric acid and risk of atrial fibrillation in the korean general population. Circ J. 2018; 82 (11): 2728-2735.
  48. Li S, Cheng J, Cui L, Gurol ME, Bhatt DL, Fonarow GC, et al. Cohort study of repeated measurements of serum urate and risk of incident atrial fibrillation. J Am Heart Assoc. 2019; 8 (13): e012020.
  49. Hong M, Park JW, Yang PS, Hwang I, Kim TH, Yu HT, et al. A mendelian randomization analysis: The causal association between serum uric acid and atrial fibrillation. Eur J Clin Invest. 2020; 50 (10): e13300.
  50. Omidvar B, Ayatollahi F, Alasti M. The prognostic role of serum uric acid level in patients with acute ST elevation myocardial infarction. J Saudi Heart Assoc. 2012; 24 (2): 73-78.
  51. Casiglia E, Tikhonoff V, Virdis A, Masi S, Barbagallo CM, Bombelli M, et al. Serum uric acid and fatal myocardial infarction: Detection of prognostic cut-off values: The URRAH (Uric Acid Right for Heart Health) study. J Hypertens. 2020; 38 (3): 412.
  52. Zuo T, Liu X, Jiang L, Mao S, Yin X, Guo L. Hyperuricemia and coronary heart disease mortality: A meta-analysis of prospective cohort studies. BMC Cardiovasc Disord. 2016; 16 (1): 1-10.
  53. Akizuki SH. Serum uric acid levels among thirty-four thousand people in Japan. Ann Rheum Dis. 1982; 41 (3): 272-274.
  54. Zhang Q, Lou S, Meng Z, Ren X. Gender and age impacts on the correlations between hyperuricemia and metabolic syndrome in Chinese. Clin Rheumatol. 2011; 30 (6): 777-787.
  55. Halperin Kuhns VL, Woodward OM. Sex differences in urate handling. Int J Mol Sci. 2020; 21 (12): 4269.
  56. Gotoh MI, Li C, Yatoh M, Iguchi AK, Hirooka Y. Serum uric acid concentrations in type 2 diabetes: Its significant relationship to serum 1, 5-anhydroglucitol concentrations. Endocr Regul. 2005; 39 (4): 119-125.
  57. Barrett-Connor EL, Cohn BA, Wingard DL, Edelstein SL. Why is diabetes mellitus a stronger risk factor for fatal ischemic heart disease in women than in men? The Rancho Bernardo Study. Jama. 1991; 265 (5): 627-631.

Author Info

Xin-Yao Liu1, Shi-Dong Guo2, Zhen-Zhou Wang3, Peng Zhong4 and Ying Bai1*
 
1Cardiovascular Center, Beijing Tongren Hospital, Capital Medical University, Beijing, China
2Emergency Department, China-Japan Friendship Hospital, Beijing, China
3Trauma Medicine Center, Peking University People’s Hospital, Beijing, China
4Department of Ultrasound, Beijing Friendship Hospital, Capital Medical University, Beijing, China
 

Citation: Liu X, Guo S, Wang Z, Zhong P, Bai Y (2021) Impact of Hyperuricemia on the Prognosis in Patients with Acute Myocardial Infarction and Atrial Fibrillation. Intern Med. 11: 346.

Received: 01-Sep-2021 Accepted: 15-Sep-2021 Published: 22-Sep-2021 , DOI: 10.35248/2165-8048.21.11.346

Copyright: © 2021 Liu X, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Sources of funding : This study was supported by grants from the National Natural Science Foundation of China (81800291), Beijing Municipal Administration of Hospitalsâ?? Youth Programme (QML20180207).