Acute myocardial infarction (AMI) is a severe form of coronary atherosclerotic heart disease, known for its rapid onset, progression, high incidence, and mortality rates.1,2 AMI is now the world’s greatest cause of death due to its continually rising mortality rate over the last ten years3,4. In China, the mortality rate of AMI was reported to be between 42.23% and 62.72% from 2002 to 2016.5 The growing population, aging demographics, and rise in long-term survivors after AMI have led to significant medical and economic burdens worldwide.1 To address this, early risk prediction tools for severe complications in AMI patients are essential.
By utilizing cardiovascular patient data and objective risk assessment, clinicians can identify potential risks and intervene promptly to mitigate complications and reduce mortality. So far, some studies have found that some single indicators including E/e ‘Ratio and Triglyceride glucose index6,7 could be for predicting the occurrence of complications and clinical outcomes in AMI.
Nomogram, a statistical models based on clinical and biological variables, are valuable tools for predicting complications, prognosis, and survival in various diseases, aiding in the development of personalized treatment plans. However, there is a lack of research utilizing nomogram to predict severe complications in AMI patients during hospitalization. The objective of this research is to examine the clinical features and laboratory markers of individuals with AMI in order to forecast the probability of severe complications.
MethodsPatientsFrom August 2020 to January 2023, all 1045 AMI patients admitted in the emergency department of Changsha Central Hospital were selected as the subjects of this study.
DefinitionThe global diagnostic standards for AMI encompass raised levels of myocardial markers in the serum (particularly troponin) surpassing the 99th percentile upper reference limit, together with one or more of the subsequent clinical signs: symptoms of ischemia, fresh ischemic ECG alterations (like recent ST-T adjustments or left bundle branch block), the appearance of pathological Q waves in the ECG, findings from imaging examinations revealing recent myocardial activity loss or recently formed regional wall motion irregularities, and verification of coronary artery thrombosis via coronary angiography or post-mortem examination.8
Severe complications of AMI include acute circulatory dysfunction, severe arrhythmia, heart failure, and death.9
Inclusion and Exclusion CriteriaCriteria for Inclusion: Patients Admitted in Emergency Department Diagnosed with AMICriteria for exclusion: Patients with AMI who expired due to concurrent aortic dissection (n=1), pulmonary embolism (n=1), stroke (n=3), inadequate data (n=16), or age< 18-year-old (n=0). A total of 21 individuals were ineligible (Figure 1).
Figure 1 Flowchart.
Abbreviation: AMI, acute myocardial infarction.
Data CollectionThe collected data includes clinical characteristics and laboratory test results of patients upon admission. The collected clinical data of patients include: general information of patients: gender, age, heart rate(HR), respiratory rate(RR), mean arterial pressure (MAP), percutaneous coronary intervention(PCI), diabetes, hypertension; laboratory indicators: triglyceride(TG), cholesterol, high-density lipoprotein(HDL), low-density lipoprotein(LDL), chlorine, ionized calcium, kalium, sodium, glucose, activated partial thromboplastin time(APTT), fibrinogen, prothrombin time(PT), international normalized ratio(INR), thrombin time(TT), urea nitrogen, creatinine, uric acid(UA), albumin, alanine aminotransferase (ALT), globulin, total bilirubin, white blood cell (WBC), lymphocyte, hematocrit, platelet (PLT), and the severe complications of AMI include death, heart failure (HF), ventricular fibrillation (VF), cardiogenic shock (CS), ventricular tachycardia (VT) and atrioventricular block (AVB).
Statistical AnalysisThe statistical findings were displayed as median values (P25~P75) with group comparisons conducted through the Mann Whitney U-test. Count data was represented as examples (%) and between-group analyses were carried out using the chi-square test. Statistical significance was denoted by P<0.05. An initial database split randomly into modeling and validation subgroups at a 7:3 ratio. Within the modeling subgroup, single-factor logistic regression was applied to identify significant independent variables (P<0.05), which were later included in a multifactor binary logistic regression model. The validation subgroup was utilized for model validation purposes. Model performance was assessed through the area under curve (AUC) of the receiver operating characteristic, calibration curve, and decision curve analysis (DCA). The area under the ROC curve, AUC, is used to evaluate the model performance. AUC>0.7 indicates that the model performance is good.10
Internal Validation is Evaluated Using Bootstrap ValidationThe logistic regression model was utilized to create a column chart, in which every coefficient from the regression was scaled to a 0–100 point system. To forecast the likelihood of severe complications, the cumulative score was determined by adding up the scores of the individual variables. Calibration curves were employed to assess the correlation between the column charts and observed probabilities. Statistical analysis was conducted with SPSS software (version 25) and R software (42.2). A significance level of p < 0.05 was established for statistical significance.
ResultGeneral Characteristics of All PatientsBased on the criteria for inclusion and exclusion, a grand total of 1024 patients with AMI were chosen, including 268 cases (26.17%) in the AMI group with severe complications and 756 cases (73.83%) in the AMI group without severe complications (Table 1). In the severe complication group (n=268) of AMI, the proportions of death, HF, VF, CS, VT and AVB accounted for 16.42% (n=44), 82.46% (n=221), 5.97% (n=16), 22.76% (n=61), 7.84% (n=21) and 5.97% (n=26), respectively. In patients with AMI, there were no notable variances observed in HDL, chlorine, sodium, APTT, globulin, total bilirubin and PLT levels between the two groups (all P>0.05). The age, WBC, lymphocyte, procalcitonin, HR, kalium, glucose, fibrinogen, PT, urea nitrogen, creatinine, UA, ALT, the proportion of female patients, diabetes and hypertension in patients without severe complications were lower than those in patients with severe complications (all P<0.05). The variables including MAP, ionized calcium, TT, albumin, and male proportion were all higher in the group with severe complications (all P<0.05). In the group without severe complications, a higher proportion of patients received PCI treatment compared to those in the group with severe complications (all P<0.05). (Table 1).
Table 1 Comparison of Baseline Data Between AMI Group with Severe Complications and AMI Group Without Severe Complications
Baseline Data Comparison Between Modeling and Validation GroupsTable 2 displayed the baseline characteristics for the modeling group (n=717) and the validation group (n=307). With the exception of glucose and PLT levels (both P<0.05), all other laboratory indicators showed no significant differences (all P>0.05) between the two groups, meeting the criteria for random assignment.
Table 2 Comparison of Baseline Data Between Modeling Group and Validation Group
Comparison of Baseline Data Between the Modeling Group with and without Severe ComplicationsTable 3 showed the comparison of baseline data between the modeling group with and without severe complications. 717 patients were included in the modeling group, including 190 cases (26.50%) in the group with severe complications and 527 cases (73.50%) in the group without severe complications. No notable variations were observed in HDL, chloride, sodium, APTT, TT, globulin, total bilirubin and PLT levels between the two groups (all P>0.05). The group without severe complications had lower levels of WBC, HR, kalium, glucose, fibrinogen, PT, urea nitrogen, creatinine, UA, ALT, total bilirubin and the proportion of females compared to the group with severe complications. (P<0.05). Age, MAP, cholesterol, LDL, TG, ionized calcium, albumin, hematocrit, lymphocyte, PLT and the male ratio was greater in the group without severe complications (P<0.05). Additionally, the rate of PCI treatment was significantly higher in the group without severe complications compared to those with severe complications (P < 0.05).
Table 3 Comparison of Baseline Data Between the Modeling Group with and without Severe Complications
Multivariate Logistic RegressionPerform statistical analysis on the indicators in the modeling group through single factor binary logistic regression analysis. Twenty-five variables were screened out, including gender, age, HR, MAP, PCI, diabetes, hypertension, TG, cholesterol, LDL, ionized calcium, kalium, glucose, APTT, fibrinogen, PT, INR, urea nitrogen, creatinine, UA, albumin, ALT, total bilirubin, and WBC (P<0.05). Include all these 25 variables in a multivariate binary logistic analysis. Ultimately, variables including TG, age, HR, MAP, diabetes, hypertension and WBC were identified as independent risk factors for severe complications in AMI patients (Table 4).
Table 4 Logistic Regression Analysis of Modeling Group
Model Establishment (Nomogram)Depending on what the modelling group’s multivariate logistic analysis revealed, TG, age, HR, MAP, diabetes, hypertension and WBC were ultimately identified as independent risk factors for severe complications in AMI patients. Establish a nomogram through R software package programming (Figure 2).
Figure 2 Nomogram.
Abbreviations: TG, triglyceride; HR, heart rate; MAP, mean artery pressure; WBC, white blood cell.
There are seven variables in a nomogram: TG, age, HR, MAP, diabetes, hypertension and WBC. With the use of charts, we can clearly show the relationships between each variable in this graphical representation of the statistical model. The probability that patients may experience major problems increases with a nomogram score.
For example, we used a simple random sampling method to analyze the clinical data of two AMI patients.
The first patient clinically diagnosed with AMI was TG: 1.17 (87.5 points), Age: 67 years old (32.5 points), HR: 112 (47.5 points), MAP (SBP: 120, DBP: 86): 97.33 (45 points), WBC: 13.50 (22.5 points), with Diabetes (17.5 points) and Hypertension (10 points). The above scores were added up to a total of 262.50 points. The risk of severe complications after AMI corresponding to 262.50 points was identified in the nomogram, and the probability of serious complications in the patient was predicted to be greater than 70%, In actual clinical practice, patients are transferred to the intensive care unit due to serious complications after myocardial infarction. The predicted results are consistent with the actual clinical manifestations of the patient.
Another patient clinically diagnosed with AMI: TG: 14.62 (20 points), Age: 56 years old (22.5 points), HR: 106 (42.5 points), MAP (SBP: 124, DBP: 84): 97.33 (45 points), WBC: 9.44 (17.5 points), without Diabetes (0 points) or Hypertension (0 points). The above scores were added up to a total of 147.50 points. The risk of serious complications after AMI corresponding to 147.50 points was identified in the nomogram, and the probability of serious complications in the patient was predicted to be less than 1%. In actual clinical practice, the patient recovered and was discharged within one week without any serious complications. The predicted results are consistent with the actual clinical manifestations of the patient.
Validation of Column Charts’ Prediction Accuracy in Modeling and Validation QueuesWith an AUC=0.791 (95% CI: 0.753–0.829), the predictive model in the modeling group demonstrated high accuracy in estimating the probability of serious complications in AMI patients (Figure 3).
Figure 3 Validation of nomogram in the modelling group, AUC=0.791 (95% CI: 0.753–0.829).
Abbreviation: AUC, the area under the receiver operating characteristic curve.
Using the repeated sample approach (n=717, sampling frequency=1000) in R software, internal validation was carried out with an absolute error of 0.011. Additionally, by creating calibration curves, we assess the optimal model’s predictive ability. The ideal model’s flawless prediction is shown by the diagonal dashed line among them. The nomogram’s performance is shown by the solid line; the stronger the prediction effect, the higher the fit with the diagonal (dashed line). The model has high calibration, as evidenced by the good consistency between the projected and actual models (Figure 4).
Figure 4 Nomogram calibration curve. Internal validation (n=717, sampling frequency=1000) with an absolute error of 0.011).
The validation queue similarly confirmed the prediction model’s accuracy, with an AUC = 0.732 (95% CI: 0.661–0.803) (Figure 5).
Figure 5 Validation of nomogram in the validation group. AUC = 0.732 (95% CI: 0.661–0.803).
Abbreviation: AUC, the area under the receiver operating characteristic curve.
Internal validation was conducted using R software repeated sampling method (n=307, sampling frequency=1000), with an absolute error of 0.044; And draw a calibration curve, The findings indicate that the model’s calibration is good because there is a rather strong agreement between the expected probability and the observed probability (Figure 6).
Figure 6 Nomogram calibration curve. Internal validation (n=307, sampling frequency=1000) with an absolute error of 0.044).
Evaluation of DCA Curve ModelDrawing DCA curves with the R 42.2 software program to assess the prediction model’s net benefit reveals that the model has a broad threshold range (0.01~0.73), a good clinical net benefit, and good applicability in clinical practice (Figure 7).
Figure 7 DCA curves of the prediction model.
Abbreviation: DCA= decision curve analysis.
DiscussionAMI is a severe cardiovascular disease that contributes significantly to global incidence and mortality rates. By conducting early assessments of the likelihood of serious complications in AMI patients, we can accurately pinpoint those requiring focused attention and prompt intervention to achieve improved clinical outcomes. This research incorporated age, HR, MAP, diabetes, hypertension, TG, and WBC as seven separate risk factors in creating a nomogram model that can forecast the likelihood of severe complications in patients with AMI, showcasing robust clinical predictive ability.
Our study found that patients with severe complications had a significantly higher WBC counts compared to those without severe complications. Previous evidence has indicated WBC, as biomarkers associated with systemic inflammatory response, plays a clear role in both the development and resolution of inflammation during AMI.11 Our research findings support the correlation between elevated levels of WBC and a negative prognosis in individuals suffering from AMI. The increase in WBC counts in circulation can lead to the release of various proteolytic enzymes that worsen local tissue damage,12 ultimately impacting myocardial remodeling and potentially leading to catastrophic consequences.13
Hypertriglyceridemia has traditionally been recognized as a risk factor for cardiovascular disease.14 Research indicates that elevated TG levels can heighten the likelihood of cardiovascular disease.15 Conversely, low TG levels are not conducive to maintaining the stability of cell membranes.16 As a result, the relationship between TG and cardiovascular disease risk has been a topic of debate. Recent studies have revealed a negative association between TG levels and adverse outcomes in patients with cardiovascular and cerebrovascular diseases.17–20 For instance, low serum TG levels have been found to have a negative correlation with in-hospital death and late outcomes in patients with ST-elevation myocardial infarction (STEMI) who are treated with PCI,17 Additionally, a decrease in serum TG levels has been identified as a predictor of cardiovascular death in individuals with HF.21 The reduction in TG during acute coronary syndromes is correlated with a rise in the occurrence of recurrent ischemia.22 This has led to the emergence of the “TG paradox” concept. Our research focused on examining the relationship between TG levels upon admission and the likelihood of severe complications in individuals diagnosed with AMI. The results of our study revealed an inverse association between TG levels and the potential for significant complications in patients suffering from AMI.
Older age has been identified as a major risk factor for developing acute coronary syndrome, and it is also associated with a higher probability of experiencing negative clinical outcomes.23 As individuals age, the incidence of cardiovascular and cerebrovascular diseases tends to increase.24 Research has shown that individuals aged 65–74 have almost a sevenfold increased risk of experiencing a heart attack compared to those in the 35–44 age bracket.25 With aging, the arterial wall becomes thicker and harder, leading to an increased risk of cardiovascular disease.26,27 Our research aligns with these findings, demonstrating a strong age dependence in cardiovascular disease.
The heart rate (HR) plays a crucial role in determining the oxygen demand of the heart muscle, affecting the flow of blood through the coronary arteries by impacting the time for filling the heart during its resting phase. The importance of HR as a prognostic factor in individuals with heart-related conditions such as heart attacks, high blood pressure, and heart dysfunction is well-known.28–30 Several studies have emphasized the role of HR as a predictor of mortality and the onset of cardiovascular disorders like high blood pressure, heart dysfunction, and heart artery blockage.31–33 Research indicates that in individuals experiencing a heart attack, higher heart rates are linked to an increased risk of cardiovascular-related death.34,35
MAP is a predictive indicator of all-cause and cardiovascular disease mortality in middle-aged and elderly individuals. Higher levels of MAP are associated with target organ damage, cardiovascular disease, and cerebrovascular disease.36–40 However, some studies have shown that patients with low MAP in AMI are more likely to experience left ventricular dysfunction.41 This finding aligns with our own research.
Diabetes has been recognized as a risk factor for AMI and is a common complication among AMI inpatients.42 Researches indicated that diabetes could increase the risk of AMI by two to four times.43 Additionally, elevated blood glucose levels can contribute to various risk factors, for example, hinder the clearance of TG-rich lipoproteins in the bloodstream. Individuals with inadequately managed diabetes have elevated TG levels in contrast to those with well-managed diabetes. Additionally, there seems to be an extended duration of postprandial hyperlipidemia in diabetic individuals, suggesting prolonged exposure of arteries to atherogenic particles.44 Our study additionally affirms the idea that diabetes heightens the likelihood of severe complications in individuals with a heart attack.
Hypertension is a significant global cardiovascular risk factor that is strongly linked to coronary artery disease. The prevalence of hypertension is high and tends to increase with age.45 The pathological and physiological links between hypertension and AMI involve endothelial dysfunction, autonomic nervous system dysfunction, impaired vascular reactivity, and genetic factors.46 Research shows that approximately 30–40% of patients with STEMI have hypertension, while the rate is even higher at around 70% for those with non-ST segment elevation myocardial infarction (NSTEMI).47,48 Our research findings align with this conclusion.
Previously researches mainly focused on the predicting single prognostic outcomes after AMI attack such as death,49 heart failure50,51 and so on. However, our study constructed a model which could predict various severe complications including acute circulatory dysfunction, severe arrhythmia, heart failure, and death after AMI. In addition, the sample size used in this study (n=1024) is relatively large, and all variables involved are commonly used indicators in clinical laboratory tests and general information of patients, with good clinical applicability.
This research has limitations that must be considered. Firstly, as a study conducted at a single center, it is crucial to recognize the necessity of adjusting for differences in countries, regions, and populations when utilizing the nomogram. When validating the model on a larger scale or in other centers, it is crucial to consider the diversity in etiologies and lifestyle habits across different regions. Secondly, conducting multicenter studies with larger sample sizes is essential to validate our findings. Secondly, the retrospective nature of our study introduces potential patient selection bias, a common limitation in such studies. Thirdly, a more comprehensive analysis comparing patient age and different types of myocardial infarction would enhance the representativeness of our research results. Fourthly, we compared the risk of severe complications in patients with AMI who underwent PCI and those who did not. However, we all know that the key to early treatment of AMI is to rebuild the infarcted blood vessel, so early PCI is crucial. Our study only focused on whether the patient underwent PCI or not. Due to the data missing, we could not compare the impact of different times of PCI on the occurrence of severe complications after AMI. Relevant studies have proved that the recovery of left ventricular ejection fraction after AMI is associated with better prognosis.52–56 However, our study lacks relevant data on left ventricular function at the initial stage and after MI, which leads to a certain limitation in our study.
ConclusionThe column chart prediction model developed based on the above seven independent risk factors has strong discriminative ability and good clinical practicality. Clinical doctors can quickly and easily assess the risk of serious complications for AMI patients upon admission through easily accessible data, and intervene early to reduce the occurrence of adverse events.
Data Sharing StatementDatasets used and/or analyzed in the present study were availed by the corresponding author on reasonable request.
Ethics approval and consent to participateThis study was conducted in accordance with Declaration of Helsinki 2002. The study was approved by institutional review board of Changsha Central Hospital of University of South China (NO.2023-045 KTSB). Due to retrospective characteristics of the study, informed consent was waived. All patient information was anonymous and confidential.
Author ContributionsAll authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas; took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.
FundingNational Key Clinical Specialty Scientific Research Project (Z2023047), Changsha Central Hospital (YNKY202306), Changsha Natural Science Foundation (kq2208445).
DisclosureThe authors report no conflicts of interest in this work.
References1. Anderson JL, Morrow DA. Acute myocardial infarction. N Engl J Med. 2017;376:2053–2064. doi:10.1056/NEJMra1606915
2. Hwang J, Lee K. Mortality and discharge outcome in acute myocardial infarction patients: a study based on Korean national hospital discharge in-depth injury survey data. Risk Manag Healthc Policy. 2024;17:2045–2053. doi:10.2147/RMHP.S472822
3. Hunziker L, Radovanovic D, Jeger R, et al. Twenty-year trends in the incidence and outcome of cardiogenic shock in AMIS plus registry. Circ Cardiovasc Interv. 2019;12(4):e007293. doi:10.1161/CIRCINTERVENTIONS.118.007293
4. Wong ND. Epidemiological studies of CHD and the evolution of preventive cardiology. Nat Rev Cardiol. 2014;11:276–289. doi:10.1038/nrcardio.2014.26
5. Du X, Patel A, Anderson CS, Dong J, Ma C. Epidemiology of cardiovascular disease in china and opportunities for improvement: JACC international. J Am Coll Cardiol. 2019;73:3135–3147. doi:10.1016/j.jacc.2019.04.036
6. Mikeladze B, Zhvania N, Nikolaishvili G. E/e’ ratio as a predictor of in-hospital complications and clinical outcomes of acute myocardial infarction. Cureus. 2024;16:e66795. doi:10.7759/cureus.66795
7. Liu H, Wang L, Zhou X, et al. Triglyceride-glucose index correlates with the occurrence and prognosis of acute myocardial infarction complicated by cardiogenic shock: data from two large cohorts. Cardiovasc Diabetol. 2024;23:337. doi:10.1186/s12933-024-02423-8
8. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol. 2012;60(16):1581–1598. doi:10.1016/j.jacc.2012.08.001
9. Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med. 2013;368:2004–2013. doi:10.1056/NEJMra1216063
10. Nahm FS. Receiver operating characteristic curve: overview and practical use for clinicians. Korean J Anesthesiol. 2022;75:25–36. doi:10.4097/kja.21209
11. Kologrivova I, Shtatolkina M, Suslova T, Ryabov V. Cells of the immune system in cardiac remodeling: main players in resolution of inflammation and repair after myocardial infarction. Front Immunol. 2021;12:664457. doi:10.3389/fimmu.2021.664457
12. Ma Y, Yabluchanskiy A, Lindsey ML. Neutrophil roles in left ventricular remodeling following myocardial infarction. Fibrogenesis Tissue Repair. 2013;6:11. doi:10.1186/1755-1536-6-11
13. Frangogiannis NG. Regulation of the inflammatory response in cardiac repair. Circ Res. 2012;110:159–173. doi:10.1161/CIRCRESAHA.111.243162
14. Miller M, Stone NJ, Ballantyne C, et al. Triglycerides and cardiovascular disease: a scientific statement from the American heart association. Circulation. 2011;123(20):2292–2333. doi:10.1161/CIR.0b013e3182160726
15. Sarwar N, Danesh J, Eiriksdottir G, et al. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation. 2007;115(4):450–458. doi:10.1161/CIRCULATIONAHA.106.637793
16. Eryurek FG, Surmen E, Oner P, Altug T, Oz H. Gamma-glutamyl transpeptidase and acetylcholinesterase activities in brain capillaries of cholesterol-fed rabbits. Res Commun Chem Pathol Pharmacol. 1990;69:245–248.
17. Cheng YT, Liu T-J, Lai H-C, et al. Lower serum triglyceride level is a risk factor for in-hospital and late major adverse events in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention- a cohort study. BMC Cardiovasc Disord. 2014;14(1):143. doi:10.1186/1471-2261-14-143
18. Li W, Liu M, Wu B, et al. Serum lipid levels and 3-month prognosis in Chinese patients with acute stroke. Adv Ther. 2008;25(4):329–341. doi:10.1007/s12325-008-0045-7
19. Khawaja OA, Hatahet H, Cavalcante J, Khanal S, Al-Mallah MH. Low admission triglyceride and mortality in acute coronary syndrome patients. Cardiol J. 2011;18:297–303.
20. Dziedzic T, Slowik A, Gryz EA, Szczudlik A. Lower serum triglyceride level is associated with increased stroke severity. Stroke. 2004;35:e151–152. doi:10.1161/01.STR.0000128705.63891.67
21. Kozdag G, Ertas G, Emre E, et al. Low serum triglyceride levels as predictors of cardiac death in heart failure patients. Tex Heart Inst J. 2013;40:521–528.
22. Correia LC, Magalhães LP, Braga JC, et al. Decrease of plasma triglycerides during the acute phase of unstable angina or non-ST elevation myocardial infarction is a marker of recurrent ischemia. Atherosclerosis. 2004;177:71–76. doi:10.1016/j.atherosclerosis.2004.05.026
23. Jiménez-Méndez C, Díez-Villanueva P, Alfonso F. Non-ST segment elevation myocardial infarction in the elderly. Rev Cardiovasc Med. 2021;22:779–786. doi:10.31083/j.rcm2203084
24. Donato AJ, Machin DR, Lesniewski LA. Mechanisms of dysfunction in the aging vasculature and role in age-related disease. Circ Res. 2018;123:825–848. doi:10.1161/CIRCRESAHA.118.312563
25. Yazdanyar A, Newman AB. The burden of cardiovascular disease in the elderly: morbidity, mortality, and costs. Clin Geriatr Med. 2009;25:563–577. doi:10.1016/j.cger.2009.07.007
26. Lakatta EG, Levy D. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: part I: aging arteries: a “set up” for vascular disease. Circulation. 2003;107:139–146. doi:10.1161/01.CIR.0000048892.83521.58
27. Lakatta EG, Levy D. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: part II: the aging heart in health: links to heart disease. Circulation. 2003;107:346–354. doi:10.1161/01.CIR.0000048893.62841.F7
28. Gillman MW, Kannel WB, Belanger A, D’Agostino RB. Influence of heart rate on mortality among persons with hypertension: the Framingham Study. Am Heart J. 1993;125:1148–1154. doi:10.1016/0002-8703(93)90128-V
29. Lonn EM, Rambihar S, Gao P, et al. Heart rate is associated with increased risk of major cardiovascular events, cardiovascular and all-cause death in patients with stable chronic cardiovascular disease: an analysis of ONTARGET/TRANSCEND. Clin Res Cardiol. 2014;103:149–159. doi:10.1007/s00392-013-0644-4
30. Vazir A, Claggett B, Jhund P, et al. Prognostic importance of temporal changes in resting heart rate in heart failure patients: an analysis of the CHARM program. Eur Heart J. 2015;36(11):669–675. doi:10.1093/eurheartj/ehu401
31. Kolloch R, Legler UF, Champion A, et al. Impact of resting heart rate on outcomes in hypertensive patients with coronary artery disease: findings from the international VErapamil-SR/trandolapril study (INVEST). Eur Heart J. 2008;29:1327–1334. doi:10.1093/eurheartj/ehn123
32. Lechat P, Hulot J-S, Escolano S, et al. Heart rate and cardiac rhythm relationships with bisoprolol benefit in chronic heart failure in CIBIS II Trial. Circulation. 2001;103:1428–1433. doi:10.1161/01.CIR.103.10.1428
33. Diaz A, Bourassa MG, Guertin MC, Tardif JC. Long-term prognostic value of resting heart rate in patients with suspected or proven coronary artery disease. Eur Heart J. 2005;26:967–974. doi:10.1093/eurheartj/ehi190
34. Seronde MF, Geha R, Puymirat E, et al. Discharge heart rate and mortality after acute myocardial infarction. Am J Med. 2014;127:954–962. doi:10.1016/j.amjmed.2014.06.034
35. Perne A, Schmidt FP, Hochadel M, et al. Admission heart rate in relation to presentation and prognosis in patients with acute myocardial infarction. Treatment regimens in German chest pain units. Herz. 2016;41:233–240. doi:10.1007/s00059-015-4355-7
36. Franklin SS, Sutton-Tyrrell K, Belle SH, Weber MA, Kuller LH. The importance of pulsatile components of hypertension in predicting carotid stenosis in older adults. J Hypertens. 1997;15:1143–1150. doi:10.1097/00004872-199715100-00012
37. Sesso HD, Stampfer MJ, Rosner B, et al. Systolic and diastolic blood pressure, pulse pressure, and mean arterial pressure as predictors of cardiovascular disease risk in Men. Hypertension. 2000;36(5):801–807. doi:10.1161/01.HYP.36.5.801
38. Domanski MJ, Davis BR, Pfeffer MA, Kastantin M, Mitchell GF. Isolated systolic hypertension: prognostic information provided by pulse pressure. Hypertension. 1999;34:375–380. doi:10.1161/01.HYP.34.3.375
39. Beloncle F, Radermacher P, Guerin C, Asfar P. Mean arterial pressure target in patients with septic shock. Minerva Anestesiol. 2016;82:777–784.
40. Zheng L, Sun Z, Li J, et al. Pulse pressure and mean arterial pressure in relation to ischemic stroke among patients with uncontrolled hypertension in rural areas of China. Stroke. 2008;39(7):1932–1937. doi:10.1161/STROKEAHA.107.510677
41. Avanzini F, Alli C, Boccanelli A, et al. High pulse pressure and low mean arterial pressure: two predictors of death after a myocardial infarction. J Hypertens. 2006;24(12):2377–2385. doi:10.1097/01.hjh.0000251897.40002.bf
42. Milazzo V, Cosentino N, Genovese S, et al. Diabetes mellitus and acute myocardial infarction: impact on short and long-term mortality. Adv Exp Med Biol. 2021;1307:153–169.
43. Abbott RD, Donahue RP, Kannel WB, Wilson PW. The impact of diabetes on survival following myocardial infarction in men vs women. THE Framingham Study Jama. 1988;260:3456–3460.
44. Coughlan BJ, Sorrentino MJ. Does hypertriglyceridemia increase risk for CAD? Growing evidence suggests it plays a role. Postgrad Med. 2000;108:77–84. doi:10.1080/19419260.2000.12277449
45. Buford TW. Hypertension and aging. Ageing Res Rev. 2016;26:96–111. doi:10.1016/j.arr.2016.01.007
46. Konstantinou K, Tsioufis C, Koumelli A, et al. Hypertension and patients with acute coronary syndrome: putting blood pressure levels into perspective. J Clin Hypertens. 2019;21(8):1135–1143. doi:10.1111/jch.13622
47. Reinstadler SJ, Eitel C, Thieme M, et al. Comparison of characteristics of patients aged 45 years with ST-elevation myocardial infarction (from the AIDA STEMI CMR Substudy). Am J Cardiol. 2016;117:1411–1416. doi:10.1016/j.amjcard.2016.02.005
48. Shah B, Bangalore S, Gianos E, et al. Temporal trends in clinical characteristics of patients without known cardiovascular disease with a first episode of myocardial infarction. Am Heart J. 2014;167:480–488e481. doi:10.1016/j.ahj.2013.12.019
49. Li P, Yao W, Wu J, et al. Development and validation of a nomogram model for predicting in-hospital mortality in non-diabetic patients with non-ST-segment elevation acute myocardial infarction. Clin Appl Thromb Hemost. 2024;30:10760296241276524. doi:10.1177/10760296241276524
50. Li X, Zhang T, Xing W. Predictive value of initial Lp-PLA2, NT-proBNP, and peripheral blood-related ratios for heart failure after early onset infarction in patients with acute myocardial infarction. Am J Transl Res. 2024;16:2940–2952. doi:10.62347/GSBB6486
51. Yu F, Xu Y, Peng J. Evaluation of a nomogram model for predicting in-hospital mortality risk in patients with acute ST-elevation myocardial infarction and acute heart failure post-PCI. Scand Cardiovasc J. 2024;58:2387001. doi:10.1080/14017431.2024.2387001
52. Chew DS, Wilton SB, Kavanagh K, et al. Left ventricular ejection fraction reassessment post-myocardial infarction: current clinical practice and determinants of adverse remodeling. Am Heart J. 2018;198:91–96. doi:10.1016/j.ahj.2017.11.014
53. Dauw J, Martens P, Deferm S, et al. Left ventricular function recovery after ST-elevation myocardial infarction: correlates and outcomes. Clin Res Cardiol. 2021;110:1504–1515. doi:10.1007/s00392-021-01887-y
54. Otero-Garcia O, Cid-álvarez AB, Juskova M, et al. Prognostic impact of left ventricular ejection fraction recovery in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention: analysis of an 11-year all-comers registry. Eur Heart J Acute Cardiovasc Care. 2021;10:898–908. doi:10.1093/ehjacc/zuab058
55. Chew DS, Heikki H, Schmidt G, et al. Change in left ventricular ejection fraction following first myocardial infarction and outcome. JACC Clin Electrophysiol. 2018;4:672–682. doi:10.1016/j.jacep.2017.12.015
56. Kim KA, Kim SH, Lee KY, et al. Predictors and long-term clinical impact of heart failure with improved ejection fraction after acute myocardial infarction. J Am Heart Assoc. 2024;13:e034920. doi:10.1161/JAHA.124.034920
留言 (0)