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| ORIGINAL ARTICLE |
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| Year : 2020 | Volume
: 2
| Issue : 2 | Page : 70-79 |
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Mortality and morbidity associated with type 2 myocardial infarction: A single-center study
Hoang H Truong1, Maiskov V Victor2, Meray A Imad2, Zhanna D Kobalava1, Usha T Parvathy3, Ibrahim Al-Zakwani4
1 Department of Internal Medicine with the Subspecialty of Cardiology and Functional Diagnostics Named After V.S. Moiseev, Institute of Medicine, Peoples' Friendship University of Russia (RUDN University), Moscow, Russia
2 Department of Internal Medicine with the Subspecialty of Cardiology and Functional Diagnostics Named After V.S. Moiseev, Institute of Medicine, Peoples' Friendship University of Russia (RUDN University); Vinogradov Moscow City Clinical Hospital, Moscow, Russia
3 MPS Hospital, Podbelskovo Street, Department of Cardiac Surgery, RUDN University, Moscow, Russia
4 Department of Pharmacology & Clinical Pharmacy, College of Medicine & Health Sciences, Sultan Qaboos University; Gulf Health Research, Muscat, Oman
| Date of Submission | 20-Jun-2020 |
| Date of Decision | 24-Jun-2020 |
| Date of Acceptance | 26-Jun-2020 |
| Date of Web Publication | 02-Sep-2020 |
Correspondence Address:
Prof. Zhanna D Kobalava
Head of the Department, Department of Internal Medicine with the Subspecialty of Cardiology and Functional Diagnostics Named after Prof. V.S. Moiseev, Institute of Medicine, RUDN University Moscow
Russia
 Source of Support: None, Conflict of Interest: None  | 1 |
DOI: 10.4103/ACCJ.ACCJ_30_20
Background: The incidence of Type 1 (T1) and Type 2 (T2) myocardial infarction (MI) varies according to the definition used. In clinical practice, approximately one third of T2MI underwent coronary angiography. It may be difficult to accurately diagnose this entity based only on clinical evidence of imbalance between oxygen supply and demand without angiographic data. Objective: The objective of this study was to assess the correlation between angiographic and clinical definitions of Type-2 versus Type-1 myocardial infarction (T2MI vs. T1MI) and prognosis. Methods: A total of 450 consecutive patients with a diagnosis of acute MI were prospectively recruited and underwent coronary angiography <24 h after the onset of symptoms. The mean follow-up was 1.9 years. Results: Atherothrombotic events were found in 275 (61.1%) patients, whereas clinical triggers were identified in 244 (54.2%) cases. T2MI was diagnosed in 175 (28.9%) patients. Rates of in-hospital (7.4% vs. 10.6%; P = 0.268) and long-term (16.6% vs. 17.1%; P = 0.886) mortality were comparable between T2MI and T1MI patients. Those with T2MI had a higher cardiac rehospitalization rate during follow-up (33.3% vs. 19.5%; P = 0.030). Reduced left ventricular ejection fraction (LVEF) was associated with increased long-term mortality (odds ratio 5.2; 95% confidence interval: 1.1–23.5; P = 0.030). GRACE score had a comparable predictive power for in-hospital mortality in both T1 and T2MI subtypes, but was poor in predicting all-cause long-term mortality in patients with T2MI (area under the receiver operating curve 0.663 vs. 0.847; P = 0.009). Conclusions: There was a discrepancy between angiographic and clinical definitions of MI types in a substantial proportion of our patient population. Reduced LVEF was a strong predictor for worse outcomes in T2MI patients. The GRACE score predicted in-hospital mortality well, but not long-term mortality in patients with T2MI.
Keywords: Atherothrombosis, coronary angiography, Type-1 myocardial infarction, Type-2 myocardial infarction
How to cite this article:
Truong HH, Victor MV, Imad MA, Kobalava ZD, Parvathy UT, Al-Zakwani I. Mortality and morbidity associated with type 2 myocardial infarction: A single-center study. Ann Clin Cardiol 2020;2:70-9 |
How to cite this URL:
Truong HH, Victor MV, Imad MA, Kobalava ZD, Parvathy UT, Al-Zakwani I. Mortality and morbidity associated with type 2 myocardial infarction: A single-center study. Ann Clin Cardiol [serial online] 2020 [cited 2023 Mar 24];2:70-9. Available from: http://www.onlineacc.org/text.asp?2020/2/2/70/294297 |
| Introduction | |  |
Type-2 myocardial infarction (T2MI) results from an imbalance between myocardial blood supply and demand, in the absence of acute atherosclerotic plaque disruption or atherothrombosis.[1] Clinical criteria, defined as provoking conditions (triggers) such as anemia, severe hypertension, and tachyarrhythmia, that can trigger myocardial ischemia have been used in defining a T2MI diagnosis in multiple studies.[2] However, more than two-thirds of patients with suspected T2MI have not undergone coronary angiography (CAG) to exclude significant coronary artery disease (CAD) atherothrombosis.[3] Thus, differentiation between T2MI and T1MI becomes difficult if based only on the clinical criteria in the absence of CAG. Moreover, differences exist in the clinical criteria used for the diagnosis of T2MI making the comparisons between studies more difficult. For example, some investigators developed a set of specific predetermined oxygen mismatch criteria [4] while others used broader criteria to define T2MI.[5],[6] Specific criteria for the diagnosis of T2MI have now been adopted and implemented in various studies.[7],[8],[9]
Although in a recent meta-analysis patients with T2MI were reported to have a worse prognosis in both short- and long-term outcomes compared to T1MI,[3],[10] no current recommendations exist on the management of T2MI. Risk stratification plays an essential role in the prevention of cardiovascular disease, including cardiovascular events such as acute coronary syndrome (ACS) and stroke [11] and provides a useful assessment of risk of developing adverse outcomes during follow-up. With regard to patients with ACS, risk stratification and prognosis assessment using the GRACE risk model (Global Registry of Acute Coronary Events) have been included in the current recommendations of the European Society of Cardiology.[11],[12] The GRACE risk scale provides prognostic value in patients presenting with ACS (C-statistic 0.84)[13] and has value in predicting risk of death within 6 months (C-statistic 0.81)[14] However, the use of the GRACE risk score applies to patients with T1MI,[15],[16] and its applicability to patients with T2MI is not well-known.
The aim of this study was to determine the incidence of T1-versus T2MI based on angiographic and clinical definitions, management, prognosis, and assess the value of the GRACE risk score in patients with T2MI.
| Methods | | |
Study design and population
This was a single-center prospective, observational, cohort study in consecutive patients with a diagnosis of acute MI undergoing CAG <24 h after the onset of symptoms. Patients were enrolled in the intensive care unit, Vinogradov Moscow clinical hospital (Moscow, Russia). [Figure 1] provides an outline of the study design and patient selection.
Data collection
The clinical and demographic characteristics were extracted from the electronic medical records (age, gender, history of hypertension, dyslipidemia, previous MI and revascularization, diabetes mellitus, and chronic kidney disease), physical examination on admission and laboratory-instrumental tests (including vital signs, Killip class, the routine cardiac blood tests, electrocardiography, echocardiography, and angiographic parameters), medications administered during hospitalization, and discharge.
Angiographic assessment
CAG was performed during the first 24 h after symptom onset according to the recent guidelines.[11],[12] The highest percentage stenosis of the main coronary arteries was assessed angiographically. Coronary artery stenosis was considered significant if it was >70% as assessed by quantitative CAG, except for the left main stem where ≥50% was considered clinically significant.[17],[18] Complexity of coronary stenosis morphology was determined as previously described.[19],[20],[21] A lesion was considered complex if it exhibited any of the following features: (1) an intraluminal filling defect consistent with thrombus, defined as abrupt vessel cutoff with persistence of contrast, or an intraluminal filling defect in a patent vessel within or next to a stenotic region with surrounding homogeneous contrast opacity; (2) plaque ulceration, defined with contrast and hazy contours beyond the vessel lumen; and (3) plaque irregularity, defined by irregular margins or overhanging edges; and impaired flow.
Definition
MI was diagnosed according to the 4th universal definition of MI,[1] defined as the detection of a rise and/or fall of cardiac biomarker values in the setting of evidence of acute myocardial ischemia. Myocardial ischemia was defined as the presence of at least one of the following criteria: Symptoms of ischemia, new significant ST/T-wave changes or left bundle-branch block, development of pathological Q-waves on electrocardiogram (ECG), imaging evidence of the new loss of viable myocardium or regional wall motion abnormality, and identification of intracoronary thrombus by angiography or autopsy.
Angiographic evidence for atherothrombosis (complex lesion) and/or in the presence of impaired flow (TIMI grade <3)[22] was considered diagnostic for T1MI. Conversely, T1MI may have also been suspected clinically in the absence of a range of well-defined triggers (anemia, infection, shock, etc.) preceding the onset of ischemic symptoms. The absence of atherothrombosis (plaque rupture) and documentation of at least one trigger were recognized as signs of T2MI. The clinical triggers used in this study were proposed by Saaby et al.[4]
Cardiac troponin I (cTnI)
The Access 2 Immunoassay System (Beckman Coulter, Atlanta, GA, USA) was used for the measurement of cardiac troponin I with the 99th percentile upper reference limit (URL) being a value of 0.02 ng/L. MI diagnosis was considered when there was a ≥20% increase (and > URL) in troponin between earlier and later samples (taken at least 6 h apart).
Inclusion and exclusion criteria
Patients with AMI and CAG within the first 24 h after symptom onset were included. Patients with Type-3, Type-4, or Type 5 MI, ACS patients with twice negative troponin test, emergency CAG (>24 h after symptom onset), who refused to perform CAG or when CAG was not performed for other reasons, and those who declined to participate, were excluded.
Calculation of GRACE risk score
The GRACE 2.0 risk score was calculated for each admitted patient.[22],[23],[24]
Endpoints
The primary endpoint was in-hospital mortality. The secondary endpoints were all-cause long-term mortality (death from any cause); nonfatal recurrent MI, recurrent revascularization, and/or unplanned rehospitalization due to cardiac or noncardiac causes. The mean follow-up time was 689 days (range from 521 to 881 days). Patients were contacted by telephone for interviews, and the hospital database was reviewed.
Ethical principles
All study protocols were approved by the local ethics committee and carried out in accordance with the declaration of Helsinki.
Statistical analysis
Statistical analysis was performed using IBM SPSS Statistics 21.0 and MedCalc 14.0 software (IBM SPSS Statistics 21.0, Chicago, IL, USA). Continuous variables were expressed as mean ± standard deviation if the data followed a normal distribution. Conversely, the variables were expressed as median and interquartile range (Q1–Q3) for variables that did not follow normal distribution. Categorical variables were presented as absolute numbers and/or percentages. Comparisons of categorical variables were performed by Chi-Square and Fisher's exact tests as appropriate, while for continuous variables by using the unpaired Student t-test and Mann–Whitney U-test, whenever appropriate. Univariate and multivariate logistic regressions were then performed to establish the independent association of studied variables with the type of MI and independent predictors of the negative outcomes, and expressed as odds ratio (OR), 95% confidence interval (CI), and P values. To evaluate the ability of the GRACE risk score to predict in-hospital and long-term mortality, the area under the curve (AUC) of the receiver operating characteristic (ROC) curves was used, with the calculation of the optimal cutoff values using the Youden index. The Hanley–McNeil test was applied to compare the AUCs. Score calibration was evaluated using the Hosmer–Lemeshow test. Statistical significance was achieved with a P < 0.05.
| Results | | |
Patient characteristics
Of 974 patients admitted with ACS, 554 patients were diagnosed with AMI. Of these 450 patients underwent CAG, T2MI was diagnosed in 175 (38.9%) patients, whereas 275 (61.1%) were diagnosed with T1MI. Baseline patient characteristics are presented in [Table 1]. Patients with T2MI were older (66.9 vs. 63.7 years; P = 0.007), more likely to be female (44.6% vs. 32.7%, P = 0.01), frequently presenting with non-ST segment elevation (75.4% vs. 28.0%; P = 0.001) with lower troponin values (2.02 vs. 6.15 ng/mL; P = 0.001) [Table 1]. Patients with T2MI also more often had a history of a prior MI (46.9% vs. 18.9%; P < 0.001) and myocardial revascularization (19.4% vs. 9.0%; P = 0.002). Left ventricular ejection fraction (LVEF) was similar in the two groups (44.3% vs. 42.3%; P = 0.071). The absence of obstructive coronary atherosclerosis (or Myocardial infarction with nonobstructive coronary arteries – MINOCA) was diagnosed in 26 (14.9%) patients with T2MI. Percutaneous coronary intervention (PCI) was performed more often in patients with T1MI compared with T2MI patients (93.5% vs. 57.7%; P < 0.001). Other demographic and clinical characteristics are listed in [Table 1]. | Table 1: Baseline demographic, clinical, laboratory, and angiographic characteristics stratified by type of myocardial infarction
Click here to view |
Concordance between angiographic and clinical definitions
Atherothrombosis or a complex coronary lesion was present in 275 (61.1%) patients, and clinical triggers were identified in 244 (54.2%). These two groups were not mutually exclusive. Among 175 T2MI patients, the most common triggers for T2MI were anemia (67 [38.3%]), atrial fibrillation [24 (13.7%)], severe hypertension [21 (12.0%)], and bronchopulmonary infection [10 (5.7%)]. The overall study population was divided into four groups: 145 (32.2%) patients had “true” T1MI (atherothrombosis +/triggers–); 114 (25.3%) were diagnosed with “true” T2MI (atherothrombosis–/triggers +); 61 (13.6%) patients did not have any atherothrombosis or triggers; and 130 (28.9%) patients had both atherothrombosis and the presence of triggers. Discordance of angiographic and clinical definition of MI type was observed in 42.5% of the patients.
Management
As shown in [Table 2], medications including antiplatelet therapy (mono or dual), angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB), statins, beta-blockers, and anticoagulants were similar among patients with T2MI and T1MI during hospitalization and at discharge. | Table 2: Medications on admission and at discharge stratified by type of myocardial infarction
Click here to view |
Multivariable prediction of T2MI
In the multivariate logistic regression analysis, the following clinical factors were independently associated with T2MI: Anemia (OR 1.8, 95% CI: 1.0–3.0, P < 0.001), left bundle branch block (OR 3.1, 95% CI: 1.2–7.8, P = 0.019), age ≥70 years (OR 1.9, 95% CI: 1.1–3.2, P = 0.014), absence of local wall motion abnormalities (OR 2.0, 95% CI: 1.2–3.4, P = 0.002), and absence of ST-segment elevation on ECG (OR 6.5, 95% CI: 3.9-10.8, P = 0.002) [Table 3]. | Table 3: Multivariate logistic regression model for the differentiation of Type-2 myocardial infarction versus Type-1 myocardial infarction
Click here to view |
Prognosis
There were no differences between T2MI and T1MI patients with regard to in-hospital mortality (7.4% vs. 10.6%; P = 0.268) and all-cause long-term mortality (16.6% vs. 17.1%; P = 0.886). For T2MI patients as shown in [Table 4], only low LVEF, (<36%) was marginally associated with in-hospital mortality (adjusted OR (aOR) 12.2; 95% CI: 0.94-158.7; P = 0.055). Low LVEF was also independently associated with all-cause long-term mortality (aOR 5.2; 95%CI: 1.1-23.5; P = 0.030) in the multivariate analysis after adjustment [Table 5]. | Table 4: Predictors of in-hospital mortality for Type-2 myocardial infarction utilizing univariate and multivariate logistic regression models
Click here to view |
T2MI patients were more frequently hospitalized due to cardiovascular causes (33.3% vs. 19.5%; P = 0.001) and noncardiovascular causes (12.6% vs. 6.5%; P = 0.029) during follow-up [Table 5]a.
GRACE risk score
ROC curves of the GRACE score used to predict in-hospital mortality in both T1 and T2MI are shown in [Figure 2]. The GRACE risk score performed well in predicting in-hospital mortality in both T1MI and T2MI with AUC of 0.89 (95% CI: 0.84–0.92) for T1MI and AUC of 0.92 (95% CI: 0.87–0.95) for T2MI, respectively; demonstrating similar predictive abilities with no significant differences (P = 0.513). The optimal cutoff value of GRACE risk score of T2MI for predicting in-hospital mortality was >136 points (sensitivity 100.0% and specificity 69%) [Table 6]. | Figure 2: Receiver operating characteristic curve of GRACE score for in-hospital mortality. T1MI: Type-1 myocardial infarction, T2MI: Type-2 myocardial infarction, AUC: Area under the curve
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 | Table 6: Value of global registry of acute coronary events risk score in mortality prediction
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With regard to all-cause long-term mortality, the discrimination of GRACE risk score was poor in T2MI in contrast to T1MI (AUC 0.66 vs. 0.85; P = 0.009) [Figure 3]. | Figure 3: Receiver operating characteristic curve of GRACE score for long-term mortality. T1MI: Type-1 myocardial infarction, T2MI: Type-2 myocardial infarction, AUC: Area under the curve
Click here to view |
| Discussion | | |
In this single-center prospective study of patients diagnosed with MI, using CAG within 24 h, angiographic and clinical definitions of MI type are discordant in a substantial proportion of patients undergoing angiography (42.5%). Second, contrary to the common perception that T2MI patients are less frequently treated with cardioprotective therapy, we observed that T2MI patients were also similarly managed with cardioprotective therapy in this study just like T1MI patients. Third, a variety of different triggers for myocardial supply and demand mismatch were identified with anemia, tachyarrhythmia, and hypertensive crisis among the most common in T2MI patients. Fourth, the clinical predictors of having T2MI were anemia, left bundle branch block, age ≥70 years, absence of local wall motion abnormalities, and absence of ST-segment elevation. Fifth, only reduced LVEF was independently associated with all-cause long-term mortality. T2MI patients were associated with a high rate of rehospitalization, and the majority of rehospitalization following T2MIs were from the cardiovascular causes. Finally, there was the comparable prognostic significance of the GRACE risk score regarding in-hospital mortality in patients with Type 2 and Type 1 MIs, but GRACE risk score was less useful for the prediction of all-cause long-term mortality for patients with T2MI.
Regarding clinical characteristics, in the recent meta-analysis of observational studies,[10] including 25,872 patients from nine studies, of whom 2,683 (10%) had T2MI, compared to T1MI patients, patients with T2MI were older (74 vs. 70 years), more likely to be female (46% vs. 33%), and more often diagnosed with non-ST-elevation MI (70.0% vs. 44.1%). The results were similar in our study, although there was higher mortality in patients with T2MI in comparison with T1MI, both in-hospital (15% vs. 4.7%; P < 0.001) and after 1 year (27% vs. 13%; P < 0.001). This could be due to the low sample size of the current study.
In the present study, the prevalence of T2MI was 39%. Wide variation in the prevalence of T2MI is reported in the literature, depending on the diagnostic criteria used between 1.6% and 74.2%.[24],[25],[26] Our study was similar to the one by Saaby et al.[4] which reported a prevalence of T2MI of 26%, probably because more specific criteria to diagnose these conditions were used. Notably, CAG performed well in only in 31 (21.5%) T2MI patients and significant CAD was found in greater than half of the cases (54.8%). Similarly, in the study by Landes et al.[8] using propensity score matching between 107 patients with T2MI and 107 patients with T1MI, the authors noted that only 29 (27.1%) of T2MI patients had been managed with CAG, and two-thirds of them (75%) had significant CAD. Importantly, when analyzing coronary lesion morphology of T2MI patients, one-third of the patients (29%) had acute plaque rupture, a feature of T1MI, which was similar to our study (28.9%). It raised the questions about the need for performing advanced imaging methods (in part, CAG) for T2MI to verify MI types and then appropriate guide-based therapy.[2],[3] Acute thrombotic coronary occlusion was present in 28.9% consistent with and labeled T1MI, whereas myocardial oxygen supply demand miss-match in the absence of plaque rupture was present in 13.6% and labeled as T2MI. Angiographic and clinical definitions of MI type were discordant in a substantial proportion of patients undergoing CAG in our study. In practice, CAG is usually performed in few cases with T2MI. In the meta-analysis by Vargas et al.,[3] including 93,194 MI patients from 20 included observational studies, of which the T2MI proportion was about 8.8%, CAG was performed in 31.5%, and 77.7% of all patients with T2MI and T1MI, respectively. By definition, T2MI can occur with or without obstructive CAD.[1]
The prevalence of CAD varies from 28% to 78% of the T2MI patients that are selected to undergo CAG.[5] The fact that the prevalence and severity of atherosclerotic lesions of the coronary arteries in the present study are comparable in both types of MI, including three-vessel CAD in over 60% of cases, is not unexpected. In 85% of cases T2MI, the prevalence of multivessel coronary lesions was 80%, similar to that reported by Higuchi et al. in a Japanese population.[27] These authors included 12,514 MI patients and studied the clinical impact of revascularization strategy in patients with T2MI. Of these, 427 (87%) with T2MI underwent CAG, of which close to 90% had significant coronary stenosis and 258 (53%) had CAG performed early. Furthermore, T2MI patients less frequently received guidelines-based therapy, including ACEI/ARB, beta-blockers, and statins, in about half of cases, while more frequently taking anti-platelet therapy (90%). However, in our study, management strategies between the two groups, including cardioprotective therapy (ACEI/ARB, beta-blockers, antithrombotic therapy, and statins) were similar except for PCI which was significantly less likely in patients with T2MI (57.7%). This could be explained by the predominance of CAD in patients with T2MI and benefit of guideline-directed therapies.[12],[13] PCIs are less likely to be performed in patients with T2MI. In the meta-analysis,[3] PCI was performed in 40.2% of T2MI patients and in 79.2% patients with T1MI. With multiple coexisting comorbidities, such as sepsis, arrhythmia, anemia, and a lack of current guidelines for T2MI, the strategy of PCI remains uncertain.[10] In clinical practice, a conservative approach was common to treat the underlying ischemic imbalance of oxygen supply and demand. This strategy may include volume adjustment, blood pressure control, transfusion of blood products, heart-rate management, and respiratory support.[1]
There was no statistically significant difference between the two groups regarding in-hospital and long-term all-cause mortality, recurrent MI, or myocardial revascularization. These findings were similar to the results of a recently published study,[28] by Neumann et al., who included 1548 patients with suspected MI (188 with T1MI and 99 with T2MI) and followed patients for up to 2 years. In this study, the differentiation between T1MI and T2MI used the 3rd universal definition and CAG was performed in 38.3% of T2MI patients. The rate of 1-year mortality was high and comparable among patients with T2MI and T1MI (13.8% vs. 9.4%; P = 0.540); however, the cardiac rehospitalization rate was higher in patients with T1MI (33.8% vs. 19.3%; P = 0.025). This may be because of the prevalence of non-significant CAD (60.5%) in T2MI patients. In the study by Baron et al.,[15] which included 20,138 MI patients, of which T2MI was present in 7.1% and T1MI was diagnosed in 88.5% of the cases. Patients with T2MI had a low rate of CAG (35.9% vs. 77.3%; P < 0.001) and were less likely to be prescribed guideline-based cardiovascular therapy, with increased 1-year mortality (hazard ratio [HR] 1.86, 95% CI: 1.66–2.08). However, after adjustment of clinical characteristics and treatment, there were no significant differences in 1-year mortality between T2MI and T1MI patients (HR 1.03, 95% CI: 0.86–1.23). This research proposes the potential role of CAG and guideline-based cardiovascular therapy in the high-risk group of T2MI patients.
With regard to risk stratification, to the best of our knowledge, the present study was the first to have use GRACE risk score to predict mortality in patients with T2MI. Celdiel et al.[6] developed the TARRACO risk score to predict the risk of death or cardiac rehospitalization at 180 days for T2MI with good discriminative accuracy (AUC 0.75, 95% CI: 0.67–0.83). It should be noted that in their study, T2MI was diagnosed using the specific criteria proposed by Saaby et al.[4] as in the current study.
T2MI patients are a heterogeneous group with varying the prognosis of cardiac and noncardiac events, in the short-term as well as during the long-term follow-up.[29] In these patients, early risk stratification plays a central role. This study showed that reduced LVEF was a powerful independent predictor of all-cause long-term mortality for T2MI patients. Left ventricular function assessment should be employed as a specific risk factor in the risk stratification of T2MI. With the poor performance of the GRACE risk score in predicting long-term mortality, our data provide new insight into risk stratification of this patient category. Further studies are needed to examine whether incorporating ejection fraction into the GRACE model could improve risk prediction using this score in patients with T2MI. The added value of LVEF assessment in non-ST-segment elevation ACS patients was described by Bosch et al.[30] that included 1,104 patients from the PRISM-plus trial registry. Adding early evaluation of LVEF to the TIMI risk score (thrombolysis in MI) improved mortality prediction (AUC 0.73 vs. 0.67) and LVEF <48% was a cutoff value with 3.3 times higher mortality rate within each TIMI risk score stratum.[30]
Until data from prospective trials becomes available to support our findings, the GRACE risk score is still recommended for risk assessment, and evaluation of LVEF for long-term risk performed more frequently, not only before discharge,[12],[13] but also as part of routine evaluation and risk stratification in T2MI patients.
Although CAG is useful for detecting atherothrombosis, it is not completely sensitive in the detection of plaque disruption. The lack of use of intravascular coronary imaging, such as optical coherence tomography or intravascular ultrasound in this study, is a limitation. However, a positive aspect of our study is the availability of angiographic data for all patients, which allowed morphological characterization of coronary lesions, and the application of criteria developed by this study to distinguish Type 1 and Type 2 MI. A second positive aspect of this study is the timing of CAG within 24 h after symptom onset, which reduces the risk of temporal uncertainty of coronary thrombosis with subsequent autologous thrombolysis. This, therefore, increases the reliability of the interpretation of CAG. This study gives new insight into angiographic and clinical definitions of MI, which maybe an important step in the development and clinical adaptation of the internationally accepted definition for T2MI.
| Conclusions | | |
This study demonstrates the discrepancy between angiographic and clinical definitions of MI in many patients undergoing CAG. In patients presenting with T2MI CAD often exists, therefore performing CAG is recommended in this group to better categorize and verify MI types, to allow better delivery of appropriate medical therapy. The GRACE risk score is useful for prediction of in-hospital death, although its predictive ability for long-term mortality is poor in this patient population.
Acknowledgment
This is an investigator-initiated single-center study conducted at the Department of Internal Medicine with the subspecialty of cardiology and functional diagnostics named after V. S. Moiseev, Institute of Medicine, Peoples' Friendship University of Russia (RUDN University), Moscow, Russian Federation.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]
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