Myocardial Infarction Methods Research Articles

Gender differences in KAsH score in acute myocardial infarction

Abstract Funding Acknowledgements None. Introduction Risk stratification at admission in patients with myocardial infarction (MI) is crucial in the prognosis assessment. KAsH score is a useful and simple tool to predict in-hospital mortality. Objective To evaluate KAsH score predictive power according to gender in patients (P) who suffered MI (either STEMI or NSTEMI) Methods Based on a single-center retrospective study, data collected from P admitted in the Cardiology department with MI between 2016 and 2019. P without or uncompleted data were excluded. We compared 2 groups: Group 1 (G1) – male patients; Group 2 (G2) – female patients. Major adverse cardiac events (MACE) were defined as the composite of nonfatal stroke, nonfatal myocardial infarction and cardiovascular death. Statistical analysis used T test, chi-square, logistic regression and ROC curve analysis. Results Among the 611 P admitted with MI mean age was 66.6±12.7 years old and 64.8% were male. G1 was younger (64.7 ±12.8 years vs 64.7±12.8, p<0.001). The groups were similar regarding the other variables that compose the KAsH score, namely Killip-Kimbal class (p=0.668), systolic blood pressure (p=0.378), and heart rate (p=0.265). The mean KAsH categorization was 1.48 for G1 and 1.54 for G2 (p=0.05). The groups were also similar regarding other (CV) factors namely arterial hypertension, diabetes mellitus, dyslipidaemia, smoking and previous MI. In general, KAsH score was able to predict in-hospital mortality in our sample p=0.03, OR 2.45, CI 1.09-5.55 but with poor accuracy (AUC 0.355). However, the score did not predict 1 year mortality (p=0.337) or 1 year readmission (p=0.943). Regarding the groups, KAsH score did not predict in-hospital mortality for G1 (p=0.465) but it did predict the occurrence of MACE events, p=0.01, OR 2.20, CI 1.20-4.09, AUC 0.634. Considering G2 KAsH score predicted in-hospital mortality p=0.02, OR 4.10, CI 1.24-13.87 but with poor accuracy (AUC 0.211). It also predicted the occurrence of MACE events p=0.001, OR 4.61, CI 1.83-11.63 with fair accuracy (AUC 0.77). Such as in G1 the score did not predict 1 year mortality or readmission (p=0.178) Conclusion In our center, KAsH score performed better in female patients in predicting in-hospital mortality and MACE events. The score also predicted MACE events in male patients, but did not predict in-hospital mortality. More studies are needed to validate additional variables to the score and to validate KAsH score as a long-term prognostic tool.

Myocardial infarction detection method based on the continuous T-wave area feature and multi-lead-fusion deep features

Objective. Myocardial infarction (MI) is one of the most threatening cardiovascular diseases. This paper aims to explore a method for using an algorithm to autonomously classify MI based on the electrocardiogram (ECG). Approach. A detection method of MI that fuses continuous T-wave area (C_TWA) feature and ECG deep features is proposed. This method consists of three main parts: (1) The onset of MI is often accompanied by changes in the shape of the T-wave in the ECG, thus the area of the T-wave displayed on different heartbeats will be quite different. The adaptive sliding window method is used to detect the start and end of the T-wave, and calculate the C_TWA on the same ECG record. Additionally, the coefficient of variation of C_TWA is defined as the C_TWA feature of the ECG. (2) The multi lead fusion convolutional neural network was implemented to extract the deep features of the ECG. (3) The C_TWA feature and deep features of the ECG were fused by soft attention, and then inputted into the multi-layer perceptron to obtain the detection result. Main results. According to the inter-patient paradigm, the proposed method reached a 97.67% accuracy, 96.59% precision, and 98.96% recall on the PTB dataset, as well as reached 93.15% accuracy, 93.20% precision, and 95.14% recall on the clinical dataset. Significance. This method accurately extracts the feature of the C_TWA, and combines the deep features of the signal, thereby improving the detection accuracy and achieving favorable results on clinical datasets.

Serum Anti-heat Shock Protein 27 Antibody Titers in Patients With Dyslipidemia: A Population-based Case-control Study

Background: Heat shock protein 27 (HSP27) is found in several cell types of adults, such as cardiomyocytes, and endothelial cells. It is expressed in response to different cellular stress conditions. HSP27 decreases the levels of reactive oxygen species (ROS) and dyslipidemia is closely associated with increased endothelial production of reactive oxygen species (ROS). Objective: Higher serum HSP27 antigen and anti-HSP27 antibodies have been reported in patients with unstable angina and myocardial infarction Methods: This population-based case-control study was conducted in 2018. We investigated serum anti-HSP27 antibody titers in all participants with dyslipidemia from the Mashhad stroke and heart atherosclerotic disorder (MASHAD) study (n=8141) and those who were healthy in terms of dyslipidemia (n=1637) using an in-house enzyme-linked immune sorbent assay (ELISA) in individuals with dyslipidemia. Findings: Anti-HSP27 titers were significantly lower in individuals with dyslipidemia compared to people without dyslipidemia (P=0.036). Conclusion: Our results revealed that the anti-HSP27 antibody titer was lower in the participants with dyslipidemia than in the negative group. However, there may be a confounding effect of drug therapy. In a subgroup of dyslipidemic subjects, we observed lower anti-HSP27 antibody titers in patients treated with some drugs (statins or corticosteroids, non-steroidal anti-inflammatory drugs [NSAIDs], or anti-diabetic and anti-hypertensive) compared to subjects untreated with these drugs.

Abstract 8905: Cardiac Troponin Thresholds and Kinetics to Differentiate Myocardial Injury and Myocardial Infarction

Background: Whilst the 99th percentile is the recommended diagnostic threshold for myocardial infarction (MI), some guidelines also advocate the use of higher troponin thresholds to rule-in MI at presentation. It is unclear whether the magnitude or change in troponin concentration can differentiate causes of myocardial injury and infarction in practice. Hypothesis: Troponin concentration alone cannot to distinguish subtypes of myocardial infarction Methods: In a secondary analysis of a multi-centre randomized controlled trial, we identified 46,092 consecutive patients presenting with suspected acute coronary syndrome without STEMI. High-sensitivity troponin I concentrations at presentation and on serial testing were evaluated. The positive predictive value (PPV) and specificity were determined at the sex-specific 99th percentile upper reference limit (URL), and rule-in thresholds of 64 ng/L and 5-fold of the URL for a diagnosis of type 1 MI. Results: Troponin concentrations were similar at presentation in type 1 (median [IQR] 91 [30-493] ng/L) and type 2 MI (50 [22-147] ng/L), and in acute (50 [26-134] ng/L) and chronic (51 [31-130] ng/L) myocardial injury (Figure A). The 99th percentile and rule-in thresholds of 64 ng/L and 5-fold URL gave a PPV of 57% (95% confidence interval [CI] 56-58%), 59% (58-61%) and 62% (60-64%), and a specificity of 96% (96-96%), 96% (96-96%) and 98% (97-98%), respectively (Figure B). The absolute, relative and rate of change in troponin concentration was highest in patients with type 1 MI (P<0.001 for all, Figure C). Discrimination improved when troponin concentration and change in troponin were combined compared to troponin concentration at presentation alone (area under curve, 0.661 versus 0.613). Conclusions: Troponin concentrations at presentation are insufficient to distinguish type 1 MI from other causes of myocardial injury or infarction in practice and should not guide management decisions in isolation.

Abstract 13194: The Effects of Methotrexate Therapy on Myocardial Infarction With ST-Segment Elevation (TETHYS Trial)

Introduction: Acute myocardial infarction provokes inflammatory activation. Methotrexate is one drug that has been shown to have anti-ischemic effects in experimental studies. Hypothesis: Methotrexate could reduce inflammation and the ischemia area in acute myocardial infarction Methods: We randomly assigned patients with myocardial infarction with ST-segment elevation to receive either methotrexate (0.05 mg/kg bolus followed by 0.05 mg/kg/h for 6 h) or matching placebo (riboflavin sodium phosphate 0.1%, in order to preserve double-blinding) at a ratio of 1:1. Patients in both groups were given a 5mg single dose of folic acid. The primary endpoint was infarct size, determined by the area under the curve (AUC) for creatine kinase (CK) release. Secondary endpoints were AUC of CK-MB and AUC of troponin I; peak CK, peak CK-MB and troponin I; B-type natriuretic peptide (BNP) level, high-sensitivity C-reactive protein (hsCRP) result and erythrocyte sedimentation rate (ESR); left ventricular ejection fraction (LVEF); TIMI frame count; Killip score; mortality and reinfarction incidence. The safety endpoint was the incidence of adverse reactions. Results: We included 84 patients. The AUC of CK was 78,861.00 in the methotrexate group and 68,088.00 in the placebo group (P=0.10). Patients given methotrexate and placebo exhibited, respectively, AUC for CK-MB of 9,803.40 and 8,037.00 (P=0.42); AUC for troponin I of 3,691.11 and 2,132.63 (P=0.09); peak CK of 2,806.00 and 2,147.00 (P=0.05), peak CK-MB of 516.00 and 462.25 (P=0.25) and peak troponin I of 121.00 and 85.05 (P=0,06). At 3 months, LVEF was lower in patients who received methotrexate (48.97±14.09%) than in patients given placebo (56.37±9.97%) (P=0.01). There were no differences in hsCRP, ESR, BNP, Killip scores or TIMI frame count. There were also no differences in reinfarction or mortality rates or in incidence of side effects, with the exception of higher median serum glutamic-pyruvic transaminase (SGPT) levels in the methotrexate group. Conclusions: Methotrexate did not reduce infarction size and worsened LVEF at 3 months.

Adiponectin is the most useful predictor for all-cause mortality and recurrence of acute coronary syndrome in patients with acute myocardial infarction

Aims: This study was designed to determine the most useful biomarker for prediction of all-cause mortality and recurrence of acute coronary syndrome (ACS) in patients with ST-segment elevation myocardial infarction Methods: This study included 254 patients who underwent primary percutaneous coronary intervention. Multiple biomarker levels, including adiponectin (APN), aldosterone, brain natriuretic peptide, epinephrine, blood glucose (BG), and C-reactive protein (CRP), were measured on the second day of admission. All patients were equally divided into tertile groups according to the biomarker levels. A Cox regression model was used to examine the prognostic impact of each biomarker. Results: During follow-up (median, 1096 days), 50 of the 254 patients died and 24 patients experienced recurrence of ACS. In the univariate analyses, death rates increased significantly with increasing levels of all biomarkers except those of BG. In the multivariate models, the highest tertile of APN and CRP levels were significant predictors of all-cause mortality (hazard ratios: APN, 5.02; p < 0.001; CRP, 3.43, p < 0.001). The rate of ACS recurrence was significantly associated with APN levels. However, the other biomarkers did not show relationships with ACS recurrence. Multivariate analyses adjusted for APN, age, body mass index, diabetes, hypertension, smoking, and dyslipidemia identified the median and highest tertile of APN levels as the only predictors of ACS recurrence (hazard ratios: median, 4.46, p = 0.024; highest, 6.63, p = 0.005). ![Figure][1] ACS-free survival estimate Conclusions: Among the established biomarkers related to patient prognosis, APN was the most useful predictor of all-cause mortality and ACS recurrence. [1]: pending:yes

A Novel and Efficient Model of Coronary Artery Ligation and Myocardial Infarction in the Mouse

coronary artery ligation to induce myocardial infarction (MI) in mice is typically performed by an invasive and time-consuming approach that requires ventilation and chest opening (classic method), often resulting in extensive tissue damage and high mortality. We developed a novel and rapid surgical method to induce MI that does not require ventilation. the purpose of this study was to develop and comprehensively describe this method and directly compare it to the classic method. male C57/B6 mice were grouped into 4 groups: new method MI (MI-N) or sham (S-N) and classic method MI (MI-C) or sham (S-C). In the new method, heart was manually exposed without intubation through a small incision and MI was induced. In the classic method, MI was induced through a ventilated thoracotomy. Similar groups were used in an ischemia/reperfusion injury model. This novel MI procedure is rapid, with an average procedure time of 1.22 ± 0.05 minutes, whereas the classic method requires 23.2 ± 0.6 minutes per procedure. Surgical mortality was 3% in MI-N and 15.9% in MI-C. The rate of arrhythmia was significantly lower in MI-N. The postsurgical levels of tumor necrosis factor-α and myeloperoxidase were lower in new method, indicating less inflammation. Overall, 28-day post-MI survival rate was 68% with MI-N and 48% with MI-C. Importantly, there was no difference in infarct size or post-MI cardiac function between the methods. this new rapid method of MI in mice represents a more efficient and less damaging model of myocardial ischemic injury compared with the classic method.

Carotid Duplex Ultrasound Findings in Patients with Coronary Artery Disease (CAD)- A Study in 50 Cases

Background: Patients with angina pectoris or myocardial infarction are more likely to experience stroke. Ischaemic stroke has been found to develop in approximately 2-5% of patients in the first 1- 2 weeks after myocardial infarction Methods: Fifty patients with coronary artery disease admitted to the National Institute of Cardiovascular Diseases (NICVD), Dhaka, were screened for presence of carotid atherosclerosis by duplex ultrasound study during the period of July 98 to August 98. Results: Carotid lesion were found in 34 patients (68%) and normal carotids found in 16 patients (32%). Age range of patients with and without carotid lesions was 56±5.39 yrs and 47±7.91 yrs respectively. Out of 34 patients, 30 were male (88.2%) and 4 were female (11.7%). 29 patients (85.3%) were smokers, 22 patients (64.7%) were hypertensive and 9 patients (26.4%) were diabetic. Dyslipidaemia was found in 16 patients (47%) and a history of transient ischaemic attack (TIA) was found in 10 patients (29.4%). A coexistent CAD on coronary (CAG) was found in 31 patients (91.1%). Conclusion: Cortaid duplex ultrasound study findings of atherosclerotic lesions in Carotid arteries are good predictors of CAD.Keywords: Carotid atherosclerosis, Carotid duplex ultrasound, Coronary artery disease. DOI: http://dx.doi.org/10.3329/cardio.v1i1.8203 Cardiovasc. j. 2008; 1(1) : 44-47