Abstract Background: Arrhythmias are considered one of the major causes of death in ST el‐ evation myocardial infarction (STEMI), particularly in the early in‐hospital phase. Pre‐ infarction angina (PIA) has been suggested to have a protective role. Objectives: To study the difference in acute electrocardiographic findings between STEMI patients with and without PIA and to assess the in‐hospital arrhythmias in both groups. Material and Methods: We prospectively enrolled 238 consecutive patients with STEMI. Patients were divided into two groups: those with or without PIA. ECG data recorded and analyzed included ST‐segment resolution (STR) at 90 min, corrected QT interval (QTc) and dispersion (QTD), T‐peak‐to‐T‐end interval (Tp‐Te), and dispersion and Tp‐Te/QT ratio. In‐hospital ventricular arrhythmias encountered in both groups were recorded. Predictors of in‐hospital arrhythmias were assessed among different clinical and electrocardiographic parameters. Results: Of the 238 patients included, 42 (17%) had PIA and 196 (83%) had no PIA. Patients with PIA had higher rates of STR (p 0.0001), while patients with no PIA had higher values of QTc (p = 0.006), QTD (p = 0.001), Tp‐Te interval (p = 0.001), Tp‐Te dispersion (p 0.0001), and Tp‐Te/QT ratio (p = 0.01) compared to those with angina preceding their incident infarction (PIA). This was reflected into significantly higher rates of in‐hospital arrhythmias among patients with no PIA (20% vs. 7%, p = 0.04). Furthermore, longer Tp‐Te interval and higher Tp‐Te/QT ratio independently pre‐ dicted in‐hospital ventricular arrhythmias. Conclusion: Pre‐infarction angina patients had better electrocardiographic measures of repolarization dispersion and encountered significantly less arrhythmic events compared to patients who did not experience PIA.

Abstract Background: Arrhythmias are considered one of the major causes of death in ST el‐ evation myocardial infarction (STEMI), particularly in the early in‐hospital phase. Pre‐ infarction angina (PIA) has been suggested to have a protective role. Objectives: To study the difference in acute electrocardiographic findings between STEMI patients with and without PIA and to assess the in‐hospital arrhythmias in both groups. Material and Methods: We prospectively enrolled 238 consecutive patients with STEMI. Patients were divided into two groups: those with or without PIA. ECG data recorded and analyzed included ST‐segment resolution (STR) at 90 min, corrected QT interval (QTc) and dispersion (QTD), T‐peak‐to‐T‐end interval (Tp‐Te), and dispersion and Tp‐Te/QT ratio. In‐hospital ventricular arrhythmias encountered in both groups were recorded. Predictors of in‐hospital arrhythmias were assessed among different clinical and electrocardiographic parameters. Results: Of the 238 patients included, 42 (17%) had PIA and 196 (83%) had no PIA. Patients with PIA had higher rates of STR (p 0.0001), while patients with no PIA had higher values of QTc (p = 0.006), QTD (p = 0.001), Tp‐Te interval (p = 0.001), Tp‐Te dispersion (p 0.0001), and Tp‐Te/QT ratio (p = 0.01) compared to those with angina preceding their incident infarction (PIA). This was reflected into significantly higher rates of in‐hospital arrhythmias among patients with no PIA (20% vs. 7%, p = 0.04). Furthermore, longer Tp‐Te interval and higher Tp‐Te/QT ratio independently pre‐ dicted in‐hospital ventricular arrhythmias. Conclusion: Pre‐infarction angina patients had better electrocardiographic measures of repolarization dispersion and encountered significantly less arrhythmic events compared to patients who did not experience PIA.

Abstract Background: Arrhythmias are considered one of the major causes of death in ST el‐ evation myocardial infarction (STEMI), particularly in the early in‐hospital phase. Pre‐ infarction angina (PIA) has been suggested to have a protective role. Objectives: To study the difference in acute electrocardiographic findings between STEMI patients with and without PIA and to assess the in‐hospital arrhythmias in both groups. Material and Methods: We prospectively enrolled 238 consecutive patients with STEMI. Patients were divided into two groups: those with or without PIA. ECG data recorded and analyzed included ST‐segment resolution (STR) at 90 min, corrected QT interval (QTc) and dispersion (QTD), T‐peak‐to‐T‐end interval (Tp‐Te), and dispersion and Tp‐Te/QT ratio. In‐hospital ventricular arrhythmias encountered in both groups were recorded. Predictors of in‐hospital arrhythmias were assessed among different clinical and electrocardiographic parameters. Results: Of the 238 patients included, 42 (17%) had PIA and 196 (83%) had no PIA. Patients with PIA had higher rates of STR (p 0.0001), while patients with no PIA had higher values of QTc (p = 0.006), QTD (p = 0.001), Tp‐Te interval (p = 0.001), Tp‐Te dispersion (p 0.0001), and Tp‐Te/QT ratio (p = 0.01) compared to those with angina preceding their incident infarction (PIA). This was reflected into significantly higher rates of in‐hospital arrhythmias among patients with no PIA (20% vs. 7%, p = 0.04). Furthermore, longer Tp‐Te interval and higher Tp‐Te/QT ratio independently pre‐ dicted in‐hospital ventricular arrhythmias. Conclusion: Pre‐infarction angina patients had better electrocardiographic measures of repolarization dispersion and encountered significantly less arrhythmic events compared to patients who did not experience PIA.

Abstract Background: Arrhythmias are considered one of the major causes of death in ST el‐ evation myocardial infarction (STEMI), particularly in the early in‐hospital phase. Pre‐ infarction angina (PIA) has been suggested to have a protective role. Objectives: To study the difference in acute electrocardiographic findings between STEMI patients with and without PIA and to assess the in‐hospital arrhythmias in both groups. Material and Methods: We prospectively enrolled 238 consecutive patients with STEMI. Patients were divided into two groups: those with or without PIA. ECG data recorded and analyzed included ST‐segment resolution (STR) at 90 min, corrected QT interval (QTc) and dispersion (QTD), T‐peak‐to‐T‐end interval (Tp‐Te), and dispersion and Tp‐Te/QT ratio. In‐hospital ventricular arrhythmias encountered in both groups were recorded. Predictors of in‐hospital arrhythmias were assessed among different clinical and electrocardiographic parameters. Results: Of the 238 patients included, 42 (17%) had PIA and 196 (83%) had no PIA. Patients with PIA had higher rates of STR (p 0.0001), while patients with no PIA had higher values of QTc (p = 0.006), QTD (p = 0.001), Tp‐Te interval (p = 0.001), Tp‐Te dispersion (p 0.0001), and Tp‐Te/QT ratio (p = 0.01) compared to those with angina preceding their incident infarction (PIA). This was reflected into significantly higher rates of in‐hospital arrhythmias among patients with no PIA (20% vs. 7%, p = 0.04). Furthermore, longer Tp‐Te interval and higher Tp‐Te/QT ratio independently pre‐ dicted in‐hospital ventricular arrhythmias. Conclusion: Pre‐infarction angina patients had better electrocardiographic measures of repolarization dispersion and encountered significantly less arrhythmic events compared to patients who did not experience PIA.

Background Bacterial infections can trigger acute coronary syndromes. This study aimed to examine bacterial footprints in the aspirate of infarct-related artery. Patients and methods We studied 140 patients with ST-elevation myocardial infarction who underwent a primary coronary intervention using thrombus aspiration catheters. The aspirate was sent for bacteriological and pathological examinations and immunoassay for pneumolysin toxin. Results Bacterial culture showed different bacteria in 14 samples. Leukocyte in ltrate was detected in all pathologically examined samples. Pneumolysin toxin was detected in only two samples. Patients with bacteria had similar baseline data as those without, except for the median age [46 (44–50) vs. 55 (47–62) years, P = 0.001, respectively], and white blood cells (WBCs) (16670 vs. 7550 cells/μl, P 0.0001, respectively). In hospital- major clinical events (death, stroke, reinfarction, lethal arrhythmia, and heart failure) were not signi cantly different between the 2 groups with and without bacteria [4 (28.6%) vs. 20 (18.6%) events, respectively, odds ratio (OR) 1.8 (95% CL: 06–6.3), P = 0.5]. Patients with bacteria, heavy in ltration, and pneumolysin had insigni cant higher events compared with those without [10/35 (28.6%) Introduction One emerging paradigm suggests that bacterial infection can contribute toward the pathogenesis of acute coronary syndromes (ACSs) [1]. The formation of platelet thrombi on the surface of complicated coronary plaques is consid- ered an essential step in the evolution of ACS [2]. Acute infections can promote the development of thrombi in var- ious ways [3]. Platelets can be activated directly by patho- gens and the in ammatory response that they elicit [4]. In addition, acute infections can cause coronary vasoconstric- tion and further narrow the lumen in atherosclerotic coro- nary segments, stimulating shear-induced platelet activity [5]. The host response to acute infections can trigger, has- ten, or facilitate ACS on the basis of generalized and local in ammatory and thrombogenic changes [6]. The clinical trials to date have not provided an adequate support for the clinical use of antibiotics in the primary or secondary prevention of coronary artery disease [7]. 0954-6928 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved. vs. 16/105 (15.2%) events, OR 2.2 (95% CL: 0.92–5.43), P = 0.13]. However, the difference was not signi cant. By multivariate analysis, bacteria, leukocyte in ltration, and pneumolysin were not predictors for in-hospital clinical events. Higher WBCs and younger age were signi cant predictors of bacterial footprints (P 0.0001 and P = 0.04, respectively). Conclusion Bacterial footprints existed in the aspirate of infarct-related artery of ST-elevation myocardial infarction patients. Predictors were higher WBCs and younger age. Bacterial markers were not predictors for in-hospital clinical events. The presence of bacterial footprints supports the infectious hypothesis of atherosclerosis.

Background Bacterial infections can trigger acute coronary syndromes. This study aimed to examine bacterial footprints in the aspirate of infarct-related artery. Patients and methods We studied 140 patients with ST-elevation myocardial infarction who underwent a primary coronary intervention using thrombus aspiration catheters. The aspirate was sent for bacteriological and pathological examinations and immunoassay for pneumolysin toxin. Results Bacterial culture showed different bacteria in 14 samples. Leukocyte in ltrate was detected in all pathologically examined samples. Pneumolysin toxin was detected in only two samples. Patients with bacteria had similar baseline data as those without, except for the median age [46 (44–50) vs. 55 (47–62) years, P = 0.001, respectively], and white blood cells (WBCs) (16670 vs. 7550 cells/μl, P 0.0001, respectively). In hospital- major clinical events (death, stroke, reinfarction, lethal arrhythmia, and heart failure) were not signi cantly different between the 2 groups with and without bacteria [4 (28.6%) vs. 20 (18.6%) events, respectively, odds ratio (OR) 1.8 (95% CL: 06–6.3), P = 0.5]. Patients with bacteria, heavy in ltration, and pneumolysin had insigni cant higher events compared with those without [10/35 (28.6%) Introduction One emerging paradigm suggests that bacterial infection can contribute toward the pathogenesis of acute coronary syndromes (ACSs) [1]. The formation of platelet thrombi on the surface of complicated coronary plaques is consid- ered an essential step in the evolution of ACS [2]. Acute infections can promote the development of thrombi in var- ious ways [3]. Platelets can be activated directly by patho- gens and the in ammatory response that they elicit [4]. In addition, acute infections can cause coronary vasoconstric- tion and further narrow the lumen in atherosclerotic coro- nary segments, stimulating shear-induced platelet activity [5]. The host response to acute infections can trigger, has- ten, or facilitate ACS on the basis of generalized and local in ammatory and thrombogenic changes [6]. The clinical trials to date have not provided an adequate support for the clinical use of antibiotics in the primary or secondary prevention of coronary artery disease [7]. 0954-6928 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved. vs. 16/105 (15.2%) events, OR 2.2 (95% CL: 0.92–5.43), P = 0.13]. However, the difference was not signi cant. By multivariate analysis, bacteria, leukocyte in ltration, and pneumolysin were not predictors for in-hospital clinical events. Higher WBCs and younger age were signi cant predictors of bacterial footprints (P 0.0001 and P = 0.04, respectively). Conclusion Bacterial footprints existed in the aspirate of infarct-related artery of ST-elevation myocardial infarction patients. Predictors were higher WBCs and younger age. Bacterial markers were not predictors for in-hospital clinical events. The presence of bacterial footprints supports the infectious hypothesis of atherosclerosis.

Background Bacterial infections can trigger acute coronary syndromes. This study aimed to examine bacterial footprints in the aspirate of infarct-related artery. Patients and methods We studied 140 patients with ST-elevation myocardial infarction who underwent a primary coronary intervention using thrombus aspiration catheters. The aspirate was sent for bacteriological and pathological examinations and immunoassay for pneumolysin toxin. Results Bacterial culture showed different bacteria in 14 samples. Leukocyte in ltrate was detected in all pathologically examined samples. Pneumolysin toxin was detected in only two samples. Patients with bacteria had similar baseline data as those without, except for the median age [46 (44–50) vs. 55 (47–62) years, P = 0.001, respectively], and white blood cells (WBCs) (16670 vs. 7550 cells/μl, P 0.0001, respectively). In hospital- major clinical events (death, stroke, reinfarction, lethal arrhythmia, and heart failure) were not signi cantly different between the 2 groups with and without bacteria [4 (28.6%) vs. 20 (18.6%) events, respectively, odds ratio (OR) 1.8 (95% CL: 06–6.3), P = 0.5]. Patients with bacteria, heavy in ltration, and pneumolysin had insigni cant higher events compared with those without [10/35 (28.6%) Introduction One emerging paradigm suggests that bacterial infection can contribute toward the pathogenesis of acute coronary syndromes (ACSs) [1]. The formation of platelet thrombi on the surface of complicated coronary plaques is consid- ered an essential step in the evolution of ACS [2]. Acute infections can promote the development of thrombi in var- ious ways [3]. Platelets can be activated directly by patho- gens and the in ammatory response that they elicit [4]. In addition, acute infections can cause coronary vasoconstric- tion and further narrow the lumen in atherosclerotic coro- nary segments, stimulating shear-induced platelet activity [5]. The host response to acute infections can trigger, has- ten, or facilitate ACS on the basis of generalized and local in ammatory and thrombogenic changes [6]. The clinical trials to date have not provided an adequate support for the clinical use of antibiotics in the primary or secondary prevention of coronary artery disease [7]. 0954-6928 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved. vs. 16/105 (15.2%) events, OR 2.2 (95% CL: 0.92–5.43), P = 0.13]. However, the difference was not signi cant. By multivariate analysis, bacteria, leukocyte in ltration, and pneumolysin were not predictors for in-hospital clinical events. Higher WBCs and younger age were signi cant predictors of bacterial footprints (P 0.0001 and P = 0.04, respectively). Conclusion Bacterial footprints existed in the aspirate of infarct-related artery of ST-elevation myocardial infarction patients. Predictors were higher WBCs and younger age. Bacterial markers were not predictors for in-hospital clinical events. The presence of bacterial footprints supports the infectious hypothesis of atherosclerosis.

Background Bacterial infections can trigger acute coronary syndromes. This study aimed to examine bacterial footprints in the aspirate of infarct-related artery. Patients and methods We studied 140 patients with ST-elevation myocardial infarction who underwent a primary coronary intervention using thrombus aspiration catheters. The aspirate was sent for bacteriological and pathological examinations and immunoassay for pneumolysin toxin. Results Bacterial culture showed different bacteria in 14 samples. Leukocyte in ltrate was detected in all pathologically examined samples. Pneumolysin toxin was detected in only two samples. Patients with bacteria had similar baseline data as those without, except for the median age [46 (44–50) vs. 55 (47–62) years, P = 0.001, respectively], and white blood cells (WBCs) (16670 vs. 7550 cells/μl, P 0.0001, respectively). In hospital- major clinical events (death, stroke, reinfarction, lethal arrhythmia, and heart failure) were not signi cantly different between the 2 groups with and without bacteria [4 (28.6%) vs. 20 (18.6%) events, respectively, odds ratio (OR) 1.8 (95% CL: 06–6.3), P = 0.5]. Patients with bacteria, heavy in ltration, and pneumolysin had insigni cant higher events compared with those without [10/35 (28.6%) Introduction One emerging paradigm suggests that bacterial infection can contribute toward the pathogenesis of acute coronary syndromes (ACSs) [1]. The formation of platelet thrombi on the surface of complicated coronary plaques is consid- ered an essential step in the evolution of ACS [2]. Acute infections can promote the development of thrombi in var- ious ways [3]. Platelets can be activated directly by patho- gens and the in ammatory response that they elicit [4]. In addition, acute infections can cause coronary vasoconstric- tion and further narrow the lumen in atherosclerotic coro- nary segments, stimulating shear-induced platelet activity [5]. The host response to acute infections can trigger, has- ten, or facilitate ACS on the basis of generalized and local in ammatory and thrombogenic changes [6]. The clinical trials to date have not provided an adequate support for the clinical use of antibiotics in the primary or secondary prevention of coronary artery disease [7]. 0954-6928 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved. vs. 16/105 (15.2%) events, OR 2.2 (95% CL: 0.92–5.43), P = 0.13]. However, the difference was not signi cant. By multivariate analysis, bacteria, leukocyte in ltration, and pneumolysin were not predictors for in-hospital clinical events. Higher WBCs and younger age were signi cant predictors of bacterial footprints (P 0.0001 and P = 0.04, respectively). Conclusion Bacterial footprints existed in the aspirate of infarct-related artery of ST-elevation myocardial infarction patients. Predictors were higher WBCs and younger age. Bacterial markers were not predictors for in-hospital clinical events. The presence of bacterial footprints supports the infectious hypothesis of atherosclerosis.

Background Bacterial infections can trigger acute coronary syndromes. This study aimed to examine bacterial footprints in the aspirate of infarct-related artery. Patients and methods We studied 140 patients with ST-elevation myocardial infarction who underwent a primary coronary intervention using thrombus aspiration catheters. The aspirate was sent for bacteriological and pathological examinations and immunoassay for pneumolysin toxin. Results Bacterial culture showed different bacteria in 14 samples. Leukocyte in ltrate was detected in all pathologically examined samples. Pneumolysin toxin was detected in only two samples. Patients with bacteria had similar baseline data as those without, except for the median age [46 (44–50) vs. 55 (47–62) years, P = 0.001, respectively], and white blood cells (WBCs) (16670 vs. 7550 cells/μl, P 0.0001, respectively). In hospital- major clinical events (death, stroke, reinfarction, lethal arrhythmia, and heart failure) were not signi cantly different between the 2 groups with and without bacteria [4 (28.6%) vs. 20 (18.6%) events, respectively, odds ratio (OR) 1.8 (95% CL: 06–6.3), P = 0.5]. Patients with bacteria, heavy in ltration, and pneumolysin had insigni cant higher events compared with those without [10/35 (28.6%) Introduction One emerging paradigm suggests that bacterial infection can contribute toward the pathogenesis of acute coronary syndromes (ACSs) [1]. The formation of platelet thrombi on the surface of complicated coronary plaques is consid- ered an essential step in the evolution of ACS [2]. Acute infections can promote the development of thrombi in var- ious ways [3]. Platelets can be activated directly by patho- gens and the in ammatory response that they elicit [4]. In addition, acute infections can cause coronary vasoconstric- tion and further narrow the lumen in atherosclerotic coro- nary segments, stimulating shear-induced platelet activity [5]. The host response to acute infections can trigger, has- ten, or facilitate ACS on the basis of generalized and local in ammatory and thrombogenic changes [6]. The clinical trials to date have not provided an adequate support for the clinical use of antibiotics in the primary or secondary prevention of coronary artery disease [7]. 0954-6928 Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved. vs. 16/105 (15.2%) events, OR 2.2 (95% CL: 0.92–5.43), P = 0.13]. However, the difference was not signi cant. By multivariate analysis, bacteria, leukocyte in ltration, and pneumolysin were not predictors for in-hospital clinical events. Higher WBCs and younger age were signi cant predictors of bacterial footprints (P 0.0001 and P = 0.04, respectively). Conclusion Bacterial footprints existed in the aspirate of infarct-related artery of ST-elevation myocardial infarction patients. Predictors were higher WBCs and younger age. Bacterial markers were not predictors for in-hospital clinical events. The presence of bacterial footprints supports the infectious hypothesis of atherosclerosis.

Background: After successful pulmonary vein isolation (PVI) for atrial brillation (AF), the left atrium (LA) undergoes reverse remodeling. However, few studies have directly studied pulmonary vein (PV) remodeling and focused on whether pre PVI-PV conditions could predict outcome of the procedure. We hypothesize that: (I) post PVI, in addition to LA remodeling the PVs undergo a parallel degree of remodeling; and (II) that PV characteristics pre PVI can be used to identify patients more likely to sustain normal sinus rhythm (NSR). Methods: Patients (n=100) scheduled for PVI had a cardiovascular magnetic resonance (CMR) imaging before and 6±2 months following PVI. PV cross sectional areas (CSA) within 0.5 cm of the ostium and LA volumes were measured. Patients were categorized as responders (R) or non-responders (NR), based on two separate 14-day Holter monitoring. Results: PVs CSA were signi cantly reduced post procedure in both groups, R (233±53 to 192±52 mm2, P0.001) and NR (241±54 to 207±44 mm2, P0.001), however, the difference between R and NR post PVI was not signi cant (192±52 to 207±44 mm2, P=0.19). Reduction in PVs CSAs post procedure moderately correlated with the 3D LA volume reduction (r=0.48, P0.001). Conclusions: PVs mirror the LA in that they signi cantly change in size following PVI yet they were not found to directly predict maintenance of NSR.