Hours Of Acute Myocardial Infarction Research Articles

Postmortem Immunohistochemical Findings in Early Acute Myocardial Infarction: A Systematic Review.

The diagnosis of early acute myocardial infarction is of particular importance in forensic practice considering the frequency of sudden cardiac death and the difficulty of positively identifying it through classical histological methods if survival is less than 6 h. This article aims to analyze potential immunohistochemical markers that could be useful in diagnosing acute myocardial infarction within the first 6 h of its onset. We conducted an extensive evaluation of the literature according to the PRISMA guidelines for reporting systematic literature reviews. We searched the Web of Science and PubMed databases from their inception to 2023 using the following keywords: "myocardial infarction" and "immunohistochemistry". Fifteen studies met the inclusion criteria. Immunohistochemical markers as complement factors and CD59, myoglobin, fibrinogen, desmin, tumor necrosis factor alpha (TNF-α), P-38, JNK (Jun N Terminal Kinase), transforming growth factor β1 (TGF-β1), cardiac troponins, fibronectin, H-FABP (heart fatty acid binding protein), dityrosine, fibronectin, CD15, IL-1β, IL-6, IL-15, IL-8, MCP-1, ICAM-1, CD18, and tryptase can be used to identify the first six hours of acute myocardial infarction. These markers are mostly studied in experimental animal models. It is necessary to conduct extensive studies on human myocardial tissue fragments, which will involve the analysis of several immunohistochemical markers and careful analysis of the available data on perimortem events, resuscitation, and postmortem intervals in the context of a uniform laboratory methodology.

Stress, Hyperglycemia, and Insulin Resistance Correlate With Neutrophil Activity and Impact Acute Myocardial Infarction Outcomes.

Introduction Acute insulin resistance (IR) and hyperglycemia are frequently observed during acute myocardial infarction (AMI), significantly influencing both immediate and long-term patient outcomes, irrespective of diabetic status. Neutrophilia and increased neutrophil activity, which are common in these scenarios, have been associated with poorer prognoses, as demonstrated in our recent findings. While it is well established that neutrophils and stress-induced hyperglycemia exacerbate inflammation and hinder recovery, the complex interplay between these factors and their combined impact on AMI prognosis remains inadequately understood. This study aims to investigate the effects of stress hyperglycemia and IR on AMI patients at the onset of the event and to elucidate the relationship between these metabolic disturbances and inflammatory markers, particularly neutrophils. Methods We conducted a longitudinal prospective study on 219 AMI patients at Elias Emergency Hospital in Bucharest, Romania, from April 2021 to September 2022. Patients were included within 24 hours of AMI with ST-segment elevation and excluded if they had acute infections or chronic inflammatory diseases. Blood samples were collected to study inflammatory biomarkers, including neutrophil extracellular traps (NETs), S100A8/A9, interleukin (IL)-1β, IL-18, and IL-6. Diabetic and pre-diabetic statuses were defined using glycated hemoglobin (HbA1c) and medical history (ADA 2019 criteria). To assess glycemic parameters, we employed the glycemia ratio (GR) and the homeostatic model assessment of insulin resistance (HOMA-IR) index, enabling a precise evaluation of stress hyperglycemia, acute IR, and their prognostic implications. Patients were stratified into groups based on GR calculations, categorized as under-average glycemia, normal glycemia, and stress hyperglycemia. Results The majority of patients in the stress hyperglycemia group exhibited an unfavorable prognosis. This group also demonstrated significantly elevated neutrophil counts and neutrophil-to-lymphocyte ratios (NLR). The GR was significantly and positively correlated with inflammation markers, including neutrophil count (Pearson's R = 0.181, P = 0.008) and NLR (Pearson's R = 0.318, P < 0.001), but showed no significant correlation with other evaluated inflammatory markers. Conclusions Our findings suggest that poor outcomes in AMI patients may be associated with stress hyperglycemia, as indicated by GR. AcuteIR, quantified by GR and HOMA-IR, exhibits a strong correlation with neutrophil count and NLR within the first 24 hours of AMI onset. However, no significant correlation was observed with other inflammatory markers, such as IL-1β, IL-18, and IL-6, underscoring the specific interplay between IR and neutrophil activity in this setting.

SERUM MYOGLOBIN AS AN EARLY DIAGNOSTIC TEST IN ACUTE MYOCARDIAL INFARCTION

Acute Myocardial Infarction is one of the leading causes of death worldwide with the prevalence of approximately three million people. In this study we have investigated Biomarkers like Serum Myoglobin, Creatine kinase MB, Lactate Dehydrogenase in Acute Myocardial Infarction within four hours and after four hours of chest pain. The possible role of Serum Myoglobin as an early indicator of Acute Myocardial Infarction. To determine if there is signicant elevation of Serum Myoglobin less than four hours of Acute Myocardial Infarction and to compare it with other biomarkers of Acute Myocardial Infarction. It is a case control study done among a study population of 80 patients presenting to Emergency department of Government Theni Medical College Hospital with complains of chest pain. The study population was divided into two groups, Cases are 40 patients with chest pain less than 4 hours of duration and Controls are 40 patients with chest pain more than 4 hours of duration. Median Age group of patients in this study was between 51 to 60 years. Sig (2-tailed) test showed statistically signicant difference in all groups namely Serum Myoglobin, Creatine kinase , Lactate Dehydrogenase distribution in cases and controls with p value &lt; 0.05. According to the present ndings in our study, the earliest Serum marker to be elevated in the case of Acute Myocardial Infarction is Serum Myoglobin.As it is not a specic marker, it can be combined with Biomarkers like Creatine Kinase and Lactate Dehydrogenase to indentify AMI at the earliest.

Rapid diagnosis of acute myocardial infarction based on reverse transcription-accelerated strand exchange amplification of miR-208a.

Acute myocardial infarction (AMI) is a prevalent cardiovascular disease associated with high morbidity and mortality, posing a significant threat to human health. Therefore, early diagnosis of AMI has become a focal point of research. MiR-208 is specifically expressed in the heart and is involved in the regulation of cardiomyocyte hypertrophy, cardiac fibrosis, and other myocardial gene expressions. It is expected to be applied in the clinical detection of AMI due to its release by damaged myocardial cells within 3 hours of AMI. In this study, we developed a denatured bubble-mediated reverse transcription-accelerated strand exchange amplification (RT-ASEA) method to detect the early biomarker miR-208a of AMI. The novel approach allowed rapid amplification of miR-208a in 15 minutes, with good performance in terms of repeatability (CV < 6%), determination limit (1 × 100 pmol L-1), and linearity (R2 = 0.9690). Based on the analysis of 42 clinical samples, a strong correlation was observed between the Ct value of miR-208a detected by the RT-ASEA method and the cTnI concentration, considered the gold standard for diagnosis of AMI. The research suggested that the RT-ASEA method could be applied to distinguish between AMI and healthy groups. The area under the receiver operating characteristic curve (AUC) was 0.9976, with a sensitivity of 96% and a specificity of 100%. Optimized RT-ASEA is a reliable and efficient method for miRNA detection. Furthermore, this study provides crucial data support for the development of miR-208a as an early biomarker for AMI, which is of great significance in life and health.

Traditional and novel diagnostic biomarkers for acute myocardial infarction

Abstract Background Acute myocardial infarction (AMI) is a leading cause of death worldwide. The first hours of acute myocardial infarction are correlated with the highest risk of death. Therefore, early diagnosis of the infarction seriously affects the efficacy of the treatment administered to the patient. Misdiagnosing patients with chest pain often leads to inappropriate admission of them as acute myocardial infarction patients. The physical examination of the patient, the electrocardiogram, and the assessment of cardiac biomarkers all play an important role in the early diagnosis of acute ischemia, along with the patient's medical history. Main body The present review highlights a number of different biomarkers that are released and elevated in blood during an acute myocardial infarction. Conclusions Analysis of cardiac biomarkers has become the first-line diagnostic tool used in the diagnosis of acute myocardial infarction. Novel markers of acute myocardial infarction, when added to routinely used markers, can provide added value not only in the earlier detection of acute myocardial infarction but also in monitoring the clinical progress of the disease, predicting its consequences, evaluating its prognosis, detecting recurrence, and managing its treatment. This leads to a lower mortality rate associated with acute myocardial infarction. cMyC, IMA, S100, and MicroRNAs can serve as markers of early diagnosis of acute myocardial infarction, whereas myeloperoxidase, sCD40L, PAPPA, and TNF-α can be used to monitor the clinical progress of the disease. In addition, H-FABP, GDF-15, F2 isoprostanes, and ST2 can serve as predictors of AMI complications and mortality. Copeptin, ST2, and SIRT can be useful as prognostic markers of acute myocardial infarction.

Spectrum of Cardiac Arrhythmias During Initial 48 Hours of Acute Myocardial Infarction Patients and their Association with in-Hospital Outcome

Objective: To determine the spectrum of arrhythmias during initial 48 hours of AMI and their impact on the in-hospital outcome.&#x0D; Study Design: Analytical Cross-sectional study.&#x0D; Place and Duration of Study: This study was conducted at a Tertiary Cardiac Center of Rawalpindi Pakistan from Jun 2021 till Jan 2022.&#x0D; Methodology: A total of (n=150) patients of Acute Myocardial Infarction (AMI) undergoing immediate or early revascularization and meeting the inclusion and exclusion criteria were included in the study. They were monitored for arrhythmias during initial 48 hours of hospitalization and their in-hospital outcomes were noted on a predesigned Performa.Chi square test applied for arrhythmia association with adverse outcome at 95% confidence interval and 5% margin of error.&#x0D; Results: This study comprised (n=117; 78%) males and (n=33; 22%) females. Mean age was 62.9 years. ST elevation MI(STEMI) constituted (n=127; 84.7%) and Non-ST Elevation MI (NSTEMI) (n=23;15.3%) of total patients. Arrhythmias documented in overall (n=122;81.3%) patients, 81.8% (n=104) in STEMI and (n=18; 77.2%) in NSTEMI. Sinus tachycardia(n=52;34.7%) was most common rhythm followed by accelerated idioventricular rhythm (n=20;13.4%) and sinus bradycardia12.7% (n=19). In-hospital mortality was (n=25;16.7%) with p-value=0.009, mostly in patients with ventricular tachycardia/ventricular fibrillation, atrial fibrillationand complete heart block. Other outcomes included (n=23;14.7%) acute left ventricular failure, (n=9; 6%) cardiogenic shock (n=5;3.3%) acute stent thrombosis, (n=2; 1.3%) cerebrovascular accident (CVA)and (n=31; 20.7%) prolonged hospitalization (p-value 0.05).&#x0D; Conclusion: Arrhythmias are common in acute myocardial infarction during initial 48 hours of presentation with sinus tachycardia being most common followed by accelerated idioventricular rhythm and sinus bradycardia. Arrhythmias are associated with increased in-hospital mortality and adverse outcome.

Glucagon-like Peptide-1 receptor Tie2+ cells are essential for the cardioprotective actions of liraglutide in mice with experimental myocardial infarction

ObjectivesGlucagon-like peptide-1 receptor (GLP-1R) agonists reduce the rates of major cardiovascular events, including myocardial infarction in people with type 2 diabetes, and decrease infarct size while preserving ventricular function in preclinical studies. Nevertheless, the precise cellular sites of GLP-1R expression that mediate the cardioprotective actions of GLP-1 in the setting of ischemic cardiac injury are uncertain. MethodsPublicly available single cell RNA sequencing (scRNA-seq) datasets on mouse and human heart cells were analyzed for Glp1r/GLP1R expression. Fluorescent activated cell sorting was used to localize Glp1r expression in cell populations from the mouse heart. The importance of endothelial and hematopoietic cells for the cardioprotective response to liraglutide in the setting of acute myocardial infarction (MI) was determined by inactivating the Glp1r in Tie2+ cell populations. Cardiac gene expression profiles regulated by liraglutide were examined using RNA-seq to interrogate mouse atria and both infarcted and non-infarcted ventricular tissue after acute coronary artery ligation. ResultsIn mice, cardiac Glp1r mRNA transcripts were exclusively detected in endocardial cells by scRNA-seq. In contrast, analysis of human heart by scRNA-seq localized GLP1R mRNA transcripts to populations of atrial and ventricular cardiomyocytes. Moreover, very low levels of GIPR, GCGR and GLP2R mRNA transcripts were detected in the human heart. Cell sorting and RNA analyses detected cardiac Glp1r expression in endothelial cells (ECs) within the atria and ventricle in the ischemic and non-ischemic mouse heart. Transcriptional responses to liraglutide administration were not evident in wild type mouse ventricles following acute MI, however liraglutide differentially regulated genes important for inflammation, cardiac repair, cell proliferation, and angiogenesis in the left atrium, while reducing circulating levels of IL-6 and KC/GRO within hours of acute MI. Inactivation of the Glp1r within the Tie2+ cell expression domain encompassing ECs revealed normal cardiac structure and function, glucose homeostasis and body weight in Glp1rTie2−/− mice. Nevertheless, the cardioprotective actions of liraglutide to reduce infarct size, augment ejection fraction, and improve survival after experimental myocardial infarction (MI), were attenuated in Glp1rTie2−/− mice. ConclusionsThese findings identify the importance of the murine Tie2+ endothelial cell GLP-1R as a target for the cardioprotective actions of GLP-1R agonists and support the importance of the atrial and ventricular endocardial GLP-1R as key sites of GLP-1 action in the ischemic mouse heart. Hitherto unexplored species-specific differences in cardiac GLP-1R expression challenge the exclusive use of mouse models for understanding the mechanisms of GLP-1 action in the normal and ischemic human heart.

The soluble major histocompatibility complex class I chain-related gene A (sMICA) as an early biomarker for diagnosing acute myocardial infarction

Introduction: It is necessary to identify tests that have high diagnostic power in the early hours of acute myocardial infarction. Objectives: In this study, we investigated the major histocompatibility complex class I chain-related molecule A (MICA) in the serum of patients with myocardial infarction (MI). Patients and Methods: In this study, 65 patients with MI were studied. Creatine phosphokinase-MB (CPK-MB), troponin I, and MICA biomarkers were measured at different times after hospitalization (0, 3, 6, 9, 12 and, 24 hours). These biomarkers were evaluated at different times after chest pain (0 to 3, 3 to 6, and more than 6 hours). Results: Serum MICA biomarker increased significantly from admission to the hospital until 3 hours. Later on, it decreased until 24 hours. However, CPK-MB biomarkers as well as troponin I, change from admission up to 24 hours. Regarding diagnostic power, it was found that the diagnostic power of MICA is high in the early hours which indicates the high diagnostic power of the test. Conclusion: The diagnostic value of MICA is significant in the early hours after MI. Therefore, due to the high accuracy of MICA in diagnosing MI, it should be used as a diagnostic test along with other tests to confirm MI in the early hours.

Oxidative Stress Markers in Young Patients with Acute Myocardial Infarction and Their Correlation with Cardiac Enzymes

Objective: The relationship between oxidative stress and acute myocardial infarction has been shown in studies. Total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) reflect the oxidative balance. The risk factors, clinical features, and prognosis of acute myocardial infarction (AMI) in young patients differ from older counterparts. This study aims to determine the oxidative stress in the young acute AMI patients and its' correlation with cardiac markers within 48 hours by the quantitative measurement of TAS, TOS, and OSI. Material and Method: In this prospective, controlled study, we included 50 patients who were 45 years old or younger and diagnosed with AMI, as well as 20 healthy individuals as the control group. TOS and TAS were measured from venous blood samples via the spectrophotometric method. The oxidative stress index was obtained from these parameters. Results: Forty-five of totally 50 patients were male, and the mean age was (36±6.8). TOS and OSI values were found significantly higher than in the control group (p=0.002, p=0.005, respectively). TAS values were found not to be different from the control group (p=0.46). A significant correlation was found between CK 0. hour (h.), and TOS 0. h., CK-MB 0. h., and TOS 0. h., CK 48. h. and OSI 48. h., CK-MB 48. h. and OSI 48. h., respectively (r=0.36, p=0.008), (r=0.46, p=0.001), (r=0.32, p=0.03), (r=0.36, p&lt;0.01). Conclusion: Oxidative stress increases in the early hours of AMI. The TOS and OSI values are correlated with cardiac markers at only some time points, and their prognostic values are limited in young AMI patients. TAS is not correlated with cardiac markers.

Macrophage migration inhibitory factor as a predictor of complications in patients with acute st-elevation myocardial infarction in acute and distant periods

Background and Aims: Acute myocardial infarction is a clinically critical disease and associated with a high incidence of adverse outcomes. It is necessary to identify new biomarkers that increase in the first hours of acute myocardial infarction and have a significant impact on cardiac function after a coronary event. The purpose of the study was to determine the prediction role of macrophage migration inhibitory factor (MIF) in development of acute ST-elevation myocardial infarction (STEMI) complications within 6 months after the event.

DYNAMICS OF ARTERIAL STIFFNESS IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION IN LONG-TERM EFFECTIVE LIPID-LOWERING THERAPY

Objective: To assess the dynamics of regional arterial stiffness by volume sphygmography in patients with primary myocardial infarction with ST segment elevation (STEMI) and without ST segment elevation (NSTEMI) on the background of long-term effective lipid-lowering therapy. Design and method: A total of 24 people with acute coronary syndrome were examined: 18 men (75%) and 6 women (25%). The diagnosis was confirmed by biomarkers of myocardial necrosis, electrocardiography, coronary angiography. STEMI was diagnosed in 91.6% of individuals. The average age was 52.88 ± 9.55 years; weight - 81.1 ± 12.6 kg; height 169.7 ± 8.9 m; BMI - 28.4 ± 4.1 kg/m2. Office pressure indicators: SBP –116.7 ± 12.23 mm Hg. and DBP –74.94 ± 8.74 mm Hg; heart rate -68.05 ± 5.16 bpm. On 7–9th day from the disease onset and after 48 weeks, the patients underwent an assessment of regional arterial stiffness using volume sphygmography (VaSera-1000, Fukuda Denshi, Japan). The following indicators were determined: the pulse wave velocity in the arteries of muscle type (B-PWV), in the arteries of elastic type on the right and left (R / L-PWV), cardio-ankle vascular index - CAVI1, which characterizes the true arterial stiffness, independent of the blood pressure level and the reflected wave. All patients were prescribed with atorvastatin 80 mg/day during the first 24–96 hours of acute myocardial infarction in addition to standard therapy. The duration of therapy was 48 weeks. If the target LDL-C level of &lt; 1.5 mmol/L was not achieved 5–6 weeks after AMI, patients were additionally prescribed with ezetimibe 10 mg daily. Results: Against the background of lipid-lowering therapy, a statistically significant decrease in PWV was observed: R-PWV decreased from 14.3 ± 2.4 to 13.2 ± 1.8 m/s (p = 0.04), L-PWV decreased from 13.8 ± 1.8 to 13.0 ± 1.4 (p = 0.04). Significant dynamics of the average R/L-PWV indicator was from 14.1 ± 2.0 to 13.0 ± 1.6 m/s (p = 0.03). There were no significant changes in CAVI and B-PWV. Conclusions: 48-week therapy with atorvastatin 80 mg in patients with primary myocardial infarction with ST segment elevation and without ST segment elevation leads to an improvement in the structural and functional properties of elastic type arteries.

Incidence of Cardiac Arrhythmias in Acute Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention and Associated Outcomes During the First 24 Hours.

BackgroundAcute myocardial infarction (AMI) is the most life-threatening manifestation of coronary artery diseases. The majority of deaths in AMI are due to arrhythmias. Therefore, the aim of this study was to evaluate the incidence and risk factors and outcomes of cardiac arrhythmias in AMI patients undergoing primary percutaneous coronary intervention (PCI) during the first 24 hours of the index hospitalization.MethodologyThis prospective observational study was conducted at the adult cardiology department of the National Institute of Cardiovascular Diseases (NICVD), Karachi, Pakistan. Patients undergoing primary PCI were included in this study. All the patients were kept under observation for the first 24 hours of AMI and monitored through telemetry system monitoring and the incidence of cardiac arrhythmias and the outcomes were recorded.ResultsA total of 110 patients were included; the mean age was 59.6±13.1 years. Most of them were male (70.9%). Arrhythmias were observed in 89.1% of the patients, with 169 episodes. The accelerated idioventricular rhythm was the most common type of arrhythmia (37.3%) followed by sinus tachycardia (36.4%), ventricular tachycardia (22.7%), and complete heart block (20.0%). Lethal arrhythmias were observed in 64.5% (71) of the patients. During the hospital course, 65.5% developed arrhythmias during arrival to balloon time, 30% during the procedure, and 53.6% within 24 hours of the procedure. The in-hospital mortality rate was 15.5% with a significant association with the development of lethal arrhythmias within 24 hours of the procedure (21.1% vs. 5.1%; p=0.026).ConclusionsThe incidence of arrhythmias within 24 hours of hospitalization is high in patients with ST-elevation myocardial infarction (STEMI) undergoing primary PCI, and it has been observed to be associated with an increased rate of in-hospital mortality.

Study of incidence and type of various arrhythmias occurring in the first 48 hours of acute myocardial infarction

Study of incidence and type of various arrhythmias occurring in the first 48 hours of acute myocardial infarction

Incidence of Hyperuricemia in Patients with Acute Myocardial Infarction - A Case-Control Study.

IntroductionVarious researches have stated the correlation between serum uric acid (sUA) and cardiovascular disease (CVD); however, no local studies are available. In this study, we will determine the prevalence of hyperuricemia in patients with acute myocardial infarction and compare with the control group.MethodsThis case-control study was conducted from March to November 2019 in the tertiary care hospital in Pakistan. In all, 119 patients with acute myocardial infarction were enrolled in this study, and 119 controls were identified from the outpatient department. Their sUA levels were measured within 24 hours of acute myocardial infarction.ResultsThe mean sUA levels were significantly higher in patients with acute myocardial infarction (AMI) in comparison to the control group (6.17 ± 2.12 vs. 5.51 ± 1.89, p-value; 0.01). Overall, there were more patients with hyperuricemia in the case group compared to the control group (47.89% vs. 33.6%, p-value = 0.04)ConclusionIn this study, after adjustment of other known factors, hyperuricemia is associated with AMI. Efforts should be made to include screening for hyperuricemia in patients with a high risk of myocardial infarction.

A Study of Arrhythmias in First 48 Hours of Acute Myocardial Infarction in a Tertiary Care Hospital

A Study of Arrhythmias in First 48 Hours of Acute Myocardial Infarction in a Tertiary Care Hospital

Amiodarone Treatment in the Early Phase of Acute Myocardial Infarction Protects Against Ventricular Fibrillation in a Porcine Model

Ventricular fibrillation (VF) occurring in the first minutes to hours of acute myocardial infarction (AMI) is a frequent cause of death and treatment options are limited. The aim was to test whether early infusion of amiodarone 10 min after onset of AMI reduced the incidence of VF in a porcine model. Eighteen female Danish landrace pigs were randomized to a control and an amiodarone group. AMI was induced by ligation of the mid-left anterior descending artery for 120 min followed by 60 min of reperfusion. VF occurred in 0/8 pigs treated with amiodarone compared to 7/10 controls (P < 0.01). Amiodarone treatment prolonged RR intervals, reduced dispersion of action potential duration in the infarcted area and mean number of ectopic beats. No negative effects on cardiac output and blood pressure were observed with amiodarone. Amiodarone qualifies as a potential drug candidate to prevent VF in the first minutes to hours of AMI.

Comparison of Ticagrelor Pharmacokinetics and Pharmacodynamics in STEMI and NSTEMI Patients (PINPOINT): protocol for a prospective, observational, single-centre study

IntroductionThe most common classification of acute myocardial infarction (AMI) is based on electrocardiographic findings and distinguishes ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI). Both types of AMI differ...

Serum Metabolic Disturbances Hailing in Initial Hours of Acute Myocardial Infarction Elucidated by NMR based Metabolomics

Serum Metabolic Disturbances Hailing in Initial Hours of Acute Myocardial Infarction Elucidated by NMR based Metabolomics

Long-Term Outcomes in Survivors of Early Ventricular Arrhythmias After Acute ST-Elevation and Non–ST-Elevation Myocardial Infarction Treated With Percutaneous Coronary Intervention

Guidelines do not recommend an implantable cardioverter defibrillator (ICD) for prevention of sudden death in patients who develop ventricular arrhythmia (VA) within 48 hours of acute myocardial infarction (AMI) if they are successfully revascularized. We aimed to determine long-term survival in a cohort of early VA survivors treated with percutaneous coronary intervention (PCI) and to determine whether certain high-risk characteristics predicted worse outcomes. This retrospective study included all patients with early VA after AMI treated with PCI at our institution from 2002 to 2012 who survived to hospital discharge. Patients who had an ICD before their index AMI and those who received ICD before hospital discharge were excluded. Overall survival in the early VA survivors was analyzed based on post-MI left ventricular ejection fraction (LVEF) (≥50% vs <50%), MI type (ST-segment elevation myocardial infarction [STEMI] vs non-ST-segment elevation myocardial infarction [NSTEMI]), and single-vessel versus multivessel disease. Baseline presenting clinical and PCI characteristics plus outcomes were compared with matched controls with PCI-treated AMI but no early VA. Of the 79 early VA survivors treated with PCI, there were no significant differences in long-term overall survival between AMI type (STEMI vs NSTEMI), single-vessel versus multivessel disease, and LVEF at time of MI (>50% vs <50%). Despite having lower presenting LVEF (46% vs 55%, p <0.001) and higher rates of cardiogenic shock (28% vs 4%; p <0.001), survivors of early VA had similar overall survival compared with PCI-treated controls whose post-AMI hospital course was not complicated by early VA (p = 0.61). In conclusion, patients with early VA treated with PCI who survive to discharge were more likely to have STEMI, lower LVEF, and cardiogenic shock. Type of AMI or the presence of systolic dysfunction or multivessel disease did not predict long-term mortality. With early PCI, early VA survivors have similar long-term prognosis compared with those without early VA.

Modern clinical retrospective on ventricular rhythm disturbances in acute myocardial infarction: Latest treatment mode according to the valid recommendations

Ventricular arrhythmias are the most common cause of mortality in patients with acute myocardial infarction. Arrhythmias in acute coronary syndrome occur because of unbalanced function of the autonomic nervous system, because of electrolyte status disturbances (hypokalemia, hypomagnesaemia, intracellular hypercalcemia) and because of slow conduction in ischemical myocardium zones. Arrhythmias contribute to acidosis and release of free oxygen radicals occurring during reperfusion of ischemic myocardium. Ventricular arrhythmias in acute myocardial infarction indicate the presence of extensive myocardial damage at a reduced left ventricular ejection fraction, and not infrequently in the formation of an aneurysm of the left ventricle. In patients with acute coronary syndrome, the most common ventricular arrhythmias are premature ventricular beats, ventricular tachycardia, ventricular flutter and fibrillation and accelerated idioventricular rhythm. Ventricular fibrillation, still the leading cause of sudden death in patients with acute coronary syndrome within the first four hours of myocardial infarction, occurs in 80 % of all ventricular fibrillations. The use of beta-blockers in the first 24 hours of acute myocardial infarction in patients with early ventricular fibrillation and tachycardia does not affect the degree of worsening heart failure and is directly associated with reduced rates of early mortality in these patients. Quick and adequate treatment of ventricular arrhythmias is a major advancement in the treatment of acute myocardial infarction.