Therapy In Myocardial Infarction Patients Research Articles

Ventricular arrhythmias occurring in myocardial infarction patients with acute ST-segment elevation within the first 24 hours after primary percutaneous coronary intervention and their prognostic value

Reperfusion therapy in myocardial infarction patients with acute ST-segment elevation significantly reduced the frequency of ventricular tachycardia and ventricular fibrillation, however, such arrhythmias still occur in 6-8% of patients, posing a threat to their lives.The aim of the study was to determine the nature of ventricular arrhythmias occurring in myocardial infarction patients with acute ST-segment elevation within the first 24 hours after primary percutaneous coronary intervention, and their prognostic value regarding the development of complications during the inpatient treatment phase. The study involved 82 individuals (mean age: 62,4±10,2 years; male: 69,23 (58,6-78,92)%, female: 30,77 (21,08-41,4)%). Within 24 hours after the infarct-related artery stenting, all patients underwent a 24-hour Holter ECG monitoring. The course of the disease was analyzed based on the presence of risk factors such as hypertension, diabetes mellitus, past COVID-19, and obesity. Ventricular rhythm disturbances were represented mainly by premature contractions. They occurred significantly more frequently in patients with arterial hypertension (883,71 (96,0; 986.0); p=0,02; p=0,03; p=0,02, compared to patients with a history of COVID-19, diabetes, and obesity, respectively) and in those with past COVID-19 (711,3 (125,0; 846,5); p=0,01; p=0,04, compared to indi­viduals with diabetes and obesity, respectively). Isolated premature ventricular complexes, pairs, triplets were recorded, and in individuals with arterial hypertension and past COVID-19 “runs” of ventricular extrasystoles and episodes of nonsustained monomorphic and even polymorphic ventricular tachycardia, such as Torsades de Pointes, (under the condition of combined risk factors) were noted; predominantly in these patients during the hospital phase such сom­plications as ventricular fibrillation and asystole,with sudden cardiac arrest developed. The obtained results is an evidence of electrical myocardial instability and indicate that myocardial infarction patients with acute ST-segment elevation, in addition to myocardial revascularization, require optimization of pharmacological treatment. The use of intravenous beta-blockers as part of complex treatment prevented the occurrence of life-threatening ventricular arrhythmias during the inpatient treatment phase.

Identifying Immune Cell Infiltration and Hub Genes During the Myocardial Remodeling Process After Myocardial Infarction.

Myocardial remodeling after myocardial infarction (MI) is a complex repair process following myocardial injury, characterized by the infiltration of multiple types of immune cells. However, the underlying molecular mechanism of myocardial remodeling after MI remains obscure. This study aimed to identify the hub differential expression genes (DEGs) of myocardial remodeling after MI and determine the distribution of immune cells infiltrating the pathology. We downloaded GSE132143, GSE151834, and GSE176092 data from the GEO database. The GSE132143 dataset was used to identify DEGs, perform functional annotation, and screen hub genes based on protein-protein interaction (PPI) analysis. The GSE151834 dataset was used to validate the expression of hub genes. CIBERSORTx analysis was performed to explore the immune microenvironment in myocardial remodeling after MI. After conducting a literature review, we selected P3H3 to confirm the expression by utilizing immunohistochemistry and qRT-PCR. Finally, the snRNA-seq data in dataset GSE176092 was used for clarifying the expression of these hub genes in various cell clusters. We found 975 DEGs in myocardial remodeling after MI. Four hub genes (P3H3, COL15A1, COL16A1, COL27A1) were identified and were verified in the GSE151834 dataset. According to immune infiltration analysis, CD4+ naive T cells, regulatory T cells, monocytes, M2 macrophages, and neutrophils were involved in the pathological process of myocardial remodeling after MI. Additionally, in vitro experiments verified that P3h3 expression was significantly elevated in myocardial remodeling after MI. The snRNA-seq data analyzed that P3h3, Col15a1, Col16a1, and Col27a1 were highly expressed in fibroblasts of post-MI. This study identified four hub genes P3H3, COL15A1, COL16A1, and COL27A1, particularly P3H3, as potential targets for targeted therapy in MI patients.

Abstract 13426: Efficacy and Safety of Hypothermia as Adjuvant Therapy for Myocardial Infarction Patients Undergoing Percutaneous Coronary Intervention: A Systematic Review and Meta-Analysis

Objective: Randomized control trials (RCT) conducted on myocardial infarction (MI) patients regarding the efficacy of therapeutic hypothermia (TH) as an adjunct to percutaneous coronary intervention (PCI) have shown inconsistent results. This study aims to compare the use of TH in patients with MI undergoing PCI with control groups. Methods: We systematically searched four databases; PubMed, Scopus, Web of Science, and Cochrane for studies conducted until March 2022. The inclusion criteria were any study design that compared TH in patients with MI undergoing PCI with a control group. Infarct size percentage and recurrent MI were primary efficacy outcomes. Mortality, major adverse cardiovascular events (MACE), and overall bleeding complications were primary safety outcomes. The risk of bias assessment of the included RCTs was conducted through Cochrane tool, while the quality of the included cohort studies was assessed by the NIH tool. The meta-analysis was performed on RevMan. Results: A total of 19 studies were included; 15 RCTs, one case-control, and three cohort studies. Infarct size percentage was significantly reduced in TH group as compared to control (MD= -1.76, 95% CI [-3.04, -0.47), p=0.007), but the TH group had a higher incidence of bleeding complications (OR= 1.88, 95% CI [1.11, 3.18), p=0.02). There were no significant differences between TH and control groups in mortality (OR= 1.06, 95% CI [0.75, 1.50), p=0.73) or recurrent MI (OR= 1.21, 95% CI [0.64, 2.30), p=0.56). Conclusion: In patients with MI, TH reduces infarct size while increasing bleeding complications. Mortality and recurrent MI outcomes are not significantly reduced.

Evaluation of ventricular tachyarrhythmias in patients with myocardial infarction after streptokinase therapy

Objectives: The occurrence of arrhythmias after myocardial infarction is associated with an increased risk of mortality. The purpose of this study was to investigate tachyarrhythmias after streptokinase therapy in myocardial infarction patients. Methods: This study was a case-control study. Among 262 patients with myocardial infarction who received streptokinase, 168 patients with ventricular tachyarrhythmia, ventricular fibrillation, or both (case group), and 94 patients without arrhythmia (control group) were selected. Their clinical information were collected by questionnaire. Data were analyzed using SPSS 20 software through chi-square test and Wilcoxon rank-sum. Results: There was no relationship between demographic variables or electrocardiogram changes and the type of arrhythmia in 168 participants in the group 1 (p > 0.05). However, there was a significant relationship between age (p = 0.04), sex (p = 0.049), diabetes (p = 0.039), hypertension (p = 0.037), history of beta-blocker use (p = 0.028), history of aspirin use (p = 0.023), number of the leads involved (p = 0.023) and occurrence of arrhythmia among the participants in the group 2. Conclusions: According to the findings of this study, patients with myocardial infarction who need to receive thrombolysis and who have any of the following conditions should be monitored by the health care staff to prevent development of ventricular tachyarrhythmias: old age, male gender, history of diabetes mellitus, hypertension or more lead involvement in their electrocardiogram.

Primary Prevention of Fatal Ventricular Arrhythmias With Implantable Cardioverter- Defibrillator Therapy – An Analysis of Implications Based on MADIT II Criteria

The primary aim of this retrospective study was to determine the proportion of patients with myocardial infarction (MI) who fulfil the criteria of the Multicenter Automatic Defibrillator Implantation Trial (MADIT) II and the implications of MADIT II criteria in practice. We performed a retrospective analysis of three hundred and ninety four admissions to the Coronary Care Unit (CCU) of the Royal Infirmary of Edinburgh. We selected those with myocardial infarction (MI) and attempted to retrieve electronic copies of their echocardiogram reports. When available, these were used to assess requirement for primary-prevention Implantable Cardioverter Defibrillator (ICD) therapy based on reported left ventricular function. One hundred and ninety patients were admitted to the CCU with a diagnosis of MI. Of these, 100 patients (51.5%) had an echocardiogram. Requirement for ICD therapy was unlikely in 87 (87%), probable in 6 (6%) and necessary in 7 (7%). Since a significant number of patients in the probable category were also likely to meet MADIT II criteria, we concluded that the proportion of patients requiring primary-prevention ICD therapy would be no less than 7% and more likely to be 13%. In the context of a busy teaching hospital, a figure of 13% for the requirement of ICD therapy in MI patients represents annual implantation activity of at least 100 per million. This is likely to have very significant resource implications.

The Association between CYP2C19 Genotype and Phenotype and the Impact on 1-year Outcomes Following Phenotype Guided-escalated Antiplatelet Therapy in Myocardial Infarction Patients with Drug Eluting Stents

The Association between CYP2C19 Genotype and Phenotype and the Impact on 1-year Outcomes Following Phenotype Guided-escalated Antiplatelet Therapy in Myocardial Infarction Patients with Drug Eluting Stents

88Oxygen therapy in myocardial infarction patients with or without diabetes mellitus - A predefined subgroup analysis from the DETO2X-AMI trial

Abstract Background In diabetes, there is an interaction between hyperglycaemia and cellular hypoxia, which may induce oxidative stress. Oxygen therapy in patients with diabetes and myocardial infarction (MI) has not been studied. Purpose Our aim was to determine the effects of supplemental oxygen in MI patients with or without diabetes. Methods The DETermination of the role of Oxygen in suspected Acute Myocardial Infarction (DETO2X-AMI) trial randomised 6629 patients with suspected myocardial infarction (MI) to receive oxygen at 6 L/min for 6–12 hours or ambient air. In this prespecified analysis involving 5010 patients with confirmed MI, 934 had known diabetes (19%). The main composite endpoint was the effect of supplemental oxygen on all-cause death, rehospitalisation with MI, or heart failure at one year in patients with diabetes. Key secondary endpoint was the comparison between patients with or without diabetes. Results In patients with diabetes, the main composite endpoint occurred in 16.2% (72 of 445) of patients allocated to oxygen compared to 16.6% (81 of 489) allocated to ambient air (hazard ratio [HR] 0.93; 95% confidence interval [CI], 0.67–1.27, P=0.81) at one year (figure). There was no statistically significant difference for the individual components of the main composite endpoint, or the rate of cardiovascular death up to one year. In comparison, corresponding endpoints in patients without diabetes were similar between the treatment groups. However, when comparing patients according to diabetes status, event rates were significantly higher in the diabetic population (main composite endpoint: HR 1.60; 95% CI, 1.32–1.93, P<0.01). Kaplan-Meier curves for main endpoint Conclusions Oxygen therapy in normoxemic MI patients did not significantly affect 1-year all-cause death, cardiovascular death, rehospitalisation with MI or heart failure, irrespective of underlying diabetes. Noteworthy, despite that the incidence of cardiovascular outcomes has declined substantially in patients with diabetes over the last decades, we still observed markedly increased event rates in patients with diabetes. Acknowledgement/Funding Swedish Heart-Lung Foundation; Swedish Research Council; Stockholm County Council

Current uses of ISACS-TC registry in Mostar

Cardiovascular disease (CVD) contributes greatly to inequalities in health in Europe. The acute myocardial infarction (MI) in hospital death rate in Bosnia and Herzegovina is three fold higher than in European Union countries before the enlargement in 2004. There is also a striking difference in mortality between Bosnia and Herzegovina and Central and East European countries that joined the EU in 2004. Rapid development of high technology treatment procedures, which followed the economic recovery of the European Union countries, still have only limited influence on the overall control of MI death rate. Large potential to control MI death rate lies in developing PCI capable network with target to rapid reperfusion therapy in MI patients. The hypothesis that social factors may contribute to explain high MI death rate is attractive, but still is an assumption. However, if confirmed, transforming such knowledge into a practical health policy would be a great challenge. A resource-saving balanced assessment approach to health technology development is warrant in Bosnia and Herzegovina. An international help is needed.

Primary coronary intervention versus thrombolytic therapy in myocardial infarction patients in the Middle East

Little is known about predictors and outcome differences of primary percutaneous coronary intervention (PPCI) and thrombolytic therapy (TT) in ST-segment elevation myocardial infarction (STEMI) patients in the Middle East. To compare predictors as well as in-hospital outcomes of PPCI and TT in STEMI patients in six Middle Eastern countries. Sixty-five hospitals (covering at least 85 % of the population) in Oman, United Arab Emirates, Qatar, Bahrain, Kuwait and Yemen. This was a prospective, multinational, multicentre, observational survey of consecutive acute coronary syndrome patients who were admitted to 65 hospitals during May 8, 2006 to June 6, 2006 and from January 29, 2007 to June 29, 2007, as part of Gulf RACE (Registry of Acute Coronary Events). Analyses were performed using univariate and multivariate statistical techniques. Predictors as well as in-hospital outcomes of PPCI and TT in STEMI patients. Out of 2,155 STEMI patients admitted to hospitals within 12 h of symptoms onset, 92 % received reperfusion (8 % PPCI and 84 % TT). TT use included reteplase (43 %), tenecteplase (30 %), streptokinase (25 %), and alteplase (2 %). Median age of the study cohort was 50 (44-58) years with majority being males (90 %). There were no significant differences in median onset time to presentation between the TT and PPCI groups (130 vs. 120 min; P = 0.422). Median door-to-needle time and door-to-balloon time were 45 min (29-75) and 75 min (58-120), respectively. Predictors of PPCI included prior PCI, hospitals with catheterization laboratory facilities as well as those involved with academia. Multivariate logistic regression model demonstrated that patients that had PPCI were less likely to have recurrent ischemic attacks than those that had TT (odds ratio, 0.18; 95 % CI, 0.06-0.56; P = 0.003). The main reperfusion strategy for STEMI patients in the Arab Middle East region is thrombolytic therapy. Predictors of primary percutaneous coronary intervention included prior percutaneous coronary intervention, hospitals with catheterization laboratory facilities as well as those involved with academia. Primary percutaneous coronary intervention resulted in significant reductions in recurrent ischemic events when compared to thrombolytic therapy.

Optimal treatment for patients after myocardial infarction: some current concepts and controversies

Acute coronary syndromes areone of the most common causes for hospitalizations in developed countries. It is estimated that there are around 1 million patients in Poland after myocardial infarction (MI) requiring medical care. Implementation of optimal treatment in these patients is a significant clinical and social problem. Clinical practice guidelines published by the European Society of Cardiology (ESC) are focused on the crucial tasks such as regular physical activity sufficient to increase exercise capacity, smoking cessation, a Mediterranean diet, intensive control of risk factors for atherosclerosis (hypertension, diabetes, hyperlipidemia), combination pharmacotherapy and in selected cases, coronary revascularization. Of particular importance is that all patients who have had an acute MI should receive optimal treatment with a combination of the drugs that are recommended as class I by the ESC guidelines. Recent registries showed that some of these drugs, including aspirin, clopidogrel, angiotensin-converting enzyme inhibitors, beta-blockers and statins, are commonly used in clinical practice in Poland. Recently, it has been highlighted that pharmacological therapy in MI patients should be extended by adding newer agents of the class I recommendations such as omega-3 acid ethyl esters and in selected patients, eplerenone.

Streptokinase promotes development of dipeptidyl peptidase IV (CD26) autoantibodies after fibrinolytic therapy in myocardial infarction patients.

Dipeptidyl peptidase IV (DPP IV) (CD26) plays a critical role in the modulation and expression of autoimmune and inflammatory diseases. We recently reported that sera from patients with rheumatoid arthritis and systemic lupus erythematosus contained low levels of DPP IV and high titers of anti-DPP IV autoantibodies of the immunoglobulin A (IgA) and IgG classes and found a correlation between the low circulating levels of DPP IV and the high titers of anti-DPP IV autoantibodies of the IgA class. Since streptokinase (SK) is a potent immunogen and binds to DPP IV, we speculated that patients with autoimmune diseases showed higher DPP IV autoantibody levels than healthy controls as a consequence of an abnormal immune stimulation triggered by SK released during streptococcal infections. We assessed this hypothesis in a group of patients suffering from acute myocardial infarction, without a chronic autoimmune disease, who received SK as part of therapeutic thrombolysis. Concomitant with the appearance of anti-SK antibodies, these patients developed anti-DPP IV autoantibodies. These autoantibodies bind to DPP IV in the region which is also recognized by SK, suggesting that an SK-induced immune response is responsible for the appearance of DPP IV autoantibodies. Furthermore, we determined a correlation between high titers of DPP IV autoantibodies and an augmented clearance of the enzyme from the circulation. Serum levels of the inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6) increased significantly after 30 days of SK administration, while the levels of soluble IL-2 receptor remained unchanged during the same period, suggesting a correlation between the lower levels of circulating DPP IV and higher levels of TNF-alpha and IL-6 in serum in these patients.

Heterogeneous changes in K currents in rat ventricles three days after myocardial infarction.

After coronary artery occlusion, surviving myocardium in and around the infarct zone plays an important role in arrhythmogenesis. Understanding the mechanisms for derangements in cardiac electrical activity at the cellular and molecular levels is important for the design of effective therapeutic strategies. To provide part of that understanding, we studied changes in K channel function and expression in rat ventricular myocardium three days after occluding the left major coronary artery. The epicardium and endocardium of infarcted region in the left ventricle and the free wall of right ventricle were separated for myocyte isolation, followed by whole-cell voltage clamp studies. Myocytes were also isolated from corresponding regions of control and sham-operated hearts and studied under the same conditions. We found that the transient outward (Ito), delayed rectifier (IK) and inward rectifier (IKI) currents have different distribution patterns in normal rat ventricular myocardium. Sham-operation did not affect any of these K currents in left ventricular myocytes, but coronary artery occlusion caused a reduction of all three. For Ito and IKI the reduction was greater in epicardial than in endocardial myocytes, but IK was reduced equally in these two cell groups. Unexpectedly, Ito and IK as well as cell capacitance were increased in right ventricular myocytes from infarcted as well as sham-operated hearts. Western blot analysis indicated that the level of Kv4 channel proteins (Kv4.2 + Kv4.3) was reduced in infarcted left ventricular myocardium, consistent with the reduction in Ito. Our data suggest that the distribution of K channels and changes in them induced by coronary artery occlusion are heterogeneous in ventricular myocardium. Understanding the molecular mechanisms for this heterogeneity and its implications in arrhythmogenesis poses a challenge in designing effective antiarrhythmic therapy for myocardial infarction patients.

Optimal intensity of oral anticoagulant therapy after myocardial infarction

Objectives.This study attempted to determine the optimal intensity of anticoagulant therapy in patients after myocardial infarction.Background.Treatment with oral anticoagulant therapy entails a delicate balance between over- (risk of bleeding) and under-anticoagulant (risk of thromboemboli). The optimal intensity required to prevent the occurrence of either event (bleeding or thromboembolic) is not known.Methods.A method was used to determine the optimal intensity of anticoagulant therapy by calculating incidence rates for either event associated with a specific international normalized ratio. The numerator included events occurring at given international normalized ratios, and the denominator comprised the total observation time.Results.The study population included 3,404 myocardial infarction patients enrolled in the ASPECT (anticoagulants in the Secondary Prevention of Events in Coronary Thrombosis) trial. Total treatment was 6,918 patient-years. Major bleeding occurred in 57 patients (0.8/100 patient-years), and thromboembolic complications in 397 (5.7/100 patient-years). The incidence of the combined outcome (bleeding or thromboembolic complications) with international normalized ratio < 2 was 8.0/100 patient-years (283 events in 3,559 patient-years), with international normalized ratios between 2 and 3, 3.9/100 patient-years (33 events in 838 patient-years); 3.2/100 patient-years (57 events in 1,775 patient-years) for international normalized ratios between 3 and 4; 6.6/100 patient-years (37 events in 564 patient-years) for international normalized ratios between 4 and 5; and 7.7/100 patient-years (14 events in 182 patient-years) for international normalized ratios >5. After adjustment for achieved international normalized ratio levels, significant predictors were higher levels of systolic blood pressure and age.Conclusions.If equal weight is given to hemorrhagic and thromboembolic complications, these results suggest that the optimal intensity of long-term anticoagulant therapy for myocardial infarction patients lies between 2.0 and 4.0 international normalized ratio, with a trend to suggest an optimal intensity of 3.0 to 4.0.

Cardiac troponin T in the diagnosis of myocardial injury.

In the last several decades serum levels of cardiac enzymes and isoenzymes have become the final arbiters by which myocardial damage is diagnosed or excluded. Because conventionally used enzymes are neither perfectly sensitive nor specific, there is need for a new sensitive and cardiospecific marker of myocardial damage. Cardiac troponin T (TnT) is a contractile protein unique to cardiac muscle and can be differentiated by immunologic methods from its skeletal-muscle isoform. An enzyme immunoassay specific for cardiac TnT is now available in a commercial kit for routine use. The biggest advantage of this assay is its cardiospecificity. TnT measurements, however, are also highly sensitive in diagnosis of myocardial injury and accurately discern even small amounts of myocardial necrosis. TnT measurements are, therefore, particularly useful in patients with borderline CK-MB and in clinical settings in which traditional enzymes fail to diagnose myocardial damage efficiently because of lack of specificity--for example, perioperative myocardial infarction or blunt heart trauma. TnT release kinetics reveal characteristics of both soluble, cytoplasmic, and structurally bound molecules. It starts to increase a few hours after the onset of myocardial damage and remains increased for several days. TnT allows late diagnosis of myocardial infarction. The diagnostic efficiency remains at 98% until 6 d after the onset of infarct-related symptoms. TnT is also useful in monitoring the effectiveness of thrombolytic therapy in myocardial infarction patients. The ratio of peak TnT concentration on day 1 to TnT concentration at day 4 discriminates between patients with successful (greater than 1) and failed (less than or equal to 1) reperfusion. TnT measurements are very sensitive and specific for the early and late diagnosis of myocardial damage and could, therefore, provide a new criterion in laboratory diagnosis of the occurrence of myocardial damage.