Examination of electrocardiographic findings in patients with left ventricular aneurysm caused by myocardial infarction

Number of pages: 130 File Format: word File Code: 31978
Year: 2014 University Degree: Master's degree Category: Paramedical
  • Part of the Content
  • Contents & Resources
  • Summary of Examination of electrocardiographic findings in patients with left ventricular aneurysm caused by myocardial infarction

    Dissertation:

    To get a doctorate

    Abstract

    Introduction: One of the rare complications of myocardial infarction that occurs in the weeks and months after it is left ventricular aneurysm, which is a thin and discrete piece of the left ventricular wall that It is raised both during systole and diastole and has a wide base. Most of the left ventricular aneurysms occur in the anterior wall and the apex, and in a small number in the posterior basal wall of the heart.

    The aim of this study is to determine the electrocardiographic findings in patients with left ventricular aneurysm caused by myocardial infarction.

    Materials and methods: This is a case series study on 60 patients. left ventricular aneurysm was performed from February 2011 to March 2012 and finally the data was analyzed using chi-square test, ANOVA and Fisher exact test in spss ver.17 software environment.

    Findings: The average age of these patients was 63.58±12.67 years. In the present study, the correlation of electrocardiogram with age, blood pressure , hyperlipidemia, smoking and the number of involved vessels were not significant, but showed a significant relationship with history of diabetes and EF percentage.

    70% of patients had ST elevation, and most patients had involvement of three coronary vessels, and 86% of patients had aneurysms in the apical and anteroapical wall.

    Conclusion: In this study, patients with higher EF The frequency of ST elevation was lower in them. Also, the average P wave height was higher in male patients and patients who did not have DM. But in this research, no significant relationship was observed between ECG, history of HTN, history of HLP, history of smoking and the number of vessels involved.

    Key words: left ventricular aneurysm, myocardial infarction, electrocardiography

    1-1- Ischemic heart diseases (IHD
    Ischemic heart diseases (IHD) is a condition in which there is insufficient blood and oxygen supply to a part of the myocardium. Specifically, IHD occurs when there is an imbalance between the supply and demand of myocardial oxygen. The most common cause of myocardial ischemia is epicardial coronary artery occlusion, which causes a regional decrease in blood flow. The myocardium and the insufficient blood supply of the myocardium fed by the coronary artery are involved [1]. 1-1-Epidemiology Ischemic heart diseases (IHD) cause the most death, disability and financial burden in developed societies. Ischemic heart diseases (IHD) are the most common and serious diseases It is chronically life-threatening in the United States. In these countries, thirteen million people suffer from ischemic heart disease, six million suffer from angina and more than seven million suffer from myocardial infarction. Genetic factors - diet rich in fat and energy - smoking - sedentary lifestyle have been associated with the emergence of ischemic heart disease. In the United States and Western Europe, the disease is increasing among the poor more than the rich because this group has adopted healthier lifestyles and primary prevention in all socioeconomic groups has moved the disease to a later time in life. Obesity-insulin resistance and type 2 diabetes are increasing and are important risk factors for ischemic heart disease. Due to urbanization in developing countries, the prevalence of IHD risk factors is rapidly increasing in these areas, and therefore most of the global burden of IHD currently occurs in low- and middle-income countries. Due to the sharp increase in ischemic heart disease in the world, it is likely that ischemic heart disease will become the most common cause of death in the world by 2020 [2]. 1-1-2- Pathophysiology The basic issue in understanding the pathophysiology of myocardial ischemia is the concept of myocardial supply and demand.Under normal conditions, for each level of oxygen demand, oxygen-rich blood is supplied to the myocardium to prevent low blood supply to myocytes and the subsequent occurrence of ischemia and infarction. The main determining factors for myocardial oxygen demand include heart rate, heart contractility, and myocardial wall tension (stress). Sufficient myocardial oxygen supply depends on satisfactory blood oxygen carrying capacity (which is dependent on breathed oxygen, pulmonary function, hemoglobin concentration and function) and sufficient coronary blood flow. Blood flow in coronary arteries is phasic and most of it occurs in diastole. About 75% of the resistance to coronary flow in three categories of arteries including:
    1) large epicardial arteries (resistance 1=1 (R
    2) pre-arteriolar vessels (R2)
    3) arterioles and capillaries inside the myocardium (R3)
    It happens. In the absence of significant atherosclerotic obstruction limiting the flow, R1 is insignificant and the main determinants of coronary resistance are R3 and R2 [3]. The normal control of coronary blood circulation is influenced and controlled by the heart's need for oxygen. This need is significantly satisfied by the ability of the coronary artery bed to change the resistance and then the blood flow, while the myocardium receives a high and almost constant amount of oxygen. In general, the resistance arterioles inside the myocardium have a large capacity for expansion (R3 and R2 decrease). For example, the change in the need for oxygen during exercise and mental stress affects the resistance of the coronary vessels and in this way supplies oxygen and raw materials to the myocardium (metabolic regulation). Also, the coronary resistance vessels adapt in response to physiological changes in blood pressure so that they can maintain the coronary blood flow at levels that are suitable for the needs of the myocardium (self-regulation). Atherosclerosis, by reducing the internal diameter of coronary arteries, when the need for blood flow increases (for example, during exercise or excitement), causes a limitation in increasing blood supply. When the decrease in the internal diameter of the vessel is severe, myocardial blood supply decreases in the baseline condition. Coronary blood flow can also be limited by spasm, clot formation in the artery, coronary embolism, and narrowing of the beginning of the vessel due to aortitis. Congenital disorders, such as the origin of the left main coronary from the pulmonary artery, may lead to ischemia and myocardial infarction in infancy, but this condition is very inaccurate in adults. Myocardial ischemia can also occur when the need for oxygen is greatly increased and the coronary blood flow is limited (like the condition seen in severe left ventricular hypertrophy due to aortic stenosis). This condition may manifest as angina, which cannot be distinguished from the pain that occurs in the context of coronary atherosclerosis due to subendocardial ischemia [4]. A decrease in oxygen carrying capacity (for example, in very severe anemia or the presence of carboxyhemoglobin) rarely leads to myocardial ischemia by itself, but this is a threshold condition. It reduces ischemia in patients with moderate coronary obstruction. Sometimes two or more causes of ischemia exist simultaneously: for example, increased oxygen demand due to left ventricular hypertrophy secondary to atherosclerosis and anemia. Abnormal contraction or non-normal expansion of coronary resistance vessels can also cause ischemia. When this causes angina, this condition is referred to as microvascular angina [5]. 1-1-3 Coronary Atherosclerosis Epicardial coronary arteries are a major site for atherosclerosis. The main risk factors for atherosclerosis, which are high LDL, low HDL, smoking, hypertension, and diabetes mellitus, interfere with the normal functioning of the vascular endothelium. These actions include: local control of vascular tone, establishment of a surface that has anticoagulant properties, and disruption of cell adhesion and diapedesis. The absence of these defenses leads to disproportionate contraction, formation of clots in the vein and abnormal reaction to monocytes and blood platelets. The latter leads to the accumulation of fat, smooth muscle cells, fibroblasts and intercellular matrix under the intima (atherosclerotic plaques), so that these plaques are created at an irregular rate in different parts of the epicardial coronary branches and ultimately lead to a reduction in the cross-sectional area of ??these vessels in different parts.
  • Contents & References of Examination of electrocardiographic findings in patients with left ventricular aneurysm caused by myocardial infarction

    List:

    Chapter One: Introduction and review of similar studies. 1

    1-1- Ischemic heart diseases (IHD. 2

    1-1-1- Epidemiology. 2

    1-1-2- Pathophysiology. 3

    1-1-3- Coronary atherosclerosis. 4

    1-1-4- Effects of ischemia. 6

    1-4-Symptomatic heart disease

    1-Unstable myocardial infarction

    1-2- Definition 9

    1-2-3- Clinical manifestations

    1-2-4- Diagnostic evaluation

    1-2-7- Treatment of unstable angina and non-ST segment elevation

    1-2-8 Conservative. 1-2-9- Long-term treatment. 20-2-10- Etiology. 20-2-10- Treatment Prinzmetal's angina. 21-2-10-4- Prognosis in Prinzmetal's angina. 22- Myocardial infarction with ST segment elevation. 22

    1-3-1- Epidemiology and importance of ST segment elevation myocardial infarction assessment. 22

    1-3-2- Pathophysiology. 23

    1-3-3- Clinical manifestations and physical findings. 25

    1-3-4-paraclinical in ST segment elevation myocardial infarction. 27

    1-3-4-1- laboratory findings. 27

    1-3-4-2- electrocardiogram. 28

    1-3-4-3- serum cardiac biomarkers. 28

    1-3-4-4- imaging of the heart. 30

    1-4- Preliminary treatment of ST segment elevation myocardial infarction. 31

    1-4-1- Pre-hospital care. 31

    1-4-2- Treatment in the emergency department. 32

    1-4-2-1- Pain control. 33

    1-4-2-2- therapeutic strategies. 34

    1-5- Treatment of ST segment elevation myocardial infarction in the hospital. 41

    1-5-1- Drug treatment. 43

    1-5-1-1- antithrombotic agents. 43

    1-5-1-2- beta blockers 45

    1-5-1-3- renin-angiotensin-aldosterone system inhibitors. 46

    1-6- Complications caused by myocardial infarction. 47

    1-6-1- ventricular dysfunction. 47

    1-6-2- Hemodynamic assessment: 48

    1-6-3- Cardiogenic shock: 49

    1-6-4- Arrhythmia. 49

    1-6-5- Ventricular prearrhythmias. 49

    1-6-7- fibrillation and ventricular tachycardia. 50

    1-6-8- Supraventricular arrhythmias. 51

    1-6-9- sinus bradycardia. 51

    1-6-10- pericarditis. 52

    1-6-11- Thromboembolism. 52

    1-6-12- Left ventricular aneurysm. 53

    1-6-12-1- Definition. 53

    1-6-12-2- History. 53

    1-6-12-3- Clinical symptoms. 54

    1-6-12-4- left ventricular aneurysm surgery. 55

    1-6-12-5- Risk factors of early death: 56

    1-6-12-6- Risk factors of late death. 57

    1-6-12-7- Survival rate 57

    1-7- Review of similar studies. 57

    Chapter Two: Materials and Methods 63

    2-1- Statement of the problem and its importance. 64

    2-2- The title of the plan. 65

    2-3- The investigated society. 65

    2-4- sample size. 65

    2-5- Study type and method. 65

    2-6- Place and time of study. 65

    2-7- Entrance criteria. 66

    2-8- Exit criteria. 66

    2-9- General purpose. 66

    2-10- Special objectives 66

    2-11- Working method 68

    2-12- Data analysis method 68

    2-13- Variables 68

    Chapter three: Findings 70

    3-1- Results. 71

    Chapter four: discussion, conclusions and suggestions. 104

    4-1- Discussion. 105

    4-2- Conclusion. 108

    4-3- Suggestions. 108

    Abstract. 109

    Resources. 110

    Source:

     

    Patrick N. Odonkor, Alina M. Grigore. Patients with Ischemic Heart Disease. Medical Clinics of North America, 2013; 97: 1033-1050

    Dan L. Longo, Dennis L. Kasper, J. Larry Jameson, Anthony S. Fauci, Stephen L. Hauser. 2012, 18th edition HARRISONS Principles of Internal Medicine. By the McGraw-Hill companies, 2012;845-8

    Dan L. Longo, Dennis L. Kasper, J. Larry Jameson, Anthony S. Fauci, Stephen L. Hauser. 2012, 18th edition2012, 18th edition HARRISONS Principles of Internal Medicine. By the Mc Graw-Hill companies, 2012;900-7

    William E. Stansfield, Mark Ranek, Avani Pendse, Jonathan C. Schisler, Shaobin Wang, Thomas Pulinilkunnil. 2014, The Pathophysiology of Cardiac Hypertrophy and Heart Failure. 51-78

    Shahbudin H. Rahimtoola, Vasken Dilsizian, Christopher M. Kramer, Thomas H. Marwick, Jean-Louis J. Vanoverschelde. Chronic Ischemic Left Ventricular Dysfunction: From Pathophysiology to Imaging and its Integration into Clinical Practice. JACC: Cardiovascular Imaging, 2008; 1: 536-555

    Florian Custodis, Stephan H. Schirmer, Magnus Baumh?kel, Gerd Heusch, Michael B?hm, Ulrich Laufs. Vascular Pathophysiology in Response to Increased Heart Rate. Journal of the American College of Cardiology, 2010; 56: 1973-1983

    Francesco Portaluppi, Bj?rn Lemmer. Chronobiology and chronotherapy of ischemic heart disease. Advanced Drug Delivery Reviews, 2007; 59 : 952-965

    Neil J. Wimmer, Benjamin M. Scirica, Peter H. Stone. The Clinical Significance of Continuous ECG (Ambulatory ECG or Holter) Monitoring of the ST-Segment to Evaluate Ischemia: A Review. Progress in Cardiovascular Diseases, 2013; 56 : 195-202

    Vivencio Barrios, Carlos Escobar, Nekane Murga, Juan Jose Quijano. Clinical profile and management of patients with chronic ischemic heart disease according to age in the population daily attended by cardiologists in Spain: The ELDERCIC study. European Journal of Internal Medicine, 2010; 21 : 180-184

    Ian Jones, Marcus Flather, Martin Johnson, Steve Barrow, D. Thompson. A description of the characteristics of patients with non-ST elevation acute coronary syndromes admitted to different settings in the 1990s. Intensive and Critical Care Nursing, 2008; 24 : 286-294

    Subroto Acharjee, Matthew T. Roe, Ezra A. Amsterdam, DaJuanicia N. Holmes, William E. Boden. Relation of Admission High-Density Lipoprotein Cholesterol Level and In-Hospital Mortality in Patients With Acute Non-ST Segment Elevation Myocardial Infarction (from the National Cardiovascular Data Registry). The American Journal of Cardiology, 2013;112: 1057-1062

    D. Fern?ndez-Bergés, V. Bertomeu-Gonzalez, P.L. S?nchez, J.M. Cruz-Fernandez, R. Arroyo, V. Barriales ?lvarez, et al. Clinical scores and patient risk stratification in non-ST elevation acute coronary syndrome. International Journal of Cardiology, 2011 ;146 : 219-224

    Cosme Garc?a-Garc?a, Isaac Subirana, Joan Sala, Jordi Bruguera, Gines Sanz, Vicente Valle, et al. Long-Term Prognosis of First Myocardial Infarction According to the Electrocardiographic Pattern (ST Elevation Myocardial Infarction, Non-ST Elevation Myocardial Infarction and Non-Classified Myocardial Infarction) and Revascularization Procedures. The American Journal of Cardiology, 2011; 108 : 1061-1067

    Stefano De Servi, Claudio Cavallini, Antonio Dellavalle, Giovanni Maria Santoro, Erminio Bonizzoni, Antonio Marzocchi .et al. Non-st-elevation acute coronary syndrome in the elderly: treatment strategies and 30-day outcome. American Heart Journal, 2004; 147 : 830-836

    Nancy M. Allen LaPointe, Anita Y. Chen, Matthew T. Roe, David J. Cohen, Deborah B. Diercks, James W. Hoekstra, et al. Relation of Patient Age and Mortality to Reported Contraindications to Early Beta-Blocker Use for Non-ST-Elevation Acute Coronary Syndrome. The American Journal of Cardiology, 2009; 104 : 1324-1329

    Marc P. Bonaca, Philippe Gabriel Steg, Laurent J. Feldman, John F. Canales, James J. Ferguson, Lars Wallentin, et al. Antithrombotics in Acute Coronary Syndromes. Journal of the American College of Cardiology, 2009; 54 : 969-984

    Ramez Nairooz, Partha Sardar, Hossam Amin, Rajesh V. Swaminathan, Luke K. Kim, Saurav Chatterjee, et al.

Examination of electrocardiographic findings in patients with left ventricular aneurysm caused by myocardial infarction