The Effects Of Coronary Artery Occlusion And Reperfusion On Myocardium

The most common physiological process leading to a myocardial infarction is the occlusion of coronary arteries by a process known as atherosclerosis. In fact, atherosclerosis is present in more than 90% of persons with coronary heart disease.1

Cardiogenic shock, according to Werden et al. (2012), is the most common cause of death from an acute myocardial infarction (AMI) and has a chance of mortality from thirty percent to eighty percent. Infarction-related cardiogenic shock (ICS) complicates approximately five to ten percent of acute myocardial infarctions (AMI) and remains the leading cause of death in patients hospitalized from an AMI (Kolte et al., 2014). Kolte et al. (2014) also states that the incidence of cardiogenic shock is higher in patients over the age of seventy-five, and has higher prevalence in women, Caucasians, Asians, and Pacific islanders. This paper will discuss the pathophysiology, clinical manifestations, tools used to diagnose, and therapeutic management of cardiogenic shock.

One of the complications of an acute MI is Left Ventricular Aneurysm (LVA) which is a localized area of myocardium with abnormal outward bulging and deformation during systole and diastole. The epidemiology occurs in 10-30% of patients after an acute MI (American Heart Association 2015). The risk factors include total occlusion of the LAD artery, females and an anterior MI. To prevent this, early revascularization is needed. The LVAs usually range from 1-8 cm.

Clearly differentiate the pathophysiology of angina and myocardial infarction, including signs and symptoms. (5 marks)

Early recognition of signs and symptoms and taking the right steps to identify, distinguish, and manage subtypes (STEMI and NSTEMI/UA) will improve Mr James outcomes (Bradley E.H., 2006)Recognizing the signs and symptoms such as chest pain or shortness of breath suggestive of an MI and obtaining an ECG as soon as possible (goal of less than 10 minutes following presentation of a patient) should be the standard of practice to manage this patient It has been demonstrated that reperfusion of the infarct-related artery in the very first hour (golden hour) of MI reduces mortality rates (Ayrik et al. 2006, Van de Werf et al. 2008). fact, every 30 minutes of delay time, the 1-year mortality risk increases by (DeLuca et al. 2004).According to triage and first assessment guidelines (Wrightet. al. 2011) Patients who complain of chest pain , pressure , tightness or heaviness require immediate assessment by the triage nurse and should be referred for further evaluation.

In the evaluation of patients with chest pain, the preliminary ECG is a more clear-cut tool for early risk stratification with more recent recommendations indicating that ECG should be performed as early as possible, within 10 minutes of ED admittance. Early indicators associated with MI or ischemic complication such as ST segment elevation or depression allows rapid treatment aligning with the indicated complication. While the ECG may reveal significant indicators in certain situations, in other circumstances findings may be limited due to low diagnostic sensitivity

49). In this light, the MSCs produce numerous bioactive molecules which facilitate tissue repair in different pathways. For instance, elevated secretion of cytokines after hUCMSC injections can increase the repairing ability of injured myocardium. Therefore, boosting the secretion and expression of tissues for repair purposes like cytokines is likely the underlying mechanism for the therapeutic properties of intramuscular injection of hUCMSCs. It is also noteworthy that exploiting the paracrine properties of MSCs averts the risks involved in intramyocardial and intracoronary

The relationship between coronary supply and myocardial demand is a very sensitive and an imbalance between them can cause a major concern in the body. If the coronary supply is less than the myocardial demand, the heart can suffer a severe spasm. The spasm cuts off the blood flow through the artery causing the heart to fail (Ischemic Heart Disease, n.d.). In contrast, if the myocardial demand exceeds the coronary supply, the heart fails once again. This is due to impaired cardiac pumping the heart experiences, an oxygen deficit of over 20 minutes causes the heart to essentially fail (Myocardial infarction) and a deficit of oxygen under 20 minutes leads to

It is important that the nurse conduct a thorough assessments when a patient presents with suspected MI. Assessments include focused physical examination to detect complications and any changes from the patient’s baseline, patient history that includes the presenting symptoms, any medical history, and the family history of heart disease. Mr. X is a 51 years old black man presented to the emergency department with severe substernal chest pain radiating to the back and neck and down the left arm. Mr. X’s risk factors for MI includes family history of CAD (mother dying of a stroke at 62 and father dying of heart attack at 58), increasing age, male gender, and race (African American native). These risk factors are non-modifiable or circumstances

ECG : ventricular rate 54 beats/min, HR varying from 39 to 60 during a 45 minute period of monitoring, infrequent PVCs, ST elevation in leads II, III and avF indicating inferior injury or ischemia secondary to acute MI.

The goal of medical management is to minimized myocardial damage, preserve myocardial function, and prevent complications. These goals are achieved by reperfusing the area by emergency use of Percutaneous Transluminal Coronary Angioplasty (PTCA) or thrombolytic medication. Minimizing myocardial damage is also accomplished by reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration, and bed rest.

Meis1 is a key regulatory protein for cardiac differentiation during embryonic development and using siRNA against Mesi1 can increase the proliferation of cardiomyocytes about threefold [145]. Additionally, siRNA administration against PLB, a key regulator of cardiac Ca2+ homeostasis, can improve cardiac function in heart failure. It was suggested from this study that down-regulation of PLB can enhance the activity of sarcoplasmic reticulum Ca2+ pump (SERCA2a) and therefore can improve the cardiac function [149-151]. Another strategy for heart regeneration is targeting the inflammatory reactions in infarcted area of myocardium. Reactive oxygen species (ROS) are the key factors in inflammatory reactions and provoking heart regeneration (i.e. cardiomyocytes apoptosis, fibroblast proliferation and myocyte hypertrophy). NADPH (Nicotinamide adenine dinucleotide phosphate) oxidase is a major source for superoxide production in infarcted myocardium that contains a catalytic subunit, Nox2

One of the major components of the SYNTAX score that enhances its predictive value on the eventual achievement of microvascular perfusion is the patency (or otherwise) of the infarct related artery (IRA). An occluded IRA has been shown to be associated with a worse post-procedural myocardial perfusion (TIMI myocardial perfusion grade of 3” 54.9% versus 18.7%”, p <0.0001). Patency of the IRA often signifies earlier spontaneous reperfusion, which reduces the actual ischemic time. As a result, infarction size is limited, and improvement in the left ventricular ejection fraction is greater in such patients, which is reflected in improved 1-year

Transplantation is a well established and often the final therapeutic option for the patients with end-stage heart and lung failure. The various advances in immunosuppression and human leucocyte antigen matching techniques have significantly reduced the incidence of acute allograft rejection, whereas the chronic allograft rejection is still difficult to treat and causes the absolute majority of terminal graft failure. Lymphatic endothelium is important in the pathogenesis of various cardiac and pulmonary diseases. However, the exact knowledge about the functions and role of lymphatic endothelium in heart and lung failure as well as after transplantation is still lacking. Therefore, the study focused on the investigation of the changes of lymphatic endothelial phenotype in patients with terminal heart failure and after heart and lung transplantation. Further, the mechanisms of lymphatic endothelial activation in the ischemia-reperfusion injury were evaluated in

When someone is possibly having a heart attack they should seek medical help immediately. They should call 9-1-1 and wait for paramedics to arrive. The patient should take their nitroglycerin and chew an aspirin if it is prescribed by a physician or a paramedic. Aspirin in the event of a heart attack will help the clot from forming more (Heart attack, 2011). If a patient is unconscious and it is suspected they are experiencing a heart attack bystanders should begin CPR until help arrives (Symptoms, 2013).