Proteins During Acute Myocardial Infarction

The Cardio Kinesiograph System (CKinG) is a novel comput-erized diagnosis system incorporating a computer model of cardiac kinesis. Cardiac Kinesis (CK) is the interpretation of heart movement or electrical activity of specialized cardiac muscle cells in response to biochemical reactions. The mechanical events occurring during the cardiac cycle consist of changes in pressure in the ventricular chamber which cause(s) blood to move in and out of the ventricle. [1] The events of the cardiac cycle start with an electrical signal and proceed through excitation-contraction coupling (which involves chemical and mechanical events) to contraction of the ventricle (pressure generation) and ejection of blood (flow) into the pulmonary and systemic circulations.

Troponin is present in heart muscle cells. If damage is done to these cells, it releases troponin into the bloodstream. The blood level of troponin, during a heart attack, increases within 3-12 hours from the onset of chest pain. It peaks between 24-48 hours and returns to a normal level over 5-14 days (Koutoukidis, Stainton & Hughson 2013, p. 506). The indicators include acute myocardial infarction, severe pulmonary embolism causing acute right heart overload, heart failure, and myocarditis. The normal value of Troponin I is <20

The result signs on 1) extent, severity and duration of episode; 2) the amount of collateral circulation; and 3) the metabolic needs of the myocardium at the time of event. Myocardial infarction almost always occurs in the left ventricle and often significantly depresses left ventricular function. The larger the infracted area, the greater the loss of contractility. Functionally, MI causes the following: 1) reduced contractility with abnormal wall motion; 2) altered left ventricular compliance; 3) reduced stroke volume; 4) reduced ejection fraction; and 5) elevated left ventricular end-diastolic pressure.

Heart failure diagnoses are carried out by a specialized medical practitioner. It comprises of holistic patient health review such as patient medical history, patients symptoms, lungs con-gestion assessment, carrying out physical activity under observation, assessing for fluid re-tention (edema) and also assessing risk factors such as Coronary artery diseases, high blood pressure, Diabetes. According to tansy (2010 1399), heart failure can be diagnosed using different test methods such as Blood tests. This helps to check for any possible diseases in the thyroid, kidney or liver that can cause heart problems (NT-proBNP). N--terminal pro-B-type natriuretic peptide is a chemical checked in the blood. When the heart is under stress BNP is secreted

Cardiac Troponins are specific to the cardiac myocyte and have central role in diagnosing ACS. They are found to be specific and sensitive, in addition they also provide prognostic information which adds to their utility in managing and diagnosing of CAD. Constant change in levels of Cardiac Troponins is required to define ACS. CKD patients with advanced disease have misfortune of having both a dramatically high rate of cardiac mortality paired with decreased ability to detect, it due to elevated Cardiac Troponin levels.[6]. mortality in dialysis patients from cardiovascular disease is substantially higher than the general population as depicted in Figure1.

The term myocarditis has been around since the beginning of the twentieth century (Dennert et al., 2008). It was during this time that the discovery of coronary artery disease was gaining recognition, the term itself however fell out of circulation (Dennert et al., 2008). In 1987 a new classification to diagnose myocarditis was introduced, it was the Dallas classification (Dennert et al., 2008). It was meant to create a standard for diagnosing but unfortunately it was not a perfect method, there were some key faults (Dennert et al., 2008). The Dallas classification did not account for sampling error, and most notably it allowed for variation in pathological interpretation (Dennert et al., 2008). Presently it is not used as a stand alone method,

Additionally, Yanir et al. (2002) reported that binding of CO to myocardial myoglobin and mitochondrial cytochrome chain enzymes might explain cardiac failure. The good response to inotropic agents and the findings of repeated echocardiographic studies support the probable diagnosis of myocardial stunning. The stunned myocytes, although unable to contribute to efficient ventricular contractility, still preserve metabolic viability suggesting that myocardial dysfunction can occur without ECG changes or elevation of enzyme levels typical of ischemia. These findings were supported with those of Aslan et al. (2005), they stated that it is not necessary to routinely measure CK, CK-MB and troponin, and perform myocardial perfusion SPECT in acute CO poisoning cases without any ECG abnormality, ischemic cardiac symptoms. In addition, Teksam et al. (2010) revealed that myocardial damage may exist with normal ECG and elevated cardiac

It binds to tropomyosin, interlocking them to form a troponin-tropomyosin complex, helping it to position on actin, while the rest of the complex modulates muscular contraction [13]. Four human cardiac TnT (cTnT) isoforms were determined. In the fetal heart, TnT1 is the mainly expressed one, TnT4 in the failing adult heart, while TnT3 is the dominant form in the adult heart [14]. The cTnT is rapidly released from injured cardiac muscles and the presence of measurable amounts of circulating cTnT can indicate cardiac damage. Therefore, serologically, cTnT is a proven diagnostic and risk biomarker in acute coronary syndromes [15]. On the other hand, histologically, cTnT is sensitive at detecting acute myocardial infarction as the infracted fibers show a low staining affinity to it [15,

1. Acute phase proteins: the liver produces these proteins as a way to signal local and systemic responses. Some of these proteins play a role in inflammation response such as fibrinogen for blood clotting and kinin for vasodilation. There are two types of acute phase proteins: positive and negative.

As stated in the European Heart Journal1,” Myocardial Infarction is defined in pathology as myocardial cell death due to prolonged ischemia”. In the pre-hospital setting, the main goal of paramedic’s is to counter act the ischemia and prevent further cell death. One of the paramedic’s drugs of choice will

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.

In acute myocardial infarction animal models, myocardial reperfusion injury accounts for more than half of the final myocardial infarction injury. Therefore, prevention of myocardial ischemia-reperfusion injury is one of the major measures for the prevention of cardiac and vascular adverse events in patients with cardiac surgery and vascular surgery. Currently, many studies focus on the prevention of ischemic-reperfusion injury, including preconditioning and postconditioning (1,2). The postconditioning measures include ischemia postconditioning, volatile anesthetic postconditioning, sufentanil postconditioning, and propofol postconditioning (3-6). In 2003, Zhao et al proposed the concept of ischemic-postconditioning to provide many rounds of

Percutaneous transluminal coronary angiography (PTCA) and thrombolysis are widely used in the treatment of acute MI in human but may have the side effects of cardiac dysfunction resulting from ischemic-reperfusion injury or “myocardial

I have enjoyed reading your post, Kerry. I agree with your analysis concerning atypical presentation of myocardial infarction. Myocardial infarction requires prompt treatment before permanent damage occurs (Mayo Clinic, 2015). It can present with insidious symptoms which may lead health care provider to mistake it for a different condition which may delay treatment (Rehman & Qazi, 2013). As you have stated, myocardial infarction may present with atypical symptoms like vomiting, shortness of breath, epigastric discomfort, falls, delirium, and general malaise. The elderly patient may not experience classic symptoms of myocardial infarction, such as chest pain (Southern Care University, 2013). Myocardial infarction in the elderly can be silent.

Myocardial Infarction or "heart attack" is the formation of ischemia that leads to necrosis or "dying" of heart tissues. This condition resulted in the deprivation of oxygen in the heart muscle that could cause the heart attack or MI. Myocardial Infarction or MI is seen in 1.5 million people each year and is also classify as the leading cause of mortality worldwide (Fuller, 2015).