How to Lower Your Risk of Death from Heart Attack?

Heart attack, also called acute myocardial infarction (AMI), can be caused by several factors, but ultimately it occurs when the coronary arteries become blocked. Heart attack starts with clogged arteries as the result of coronary artery disease, triggered by the formation of blood clot (thrombus).

If the coronary arteries, which take oxygen-rich blood and nutrition to your heart, become blocked, the cardiac muscle tissue will be damaged due to shortage of oxygen supply and the metabolic waste cannot be excreted. Additionally, biochemical changes, affected by several factors such as the severity of ischemia (an inadequate blood supply to the cardiac muscles), age, and sex, will follow the process. These biochemical changes include:

- Changes during the first second. Shortage of blood flow to the cardiac muscles (ischemia) that occurs quickly will result in biochemical changes within the body.

- Changes during the first minute. Impeded blood flow will disrupt the disposal of metabolic excretes and lead to a build-up. The changes occur during the first minute may go back to normal (reversible), for example cleaning the clogging and blood flow reperfusion may restore the cell function into normal. However, prolonged clogging will result in permanent damage (irreversible).

- Changes due to permanent damage (irreversible). The damage is marked by the release of substance such as enzyme and protein. The substances will enter blood flow and the level is measurable.

Patients with coronary artery disease may experience symptoms called angina pectoris. Also, there will not be any suspicious symptoms, categorized as silent myocardial ischemia. The common symptom is chest pain. Chest pain occurring when patients are resting is classified as unstable angina, an acute syndrome closely related to torn plaque, platelet aggregation, and formation of blood clot (thrombus). Unstable angina caused by totally clogged coronary arteries becomes myocardial infarction (MI).

Early detection using cardiac biomarker

Correct detection and medication for patients with unstable angina will reduce the risk of heart attack and lower the mortality rate. For diagnosing and determining the risk level to detect the disease development, there must be adequate biomarkers. At present, aside from establishing diagnosis for unstable angina and MI and assessing the risk, biomarkers have also been used for infarct sizing (determine the infarct size), post-thrombolytic therapy reperfusion monitoring, torn plaque detection, blood vessels inflammation, cardiac muscles ischemia, up to the emergence of acute condition in unstable angina or MI.

Cardiac biomarker can be used to determine the size and severity of myocardial infarction. Determining the size is useful for the future management of patients with myocardial infarction. High sensitivity biomarker development is useful to determine mild damage within the cardiac muscle in unstable angina, for instance, because differentiating unstable angina from MI is important for patient treatment.

- Myoglobin

Myoglobin is an oxygen-binding heme protein, having structure which resembles hemoglobin, located primarily in cardiac and skeletal muscles (skeleton). Damaged cells occur during AMI will release myoglobin to blood flow. On patients with AMI, the myoglobin level may increase up to 10 times above normal. Myoglobin level will rise 2 hours after the onset of chest pain and reach the peak within 6-9 hours, but then return to normal 24-36 hours after experiencing infarction. Whereas CK-MB level will be abnormal 6 hours after the attack and reach the peak 12-24 hours and will return to normal after 48 hours. Myoglobin is the initial marker for AMI diagnosis.

- Creatine Kinase-MB Mass (CK-MB Mass)

AMI cannot be detected simply through echocardiography (ECG) in about 20% of the patients. Therefore, a biochemical parameter test is needed to help establishing diagnosis, such as CK-MB test. The CK-MB mass test provides better result compared to the former CK-MB enzyme activity test, it improves sensitivity for MI diagnosis so it can be established within 8-48 hours. Additionally, CK-MB mass is useful to determine the success or failure of thrombolytic therapy, thus different treatment can be conducted immediately.

About 5-20% of patients with unstable angina usually develop MI or experience sudden death within a year. Further research shows that the fatal impacts usually involve microinfarct. The CK-MB mass test is able to detect ischemia extension on patients with unstable angina. Research on CK-MB mass used in determining the risk of MI reports that the CK-MB mass can detect a group of patients with heart ischemia and development of serious diseases which cannot be detected by routine diagnostic procedure.

- Cardiac Troponin T

Cardiac Troponin T (cTnI) is the most sensitive and specific cardiac marker for AMI diagnosis. cTnI is released into the blood 4-8 hours after the onset of chest pain. It will reach the peak 14-36 hours after AMI and continues to rise up for 3-7 days. Due to this prolonged increase, cTnI is able to detect patients with AMI that emerges slowly. Some researches reveal that cTnI is a good biomarker to achieve reperfusion after the thrombolytic therapy.

A better and comprehensive understanding on pathophysiology and treatment of acute coronary syndrome (ACS), encourages the scientists and diagnostic companies to improve or search for new cardiac markers. A more complete clinical testing involving a thrombolytic therapy indicates the need of early diagnosis of AMI and the risk level of unstable angina. The thrombolytic therapy is useful to treat patients with AMI, while a late therapy will result in fatal impacts. An adequate combination of cardiac markers enables early detection of AMI symptoms and also reduces the death rate caused by heart attack.