Myocardial Infarction

Laboratory Evaluation - Cardiac Biomarkers Troponin I & T

Cardiac troponin I and T are proteins unique to myocardial muscle cells, and are only released into circulation after myocardial cell injury. (Troponin is found in any muscle tissues. these levels are usually very low so when elevated, its very sensitive) Elevated (positive) troponin levels (cardiac TnI and TnT via immunoassay) are considered diagnostic of an acute MI (best sensitivity and specificity of the cardiac biomarkers) Levels rise within 3-12 hours after onset of chest pain, peak within 24 to 48 hours, and remain elevated for 1-3 weeks. Note: Elevated troponin levels in the absence of ECG changes (e.g., without ST elevation) is a risk factor for dying from a future cardiac event ***Troponin might pick up something that is happening that is not picking up on ECG

Repair and resolution

Coagulative necrosis develops at site of infarct. Inflammation leads to scar tissue deposition at the site of infarct

Causes of MI

Coronary Atherosclerosis (CAD) {high ldl, low hdl, diabetes, overweight, no exercise, smoking, dyslipidemia}

Less Common cause of MI

Coronary artery emboli, (i.e. atrial fib causing clots, DIC, sepsis), aortic dissection with retrograde involvement of the coronary arteries, coronary vasospasm (Usually reversible), coronary artery trauma, cocaine and other illicit drug use (Causes vasospasm), Prescription and over the counter medications (Antibiotics, beta blockers),

Other Labs FOR MI

Glucose- increased due to stress response CBC- want to check for anemia Chemistry profile-check for creatine-watch for perfusion of kidney Lipid profile

Precipitating conditions include factors that reduce the oxygen content of the blood:

Hypoxemia (altitude, pulmonary disease), Anemia

Reperfusion injury

If the hypoxic myocardial tissue is reperfused (thrombolytic therapy or percutaneous coronary intervention), further cardiac injury occurs due to oxidative stress. Introducing oxygen to tissue that has been hypoxic causes the formation of reactive oxygen species (i.e., free radicals) Note: Microvascular (capillary) obstruction due to microthrombi, small plaque fragments, lipids, and or endothelial injury can reduce effectiveness of reperfusion. (Hypoxic cells produce xanthine oxidase ---- catalyzes reaction of O2 into oxygen free radicals, Free radicals could go into a tissue that might have survived and kill it. Some patients with MI's sometimes die a few hours later...possibility from reperfusion injury)

Why do patients with left ventricular failure (LVF) experience dyspnea and hypoxemia?

Increased hydrostatic pressures in the pulmonary capillaries leads to pulmonary edema.

Which of the following hemodynamic changes occur in left ventricular failure (LVF) that is systolic in nature?

Increased left ventricular preload

Inflammation (Inflammation makes things worse when there is not an infection)

Neutrophils release a myriad of inflammatory mediators, some of which can cause myocardial cell injury (e.g., NO, IL-1, TNF, etc) Neutrophils also release reactive oxygen species (ROS) and lysosomal enzymes during phagocytosis, which also contributes to myocardial cell injury

How does activation of the sympathetic nervous system help the body maintain blood pressure in left ventricular failure?

Norepinephrine stimulates alpha-1 receptors which results in arterial vasoconstriction.

C-Reactive Protein (CRP) (Wouldn't use this to diagnose a MI)

Plasma protein (acute phase reactant) that is released by the liver during inflammation Elevations greater than 1 mg/L are associated with increased risk of cardiovascular disease. Any level > 3 mg/L is associated with a high risk for heart disease Elevated CRP is a reliable predictor of degree of heart failure and mortality following an AMI, but lacks specificity because it is a general marker for inflammation. (used to predict cardiovascular risk and risk of death from cardiovascular disease )

the following condition does not precipitate a myocardial infarction by increasing myocardial demand,

ANEMIA

Myoglobin

An intracellular protein similar to hemoglobin that is released after myocardial cell injury (Released when muscle cells are injured or die) Rises in myoglobin are very sensitive, but not very specific to acute MI (this test is not very specific because other cells contain myoglobin)

Why is an elevation in the plasma levels of B-type natiuretic peptide (BNP) an indication that a patient may have heart failure?

BNP is released when the kidneys retain fluid to compensate for the drop in CO and blood pressure.

Clinical Consequences of MI: Functional impairment depends on location and severity of infarct

Decreased ventricular (and atrial) contractility Conduction disturbances (i.e. Causing damage to SA/AV/etc fibers can end up with arrhythmias) Ischemic pain (hypoxic enhances our pain mainly from lactic acid)

Which of the following laboratory indicators can be used to predict the risk of death from cardiovascular disease in the weeks and months following an acute MI?

Elevated CRP

CK-MB

Enzyme found primarily in myocardial muscle cells that is released after cell injury Sensitivity of test is improved by using the CK-MB/total CK index (ratio > 5 indicates cardiac source of CK-MB) Rises 3-12 hours after the MI, peaking in 24 hours, and disappearing in 2-3 days.

Precipitating conditions include factors that increase metabolic demand (These arteries can't dilate because of the plaque)

Extreme physical demand, HTN (Increase in LV afterload), Aortic stenosis (Can also occur on the valve)

Lactate dehydrogenase (LDH)

LDH is an intracellular enzyme (present in the cytoplasm of all cells) that catalyzes the process of converting pyruvate to lactate. It is also found in the plasma. LDH-1 is an isoenzyme of LDH that is primarily found in cardiac muscle cells. LDH-2 is the isoenzyme primarily found in the plasma. An elevation of LDH-1 (or an increase in the ratio of LDH-1 to LDH-2) is indicative of myocardial cell injury. Sensitivity is high, but specificity is not as good as troponin I. Rises at 10-12 hours, peaks at 48-72 hours, returns to normal within 10-12 days.

The accumulation of which molecule causes ischemic pain in a myocardial infarction?

Lactic Acid

Define Myocardial Infarction

Severe reduction of coronary artery blood flow leading to myocardial cell death

An 74 year-old-male who presents to the ED with chest pain, nausea and syncope is diagnosed as having an acute myocardial infarction. In the cardiac catheterization lab, two stents are placed in branches of the left coronary artery. On follow up, there is evidence of necrotic cardiac muscle tissue. It is suspected that the cardiac reperfusion contributed to this injury. What is the primary cause of reperfusion injury?

The formation of xanthium oxidase in hypoxic tissue causes the formation of free radicals when oxygen is reintroduced.

How does activation of the renin-angiotensin-aldosterone system help the body maintain blood pressure in left ventricular failure?

The hormones released increase systemic vascular resistance and blood volume.

Which of the following is a common factor contributing to the development of myocardial infarction?

Thrombus formation within the arherosclerotic coronary artery

Patho of MI: Infarction of an atherosclerotic coronary artery generally occurs due to the following circumstances:

Thrombus forms on the rough surface of the plaque, Wall of an atherosclerotic coronary artery ruptures, Long-term obstruction of coronary artery by plaque, Plaque embolus obstructs coronary artery

Hypoxic injury

Within 10 seconds of infarction see hypoxic injury to myocardial cells. Consequences of anaerobic metabolism include decreased ATP production & lactic acid formation. (lysosomes leads to cells auto digest) REVIEW HYPOXIC INJURY MODULE Anaerobic metabolism is insufficient - after 20 minutes of complete occlusion, irreversible injury and cell death begins in the affected areas. (Unlike many other tissues cardiac muscles cannot regenerate