Myocardial Ischemia and Its Causes

Partial blockage of coronary arteries resulting in reduced oxygen to heart muscle.

Coronary atherosclerosis, vasospasms, reduced oxygen supply, and increased myocardial demand are all causes of insufficient blood flow to the heart.

Buildup of plaque in the coronary arteries, narrowing the vessel and reducing blood flow.

Sudden contractions of the coronary arteries, reducing blood flow.

Intermittent chest pain relieved by rest or medication, following a predictable pattern.

Chest pain that intensifies, increases in frequency or duration, and is not relieved by rest or medication.

Severe reduction in coronary blood flow leading to complete blockage and heart cell death (infarction).

Coronary atherosclerosis, emboli, vasospasm, trauma, and factors increasing metabolic demand, or decreasing blood oxygen are causes.

Various schemes classify MI types for treatment considerations.

Categorizes Myocardial Infarctions (MIs) based on the extent of damage. Transmural involves whole heart wall; non-transmural affects inner or partial sections.

A type of MI where the electrocardiogram (ECG) shows ST-segment elevation, indicating complete blockage and tissue death

A type of MI where the ECG does not show ST-segment elevation; partial or intermittent blockage.

A standardized classification of MI, dividing it into subtypes based on cause and clinical presentation to improve diagnostic accuracy of MI.

MI related to acute blockage of arteries by blood clots (atherothrombosis).

MI due to reduced blood flow to the heart (supply-demand mismatch), not from acute blockage.

MI leading to sudden cardiac death, often with symptoms and specific EKG changes before troponin test results.

MI occurring during a procedure to open blocked coronary arteries.

MI caused by a blood clot after a stent.

MI due to narrowed arteries (restenosis) after procedures.

MI related to coronary artery bypass graft (CABG) surgery.

Damage to heart cells due to lack of oxygen; occurs within 10 seconds of a blocked artery.

Blocking of the artery supplying the heart, which leads to myocardial injury and cell death

The body's response to tissue damage or infection, characterized by redness, swelling, heat, and pain. Neutrophils release inflammatory mediators and reactive oxygen species (ROS), causing myocardial cell damage during this process.

Damage to heart muscle cells, resulting from inflammation (release of inflammatory mediators & ROS) or reperfusion injury (reintroduction of oxygen to previously hypoxic tissue).

Further cardiac damage that occurs when blood flow is restored to hypoxic (oxygen-starved) tissue, leading to oxidative stress.

Highly reactive molecules containing oxygen and capable of damaging cells.

Proteins found only in heart muscle cells. Their presence in the blood indicates myocardial injury.

Acute Myocardial Infarction - Heart attack

Substances in the blood that indicate heart damage. Troponin I and T are common examples.

A type of cell death that occurs at the site of an infarction (heart tissue death).

Formation of scar tissue at the site of infarct (heart attack) due to inflammation.

High levels of troponin in the blood, without ECG changes, indicate increased risk of future heart problems.

Enzyme found mostly in heart muscle cells. Released after heart injury.

Ratio of CK-MB to total CK. A ratio greater than 5 suggests heart as the source of the enzyme.

Protein released after heart muscle damage, very sensitive but not specific for heart attack.

Liver-produced protein, elevated levels linked to inflammation and increased heart disease risk.

Enzyme found in all cells, including heart cells, elevated LDH-1 suggests heart damage.

A ratio used to determine if the elevation in LDH is due to heart damage.

High blood sugar levels, linked to heart disease risk.

Increased white blood cell count, often linked with inflammation.

High potassium levels in the blood, linked to heart function abnormalities.

Partial blockage of coronary arteries, reducing oxygen supply to the heart muscle.

Plaque buildup in coronary arteries, narrowing the vessel and reducing blood flow.

Sudden contraction of coronary arteries, restricting blood flow.

Low blood oxygen levels, often due to lung disease.

Heart's oxygen needs exceed its supply, often due to tachycardia or increased workload.

A condition where atherosclerosis narrows coronary arteries, reducing blood flow.

When the heart's need for oxygen exceeds the oxygen available to it.

Lack of oxygen to the heart muscle cells.

Reduced ability of the heart's lower chambers to pump blood.

Problems with the electrical signals that control heart contractions.

Intermittent chest pain that follows a predictable pattern, relieved by rest.

Severe chest pain lasting longer than typical angina and not relieved by rest.

Heart attack; Complete blockage of blood supply to the heart muscle, causing cell death.

Heart attack where the entire heart wall is damaged.

Heart attack where damage is limited to parts of the heart wall.

A heart attack without ST-segment elevation on an ECG.

A heart attack with ST-segment elevation on an ECG, indicating a complete blockage.

A system to classify heart attacks based on cause and clinical presentation.

Heart attack caused by a blood clot in an artery.

Heart attack due to reduced blood flow, not from a blood clot.

Heart attack leading to sudden cardiac death.

Heart attack during a procedure to open blocked arteries.

Heart attack due to a blood clot after a stent.

Heart attack due to restenosis (narrowing) after procedures.

Heart attack related to bypass surgery.

Plaque buildup in the coronary arteries, reducing blood flow.

A condition where atherosclerosis narrows coronary arteries, reducing blood flow.

High levels of troponin in the blood, indicating heart damage.

Additional heart damage that arises when blood flow is restored to previously oxygen-deprived tissue.

Harmful effect of excessive reactive oxygen species (ROS) formation.

Excessive calcium influx into cells, leading to cellular dysfunction and injury.

Body's response to reperfusion, resulting in further tissue damage.

Proteins found only in heart muscle cells; elevated levels indicate heart damage.

Substances in the blood that indicate damage to the heart.

Enzyme found primarily in heart muscle; elevated levels indicate heart damage.

An enzyme primarily found in heart muscle. Elevated levels indicate potential heart injury.

A ratio greater than 5 suggests a myocardial infarction (heart attack) is likely.

CK-MB levels start rising 4-6 hours after a heart attack, peak after 24 hours, and return to normal within 2-3 days.

A protein found in muscles that is released after muscle damage, including heart muscle.

Myoglobin levels increase very quickly after a heart attack. It's one of the first markers to rise.

A protein the liver releases in response to inflammation. Elevated levels associate with heart attack severity.

A type of LDH enzyme primarily found in cardiac muscle cells. Elevated levels can indicate heart damage.

This ratio helps determine if elevated LDH levels are due to heart damage.

Acute Myocardial Infarction (heart attack).

Damage to heart muscle cells due to lack of oxygen, occurring within 10 seconds of blocked blood flow.

The process cells use without oxygen to produce energy.

Cellular energy production through metabolic processes, crucial for cell function.

A byproduct of anaerobic metabolism, contributing to cellular acidity.

Impaired function of the important cell pump, leading to cellular fluid imbalance.

Impaired calcium removal from cells, leading to dangerous calcium buildup in cells.

Damage to the energy-producing part of the cell.

Harmful enzymes released from lysosomes (cell trash disposal system), leading to self-destruction.

Irreversible damage to heart muscle cells beyond 20 minutes without oxygen.

The limited ability of cardiac muscle tissue to replace damaged cells.

Body's response to damage, involving neutrophils and inflammatory mediators, potentially damaging heart further.

Substances released during inflammation that can harm myocardial cells.

Harmful molecules produced during inflammation, damaging myocardial cells.

Immune cells that release inflammatory mediators and ROS during inflammation.

Damage to heart muscle cells, from inflammation or reperfusion.