Alterations of CV Function II

Partial blockage of coronary arteries, leading to reduced blood flow to the heart muscle.

Buildup of plaque in coronary arteries, narrowing the vessels.

A condition caused by atherosclerosis, narrowing the coronary arteries.

Contraction of coronary arteries, reducing blood flow.

Low level of oxygen in the blood.

Low red blood cell count.

Higher workload on heart muscle, requiring more oxygen.

Heart attack; complete blockage of a coronary artery leading to death of heart tissue.

Insufficient oxygen supply to the heart muscle, hindering ATP production for normal function.

Intermittent chest pain, predictable in pattern and duration, relieved by rest or medication.

Severe chest pain lasting 15–20 minutes, not relieved by rest or medication, a warning sign for heart attack.

Heart attack affecting the entire heart wall.

Heart attack limited to the inner layer of the heart wall.

When heart muscle lacks oxygen, it switches to anaerobic metabolism, producing less energy (ATP) and lactic acid. This is inefficient and leads to cell damage.

Hypoxia disrupts the Na+-K+ pump, causing sodium to build up inside the heart cells. This leads to cell swelling.

Hypoxia also impacts the Ca2+ pump, leading to calcium buildup inside heart cells. This damages mitochondria and can trigger cell death.

Hypoxia causes lysosomes to release enzymes, leading to autodigestion (self-destruction) of heart cells.

Neutrophils, the immune system's first responders, can actually damage heart cells during inflammation. They release chemicals and enzymes that can contribute to injury.

Myocardial infarction (MI) without ST-segment elevation on the electrocardiogram (ECG).

Elevated troponin with at least one value > 99%ile.

MI related to acute athero-thrombosis of the artery feeding the infarcted myocardium.

MI due to supply-demand mismatch not related to acute athero-thrombosis.

Coronary atherosclerosis, emboli, aortic dissection, vasospasm, trauma, drug use, and medications.

Factors that increase metabolic demand (physical activity, hypertension, aortic stenosis) or reduce blood oxygen (hypoxemia, anemia).

Thrombus formation, plaque rupture, chronic obstruction, or embolus blocking the coronary artery.

Damage that occurs when blood flow is restored to ischemic tissue, paradoxically causing further injury.

Formation of reactive oxygen species (ROS) like OH-, O2-, ONOO-, and H2O2 during reperfusion, damaging cell membranes and proteins.

Increased calcium influx during reperfusion, leading to mitochondrial damage, reduced ATP production, and further damage.

Neutrophils adhere to the reperfused tissue, releasing cytokines and proteases, contributing to damage.

Functional impairment based on infarct size, decreased ventricular contractility, ischemic pain, and conduction disturbances.

Troponin I is specific to cardiac muscle, while Troponin T is found in both cardiac and skeletal muscle. Elevated levels of both indicate myocardial damage.

CK-MB, a specific enzyme found primarily in cardiac muscle, is elevated after myocardial injury and reflects the extent of damage.

Troponin levels rise 2-3 hours after injury, peaking at 12-48 hours and remaining elevated for 4-10 days.

A ratio used to diagnose AMI. A ratio above 5 indicates a high probability of AMI.

CK-MB levels rise 4-6 hours after AMI, peaking at 24 hours and returning to normal after 2-3 days.

Myoglobin, a protein found in muscle cells, is released when muscle cells are injured. Myoglobin levels rise rapidly after an AMI, but it is not specific for heart damage.

CRP is an inflammatory protein that rises after an ischemic event, indicating damage to the heart. Higher levels are associated with increased risk of heart attack and mortality.

LDH-1, an enzyme primarily found in heart muscle cells, increases when heart cells are injured. Higher LDH-1 levels indicate possible myocardial cell injury.

LDH, while sensitive for AMI, has a low specificity, leading to a high false positive rate.

Isoenzymes are different forms of an enzyme that catalyze the same reaction. LDH-1 is found mainly in heart muscle, while LDH-2 is in plasma.

CRP levels are associated with risk of cardiovascular disease: <1.0 mg/L is low risk, 1.0-2.9 mg/L is intermediate risk, and >3.0mg/L is high risk.