Myocardial Ischemia Past Paper PDF

Myocardial Ischemia *Partial blockage of one or more branches of the left or right coronary artery* [Causes] **Coronary atherosclerosis (coronary artery disease)** Repetitious endothelial injury with the resulting inflammatory response in the blood vessel wall results in a buildup of fibrous cap...

Myocardial Ischemia *Partial blockage of one or more branches of the left or right coronary artery* [Causes] **Coronary atherosclerosis (coronary artery disease)** Repetitious endothelial injury with the resulting inflammatory response in the blood vessel wall results in a buildup of fibrous caps and plaque, which restricts blood flow to coronary arteries. **Other causes/contributing factors include**: Vasospasms of coronary artery (called Prinzmetal or variant angina) Decreased oxygen supply to myocardium (e.g., hypoxemia, anemia) Increased myocardial demand (increased heart rate or CO) [Pathophysiology ] Coronary atherosclerosis results in myocardial ischemia Oxygen demand of ventricle exceeds oxygen supply in the coronary arteries [Clinical Consequences] **Decreased ventricular contractility** **Conduction disturbances** **Ischemic Pain** Stable angina pectoris *Intermittent chest pain occurring with the same pattern of onset, duration and intensity* Unstable angina pectoris *Chest pain lasting 15 to 20 minutes not relieved by rest, position change, or nitroglycerin* Myocardial Infarction *Severe reduction of coronary artery blood flow leading to myocardial cell death* [Causes] Coronary atherosclerosis (coronary artery disease) *Other less common causes include*: *Precipitating conditions include factors that increase metabolic demand*: *Precipitating conditions include factors that reduce the oxygen content of the blood*: [Types ] *There are several schemes used to classify types of MI for the purpose of directing treatment. (Don't memorize)* +-----------------------------------+-----------------------------------+ | *Classification* | *Description of Categories* | +===================================+===================================+ | Morphologic | **Transmural**: necrosis extends | | | throughout the entire wall of the | | | myocardium | | | | | | **Non-transmural**: necrosis is | | | limited to the endocardium or | | | subendocardium (most frequent), | | | or a segment of the myocardium. | +-----------------------------------+-----------------------------------+ | STEMI vs. NSTEMI | **STEMI**: MI in the presence of | | | ST segment elevation on the ECG | | | | | | **NSTEMI**: no ST segment | | | elevation | +-----------------------------------+-----------------------------------+ | Fourth Universal Definition of | **Myocardial Injury:** Elevated | | Myocardial Infarction (2018) | troponin with at least one value | | | \> 99 %ile | | | | | | **Type 1**: MI related to acute | | | athero-thrombosis of artery | | | feeding the infarcted myocardium | | | | | | **Type 2**: Supply-demand | | | mismatch unrelated to acute | | | athero-thrombosis | | | | | | **Type 3**: Cardiac death in | | | patients with symptoms suggestive | | | of myocardial ischemia and | | | presumed new ischemic EKG changes | | | before troponin levels available | | | or abnormal | | | | | | **Type 4a**: MI associated with | | | percutaneous coronary | | | intervention | | | | | | **Type 4b:** MI related to stent | | | thrombosis | | | | | | **Type 4c:** MI related to | | | restenosis | | | | | | **Type 5**: MI related to CABG | +-----------------------------------+-----------------------------------+ [Pathophysiology ] Infarction of an atherosclerotic coronary artery generally occurs due to the following circumstances: **Hypoxic injury** Within 10 seconds of infarction, see hypoxic injury to myocardial cells. Consequences of anaerobic metabolism include decreased ATP production & lactic acid formation. Anaerobic metabolism is insufficient - after 20 minutes of complete occlusion, irreversible injury and cell death begins in the affected areas. **Inflammation** 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 **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. **\ ** **Repair and resolution** Coagulative necrosis develops at site of infarct. Inflammation leads to scar tissue deposition at the site of infarct (and other changes in the surrounding tissue described on the next page). [Clinical Consequences] *Functional impairment depends on location and severity of infarct* Decreased ventricular (and atrial) contractility Conduction disturbances Ischemic pain [\ 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.* 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 2-3 hours after onset of chest pain, peak within 12 to 48 hours, and remain elevated for 4-10 days. *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* **CK-MB (Creatine Kinase -- muscle and brain type)** *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 4-6 hours after the MI, peaking in 24 hours, and disappearing in 2-3 days. **Myoglobin** *An intracellular protein similar to hemoglobin that is released after myocardial cell injury* Rises in myoglobin are very sensitive, but not very specific to acute MI **\ ** **C-Reactive Protein (CRP)** *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. **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.* **FYI - Other Lab Findings** Elevated glucose CBC -- Elevated WBC count Chemistry -- Elevated potassium Lipid profile -- see 'atherosclerosis'