ST elevation myocardial infarction pathophysiology
| Myocardial Infarction Pathophysiology | |
| ICD-10 | I21-I22 |
|---|---|
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
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Plaque rupture
Shown above are multiple slices of the LAD. The proximal LAD is located to the left. Plaque rupture with thrombus formation begins in the second slice of the LAD.
Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. Blood stream column irregularities visible on angiographies reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote a thrombus (blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of downstream myocardium).
If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells die (chiefly through necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that another form of cell death called apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.[1] As a result, the patient's heart can be permanently damaged. This scar tissue also puts the patient at risk for potentially life threatening arrhythmias.
In ST segment myocaridal infarction (STEMI), the ST segments on the ECG are by definition elevated and there is myonecrosis (death of myocytes) as reflected by elevation of biomarkers such as creatine kinase MB fraction (CK-MB) or troponin T or I (tn)). This is in contrast to non ST elevation myocardial infarction (NSTEMI) where there is myonecrosis but no ST segment elevation on the ECG. STEMI is one of three variants of acute coronary syndrome (the others being non ST elevation MI and unstable angina), which is often (but by no means always) a manifestation of atherosclerotic coronary artery disease.
ST Segment Elevation Does Not Always Signify a Myocardial Infarction
ST segment elevation should alert the clinician to the possibility of myocardial injury, however, there are a variety of conditions that cause ST segment elevation which are not associated with myonecrosis.
Differential Diagnosis of Causes of ST Segment Elevation in the Absence of Myonecrosis
Acute epicardial artery occlusion by thrombus is certainly one cause of ST segment elevation, but other causes of ST segment elevation which are not associated with myonecrosis include the following: (listed in alphabetical order) [2][3]
- Aneurysm of the ventricle can result in persistent ST segment elevation that can be exacerbated with tachycardia.
- Balloon inflation in a coronary artery during percutaneous coronary intervention
- Coronary artery rupture during percutaneous coronary intervention
- Early repolarization is a normal variant that can result in ST segment elevation. It is more common in males of younger age. The ST elevation is exacerbated by bradycardia.
- Hyperkalemia known as the "dialyzable current of njury" hyperkalemia may cause hyperacute ECG changes due to changes in membrane polarity
- Left bundle branch block is associated with ST segment elevation in those leads that are discordant to the QRS. Stated differently, if the QRS is predominantly of a negative deflection, it is normal to observe ST segment elevation in the same leads. The presence of ST elevation in leads where the QRS deflection is upright (concordance) may be a marker of myocardial injury.
- Myopericarditis can cause injury to the subepicardial myocytes and ST segment elevation.
- Myocarditis can cause injury to the subepicardial myocytes and ST segment elevation.
- Pericardiocentesis when the needle comes into contact with the myocardium, there can be ST segment elevation reflecting local injury of the myocardium.
- Pericarditis can cause injury to the subepicardial myocytes and ST elevation.
- Prinzmetal's angina is associated with ST segment elevation due to transient epicardial coronary artery spasm either in the absence or presence of atherosclerosis. If the condition persists long enough, myonecrosis can be observed.
- Stroke Intracranial hemorrhage can in some cases cause ST segment elevation due to direct myocyte injury from a hyperadrenergic stimulation emanating from the central nervous system.
Differential Diagnosis of Causes of ST Segment Elevation in the Presence of Myonecrosis (STEMI)
While plaque rupture is the most common cause of ST segment elevation MI, other conditions can cause ST elevation and myocardial necrosis. In order to expeditiously treat an alternate underlying cause of myonecrosis, it is important to rpadily identify conditions other than plaque rupture that may also cause ST elevation and myonecrosis. Indeed, the management of some of these conditions might be differ substantially from that of plaque rupture: cocaine induced STEMI would not be treated with beta-blockers, and myocardial contusion would not be treated with an antithrombin. These conditions include the following:
| Cardiovascular | Aortic dissection more often extends to occlude the ostium of the right coronary artery
Aortic stenosis can cause subendocardial ischemia and infarction if demand grossly exceeds supply
|
| Chemical / poisoning | Carbon monoxide poisoning |
| Dermatologic | No underlying causes |
| Drug Side Effect | Oral contraceptive pills, particularly among women who smoke |
| Ear Nose Throat | A recent upper respiratory tract infections has been associated with a 4.9 fold rise in the risk of MI |
| Endocrine | Thyrotoxicosis |
| Environmental | Blizzards and snow shoveling, and inhalation of fine particulate matter in areas with air pollution and high traffic have been identified as triggers of MI. |
| Gastroenterologic | A heavy meal has been associated with a 4 fold rise in the risk of MI, and it is not clear if this is mediated by hyperadrenergic tone[4]; |
| Genetic | Familial hypercholesterolemia |
| Hematologic | Disseminated intravascular coagulation (DIC) |
| Iatrogenic | Epinephrine overdose
Sudden withdrawal of Beta blockers or nitrates |
| Infectious Disease | A recent upper respiratory tract infections has been associated with a 4.9 fold rise in the risk of MI
Infectious endocarditis may STEMI as a result of embolization |
| Musculoskeletal / Ortho | No underlying causes |
| Neurologic | No underlying causes |
| Nutritional / Metabolic | A heavy meal has been associated with a 4 fold rise in the risk of MI and it is not clear if this is mediated by hyperadrenergic tone[4];
Mucopolysaccharidoses or Hurler disease Thiamine deficiency has been associated with ST elevation and myonecrosis [5] [6] [7] |
| Obstetric/Gynecologic | Spontaneous coronary dissection in the setting of pregnancy |
| Oncologic | Radiation therapy can accelerate atherosclerosis particularly in the distribution of the left anterior descending artery; |
| Opthalmologic | No underlying causes |
| Overdose / Toxicity | Cocaine ingestion which may result in direct myocyte injury due to an adrendergic surge, vasoconstriction of the microvasculature or plaque rupture and thrombus formation;
Marijuana ingestion has been identified as a trigger of MI. |
| Psychiatric | Anger, anxiety, bereavement, work-related stress, earthquakes, bombings and other psychosocial stressors have been identified as triggers of MI, and it is not clear if the mechanism is plaque rupture or hyperadrenergic tone;
Stress cardiomyopathy or Broken heart syndrome causes ST segment elevation most often in the anterior precordium and is thought to be due to direct myocyte injury from a hyperadrenergic stimulation emanating from the central nervous system. |
| Pulmonary | A recent upper respiratory tract infections has been associated with a 4.9 fold rise in the risk of MI |
| Renal / Electrolyte | Homocystinuria |
| Rheum / Immune / Allergy | Takayasus |
| Sexual | Sexual activity has been identified as a trigger of MI |
| Trauma | Both penetrating and non-penetrating trauma to the heart or myocardial contusion, commotio cordis can be associated with ST elevation and myonecrosis. |
| Urologic | No underlying causes |
| Miscellaneous | Hypotension particularly if it is prolonged |
Histopathological Findings
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Coronary artery: Atherosclerosis: Micro H&E med mag; A good example of plaque rupture with thrombosis.
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Right coronary artery: Ruptured Plaque: Micro low mag H&E; Ruptured plaque with foam cell lesion (near rupture site).
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Right coronary artery: Atherosclerosis Plaque Ruptured with Thrombus: Micro low mag H&E; an excellent view of ruptured plaque with thrombus and some old fibrin in it.
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Right coronary artery: Atherosclerosis Plaque Ruptured with Thrombus: Micro low mag trichrome.
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Right coronary artery: Atherosclerosis Plaque Ruptured: Micro low mag H&E; large plaque with hemorrhage; (an excellent example of hemorrhage).
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Coronary artery: Atherosclerosis: Micro H&E low mag injected artery fairly typical uncomplicated atheromatous plaque
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Coronary artery: Atherosclerosis: Micro H&E low mag, injected artery has typical fibrous plaque with small hemorrhage in atheroma.
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Coronary artery: Atherosclerosis: Micro H&E low mag, injected artery is a very good example of marked lumen stenosis due to typical fibrous plaque with calcification
Gross Findings
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Left anterior descending coronary artery: Atherosclerosis Plaque Ruptured with Thrombosis: Gross; natural color; four cross sections, close-up view (acute anterior myocardial infarction with rupture)
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Coronary artery: Atherosclerotic Plaque: Gross natural color close-up view of a typical plaque
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Coronary Atherosclerosis: Gross, natural color, close-up view of large atherosclerotic plaque with soft atheroma (a quite good example in 54yo male. Smoker with hypertension). This slide shows the left main artery
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Coronary artery: Atherosclerotic Plaque: Gross, natural color, close-up view of plaque with atheroma core causing more than 90% lumen occlusion (an excellent example)
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Coronary artery: Atherosclerotic Plaque with Hemorrhage and Thrombosis: Gross, natural color, cross section, close-up, an excellent example of right coronary artery in 71yo female.
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Coronary artery: Atherosclerotic Plaque with Hemorrhage and Thrombosis: Gross, natural color, cross sections; there is excellent example of hemorrhagic plaque and thrombus at and just below the origin of first diagonal artery. Another one (a more acute one) was in the right coronary artery.
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Coronary artery: Atherosclerotic Plaque with Thrombus: Gross natural color, close-up of cross section.
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Coronary artery: Atherosclerotic Plaque with Hemorrhage: Gross fixed tissue, cross sections. LAD and 1st diagonal with large plaques and several apparent areas of hemorrhage.
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Coronary artery: Atherosclerosis: Gross, an excellent close-up atherosclerosis with hemorrhage into plaque.
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Coronary artery: Atherosclerosis: Gross, cross sections coronary artery with hemorrhage into plaque (image shows full length of the artery).
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Coronary artery: Atherosclerosis: Gross, cross sections of artery showing plaques (an excellent example)
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Coronary artery: Atherosclerosis: Gross natural color in situ cross section with large fibrocalcific plaque with hemorrhage (an excellent example)
The Time Dependent Wavefront of Necrosis
Irreversible injury of ischemic myocytes occurs first in the subendocardial zone. With more extended ischemia, a wavefront of cell death moves through the myocardium to involve progressively more of the transmural thickness of the ischemic zone. The precise location, size, and specific morphologic features of an acute myocardial infarction depend on:
- The location, severity, and rate of development of coronary atherosclerotic obstructions,
- The size of the vascular bed perfused by the obstructed vessels
- The duration of the coronary artery occlusion
- The metabolic / oxygen needs of the myocardium at risk,
- The extent of collateral blood vessels
Decrease of ATP levels in myocytes in reaction to ischemia starts within seconds and causes loss of contractility in first two minutes. If ischemia persists, ATP levels reduced to its half level within 10 minutes and to 1/10 within 40 minutes. Irreversible cell injury occurs between 20-40 minutes and microvascular level injury starts if ischemia lasts more than an hour.[8]
Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib / VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death.
Another life threatening arrhythmia is ventricular tachycardia (V-Tach / VT), which may or may not cause sudden cardiac death. However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which is particularly bad for the patient experiencing acute myocardial infarction.
The cardiac defibrillator is a device that was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.
Videos
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References
- ↑ Krijnen PA, Nijmeijer R, Meijer CJ, Visser CA, Hack CE, Niessen HW. (2002). "Apoptosis in myocardial ischaemia and infarction". J Clin Pathol. 55 (11): 801–11. PMID 12401816.
- ↑ Wang K, Asinger RW, Marriott HJ (2003). "ST-segment elevation in conditions other than acute myocardial infarction". N. Engl. J. Med. 349 (22): 2128–35. doi:10.1056/NEJMra022580. PMID 14645641. Unknown parameter
|month=ignored (help) - ↑ Ako J, Honda Y, Fitzgerald PJ (2004). "Conditions associated with ST-segment elevation". N. Engl. J. Med. 350 (11): 1152–5, author reply 1152–5. doi:10.1056/NEJM200403113501118. PMID 15014192. Unknown parameter
|month=ignored (help) - ↑ 4.0 4.1 Lipovetzky N, Hod H, Roth A, Kishon Y, Sclarovsky S, Green MS (2004). "Heavy meals as a trigger for a first event of the acute coronary syndrome: a case-crossover study". Isr. Med. Assoc. J. 6 (12): 728–31. PMID 15609883. Unknown parameter
|month=ignored (help) - ↑ Kawano H, Koide Y, Toda G, Yano K (2005). "ST-segment elevation of electrocardiogram in a patient with Shoshin beriberi". Intern. Med. 44 (6): 578–85. PMID 16020883. Unknown parameter
|month=ignored (help) - ↑ Hundley JM, Ashburn LL, Sebrell WH. The electrocardiogram in chronic thiamine deficiency in rats. Am J Physiol 144: 404–414, 1954.
- ↑ Read DH, Harrington DD (1981). "Experimentally induced thiamine deficiency in beagle dogs: clinical observations". Am. J. Vet. Res. 42 (6): 984–91. PMID 7197132. Unknown parameter
|month=ignored (help) - ↑ Robbins Pathologic Basis of Disease, Kumar V, 7th ed
Additional Resources
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External Links
- The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research
- Clinical Trial Results: An up to date resource of Cardiovascular Research
- Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study from the United States National Heart, Lung and Blood Institute
- Heart Attack overview from MedlinePlus
- Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada
- A Regional PCI and Resource Center for STEMI
- STEMI Systems' Quarterly newsletter
- American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.
- American Heart Association's Heart Attack web site