ST elevation myocardial infarction pathophysiology

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Myocardial Infarction Pathophysiology
Shown in yellow is atherosclerotic plaque, in red is clot that has formed inside the ruptured plaque and in the lumen of the coronary artery.
ICD-10 I21-I22
ICD-9 410
DiseasesDB 8664
MedlinePlus 000195
eMedicine med/1567  emerg/327 ped/2520

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Please Join in Editing This Page and Apply to be an Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

The role of plaque rupture in ST elevation myocardial infarction

Atherosclerosis or "hardening of the arteries" is the gradual buildup of cholesterol and fibrous tissue (collagen and smooth muscle cells) throughout the vascular tree. When there is localized accumulation of lipids and scar tissue, this is called a "plaque". Somewhat paradoxically, it is not the most severe plaque narrowings that lead to ST elevation MI. Pathology studies indicate that it is often mild to-moderate, lipid laden, inflammed plaques that are the ones that most likely to rupture and cause an ST elevation MI (STEMI) or a non ST elevation MI (NSTEMI). [1] The role of plaque rupture in STEMI and NSTEMI is supported by studies demonstrating that plaque rupture is present in about 70% and superficial erosion is present in 30% of patients who die suddenly in whom there is documented coronary artery disease. [2] Exposure of the blood stream to the thrombogenic components of the plaque leads to activation of the coagulation cascade and thrombus formation. In STEMI, the clot completely occludes the epicardial artery, and there is a complete lack of blood flow to the involved territory. This causes transmural injury and ST elevation. In NSTEMI, there is partial obstruction with embolization. This causes ischemia and subendocardial injury that are manifested by ST depression.

Shown below 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.

Shown below is a magnified view of the second slice from the left. In yellow is atherosclerotic plaque, in red is clot that has formed inside the ruptured plaque and in the lumen of the coronary artery.

Te following are excellent videos demonstrating the underlying pathophysiology:

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The consequence of plaque rupture and vessel occlusion: The Time Dependent Wavefront of Necrosis

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.[3] 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) [4][5]

  • 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
  • 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

Anabolic steroids

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[6];
Genetic Familial hypercholesterolemia
Hematologic Disseminated intravascular coagulation (DIC)

Hypercoagulable states

Polycythemia vera

Thrombocytosis

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[6];

Amyloidosis

Fabry disease

Homocystinuria

Mucopolysaccharidoses or Hurler disease

Pseudoxanthoma elasticum

Thiamine deficiency has been associated with ST elevation and myonecrosis [7] [8] [9]

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

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Gross Findings

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology






The Time Dependent Wavefront of Necrosis

Time dependent wavefront of necrosis working its way from the subendocardium to the subepicardium
Time dependent wavefront of necrosis working its way from the subendocardium to the subepicardium

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:

  1. The location, severity, and rate of development of coronary atherosclerotic obstructions,
  2. The size of the vascular bed perfused by the obstructed vessels
  3. The duration of the coronary artery occlusion
  4. The metabolic / oxygen needs of the myocardium at risk,
  5. 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.[10]

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.


References

  1. Falk E, Shah PK, Fuster V (1995). "Coronary plaque disruption". Circulation. 92 (3): 657–71. PMID 7634481. Unknown parameter |month= ignored (help)
  2. Burke AP, Farb A, Malcom GT, Liang YH, Smialek J, Virmani R (1997). "Coronary risk factors and plaque morphology in men with coronary disease who died suddenly". N. Engl. J. Med. 336 (18): 1276–82. PMID 9113930. Unknown parameter |month= ignored (help)
  3. 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.
  4. 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)
  5. 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)
  6. 6.0 6.1 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)
  7. 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)
  8. Hundley JM, Ashburn LL, Sebrell WH. The electrocardiogram in chronic thiamine deficiency in rats. Am J Physiol 144: 404–414, 1954.
  9. 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)
  10. Robbins Pathologic Basis of Disease, Kumar V, 7th ed

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