B P5 C37 ST-Elevation Myocardial Infarction: Pathophysiology and Clinical Evolution Flashcards
Type of MI
Demonstration of acute atherothrombosis in the artery supplying the infarcted myocardium
Type 1
Acute myocardial infarction should be used when there is acute myocardial injury with clinical evidence of acute myocardial ischemia and with detection of a rise and/or fall of cTn values with at least one value above the 99th percentile URL and at least one of the following:
• Symptoms of myocardial ischemia
• New ischemic ECG changes
• Development of pathologic Q waves
• Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology
• Identification of a coronary thrombus by angiography or autopsy (not for type 2 or 3 MIs)
An imbalance between myocardial oxygen supply and demand unrelated to acute atherothrombosis meets criteria for _________
Type 2 MI
Cardiac death in patients with symptoms suggestive of myocardial ischemia and presumed new ischemic ECG changes before cTn values become available or abnormal meets criteria for ____________
Type 3 MI
Percutaneous coronary intervention (PCI)-related MI is termed _______________
Type 4a MI
Type 4b MI ______________
Type 4c MI ______________
Type 4 MI include type 4b MI stent thrombosis and type 4c MI restenosis that both meet type 1 MI criteria.
Coronary artery bypass grafting (CABG) related MI is termed _______________
Type 5 MI
Coronary procedure related MI </= 48 hr after the index procedure is arbitrarily defined by an elevation of cTn values > ___ times for type 4a MI and >___ for type 5 MI of the 99th percentile URL in patients with normal baseline values.
> 5x: type 4a
> 10x: type 5
Patients with preprocedural cTn values, in whom the preprocedural cTn level is stable (<20% variation) or falling, must meet the criteria for a >5 or >10 fold increase and manifest a change from the baseline value of >_____%.
> 20%
Criteria for prior or silent /unrecognized MI
- Abnormal Q waves +/- symptoms in the absence of nonischemic causes.
- Imaging evidence of loss of viable myocardium in a pattern consistent with ischemic etiology.
- Pathoanatomical findings of a prior MI.
Management and outcomes of patients with STEMI appear to vary substantially depending on the volume of such patients cared for within a hospital system.
_____ have lower STEMI mortality rates.
Conversely, patients with STEMI _____ have higher mortality rate
LOWER STEMI Mortality:
Hospitals with a high clinical volume
High rate of invasive procedures
Top ranking in quality reports
HIGHER MORTALITY RATE:
Not cared for by a cardiovascular specialist
The highest risk of ischemic complications following MI occurs within ____ days, after which the risk becomes fairly linear. This pattern is most evident in patients older than 80 years
180 days
Identify type of MI:
Any one of the following criteria meets the diagnosis for prior or silent/ unrecognized MI:
• Abnormal Q waves with or without symptoms in the absence of nonischemic causes.
• Imaging evidence of loss of viable myocardium in a pattern consistent with ischemic etiology.
• Pathoanatomical findings of a prior MI.
Prior or silent/unrecognized myocardial infarction
Cause of myocardial injury related to AMI
Atherosclerotic plaque disruption with thrombosis
Most ACSs result from coronary atherosclerosis, generally with superimposed coronary thrombosis caused by_____
Rupture or erosion of an atherosclerotic lesion
Thus, equating the lipid-rich, thin-capped plaque with “vulnerability” is a misnomer. Other morphologic characteristics associated with rupture-prone plaque include _____.
Expansive remodeling that minimizes luminal obstruction (mild stenosis by angiography)
Neovascularization (angiogenesis)
Plaque hemorrhage
Adventitial inflammation
“Spotty” pattern of calcification
Infarction alters the sequence of depolarization ultimately reflected as changes in the QRS-T complex.
The most characteristic change in QRS that develops in most patients with STEMI is the evolution of _____ in leads that interrogate the infarct zone.
Q waves
In a minority of patients with ST elevation, no Q waves develop but other abnormalities in the QRS complex occur frequently, such as diminution in R wave height and notching or splintering of the QRS
Myocardial injury related to acute myocardial ischemia because of oxygen supply/demand imbalance
Identify causes with reduced myocardial perfusion
• Coronary artery spasm, microvascular dysfunction
• Coronary embolism
• Coronary artery dissection
• Sustained bradyarrhythmia
• Hypotension or shock
• Respiratory failure
• Severe anemia
Causes of Increased myocardial oxygen demand
Sustained tachyarrhythmia
Severe hypertension with or without left ventricular hypertrophy
Gross alterations in the myocardium appear _____ hours after the onset of necrosis, but a variety of histochemical stains can identify zones of necrosis after only _____ hours.
6-12 hours: Gross alterations
2-3 hours: Histochemical stains
Within hours of death from MI, the presence of an infarct can often be detected by immersing slices of myocardium in triphenyltetrazolium chloride (TTC), which turns noninfarcted myocardium a _____ color due to preserved lactate dehydrogenase activity while the infarcted area _____
Birck-red color: NONINFARCTED
Unstained: INFARCTED
An MI can often be identified at _____ hours as a red-blue area of disco-oration caused by edema and extravasated blood.
By day ____, an infarct is rimmed by a zone of granulation tissue as it eventually evolves into a fibrous scar.
12-24 hours: RED-BLUE AREA
DAY 7
Approximate time of onsent of key events in ischemic cardiac myocytes
Onset of ATP depletion:
Loss of contractility:
ATP reduced
to 50% of normal:
to 10% of normal:
Irreversible cell injury:
Microvascular injury:
Onset of ATP depletion: Seconds
Loss of contractility: <2 min
ATP reduced
to 50% of normal: 10 min
to 10% of normal: 40 min
Irreversible cell injury: 20–40 min
Microvascular injury: > 1 hr
Myocardial relaxation-contraction is compromised within a minute after the onset of severe ischemia with loss of systolic function, and irreversible cell injury begins within as early as _____________
20 minutes
Irreversible cell death usually occurs in the ischemic region in _____ hrs in the absence of reperfusion or sufficient collateral circulation
6 hours
ECG criteria for ST Elevation
New ST elevation at the J point in two contiguous leads with the following cut points:
• ≥0.1 mV in all leads (except V2 –V3 )
• In leads V2 –V 3 the following cut points apply:
• ≥0.2 mV in men ≥40 years
• ≥0.25 mV in men <40 years
• ≥0.15 mV in women
ECG manifestations of ST Depression and T Wave Changes
• New horizontal or downsloping ST depression ≥0.05 mV in two contiguous leads
• T wave inversion ≥0.1 mV in two contiguous leads with a prominent R wave or R/S ratio >1
Electrocardiographic Manifestations of Ischemia in the Setting of Left Bundle Branch Block
Electrocardiographic Criterion
ST-segment elevation ≥1 mm and concordant with the QRS complex (5 points)
ST-segment depression ≥1 mm in lead V1 , V2 , or V3 (3 points)
ST-segment elevation ≥5 mm and discordant with the QRS complex (2 points)
A score of ≥3 had a specificity of 98% for acute MI
Electrocardiographic Changes Associated With Previous Myocardial
Infarction (in the Absence of Left Ventricular Hypertrophy and Left Bundle Block)
Any Q wave in leads V2 –V 3 ≥0.02 sec or a QS complex in leads V 2 and V3
Q wave ≥0.03 sec and ≥0.1-mV deep or QS complex in leads I, II, aVL, aVF, or V4 –V 6 in any 2 leads of a contiguous lead grouping (I, aVL; V1 –V6 ; II, III, aVF)
R wave ≥0.04 sec in V1 –V 2 and R/S ≥1 with a concordant positive T wave in absence of a conductions defect
Ultrastructural changes appear within several minutes after the onset of ischemia. If reperfusion occurs, these early changes can reverse.
Irreversible damage usually requires a reduction of flow to less than ___% of normal for _____ minutes.
<10% of normal for 20-30 minutes
In experimental infarction, the earliest ultrastructural changes in cardiac muscle after ligation of a coronary artery, noted within _____ minutes, is a reduction in the size and number of glycogen granules, myofibrillar relaxation, intracellular edema, and swelling and distortion of the transverse tubular system, sarcoplasmic reticulum, and mitochondria.
Changes after _____ minutes of occlusion include myocyte swelling,swelling and internal disruption of mitochondria, development of amorphous (flocculent) aggregation and margin- ation of nuclear chromatin, and relaxation of myofibrils.
After 20 minutes to 2 hours of ischemia, the changes in some cells become irreversible
20 minutes
Reduction in the size and number of glycogen granules
Myofibrillar relaxation
Intracellular edema
Swelling and distortion of the transverse tubular system, sarcoplasmic reticulum, and mitochondria
60 minutes
Myocyte swelling
Swelling and internal disruption of mitochondria
Development of amorphous (flocculent) aggregation and margination of nuclear chromatin
Relaxation of myofibrils.
_____ necrosis results from severe, persistent ischemia and is usually present in the central region of infarcts.
Coagulation necrosis
The tissue exhibits:
Stretched myofibrils
Many cells with pyknotic nuclei
Congested microvessels
Phagocytosis of necrotic muscle cells
Mtochondrial damage occurs, but no calcification is evident
This form of myocardial necrosis, also termed ______________________, results primarily from severe ischemia followed by reflow
The entire infarct may show this form of necrosis after reperfusion
Contraction band necrosis or coagulative myocytolysis
It is characterized by:
Hypercontracted myofibrils with contraction bands and mitochondrial damage, frequently with calcification
Marked vascular congestion
Healing by lysis of muscle cells
Ischemia without necrosis generally causes no acute changes visible on light microscopy, but severe prolonged ischemia can result in myocyte vacuolization, often termed _____.
Myocytolysis
Prolonged severe ischemia, which is potentially reversible, causes cloudy swelling, as well as hydropic, vascular,and fatty degeneration.
An additional pathway of myocyte death involves ______, a form of programmed cell death. In contrast to coagulation necrosis, myocytes undergoing apoptosis exhibit shrinkage, and fragmentation of DNA without the usual cellular infiltrate indicative of inflammation.
Apoptosis
Early reperfusion of the myocardium evolving from ischemia to infarction (i.e., within _____ minutes) can prevent necrosis. Beyond this early stage, the number of salvaged myocytes—and therefore the amount of salvaged myocardial tissue (area of necrosis/area at risk)— relates directly to the duration of coronary artery occlusion, the level of myocardial oxygen consumption, and collateral blood flow
Within 15-20 mins
While all patients who achieve reperfusion as soon as possible to preserve viable, but at risk, myocardium, the reperfusion of tissue per- fusion can induce arrhythmias and potential for “reperfusion injury,” which has been estimated to account for up to _____% of the ultimate infarct size.
50%
The physiology of reperfusion injury is likely multifactorial and includes:
Pathologic findings of reperfusion injury include widespread myocardial hemorrhage and contraction bands.
Release of cytotoxic mitochondrial content
Myocyte hypercontractility due to Ca2+ excess
Reactive oxygen species
Leukoyte aggregation
Platelet and complement activation
Approximately _____% of STEMI cases will have a total occlusion of the infarct-related vessel on initial angiogram
90%
Factors that influence the viability of myocardial cells distal to the occlusion:
Collateral blood flow
Level of myocardial metabolism
Presence and location of stenoses in other coronary arteries
Rate of development of the obstruction, and quantity of myocardium supplied by the obstructed vessel
Approximately ________ of patients with inferior infarction have some involvement of the right ventricle
Isolated ______
30% to 50%
3% to 5%
The classic presentation of an RV infarct:
Hypotension, clear lung fields, and elevated jugular venous pressures
Acute management of RV infarction complicated by cardiogenic shock includes judicious volume replacement, early revascularization, maintenance of atrioventricular synchrony, and in refractory cases, mechanical circulatory support.
In contrast to the left ventricle, the right ventricle can sustain long periods of ischemia but still demonstrate excellent recovery of contractile function after reperfusion.
Infarction of the atria occurs in up to 10% of patients with STEMI if ______________ is used as the criterion
Isolated atrial infarction?
In conjunction with ventricular infarction?
PR segment displacement
<5%
Approx 15%
Atrial infarction is more common on the _____ side, occurs more frequently in the _____ of the atrium, and can result in thrombus formation
Right than the left
Atrial appendages than in the lateral or posterior walls
The _________________ is a principal determinant of the infarct size
Magnitude of coronary collateral flow
_______________ defined as evidence of MI (positive cardiac b marker and corroborative clinical evidence of infarction due to ischemia) with angiographically normal or near-normal coronary arteries (the absence of obstructive CAD on angiography [i.e., no coronary artery stenosis ≥50%] in any potential infarct-related artery), and no other explanation for the presentation
Myocardial infarction with nonobstructive coronary arteries (MINOCA)
_______________, _______________, ______________ are common MINOCA etiologies affecting the epicardial arteries, as are plaque erosion and plaque rupture not discerned by standard angiography
Coronary artery spasm, plaque erosion or rupture, and coronary dissection
Two most common myocardial or microvascular mimickers of MI
Myocarditis
Takotsubo CMP
Compared to patients with atherosclerotic-mediated MI, patients with MINOCA tend to be younger, and more often ____________, black Maori or Pacific race, or Hispanic, with relatively few coronary risk factors except a ___________________
Female
History of cigarette smoking
In general, patients who have survived STEMI without evidence of significant CAD have a ________________ and better long-term outlook than those with atherosclerotic-mediated STEMI; in-hospital mortality is approximately 60% lower, and 1-year mortality, 40% lower.
Smaller infarct sizes
_______________ can result from embolization into a coronary artery.
_______________ of coronary arteries can occur secondary to chest wall trauma or hypercoagulable states.
Embolic/Thrombotic coronary arterial occlusions
The causes of coronary embolism are numerous: infective endocarditis and nonbacterial thrombotic endocarditis (see Chapter 80), prolapsed mitral valve, or myxoma, mural thrombi, prosthetic valves, neoplasms, air introduced at cardiac surgery, and calcium deposits from manipulation of calcified valves at surgery.
In situ thrombosis
___________________ medial dissection or rupture in the vasa vasorum, often in the setting of some physical or emotional stress in patients with some predisposition, that leads to intramural hemorrhage and subsequent coronary occlusion by the hematoma itself or a dissection flap.
SCAD
may account for 25% to 33% of MIs in women younger than 50 years old
Type of SCAD
_____________ classic appearance of contrast dye staining of arterial wall with multiple radiolucent lumen
Type 1
Rarer causes include _____, which can produce marked narrowing or occlusion of one or both coronary ostia, whereas Takayasu arteritis can result in obstruction of the coronary arteries
Syphilitic aortitis
________________ involves transient wall motion abnormalities involving the LV apex and midventricle
Occurs in the absence of obstructive epicardial CAD and can mimic STEMI, but should not be considered a subtype of MINOCA as it has a specific pathophysiology that likely reflects neurocardiogenic myocardial stunning
Acute stress cardiomyopathy, also termed transient LV apical ballooning syndrome or takotsubo cardiomyopathy
Typically, an episode of physical or psychological stress precedes the development of takotsubo cardiomyopathy, although some cases lack an evident precipitant. More than half of patients presenting with takotsubo cardiomyopathy have an active or history of a neurologic or psychiatric disorder, potentially linking neurologic-mediated vasoconstriction.
Most common variant of stress cardiomyopathy
Apical ballooning (75-80%)
Others:
Midventricular (10-20%) - severe LVD, acute HF
Basal or inverted (5%)
Biventricular (<0.5%)
Focal dysfunction (Rare) - benign, more associated with chest pain
Dilation of the left ventricle elevates ________________ and elevates ________________
Ventricular wall tension
Myocardial oxygen consumption
