This document summarizes a seminar on ST-elevation myocardial infarction (STEMI). The seminar objectives were to define STEMI, describe its pathophysiology and presentations, understand diagnostic tests and their interpretation, diagnose and manage complications, and ensure appropriate secondary prevention. The seminar covered the epidemiology, pathophysiology, clinical features, investigations including ECG and cardiac biomarkers, management including reperfusion therapies, complications and post-STEMI risk stratification.
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Seminar on STEMI.pptx
1. Seminar on
STEMI
Presenter:- Dr. Misale H. (IM/RI)
Moderator:- Dr. Chala J. (Internist, Assistant prof. of
Internal Medicine)
June 13 , 2023
6/13/2023 1
3. Define STEMI and describe the pathophysiology and varied clinical
presentations.
Understand different investigation modalities and their interpretation
and significance.
Diagnose and detect complications early and manage accordingly.
Asses different guidelines and their recommendation on the
management of STEMI.
Ensure STEMI patients are discharged on appropriate secondary
prevention.
6/13/2023 3
4. The term acute coronary syndrome (ACS) is a unifying construct
representing a pathophysiologic and clinical spectrum culminating in
acute myocardial ischemia.
Unstable angina (UA), Non ST Elevation Myocardial Infarction
(NSTEMI) and ST Elevation Myocardial Infarction (STEMI)
collectively constitute the diagnosis of Acute Coronary Syndrome
(ACS).
STEMI caused by most severe occlusion of a coronary artery
6/13/2023 4
5. 605,000 patients experience a new AMI,& 200,000 experience a
recurrent AMI each year in US
In-hospital mortality rate declined from 10%-5%
The 1-year mortality rate after AMI is ∼15%. Mortality is
approximately fourfold higher in elderly patients (aged >75) as
compared with younger patients
Epidemiologic studies indicate there has been a shift in the pattern of
AMI more patients with NSTEMI
6/13/2023 5
14. STEMI usually occurs when coronary blood flow decreases abruptly
after a thrombotic occlusion of a coronary artery previously affected
by atherosclerosis.
In most cases, STEMI occurs when the surface of an atherosclerotic
plaque becomes disrupted and conditions favor thrombogenesis.
Irreversible damage usually requires a reduction of flow to less than
10% of normal for 20 to 30 minutes.
6/13/2023 14
16. Chest pain:- The pain is deep, visceral (heavy, squeezing, and
crushing)Occur at rest and lasts 30 minutes Severe, frequent,
central portion of the chest radiates to the arms, back, lower jaw, and
neck, xiphoid and epigastrium
Angina equivalent:- Sudden breathlessness with pulmonary edema,
Sudden loss of consciousness, confusional state, anxiety, profound
weakness, diaphoresis, nausea, vomiting, epigastric pain, sensation of
impending doom
Painless or atypical chest pain commonly occurs in
elderly, women, diabetic patients, prior MI
6/13/2023 16
18. 1) ECG
2) Serum cardiac biomarkers
3) cardiac imaging
4) Non specific markers of tissue necrosis & inflammation
When evaluating the results of diagnostic tests for STEMI
the temporal phase of the infarction must be considered
Acute ( first few hours-7 days)
Healing(7-28 days)
Healed (>29 days)
6/13/2023 18
19. Important initial evaluation of patients with ACS.
Diagnosis of STEMI
Serial ECG and Additional imaging might be needed.
Localization of MI
Prognosis and success of reperfusion.
POOR prognosis indicators on ECG
Conduction problems ( LBBB and RBBB)
Q wave
Additional ST-depression ( Ischemia at distance)
6/13/2023 19
26. Proteins released from necrotic heart muscle after MI.
1) Cardiac troponin:- has three components; cTnT, cTnI and cTnC.
Detected after 3 hours of symptom onset & may persist for up to 7-
10days (cTnI) and 14days (cTnT).
A rise and/or fall of cTn with at least one cutoff values >99th
percentile of the upper reference limit (the highest value seen in
99% of a reference population not suffering from MI)
Serial cTn values (repeat after 3-6 hr) helps to quantify the
magnitude of changes (δ) in cTn values, obtained by serial
measurement (20%)
6/13/2023 26
27. 2. Creatinine Kinase
CK rises within 4–8 h and generally returns to normal by 48–72 h
lacks specificity for MI
used for early timing and detection of reinfarction
CK-MB has the advantage over total CK and more specific
For diagnosis, Cutoff values, in a rise/fall pattern above 99 percentile for
a given sex-specific reference level for two consecutive samples
A ratio of CK-MB mass to CK activity ≥2.5 suggests the source is
myocardial rather than a skeletal muscle
6/13/2023 27
31. General outlines of therapy
Treatment at the time of onset of STEMI
Pre-hospital care
Diagnosis and management at ER
Reperfusion therapy
In-hospital management
Medications
Device and surgical therapy
31
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32. General measures
Admission:- ICU, Coronary care unit with ECG monitoring
Activity:- bed rest for the first 6–12 h
Diet:-either NPO or only clear liquids by mouth for the first 4–12 hr.
Bowel management:- high fiber diet, stool softener
Oxygen therapy:- SpO2 < 90%(2-4 L/min for 6-12hs)
Sedation
6/13/2023 32
33. Antiplatelet:- ASA, Clopidogrel
Anticoagulants:- UFH or enoxaparin, Warfarin (extensive
anteroseptal AMI, mural thrombus, low LVEF)
Reperfusion therapy:- fibronolysis; PCI,CABG
Control of cardiac discomfort
Nitroglycerine 0.4 mg SL every 5 min up to 3 doses
Morphine 2-4mg every 5 minutes
Beta blocker(Metoprolol 5mg IV every 2-5min max 3 doses
followed by 50 mg po every 6hr for 48 hrs followed by
100mg every 12 hrs
6/13/2023 33
35. While the central zone of the infarct contains necrotic tissue that is
irretrievably lost, the fate of the surrounding ischemic myocardium
(ischemic penumbra) may be improved by
• timely restoration of coronary perfusion
• reduction of myocardial O2 demands
• prevention of the accumulation of noxious metabolites
• blunting of the impact of mediators of reperfusion injury (e.g., calcium
overload and oxygen-derived free radicals).
Spontaneous recanalization occurs in up to 1/3rd of patients
beginning at 12 to 24 hours.
6/13/2023 35
38. I. Primary PCI
Angioplasty and/or stenting without preceding fibrinolysis
advantage of being applicable to patients who have contraindications
to fibrinolytic therapy
more effective than fibrinolysis in opening occluded coronary arteries.
Compared with fibrinolysis, primary PCI is generally preferred when
the diagnosis is in doubt
cardiogenic shock is present
bleeding risk is increased
symptoms have been present for at least 2–3 h when the clot is more
mature and less easily lysed by fibrinolytic drugs.
6/13/2023 38
39. II. Rescue PCI
◦ PCI after failed or persistent severe stenosis following fibrinolysis
◦ Early invasive angiography and revascularization has shown to decrease
mortality, MI recurrence and HF in patients with failed fibrinolysis.
III. Delayed Angiography and PCI
◦ Patients with previous fibrinolysis are candidates for angiography
39
6/13/2023
42. If no contraindications are present fibrinolytic therapy should ideally
be initiated within 30 min of presentation.
The principal goal of fibrinolysis is prompt restoration of full
coronary arterial patency.
The fibrinolytic agents are tenecteplase (TNK), reteplase (rPA),
tissue plasminogen activator (tPA), streptokinase.
All act by promoting the conversion of plasminogen to plasmin,
which subsequently lyses fibrin thrombi
6/13/2023 42
46. Indications
In patients with STEMI and coronary anatomy not amenable to PCI who
have ongoing or recurrent ischemia, cardiogenic shock, severe HF, or
other high-risk features (left main disease) (Class IB)
MI-related complications: VSD, MR (At the time of repair) (Class IB)
Emergency CABG ( 24 – 48 hours) has higher mortality
Patients with hemodynamic deterioration or who are at high risk of
recurrent ischemic events should be operated on without waiting for the
full recovery of platelet function following discontinuation of DAPT.
For all other patients, a waiting period of 3–7 days may be the best
compromise
46
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47. I. TIMI grade flow:- Describes flow in the infarct artery, By 60-90min.
II. TIMI Frame count:- Qualitative information
III. ECG:- Resolution of STE has high PPV for reperfusion. (90%)
47
6/13/2023
Failed reperfusion:-
Resolution of STE by <50% in the worst lead at 60-90min,
persistent chest pain and absence of reperfusion arrhythmia by
2 hours. Consider rescue PCI.
Coronary artery re occlusion
Re-elevation of ST segments and/or recurrent chest pain or
the development of recurrent ischemia
50. 1) Antithrombotic therapy
◦ primary goal- to maintain patency of the infarct-related artery.
◦ Secondary goal- to reduce the tendency to thrombosis
Patients with anterior MI, LVEF<30%, history of embolism,
evidence of mural thrombus or aneurysm, atrial fibrillation, heart
failure should receive full therapeutic levels of anticoagulant
therapy (LMWH or UFH) while hospitalized, followed by at least
3 months of warfarin therapy.
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52. The benefits of beta blockers in patients with STEMI can be
divided into those that occur immediately when the drug is given
acutely and those that occur over the long term when the drug is
given for secondary prevention after an infarction.
The chronic routine use of oral beta–adrenoceptor blockers for at
least 2 years after STEMI is supported.
Patients with initial contraindications to the use of beta blockers in
the first 24 hours after STEMI should be reevaluated to determine
their subsequent eligibility.
6/13/2023 52
54. Class I
An ACE inhibitors should be administered within the first 24
hours to all patients with STEMI with anterior location, HF and
LVEF40% (LOE A)
An angiotensin receptor blocker (ARB) should be given to
patients with STEMI who have indications for but are intolerant
of ACE inhibitors. (LOE B)
An aldosterone antagonist should be given to patients with
STEMI and no contraindications who are already receiving an
ACE inhibitor and beta blocker and who have LVEF 40% and
either symptomatic HF or diabetes mellitus. (LOE B)
6/13/2023 54
55. Treatment with statins in patients stabilized after an ACS,
including STEMI, lowers the risk of coronary heart disease
death, recurrent MI, stroke, and the need for coronary
revascularization.
Class I
High-intensity statin therapy should be initiated or continued in
all patients with STEMI and no contraindications to its use.
(LOE B)
6/13/2023 55
57. The prognosis in STEMI is largely related to the occurrence
of two general classes of complications:
1. electrical complications (arrhythmias)
2. mechanical complications (“pump failure”).
Early Complication (<1 Week)
Late Complications(>1 Week Post-MI)
6/13/2023 57
65. The onset of cardiogenic shock due to mechanical complications
after STEMI is bimodal; most cases occur within 24 hours
When the abnormally contracting segment is
>15% of the myocardium, the EF may decline
>25% of the myocardium Clinical HF accompanies
>40% of the LV myocardium usually leads to
cardiogenic shock, often fatal.
6/13/2023 65
67. Killip classification of heart failure in STEMI
Class I:- no signs of pulmonary or venous congestion (0-5% )
Class II:- moderate heart failure (rales at the ,S3 gallop, tachypnea
raised JVP & hepatic congestion. (m- 10-20% )
Class III:- severe heart failure with pulmonary edema. (35-54%)
Class IV:- shock with systolic pressure <90 mmH and
evidence of peripheral vasoconstriction, peripheral
cyanosis, mental confusion, and oliguria. (85–95%)
6/13/2023 67
69. RV infarction complicates the course of approximately one third of
patients with inferior STEMI, is most often due to proximal
occlusion of the right coronary artery, and is associated with a
higher mortality risk.
The clinical triad are- hypotension, clear lung fields, and elevated
jugular venous pressure is characteristic
Treatment includes maintenance of RV preload, reduction of RV
afterload, inotropic support if needed, and immediate reperfusion.
Nitrates and diuretics should be avoided.
Restoration of atrioventricular (AV) synchrony or cardioversion
from AF may be needed.
6/13/2023 69
70. Class I
1) Anticoagulant therapy with a vitamin K antagonist should be
provided to patients with STEMI and AF with CHADS2 score 2,
mechanical heart valves, venous thromboembolism, or
hypercoagulable disorder. (LOE C)
2) The duration of triple antithrombotic therapy with a
vitamin K antagonist, aspirin, and a P2Y12 receptor
inhibitor should be minimized to the extent possible
to limit the risk of bleeding. (LEO C)
Complicates STEMI in ~10% of cases contribute to death in 25%
of patients with STEMI who die after admission to the hospital.
6/13/2023 70
71. Class I
1) Aspirin is recommended for treatment of pericarditis after
STEMI.(LOE: B)
Early Infarct-associated Pericarditis
Late or Post-cardiac Injury Pericarditis (Dressler Syndrome)
Aspirin at 650 mg orally as often as every 4 hours may be
necessary. NSAIDs and steroids should be avoided because they
may interfere with myocardial scar formation.
Anticoagulation should be avoided.
6/13/2023 71
72. Early risk stratification
I. GRACE risk model:
8 independent estimating factors &
their summation predicts in hospital
mortality & 6month mortality after ACS
Grace score 108 or less low risk
Grace score 109-140 intermediate risk
Grace score 140 or more high risk
6/13/2023 72
1. Age
2. Killip class
3. Systolic blood
pressure
4. Presence of ST-
segment deviation
5. Cardiac arrest during
presentation
6. Serum creatinine
concentration
7. Elevated serum
cardiac biomarkers
8. Heart rate
73. II. TIMI risk score: 8 components predicts 30 day mortality
6/13/2023 73
74. Atypical clinical presentation of AMI:- most of the time the
diagnosis is missed and delayed, so be cautious in such cases.
ECG and STEMI diagnosis:-In some cases, patients may have
coronary artery occlusion/global ischemia in the absence of
characteristic ST elevation, in such patients with clinical presentation
compatible with ongoing myocardial ischemia, a primary PCI
strategy should be followed.
6/13/2023 74
75. 1. Harrison principle of internal medicine 21st edition
2. Braunwalds heart disease 12th edition
3. 2017 ESC Guidelines for the management of acute myocardial
infarction in patients presenting with ST-segment elevation
4. 2013 ACCF/AHA Guideline for the Management of ST-Elevation
Myocardial Infarction
5. Uptodate 2023
6/13/2023 75
MI occurs when the heart tissue dies as a result of a lack of blood flow
STEMI diagnosed in the presence of positive cardiac biomarkers, ST segment elevation and symptoms of ischemia
Among unselected patients presenting with acute chest pain to the emergency department, disease prevalence can be expected to be the following: 5-10% STEMI, 15-20% NSTEMI, 10% unstable angina, 15% other cardiac conditions, and 50% non-cardiac diseases.
The incidence of NSTEMI is rising due to the increasing burden of obesity, diabetes, and chronic kidney disease in an aging population and the Increasing detection of myocardial necrosis by troponin whereas the incidence of STEMI is declining due to greater use of aspirin, statins, and less smoking.
European Society of Cardiology/ACCF/AHA/World Heart Federation Task Force for the Universal Definition of Myocardial Infarction
Type 1 Vs 2: Type 1 has athero-thrombus
Type 2 Vs Myocardial Injury may coexist
Acute MI requires a rising and/or falling pattern of cTn values but in non-ischemic myocardial injury cTn values may be stable and unchanging.
Type 3 MI is diagnosed and a subsequent autopsy reveals recent evidence of an MI, with a fresh or recent thrombus in the infarct-related artery, the type 3 MI should be reclassified to a type 1 MI.
Type 4a: no symptoms of ischemia in defn.
Type 4b: same defn. as type 1 but with stent/scaffold
Type 4c: same defn. as type 1 but with in-stent restenosis, or restenosis following balloon angioplasty in the infarct territory
Type 5: no ischemic symptoms or ECG changes except Q waves
These risk factors(novel) are important for 3 reasons. 1. Ability to accurately predict the CVD risk of a specific individual based on his or her conventional risk factor profile is limited. 2. The risk prediction using conventional risk factors may not always be accurate as it is not possible to explain all myocardial infarctions. It has been found that only around 50% case of acute coronary events can be explained with these conventional risk factors.
3. The risk of CVD varies among different ethnic groups, and novel risk factors may partly explain this variation.
Approximate Time of Onset of Key Events in Ischemic Cardiac Myocytes FEATURE TIME
Onset of ATP depletion Seconds
Loss of contractility <2 min
ATP reduced to
50% of normal 10 minto
10% of normal 40 min
Irreversible cell injury 20–40 min
Microvascular injury >1 hr
The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of the disrupted plaque Factors VII and X are activated conversion of prothrombin to thrombin convertion of fibrinogen to fibrin. Fluid-phase and clot-bound thrombin autoamplification reaction
Myocardial damage depends on
The territory supplied by the affected vessel
Whether or not the vessel becomes totally occluded
The duration of coronary occlusion
The quantity of blood supplied by collateral vessels to the affected tissue
The demand for oxygen of the myocardium whose blood supply has been suddenly limited
inferior STEMI Associated with weakness, sweating, nausea, vomiting, epigastric pain Nausea and vomiting may occur, presumably because of activation of the vagal reflex or
stimulation of LV receptors as part of the Bezold-Jarisch reflex(bradycardia, hotn, apnea) No radiation to below umbilicus and trapezius
Appreance of arrhythmias
peripheral embolization
sudden unexplained hypotension
Signs of sympathetic activation: Pallor, Sweating,Tachycardia
Signs of vagal activation: Vomiting, Bradycardia
friction rubs can be heard within 24 hours or as late as 2 weeks after onset of infarction Delayed onset of the rub and the associated discomfort of pericarditis (as late as 3 months after infarction) characterizes the now rare post-MI (Dressler) syndrome. Signs of impaired myocardial function
Hypotension, oliguria, cold periphery
Narrow pulse pressure
Raised JVP, third heart sound
Lung Crepitation
Sign of tissue damage: Fever
Complications: Murmur, Pericardial rub
Elevation of the white blood cell count usually develops within 2 hours after the onset of chest pain, reaches a peak 2 to 4 days after infarction, and returns to normal in 1 week; the peak leukocyte count generally ranges between 12 and 15 × 103/mL but occasionally rises to as high as 20 × 103/mL in patients with large STEMI. The fall in HDL cholesterol after STEMI is greater than the fall in total cholestero
ECG is an integral part of the diagnostic workup of patients with suspected MI
Should be done within 10 min after first medical contact
reduce the time to diagnosis and treatment, and
can facilitate the triage of STEMI patients to hospitals with PCI capability
serial ECG acquisition can provide critical information, particularly if the ECG at initial presentation is non-diagnostic.
Serial or continuous ECG recordings may be helpful in determining reperfusion or reocclusion status.
Q wave on the ECG is more dependent on the volume of infarcted tissue rather than the transmurality of infarction. An initial Q wave or abnormal R wave develops over a period of several hours to days.
Within the first 1-2 weeks (or less), the ST segment gradually returns to the isoelectric baseline, the R wave amplitude becomes markedly reduced, and the Q wave deepens.
In addition, the T wave becomes inverted.
Patients with an abnormal R wave in V1 (0.04 second in duration and/or R/S ratio ≥1 in the absence of preexcitation or RV hypertrophy) and
inferior or lateral Q waves have an increased incidence of isolated occlusion of a dominant left circumflex coronary artery without collateral circulation ST-segment elevations in aVR, reflecting the basal intraventricular septum, can be observed in up to 30% of STEMIs and identifies patients with a higher likelihood of left main coronary artery or multivessel disease and worse outcomes.
Cardiac troponin levels rise to about 20–50 times the upper reference limit in patients who have a “classic” acute myocardial infarction (MI) Acute Myocardial Infarction ♠ Burns
♠ Myocarditis and Myopericarditis ♠ Sepsis
♠ Pulmonary Embolism ♠ Renal Failure
♠ Acute CNS Event ♠ Rhabdomyolysis
♠ Sympathomimetic Ingestions ♠ Shock
♠ Congenital Coronary Anomalies ♠ Cardiomyopathies
♠ Extreme Physical Exertion
♠ Acute Congestive Failure (Pulmonary Edema)
Detection of a rise and fall in cTnT or cTnI in the appropriate clinical setting is the cornerstone of the diagnostic criteria for MI
The rise in B type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) after STEMI correlates with infarct size and regional wall motion abnormalities
Troponin T vs I – both equivalent in diagnostic and prognostic abilities ( except in renal failure – Trop T less sensitive)
detected by highly specific monoclonal Abs.
If the cTn concentrations are elevated but stable or declining at the time of the recurrent symptoms, then an elevation of greater than 20% indicates a reinfarction Measuring concurrent CKMB may help identify early reinfarction because CKMB levels decline much faster than cTn.
Radionuclide imaging
Myocardial perfusion imaging with [201Tl] or [99mTc]-sestamibi
reveals a defect (“cold spot”) in transmural infarct.
It cannot distinguish acute infarcts from chronic scars
Radionuclide ventriculography, with [99mTc]-labeled RBC shows
wall motion disorders
reduction in the ventricular ejection fraction
High-resolution cardiac MRI
late enhancement (gadolinium) is administered and images are obtained after a 10-min delay shows bright signal in areas of infarction
foods that are high in K, Mg, and fiber, but low in Na Management of Diabetes mellitus and hypertriglyceridemia
Bed rest + narcotics => constipation
Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A2 levels is achieved by buccal absorption of a chewed 160–325-mg tablet in the emergency department.
In addition to diminishing or abolishing chest discomfort, nitroglycerin may be capable of both decreasing myocardial oxygen demand (by lowering preload) and increasing myocardial oxygen supply (by dilating infarct-related coronary vessels or collateral vessels).
Morphine also has a vagotonic effect and may cause bradycardia or advanced degrees of heart block, particularly in patients with inferior infarction.
Oral beta blocker therapy should be initiated in the first 24 h for patients who do not have any of the following: (1) signs of heart failure, (2) evidence of a low-output state, (3) increased risk for cardiogenic shock, or (4) other relative contraindications to beta blockade (PR interval >0.24 s, second- or third-degree heart block, active asthma, or reactive airway disease)
provided the patient has a heart rate >60 beats/min, systolic pressure >100 mmHg, a PR interval <0.24 s, and rales that are no higher than 10 cm up from the diaphragm. The addition of the P2Y12 inhibitor clopidogrel to background treatment with aspirin to STEMI patients reduces the risk of clinical events (death, reinfarction, stroke) and, in patients receiving fibrinolytic therapy, has been shown to prevent reocclusion of a successfully reperfused infarct artery
# Protection of the ischemic myocardium by…
# Glucocorticoids and nonsteroidal anti-inflammatory agents, with the exception of aspirin, should be avoided in patients with STEMI.
They can impair infarct healing and
increase the risk of myocardial rupture, and
their use may result in a larger infarct scar. In addition,
they can increase coronary vascular resistance, thereby potentially reducing flow to ischemic myocardium.
Compared with fibrinolytic therapy, primary PCI produces
higher rates of infarct artery patency
higher TIMI 3 flow, and access site bleeding
lower rates of recurrent ischemia, reinfarction
Lower emergency repeat revascularization procedures, intracranial hemorrhage (ICH), and death
primary PCI is generally preferred when the diagnosis is in doubt, cardiogenic shock is present, bleeding risk is increased, or symptoms have been present for at least 2–3 h when the clot is more mature and less easily lysed by fibrinolytic drugs.
(bare-metal stent [BMS] drug-eluting stent [DES])
BMS should be used in patients with high bleeding risk, inability to comply with 1 year of dual antiplatelet therapy (DAPT), or anticipated invasive or surgical procedures in the next year.
These drugs all act by promoting the conversion of plasminogen to plasmin, which subsequently lyses fibrin thrombi.
fibrin-specific agents, such as tPA, and non-fibrin-specific agents, such as streptokinase
When assessed angiographically, flow in the culprit coronary artery is described by a simple qualitative scale called the Thrombolysis in Myocardial Infarction (TIMI) grading system: grade 0 indicates complete occlusion of the infarct-related artery; grade 1 indicates some penetration of the contrast material beyond the point of obstruction, but without perfusion of the distal coronary bed; grade2 indicates perfusion of the entire infarct vessel into the distal bed, but with flow that is delayed compared with that of a normal artery; and grade 3 indicates full perfusion of the infarct vessel with normal flow.
tPA and the other relatively fibrin-specific plasminogen activators, rPA and TNK, are more effective than streptokinase at restoring full perfusion
The current recommended regimen of tPA consists of a 15mg bolus followed by 50 mg intravenously over the first 30 min, followed by 35 mg over the next 60 min.
Streptokinase is administered as 1.5 million units (MU) intravenously over 1 h.
rPA is administered in a double-bolus regimen consisting of a 10-MU bolus given over 2–3 min, followed by a second 10-MU bolus 30 min later
Waiting period of 3–7 days may be the best compromise (at least 3 days following interruption of ticagrelor, 5 days for clopidogrel, and 7 days for prasugrel), while it is recommended that aspirin is continued. The first aspirin administration post-CABG is recommended 6–24 h after surgery in the absence of ongoing bleeding events.
Emergency CABG ( 24 – 48 hours) has higher mortality
Patients with hemodynamic deterioration or who are at high risk of recurrent ischemic events (i.e. patients with a large area of myocardium at jeopardy due to critical coronary stenosis or recurrent ischemia) should be operated on without waiting for the full recovery of platelet function following discontinuation of DAPT.
For all other patients, a waiting period of 3–7 days may be the best compromise
Mortality steadily increases as TIMI flow grade decreases
Persistent STE may show high risk of LV dysfunction and mortality.
Thrombolysis in Myocardial Infarction (TIMI) grading system:
Grade 0 complete occlusion of the infarct-related artery;
Grade 1 some penetration of the contrast material beyond the point of obstruction, but without perfusion of the distal coronary bed;
Grade 2 perfusion of the entire infarct vessel into the distal bed, but with flow that is delayed compared with that of a normal artery; and
Grade 3 full perfusion of the infarct vessel with normal flow.
Inhibitors of the P2Y 12 ADP receptor
reduces the risk of clinical events (death, reinfarction, stroke)
prevent reocclusion of a successfully reperfused infarct artery.
prasugrel and ticagrelor, are more effective than clopidogrel in preventing ischemic complications in STEMI patients undergoing PCI
Glycoprotein IIb/IIIa receptor inhibitors
for preventing thrombotic complications in patients with STEMI undergoing PCI
primary goal- to maintain patency of the infarct-related artery.
10% of restoring TIMI grade 3 flow
Secondary goal- to reduce the tendency to thrombosis
(mural thrombus and deep venous thrombosis).
Figure 3 Algorithm for DAPT in patients with coronary artery disease. ACS = acute coronary syndrome, BMS = bare-metal stent; BRS = bioresorbable vascular scaffold; CABG = Coronary artery
bypass graft; DCB = drug-coated balloon; DES: drug-eluting stent; PCI = percutaneous coronary intervention; Stable CAD = stable coronary artery disease.
High bleeding risk is considered as an increased risk of spontaneous bleeding during DAPT (e.g. PRECISE-DAPT score >_25).
Colour-coding refers to the ESC Classes of Recommendations (green = Class I; yellow = Class IIa; orange = Class IIb).
Treatments presented within the same line are sorted in alphabetic order, no preferential recommendation unless clearly stated otherwise.
1: After PCI with DCB 6 months. DAPT should be considered (Class IIa B).
2: If patient presents with Stable CAD or, in case of ACS, is not eligible for a treatment with prasugrel or ticagrelor.
3: If patient is not eligible for a treatment with prasugrel or ticagrelor.
4: If patient is not eligible for a treatment with ticagrelor.
ACE inhibitors reduce the mortality rate after STEMI, and the mortality benefits are additive to those achieved with aspirin and beta blockers.
The maximum benefit is seen in high-risk patients (those who are elderly or who have an anterior infarction, a prior infarction, and/or globally depressed LV function), but evidence suggests that a short-term benefit occurs when ACE inhibitors are prescribed unselectively to all hemodynamically stable patients with STEMI (i.e., those with a systolic pressure >100 mmHg). Duration is indefinitely
This difference is related to the fact that heart block in inferior infarction is commonly a result of increased vagal tone and/ or the release of adenosine and therefore is transient. In anterior wall infarction, however, heart block is usually related to ischemic malfunction of the conduction system, which is commonly associated with extensive myocardial necrosis.
First-degree AV block does not require treatment
Highgrade AV block with inferior/posterior STEMI usually is transient and associated with a narrow complex/junctional escape rhythm that can be managed conservatively
Atropine 0.5mg-1mg every 5 minute max 3mg
Prophylactic placement of a temporary pacing system is recommended for high-grade AV block and/or new bundle-branch (especially LBBB) or bifascicular block in patients with anterior/lateral MI
permanent pacing for persistent AV block or bundle-branch block after STEMI
Atrial Fibrillation
Is the most common supraventricular arrhythmia
Occurs in 8% to 22% of patients with STEMI
higher rates in elderly patients and those with HF and hypertension.
For those with pump failure, 15% of cases occur at time of presentation, and 85% develop during hospitalization
Class I patients have no rales and third heart sound (S3).
Class II patients have rales, but only to a mild to moderate degree (<50% of lung fields), and may or may not have an S3.
Class III patients have rales in more than half of each lung field and frequently have pulmonary edema.
Class IV patients have cardiogenic shock.
HF after STEMI is an indication for angiography with intent to proceed with revascularization if not previously performed.
Medical treatment is based on the use of diuretics, vasodilators, and inotropic agents when required, Inhibitors of the renin angiotensin-aldosterone system , and the indications for beta-blocker therapy should be evaluated continuously throughout the hospital course.
