AMI Flashcards
A 65-year-old hypertensive woman without CVRFs is admitted to ICU for suspected non-ST elevation myocardial infarction (Non-STEMI) based on chest discomfort, non-specific ECG changes and mildly elevated high-sensitivity troponin [48 ng/L (ULN <14 ng/L)]. She is on Vitamin K antagonists (VKA) for atrial fibrillation and the INR is 2.9. Her ventricular rate is poorly controlled (150/min) in the absence of signs of heart failure. Kidney function is normal. Echocardiography shows normal LV systolic function in the absence of regional wall motion abnormalities and a moderate LV hypertrophy.
Which ONE of the following statements are applicable to this patient?
Select one:
a.
The patient more likely to have a Takotsubo Syndrome
b.
These symptoms indicate unstable angina (UA) as the more likely diagnosis
c.
The patient more likely to have a Non-STEMI type 2.
d.
These symptoms strongly suggests that this patient be part of a subgroup referred to as MINOCA (MI with non-obstructive coronary arteries).
Incorrect!
e.
The patient more likely to have a Non-STEMI type 1
Takotsubo and UA are not a diagnostic consideration because of echocardiography findings and elevated high-sensitivity troponin respectively.
More likely this patient to have an Type2MI strongly related to atrial fibrillation with rapid ventricular rate and left ventricular hypertrophy. Type 2 MI, is defined as an MI driven by a myocardial oxygen supply and demand mismatch in the absence of coronary thrombosis. Therefore, the key features to diagnose a type 2 MI (more properly secondary ischaemic cardiac injury), can be summarised as follows:
An elevated but changing troponin value Clinical features inconsistent with type 1 acute MI Clinical conditions known to increase the oxygen demand or decrease the oxygen supply like tachycardia Potentially confounding clinical conditions or comorbidities that are potentially associated or known to be associated with myocardial injury Absence of symptoms and/or signs indicating other nonischemic causes of troponin elevations like myocarditis.
Is less likely to have a Type1MI or a Myocardial infarction with non-obstructive coronary arteries (MINOCA). Type 1 MI is characterized by atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequent myocardial necrosis. The patient may have underlying severe coronary artery disease (CAD) but, on occasion (i.e. 5–20% of cases), there may be non-obstructive coronary atherosclerosis or no angiographic evidence of CAD, particularly in women.
A patient with MINOCA meets diagnostic criteria for a classic myocardial infarction (MI), including rise and/or fall of troponin associated with one of the following: symptoms of myocardial ischemia, electrocardiographic changes consistent with ischemia (new ST changes or new left bundle branch block), new pathologic Q waves, loss of viable myocardium, or new wall motion abnormality, and identification of intracoronary thrombus by angiogram or autopsy. MINOCA is differentiated from a typical MI by angiographically proving normal or near normal coronary arteries.
A 64-year-old woman was admitted to Intensive Care Unit (ICU) with no prior history of cardiovascular disease who underwent open surgical repair of an abdominal aortic aneurism 48 h earlier. An increase in high-sensitivity troponin from 110 to 220 ng/L (ULN <14 ng/L) was observed within 24 h of surgery. The patient did not have chest pain but is receiving morphine. The ECG is normal. Her haemoglobin level is 8.5 g/dL. Echocardiography shows normal left ventricular (LV) function in the absence of regional wall motion abnormalities. Which statements are applicable to this scenario
A. This patient suffered a perioperative myocardial infarction (M) type 2
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B. Takotsubo cardiomyopathy can be included among the differential diagnoses
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C. Additional information regarding the intraoperative course (e.g. hypotension, major bleeding, arrhythmias) is necessary to differentiate Type 1 MI from Type 2 MI.
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D. Teamwork discussion with the surgeon is needed to assess the risks and benefits of early therapy in this patient
Answer
Type 2 myocardial infarction (T2MI) refers to myocardial necrosis caused by an imbalance in myocardial oxygen supply and demand and in the absence of acute coronary thrombosis.
T2MI requires detection of a rise and/or fall of cardio-troponin (cTn) values with at least one value above the 99th percentile URL, and evidence of an imbalance between myocardial oxygen supply and demand unrelated to coronary thrombosis, requiring at least one of the following:
Symptoms of acute myocardial ischaemia New ischaemic ECG changes Development of pathological Q waves Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology
Accordingly to guidelines, non-invasive testing should be performed to document myocardial ischaemia.
Takotsubo cardiomyopathy (TTC) is not a diagnostic consideration because echocardiographic findings. Echocardiography is a widely available, first-line, non-invasive imaging technique appropriate both in emergency setting to confirm diagnosis of TTC, assess for various potential acute complications, and in serial follow-up to track myocardial recovery. During the acute phase of TTC, trans-thoracic echocardiography (TTE) examination may detect a large area of dysfunctional myocardium usually extending beyond the territory of distribution of a single coronary artery. The pathophysiology of TTC is not well understood, but a sudden massive surge of catecholamines such as adrenaline and norepinephrine from extreme stress; either physical or emotional. There may be ECG changes mimicking a myocardial infarction and also modest elevation of Cardiac Troponin levels. Cardiac catheterization usually shows absence of significant coronary artery disease. The treatment of TTC is generally supportive in nature, and is dependent on whether patients experience heart failure or acute hypotension and shock. Despite the grave initial presentation in some of the patients, most of the patients survive the initial acute event and left ventricular function normalizes within next 4-12 weeks.
The patient in the case vignette has elevations of Cardiac Troponins which are consistent with myocardial injury. Peri-operative hypotension and cardiac arrhythmias may result in myocardial demand-supply mismatch and result in Type-2 MI. She was receiving peri-operative morphine, which may have suppressed the chest-pain symptoms. She had undergone a major vascular surgery which may represent a significant physical stress trigger for TTC. Teamwork between between intensivist, cardiologists and surgeons improves the individual patient’s clinical situation and procedures-related risks and provide the best treatment strategy.
Regarding acute coronary syndromes
A. Non-occlusive coronary thrombosis typically results in ST-segment depressions and/or T wave inversions
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B. Occlusive coronary thrombosis is typically responsible for ST-segment elevations
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C. The presence of pathologic Q waves reliably indicates the transmural involvement of myocardial infarction
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D. Q waves develop in approximately 75% of patients with ST-segment elevation myocardial infarction who do not undergo acute reperfusion interventions
Answer
Plaque rupture and plaque erosion are mechanisms that lead to coronary thrombosis and acute coronary syndromes. When the resulting intracoronary thrombus is only partially occlusive, ST-segment depressions or T wave inversions (or both) commonly develop. When the thrombus is completely occlusive, ST-segment elevations typically occur. In the latter setting, Q waves subsequently form in approximately 75% of patients who are not treated with fibrinolysis or acute mechanical coronary revascularization. In the remaining 25%, other ECG manifestations may develop, including reduction of the R wave height or notching of the QRS complex.
In the pre-fibrinolytic era, it was common to divide patients with myocardial infarction (MI) into those experiencing either a “Q wave MI” (now called “ST-segment elevation MI”) or a “non–Q wave” MI (now called “non–ST-segment elevation MI”) based on the evolution of the ECG over several days. Q wave infarction was considered to be synonymous with the pathology of a transmural infarction, whereas non–Q wave infarctions were considered to involve only the subendocardial layer. However, contemporary studies using cardiac magnetic resonance imaging indicate that the development of a Q wave on the ECG is determined more by the size of the infarct than the depth of mural involvement.
A patient is admitted to the hospital because of paroxysmal atrial fibrillation, which responds quickly to pharmacological cardioversion. During the tachycardia, the patient complained of a vague chest discomfort. In sinus rhythm he is completely asymptomatic and has a good exercise capacity. Yet, a mild troponin elevation is noted a few hours after sinus rhythm restoration. Which statements are applicable to this scenario?
A. Troponin elevation per se is not sufficient for the diagnosis of myocardial infarction (MI).
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B. In the presence of poorly controlled ventricular rate during atrial fibrillation, troponin elevation may be secondary to a myocardial oxygen supply/demand mismatch and may not be related to plaque rupture.
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C. Additional information is necessary to differentiate type 1 myocardial infarction (MI) from type 2 MI.
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D. Routine invasive management in patients with the mentioned presentation is indicated
Answer
Cardiac troponins are elevated in a significant proportion of patients with atrial fibrillation (AF) that predicts a worse outcome and greater cardio-embolic risk independently of the other known risk factors. Such elevation does not necessarily represent the expression of an ongoing acute coronary event.
This data is not conclusive about the meaning of troponin elevation in the setting of AF. Perhaps troponin increase is due to AF per se, or is caused by coexistent cardiovascular risk factors. Therefore investigations to detect ischaemia should be considered in patients with atrial fibrillation and elevated cardiac troponin levels.
Accordingly to recent guidelines, non-invasive testing should be first performed to document myocardial ischaemia.
Which ONE of the following describes a patient with a non-ST elevation myocardial infarction Type 1?
Select one:
a.
Acute onset rest angina with a normal ECG and elevated cardiac biomarkers
Correct!
b.
Rest angina with 2 mm ST elevation in leads V1-V4 and elevated cardiac biomarkers
c.
Exertional angina that is new onset with 1 mm ST depression in leads V5 and V6. Normal cardiac biomarkers
d.
Rest angina with 2 mm ST depression in the inferior leads and normal cardiac biomarkers
e.
Acute onset rest angina with 1 mm ST elevation in the inferior leads and normal cardiac biomarkers
A non-ST elevation myocardial infarction (Non-STEMI) is defined as anginal symptoms at rest that result in myocardial necrosis as identified by elevated cardiac biomarkers with no ST segment elevation on the 12-lead electrocardiogram. ECG changes may include transient ST-segment elevation, persistent or transient ST-segment depression, T-wave inversion, flat T waves or pseudo-normalization of T waves or the ECG may be normal.
The clinical spectrum of Non-STEMI may range from patients free of symptoms at presentation to individuals with ongoing ischaemia, electrical or haemodynamic instability or cardiac arrest. The pathological correlate at the myocardial level is cardiomyocyte necrosis (Non-STEMI) or, less frequently, myocardial ischaemia without cell loss (unstable angina).
Type 1 MI is characterized by atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequent myocardial necrosis. The patient may have underlying severe coronary artery disease (CAD) but, on occasion (i.e. 5–20% of cases), there may be non-obstructive coronary atherosclerosis or no angiographic evidence of CAD, particularly in women.
Type 2 MI is myocardial necrosis in which a condition other than coronary plaque instability contributes to an imbalance between myocardial oxygen supply and demand. Mechanisms include coronary artery spasm, coronary endothelial dysfunction, tachyarrhythmias, bradyarrhythmias, anaemia, respiratory failure, hypotension and severe hypertension. In addition, in critically ill patients and in patients undergoing major non-cardiac surgery, myocardial necrosis may be related to injurious effects of pharmacological agents and toxins.
The universal definition of MI also includes type 3 MI (MI resulting in death when biomarkers are not available) and type 4 and 5 MI (related to percutaneous coronary intervention [PCI] and coronary artery bypass grafting [CABG], respectively).
A 54-year-old patient with multiple cardiovascular risk factors (i.e. smoking, hypertension) presents with persistent severe typical retrosternal chest pain lasting for 1 h at the time of Emergency Room admission. He is haemodynamically stable and the initial physical examination is unremarkable. The 12-lead ECG shows no ST deviation while chest pain persists. What are the most important next diagnostic steps?
A. A second ECG recording shortly after (e.g. in 10 min)
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B. Await results of D-dimers and troponin measurements
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C. Recording of additional ECG leads (V7 – V9 and V3R and V4R)
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D. CT scan to exclude aortic dissection or pulmonary embolism
Answer
Recording additional leads (V7–V9 and V3R and V4R) and, if no ST elevations are detected, a second ECG recording in about 10 min is the most helpful step in this patient with suspected on-going myocardial ischemia. The use of additional leads may help detect acute MI, as approximately 50% of acute occlusions of the left circumflex artery may not cause ST-segment elevation in the standard 12-lead ECG.
In the presence of chest pain, ECG changes suggestive of an acute myocardial infarction include:
A. Saddle shaped ST segment elevations in all leads
Answer
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B. New left bundle branch block or complete heart block
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C. Deep T wave inversions in the anterior leads
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D. Ventricular tachycardia
Answer
Saddle shaped ST segment elevations are seen in pericarditis. They are often widespread. The ST elevations in myocardial infarction are dome shaped, and usually confined to specific leads reflecting the area of infarction. New onset left bundle branch block in a patient with chest-pain also strongly suggests acute MI. New complete heart block may be the presenting feature of a silent myocardial infarction. Deep symmetrical T wave inversions are seen in non-STEMI. An acute MI may present with ventricular tachycardia.
A 70-year-old man was brought urgently to the cardiac catheterization laboratory in the setting of an acute ST-elevation myocardial infarction. She had presented with chest pain and epigastric discomfort. His heart rate is 54 beats/min and his blood pressure 86/52 mm Hg with jugular venous distension. Coronary angiography demonstrated ostial occlusion of a dominant right coronary artery, without significant left-sided coronary artery disease.
A. Isolated infarction of the right ventricle, without left ventricular involvement, is likely
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B. The abnormal heart rate and blood pressure are likely a consequence of vagal stimulation
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C. ST-segment elevation is expected in lead V4R
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D. ST-segment elevation in leads V1 and V2 would be expected to accompany inferior ST elevation
Answer
Proximal occlusion of a dominant right coronary artery (RCA) leads to infarction of the left ventricular (LV) inferior wall, but often also involves the posterior wall, the right ventricle, and portions of the conduction system, which are all supplied by branches of the RCA. ST-segment elevation in leads II, III, and aVF is the sine qua non of infarction of the inferior wall. If the posterior wall is involved, ST-segment depression is usually evident in V1 and V2 reflecting a current of injury on the side of the heart opposite those leads. Very proximal occlusion of the RCA is often accompanied by right ventricular (RV) infarction because the RV arterial branch arises near the origin of that vessel.
If RV infarction is present, right-sided precordial electrocardiographic leads, particularly V4R, often demonstrate ST-segment elevation as well. ST elevation may also be seen in lead V1, which is the only standard precordial ECG lead that looks directly at the right ventricle.
Sinus bradycardia may occur, especially in inferior or posterior infarction. This arrhythmia, when accompanied by hypotension, may arise from stimulation of cardiac vagal afferent fibbers, which are present in the inferoposterior left ventricle. Sinus bradycardia may reflect ischemia of the sinoatrial artery, which arises from the RCA in 60% of the population.
Which of the following ECG patterns is consistent with those seen in the setting of non-ST elevation myocardial infarction?
Select one:
a.
Isolated T wave flattening or inversion
b.
Wellen’s phenomenon (biphasic or deeply inverted T waves in the anterior precordial leads)
c.
Down-sloping ST segment depression
d.
Normal ST segments and T waves
e.
All of the above
Changes on ECG in patients with NSTE-ACS include ST depression, transient ST-elevation, or new T-wave inversion. The ECG can be relatively normal or initially non-diagnostic; if this is the case, the ECG should be repeated (eg, at 15- to 30-minute intervals during the first hour), especially if symptoms recur. A normal ECG does not exclude ACS and occurs in 1% to 6% of such patients. A normal ECG may also be associated with left circumflex or right coronary artery occlusions, which can be electrically silent (in which case posterior electrocardiographic leads [V7 to V9] may be helpful).
Wellen’s phenomenon frequently indicates a significant stenosis in the proximal left anterior descending coronary artery.
Which ONE of the following statements describes a patient with a myocardial infarction that is Killip Class IV?
Select one:
a.
Pulmonary oedema. Arterial capillary pressure > 18 mmHg Cardiac Index > 2,2 l/min/m2
b.
Findings of mild to moderate heart failure (S3 gallop, rales < half-way up lung fields or elevated jugular venous pressure)
c.
Cardiogenic shock defined as systolic blood pressure < 90 mmHg and signs of hypoperfusion such as oliguria, cyanosis and sweating
Correct!
d.
No evidence of heart failure. Arterial capillary pressure < 15-18 mmHg Cardiac Index > 2,2 l/min/m2
e.
Hypotension and bradycardia in the evolution of a inferior STEMI
The Killip Classification is frequently used to predict mortality during STEMI. First published in 1967, this system focuses on physical examination and the development of heart failure to predict risk as described below:
Class I: No evidence of heart failure (mortality 6%) Class II: Findings of mild to moderate heart failure (S3 gallop, rales < half-way up lung fields or elevated jugular venous pressure (mortality 17%) Class III: Pulmonary oedema (mortality 38%) Class IV: Cardiogenic shock defined as systolic blood pressure < 90 mmHm and signs of hypoperfusion such as oliguria, cyanosis, and sweating. (Mortality 81%)
The original data from 1967 showed the above mortality rate in each class. This was before reperfusion therapy (thrombolytics and/or PCI). With advances in therapy, the mortality rates have declined about 30-50% in each class.
A 57-year-old man with a history of hypertension and elevated LDL cholesterol presents to the emergency room with the acute substernal chest pressure. His blood pressure is 159/95 mm Hg and the heart rate is 93 beats/min. The ECG shows sinus rhythm with a prominent R wave in lead V2, 0.5 mm of ST elevation in lead III, and 2 mm of horizontal ST depression in leads V1–V3. The following would be diagnostically useful to plan an immediate course of action.
A. A second 12 leads-ECG recording shortly after (e.g. in 10 min)
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B. Recording of additional ECG leads (V7 – V9 and V3R and V4R)
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C. Obtain a chest computed tomography (CT) to assess for pulmonary embolism
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D. Await results of serum cardiac biomarkers
Answer
The clinical presentation is concerning for an acute coronary syndrome and rapid evaluation of the ECG is critical to detect whether an acute ST-segment elevation myocardial infarction (STEMI) is present, which would warrant immediate coronary revascularization. The ECG in this patient is not diagnostic for STEMI, with <1 mm of ST elevation in only one lead (III). However, the presence of ST depressions and a prominent R wave in the anterior precordial leads should raise suspicion for an acute ST elevation myocardial infarction in the posterior territory. In this circumstance, posteriorly placed ECG leads (V7 –V9) placed from the posterior axillary line to the left border of the spine would be helpful to evaluate for true posterior ST elevations. A second ECG recording in about 10 min is helpful step in this patient with suspected on-going myocardial ischemia
Right-sided precordial leads are useful to detect right ventricular involvement in the setting of an inferior STEMI. Awaiting the results of cardiac biomarkers would delay care. Diagnostic tests should focus first on an acute coronary syndrome rather than pulmonary embolism, based on the presenting clinical symptoms.
A 68-year-old woman with a history of hypertension presents to the emergency department with dyspnoea and nausea. The electrocardiogram shows anterolateral ST-segment depressions, and the initial serum measurement of high-sensitive cardiac troponin T (hs-cTnT) is elevated. Regarding women who present with acute coronary syndromes (ACS)
A. Women with ACS are more likely to present earlier in the course of symptoms and are admitted to the hospital for the evaluation of chest pain less often than men
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B. Most women presenting with an acute myocardial infarction do not describe chest pain
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C. Women who present with chest discomfort are more likely than men to have non-atherosclerotic causes of ischemia, such as coronary vasospasm
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D. Women presenting with myocardial infarction are more likely than men to have accompanying cardiovascular comorbidities
Answer
With regard to men, women experiencing an acute coronary syndrome more frequently describe milder symptoms and are more likely to have “atypical” and often nonspecific symptoms, including dyspnoea, pain or discomfort in other body locations, nausea, or generalized weakness. Despite gender differences the vast majority of women with acute myocardial infarctions frequently report chest pain.1 In addition, women presenting with myocardial infarctions typically have more comorbidities (e.g., hypertension), and often present later in the course of symptoms than men. Women are hospitalized more frequently than men for the evaluation of chest pain, but women who present with chest discomfort are more likely to have a nonatherosclerotic cause of ischemia, including stress “takotsubo” cardiomyopathy, coronary vasospasm and spontaneous coronary artery dissection.
A 70-year-old patient with hypertension and hypercholesterolemia as cardiovascular risk factors (CVRFs) presents to the Emergency Room with typical chest pain, palpitations, ST depression on ECG and troponin rise. Regarding the underlying process
A. The underling process is definitely a rupture of a coronary atherosclerotic plaque with complete occlusive intracoronary thrombosis
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B. An extra-coronary condition may contribute to an imbalance between myocardial oxygen supply
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C. The patient described may have other cardiovascular conditions
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D. This may be due to other coronary aetiologies not associated with plaque instability
Answer
In contrast to ST elevation myocardial infarction (STEMI), where a totally occlusive intracoronary thrombosis is the paradigm at early angiography, patients with NonSTEMI have a relatively low prevalence of occlusive thrombosis. Transient coronary occlusion, increased vasoreactivity, microembolization, and platelet-mediated damage, alone or in combination, may have a particularly significant contribution to myocardial injury in NonSTEMI patients
According to the universal definition of myocardial infarction (MI), two main subtypes of Non-STelevation MI (Non-STEMI) have to be differentiated: type 1 MI, characterized by any of the processes of rupture, ulceration, fissuring or erosion of a coronary atherosclerotic plaque and type 2 MI, in which an extra-coronary condition contributes to an imbalance between myocardial oxygen supply and demand (e.g. tachycardia, anaemia or hypotension). Type 2 MI also includes two coronary aetiologies not associated with plaque instability: coronary spasm and coronary embolism. The patient described may have, among other conditions conditions, severe aortic stenosis or intermittent atrial fibrillation.
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A possible diagnosis of acute myocardial infarction should be considered in the following situations:
A. New onset of complete heart block
Answer
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B. Sudden severe left ventricular failure
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C. Sudden death
Answer
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D. Severe burning of epigastric pain
Answer
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All of these conditions can be presentations of acute MI. In the elderly, diabetics and patients in renal failure silent myocardial infarction can occur. These may present as left ventricular failure, or severe dysrhythmias. Epigastric burning pain mimicking ulcer disease represents an angina-equivalent symptom in some patients with Acute Coronary Syndrome.
A 65-year-old patient with multiple cardiovascular risk factors (CVRFs) presents to the emergency room with typical acute chest pain refractory to the administration of beta- blockers and sublingual nitrates. The pain started 2 h prior to admission, has lasted for a total of 3 h and is on-going. The first high-sensitivity cardiac troponin was slightly elevated while the ECG showed no frank ST elevation.
What is the most appropriate treatment in this case.
Select one:
a.
Pain control with morphine (iv or sc)
b.
Fibrinolytic therapy is indicated if cardiac catheterization is not immediately available
c.
Immediate coronary-angiography
d.
Intravenous nitrates substantially relieve chest pain
Incorrect!
e.
Dual antiplatelet therapy and anticoagulation should be initiated immediately
The patient has on-going ischemia refractory to initial treatment. According to the guidelines, he needs to undergo immediate coronary angiography. He may have occlusion of a main coronary artery (i.e. the left circumflex coronary artery) or a branch, which may be silent on 12-lead ECG. As a consequence, he is at risk of life-threatening arrhythmias and of deterioration of cardiac function.
Additional ECG leads (V7–V9 and V3R and V4R) may detect ST elevation. Visualization of regional wall motion abnormalities on transthoracic echocardiography (TTE), while not mandatory, is useful to reinforce the suspicion.
