Chapter 38, 39 Flashcards
1
Q
Which of the following is the characteristic of red thrombi?
A. lipid poor
B. happens in plaque erosion
C. Macrophage predominance
D. all of the above
A
C
2
Q
What is the primary goal in the management of STEMI?
A
Primary Percutaneous Coronary Intervention
To restore blood flow to the infarct zone quickly to prevent further loss of functioning myocytes.
3
Q
What is the preferred method of reperfusion therapy in STEMI?
A
Primary percutaneous coronary intervention (PCI) if performed promptly by an experienced team.
4
Q
Which of the following time from onset of ischemic symptoms to reperfusion is correctly matched?
A. total ischemic time should be kept <120 minutes
B. arrived at PCI-capable- 90 minutes door-balloon time
C. arrived at non-PCI-capable- door-to-needle time - 30 minutes or less
D. all of the above
A
D
5
Q
When is most deaths associated with STEMI happen?
A
within the first hour of its onset
cause: usually from ventricular fibrillation
6
Q
What is the outcome of prehospital fibrinolysis according to a meta-analysis?
A
17% mortality reduction
7
Q
What is the recommended door-to-needle time for initiation of fibrinolytic therapy?
A
30 minutes or less
8
Q
What is the recommended door-to-device time for percutaneous coronary perfusion?
A
90 minutes or less
9
Q
What is the benefit of morphine in STEMI management?
A
Improves pulmonary edema
It relieves pain and reduces the work of breathing by causing peripheral arterial and venous dilation.
Decreases HR- withdrawal of sympathetic tone and augmentation of vagal tone
10
Q
What should be avoided in patients with suspected right ventricular infarction?
A
Sublingual nitroglycerin.
11
Q
What are the contraindications for early IV beta blockers in STEMI patients?
A
- Heart failure
- Hypotension (systolic BP <90 mm Hg)
- Bradycardia (HR <60 beats/min)
- Significant atrioventricular block.
12
Q
When to start oxygen therapy in STEMI management?
A
Arterial hypoxemia (SaO2 <90%)
13
Q
What are the approaches to limit infarct size in STEMI?
A
- Early reperfusion
- Reduction of myocardial energy demands
- Manipulation of energy production sources
- Prevention of reperfusion injury.
14
Q
What is myocardial stunning?
A
A period of postischemic contractile dysfunction that occurs after successful reperfusion.
15
Q
What are the types of reperfusion injury?
A
- Lethal reperfusion injury
- Vascular reperfusion injury
- Stunned myocardium
- Reperfusion arrhythmias.
16
Q
What is remote ischemic conditioning (RIC)?
A
Transient ischemia produced in other vascular beds that may reduce reperfusion injury.
17
Q
How ofter is spontaneous recanalization of an occluded infarct-related artery happen?
A
Happens in 1/3 of patients
18
Q
What is the recommended initial dose of morphine for STEMI patients?
A
4 to 8 mg intravenously
then 2-8mg IV q5-15 minutes
contraindication: documented morphine hypersensitivity
19
Q
What is the role of beta-adrenergic blocking agents in STEMI management?
A
They aid in relief of ischemic pain and reduce infarct size and life-threatening arrhythmias.
20
Q
Fill in the blank: The American Heart Association (AHA) has initiated programs to improve STEMI care, focusing on reducing total _______ time.
A
ischemic.
<120 minutes
21
Q
True or False: The efficacy of fibrinolytic agents increases as coronary thrombi mature over time.
A
False.
22
Q
What is the primary tool for screening patients with possible acute coronary syndrome (ACS) for STEMI?
A
Initial 12-lead ECG.
23
Q
What is the effect of timing on the beneficial effects of interventions after reperfusion?
A
Beneficial effects decline rapidly after 45 to 60 minutes of reperfusion.
24
Q
What is the concept of remote ischemic conditioning (RIC)?
A
Transient ischemia in other vascular beds may reduce reperfusion injury.
25
What is postconditioning?
Introducing brief, repetitive episodes of ischemia alternating with reperfusion to activate cellular protective mechanisms.
26
What is a common transient arrhythmia seen in patients with inferior infarcts during acute reperfusion?
Transient sinus bradycardia.
27
What reflex may be activated during hypotension and bradycardia following reperfusion?
Bezold-Jarisch reflex.
28
What arrhythmias may follow successful reperfusion?
* Premature ventricular contractions (PVCs)
* Accelerated idioventricular rhythm
* Nonsustained VT
29
True or False: Rhythm disturbances after reperfusion always indicate inadequate coronary flow restoration.
False.
## Footnote
indicate reperfusion
30
When is the administration of a fibrinolytic indicated for STEMI?
If time from first medical contact to primary PCI is anticipated to exceed 120 minutes and within 12 hours of onset.
31
What is the formula for TIMI frame count measure?
21/ (observed TIMI frame count) x 1.7
32
What are the four major impediments to normalization of myocardial perfusion?
* Ischemia-related injury
* Reperfusion-related injury
* Distal embolization
* Individual susceptibility of the microcirculation to injury
33
What does electrocardiographic ST-segment resolution indicate?
High positive predictive value for infarct artery patency.
## Footnote
>90%
34
What is a poor predictor of infarct-related artery occlusion?
Persistent ST-segment elevation after reperfusion
## Footnote
>identifies patients with higher risk for LV Dysfunction and mortality (microvascular damage in the infarct zone)
35
What do defects in perfusion patterns seen with contrast-enhanced echocardiography correlate with?
Regional wall motion abnormalities and lack of myocardial viability on dobutamine stress echo
36
What is the TIMI myocardial perfusion (TMP) grade used for?
To assess myocardial perfusion abnormalities
>TMP angiographic method for assessing myocardial perfusion
>abnormalities correlate with unfavorable ventricular remodelling and risk for mortality (even after adjusting for TIMI frame count and TIMI grade flow)
37
What does the myocardial salvage index represent?
The difference between initial and final perfusion defects.
38
What is the most serious complication of fibrinolytic therapy?
Intracranial hemorrhage.
39
What does the Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group indicate about early IV fibrinolysis?
It improves survival in patients with STEMI.
40
What is the effect of fibrinolytic therapy on mortality in elderly patients?
Controversial, with increased risk for cardiac rupture.
41
What do fibrinolytic agents do?
Convert proenzyme plasminogen to active enzyme plasmin.
42
What is the recommendation for patients with ongoing ischemia but initially seen late (>12 hours)?
Better managed with PCI than fibrinolytic therapy.
43
What is the effect of heparin on mortality in STEMI patients?
Lower risk for reinfarction, pulmonary embolism, and stroke.
44
What is the recommendation for patients in cardiogenic shock regarding revascularization?
Immediate revascularization of the infarct artery is preferred.
45
What is the recommendation for patients with a prolonged time from the onset of symptoms to initiation of reperfusion therapy?
PCI is preferable, especially if seen 12 to 24 hours after symptom onset.
46
What should be done for patients who are not eligible for reperfusion therapy?
Aspirin and antithrombin therapy should be prescribed.
47
What is the rationale for administering anticoagulant therapy to STEMI patients?
To maintain patency of the infarct-related artery and prevent thromboembolic complications.
48
What is the definition of myocardial 'no-reflow'?
A state of reduced myocardial perfusion after reopening an epicardial artery.
49
What is the recommended strategy for patients with an increased risk for bleeding?
Favor a PCI-based reperfusion strategy.
50
What is the general mortality rate for urgent or emergency CABG within 24 to 48 hours of STEMI?
Between 12% and 15%.
51
What effect does heparin have on mortality in STEMI patients?
Heparin shows a lower risk for reinfarction, pulmonary embolism, and stroke in STEMI patients not treated with fibrinolytic therapy.
## Footnote
Evidence supports the administration of heparin for such patients.
52
What did the ISIS-2 trial conclude about aspirin in STEMI patients?
Aspirin alone significantly reduces mortality in STEMI patients.
## Footnote
The trial showed a reduction of 23% in mortality, additive to a 25% reduction from fibrinolytics.
53
What were the findings of the meta-analysis regarding heparin versus aspirin?
For every 1000 patients treated with heparin versus aspirin alone, there were five fewer deaths and three fewer recurrent infarctions, but three more major bleeding episodes occurred.
## Footnote
P = 0.03 indicates statistical significance.
54
What are the factors associated with major hemorrhagic events with heparin?
Major hemorrhagic events occur more frequently in patients with:
* Low body weight
* Advanced age
* Female sex
* Prolonged APTT (>90 to 100 seconds)
* Invasive procedures
## Footnote
Interpretation of APTT may be complicated by fibrinolytic therapy.
55
What is a disadvantage of heparin in treatment?
Heparin's disadvantages include:
* Dependency on antithrombin III
* Sensitivity to platelet factor 4
* Inability to inhibit clot-bound thrombin
* Marked interpatient variability
* Need for frequent APTT monitoring
## Footnote
These factors complicate its clinical use.
56
How do direct thrombin inhibitors compare to heparin in patients undergoing fibrinolysis?
Direct thrombin inhibitors like hirudin or bivalirudin reduce recurrent MI incidence by 25% to 30% compared with heparin, but do not reduce mortality.
## Footnote
They also cause higher major bleeding rates.
57
What was the outcome of the HORIZONS-AMI trial regarding bivalirudin?
Bivalirudin reduced the 30-day rate of major bleeding or major adverse CV events compared to heparin plus GP IIb/IIIa inhibitors.
>increased the early risk for stent thrombosis
## Footnote
It also reduced mortality at 30 days and 1 year.
58
What is the primary role of low-molecular-weight heparins (LMWH) in STEMI management?
LMWH serves as an adjunct to fibrinolytic therapy in STEMI management.
## Footnote
They do not improve early reperfusion rates but reduce reocclusion and reinfarction.
59
What did the ASSENT 3 trial find regarding enoxaparin in STEMI patients?
Enoxaparin reduced 30-day mortality and in-hospital reinfarction compared to UFH.
## Footnote
This was achieved with a 30-mg IV bolus followed by SC injections.
60
What did the OASIS-6 trial conclude about fondaparinux?
In patients with STEMI, particularly those not undergoing primary percutaneous coronary intervention, fondaparinux significantly reduces mortality and reinfarction without increasing bleeding and strokes.
## Footnote
It was evaluated as a specific factor Xa antagonist.
61
What is recommended for anticoagulant therapy during primary PCI?
UFH or bivalirudin is recommended, with a preference for bivalirudin for high-risk bleeding patients.
## Footnote
Fondaparinux is not recommended as the sole anticoagulant.
62
What is the suggested regimen for anticoagulation with fibrinolysis?
IV UFH bolus of 60 units/kg followed by infusion at 12 units/kg/hr for 48 hours, adjusted to maintain APTT at 1.5 to 2 times control.
## Footnote
Enoxaparin or fondaparinux is preferred when the administration of an anticoagulant for longer than 48 hours is planned in patients with STEMI treated with a fibrinolytic
This regimen is effective in fibrinolytic therapy.
63
What should be administered to patients treated with fondaparinux undergoing PCI?
Co-administration of an additional anti-thrombin agent with anti-factor IIa activity is required.
## Footnote
This is to mitigate the risk of catheter-related thrombosis.
64
What is the role of antiplatelet therapy in STEMI management?
Antiplatelet therapy is crucial for preventing thrombus formation in response to coronary artery plaque disruption.
## Footnote
Platelets play a major role in the early phase of thrombus formation.
65
What is the recommended initial aspirin dose for STEMI patients?
Patients should chew 162-325 mg of non-enteric-coated aspirin initially.
## Footnote
Afterward, the dose should be reduced to 75-162 mg for maintenance.
66
What did the TRITON-TIMI 38 trial reveal about prasugrel?
Prasugrel was superior to clopidogrel in reducing the risk of CV death, MI, or stroke in STEMI patients.
## Footnote
It showed a 32% reduction at 30 days.
67
What are the findings of the PLATO trial regarding ticagrelor?
Ticagrelor reduced the primary endpoint of CV death, recurrent MI, or stroke by 13% compared to clopidogrel.
## Footnote
It also resulted in a 26% reduction in stent thrombosis.
68
What are the implications of the CURRENT-OASIS 7 trial regarding aspirin dosing?
No difference in efficacy or safety was found between 81 mg and 325 mg doses of aspirin.
## Footnote
This informs optimal dosing strategies.
69
What is the management approach for STEMI patients in coronary care units?
Coronary care units enable continuous monitoring and immediate treatment of arrhythmias, improving patient outcomes.
## Footnote
Intermediate care telemetry units are also utilized for stable patients.
70
What should clinical staff address for STEMI patients regarding lifestyle?
Patient concerns about prognosis and lifestyle changes, particularly diet, should be addressed for secondary prevention.
## Footnote
This is part of general management measures.
71
How soon can stabilized STEMI patients begin physical activity?
Stabilized patients can be out of bed within 12 hours and use a bedside commode soon after admission.
## Footnote
Activity progression depends on clinical status.
72
What should be discontinued in patients with abnormal mental status?
Narcotics and beta blockers
## Footnote
Haloperidol can be used safely in STEMI patients if needed.
73
When can stabilized STEMI patients start mobilizing?
Within 12 hours of admission
## Footnote
Patients can use a bedside commode soon after if not hemodynamically compromised.
74
What are the benefits of early mobilization in STEMI patients?
Psychological and physical benefits with minimal medical risk
## Footnote
Vital signs should be monitored during early mobilization.
75
What are the immediate and long-term benefits of beta blockers for STEMI patients?
Reduce free fatty acids and improve secondary prevention
## Footnote
Elevated FFA levels can augment myocardial oxygen consumption.
76
What did early trials of beta blockers in acute MI suggest?
Benefits in reducing mortality, reinfarction, and cardiac arrest
## Footnote
These trials were conducted before reperfusion strategies.
77
What was the outcome of the COMMIT trial regarding metoprolol?
Reduced reinfarction and ventricular fibrillation episodes
## Footnote
There were more cardiogenic shock incidents in the metoprolol group.
78
What is the recommended timing for administering oral beta blockers to STEMI patients?
Within the first 24 hours
## Footnote
This is provided there are no contraindications.
79
Name some beta blockers favorable for STEMI treatment.
* Metoprolol
* Atenolol
* Carvedilol
* Timolol
* Alprenolol
## Footnote
Propranolol and esmolol are likely beneficial as well.
80
What are the major contraindications for ACE inhibitors in STEMI patients?
* Hypotension with adequate preload
* Hypersensitivity
* Pregnancy
## Footnote
Adverse reactions can include hypotension, cough, and angioedema.
81
What is the effect of ACE inhibitors in selective trials for STEMI patients?
26% reduction in the risk of death
## Footnote
Selective trials showed greater benefits with long-term therapy.
82
What was observed in the VALIANT trial regarding valsartan?
Mortality rates were similar among valsartan, valsartan plus captopril, and captopril alone
## Footnote
Combination therapy caused more adverse effects.
83
What is the role of nitrates in STEMI treatment?
Reduce ventricular filling pressure and improve coronary blood flow
## Footnote
Nitrates do not improve survival in STEMI patients.
84
What are the recommendations for nitroglycerin use in STEMI patients?
Indicated for persistent pain relief and as a vasodilator in LV failure or hypertension
## Footnote
Nitrates are not prescribed beyond 48 hours without angina or LV failure.
85
What are the potential risks of calcium channel antagonists in acute STEMI?
Increased mortality risk
## Footnote
Especially with short-acting dihydropyridines.
86
What should be monitored regarding magnesium levels in STEMI patients?
Maintain serum magnesium levels of 2 mEq/L or greater
## Footnote
A functional magnesium deficit may increase arrhythmia risk.
87
What is the recommended blood glucose level to maintain during STEMI?
Below 180 mg/dL
## Footnote
Avoid hypoglycemia; intensive insulin therapy is not routinely recommended.
88
What are the four major hemodynamic subsets identified in acute MI patients?
* Normal perfusion and no pulmonary congestion
* Normal perfusion with pulmonary congestion
* Decreased perfusion without pulmonary congestion
* Decreased perfusion with pulmonary congestion
89
What is the management recommendation for hypotension with bradycardia?
Atropine and reverse Trendelenburg position
## Footnote
Atropine should be given at 1 mg IV at intervals of 3-5 minutes.
90
What is indicated if a patient has a hyperdynamic state with elevated heart rate and blood pressure?
Beta blockers
## Footnote
This counters excessive sympathetic activation.
91
What does left ventricular dysfunction indicate in STEMI patients?
Critical predictor of mortality
## Footnote
It encompasses both systolic and diastolic dysfunction.
92
What is the recommended administration of IV fluids for suspected hypovolemia?
IV fluids at 3-5 mins interval up to 3 mg total
## Footnote
Reverse Trendelenburg position may also be employed.
93
What is indicated in a hyperdynamic state with elevated heart rate and normal or low LV filling pressure?
Beta blockers
## Footnote
This condition is often due to pain or anxiety.
94
What is a critical predictor of mortality after STEMI?
Left ventricular (LV) dysfunction
## Footnote
It includes both systolic and diastolic dysfunction.
95
What can cause pulmonary venous hypertension and congestion in STEMI patients?
LV diastolic dysfunction
## Footnote
Symptoms worsen as LV injury increases.
96
What are key predictors of symptomatic LV dysfunction or cardiogenic shock?
* Large infarct size
* Advanced age
* Dysglycemia
* Delays in revascularization
97
What is the initial management focus for high LV filling pressure and low cardiac index?
Reducing ventricular preload and afterload
## Footnote
Invasive monitoring can guide therapy.
98
How should hypoxemia in STEMI complicated by heart failure be managed?
Administer supplemental oxygen if SaO₂ is below 85-90%
## Footnote
Excessive oxygen can worsen ischemia.
99
What is the effect of intravenous furosemide in STEMI patients?
Reduces left ventricular (LV) wall tension and improves cardiac function
## Footnote
Administered in doses of 10 to 40 mg every 3-4 hours.
100
What are the goals of afterload reduction in STEMI patients with heart failure?
* Reduction of LV afterload
* Avoidance of excessive systemic arterial hypotension
* Avoidance of excessive reduction of ventricular filling pressure
101
What is the initial dosage of nitroglycerin in STEMI patients?
10 to 15 μg/min, with increments of 10 μg/min every 5 minutes
## Footnote
Adjust until improved hemodynamics or specific blood pressure goals are achieved.
102
What is recommended for long-term management of STEMI patients with persistent heart failure?
Inhibition of the renin-angiotensin-aldosterone system (RAAS)
## Footnote
This includes ACE inhibitors, ARBs, and aldosterone antagonists.
103
What benefits do SGLT2 inhibitors offer in patients post-MI?
Reduce hospitalizations for heart failure, cardiovascular death, and serious renal outcomes
## Footnote
They are beneficial regardless of diabetes status.
104
What is a primary use of digitalis in heart failure management?
To manage supraventricular tachyarrhythmias
## Footnote
Particularly when standard therapies fail.
105
What are the considerations for vasoactive medication in acute myocardial infarction?
Maintain cardiac output, blood pressure, and end-organ perfusion
## Footnote
Inotropic agents and vasopressors may be necessary.
106
What is the dose-dependent effect of dopamine?
* Low doses: stimulate dopaminergic receptors
* Moderate doses: activate beta1 receptors
* High doses: stimulate alpha1 receptors
107
What is a notable finding regarding norepinephrine in recent studies?
Recommended over dopamine for MI and shock patients
## Footnote
Especially except in cases of relative bradycardia.
108
What is the role of epinephrine in severe cases?
Used for refractory shock, anaphylaxis, or cardiac arrest
## Footnote
May lead to higher rates of return of spontaneous circulation.
109
What is a characteristic of milrinone?
A phosphodiesterase inhibitor with inotropic and vasodilating effects
## Footnote
Useful in cardiogenic shock without significant hypotension.
110
What is the primary action of vasopressin (ADH)?
Causes arterial smooth muscle contraction through V1 receptor agonism
## Footnote
Typically used for refractory vasodilatory shock.
111
What is a significant drawback of phenylephrine?
Causes potent vasoconstriction
## Footnote
Rarely used in cardiogenic shock due to this effect.
112
What is cardiogenic shock?
Cardiogenic shock is characterized by congestion and inadequate tissue or end-organ perfusion due to cardiac insufficiency, leading to decreased oxygen and nutrient delivery.
113
What percentage of cardiogenic shock cases following myocardial infarction (MI) result from left ventricular dysfunction?
About 80% of cardiogenic shock cases following MI result from left ventricular dysfunction.
114
What are the common histories of patients with cardiogenic shock complicating STEMI?
Patients often have a history of diabetes mellitus, previous MI, or heart failure.
115
What is the typical in-hospital mortality rate for patients with cardiogenic shock?
The in-hospital mortality rate remains high, at 30% to 50%.
116
List the criteria for diagnosing cardiogenic shock.
* Hypotension: Systolic BP below 80 or 90 mm Hg
* Inadequate cardiac index: Less than 1.8 liters/min/m² without support
* Elevated end-diastolic pressures
* End-organ hypoperfusion
117
True or False: Misestimated left ventricular end-diastolic pressure can occur in cases of marked mitral regurgitation.
True
118
What immediate evaluations are crucial for patients with cardiogenic shock?
Immediate hemodynamic, angiographic, and echocardiographic evaluations are crucial.
119
What agents are typically used in the medical management of cardiogenic shock?
Inotropic and vasopressor agents are used to maintain mean arterial pressure and enhance cardiac output.
120
What are the theoretical benefits of mechanical circulatory support (MCS)?
* Maintaining end-organ perfusion
* Reducing intracardiac filling pressures
* Decreasing left ventricular volumes
* Augmenting coronary perfusion
121
What does intra-aortic balloon (IAB) counterpulsation aim to improve in patients with cardiogenic shock?
IAB counterpulsation aims to reduce preload, increase coronary blood flow, and improve cardiac performance.
122
What did the largest randomized trial find regarding IAB counterpulsation in patients with cardiogenic shock?
The trial found no overall survival benefit in patients with cardiogenic shock secondary to myocardial infarction.
123
What is the role of percutaneous left ventricular assist devices (LVADs) in cardiogenic shock management?
They provide advanced temporary mechanical circulatory support but have not shown a proven survival benefit.
124
What are the complications associated with mechanical circulatory support (MCS)?
* Vascular damage
* Ischemia
* Thrombocytopenia
* Infection
* Mechanical failure
125
What did the SHOCK study assess regarding early revascularization for myocardial infarction complicated by cardiogenic shock?
It assessed the effects of early revascularization by CABG or angioplasty versus initial medical stabilization.
126
What does the CULPRIT-SHOCK trial highlight about revascularization in cardiogenic shock?
Infarct artery-only revascularization may be preferable in the context of cardiogenic shock.
127
What is the importance of multidisciplinary teams in managing cardiogenic shock?
They improve outcomes through a protocolized, team-based approach.
128
What are the clinical features of right ventricular (RV) infarction?
* Elevated right-sided heart filling pressures
* Normal or slightly raised left ventricular filling pressures
* Decreased RV systolic and pulse pressures
129
What is a key diagnostic feature of RV infarction?
Elevated RV filling pressures and ST-segment elevation in right precordial leads on ECG.
130
What medications should be avoided in RV infarction due to the risk of worsening hypotension?
Nitrates, morphine, and diuretics should be avoided.
131
What is the clinical course of free wall rupture?
It varies from catastrophic leading to tamponade and immediate death to subacute with symptoms like nausea and hypotension.
132
What is a pseudoaneurysm?
A pseudoaneurysm results from an incomplete rupture of the heart where organized thrombus and pericardium seal the rupture.
133
What imaging techniques can be used to diagnose pseudoaneurysms?
* Echocardiography
* Contrast-enhanced angiography
* Cardiac magnetic resonance (CMR)
* Computed tomography (CT)
134
What is the treatment approach for critically compromised hemodynamics due to free wall rupture?
Immediate surgical resection of the necrotic and ruptured myocardium with primary reconstruction is essential.
135
What are the risk factors for rupture of the interventricular septum?
* Lack of collateral network development
* Advanced age
* Female sex
* Chronic kidney disease
136
What is the clinical presentation of a new rupture of the interventricular septum?
A new, harsh, loud holosystolic murmur at the lower left sternal border, usually with a thrill.
137
What condition underlies the rupture of the ventricular septum?
Transmural infarction
## Footnote
Transmural infarction is a type of heart attack that affects the entire thickness of the heart muscle.
138
What are the characteristics of a ventricular septal rupture?
Rupture can range from one to several centimeters, can be a direct opening or irregular and serpiginous
## Footnote
Anterior infarctions typically result in apical ruptures, while inferior infarctions often cause basal septal perforations, which have a worse prognosis.
139
List risk factors for ventricular septal rupture.
* Lack of collateral network development
* Advanced age
* Female sex
* Chronic kidney disease
140
What is the clinical presentation of a ventricular septal rupture?
A new, harsh, loud holosystolic murmur at the lower left sternal border, usually with a thrill
## Footnote
Biventricular failure typically occurs within hours to days.
141
What diagnostic tool is used to visualize a ventricular septal rupture?
Echocardiography with Color Flow Doppler
## Footnote
It is used to visualize the defect.
142
What is the mortality rate associated with ventricular septal rupture?
40% to 75%
## Footnote
Survival depends on the degree of ventricular function impairment and the defect size.
143
What are the common treatment methods for a ventricular septal rupture?
* Surgical Repair
* Transcatheter Closure
144
What is a rare but often fatal complication of transmural MI?
Rupture of a Papillary Muscle
## Footnote
It can lead to sudden massive mitral regurgitation.
145
What are the types of papillary muscle rupture?
* Complete Transection
* Partial Rupture
146
Which papillary muscle is more frequently ruptured and why?
Posteromedial Papillary Muscle due to its singular blood supply
## Footnote
Often follows an inferior wall infarction.
147
What symptoms indicate a rupture of a papillary muscle?
Increasingly severe heart failure and holosystolic murmur
## Footnote
Murmur may be unimpressive or absent in cases of acute MR due to rapid equalization of pressures.
148
What is the role of transthoracic echo (TTE) in diagnosing papillary muscle rupture?
Can promptly recognize MR secondary to partial or complete rupture of a papillary muscle
149
Fill in the blank: Color Flow Doppler Echocardiography is used to distinguish between _______ and mitral regurgitation.
ventricular septal rupture
150
What is indicated by a 'step-up' in oxygen saturation during right-heart catheterization?
Ventricular Septal Rupture
## Footnote
Acute MR lacks this step-up but may show tall c-v waves in pulmonary capillary and pulmonary arterial pressure tracings.
151
What is the management approach upon recognizing a major mechanical complication of STEMI?
Invasive Monitoring
## Footnote
Vasodilator therapy and inotropic agents may also be used.
152
What is the recommended treatment for unstable VT or VF?
Rapid electrical cardioversion and possibly IV amiodarone
153
What factors increase the risk of ventricular arrhythmias during acute coronary occlusion?
Inhomogeneity in ischemic myocardium
## Footnote
VT or VF later in STEMI is associated with transmural infarction, LV dysfunction, and hemodynamic deterioration.
154
What is the prognosis for patients experiencing VT/VF after STEMI?
Higher mortality, particularly with late VT/VF
## Footnote
Adjusted mortality risk at 90 days is increased twofold for early VT/VF and sixfold for late VT/VF.
155
True or False: Sinus bradycardia is uncommon in early STEMI phases.
False
## Footnote
It is common, especially with inferior/posterior infarctions.
156
What management is recommended for isolated sinus bradycardia without hypotension?
Observe
## Footnote
Administer IV atropine if heart rate <40-50 beats/min with hypotension.
157
What is the main concern with beta blockers in patients with tachycardia due to pump failure?
They are contraindicated.
158
What is a common cause of sinus tachycardia in STEMI patients?
Augmented sympathetic activity
## Footnote
Common causes include anxiety, persistent pain, and LV failure.
159
What is the typical management for atrial flutter and fibrillation in STEMI?
Treat as in other settings, consider cardioversion if causing hypotension, ischemia, or heart failure
160
What are common complications following an MI?
* Recurrent Chest Discomfort
* Recurrent Ischemia and Reinfarction
161
What is a diagnostic challenge in distinguishing new myocardial infarction from extension of the initial necrosis?
Elevated cardiac markers from the initial event can complicate diagnosis
162
What is the benefit of primary PCI for STEMI compared to fibrinolysis?
Results in less post-infarction angina and reinfarction
163
What is the primary benefit of PCI for STEMI compared to fibrinolysis?
Less post-infarction angina and reinfarction.
## Footnote
Primary PCI offers a more effective strategy in managing STEMI outcomes.
164
How can high-risk patients treated with fibrinolysis benefit within 6 hours?
They show fewer ischemic complications when followed by subsequent PCI.
## Footnote
This highlights the importance of timely intervention.
165
What is the current rate of recurrent ischemic events due to improved stent designs and therapies?
Under 5%.
## Footnote
Advances in technology have significantly improved patient outcomes.
166
What complicates the diagnosis of myocardial infarction within 24 hours?
Elevated cardiac markers from the initial event.
## Footnote
This can lead to misinterpretation of subsequent symptoms.
167
What does dynamic ST-segment elevation suggest?
Recurrent infarction.
## Footnote
Monitoring ST-segment changes is crucial in acute settings.
168
What are angiographic predictors of reinfarction?
* Final coronary stenosis >30%
* PCI-related dissection or thrombus
* Multivessel disease
* Extensive stent length
## Footnote
These factors help assess the risk of future events.
169
What is linked to higher short-term morbidity and mortality post-infarction?
Post-infarction angina, whether persistent or intermittent.
## Footnote
This emphasizes the need for effective management strategies.
170
What is recommended for urgent catheterization in recurrent ST-segment elevation?
Unless pericarditis or other complications are confirmed.
## Footnote
Prompt intervention is critical in managing recurrent ischemia.
171
How are recurrent ischemia symptoms managed if there is no ST elevation?
With SL or IV nitroglycerin and IV beta blockers.
## Footnote
This approach addresses symptoms effectively while monitoring the patient.
172
When is pericardial effusion commonly observed?
anterior or lateral STEMI
larger infarcts
significant LV dysfunction
## Footnote
This condition can often resolve without significant intervention.
173
What are distinguishing features of pericarditis?
* Pain radiating to the trapezius ridge
* Worsened by deep inspiration
* Relieved by sitting up and leaning forward
## Footnote
Recognizing these symptoms aids in accurate diagnosis.
Transmural MI can cause acute fibrinous pericarditis.
174
What is the traditional treatment for pericarditis?
* High-dose aspirin (650 mg every 4 hours)
* Proton pump inhibitor
* Colchicine
## Footnote
NSAIDs and steroids are avoided within 4 weeks due to potential interference with healing
>anticoagulation is not an absolute contraindication (discontinue if PE 1 cm or more)
175
What is Dressler Syndrome?
Occurs 1 to 8 weeks post-MI with symptoms like malaise, fever, and pericardial discomfort.
## Footnote
This condition reflects an immune response after myocardial infarction.
Pericarditis can occur from first day to 8 weeks post STEMI
176
What is the incidence of pulmonary embolism in STEMI patients historically?
Historically, >20% of autopsied STEMI patients had PE.
## Footnote
Early mobilization and anticoagulation have significantly reduced this incidence.
177
What increases the mortality risk associated with left ventricular aneurysms?
Ventricular tachyarrhythmias and heart failure
## Footnote
Management includes prompt reperfusion to reduce aneurysm incidence.
178
What is the recommended duration of anticoagulation for patients with mural thrombi?
3 to 6 months
## Footnote
This helps reduce the risk of thrombus development
>LV thrombus form due to stasis and endocardial inflammation; early formation (48-72 hours = hihg mortality)
>15% in STEMI, 25% in anterior MI
>4x increased risk of embolic events
179
What are the key components of cardiac rehabilitation?
* Medical surveillance
* Nutritional counseling
* Hypertension and diabetes management
* Smoking cessation
* Psychosocial support
* Exercise training
## Footnote
Cardiac rehabilitation significantly improves patient outcomes.
180
What is the target LDL for patients with acute coronary syndrome?
Ideally <55 mg/dL
## Footnote
Managing lipid profiles is crucial for secondary prevention.
181
What is the preferred maintenance dose of aspirin for STEMI patients?
81 mg daily
## Footnote
Aspirin is recommended indefinitely unless contraindicated.
182
Which trial demonstrated the benefit of adding ezetimibe to statin therapy?
IMPROVE-IT Trial
## Footnote
This combination reduces recurrent cardiovascular events.
183
Name the Trial:
Tested whether encainide, flecainide, or moricizine suppressed ventricular arrhythmias detected on ambulatory electrocardiographic monitoring would reduce the risk for cardiac arrest and death
CAST trial
Cardiac Arrhythmia Suppression Trial
## Footnote
>increased mortality in the active treatment groups
>other trials: SWORD, CAMIAT, EMIAT- incerased mortality in the treatment group
184
Why NSAIDs should be avoided in post-STEMI patients?
They increase the risk of atherothrombotic events and should be avoided.
## Footnote
If necessary, use the lowest effective dose for the shortest time.
185
What is the mortality rate associated with cardiogenic shock post-STEMI?
Over 30%
## Footnote
This highlights the critical nature of managing cardiogenic shock effectively.
186
Identify
## Footnote
A. Plaque rupture of a necrotic core with an overlying thin-ruptured cap represents the most frequent pathophysiologic process leading to an acute coronary syndrome
B. Plaque erosion with a thrombus in direct contact with an intimal plaque that is rich in smooth muscle cells and proteoglycan matrix is shown.
C. The least common plaque morphology is the calcified nodule, which is a heavily calcified plaque with a surrounding area of fibrosis. There are breaks in the calcified plate of the plaque with bone formation and interspersed fibrin, with a disrupted fibrous cap and overlying thrombus. A calcified nodule as the basis of an acute coronary syndrome is more common in older men than in women or younger patients.
187
What are the causes of delay in seeking medical attention in STEMI?
older age,
female sex, black race, low socioeconomic or
uninsured status, history of angina or diabetes, and
consulting others before seeking help.
188
What is the drug of choice for analgesia in STEMI?
Morphine
## Footnote
>initial dose: 4-8 mg can be administered intravenously initially,
>followed by doses of 2-8 mg repeated at intervals of 5 to 15 minutes until the pain is relieved or side effects emerge—hypotension, depression of respiration, or vomiting
>contraindications to morphine: well- documented morphine
hypersensitivity
189
What does a persistent ST elevation signifies?
A. presence of LV thrombus
B. signifies LV aneurysm
C. indicates large infarct with RWMA
D. All of the above
C
190
Cause of LV aneurysm:
Total occlusion of a poorly collateralized LAD
## Footnote
Treatment: Surgical aneurysmectomy generally succeeds only if contractile performance in the nonaneurysmal portion of the left ventricle is relatively preserved
>residual LV aneurysm after STEMI may warrant long-term oral anticoagulation
191
What are the class I indications for PCI after fibrinolytic therapy?
Cardiogenic shock or acute heart failure that develops after initial evaluation (IB)
Intermediate -or high risk findings on predischarge non-invasive ischemia testing
Spontaneous or easily provoked myocardial ischemia
192
Dose of tenectelase:
<60kg
60-69kg
70-79kg
80-89kg
90kg up
<60kg- 30mg
60-69kg- 35mg
70-79kg- 40 mg
80-89kg- 45 mg
90kg up- 50 mg
193
Recommendation for PCI if fibrinolysis failed?
Rescue PCI
Class I
194
Recommendation for PCI if fibrinolysis is successful?
Early angiography
Class I
195
Based on the design of these 2 trials, when administered concurrently with fibrinolytic as the reperfusion strategy, clopidogrel is recommended to be administered with a loading dose (300 mg, then 75 mg daily) for patients <75 years of age and starting without a loading dose (75 mg daily) for patients <75 years of age.
CLARITY (Clopidogrel as Adjunctive Reperfu- sions Therapy)-TIMI 28 trial
COMMIT (Clopidogrel and Metoprolol in Myocardial Infarction Trial)
## Footnote
In patients treated with a fibrinolytic agent who are undergoing subsequent PCI, either clopidogrel or ticagrelor (age <75 years, within 24 hours after a fibrinolytic agent) or prasugrel (>24 hours after a fibrinolytic agent) are alternatives to support PCI.
196
Dosing of Parenteral Anticoagulation in ACS
197
Based on this trial, when bivalirudin is used to support PPCI for STEMI, a postprocedure 2- to 4-hour infusion at full dose is recommended.
BRIGHT-4 (Bivalirudin with Pro- longed Full-Dose Infusion during PPCI versus Heparin) trial
## Footnote
both NSTE-ACS and STEMI
standard bolus and dosing (0.75 mg/kg, then 1.75 mg/kg per hour) plus a post-PCI infusion at the full dose (1.75 mg/kg per hour) for 2 to 4 hours
198
Name the study:
Bivalirudin was noninferior to UFH plus glycoprotein IIb/IIIa inhibitor for the risk of MACE and superior with respect to 30-day major bleeding
(NSTEMI)
ACUITY (A Comparison of Angiomax Versus Heparin in Acute Coronary Syndromes) trial
199
Bivalirudin was compared against UFH alone.
No significant difference was observed between the 2 arms with respect to 30-day ischemic or bleeding events.
MATRIX (Minimizing Adverse Hemorrhagic Events by Transradial Access Site and Systemic Implementation of AngioX)
200
Name the trial:
An increase was observed in the rate of catheter-related thrombus with fondaparinux compared with enoxaparin (0.9% versus 0.4%)
OASIS-5 and 6 (The Safety and Efficacy of Fondaparinux versus Control Therapy in Patients with STEMI) trial
## Footnote
In patients with STEMI who are not likely to undergo an invasive approach, fondaparinux is an alternate anticoagulant that can be used.
201
