CONTENTS
- Approach to the deteriorating post-MI patient
- Retroperitoneal hematoma
- Re-infarction
- Post-MI pericarditis
- Mechanical complications
- Tachyarrhythmia
- Bradyarrhythmia
- Podcast
- Questions & discussion
- Pitfalls
differential diagnosis for deterioration s/p MI
- Reinfarction (e.g., in-stent thrombosis).📖
- Rupture:
- Post-MI Pericarditis (Post-cardiac injury syndrome).📖
- Hemorrhage (e.g., retroperitoneal hemorrhage 📖).
- Medication effect (e.g., beta-blockers, ACE-inhibitors, diuretics).
- Arrhythmia.
- Other complications:
- Pneumothorax.
- Aortic dissection.
- Pulmonary embolism.
- Infection (e.g., ventilator-associated pneumonia, line infection).
- Dynamic LV outflow tract obstruction (LVOTO).
investigation of delayed deterioration
- Review any recent interventions (e.g., medications, procedures).
- ECG (new ischemia?).
- Auscultation:
- ? New murmur (mitral regurgitation, VSD).
- ? Pericardial friction rub.
- Echocardiogram:
- ? Pericardial effusion (pericarditis, ventricular wall rupture).
- ? New mitral regurgitation.
- ? New aortic regurgitation (may suggest aortic dissection).
- ? Fall in ejection fraction or new wall motion abnormality (reinfarction, excess beta-blockers).
- ? Evidence of VSD (color doppler shows flow across septum).
- ? Hypovolemia (hemorrhage, over-diuresis).
- ? RV dilation (RV infarction, PE, VSD).
epidemiology
- One of the most common complications (~1/200 procedures).
- Only occurs with femoral access (#RadialFirst).
- Usually occurs very early following catheterization.
presentation
- Severe hemorrhage manifests with hypotension and/or shock.
- Pain may occur in the abdomen, back, or flank. Tenderness or fullness may be noted.
- Less severe hematoma may present in a delayed fashion, with falling hemoglobin and hematoma tracking over abdomen/flank.
- Can present as jaundice and abnormal liver function tests (elevated lactate dehydrogenase, AST, and unconjugated bilirubin)
differential diagnosis
- Bleeding elsewhere (e.g., gastrointestinal bleed due to anticoagulation).
- Vasovagal reaction.
- Other causes of shock. 📖
diagnostic tests
- CT angiogram – the study should be specifically protocoled to evaluate for active extravasation.
- Performing a non-angiogram CT scan has little or no value. Merely identifying the hemorrhage isn't helpful, as this doesn't guide the next step in management. (28707444)
treatment
- (1) Supportive measures should be instituted without delay:
- PRBC transfusion (type & cross-match, stay 2-4 units ahead).
- Interruption of anticoagulation (e.g., if patient on a heparin infusion). For hemorrhagic shock, anticoagulation reversal may be considered (although this must be weighed against the risk of coronary stent thrombosis).
- (2) Interventional management:
- Definitive control can generally be achieved by interventional radiology or interventional cardiology. Techniques will vary depending on the nature of the bleed, but may include coil embolization or placement of a covered stent.
- Perhaps the most important indication for intervention is ongoing extravasation of blood seen on CT scan.
- Most patients don't require interventional therapy. Rather, with conservative management most bleeds will tamponade eventually.
- (3) Vascular surgery?
- Theoretically this is a third-line treatment, if all else fails.
presentation
- Recurrent ischemic symptoms (e.g., anginal chest pain).
- In-stent thrombosis may cause severe transmural infarction.
differential diagnosis
- Type-II MI due to another aggravating factor (e.g., anemia, hemorrhage).
- Pericarditis.
- Pulmonary embolism.
diagnostic tests
- EKG may show new ischemic changes.
- Troponin may re-elevate, but this is often difficult to discern in the context of previously elevated troponin values.
- Echocardiography may reveal a new wall motion abnormality.
- The key is comparison to the last EKG and echocardiogram obtained:
- Some patients with poor reperfusion following their initial MI will have have persistent ST elevation (which may eventually evolve into an LV-aneurysm pattern on the EKG). This pattern of persistent ST elevation doesn't represent represent re-infarction.
treatment
- (a) In-stent thrombosis requires immediate repeat PCI.
- (b) Type-II MI may be treated in the usual fashion (e.g., beta-blocker to reduce myocardial oxygen demand, possibly nitroglycerine).
early infarct-related pericarditis
- Occurs within the first 4 days after MI (due to transmural necrosis that directly causes pericardial inflammation).
- Diagnosis: Diagnostic criteria are the same as for late pericarditis (listed below).
- Treatment:
- This is mostly transient and self-limiting.
- Treatment may include aspirin 500 mg q8-12 hours.
- Therapy beyond 5-7 days usually isn't required. (ESC 2023, 37622654)
late pericarditis, aka post-cardiac injury (Dressler) syndrome
This may solely include pericarditis, or it may involve a combination of pericarditis plus pleural effusions (pleuropericarditis).
epidemiology
- Rare.
- Occurs between one week to three months after MI (most frequently after 1-2 weeks).(ESC 2023, 37622654)
presentation
- Chest pain, typically pleuritic (different in quality from original ischemic pain).
- Radiation to trapezius ridge supports pericarditis.
- May improve with leaning forward.
- Fever is often seen.
- Tamponade is rare.
diagnostic tests
- Auscultation may reveal pericardial friction rub.
- EKG may reveal diffuse ST elevation.
- Echocardiogram may reveal pericardial effusions (although these may also occur in the absence of pericarditis).
- CXR may reveal pleural effusion and pneumonitis.
- Lab evaluation may show leukocytosis (which is neither sensitive nor specific).
diagnostic criteria for pericarditis
- Two of the following support the diagnosis of pericarditis: (ESC 2023, 37622654)
- Pleuritic chest pain (>80%).
- Pericardial friction rub (>60%).
- Suggestive EKG changes.
- New or worsening pericardial effusion (>70%).
differential diagnosis
- Re-infarction.
- Ventricular free wall rupture (may be suggested by pericardial effusion >1 cm).
- Pulmonary embolism.
treatment
- First line therapy is high-dose aspirin:
- 500-1000 mg every 6-8 hours, until symptomatic improvement.
- Then taper by 250-500 mg every two weeks. (ESC 2023, 37622654)
- A proton pump inhibitor should be given to prevent gastric ulceration.
- Colchicine:
- Pericardial effusion isn't a contraindication to the use of antithrombotics and/or anticoagulants if these are otherwise indicated. (ESC 2023, 37622654)
epidemiology
- Rare, usually occurs within a week of MI.
- Typically occurs with inferior or posterior MI, affecting the posteromedial valve leaflet (figure above).
- Can occur with relatively small infarctions in about half of cases.
- Rupture accounts for more than half of acute, severe mitral regurgitation that occurs after MI. (33295949)
presentation
- Dyspnea, respiratory failure due to pulmonary edema.
- Hypotension/shock.
- The initial MI may be mild, so patients may present initially with ruptured papillary muscle.
- In this presentation, the initial findings are often those of acute heart failure.
- 💡 Whenever a patient with heart failure is encountered with normal ejection fraction, be sure to investigate valvular function with color doppler.
diagnostic tests
- Lung ultrasound and/or chest radiograph shows cardiogenic pulmonary edema. Dysfunction of the posterior mitral valve leaflet may cause asymmetric pulmonary edema, which predominantly involves the right upper lobe.
- Echocardiography
- Generally shows mitral regurgitation with a flail leaflet. However, this can be missed if there is a narrow and eccentric regurgitant jet. Transthoracic echocardiography only has a sensitivity of ~80%, so transesophageal echocardiography may be needed.(30987913)
- Ejection fraction is often normal or elevated (due to unloading effect of mitral regurgitation). (Griffin 2022)
- ECG may be relatively benign. Shock which is disproportionate to ECG changes suggests acute mitral regurgitation. (Griffin 2022)
- (On auscultation, the murmur may be unimpressive or absent, due to rapid pressure equalization between the left ventricle and left atrium.)
differential diagnosis
- Ventricular septal defect can present in a similar fashion.
- Causes of acute mitral regurgitation after MI:
- (1) Rupture of chordae tendineae.
- (2) Papillary muscle dysfunction is common following MI (usually due to inferior MI).
- (3) Mitral valve annulus dilation, due to dilation of the left ventricle.
- (4) Anterior MI with dynamic LV outflow tract obstruction (LVOTO) and systolic anterior motion of the mitral valve.
treatment
- Temporary stabilization:
- Afterload reduction reduces regurgitation. However, in patients with profound hypotension, norepinephrine may be required to maintain a minimal blood pressure consistent with life.
- Inotrope may be required.
- Intra-aortic balloon pump may be considered (but shouldn't delay surgery).
- Noninvasive ventilation or intubation may be required for management of pulmonary edema. (33295949)
- Operative intervention is required:
- (1) Generally this consists of emergent surgery.
- If the patient hasn't been revascularized, this surgery should ideally be a combined CABG plus mitral valve repair/replacement.
- (2) Transcatheter mitral valve repair may be another option. (33295949)
- (1) Generally this consists of emergent surgery.
epidemiology
- Rare (~0.3%), typically within the first week post-MI. There may be a bimodal incidence, with the first peak within <24 hours and the second after 3-5 days. (33295949, Griffin 2022)
- Often follows a large anterior infarct, but the rate may be similar among either anterior or inferior MIs.
presentation
- Dyspnea that may be accompanied by cardiogenic pulmonary edema.
- Sudden hemodynamic deterioration.
- Recurrent anginal chest pain (due to myocardial strain).
diagnostic tests
- Auscultation: Loud, holosystolic, harsh murmur might be heard.
- Echocardiogram:
- RV volume overload (dilation).
- Doppler echo may show flow across ventricle.
- Inferior or lateral infarction may cause basal VSDs that can be missed on routine transthoracic echocardiography. (33295949)
- Best views:
- Basal VSD: parasternal long-axis with medial angulation; apical long-axis, subcostal four-chamber view, parasternal short-axis.
- Apical VSD: apical 4-chamber. (Griffin 2022)
differential diagnosis
- Presentation most similar to papillary muscle rupture.
- Hemodynamic deterioration with RV dilation may mimic PE.
treatment
- Stabilization:
- Afterload reduction with a systemic vasodilator may favor blood flow from the left ventricle to the aorta (instead of refluxing into the right ventricle) – if the systemic blood pressure is high enough to tolerate this. Alternatively, for patients with profound hypotension, norepinephrine may be required to achieve a blood pressure compatible with life.
- Inotropic support is often needed.
- Intra-aortic balloon pump may be considered, but shouldn't delay surgery.
- Cardiogenic pulmonary edema may be stabilized temporarily with noninvasive ventilation. Caution is required with intubation, as this may precipitate cardiovascular collapse.
- Repair:
- Even small VSDs should be repaired (they may suddenly enlarge). Historical series suggest a mortality of ~95% without surgery. (10618300)
- Surgery is generally preferred, but transcatheter closure is another option. In some cases, transcatheter closure may be used to stabilize the patient as a bridge to definitive surgical repair. Complications of percutaneous VSD closure may include persistent shunting, arrhythmias, tamponade, bleeding, device embolization, hemolysis, and tricuspid leaflet chordal rupture. (33295949)
epidemiology
- Rare.
- Typically occurs in the context of a large anterior MI with an occluded LAD (although LCX causes 40% of ruptures and RCA occlusion causes 18%).(30987913)
- Generally occurs within the first 1-2 weeks.
- Risk factors include:
- Single-vessel transmural infarction.
- Late or incomplete reperfusion.
- Female gender.
- No prior MI or angina.
- Age >70 years. (Griffin 2022)
presentation
- Two types of presentation are described in the surgical literature as “blowout” or “oozing” presentations. (33295949) Overall, the presentation tends to mimic pericardial tamponade.
- Sudden rupture: Acute tamponade, cardiac arrest due to pulseless electrical activity.
- Subacute rupture: Chest pain, dyspnea, vomiting, fluctuating hemodynamic instability.
ECG
- May see variety of findings:
- Persistent STE is often seen (due to failure to re-perfuse).
- Recurrent STE or STD may occur.
- New Q-waves may be seen.
- Overall, this may be misleading (potentially pointing towards re-infarction or pericarditis).
echocardiography
- Pericardial effusion:
- Sensitive, but nonspecific in the context of MI.
- The presence of internal echoes or echogenic masses (clot) within pericardial effusion increases specificity.
- Contrast echocardiography may show extravasation of contrast material into the pericardium.
- Additional diagnostic features are similar to other causes of tamponade. 📖
differential diagnosis
- Post-MI pericarditis may cause a pericardial effusion.
- Aortic dissection may cause hemorrhagic tamponade.
treatment
- In tamponade, pericardiocentesis may be used as bridge to surgery. However, there is also a risk that pericardiocentesis could increase blood pressure and the pressure gradient across the myocardium, causing the wall rupture to extend further.(30987913) If echocardiography shows that the pericardium contains predominantly clotted blood, then pericardiocentesis is likely to fail. (33295949)
- Hemodynamic optimization (e.g., fluid, inotropes). However, avoid hypertension as that could theoretically aggravate bleeding from the left ventricle.
- Emergent surgical repair is generally required. Mortality with medical management is quoted at ~90%. (33295949)
- This is essentially a contained rupture of the LV (clot and pericardium seal off the rupture).
- Clinical presentation:
- May include dyspnea or chest pain.
- Thrombus formation with embolization may lead to systemic infarction(s).
- Ventricular arrhythmias may occur. (Griffin 2022)
- ECG:
- May show persistent ST elevation.
- May show regional pericarditis.
- Most often, ECG is nonspecific. (Griffin 2022)
- Diagnosis is often based on echocardiography (compared to a true aneurysm, the neck is generally narrower). In some cases, cardiac CT scan or cardiac MRI may help clarify the anatomy. (33295949)
- Don't be misled by the “aneurysm” verbiage – this is extremely dangerous.
- Treatment: overall, similar to the management of a subacute myocardial rupture. Stabilize the patient and consult cardiothoracic surgery.
These two pathologies are very closely linked, with LV thrombus usually complicating the presence of an LV aneurysm.
epidemiology
- LV aneurysm and thrombus both have an incidence of roughly ~10%.
- These tend to occur following transmural, anterior wall MI.
- The incidence of LV thrombus increases over the first two weeks following MI. (ESC 2023, 37622654)
symptoms
- LV aneurysm may lead to additional symptoms:
- Heart failure (due to abnormal ventricular geometry, for example functional mitral regurgitation).
- Recurrent ventricular arrhythmias. (Griffin 2022)
- LV thrombus may manifest with distal embolization (e.g., stroke).
diagnosis
- ECG in LV aneurysm often reveals persistent STE with shallow TWI.
- Echocardiography is the front-line screening test. However, echocardiography may be equivocal for thrombus formation.
- Cardiac MRI is the definitive gold-standard test. Cardiac MRI should be utilized if echocardiography yields unclear results. (ESC 2023, 37622654)
treatment
- LV aneurysm:
- Treatment involves standard post-MI therapies (e.g., ACE-inhibitor or ARB may be especially useful to avoid aneurysm expansion).
- It's controversial whether to anticoagulate patients for LV aneurysm without an identified thrombus, especially in the context of a patient who is already on dual antiplatelet therapy. (Griffin 2022)
- LV thrombus:
- Anticoagulation is indicated (e.g., heparin infusion initially, with transition to chronic oral anticoagulation).
- The duration of therapy may typically range from 3-6 months. Repeat imaging is important to ensure resolution. (ESC 2023, 37622654)
epidemiology
- May represent recurrence of pre-existing paroxysmal AF, or new-onset AF.
- Risk factors include:
- History of atrial fibrillation.
- Congestive heart failure, LV dysfunction.
treatment
- Management is similar to atrial fibrillation in general.📖
- If AF appears to trigger hemodynamic instability or ischemia, consider electrical cardioversion.
- For new-onset AF in the context of MI, this could tip the balance a bit towards considering rhythm control (as opposed to rate control). With resolution of transient instability due to MI, hopefully sinus rhythm could be sustained.
- Beta-blockade may be useful if hemodynamically tolerated (and would generally be preferable to diltiazem).
PVCs (premature ventricular contractions)
background
- >10 PVCs per hour predict higher long-term mortality.
- The CAST trials demonstrated that arrhythmia suppression using class IC antiarrhythmics increased mortality (encainide, flecainide, and moricizine). Elevated mortality could be explainable by the proarrhythmic properties of IC agents.
- The CAMIAT trial (Canadian Amiodarone Myocardial Infarction Arrhythmia Trial) evaluated the role of amiodarone in patients with frequent PVCs or one run of VT. Amiodarone reduced the risk of resuscitated ventricular fibrillation or arrhythmic death from 7% to 4.5% (p = 0.016). (9078198) However, this result required long term therapy with amiodarone. A meta-analysis of 13 trials of amiodarone among patients with heart failure or following MI found a reduction in mortality. (9371164)
management of frequent PVCs and/or NSVT
- Repeat an ECG to evaluate for any acute ischemic changes.
- Electrolytes should be monitored and repleted (target Mg >2 mg/dL, K >3.5 mEq/L).
- Beta-blockade may be the optimal therapy if the patient is hemodynamically stable enough to tolerate.
- Discussion on the role of beta-blockade s/p MI: 📖.
- Amiodarone could be considered in selected situations:
- Ectopy is causing symptoms or hemodynamic compromise. (Hurst 15e)
- Escalating pattern of ventricular ectopy, long runs of NSVT that almost meet criteria for sustained VT). (37009192)
NSVT (nonsustained ventricular tachycardia)
- NSVT is defined as wide-complex tachycardia lasting <30 seconds, terminating spontaneously, and not causing hemodynamic collapse.
- Early NSVT (<48 hours after MI) may not be associated with a risk of sudden cardiac death, since this reflects transient elevated automaticity or triggered activity in the ischemic myocardium. NSVT after 48 hours is more likely to reflect scar formation, which may associate with an elevated long-term risk of sudden cardiac death. (37009192)
- Management of NSVT is similar to the management of PVCs as discussed in the section above. ☝️
sustained monomorphic VT
definition
- Sustained monomorphic VT is defined as ventricular tachycardia which lasts >30 seconds or causes hemodynamic collapse.
- Note that if the rate is low (<~110 b/m) this may represent accelerated idioventricular rhythm (AIVR 📖) – which is typically a benign arrhythmia associated with reperfusion.
diagnosis
- Following MI, any monomorphic, wide-complex tachycardia is exceedingly likely to be VT and should generally be treated as such.
- (Further discussion of the approach to wide-complex tachycardia: 📖.)
treatment: initial considerations
- Initial management is based on ACLS algorithms (DC Cardioversion for unstable patients versus amiodarone for hemodynamically stable patients). Following conversion to sinus rhythm, patients will often be treated with an amiodarone infusion to prevent recurrence. Lidocaine 💊 may be used as a second-line anti-arrhythmic (with typical dosing including a bolus of ~100 mg followed by 1-4 mg/min infusion).
- Ischemia should be considered as a potential underlying cause, and treated if appropriate (e.g., with percutaneous coronary intervention).
- Electrolyte abnormalities should be corrected (e.g. target Mg >2 mg/dL and K >3.5 mM).
- Avoid beta-agonists wherever possible (e.g., dobutamine, epinephrine). Beta-blockers should be considered if hemodynamics will tolerate them (noting that beta-blockers are supported by the most robust evidence to reduce post-MI ventricular arrhythmias). 📖
- Treat conditions which may be increasing sympathetic tone (e.g., pain or anxiety). This is an especially important consideration among patients who are intubated and may be unable to report these symptoms.
- For recurrent arrhythmias refractory to therapy, see the section on VT storm. 📖
treatment: longer term considerations
- Early VT (<48 hours post MI) may not require ongoing antiarrhythmic therapy, especially if the patient can be successfully revascularized.
- Late VT (>48 hours post MI) raises concern about the presence of myocardial scar tissue. These patients may benefit from longer periods of antiarrhythmic therapy and perhaps from an implanted cardioverter-defibrillator (ICD). Electrophysiology consultation can help sort this out.
polymorphic VT due to active ischemia
- Basics: Polymorphic VT often reflects active myocardial ischemia. It may be most common early in the course of a myocardial infarction (e.g., <48 hours after MI).
- Differential diagnosis: If the QTc is significantly prolonged, the differential diagnosis includes torsade de pointes. However, this can get confusing, because myocardial ischemia itself may prolong the QT interval somewhat. Torsade isn't particularly common among patients with acute MI, but it may be caused by various QT-prolonging medications (e.g., sotalol or dofetilide).
- Treatment:
- Optimal treatment may be reperfusion (electrical instability is an indication for PCI).
- Anti-arrhythmic therapies may be similar to monomorphic VT (see above).
- If there is a concern regarding possible torsade de pointes, administration of IV magnesium is safe and reasonable. (Management of torsade is discussed here: 📖)
- The key aspect of sinus tachycardia is evaluation and treatment of the underlying cause of the sinus tachycardia. In the context of MI, common causes of tachycardia could include:
- Anxiety and/or pain.
- Systolic heart failure with compensatory tachycardia.
- Beta-adrenergic medications.
- Anemia related to post-PCI bleeding; hypovolemia.
- Pericardial tamponade.
- Hypoglycemia.
- (Further discussion of the causes of sinus tachycardia is here: 📖)
- Evaluation should include bedside echocardiography.
- Beta-blockers should generally be reserved until a complete evaluation of the potential causes of sinus tachycardia has been performed. Cautious beta-blockade may be considered once the following factors have been established:
- Absence of any other treatable cause of sinus tachycardia, especially:
- Reasonable ejection fraction.
- Absence of hypovolemia or acute hemorrhage.
- Robust blood pressure with reassuring shock index (e.g., HR/SBP < ~0.8).
- Absence of any other treatable cause of sinus tachycardia, especially:
basics
- Sinus bradycardia is usually associated with inferior MI, typically due to proximal occlusion of the right coronary artery.
- Bradycardia may result from ischemic injury to the SA node, or increased vagal tone due to stimulation of nerves adjacent to the AV node (Bezold-Jarisch phenomenon). (34957766)
- Bradycardia is usually responsive to medical therapies and resolves within 24 hours. (34957766)
investigation
- Consider alternative causes of sinus bradycardia as discussed here (especially medications): 📖
management
- Emergent treatment of hemodynamically unstable bradycardia is discussed here: 📖.
- Infusion of an inotrope is often adequate for initial therapy:
- Epinephrine infusion may be suitable for patients with hypotension.
- Dobutamine may be reasonable for patients with preserved blood pressure, yet impaired perfusion.
- Atropine or glycopyrrolate may be effective for patients with bradycardia due to excessive vagal tone. (34957766)
- Persistent bradycardia (>72 hours) might rarely require a permanent pacemaker. (37009192)
heart block due to inferior MI
- Pathophysiology:
- Generally due to ischemia involving the AV node and/or elevated vagal tone.
- The AV node has dual circulation, so generally it is resistant to true infarction and will eventually recover. (Sadhu 2023)
- Clinical presentation:
- Patients often have a junctional escape rhythm (narrow-complex, with heart rate 40-60 b/m).
- Heart block is usually transient (resolving within a week).
- Treatment:
- (Immediate management: see the chapter on bradycardia. 📖)
- Bradycardia may respond to atropine, especially if occurring early in course of MI. Alternative or additional therapies may include an epinephrine or dobutamine infusion.
- This can generally be managed conservatively (without transvenous wire insertion). Recovery usually occurs relatively quickly, especially following revascularization.
- Rarely, heart block may persist for 1-2 weeks. This may be responsive to theophylline or aminophylline. (Sadhu 2023)
heart block due to anterior MI
- Pathophysiology:
- Generally reflects septal myocardial necrosis resulting from a very proximal LAD occlusion.
- The block is located below the AV node.
- Clinical presentation:
- May develop abruptly, or can be preceded with RBBB with either LAFB or LPFB (bifascicular block).
- Often causes instability (or associated with instability).
- Treatment:
- (Immediate management: see the chapter on bradycardia. 📖)
- ⚠️ Block below the AV node can be exacerbated by atropine, so this should be avoided. (37009192, Griffin 2022)
- Indications to consider transvenous pacing may include:
- (a) Mobitz II or higher grade block.
- (b) New bundle-branch block (especially LBBB).
- (c) Bifascicular block (RBBB plus either LAHB or LPFB, or alternating RBBB and LBBB).
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- For suspected retroperitoneal hemorrhage, obtain a stat CT angiogram (make sure the study is protocoled as an angiogram).
- For decompensation after myocardial infarction, echocardiogram is critical to evaluate for a diverse range of complications.
- Some patients may present to the hospital with heart failure due to a ruptured chordae tendineae (following a silent or mildly symptomatic myocardial infarction). For patients with heart failure and a normal appearing ventricle, look carefully for a small eccentric regurgitant jet from the mitral valve.
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References
- 10618300 Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, Vahanian A, Califf RM, Topol EJ. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal defect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation. 2000 Jan 4-11;101(1):27-32. doi: 10.1161/01.cir.101.1.27 [PubMed]
- 26295381 Bajaj A, Sethi A, Rathor P, Suppogu N, Sethi A. Acute Complications of Myocardial Infarction in the Current Era: Diagnosis and Management. J Investig Med. 2015 Oct;63(7):844-55. doi: 10.1097/JIM.0000000000000232 [PubMed]
- 28707444 Safian RD. Current approaches to retroperitoneal hemorrhage: Too little, too late. Catheter Cardiovasc Interv. 2017 Jul;90(1):112-113. doi: 10.1002/ccd.27168 [PubMed]
- 30987913 Montrief T, Davis WT, Koyfman A, Long B. Mechanical, inflammatory, and embolic complications of myocardial infarction: An emergency medicine review. Am J Emerg Med. 2019 Jun;37(6):1175-1183. doi: 10.1016/j.ajem.2019.04.003 [PubMed]
- 33295949 Gong FF, Vaitenas I, Malaisrie SC, Maganti K. Mechanical Complications of Acute Myocardial Infarction: A Review. JAMA Cardiol. 2021 Mar 1;6(3):341-349. doi: 10.1001/jamacardio.2020.3690 [PubMed]
- 37009192 Frampton J, Ortengren AR, Zeitler EP. Arrhythmias After Acute Myocardial Infarction. Yale J Biol Med. 2023 Mar 31;96(1):83-94. doi: 10.59249/LSWK8578 [PubMed]
- 37622654 Byrne RA, Rossello X, Coughlan JJ, Barbato E, Berry C, Chieffo A, Claeys MJ, Dan GA, Dweck MR, Galbraith M, Gilard M, Hinterbuchner L, Jankowska EA, Jüni P, Kimura T, Kunadian V, Leosdottir M, Lorusso R, Pedretti RFE, Rigopoulos AG, Rubini Gimenez M, Thiele H, Vranckx P, Wassmann S, Wenger NK, Ibanez B; ESC Scientific Document Group. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J. 2023 Oct 12;44(38):3720-3826. doi: 10.1093/eurheartj/ehad191 [PubMed]