a b s t r a c t

Introduction: Despite the declining incidence of coronary heart disease (CHD) in the United States, acute myocar- dial infarction (AMI) remains an important clinical entity, with many patients requiring emergency department (ED) management for mechanical, inflammatory, and embolic complications.

Objective: This narrative review provides an evidence-based summary of the current data for the emergency medicine evaluation and management of post myocardial infarction mechanical, inflammatory, and embolic complications.

Discussion: While 30-day mortality rate after AMI has decreased in the past two decades, it remains significantly elevated at 7.8%, owing to a wide variety of subAcute complications evolving over weeks. Mechanical complica- tions such as ventricular free wall rupture, ventricular septal rupture, mitral valve regurgitation, and formation of left ventricular aneurysms carry significant morbidity. Additional complications include ischemic stroke, heart failure, renal failure, and cardiac dysrhythmias. This review provides several guiding principles for management of these complications. Understanding these complications and an approach to the management of various com- plications is essential to optimizing patient care.

Conclusions: Mechanical, inflammatory, and embolic complications of AMI can result in significant morbidity and mortality. Physicians must rapidly diagnose these conditions while evaluating for other diseases. In addition to understanding the natural progression of disease and performing a focused physical examination, an electrocar- diogram and bedside echocardiogram provide quick, noninvasive determinations of the underlying pathophys- iology. Management varies by presentation and etiology, but close consultation with cardiology and cardiac surgery is recommended.

Introduction

Atherosclerotic cardiovascular disease is the leading cause of death around the world [1]. Despite the declining incidence of coronary heart disease (CHD) in the United States over the last few decades many, but not all, observational studies have found no reduction in the incidence of acute myocardial infarction (AMI), accounting for 208 cases per 100,000 person-years, with roughly 22% representing ST- segment elevation myocardial infarction (STEMI) [2]. While 30-day mortality rate after AMI has decreased in the past two decades, it re- mains significantly elevated at 7.8% [2].

Complications of AMI include a wide variety of mechanical, embolic,

ischemic, dysrhythmic, and Inflammatory processes evolving over

* Corresponding author.

E-mail address: [email protected] (B. Long).

weeks. These complications are associated with significantly increased morbidity and mortality [3,4]. Following the widespread adoption of in- terventional percutaneous coronary intervention (PCI) as the preferred treatment for acute STEMI, the incidence of these complications has been reduced significantly to under 1% [3,4]. This includes ventricular free wall rupture (VFWR) with an incidence of 0.52%, Papillary muscle rupture with an incidence of 0.26%, and ventricular septal rupture (VSR) with a 0.17% incidence [3,4]. Acute mitral valve regurgitation (MR) after AMI is most commonly secondary to left ventricular dilata- tion or papillary muscle rupture (PMR) and is associated with a mortal- ity rate of up to 24% at 30 days [5]. Dysrhythmias, most commonly atrial fibrillation, ventricular fibrillation, and ventricular tachycardia, affect nearly 21% of this population [6]. Ischemic complications can affect the kidneys resulting in renal failure, the brain in the form of embolic strokes secondary to dysrhythmias, and the heart with the formation of left ventricular (LV) aneurysm [7-9]. Ischemic complications may also include Stent thrombosis and secondary heart failure with subse- quent exacerbations [10,11].

https://doi.org/10.1016/j.ajem.2019.04.003 0735-6757/

Methods

Authors searched PubMed and Google Scholar for articles using the keywords “myocardial infarction” OR “acute coronary syndrome” OR “acute coronary syndromes” AND “complications”, AND “emergency” for production of this narrative review. Authors included case reports and series, retrospective and prospective studies, systematic reviews and meta-analyses, clinical guidelines, and other narrative reviews. The literature search was restricted to studies published in English. Ini- tial literature search revealed over 600 articles. Authors reviewed all rel- evant articles and decided which studies to include for the review by consensus, with focus on emergency medicine-relevant articles, includ- ing guidelines. A total of 177 resources were selected for inclusion in this review. As this is a narrative review, authors did not pool individual study data.

Discussion

Ventricular free wall rupture

Etiology

VFWR occurs in 0.5-2.7% of patients following AMI and contributes to 20-30% of AMI-related deaths [12-16]. Following the advent of PCI and thrombolytic agents, the incidence of late VFWR occurring at least 1 day after MI has diminished, although this may be under-reported due to decreased autopsy rates during the same time [17]. Patients with VFWR typically present within the first week after an AMI [12,13,18]. Subacute or late-occurring VFWRs present 1-3 days after an AMI and account for up to one third of VFWRs [19,20]. Altogether, 50% present within the first 5 days after MI, with 90% presenting within the first 2 weeks [20,21]. However, rupture has been reported to occur up to 1 month post-AMI [22,23]. Left VFWR accounted for 1.7% of pa- tients in cardiogenic shock from the SHOCK registry [18]. Early VFWR occurring within the first 24 h is due to full-thickness rupture associated with a small myocardial tear [4]. This myocardial tear may temporarily become covered by clot or late-developing pericardial adhesions [4]. In contrast, subacute or late-occurring VFWRs present 1-3 days after an AMI due to a slow erosion of the border zone between healthy and in- farcted myocardium, progressing to a full-thickness rupture [4].

As with ventricular septal rupture (VSR), VFWRs may be further classified as simple or complex, and can involve the anterior or lateral and posterior LV wall [13,18,20]. Simple VFWRs are direct through- and-through defects, while complex VFWRs are characterized by ser- piginous dissection tracts extending from the primary tear of the rup- ture [24]. The lateral and posterior wall AMIs are theorized to be more prone to free wall rupture but are less prevalent due to the overall higher proportion of anterior wall AMIs [25]. Inferior infarctions are present in the majority of subacute VFWRs [19,26]. The infarcted coro- nary distribution leading to VFWRs has been reported as the circumflex coronary artery (LCX) in 40% of cases, left anterior descending artery (LAD) in 42% of cases, and the right coronary artery in 18% of cases [27].

Risk factors

Risk factors for VFWRs include Female gender, age N55 (most com- monly 65-70), hypertension, large infarct size, single vessel disease (usually a completely occluded vessel), transmural infarction, pseudoaneurysm formation, and delayed or incomplete revasculariza- tion [12,28-34]. VFWRs are more likely to occur following a first AMI in patients without prior history of angina, suggesting that these pa- tients have limited development of a collateral coronary Blood supply [35-38].

Clinical presentation and diagnosis

The emergency physician must have a high index of suspicion, as Timely diagnosis and management are vital to the survival of this

high-risk population. Clinical presentation varies, and patients may present with prolonged episodes of angina lasting for 6 h or more [13,30,39]. Some patients have sentinel anginal episodes lasting N30-60 min in the preceding days [30,39]. In these instances, continued ischemia may trigger VFWR as the initial infarction extends transmurally [40]. Persistent Arterial hypertension does not appear to affect the development of VFWRs; however, physical exertion-such as persistent coughing, retching, or excessive straining during defeca- tion-is thought to play a role [4,39]. These patients may also present with syncope, dyspnea, or hypotension after a silent AMI complicated by VFWR and subsequent Pericardial tamponade [39]. hemodynamic stability depends on the amount of accumulated pericardial bleeding, rate of bleeding, and presence of a clot sealing any pericardial leaks [41]. Patients with rapid accumulation of pericardial blood may suffer from sudden electromechanical dissociation and death [39]. VFWR pa- tients may present in extremis, characterized by any combination of tamponade, hypotension with associated hemorrhage, or stigmata of low cardiac output [39,42-44]. Physical examination findings may be consistent with cardiac tamponade, including jugular venous disten- sion, Pulsus paradoxus, hypotension, and diminished heart sounds [20,45].

The electrocardiogram (ECG) has a limited specificity for diagnosing VFWR, but may reveal low voltages throughout, or the presence of elec- trical alternans [46]. The cardiac rhythms found in VFWR most com- monly include junctional rhythms, asystole, pulseless electrical activity, Sinus bradycardia, complete heart block, or idioventricular rhythms [40]. Other possible ECG findings include persistent ST- segment elevation (N0.3 mV) and pseudonormalization of pre-existing negative precordial T waves up to 3 days post-AMI [40]. Within the lit- erature, ST-segment elevation in leads other than the infarction-related leads is a sensitive marker for an impending free wall rupture [47]. It is important to note, however, that the aforementioned findings vary with the location of infarction. The presence of an intraventricular conduc- tion delay may be less prevalent in patients with VFWR, although the subsequent development of a new conduction delay may portend in- creased risk for rupture [28,36,40].

Echocardiography will demonstrate a pericardial effusion with signs

of cardiac tamponade, including diastolic Right ventricular collapse (high specificity), systolic Right atrial collapse (earliest sign), a plethoric inferior vena cava with minimal Respiratory variation (high sensitivity), and exaggerated respiratory cycle changes in mitral and Tricuspid valve in-flow velocities as a surrogate for pulsus paradoxus [4,48]. Presence of increased echogenicity within the pericardium suggests presence of a hematoma developing into a fibrin clot [25,49]. Chest radiography is poorly diagnostic of free wall rupture and associated pericardial effusion but may be a useful adjunct to assess for other potential etiologies for the patient’s presentation [50]. Computed tomography angiography, while not routinely necessary for the diagnosis, may be useful for surgi- cal planning, determining the extent of rupture, and excluding aortic dissection in stable patients [51-53].

Management

Management of VFWR centers on Hemodynamic resuscitation and emergent surgical intervention [4,25,54]. Early consultation with the cardiothoracic surgical team and rapid mobilization of the operating room is essential [4,20]. Intravascular resuscitation with intrave- nous crystalloids or blood products and hemodynamic support with va- sopressors and/or inotropes should be initiated in hemodynamically unstable patients, but this should not delay definitive treatment [20].

While pericardiocentesis (PC) provides rapid improvement in the

patient’s hemodynamics by relieving the underlying tamponade physi- ology, emergent PC in these patients remains controversial [55]. By re- lieving the tamponade, there is a reflex increase in blood pressure and subsequent tension on the LV myocardium, which may convert a small tear to a full-thickness VFWR [4]. As PC can only act in a

temporizing fashion, it should be reserved for those patients in extremis refractory to supportive therapy en route to the OR [20,55].

Prognosis

Prognosis for all VFWR remains poor, with a mortality rate between 75 and 94% [56]. However, patients with subacute VFWRs are less likely to experience rapid Hemodynamic deterioration [20]. In a prospective study of 1247 consecutive patients with AMI that included 33 patients with subacute VFWR, 76% (25 of 33) survived their initial surgical re- pair, with 48.5% (16) of them becoming long-term survivors [32]. This rate of successful surgical management has been demonstrated in sev- eral small series as well [57,58].

Ventricular septal rupture (VSR)

Etiology

VSR, a defect in the intraventricular septum, is typically caused by is- chemic necrosis and causes up to 4.6% of cardiogenic shock after an AMI [20,59]. Before the current era of thrombolysis and PCI, VSR occurred in approximately 1-2% of patients with AMI; however, the current inci- dence is closer to 0.17% [36,60,61]. VSR, much like VFWR, represents a transmural infarction of the myocardium and may be subdivided into simple or complex presentations [4,21]. Simple VSRs consists of an abrupt, slit-like “through-and-through” intraventricular defect occur- ring at the same level of both ventricles. A complex VSR is characterized by disruption of the intraventricular septum followed by hemorrhage formation and development of a meshwork of channels connecting the ventricles [4]. Location of the VSR may provide an indication as to VSR subtype, with complex forms associated with posteroinferior in- farctions and simple forms more commonly seen following anterior in- farctions [20].

Risk factors

Risk factors for the development of VSR and subsequent mortality mirror those of VFWR, including hypertension, elevated body mass index, anterior wall AMI, increased age, female gender, first AMI, single vessel occlusion, and absence of smoking history [17,62-65]. Histori- cally, VSR is most commonly associated with ischemia of the anterior or anterolateral distributions supplied by the LAD, occurring in 60% of cases [60,66]. Comparatively, occlusion of the dominant RCA or LCX ac- counts for VSR formation in up to 40% of cases [20].

Clinical presentation and diagnosis

As shown in the SHOCK trial and further validated by APEX-MI and GUSTO-I, VSR timecourse is variable, but the large majority of patients will present within the first week following an AMI, with a median time to presentation of 16 h [21,67-69]. Patients characteristically pres- ent for the first time following an AMI and are clinically stable before experiencing the sudden onset of recurrent angina followed by short- ness of breath secondary to the creation of a left-to-right shunt (LRS) through the VSR [4,20]. This LRS typically leads to acute pulmonary edema with right sided heart failure, and patients decompensate rapidly into cardiogenic shock characterized by oliguria (81% of patients) and cold, poorly perfused extremities (83%) [4,20,68]. Physical examination reveals a palpable parasternal thrill in approximately one half of presen- tations, with a new, harsh pan-systolic murmur radiating to the apex and base best heard at the left lower sternal border occurring in up to 90% of cases [70-73]. In comparison, Mitral regurgitation, which may present similarly or occur concomitantly, has a mid-frequency pansystolic murmur best heard at the apex [73]. Other physical exami- nation findings are secondary to increased right-sidED flow and subse- quent right-sided failure, including jugular venous distention, a left or right S3 gallop, tricuspid regurgitation with cannon A waves, and possi- bly a loud pulmonic component of the second heart sound [73,74].

STEMI is present in the majority of patients with VSR, and anterior STEMI (60% of patients) is more common than inferior STEMI (40%)

[20,68]. There is an associated atrioventricular or infranodal conduction abnormality in 40% of cases [4,20,75]. Chest radiography lacks specific- ity and sensitivity for diagnosing VSR but may show cardiomegaly, pul- monary congestion, or a pleural effusion [20].

When the emergency clinician suspects VSR, point-of-care transtho- racic (TTE) or transesophageal echocardiography with color-flow Doppler is the imaging modality of choice for early diagnosis and ther- apy guidance [76,77]. Echocardiography is able to determine the size and site of VSR, assess the magnitude of the LRS as well as biventricular function, and evaluate for any concurrent papillary muscle rupture or MR [4,20]. Both the sensitivity and specificity of TTE with color-flow Doppler reach 100% within the literature [78,79]. Characteristic findings on TTE include Right ventricular dilation, pulmonary hypertension, per- foration of the ventricular septum, and demonstration of left-to-right flow across the septum on color-flow Doppler [74]. Magnitude of the LRS can be assessed by comparing flow across the aortic and pulmonic valves [4,80,81]. Unless there is a large territory of infarction or pre- existing dysfunction, TTE reveals a hyperdynamic left ventricle [74]. While TTE remains the most accessible bedside technique, TEE should be considered in those patients in which the TTE is undiagnostic and there remains a high index of suspicion [74].

Management

Due to the significant morbidity and mortality associated with un- treated VSR, consultation with interventional cardiology and cardiac surgery is essential, as early closure via surgery or percutaneous inter- vention improves outcomes, even in the hemodynamically stable pa- tient [20]. Patients presenting with VSR commonly present in extremis secondary to cardiogenic shock and fulminant pulmonary edema, necessitating the use of non-invasive ventilation (NIV) or defin- itive airway management [4]. However, these patients are at high risk for peri-intubation mortality and should be hemodynamically opti- mized prior to intubation if possible.

Treatment depends on patient blood pressure and perfusion. Tem- porizing management for Hypertensive patients with VSR includes re- ducing LRS and increasing LV stroke volume via afterload reduction. Afterload reduction is initially achieved by pharmacologic means with intravenous nitrates, which have the advantage of being rapidly titrat- able [4,74]. Phosphodiesterase-3 inhibitors, such as milrinone, may be used as an inodilator, providing afterload reduction while simulta- neously increasing myocardial contractility [82-84]. However, milrinone is slow in onset with a long half-life and may not be readily available in the emergency department. Dobutamine is another viable option for inodilation [85]. If available, Pulmonary vasodilators, such as inhaled nitric oxide, may benefit patients with significant right ven- tricular dysfunction [86]. However, afterload reduction should be avoided in patients presenting with hypotension [20]. In patients unable to tolerate afterload reduction, inotropic support may be necessary [4]. hypotensive patients may require vasopressors, such as norepineph- rine, to improve Peripheral perfusion and ensure adequate Coronary blood flow to maintain adequate cardiac output for end-organ perfusion [20,74,82].

Non-pharmacologic measures for afterload reduction include the use of an intra-aortic balloon pump which also augments coro- nary blood flow, Impella placement, and veno-arterial extracorporeal membrane oxygenation , which also augments cardiac output [87-91]. IABP decreases afterload, thereby reducing the degree of LRS, and increases cardiac output, systemic pressures, and end-organ perfu- sion. Hemodynamic optimization should not delay definitive treatment via percutaneous closure device or primary surgical treatment [4,20,74].

Prognosis

Thirty day mortality for patients with VSR approaches 87% in those with VSR and concomitant cardiogenic shock, and VSR is always fatal in patients who do not receive operative repair [68,92]. Though there is a high mortality associated with Surgical repair of VSR (~43%), there

are favorable long-term outcomes in operative survivors with a 5-year cumulative survival of 57% [90,93]. Patients should be referred to sur- gery or percutaneous closure as soon as possible.

Mitral valve regurgitation (MR)

Etiology

Acute MR remains a prominent complication of AMI, accounting for 8.3% of cardiogenic shock presentations per the SHOCK registry [59,94]. While mild to moderate MR is found in up to 45% of patients following an AMI, it is generally well tolerated, transient, and asymptomatic [5]. However, acute MR with subsequent cardiogenic shock following papil- lary muscle rupture or LV dilation is a life-threatening diagnosis [95,96]. The underlying pathophysiology of acute MR following an AMI may be categorized as mechanical or functional in nature. Functional MR occurs secondary to LV dilation with concomitant mitral valve annular dilation, or poor leaflet valve coaptation due to papillary Muscle dysfunction with resultant segmental Wall motion abnormality at the muscle inser- tion site [97-99]. This functional MR is seen in even slight modification of LV geometry in the presence of regional wall motion abnormalities [100].

Conversely, structural MR may occur due to chordae rupture, papil- lary muscle dysfunction, or PMR leading to a flail mitral valve leaflet [4,20]. Structural MR is closely tied to coronary anatomy, as the posteromedial papillary muscle has a singular arterial supply via the posterior descending artery which arises from the RCA or the LCX in right and left dominant systems, respectively [20,101,102]. The antero- lateral papillary muscle is 6-12 times less likely to suffer rupture, as it receives duel blood supply from the LAD and LCX [20,70].

Risk factors

Patients presenting with cardiogenic shock secondary to acute MR are more likely to have an RCA lesion with right dominant circulation, as well as preexisting coronary artery disease and diabetes [96]. Addi- tional risk factors for development of acute MR include female gender, increased age, and presence of cerebrovascular disease [96].

Clinical presentation and diagnosis

MR most commonly occurs within 2-7 days post-AMI, with a me- dian time to onset of 13 h [4,94]. Clinical presentation varies according to degree of MR, with fulminant MR following PMR characterized by acute pulmonary edema, hypotension, and cardiogenic shock [4]. Phys- ical examination is non-specific and does not identify 50% of patients with moderately severe to severe MR [96]. However, the presence of a soft pansystolic murmur heard loudest at the cardiac apex, with a dia- stolic component and radiation to the left axilla, may be suggestive of MR [4,20,73]. However, the characteristic murmur may be absent in pa- tients with impaired LV systolic function or elevated left atrial pressure [103].

ECG may show tachycardia, or confirm the presence of a posterior or inferior AMI, while chest radiography may reveal pulmonary edema with right upper lobe predominance suggestive of increased flow in the right superior pulmonary vein [4,104]. Bedside echocardiography with color-flow Doppler is the imaging modality of choice for initial di- agnosis of MR, Clinical monitoring, and surgical planning [4]. TTE may reveal the size and direction of the regurgitant jet via color-Doppler, while it is possible to visualize flail leaflets and evidence of malcoaptation [103]. Likewise, TTE may help distinguish between VSR and PMR with associated MR, while evaluating biventricular function [4,105]. The presence of MR with normal LV size is highly suggestive of acute MR [103]. While TTE is useful, and often the initial imaging mo- dality, it has a sensitivity between 65 and 85% for diagnosing PMR [106]. Therefore, TEE may be necessary if there remains a high index of suspi- cion PMR not diagnosed by TTE [20].

Management

Prompt diagnosis and emergent surgical correction of MR are vital to improve survival [4,107]. Immediate stabilization involves management of pulmonary edema, necessitating the use of Non-invasive ventilation or definitive airway management via endotracheal intubation [4]. The goals of temporizing medical management is to increase for- ward flow from the left ventricle and decrease the amount of MR. Nitro- prusside or nitroglycerin can be used to provide vasodilation and afterload reduction as tolerated by the blood pressure. Inodilators such as dobutamine, are helpful by improving both contractility and va- sodilation to improve forward flow. Vasopressors, such as norepineph- rine, may be needed to maintain blood pressure despite the adverse effect of increasing afterload. If patients are hypertensive with pulmo- nary edema, vasodilator therapy with nitrates is recommended [20,108]. Maintaining ventricular function is vital by avoiding cardiodepressant drugs including beta-blockers, as well as augmenting cardiac output via catecholamine inotropes such as dobutamine [4,103]. Diuretics, as well as hemofiltration, may be used in patients with acute pulmonary edema and pulmonary congestion [4]. Similarly to patients with VSR, Mechanical circulatory support in the form of IABP, Impella placement, or ECMO may prove useful [89,109-113]. While the decision for primary surgical repair is largely based on the se- verity of MR and Underlying etiology (functional vs. structural), it is im- portant to involve the surgical specialists as well as interventional cardiology [4,20].

Prognosis

Prognosis for acute MR following AMI remains poor, with a mortality rate of 75% at 24 h and 95% at 2 weeks if left untreated [114]. Operative mortality approaches 39%, with an in-hospital mortality of 55% [59,94].

Post-myocardial infarction pericarditis (PMIP)

Etiology

PMIP, also known as postmyocardial infarction syndrome or Dressler’s Syndrome (DS), is a form of pericarditis presenting with or without pericardial effusion after an AMI [115]. However, PMIP repre- sents a small part of the post-cardiac injury syndrome (PCIS), which ex- pands to include post-traumatic pericarditis secondary to iatrogenic causes such as PCI and postpericardiotomy syndrome following cardiac surgery [116]. While the exact pathophysiology of PMIP remains un- known, it is presumed to be triggered by initial insult to pericardial me- sothelial cells as well as minor bleeding into the pericardial space, releasing cardiac antigens, stimulating an inflammatory and autoim- mune response in predisposed patients [115,116]. This inflammation causes a spectrum of clinical presentation ranging from simple, uncom- plicated pericarditis to more complicated disease including cardiac tamponade, Pleural effusions, and/or pleuropericarditis [115,116].

Two time-related forms of PMIP are recognized. Early PMIP occurs within the first 2-4 days after an AMI, and late PMIP typically presents after the first week following an AMI [117]. Historically, the incidence of early PMIP was thought to occur in 10-20% of post-AMI patients [117], although this has decreased to an incidence of roughly 6% in the post-thrombolytic era [118,119]. Conversely, late PMIP, formerly known as DS, had an incidence of 3-4% in the past [120], but contempo- rary studies show an incidence of b1% [117,119].

Risk factors

The risk factors for the development of PMIP include delayed reper- fusion, higher cardiac biomarkers, larger infarction size, younger age, anterior location of ischemia, inferior infarcts accompanied by right ventricular involvement, and more frequently reduced left ventricular ejection fraction [121-124].

Clinical presentation/diagnosis

Patients who develop PMIP typically present with signs and symp- toms similar to those seen in patients presenting with acute pericarditis and/or pericardial effusion [115,116,124]. Most patients present with sharp, pleuritic chest pain that is centrally located (N80%), low-grade fever (N50-60%), and dyspnea (50-60%) [116,125]. Clinical evaluation may reveal leukocytosis, elevated inflammatory markers such as eryth- rocyte sedimentation rate and C-reactive protein (N80%), the presence of a pericardial effusion (N80%), new pleural effusion with or without pulmonary infiltrates (N60%), and evidence of a pericardial or pleural rub (30-60%) [116,125]. ECG changes are present in 60-80% of cases of pericarditis in different series [115]. Elevated troponin levels may re- veal myocardial involvement and the presence of myopericarditis [126]. Typical ECG changes seen in pericarditis, including diffuse ST seg- ment elevations in association with PR segment depressions, are often masked by post-AMI changes [116,127]. However, ST segment elevation with persistently upright T waves or T waves that become upright after having been inverted suggest PMIP [128,129]. Chest radiography is typ- ically normal in patients with PMIP but may show new-onset pleural ef- fusion or pulmonary infiltrates and an enlarged cardiac silhouette, present in pericardial effusions N200 mL [115,116,127]. TTE should be performed in patients with PMIP, specifically to evaluate for pericardial effusion, as well as evidence of tamponade [130,131]. Patients with a PMIP and effusions N10 mm are at significantly increased risk of sub-

acute VFWR [130,131].

There are no formalized criteria for diagnosing PMIP [115,116]. However, the diagnosis requires the presence of a prior injury to the pericardium, myocardium, or pleura and evidence of pleuroPericardial inflammation (Table 1) [116].

Management

While there is little literature to guide treatment for PMIP, manage- ment principles may be extrapolated from studies evaluating acute pericarditis. For patients presenting with early PMIP, which is usually self-limited, the recommended approach is to avoid using NSAIDs for the initial 7-10 days post-AMI, with the exception of once daily aspirin for secondary prevention [132]. For those with severe symptoms requir- ing analgesia, acetaminophen remains the preferred agent, with high- dose aspirin second line [132].

Treatment for late occurring PMIP is mostly supportive, with medi- cal management including Non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids [115-117]. Aspirin should be preferentially used in patients with PMIP due to the patient’s require- ment for Antiplatelet therapy, as well as the fact that the anti- inflammatory actions of other NSAIDs may interfere with myocardial healing and scar formation [115,133-136]. Indomethacin should be avoided, as it decreases coronary blood flow [136]. High-dose aspirin (800 mg orally every 6-8h for 7-10 days followed by gradual tapering of the dose by 800 mg per week for 3 weeks) has been shown to be ef- ficacious in multiple studies [127,137,138]. Ibuprofen, which has been shown to increase coronary flow, may be prescribed at a dose of 600 to 800 mg every 6-8 h, with tapering of the total daily dose by 400 to 800 mg every week for a treatment period of 3-4 weeks [124]. Gastric protection, commonly with a proton pump inhibitor, should be pro- vided in all patients treated with an NSAID [115].

Colchicine (0.5 mg BID for patients N70 kg and 0.5 mg once daily for patients b70 kg for 4-6 weeks) has been shown to be effective in reliev- ing pain in patients with acute pericarditis and preventing recurrences,

Table 1

Diagnostic features of post-myocardial infarction pericarditis.

Evidence of prior pericardial, myocardial, or pleural injury, plus

• Pericarditis +- pericardial or pleural effusion

• Evidence of inflammation without alternative etiology

and it may play a role in PMIP prevention [138-140]. Treatment with colchicine is recommended by multiple guidelines [115,141,142]. How- ever, colchicine should be avoided in those patients at risk for bone mar- row suppression, as well as those with liver disease, gastrointestinal motility disorders, and renal insufficiency [115]. Low-dose corticoste- roid therapy (i.e. prednisone 0.2-0.5 mg/kg/day for four weeks followed by a taper) has been shown to be effective in patients in whom aspirin/ NSAIDs are contraindicated, and those who have failed to respond to more Conservative therapy [115,116,143]. If steroids are used, dosages must be tapered very slowly to avoid recurrences of PMIP [138]. In the case of PMIP complicated by cardiac tamponade, PC is indicated [115,117,124].

Prognosis

While the prognosis of PMIP is good for the majority of patients, there remains a recurrence rate of 10-15% [116]. Inpatient admission is not necessary for all patients with PMIP; however, patients with high-risk features should be hospitalized [137,144]. These include pa- tients with leukocytosis, fever (temperature N 38 ?C), immunosup- pressed state, subacute course (symptoms developing over days to weeks), concurrent oral anticoagulant use, elevated troponin levels, large effusion or tamponade, and aspirin or NSAID failure [115,144].

Left ventricular aneurysm (LVA)

Etiology

AMI may be complicated by the formation of a LVA, broadly defined as a large area of abnormal left ventricular akinesia or dyskinesia that causes a reduction in LV ejection fraction [145-147]. LVAs characteristi- cally are a well-delineated, thin, scarred, fibrotic wall containing ne- crotic myocardium secondary to a healing transmural AMI [148]. This is in contrast to a LV pseudoaneurysm, which represents a VFWR contained by the surrounding pericardium [39]. While the mechanism of LVA formation is not completely elucidated, there appears to be a component of transmural infarction with poor collateral blood supply or incomplete coronary reperfusion, followed by a period of increased wall stress in the month following an AMI [145]. This increased wall stress may arise from preserved contractility of adjacent myocardium, ventricular dilation, decreased wall thickness, or a combination thereof [145,149].

Approximately 85% of LVAs are anterolateral in nature, correspond- ing to the territory perfused by the LAD artery, with 5-10% located pos- teriorly in the distribution of the RCA, and the remaining LVAs arising from the lateral myocardium supplied by the obtuse marginal arteries [147,150]. Historically LVA was thought to develop in up to 35% of pa- tients following an AMI [151], but current literature reports an inci- dence between 8 and 15%, likely due to contemporary Reperfusion strategies [149,152,153].

Risk factors

Risk factors for LVA formation include female gender, absence of previous angina, Single-vessel disease, total LAD occlusion, hyperten- sion, and incomplete reperfusion [149,154].

Clinical presentation/diagnosis

Clinical presentation varies and is often nonspecific. Small and moderate-sized aneurysms are often asymptomatic, while large LVAs present with persistent dyspnea and evidence of heart failure [145]. The paradoxical movement of the LVA during systole results in de- creased cardiac output related to both systolic and diastolic dysfunction [145]. A portion of the LV volume is retained in the poorly-contractile LVA instead of flowing through the aortic valve while the fibrotic wall stiffens, impairing diastolic relaxation [155-157]. This increased myo- cardial tension and wall stiffening cause increased oxygen demand, which may lead to further myocardial ischemia. Myocardial ischemia and increased stretch lead to enhanced automaticity and increased

ventricular activity [158]. Symptoms related to ventricular dysrhythmias occur in up to 44%% of patients, with the clinical presentation ranging from palpitations to syncope and sudden cardiac death [159-161]. Some degree of functional mitral valve dysfunction is present due to the distorted LV geometry and dyskinetic movement in these patients [145]. Similarly, an LVA may enlarge over time and rupture, although this is a rare event owing to the dense fibrotic wall [162]. Over half of pa- tients with LVAs have a mural thrombus on autopsy or surgery, due to the stasis of flow in the aneurysmal cavity as well as the procoagulant nature of the fibrotic tissue within the LVA [163,164]. Systemic embolization oc- curs in 13.7% of these patients [165]. Palpation of the chest may demon- strate an apical systolic thrust or the presence of a double impulse. A third or fourth heart sound may be present as well. There may be an apical pansystolic murmur in the case of concomitant mitral regurgitation.

ECG usually shows persistent ST segment elevations; however, this finding does not necessarily imply the presence of an LVA [166]. The fre- quency of ST elevations ranges from 84 to 100% in patients with known LVA [167,168]. While the presence of ST elevations is highly sensitive for LVA, specificity is limited, as post-AMI ST elevations may be due to ven- tricular hypertrophy, left axis deviation, scarring, or Left bundle branch block [167].

While the presence of an LVA may be suspected from chest radiogra- phy, it is poorly sensitive for evaluation of a suspected LVA [169]. Echo- cardiography is the imaging modality of choice and will typically show a dyskinetic LV wall with diastolic deformity [170]. Mural thrombus and LV wall calcification may be suggestive of LVA. TTE can also evaluate as- sociated mitral valve dysfunction and differentiate a true aneurysm from pseudoaneurysm by detecting any discontinuity in the myocar- dium, indicative of myocardial perforation and pseudoaneurysm forma- tion [171]. In cases in which echocardiography is not diagnostic, cardiac CTA may confirm the diagnosis and may be helpful to distinguish be- tween a true and pseudoaneurysm [172].

Management

Management of an LVA focuses on medical therapy for associated complications and consideration of an aneurysmectomy. Asymptomatic small to moderately sized LVAs may be managed medically in consulta- tion with cardiology and cardiac surgery; however, the role for medical management for symptomatic patients or those with asymptomatic large aneurysms is uncertain [145]. Additional surgical indications in- clude intractable ventricular dysrhythmias, severe angina, heart failure unresponsive to medical management, and systemic embolization in patients who cannot take oral anticoagulants [132,145]. Therapy for symptomatic patients includes afterload reduction for those with LV en- largement, anti-ischemic medications for angina, and parenteral anticoagulation if there is thrombus present within the aneurysm or LV. Preferred agents for parenteral anticoagulation include unfractionated heparin or low-molecular weight heparin, which should be continued until effective anticoagulation with warfarin is achieved [173]. Although isolated case reports have reported efficacy with off- label use of direct oral anticoagulants in this population, further studies are needed before adopting this practice [174]. Cardiology and cardiac surgery consultations may help guide therapeutic management and consideration for surgical repair in these patients.

Prognosis

The prognosis and natural history for patients with LVA in the con- temporary era is improved, with an anticipated 5 year survival rate of up to 90% for medically treated small to moderate sized LVAs [175]. The 30-day mortality following surgical LVA repair ranges from 2 to 8%, with 5 year survival ranging from 73 to 90% [145].

Additional complications

There remains a variety of subacute complications, including acute ischemic stroke, acute renal failure, congestive heart failure, and cardiac

dysrhythmias. While the presentation, evaluation, and management of these conditions in patients following AMI are similar to the general population, there are important epidemiological differences. For in- stance, the rate of ischemic stroke is increased in the subacute post- AMI period, with 12.2 ischemic strokes occurring per 1000 AMIs at 30 days [176]. This represents roughly a 44-fold increase compared to the general population [177]. While the incidence of acute heart failure following AMI has diminished from approximately 16 per 100 person years in 1998 to 14 per 100 person-years in 2010, survival remains poor, with a 1 year mortality rate of 45.5% [178]. Additionally, these pa- tients are at high risk for sudden death secondary to sustained ventric- ular dysrhythmias, which account for roughly 50% of all deaths in the post-AMI period [179]. Atrial fibrillation is the most common sustained cardiac dysrhythmia, with an incidence of 6-21% [6]. Acute kidney in- jury (AKI) is a well-described complication of AMI, affecting up to 19.4% of patients, including 7.1% with mild, 7.1% with moderate, and 5.2% with severe AKI [180]. In patients following PCI, stent thrombosis is uncommon, occurring in 1.4% of patients within 30 days of placement, but carries a mortality rate of 20-45% [181,182].

Conclusions

Despite improvements in reperfusion therapy and medical manage- ment, the 30-day mortality rate after AMI remains significantly elevated at 7.8%, secondary to a variety of both acute and subacute complications [2]. These complications include a wide variety of mechanical, embolic, ischemic, dysrhythmic, and inflammatory processes evolving over weeks after an AMI. Patients may present to the acute care setting with VFWR, VSR, acute mitral valve dysfunction, LVA, and PMIP [3,4]. Dysrhythmias, most commonly atrial fibrillation, as well as Ischemic events such as renal failure or stroke affect these patients. In addition to understanding the natural progression of disease and performing a focused physical examination, an ECG and bedside echocardiogram pro- vide quick, noninvasive determinations of the underlying pathophysiol- ogy. Management varies by presentation and etiology, but close consultation with cardiology as well as cardiac surgery, when indicated, is recommended.

Conflicts of interest

None.

Acknowledgements

WTD, TM, BL, and AK conceived the idea for this manuscript and con- tributed substantially to the writing and editing of the review. Dr. Wil- liam Brady approved the idea and construction of this review. This manuscript did not utilize any grants or funding, and it has not been presented in abstract form. This clinical review has not been published, it is not under consideration for publication elsewhere, its publication is approved by all authors and tacitly or explicitly by the responsible au- thorities where the work was carried out, and that, if accepted, it will not be published elsewhere in the same form, in English or in any other language, including electronically without the written consent of the copyright-holder. This review does not reflect the views or opinions of the U.S. government, Department of Defense, U.S. Army, U.S. Air Force, or SAUSHEC EM Residency Program.

References

1. Barquera S, Pedroza-Tobias A, Medina C, Hernandez-Barrera L, Bibbins-Domingo K, Lozano R, et al. Global overview of the epidemiology of atherosclerotic cardiovascu- lar disease. Arch Med Res. 2015;46(5):328-38.
2. Yeh RW, Sidney S, Chandra M, Sorel M, Selby JV, Go AS. Population trends in the in- cidence and outcomes of acute myocardial infarction. N Engl J Med 2010;362(23): 2155-65.
3. French JK, Hellkamp AS, Armstrong PW, Cohen E, Kleiman NS, O’Connor CM, et al. mechanical complications after percutaneous coronary intervention in ST-

   elevation myocardial infarction (from APEX-AMI). Am J Cardiol. 2010;105(1): 59-63.

   Kutty RS, Jones N, Moorjani N. Mechanical complications of acute myocardial in- farction. Cardiol Clin 2013;31(4):519-31 [vii-viii].

4. Aronson D, Goldsher N, Zukermann R, Kapeliovich M, Lessick J, Mutlak D, et al. Is- chemic mitral regurgitation and risk of heart failure after myocardial infarction. Arch Intern Med 2006;166(21):2362-8.
5. Schmitt J, Duray G, Gersh BJ, Hohnloser SH. Atrial fibrillation in acute myocardial infarction: a systematic review of the incidence, clinical features and prognostic implications. Eur Heart J 2009;30(9):1038-45.
6. Dutta M, Hanna E, Das P, Steinhubl SR. Incidence and prevention of ischemic stroke following myocardial infarction: review of current literature. Cerebrovasc Dis 2006;22(5-6):331-9.
7. Putaala J, Nieminen T. stroke risk period after acute myocardial infarction revised. J Am Heart Assoc 2018;7(22):e011200.
8. Shacham Y, Steinvil A, Arbel Y. Acute kidney injury among ST elevation myocardial infarction patients treated by primary percutaneous coronary intervention: a mul- tifactorial entity. J Nephrol 2016;29(2):169-74.
9. Beinart R, Abu Sham’a R, Segev A, Hod H, Guetta V, Shechter M, et al. The incidence and Clinical predictors of early stent thrombosis in patients with acute coronary syndrome. Am Heart J. 2010;159(1):118-24.
10. Torabi A, Cleland JG, Rigby AS, Sherwi N. Development and course of heart failure after a myocardial infarction in younger and older people. J Geriatr Cardiol 2014; 11(1):1-12.
11. Wehrens XH, Doevendans PA. Cardiac rupture complicating myocardial infarction. Int J Cardiol 2004;95(2-3):285-92.
12. Oliva PB, Hammill SC, Edwards WD. Cardiac rupture, a clinically predictable com- plication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22(3):720-6.
13. Keeley EC, de Lemos JA. Free wall rupture in the elderly: deleterious effect of fibri- nolytic therapy on the ageing heart. Eur Heart J 2005;26(17):1693-4.
14. Moreno R, Lopez de Sa E, Lopez-Sendon JL, Garcia E, Soriano J, Abeytua M, et al. Fre- quency of left ventricular free-wall rupture in patients with acute myocardial in- farction treated with primary angioplasty. Am J Cardiol 2000;85(6):757-60, [A8].
15. Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, et al. Cardiac rupture com- plicating acute myocardial infarction in the direct percutaneous coronary interven- tion reperfusion era. Chest. 2003;124(2):565-71.
16. Hutchins KD, Skurnick J, Lavenhar M, Natarajan GA. Cardiac rupture in acute myo- cardial infarction: a reassessment. Am J Forensic Med Pathol 2002;23(1):78-82.
17. Slater J, Brown RJ, Antonelli TA, Menon V, Boland J, Col J, et al. Cardiogenic shock due to cardiac free-wall rupture or tamponade after acute myocardial infarction: a re- port from the SHOCK Trial Registry. Should we emergently revascularize occluded coronaries for cardiogenic shock? J Am Coll Cardiol 2000;36(3 Suppl A):1117-22.
18. Purcaro A, Costantini C, Ciampani N, Mazzanti M, Silenzi C, Gili A, et al. Diagnostic criteria and management of subacute ventricular free wall rupture complicating acute myocardial infarction. Am J Cardiol. 1997;80(4):397-405.
19. Ng R, Yeghiazarians Y. Post myocardial infarction cardiogenic shock: a review of current therapies. J Intensive Care Med 2013;28(3):151-65.
20. Crenshaw BS, Granger CB, Birnbaum Y, Pieper KS, Morris DC, Kleiman NS, et al. Risk factors, angiographic patterns, and outcomes in patients with ventricular septal de- fect complicating acute myocardial infarction. GUSTO-I (Global Utilization of Strep- tokinase and TPA for Occluded Coronary Arteries) Trial Investigators. Circulation. 2000;101(1):27-32.
21. Pollak H, Diez W, Spiel R, Enenkel W, Mlczoch J. Early diagnosis of subacute free wall rupture complicating acute myocardial infarction. Eur Heart J 1993;14(5): 640-8.
22. Mann JM, Roberts WC. Rupture of the left ventricular free wall during acute myo- cardial infarction: analysis of 138 necropsy patients and comparison with 50 nec- ropsy patients with acute myocardial infarction without rupture. Am J Cardiol 1988;62(13):847-59.
23. Batts KP, Ackermann DM, Edwards WD. Postinfarction rupture of the left ventricu- lar free wall: clinicopathologic correlates in 100 consecutive autopsy cases. Hum Pathol 1990;21(5):530-5.
24. Haddadin S, Milano AD, Faggian G, Morjan M, Patelli F, Golia G, et al. Surgical treatment of postinfarction left ventricular free wall rupture. J Card Surg. 2009;24(6):624-31.
25. Blinc A, Noc M, Pohar B, Cernic N, Horvat M. Subacute rupture of the left ventricular free wall after acute myocardial infarction. Three cases of long-term survival with- out emergency surgical repair. Chest 1996;109(2):565-7.
26. Markowicz-Pawlus E, Nozynski J, Duszanska A, Hawranek M, Jarski P, Kalarus Z. The impact of a previous history of ischaemic episodes on the occurrence of left ventricular free wall rupture in the setting of myocardial infarction. Kardiol Pol 2012;70(7):713-7.
27. Figueras J, Curos A, Cortadellas J, Sans M, Soler-Soler J. Relevance of electrocardio- graphic findings, heart failure, and infarct site in assessing risk and timing of left ventricular free wall rupture during acute myocardial infarction. Am J Cardiol 1995;76(8):543-7.
28. Melchior T, Hildebrant P, Kober L, Jensen G, Torp-Pedersen C. Do diabetes mellitus and systemic hypertension predispose to left ventricular free wall rupture in acute myocardial infarction? Am J Cardiol 1997;80(9):1224-5.
29. Figueras J, Cortadellas J, Calvo F, Soler-Soler J. Relevance of delayed hospital admis- sion on development of cardiac rupture during acute myocardial infarction: study in 225 patients with free wall, septal or papillary muscle rupture. J Am Coll Cardiol 1998;32(1):135-9.
30. Pretre R, Ye Q, Grunenfelder J, Zund G, Turina MI. Role of myocardial revasculariza- tion in postinfarction ventricular septal rupture. Ann Thorac Surg 2000;69(1): 51-5.
31. Lopez-Sendon J, Gonzalez A, Lopez de Sa E, Coma-Canella I, Roldan I, Dominguez F, et al. Diagnosis of subacute ventricular wall rupture after acute myocardial infarc- tion: sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria. J Am Coll Cardiol 1992;19(6):1145-53.
32. Pollak H, Mlczoch J. Effect of nitrates on the frequency of left ventricular free wall rupture complicating acute myocardial infarction: a case-controlled study. Am Heart J 1994;128(3):466-71.
33. Shiyovich A, Nesher L. Contained left ventricular free wall rupture following myo- cardial infarction. Case Rep Crit Care 2012;2012:467810.
34. Herlitz J, Samuelsson SO, Richter A, Hjalmarson A. Prediction of rupture in acute myocardial infarction. Clin Cardiol 1988;11(2):63-9.
35. Pohjola-Sintonen S, Muller JE, Stone PH, Willich SN, Antman EM, Davis VG, et al. Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size. Am Heart J. 1989;117(4):809-18.
36. Yoshikawa T, Inoue S, Abe S, Akaishi M, Mitamura H, Ogawa S, et al. Acute myocar- dial infarction without warning: clinical characteristics and significance of preinfarction angina. Cardiology. 1993;82(1):42-7.
37. Cheriex EC, de Swart H, Dijkman LW, Havenith MG, Maessen JG, Engelen DJ, et al. Myocardial rupture after myocardial infarction is related to the perfusion status of the infarct-related coronary artery. Am Heart J. 1995;129(4):644-50.
38. Figueras J, Cortadellas J, Soler-Soler J. Left ventricular free wall rupture: clinical pre- sentation and management. Heart 2000;83(5):499-504.
39. Birnbaum Y, Chamoun AJ, Anzuini A, Lick SD, Ahmad M, Uretsky BF. Ventricular free wall rupture following acute myocardial infarction. Coron Artery Dis 2003; 14(6):463-70.
40. Mahilmaran A, Nayar PG, Sheshadri M, Sudarsana G, Abraham KA. Left ventricular pseudoaneurysm caused by Coronary spasm, myocardial infarction, and myocardial rupture. Tex Heart Inst J 2002;29(2):122-5.
41. Figueras J, Curos A, Cortadellas J, Soler-Soler J. Reliability of electromechanical dis- sociation in the diagnosis of left ventricular free wall rupture in acute myocardial infarction. Am Heart J 1996;131(5):861-4.
42. Che J, Li G, Chen K, Liu T. Post-MI free wall rupture syndrome. Case report, literature review, and new terminology. Clin Case Rep 2016;4(6):576-83.
43. Roberts JD, Mong KW, Sussex B. Successful management of left ventricular free wall rupture. Can J Cardiol 2007;23(8):672-4.
44. Honasoge AP, Dubbs SB. Rapid fire: pericardial effusion and tamponade. Emerg Med Clin North Am 2018;36(3):557-65.
45. Honda S, Asaumi Y, Yamane T, Nagai T, Miyagi T, Noguchi T, et al. Trends in the clin- ical and pathological characteristics of cardiac rupture in patients with acute myo- cardial infarction over 35 years. J Am Heart Assoc. 2014;3(5):e000984.
46. Wehrens XH, Doevendans PA, Widdershoven JW, Dassen WR, Prenger K, Wellens HJ, et al. Usefulness of sinus tachycardia and ST-segment elevation in V(5) to iden- tify impending left ventricular free wall rupture in inferior wall myocardial infarc- tion. Am J Cardiol. 2001;88(4):414-7.
47. Alerhand S, Carter JM. What echocardiographic findings suggest a pericardial effu- sion is causing tamponade? Am J Emerg Med 2019;37(2):321-6.
48. Perez-Casares A, Cesar S, Brunet-Garcia L, Sanchez-de-Toledo J. Echocardiographic evaluation of pericardial effusion and cardiac tamponade. Front Pediatr 2017;5:79.
49. Eisenberg MJ, Dunn MM, Kanth N, Gamsu G, Schiller NB. Diagnostic value of chest radiography for pericardial effusion. J Am Coll Cardiol 1993;22(2):588-93.
50. Onoda N, Nonami A, Yabe T, Doi YL, Fujita Y, Yamamoto S, et al. Postinfarct cardiac free wall rupture detected by Multidetector computed tomography. J Cardiol Cases. 2012;5(3):e147-e9.
51. Hoshino A, Yokoya S, Enomoto S, Kawahito H, Kurata H, Nakahara Y, et al. [Survivor of blow out type of free wall rupture: multislice computed tomographic detection of myocardial rupture in a case of small myocardial infarction]. J Cardiol 2007;49 (2):97-102.
52. Brenes JA, Keifer T, Karim RM, Shroff GR. Adjuvant role of CT in the diagnosis of post-infarction left ventricular free-wall rupture. Cardiol Res 2012;3(6):284-7.
53. Mantovani V, Vanoli D, Chelazzi P, Lepore V, Ferrarese S, Sala A. Post-infarction car- diac rupture: surgical treatment. Eur J Cardiothorac Surg 2002;22(5):777-80.
54. Kumar R, Sinha A, Lin MJ, Uchino R, Butryn T, O’Mara MS, et al. Complications of pericardiocentesis: a clinical synopsis. Int J Crit Illn Inj Sci 2015;5(3):206-12.
55. Figueras J, Alcalde O, Barrabes JA, Serra V, Alguersuari J, Cortadellas J, et al. Changes in hospital mortality rates in 425 patients with acute ST-elevation myocardial infarction and cardiac rupture over a 30-year period. Circulation. 2008;118(25):2783-9.
56. Zoffoli G, Battaglia F, Venturini A, Asta A, Terrini A, Zanchettin C, et al. A novel ap- proach to ventricular rupture: clinical needs and surgical technique. Ann Thorac Surg. 2012;93(3):1002-3.
57. Flajsig I, Castells y Cuch E, Mayosky AA, Rodriguez R, Calbet JM, Saura E, et al. Sur- gical treatment of left ventricular free wall rupture after myocardial infarction: case series. Croat Med J 2002;43(6):643-8.
58. Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA, et al. Cardiogenic shock complicating acute myocardial infarction-etiologies, management and out- come: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK? J Am Coll Cardiol. 2000;36(3 Suppl A): 1063-70.
59. Radford MJ, Johnson RA, Daggett WM, Jr., Fallon JT, Buckley MJ, Gold HK, et al. Ven- tricular septal rupture: a review of clinical and physiologic features and an analysis of survival. Circulation. 1981;64(3):545-53.
60. Holmes DR, Jr., Bates ER, Kleiman NS, Sadowski Z, Horgan JH, Morris DC, et al. Con- temporary reperfusion therapy for cardiogenic shock: the GUSTO-I trial experience. The GUSTO-I Investigators. Global Utilization of Streptokinase and Tissue Plasmin- ogen Activator for Occluded Coronary Arteries. J Am Coll Cardiol 1995;26(3): 668-74.
61. Skillington PD, Davies RH, Luff AJ, Williams JD, Dawkins KD, Conway N, et al. Surgi- cal treatment for infarct-related ventricular septal defects. Improved early results combined with analysis of late functional status. J Thorac Cardiovasc Surg 1990; 99(5):798-808.
62. Hutchins GM. Rupture of the interventricular septum complicating myocardial in- farction: pathological analysis of 10 patients with clinically diagnosed perforations. Am Heart J 1979;97(2):165-73.
63. Daggett WM, Buckley MJ, Akins CW, Leinbach RC, Gold HK, Block PC, et al. Im- proved results of surgical management of postinfarction ventricular septal rupture. Ann Surg. 1982;196(3):269-77.
64. Serpytis P, Karvelyte N, Serpytis R, Kalinauskas G, Rucinskas K, Samalavicius R, et al. Post-infarction ventricular septal defect: risk factors and early outcomes. Hellenic J Cardiol 2015;56(1):66-71.
65. Skehan JD, Carey C, Norrell MS, de Belder M, Balcon R, Mills PG. Patterns of coro- nary artery disease in post-infarction ventricular septal rupture. Br Heart J 1989; 62(4):268-72.
66. Toma M, Fu Y, Ezekowitz JA, McAlister FA, Westerhout CM, Granger CB, et al. Does silent myocardial infarction add prognostic value in ST-elevation myocardial in- farction patients without a history of prior myocardial infarction? Insights from the Assessment of Pexelizumab in Acute Myocardial Infarction (APEX-AMI) Trial. Am Heart J. 2010;160(4):671-7.
67. Menon V, Webb JG, Hillis LD, Sleeper LA, Abboud R, Dzavik V, et al. Outcome and profile of ventricular septal rupture with cardiogenic shock after myocardial infarc- tion: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol 2000;36(3 Suppl A): 1110-6.
68. Glancy DL, Khuri BN, Mustapha JA, Menon PV, Hanna EB. Myocardial infarction with ventricular septal rupture and cardiogenic shock. Proc (Bayl Univ Med Cent) 2015;28(4):512-3.
69. Reeder GS. Identification and treatment of complications of myocardial infarction. Mayo Clin Proc 1995;70(9):880-4.
70. Topaz O, Taylor AL. Interventricular septal rupture complicating acute myocardial infarction: from pathophysiologic features to the role of invasive and noninvasive diagnostic modalities in current management. Am J Med 1992;93(6):683-8.
71. Lemery R, Smith HC, Giuliani ER, Gersh BJ. Prognosis in rupture of the ventricular septum after acute myocardial infarction and role of early surgical intervention. Am J Cardiol 1992;70(2):147-51.
72. Maganti K, Rigolin VH, Sarano ME, Bonow RO. Valvular heart disease: diagnosis and management. Mayo Clin Proc 2010;85(5):483-500.
73. Jones BM, Kapadia SR, Smedira NG, Robich M, Tuzcu EM, Menon V, et al. Ventricular septal rupture complicating acute myocardial infarction: a contemporary review. Eur Heart J. 2014;35(31):2060-8.
74. Vlodaver Z, Edwards JE. Rupture of ventricular septum or papillary muscle compli- cating myocardial infarction. Circulation 1977;55(5):815-22.
75. Vargas-Barron J, Molina-Carrion M, Romero-Cardenas A, Roldan FJ, Medrano GA, Avila-Casado C, et al. Risk factors, echocardiographic patterns, and outcomes in pa- tients with acute ventricular septal rupture during myocardial infarction. Am J Cardiol 2005;95(10):1153-8.
76. Evrin T, Unluer EE, Kuday E, Bayata S, Surum N, Eser U, et al. Bedside echocardiog- raphy in Acute myocardial infarction patients with hemodynamic deterioration. J Natl Med Assoc. 2018;110(4):396-8.
77. Smyllie JH, Sutherland GR, Geuskens R, Dawkins K, Conway N, Roelandt JR. Doppler color flow mapping in the diagnosis of ventricular septal rupture and acute mitral regurgitation after myocardial infarction. J Am Coll Cardiol 1990;15(6):1449-55.
78. Fortin DF, Sheikh KH, Kisslo J. The utility of echocardiography in the diagnostic strategy of postinfarction ventricular septal rupture: a comparison of two- dimensional echocardiography versus Doppler color flow imaging. Am Heart J 1991;121(1 Pt 1):25-32.
79. Awasthy N, Radhakrishnan S. Stepwise evaluation of left to right shunts by echo- cardiography. Indian Heart J 2013;65(2):201-18.
80. Konstantinides S, Geibel A, Kasper W, Just H. Noninvasive estimation of right ven- tricular systolic pressure in postinfarction ventricular septal rupture: an assess- ment of two Doppler echocardiographic methods. Crit Care Med 1997;25(7): 1167-74.
81. Murday A. optimal management of acute ventricular septal rupture. Heart 2003;89

    (12):1462-6.

    Malhotra A, Patel K, Sharma P, Wadhawa V, Madan T, Khandeparkar J, et al. Tech- niques, timing & prognosis of post infarct ventricular septal repair: a re-look at old dogmas. Braz J Cardiovasc Surg 2017;32(3):147-55.

82. Tariq S, Aronow WS. Use of inotropic agents in treatment of systolic heart failure. Int J Mol Sci 2015;16(12):29060-8.
83. Bayram M, De Luca L, Massie MB, Gheorghiade M. Reassessment of dobutamine, dopamine, and milrinone in the management of acute heart failure syndromes. Am J Cardiol 2005;96(6A):47G-58G.
84. George I, Xydas S, Topkara VK, Ferdinando C, Barnwell EC, Gableman L, et al. Clin- ical indication for use and outcomes after inhaled nitric oxide therapy. Ann Thorac Surg. 2006;82(6):2161-9.
85. Kettner J, Sramko M, Holek M, Pirk J, Kautzner J. Utility of intra-aortic balloon pump support for ventricular septal rupture and acute mitral regurgitation complicating acute myocardial infarction. Am J Cardiol 2013;112(11):1709-13.
86. Rob D, Spunda R, Lindner J, Rohn V, Kunstyr J, Balik M, et al. A rationale for early extracorporeal membrane oxygenation in patients with postinfarction ventricular septal rupture complicated by cardiogenic shock. Eur J Heart Fail 2017;19 Suppl 2:97-103.
87. Sheu JJ, Tsai TH, Lee FY, Fang HY, Sun CK, Leu S, et al. Early extracorporeal mem- brane oxygenator-assisted primary percutaneous coronary intervention improved

    30-day clinical outcomes in patients with ST-segment elevation myocardial infarc- tion complicated with profound cardiogenic shock. Crit Care Med. 2010;38(9): 1810-7.

    Arnaoutakis GJ, Zhao Y, George TJ, Sciortino CM, McCarthy PM, Conte JV. Surgical repair of ventricular septal defect after myocardial infarction: outcomes from the Society of thoracic surgeons national database. Ann Thorac Surg 2012;94(2): 436-43 [discussion 43-4].

88. La Torre MW, Centofanti P, Attisani M, Patane F, Rinaldi M. Posterior ventricular septal defect in presence of cardiogenic shock: early implantation of the Impella re- cover LP 5.0 as a bridge to surgery. Tex Heart Inst J 2011;38(1):42-9.
89. Poulsen SH, Praestholm M, Munk K, Wierup P, Egeblad H, Nielsen-Kudsk JE. Ven- tricular septal rupture complicating acute myocardial infarction: clinical character- istics and contemporary outcome. Ann Thorac Surg 2008;85(5):1591-6.
90. Jeppsson A, Liden H, Johnsson P, Hartford M, Radegran K. Surgical repair of post in- farction ventricular septal defects: a national experience. Eur J Cardiothorac Surg 2005;27(2):216-21.
91. Thompson CR, Buller CE, Sleeper LA, Antonelli TA, Webb JG, Jaber WA, et al. Cardio- genic shock due to acute severe mitral regurgitation complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we use emergently revascularize Occluded Coronaries in cardiogenic shocK? J Am Coll Cardiol 2000; 36(3 Suppl A):1104-9.
92. Kishon Y, Oh JK, Schaff HV, Mullany CJ, Tajik AJ, Gersh BJ. Mitral valve operation in postinfarction rupture of a papillary muscle: immediate results and long-term follow-up of 22 patients. Mayo Clin Proc 1992;67(11):1023-30.
93. Tcheng JE, Jackman JD, Jr., Nelson CL, Gardner LH, Smith LR, Rankin JS, et al. Out- come of patients sustaining acute ischemic mitral regurgitation during myocardial infarction. Ann Intern Med 1992;117(1):18-24.
94. Glasson JR, Komeda M, Daughters GT, Bolger AF, Karlsson MO, Foppiano LE, et al. Early systolic mitral leaflet “loitering” during acute ischemic mitral regurgitation. J Thorac Cardiovasc Surg. 1998;116(2):193-205.
95. Lai DT, Tibayan FA, Myrmel T, Timek TA, Dagum P, Daughters GT, et al. Mechanistic insights into posterior mitral leaflet inter-scallop malcoaptation during acute ische- mic mitral regurgitation. Circulation. 2002;106(12 Suppl 1):I40-I5.
96. Kimura T, Roger VL, Watanabe N, Barros-Gomes S, Topilsky Y, Nishino S, et al. The unique mechanism of functional mitral regurgitation in acute myocardial infarc- tion: a prospective dynamic 4D quantitative echocardiographic study. Eur Heart J Cardiovasc Imaging. 2018.
97. Lamas GA, Mitchell GF, Flaker GC, Smith SC, Jr., Gersh BJ, Basta L, et al. Clinical sig- nificance of mitral regurgitation after acute myocardial infarction. Survival and Ventricular Enlargement Investigators. Circulation. 1997;96(3):827-33.
98. Voci P, Bilotta F, Caretta Q, Mercanti C, Marino B. Papillary muscle perfusion pat- tern. A hypothesis for ischemic papillary muscle dysfunction. Circulation 1995;91 (6):1714-8.
99. Jain SK, Larsen TR, Darda S, Saba S, David S. A forgotten devil; rupture of mitral valve papillary muscle. Am J Case Rep 2013;14:38-42.
100. Stout KK, Verrier ED. Acute valvular regurgitation. Circulation 2009;119(25): 3232-41.
101. Raman S, Pipavath S. Images in clinical medicine. Asymmetric edema of the upper lung due to mitral valvular dysfunction. N Engl J Med 2009;361(5):e6.
102. Gueret P, Khalife K, Jobic Y, Fillipi E, Isaaz K, Tassan-Mangina S, et al. Echocardio- graphic assessment of the incidence of mechanical complications during the early phase of myocardial infarction in the reperfusion era: a French multicentre prospective registry. Arch Cardiovasc Dis. 2008;101(1):41-7.
103. Czarnecki A, Thakrar A, Fang T, Lytwyn M, Ahmadie R, Pascoe E, et al. Acute severe mitral regurgitation: consideration of papillary muscle architecture. Cardiovasc Ul- trasound. 2008;6:5.
104. Chevalier P, Burri H, Fahrat F, Cucherat M, Jegaden O, Obadia JF, et al. Perioperative outcome and long-term survival of surgery for acute post-infarction mitral regurgi- tation. Eur J Cardiothorac Surg. 2004;26(2):330-5.
105. Chen EP, Bittner HB, Davis Jr RD, Van Trigt 3rd P. Milrinone improves pulmonary hemodynamics and right ventricular function in chronic pulmonary hypertension. Ann Thorac Surg 1997;63(3):814-21.
106. Dekker AL, Reesink KD, van der Veen FH, van Ommen GV, Geskes GG, Soemers AC, et al. Intra-aortic balloon pumping in acute mitral regurgitation reduces aortic im- pedance and regurgitant fraction. Shock. 2003;19(4):334-8.
107. Arnaiz-Garcia ME, Dalmau-Sorli MJ, Gonzalez-Santos JM, Perez-Losada ME, Sastre- Rincon JA, Hernandez-Hernandez J, et al. Veno-arterial extracorporeal membrane oxygenation as a bridge for enabling surgery in a patient under cardiogenic shock due to acute mitral prosthesis dysfunction. J Saudi Heart Assoc. 2018;30 (2):140-2.
108. Staudacher DL, Bode C, Wengenmayer T. Severe mitral regurgitation requiring ECMO therapy treated by interventional valve reconstruction using the MitraClip. Catheter Cardiovasc Interv 2015;85(1):170-5.
109. Kim TS, Na CY, Baek JH, Kim JH, Oh SS. Preoperative extracorporeal membrane ox- ygenation for severe ischemic mitral regurgitation — 2 case reports. Korean J Thorac Cardiovasc Surg 2011;44(3):236-9.
110. Dixon SR, Henriques JP, Mauri L, Sjauw K, Civitello A, Kar B, et al. A prospective fea- sibility trial investigating the use of the Impella 2.5 system in patients undergoing high-risk percutaneous coronary intervention (the PROTECT I Trial): initial U.S. ex- perience. JACC Cardiovasc Interv 2009;2(2):91-6.
111. Wei JY, Hutchins GM, Bulkley BH. Papillary muscle rupture in fatal acute myocar- dial infarction: a potentially treatable form of cardiogenic shock. Ann Intern Med 1979;90(2):149-52.
112. Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, et al. Pericardial disease: diagnosis and management. Mayo Clin Proc. 2010;85(6): 572-93.
113. Imazio M, Hoit BD. Post-cardiac injury syndromes. An emerging cause of pericar- dial diseases. Int J Cardiol 2013;168(2):648-52.
114. Indik JH, Alpert JS. Post-myocardial infarction pericarditis. Curr Treat Options Cardiovasc Med 2000;2(4):351-6.
115. Welin L, Vedin A, Wilhelmsson C. Characteristics, prevalence, and prognosis of postmyocardial infarction syndrome. Br Heart J 1983;50(2):140-5.
116. Lichstein E, Arsura E, Hollander G, Greengart A, Sanders M. Current incidence of postmyocardial infarction (Dressler’s) syndrome. Am J Cardiol 1982;50(6):1269-71.
117. Dressler W. The post-myocardial-infarction syndrome: a report on forty-four cases. AMA Arch Intern Med 1959;103(1):28-42.
118. Lador A, Hasdai D, Mager A, Porter A, Goldenberg I, Shlomo N, et al. Incidence and prognosis of pericarditis after ST-elevation myocardial infarction (from the acute coronary syndrome Israeli survey 2000 to 2013 registry database). Am J Cardiol. 2018;121(6):690-4.
119. Correale E, Maggioni AP, Romano S, Ricciardiello V, Battista R, Salvarola G, et al. Comparison of frequency, diagnostic and prognostic significance of pericardial in- volvement in acute myocardial infarction treated with and without thrombolytics. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico (GISSI). Am J Cardiol 1993;71(16):1377-81.
120. Wall TC, Califf RM, Harrelson-Woodlief L, Mark DB, Honan M, Abbotsmith CW, et al. Usefulness of a pericardial friction rub after thrombolytic therapy during acute myocardial infarction in predicting amount of myocardial damage. The TAMI Study Group. Am J Cardiol. 1990;66(20):1418-21.
121. Mehrzad R, Spodick DH. Pericardial involvement in diseases of the heart and other contiguous structures: part I: pericardial involvement in infarct pericarditis and peri- cardial involvement following myocardial infarction. Cardiology 2012;121(3):164-76.
122. Wessman DE, Stafford CM. The postcardiac injury syndrome: case report and re- view of the literature. South Med J 2006;99(3):309-14.
123. Imazio M, Cooper LT. Management of myopericarditis. Expert Rev Cardiovasc Ther 2013;11(2):193-201.
124. Imazio M, Spodick DH, Brucato A, Trinchero R, Adler Y. Controversial issues in the management of pericardial diseases. Circulation 2010;121(7):916-28.
125. Oliva PB, Hammill SC, Talano JV. T wave changes consistent with epicardial involve- ment in acute myocardial infarction. Observations in patients with a postinfarction pericardial effusion without clinically recognized postinfarction pericarditis. J Am Coll Cardiol 1994;24(4):1073-7.
126. Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis. Ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocar- dial infarction. Circulation 1993;88(3):896-904.
127. Figueras J, Juncal A, Carballo J, Cortadellas J, Soler JS. Nature and progression of peri- cardial effusion in patients with a first myocardial infarction: relationship to age and free wall rupture. Am Heart J 2002;144(2):251-8.
128. Figueras J, Barrabes JA, Serra V, Cortadellas J, Lidon RM, Carrizo A, et al. Hospital outcome of moderate to severe pericardial effusion complicating ST-elevation acute myocardial infarction. Circulation. 2010;122(19):1902-9.
129. O’Gara PT, Kushner FG, Ascheim DD, Casey DE, Jr., Chung MK, de Lemos JA, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarc- tion: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127(4):e362-425.
130. Jugdutt BI, Basualdo CA. Myocardial infarct expansion during indomethacin or ibu- profen therapy for symptomatic post infarction pericarditis. Influence of other pharmacologic agents during early remodelling. Can J Cardiol 1989;5(4):211-21.
131. Hammerman H, Kloner RA, Schoen FJ, Brown Jr EJ, Hale S, Braunwald E. Indomethacin-induced scar thinning after experimental myocardial infarction. Cir- culation 1983;67(6):1290-5.
132. Brown Jr EJ, Kloner RA, Schoen FJ, Hammerman H, Hale S, Braunwald E. Scar thin- ning due to ibuprofen administration after experimental myocardial infarction. Am J Cardiol 1983;51(5):877-83.
133. Schifferdecker B, Spodick DH. Nonsteroidal anti-inflammatory drugs in the treat- ment of pericarditis. Cardiol Rev 2003;11(4):211-7.
134. Imazio M, Demichelis B, Parrini I, Giuggia M, Cecchi E, Gaschino G, et al. Day- hospital treatment of acute pericarditis: a management program for outpatient therapy. J Am Coll Cardiol 2004;43(6):1042-6.
135. Imazio M, Bobbio M, Cecchi E, Demarie D, Demichelis B, Pomari F, et al. Colchicine in addition to conventional therapy for acute pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation. 2005;112(13):2012-6.
136. Imazio M, Brucato A, Forno D, Ferro S, Belli R, Trinchero R, et al. Efficacy and safety of colchicine for pericarditis prevention. Systematic review and meta-analysis. Heart. 2012;98(14):1078-82.
137. Imazio M, Adler Y. Treatment with aspirin, NSAID, corticosteroids, and colchicine in acute and recurrent pericarditis. Heart Fail Rev 2013;18(3):355-60.
138. Adler Y, Charron P, Imazio M, Badano L, Baron-Esquivias G, Bogaert J, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: the Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC) Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015;36(42):2921-64.
139. Lilly LS. Treatment of acute and recurrent idiopathic pericarditis. Circulation 2013; 127(16):1723-6.
140. Imazio M, Brucato A, Cumetti D, Brambilla G, Demichelis B, Ferro S, et al. Corticoste- roids for recurrent pericarditis: high versus low doses: a nonrandomized observa- tion. Circulation. 2008;118(6):667-71.
141. Imazio M, Cecchi E, Demichelis B, Ierna S, Demarie D, Ghisio A, et al. Indicators of poor prognosis of acute pericarditis. Circulation. 2007;115(21):2739-44.
142. Antunes MJ, Antunes PE. Left-ventricular aneurysms: from disease to repair. Expert Rev Cardiovasc Ther 2005;3(2):285-94.
143. Buckberg GD. Defining the relationship between akinesia and dyskinesia and the cause of left ventricular failure after anterior infarction and reversal of remodeling to restoration. J Thorac Cardiovasc Surg 1998;116(1):47-9.
144. Mickleborough LL, Merchant N, Ivanov J, Rao V, Carson S. Left ventricular recon- struction: early and late results. J Thorac Cardiovasc Surg 2004;128(1):27-37.
145. Dubnow MH, Burchell HB, Titus JL. Postinfarction ventricular aneurysm. A clinicomorphologic and electrocardiographic study of 80 cases. Am Heart J 1965; 70(6):753-60.
146. Tikiz H, Atak R, Balbay Y, Genc Y, Kutuk E. Left ventricular aneurysm formation after anterior myocardial infarction: clinical and angiographic determinants in 809 pa- tients. Int J Cardiol 2002;82(1):7-14 [discussion -6].
147. Tavakoli R, Bettex D, Weber A, Brunner H, Genoni M, Pretre R, et al. Repair of postinfarction dyskinetic LV aneurysm with either linear or patch technique. Eur J Cardiothorac Surg. 2002;22(1):129-34.
148. Mills NL, Everson CT, Hockmuth DR. Technical advances in the treatment of left ventricular aneurysm. Ann Thorac Surg 1993;55(3):792-800.
149. Faxon DP, Ryan TJ, Davis KB, McCabe CH, Myers W, Lesperance J, et al. Prognostic significance of angiographically documented left ventricular aneurysm from the Coronary Artery Surgery Study (CASS). Am J Cardiol. 1982;50(1):157-64.
150. Antunes PE, Silva R, Ferrao de Oliveira J, Antunes MJ. Left ventricular aneurysms: early and long-term results of two types of repair. Eur J Cardiothorac Surg 2005; 27(2):210-5.
151. Tikiz H, Balbay Y, Atak R, Terzi T, Genc Y, Kutuk E. The effect of thrombolytic therapy on left ventricular aneurysm formation in acute myocardial infarction: relationship to successful reperfusion and vessel patency. Clin Cardiol 2001;24(10):656-62.
152. Kitamura S, Kay JH, Krohn BG, Magidson O, Dunne EF. Geometric and functional ab- normalities of the left ventricle with a chronic localized noncontractile area. Am J Cardiol 1973;31(6):701-7.
153. Nicolosi AC, Spotnitz HM. Quantitative analysis of regional systolic function with left ventricular aneurysm. Circulation 1988;78(4):856-62.
154. Klein MD, Herman MV, Gorlin R. A hemodynamic study of left ventricular aneu- rysm. Circulation 1967;35(4):614-30.
155. Harken AH. Surgical treatment of cardiac arrhythmias. Sci Am 1993;269(1):68-74.
156. Grondin P, Kretz JG, Bical O, Donzeau-Gouge P, Petitclerc R, Campeau L. Natural history of Saccular aneurysms of the left ventricle. J Thorac Cardiovasc Surg 1979;77(1):57-64.
157. Friedman BM, Dunn MI. Postinfarction ventricular aneurysms. Clin Cardiol 1995;18

     (9):505-11.

     Benediktsson R, Eyjolfsson O, Thorgeirsson G. Natural history of chronic left ventricular aneurysm; a population based cohort study. J Clin Epidemiol 1991;44(11):1131-9.

158. Vlodaver Z, Coe JI, Edwards JE. True and false left ventricular aneurysms. Propensity for the latter to rupture. Circulation 1975;51(3):567-72.
159. Keeley EC, Hillis LD. Left ventricular mural thrombus after acute myocardial infarc- tion. Clin Cardiol 1996;19(2):83-6.
160. Reeder GS, Lengyel M, Tajik AJ, Seward JB, Smith HC, Danielson GK. Mural throm- bus in left ventricular aneurysm: incidence, role of angiography, and relation be- tween anticoagulation and embolization. Mayo Clin Proc 1981;56(2):77-81.
161. Murphy JG, Wright RS, Barsness GW. Ischemic left ventricular aneurysm and anticoagulation: is it the clot or the plot that needs thinning? Mayo Clin Proc 2015;90(4):428-31.
162. Engel J, Brady WJ, Mattu A, Perron AD. Electrocardiographic ST segment elevation: left ventricular aneurysm. Am J Emerg Med 2002;20(3):238-42.
163. Cohn K, Dymnicka S, Forlini FJ. Use of the electrocardiogram as an aid in screening for left ventricular aneurysm. J Electrocardiol 1976;9(1):53-8.
164. Ford RV, Levine HD. The electrocardiographic clue to ventricular aneurysm. Ann In-

     tern Med 1951;34(4):998-1016.

     Kittredge RD, Gamboa B, Kemp HG. Radiographic visualization of left ventricular aneurysms on lateral chest film. AJR Am J Roentgenol 1976;126(6):1140-6.

165. Arvan S, Varat MA. Persistent ST-segment elevation and left ventricular wall abnor-

     malities: a 2-dimensional echocardiographic study. Am J Cardiol 1984;53(11):1542-6.

     Zoffoli G, Mangino D, Venturini A, Terrini A, Asta A, Zanchettin C, et al. Diagnosing left ventricular aneurysm from pseudo-aneurysm: a case report and a review in lit- erature. J Cardiothorac Surg 2009;4:11.

166. Gopal A, Pal R, Karlsberg RP, Budoff MJ. Left Ventricular pseudoaneurysm by cardiac CT angiography. J Invasive Cardiol 2008;20(7):370-1.
167. Delewi R, Zijlstra F, Piek JJ. Left ventricular thrombus formation after acute myocar- dial infarction. Heart 2012;98(23):1743-9.
168. Degheim G, Berry A, Zughaib M. Off label use of direct oral anticoagulants for left ventricular thrombus. Is it appropriate? Am J Cardiovasc Dis 2017;7(5):98-101.
169. Mourdjinis A, Olsen E, Raphael MJ, Mounsey JP. Clinical diagnosis and prognosis of ventricular aneurysm. Br Heart J 1968;30(4):497-513.
170. Witt BJ, Ballman KV, Brown Jr RD, Meverden RA, Jacobsen SJ, Roger VL. The incidence of stroke after myocardial infarction: a meta-analysis. Am J Med 2006;119(4):354 e1-9.
171. Witt BJ, Brown Jr RD, Jacobsen SJ, Weston SA, Yawn BP, Roger VL. A community- based study of stroke incidence after myocardial infarction. Ann Intern Med 2005;143(11):785-92.
172. Chen J, Hsieh AF, Dharmarajan K, Masoudi FA, Krumholz HM. National trends in heart failure hospitalization after acute myocardial infarction for Medicare benefi- ciaries: 1998-2010. Circulation 2013;128(24):2577-84.
173. Uretsky BF, Sheahan RG. Primary prevention of sudden cardiac death in heart fail- ure: will the solution be shocking? J Am Coll Cardiol 1997;30(7):1589-97.
174. Parikh CR, Coca SG, Wang Y, Masoudi FA, Krumholz HM. long-term prognosis of acute kidney injury after acute myocardial infarction. Arch Intern Med 2008;168(9):987-95.
175. Reejhsinghani R, Lotfi AS. Prevention of stent thrombosis: challenges and solutions. Vasc Health Risk Manag 2015;11:93-106.
176. Holmes DR, Jr., Kereiakes DJ, Garg S, Serruys PW, Dehmer GJ, Ellis SG, et al. Stent thrombosis. J Am Coll Cardiol. 2010;56(17):1357-65.