Mechanical Complication of Myocardial Infaction

ARTICLE IN PRESS
REVIEW
Mechanical Complications of Myocardial Infarction

Andrew Murphy, MD, Sheldon Goldberg, MD
Pennsylvania Hospital of the University of Pennsylvania Health System, Philadelphia, PA.
ABSTRACT
Mechanical complications of myocardial infarction include rupture of a papillary muscle, ventricular sep-
tum, and free wall. Since the advent of acute coronary reperfusion, there has been a significant reduction
in the incidence of these complications. One must have a high index of suspicion for a mechanical compli-
cation in any patient who develops cardiogenic shock in the days following a myocardial infarction. The
most important diagnostic investigation in evaluation of these complications is echocardiography.
Although there is a role for mechanical circulatory support, urgent surgical repair is required in most cases.
We will review the predictors, clinical features, diagnostic, and management strategies in patients with
these complications.
Published by Elsevier Inc. The American Journal of Medicine (2022) 000:1−9
KEYWORDS: Cardiogenic shock; Free wall rupture; Myocardial infarction; Papillary muscle rupture; Ventricular
septal rupture
INCIDENCE IN THE PRE- AND POSTREPERFUSION 0.2% in the reperfusion era.3-7 The incidence of ventricular
ERA septal rupture complicating acute myocardial infarction in
Rupture of the left ventricular myocardium during the course the pre-reperfusion era was approximately 2% and 0.17%-
of an acute myocardial infarction may affect the free wall, the 0.31% in the reperfusion era.8,9 In the pre-reperfusion era,
interventricular septum, or the papillary muscles. When a rup- the incidence of papillary muscle rupture after myocardial
ture occurs, it is referred to as a mechanical complication of infarction was between 1% and 5% and is between 0.2%
acute myocardial infarction. All mechanical complications and 0.3% in the reperfusion era (Figure 1).10
may lead to cardiogenic shock. Since the advent of coronary A study examining the effect of timing of reperfusion by
reperfusion, the incidence of mechanical complications has primary coronary angioplasty on mechanical complications
declined. Even though mortality remains high, their recogni- in acute myocardial infarction divided patients into 3
tion is important because survivors who have undergone groups: early reperfusion (fewer than 12 hours), late reper-
repair may have a good long-term prognosis.1 fusion (more than 12 hours), and failed reperfusion. The
Mechanical complications occur infrequently but are incidence of mechanical complications was highest in the
important predictors of prognosis following myocardial failed reperfusion group (early 1.4%; late 1.8%; failed
infarction. They most commonly occur within the first 5.0%; P < .01). Successful late reperfusion is associated
week after myocardial infarction.2 Multiple studies have with reduced risk of mechanical complications in patients
demonstrated the benefit of reperfusion in reducing the inci- with acute myocardial infarction (Figure 3).12
dence of mechanical complications. The incidence of free In a retrospective observational study that examined the
wall rupture after myocardial infarction in the pre-reperfu- incidence and characteristics of myocardial infarction-associ-
sion era was between 2% and 6.2% and has declined to ated mechanical complications, factors associated with
mechanical complications were advanced age, poor nutritional
status, high Killip class, delayed diagnosis of myocardial
Funding: None.
Conflicts of Interest: None. infarction, high lactate concentration, low thrombolysis in
Authorship: Both authors had access to the data and a role in writing myocardial infarction flow grade, and single-vessel disease.13
this manuscript. In a study that evaluated all ST-elevation myocardial
Requests for reprints should be addressed to Andrew Murphy, MD, infarction (STEMI) and non-ST-elevation myocardial infarc-
Internal Medicine, Pennsylvania Hospital of the University of Pennsylva-
tion hospitalizations in the National Inpatient Sample data-
nia Health System, 800 Spruce St., Philadelphia, PA 19107.
E-mail address: andrew.murphy2@pennmedicine.upenn.edu base (2003 to September 2015), the rates of in-hospital
0002-9343/Published by Elsevier Inc.

https://doi.org/10.1016/j.amjmed.2022.08.017
Descargado para Anonymous User (n/a) en Cayetano Heredia Pervuvian University de ClinicalKey.es por Elsevier en octubre 07, 2022. Para uso
personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2022. Elsevier Inc. Todos los derechos reservados.
ARTICLE IN PRESS
2 The American Journal of Medicine, Vol 000, No 000, && 2022
mortality in patients with mechanical complications were Clinical Presentation

42.4% after STEMI and 18.0% after non-STEMI (Figure 2). The clinical presentation of papillary muscle rupture is acute
Patients who developed mechanical complications after myo- onset hypotension and respiratory distress due to pulmonary
cardial infarction had higher rates of in-hospital mortality, edema, occurring within 2 to 7 days after an inferior
cardiogenic shock, acute kidney injury, hemodialysis, and STEMI.17 However, signs and symptoms are quite variable,
respiratory complications compared with those without ranging from mild dyspnea to cardiopulmonary arrest. Hemo-
mechanical complications.11 dynamic stability depends on the
integrity of the subvalvular appara-
PAPILLARY MUSCLE CLINICAL SIGNIFICANCE tus, degree of mitral regurgitation,
RUPTURE and the extent and location of myo-
Rupture of the left ventricular myocar- cardial damage.18 Complete papillary
dium during the course of an acute muscle rupture generally results in
Risk Predictors
myocardial infarction may affect the cardiogenic shock and death, while
In an observational study that
examined clinical and angio-
free wall, the interventricular septum, partial rupture usually presents with
or the papillary muscles. pulmonary congestion without shock.
graphic difference between
patients with and without papil- When a rupture occurs, it is referred to Approximately 80% of ruptures
lary muscle rupture, patients with as a mechanical complication of acute occur within 10
7 days after myocardial
myocardial infarction and may lead to infarction.
papillary muscle rupture were
found to be older (67 vs 60 years, cardiogenic shock.
P < .005), have a lower rate of Since the advent of coronary reperfu-
diabetes mellitus (7% vs 38%,
Diagnosis (Noninvasive and
sion, the incidence of mechanical
P < .005), and lower rate of prior Catheterization Findings)
complications has declined, but recog-
angina or myocardial infarction The classic physical examination
nizing them is important.
(24% vs 50%, P < .005). The finding of papillary muscle rupture is
incidence of multivessel disease a holosystolic murmur loudest at the
was higher in patients without apex, radiating to the axilla.2 How-
papillary muscle rupture (87% vs 56%, P < .06).12 In a ever, a murmur may be inaudible. The explanation for an
separate study, patients with papillary muscle rupture inaudible murmur in severe mitral regurgitation is due to a
were found to have a higher prevalence of systemic rapid increase in pressure in the left atrium coupled with a
hypertension and inferior myocardial infarction than large regurgitant orifice resulting in insufficient turbulence to
those from a control group (Figure 4). 13 create a murmur.17 Chest radiography demonstrates pulmo-
Autopsy analysis has shown that the posteromedial pap- nary edema.19
illary muscle ruptures 3 times more frequently than the Transthoracic echocardiography (TTE) usually demon-
14 strates a flail segment of the mitral valve and often a sev-
anterolateral muscle (73% and 27%, respectively). The
anterolateral papillary muscle is less vulnerable to rupture ered papillary muscle head may be seen moving freely.17 A
due to its dual blood supply from the left anterior descend- hyperdynamic contraction pattern in the noninfarcted area
15 occurs as a result of ventricular contraction against the low
ing artery and circumflex artery. The posteromedial papil-
lary muscle is more prone to ischemia and rupture due to its impedance left atrium.17 A diagnosis by TTE may not be
dependence on single blood supply from the posterior
descending artery.15,16
Figure 2 The incidence of mechanical complications

in STEMI and NSTEMI patients in the reperfusion
Figure 1 The incidence of mechanical complications era.11 NSTEMI = non-ST-elevation myocardial infarc-
in the pre and postreperfusion eras. FWR = free wall tion; STEMI = ST-elevation myocardial infarction.
rupture; PMR = papillary muscle rupture; VSR = ven- FWR = free wall rupture; PMR = papillary muscle rup-
tricular septal rupture. ture; VSR = ventricular septal rupture.
ARTICLE IN PRESS
Murphy and Goldberg Mechanical Complications of Myocardial Infarction 3
Figure 3 Relationship between timing of reperfusion

and incidence of MCs. MC = mechanical complication.
Figure 5 Pulmonary artery catheter wedge tracing in
PMR. PCWP of 25 mm Hg with V waves > 50 mm
Hg (arrow). Note the timing of the V wave, after the
possible in some patients due to technical difficulties in T wave on the ECG.22 ECG = electrocardiogram;
PCWP = pulmonary capillary wedge pressure;
obtaining adequate quality images. Transesophageal echo-
PMR = papillary muscle rupture.
cardiogram examination of the left ventricle is useful in the
diagnosis of papillary muscle rupture, especially in those
patients in whom the ruptured head does not prolapse into
the left atrium.20 trial registry, approximately 10% of patients who presented
Right heart catheterization has limited use in the diagno- with shock after STEMI presented with severe mitral regur-
sis of acute mitral regurgitation but can be useful in differ- gitation and had an overall hospital mortality of 55%. Mor-
entiating it from ventricular septal rupture (see Table). The tality with medical treatment alone was 71% compared
pulmonary capillary wedge pressure in papillary muscle with 40% with surgery.21,24 Mortality and ventricular func-
rupture is typically very high. Large systolic V waves may tion are improved with surgery compared with medical
be seen in both papillary muscle rupture and ventricular therapy alone.21 Coronary artery bypass grafting should be
septal rupture. This is due to enhanced left atrial filling done at the same time as mitral valve surgery.21
retrograde from the left ventricle or antegrade from the pul- In a study that compared mitral valve replacement and
monary circulation as a result of left to right shunting.21 repair in partial papillary muscle rupture after myocardial
(See Figure 5) infarction, mitral valve repair for partial rupture was reli-
able with good short- and long-term results, provided
Prevention, Treatment, and Prognosis

All patients with papillary muscle rupture should be consid-
ered for urgent surgery.23 While emergency surgery is
arranged, stabilizing measures include an intra-aortic bal-
loon pump (IABP), inotropic support, and afterload reduc-
tion to reduce regurgitant volume and pulmonary
congestion. In the Should We Use Emergently Revascular-
ize Occluded Coronaries in Cardiogenic Shock? (SHOCK)
Figure 6 Diagnostic approach to PMR.

Figure 4 Comparison of clinical and angiographic fea- PMR = papillary muscle rupture; RHC = right heart
tures between patients with and without PMR. catheteriation; TEE = transesophageal echocardiogra-
PMR = papillary muscle rupture. phy; TTE = transthoracic echocardiography.
ARTICLE IN PRESS
Figure 7 Risk predictors of VSD in acute MI with odds

ratios and confidence intervals. MI = myocardial infarc-
tion; VSD = ventricular septal defect.
Figure 8 Physiologic complications of VSR.

VSR = ventricular septal rupture.
adjacent tissue is not friable and established repair techni-
ques are used.25
Preoperative inotropic drug support and mitral valve Another study demonstrated that advanced age, anterior
replacement without preservation of the subvalvular appara- infarct location, female sex, no current smoking, hyperten-
tus are strong independent predictors of a lower survival in sion, extensive coronary artery disease, and no previous
patients undergoing mitral valve surgery for papillary muscle myocardial infarction or angina are important predictors of
rupture after myocardial infarction. Whenever possible, the ventricular septal defect.3,27-29
subvalvular apparatus should be preserved (Figure 6).10 In a study that examined cardiac angiography in 91
patients with ventricular septal defect after myocardial
infarction compared to 123 stable survivors who had a posi-
VENTRICULAR SEPTAL DEFECT tive submaximal exercise test early after infarction, patients
with ventricular septal rupture had more extensive left ven-
Risk Predictors tricular damage with aneurysm formation. Coronary angi-
Independent clinical predictors for development of ventric- ography showed more single than triple vessel disease. In
ular septal defect are age (odds ratio [OR] 2.19, 95% confi- the comparison group there was more triple-vessel disease
dence interval [CI] 1.62 to 2.98; P < .001), female gender than single-vessel disease. Angiographically demonstrable
(OR 5.07, 95% CI 2.7 to 9.98; P < .001), and lack of previ- collaterals to the infarct territory were absent or faint in
ous angina (OR 2.11, 95% CI 1.12 to 4.29; P = .021). Two 82% of those with septal rupture. Well-developed collater-
electrocardiographic variables predict development of acute als were seen in two-thirds of the comparison group. These
ventricular septal defect: the magnitude of ST deviation in patterns of coronary disease suggest that ventricular septal
lead III (OR 1.55, 95% CI 1.12 to 2.21l P = .007) and in rupture is more likely in patients with coronary occlusion
lead V2 (P < .001); see Figure 7.26 and little or no collateral support to the infarct territory.29
Table
Echocardiographic findings Angiographic findings (compared Right heart catheterization
to patients who did not develop findings
the complication)
Papillary muscle rupture Flail segment of mitral valve Lower incidence of multivessel Low pulmonary arterial oxygen
Severed papillary muscle head disease saturation
Large V waves
Very high PCWP
Ventricular septal rupture Turbulent flow traversing the Lower incidence of multivessel Normal or elevated pulmonary
ventricular septum during disease arterial oxygen saturation
systole Lower rate of collateral circula- Large V waves
tion to infarct territory
PCWP = pulmonary capillary wedge pressure.
ARTICLE IN PRESS
a systolic murmur in the setting of acute myocardial infarc-

tion.30 Ventricular septal rupture can be identified by turbu-
lent flow traversing the ventricular septum during systole.31
Transesophageal echocardiogram is a useful and safe
adjunct to transthoracic imaging for diagnosis and may
improve diagnostic accuracy and image quality.32
Right heart catheterization can provide diagnostic infor-
mation if echocardiography is equivocal (see Table).19 A
demonstrated “step-up” between samples taken from the
right atrium and pulmonary artery confirms the presence of
a ventricular shunt.18 The ratio of flow between the pulmo-
Figure 9 Findings from an oximetry run per- nary and systemic circulations provides an estimate of the
formed in a patient with a large VSD.33 size of the shunt. The excess pulmonary blood flow repre-
VSD = ventricular septal defect. sents the amount of blood passing through the defect.19
Oxygen saturation samples are taken simultaneously to
estimate the pulmonary to systemic flow ratio from
Clinical Presentation the right atrium, pulmonary artery, and systemic artery
Ventricular septal defect after myocardial infarction most (Figures 9-11). A pulmonary to systemic flow ratio greater
commonly occurs within the first week after a myocardial than 2 suggests a large shunt. A normal or high pulmonary
infarction, with a mean time interval of 3 to 5 days. Ventric- artery saturation in a patient with cardiogenic shock is a
ular septal rupture causes left to right shunting with classic finding in patients with ventricular septal rupture
increased pulmonary blood flow and left ventricular volume after myocardial infarction.19
overload.27 Ventricular septal defect after myocardial Pulmonary blood flow (Qp) is calculated using the fol-
infarction generally presents with acute onset heart failure, lowing formula with PV indicating pulmonary vein and PA
chest pain, and hypotension.27 These features may be diffi- indicating pulmonary artery:33
cult to differentiate from that of acute mitral regurgitation. O2 consumption ðmL per minÞ
Qp ðL per minÞ ¼
One important difference is that in ventricular septal rupture ½PV O2 content ðmL per LÞ ½PA O2 content ðmL per LÞ
after myocardial infarction, patients may be comfortable
while supine, and acute pulmonary edema is generally less According to Fick’s principle, cardiac output (CO) is
severe than in papillary muscle rupture (Figure 8).17 calculated using the same formula, with SA indicating sys-
temic artery and MV indicating mixed venous:33
O2 consumption ðmL per minÞ
Diagnosis (Noninvasive and Angiographic CO ðL per minÞ ¼
½SA O2 content ðmL per LÞ ½MV O2 content ðmL per LÞ
Patterns)
A left to right shunt associated with ventricular septal rup-
ture produces a holosystolic murmur, which is loudest along
the left parasternal border and may be associated with a Prevention, Treatment, and Prognosis
thrill.27 In the setting of cardiogenic shock, the flow across Afterload reduction is critical in ventricular septal rupture
the defect may be inadequate to produce a thrill or a mur- and can be achieved with pharmacologic and mechanical
mur. A third heart sound may be present. TTE echocardiog- measures. Intravenous nitrates such as nitroprusside are
raphy with Doppler imaging is the diagnostic investigation beneficial in improving cardiac index and can be titrated
of choice with a sensitivity and specificity of 100%.30 The intravenously often without causing a significant change in
combination of 2-dimensional echocardiography and Dopp- systemic arterial pressure.21,34 Nonpharmacologic measures
ler color flow mapping is sensitive and specific for the dif- include an IABP,21 axial flow pumps, and extracorporeal
ferentiation of postinfarction ventricular septal rupture and membrane oxygenation (ECMO).35,36 In a computer simu-
acute mitral regurgitation and is the optimal method for lation that examined hemodynamic effects of mechanical
defining the underlying pathology in patients who develop circulatory support devices in patients with ventricular
Figure 10 Diagnostic approach to VSR. VSR = ventricular septal rupture; TEE = transesophageal echocardiog-
raphy; TTE = transthoracic echocardiography.
ARTICLE IN PRESS
Figure 11 Echocardiographic, angiographic, and right heart catheterization findings of PMR and VSR. PMR = papillary
muscle rupture; VSR = ventricular septal rupture.
septal defect after myocardial infarction, Impella 5.0 pro- mortality if repair was delayed until after 7 days. Mortality
vided the greatest degree of reduction in pulmonary capil- was highest (>60%) in patients who underwent surgery in
lary wedge pressure and shunt volume.35 A case report the first 24 hours. The improved outcome with delayed sur-
examining effects of intraoperative implantation of Impella gery may be related to evolution of the infarct and
5.5 SmartAssist in ventricular septal defect after myocardial improved stability of the cardiac tissue allowing a more
infarction with cardiogenic shock concluded that the effective repair but is also a representation of survival bias
Impella axial flow pump lowers pulmonary arterial and because early surgery is usually performed on individuals
wedge pressure, reduces mitral regurgitation, and supports with marked hemodynamic instability. The clinician must
the stunned ventricle with improvement of cardiac index weigh the known risk of early surgery against the risk of
after early surgical ventricular septal defect closure.36 For postponing surgery and clinical deterioration. In general,
patients who are hemodynamically unstable, delayed surgi- immediate surgery is preferred in hemodynamically unsta-
cal repair with ECMO for hemodynamic support is an ble patients. In hemodynamically stable patients with a
option.27 However, stabilizing measures should not delay large ventricular septal defect, mechanical circulatory
surgical treatment.
Surgical repair with coronary artery bypass grafting for
ventricular septal rupture after myocardial infarction is a
class 1 recommendation.21 In select cases, transcatheter
approach can provide immediate closure of the defect and
early hemodynamic stabilization.27 Percutaneous transcath-
eter ventricular septal defect closure allows immediate sep-
aration of pulmonary and systemic circulation by
diminishing trans-septal flow. In patients with advanced
age and multiple comorbidities, transcatheter closure is an
option.27
Mortality of patients with ventricular septal defect in the
STS database varied significantly depending on timing of
Figure 12 Risk predictors of FWR in acute MI.
surgery. Patients who underwent surgery within 7 days of FWR = free wall rupture; MI = myocardial infarction.
presentation had a 54.1% mortality compared with 18.4%
ARTICLE IN PRESS
Clinical presentation of free wall rupture depends if the

rupture is complete or incomplete. Free wall rupture may
present as hemorrhage, tamponade, hypotension, cardio-
genic shock, or sudden death.19 Sudden onset of pain fol-
lowing coughing or straining may be suggestive of free
wall rupture.19 Pulseless electrical activity has a predictive
accuracy of 95% for diagnosing free wall rupture in patients
with a first myocardial infarction without overt heart fail-
ure.42 Rarely, free wall rupture may lead to the formation
of a pseudoaneurysm due containment by epicardial clots
or pericardial adhesions.43
Diagnosis (Noninvasive and Angiographic

Patterns)
Diagnostic investigations are not always a priority given the
nature of free wall rupture. The definitive diagnosis is usu-
ally made at surgery.43 However, if time allows, echocardi-
ography is the modality of choice, with a sensitivity and
Figure 13 Echocardiographic features of cardiac tam- specificity of 93%-98%. Echocardiographic features
ponade. IVC = interior vena cava. include a pericardial collection with signs of cardiac tampo-
nade, including collapse of the right atrium and ventricle in
diastole, a dilated inferior vena cava, and marked respira-
tory variation in mitral and tricuspid valve inflow.19 In left
support and delayed surgery after 7 days is preferred. In
ventricular pseudoaneurysm, Doppler can demonstrate the
hemodynamically stable patients with a small ventricular
discontinuity of the ventricular wall and highlight the dis-
septal defect, delayed surgery as long as possible is
tinctive bidirectional flow between the extracardiac echo-
preferred.37-39
free space and the left ventricle.43
Poor prognostic factors in patients with ventricular sep-
Right heart catheterization at the bedside would demon-
tal rupture include development of cardiogenic shock, right
ventricular dysfunction, and inferior infarct location.40 strate the hemodynamic abnormality of cardiac tamponade
Patients who are treated medically have a very poor progno- with equalization of right atrial, right ventricular diastolic
and pulmonary capillary wedge pressures (Figure 13).19
sis with a mortality rate of 94% within 30 days.27,40
Prevention, Treatment, and Prognosis

FREE WALL RUPTURE The most important determinants in preventing free wall
Risk Predictors rupture are successful early reperfusion and the presence of
In a study that evaluated predictors of free wall rupture in collateral circulation.21
reperfused acute myocardial infarction, the following charac- Emergency surgical repair is the preferred treatment of
teristics were associated with a higher rate of free wall rupture free wall rupture.21 Emergency pericardiocentesis may pro-
in the univariable analysis: age greater than 70 (5.2% vs vide hemodynamic short-term improvement by relieving the
1.2%, P < .001), female gender (5.1% vs. 1.8%, P = .006), tamponade. However, it can cause a dangerous increase in
anterior location (3.3% vs 1.4%, P = .02), and treatment blood pressure with increased tension on damaged myocar-
>2 hours after symptom onset (3.6% vs 1.7%, P = .043). In dium, with the potential for extension of a small tear to a rup-
the multivariable analysis, age >70 (OR 4.12, 95% CI 3.04 to ture.19 In preparation for surgery, hemodynamic stabilization
8.62, P < .001) and anterior location (OR 2.91, 95% CI: 1.36 may require inotropes, intravenous fluids and IABP. In the
to 6.63, P = .008) were independent risk factors of free wall presence of refractory cardiac arrest, ECMO may be useful to
rupture, and treatment with percutaneous coronary interven- provide a chance for definitive surgical treatment.43
tion was an independent protective factor (OR 0.46, 95% CI Two surgical approaches can be used: sutureless and
0.22 to 0.96, P = .0371); see Figure 12.41 sutured repair. Sutured approaches include linear closure,
infarctectomy and closure, and patch covering.43 The avail-
ability of tissue adhesive materials and surgical glues have
Clinical Presentation made the sutureless technique more popular. Surgical princi-
The frequency of free wall rupture has 2 peaks: an early peak ples in free wall rupture are to relieve tamponade, close the
within 24 hours and a late peak from 3 to 5 days after STEMI. tear or stop the bleeding, anchor the repair on healthy tissue,
Early rupture is related to the initial evolution of infarction and minimize distortion of heart geometry while preventing
before significant collagen deposition and late rupture is recurrence of rupture or pseudoaneurysm formation.43
related to expansion of the infarct-related ventricular wall.21 Free wall rupture is associated with 20% mortality.19
ARTICLE IN PRESS
CONCLUSION 14. Barbour DJ, Roberts WC. Rupture of a left ventricular papillary mus-
The incidence of mechanical complications has decreased cle during acute myocardial infarction: analysis of 22 necropsy
patients. J Am Coll Cardiol 1986;8(3):558–65. https://doi.org/
markedly in the era of coronary reperfusion. A high index
10.1016/s0735-1097(86)80182-6.
of suspicion is required for prompt diagnosis so that optimal 15. Bouma W, Wijdh-den-Hamer IJ, Koene BM, et al. Predictors of in-
therapy can be instituted in a timely fashion. The improve- hospital mortality after mitral valve surgery for post-myocardial
ment in surgical and catheter based techniques have infarction papillary muscle rupture. J Cardiothorac Surg 2014;9:171.
resulted in significant reductions in mortality. Efforts https://doi.org/10.1186/s13019-014-0171-z.
16. Estes EH Jr, Dalton FM, Entman ML, Dixon HB 2nd, Hackel DB. The
directed at earlier diagnosis and initiation of reperfusion
anatomy and blood supply of the papillary muscles of the left ventri-
therapy of acute myocardial infarction offer the best hope cle. Am Heart J 1966;71(3):356–62. https://doi.org/10.1016/0002-
for avoiding these life-threatening complications. 8703(66)90475-3.
17. Reeder GS. Identification and treatment of complications of myocar-
References dial infarction. Mayo Clin Proc 1995;70(9):880–4. https://doi.org/
10.1016/S0025-6196(11)63946-3.
1. Brunschwig T, Eberli FR, Herren T. Mechanische Komplikationen bei
18. G€uvenç RC, G€uvenç TS. Clinical presentation, diagnosis and manage-
akutem Myokardinfarkt [Mechanical complications of acute myocar-
ment of acute mitral regurgitation following acute myocardial infarc-
dial infarction]. Z Kardiol 2004;93(11):897–907. https://doi.org/
tion. J Acute Dis 2016;5(2):96–101.
10.1007/s00392-004-0133-x.
19. Kutty RS, Jones N, Moorjani N. Mechanical complications of acute
2. Gong FF, Vaitenas I, Malaisrie SC, Maganti K. Mechanical complica-
myocardial infarction. Cardiol Clin 2013;31(4):519–31. https://doi.
tions of acute myocardial infarction: a review. JAMA Cardiol 2021;6
org/10.1016/j.ccl.2013.07.004.
(3):341–9. https://doi.org/10.1001/jamacardio.2020.3690.
20. Moursi MH, Bhatnagar SK, Vilacosta I, San Roman JA, Espinal MA,
3. Feneley MP, Chang VP, O’Rourke MF. Myocardial rupture after acute
Nanda NC. Transesophageal echocardiographic assessment of papil-
myocardial infarction. Ten year review. Br Heart J 1983;49(6):550–6.
lary muscle rupture. Circulation 1996;94(5):1003–9. https://doi.org/
https://doi.org/10.1136/hrt.49.6.550.
10.1161/01.cir.94.5.1003.
4. Lopez-Send on J, Gonzalez A, Lopez de Sa E, et al. Diagnosis of sub-
21. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines
acute ventricular wall rupture after acute myocardial infarction: sensi-
for the management of patients with ST-elevation myocardial infarc-
tivity and specificity of clinical, hemodynamic and echocardiographic
tion−executive summary. A report of the American College of Cardi-
criteria. J Am Coll Cardiol 1992;19(6):1145–53. https://doi.org/
ology/American Heart Association Task Force on Practice Guidelines
10.1016/0735-1097(92)90315-e.
(Writing Committee to revise the 1999 guidelines for the management
5. Becker RC, Gore JM, Lambrew C, et al. A composite view of cardiac
of patients with acute myocardial infarction). J Am Coll Cardiol
rupture in the United States National Registry of Myocardial Infarc-
2004;44(3):671–719. https://doi.org/10.1016/j.jacc.2004.07.002. Erra-
tion. J Am Coll Cardiol 1996;27(6):1321–6. https://doi.org/10.1016/
tum in: J Am Coll Cardiol. 2005;45(8):1376.
0735-1097(96)00008-3.
22. Labrada L, Patil A, Kumar J, et al. Papillary muscle rupture complicat-
Tag edP 6. Pappas PJ, Cernaianu AC, Baldino WA, Cilley JH Jr, DelRossi AJ.
ing acute myocardial infarction: a tale of teamwork. JACC Case Rep
Ventricular free-wall rupture after myocardial infarction. Treatment
2020;2(15):2283–8. https://doi.org/10.1016/j.jaccas.2020.08.027.
and outcome. Chest 1991;99(4):892–5. https://doi.org/10.1378/
23. Damluji AA, van Diepen S, Katz JN, et al. Mechanical complications
chest.99.4.892.
of acute myocardial infarction: a scientific statement from the Ameri-
7. Slater J, Brown RJ, Antonelli TA, et al. Cardiogenic shock due to car-
can Heart Association. Circulation 2021;144(2):e16–35. https://doi.
diac free-wall rupture or tamponade after acute myocardial infarction:
org/10.1161/CIR.0000000000000985.
a report from the SHOCK Trial Registry. Should we emergently revas-
24. Thompson CR, Buller CE, Sleeper LA, et al. Cardiogenic shock due to
cularize occluded coronaries for cardiogenic shock? J Am Coll Car-
acute severe mitral regurgitation complicating acute myocardial
diol 2000;36(3 Suppl A):1117–22. https://doi.org/10.1016/s0735-1097
infarction: a report from the SHOCK Trial Registry. Should we use
(00)00845-7.
emergently revascularize occluded coronaries in cardiogenic shock? J
8. Kinkel CR, Selene Janette SP, Arias ER, et al. Ventricular septal rup-
Am Coll Cardiol 2000;36(3 Suppl A):1104–9. https://doi.org/10.1016/
ture complicating acute myocardial infarction: interesting case and
s0735-1097(00)00846-9.
review. Cardiovasc Thorac Surg 2019;4(1):1–5. https://doi.org/
25. Bouma W, Wijdh-den Hamer IJ, Klinkenberg TJ, et al. Mitral valve
10.15226/2573-864X/4/1/00154.
repair for post-myocardial infarction papillary muscle rupture. Eur J
9. Moreyra AE, Huang MS, Wilson AC, et al. Trends in incidence and
Cardiothorac Surg 2013;44(6):1063–9. https://doi.org/10.1093/ejcts/
mortality rates of ventricular septal rupture during acute myocardial
ezt150.
infarction. Am J Cardiol 2010;106(8):1095–100. https://doi.org/
26. Birnbaum Y, Wagner GS, Gates KB, et al. Clinical and electrocar-
10.1016/j.amjcard.2010.06.013.
diographic variables associated with increased risk of ventricular sep-
10. Bouma W, Wijdh-den-Hamer IJ, Koene BM, et al. Long-term survival
tal defect in acute anterior myocardial infarction. Am J Cardiol
after mitral valve surgery for post-myocardial infarction papillary
2000;86(8):830–4.
muscle rupture. J Cardiothorac Surg 2015;10:11.
27. Shahreyar M, Akinseye O, Nayyar M, Ashraf U, Ibebuogu UN. Post-
11. Elbadawi A, Elgendy IY, Mahmoud K, et al. Temporal trends and out-
myocardial infarction ventricular septal defect: a comprehensive
comes of mechanical complications in patients with acute myocardial
review. Cardiovasc Revasc Med 2020;21(11):1444–9.
infarction. JACC Cardiovasc Interv 2019;12(18):1825–36. https://doi.
28. Crenshaw BS, Granger CB, Birnbaum Y, et al. Risk factors, angio-
org/10.1016/j.jcin.2019.04.039.
graphic patterns and outcomes in patients with ventricular septal
12. Calvo FE, Figueras J, Cortadellas J, Soler-Soler J. Severe mitral regur-
defect complicating acute myocardial infarction. Circulation
gitation complicating acute myocardial infarction. Clinical and angio-
2000;101:27–32.
graphic differences between patients with and without papillary
29. Skehan JD, Carey C, Norrell MS, et al. Patterns of coronary artery dis-
muscle rupture. Eur Heart J 1997;18(10):1606–10. https://doi.org/
ease in post-infarction ventricular septal rupture. Heart 1989;62:
10.1093/oxfordjournals.eurheartj.a015140.
268–72.
13. Figueras J, Calvo F, Cortadellas J, Soler-Soler J. Comparison of
30. Smyllie JH, Sutherland GR, Geuskens R, Dawkins K, Conway N,
patients with and without papillary muscle rupture during acute myo-
Roelandt JR. Doppler color flow mapping in the diagnosis of ventricu-
cardial infarction. Am J Cardiol 1997;80(5):625–7. https://doi.org/
lar septal rupture and acute mitral regurgitation after myocardial
10.1016/s0002-9149(97)00435-9.
ARTICLE IN PRESS
infarction. J Am Coll Cardiol 1990;15(6):1449–55. https://doi.org/ 37. Jones BM, Kapadia SR, Smedira NG, et al. Ventricular septal rupture
10.1016/s0735-1097(10)80038-5. complicating acute myocardial infarction: a contemporary review. Eur
31. Harrison MR, MacPhail B, Gurley JC, et al. Usefulness of color Dopp- Heart J 2014;35(31):2060–8. https://doi.org/10.1093/eurheartj/ehu248.
ler flow imaging to distinguish ventricular septal defect from acute 38. Arnaoutakis GJ, Zhao Y, George TJ, Sciortino CM, McCarthy PM,
mitral regurgitation complicating acute myocardial infarction. Am J Conte JV. Surgical repair of ventricular septal defect after myocardial
Cardiol 1989;64(12):697–701. https://doi.org/10.1016/0002-9149(89) infarction: outcomes from the Society of Thoracic Surgeons National
90750-9. Database. Ann Thorac Surg 2012;94(2):436–43. https://doi.org/
32. Obarski TP, Rogers PJ, Debaets DL, Murcko LG, Jennings MR. 10.1016/j.athoracsur.2012.04.020. discussion 443-444.
Assessment of postinfarction ventricular septal ruptures by transeso- 39. Papalexopoulou N, Young CP, Attia RQ. What is the best timing of
phageal Doppler echocardiography. J Am Soc Echocardiogr 1995;8(5 surgery in patients with post-infarct ventricular septal rupture? Inter-
Pt 1):728–34. https://doi.org/10.1016/s0894-7317(05)80388-8. act Cardiovasc Thorac Surg 2013;16(2):193–6. https://doi.org/
33. Baim-Donald S, Grossman W. Shunt detection and quantification. 10.1093/icvts/ivs444.
Grossman’s Cardiac Catheterization, Angiography, and Intervention. 40. Moreno N, Silva JC, Andrade A. Complicated transcatheter closure of
Philadelphia, PA: Lippincott Williams & Wilkins; 2000:87. postinfarction ventricular acute septal defect. J Invasive Cardiol
34. Tecklenberg PL, Fitzgerald J, Allaire BI, Alderman EL, Harrison DC. 2011;23(10). E244-246.
Afterload reduction in the management of postinfarction ventricular 41. Moreno R, Lopez-Sendon J, Garcıa E, et al. Primary angioplasty
septal defect. Am J Cardiol 1976;38(7):956–8. https://doi.org/ reduces the risk of left ventricular free wall rupture compared with
10.1016/0002-9149(76)90809-2. thrombolysis in patients with acute myocardial infarction. J Am Coll
35. Pahuja M, Schrage B, Westermann D, Basir MB, Garan AR, Burkhoff Cardiol 2002;39(4):598–603.
D. Hemodynamic effects of mechanical circulatory support devices in 42. Figueras J, Curos A, Cortadellas J, Soler-Soler J. Reliability of elec-
ventricular septal defect. Circ Heart Fail 2019;12(7):e005981. https:// tromechanical dissociation in the diagnosis of left ventricular free
doi.org/10.1161/CIRCHEARTFAILURE.119.005981. wall rupture in acute myocardial infarction. Am Heart J 1996;131
36. Madjarov JM, Katz MG, Madzharov S, Fazal S, Robicsek F. Advan- (5):861–4. https://doi.org/10.1016/s0002-8703(96)90165-9.
tages of intraoperative implantation of Impella 5.5 SmartAssist in the TagedP43. Matteucci M, Fina D, Jiritano F, et al. Treatment strategies for post-
management of acute post-infarction ventricular septal defect with infarction left ventricular free-wall rupture. Eur Heart J Acute Cardi-
cardiogenic shock. J Cardiothorac Surg 2021;16(1):132. https://doi. ovasc Care 2019;8(4):379–87. https://doi.org/10.1177/
org/10.1186/s13019-021-01513-y. 2048872619840876.

Mechanical Complication of Myocardial Infaction

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Mechanical Complication of Myocardial Infaction

Uploaded by

Copyright:

Available Formats

ARTICLE IN PRESS

Mechanical Complications of Myocardial Infarction

0002-9343/Published by Elsevier Inc.

mortality in patients with mechanical complications were Clinical Presentation

Figure 2 The incidence of mechanical complications

Figure 3 Relationship between timing of reperfusion

Prevention, Treatment, and Prognosis

Figure 6 Diagnostic approach to PMR.

Figure 7 Risk predictors of VSD in acute MI with odds

Figure 8 Physiologic complications of VSR.

PCWP = pulmonary capillary wedge pressure.

a systolic murmur in the setting of acute myocardial infarc-

Clinical presentation of free wall rupture depends if the

Diagnosis (Noninvasive and Angiographic

Prevention, Treatment, and Prognosis

You might also like