Acute myocardial infarction: Mechanical complications

INTRODUCTION — Rupture of the left ventricular free wall, rupture of the interventricular septum, and acute mitral regurgitation due to papillary muscle necrosis are three potentially lethal mechanical complications of acute myocardial infarction (MI). In this topic, acute MI refers to both ST-elevation MI (STEMI) and non-ST-elevation MI (NSTEMI).

This topic will discuss these three complications, which have many similar clinical characteristics. Other potentially devastating complications of acute MI are discussed separately:

●(See "Conduction abnormalities after myocardial infarction".)

●(See "Right ventricular myocardial infarction".)

●(See "Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction".)

●(See "Pericardial complications of myocardial infarction".)

●(See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction".)

●(See "Left ventricular thrombus after acute myocardial infarction".)

GENERAL COMMENTS — Acute MI results in the loss of functioning left (and right) ventricular myocardium. As the amount of healthy myocardium decreases, there is a progressive fall in the left ventricular ejection fraction. Cardiogenic shock may be seen when there is severe left ventricular dysfunction. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction", section on 'Pathophysiology' and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)

Rupture of the left ventricular free wall, rupture of the interventricular septum, and acute mitral regurgitation are the three mechanical complications of acute MI. These potentially lethal complications may occur with large MIs or with lesser degrees of ventricular dysfunction if the location of the infarct is critically placed. They are grouped together, as they have rupture or tearing of necrotic myocardium as part of their underlying pathophysiology. They often lead to cardiogenic shock.

Incidence — The true incidence of the three mechanical complications may differ from reported incidence due to underreporting, miscoding, or variation in the populations studied. It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI [1]. Among patients with STEMI, ventricular septal rupture is the most common and occurs with a frequency of about 1 in 1000 [1,2]. Free wall rupture is the least common.

Reperfusion therapy has lowered the incidence of these mechanical complications. For example, prior to the widespread use of reperfusion, rupture of the free wall occurred in about 2 percent (or perhaps higher) of acute MIs. The incidence of free wall rupture in patients treated with fibrinolytic therapy emerged to be much lower than in patients treated conservatively. Accordingly, the incidence declined progressively from 1977 to 1982 (above 4 percent) to 2001 to 2006 (about 2 percent) [3]. Rates less than 1 percent were seen after successful reperfusion [4]. In regions where reperfusion therapy is widely used, there is some evidence to suggest that rates have not fallen significantly since 2003 [1].

The best estimate of the incidence of the individual complications comes from a 2019 study of over 9,000,000 MI hospitalizations between 2003 and 2015 in the United States [1]:

●Ventricular septal rupture occurred in only 0.21 percent of the STEMI and 0.04 percent of the NSTEMI populations.

●Papillary muscle rupture occurred in only 0.05 percent of the STEMI and 0.01 percent of the NSTEMI populations.

●Free wall rupture occurred in only 0.01 percent of the STEMI and 0.01 percent of the NSTEMI populations.

There was an increase in the risk of mechanical complications during the coronavirus 2019 (COVID-19) pandemic [5]. Potential mechanisms include delay in presentation and lack of access to hospital facilities. Outcomes of surgical treatment, however, were similar to those in the pre-COVID-19 era [6].

Prognosis — Mechanical complications are associated with high in-hospital mortality even if timely surgical or interventional repair is performed. One study found an in-hospital mortality rate of 42.4 percent after STEMI and 18 percent after NSTEMI [1].

It has been estimated that about 10 to 15 percent of in-hospital deaths from acute MI are attributable to one of these [7], with cardiogenic shock without a mechanical complication being responsible for most of the rest.

Mortality has decreased progressively over time, from 94 to 75 percent, despite an increasing age of this cohort [3,8,9].

The following comments apply to the specific mechanical complication:

●In an analysis of the CAUTION registry of post-MI mechanical complications from the Netherlands from 2001 to 2018, patients that had surgery for papillary muscle rupture had an in-hospital mortality rate of 24.8 percent. The mean age was 66.9 (standard deviation 10.5 years), mitral valve replacement was performed in 82.7 percent, and additional coronary artery bypass graft surgery in 57 percent. During the study period, there was no change in in-hospital mortality [10].

●Without surgical repair of postinfarction ventricular septal rupture, 90 percent of patients die within two months. The current mortality of surgically treated ventricular septal rupture closure is as high as 50 percent [11,12]. In two prospective registries, the mortality rates were as high as 81 to 100 percent for patients with ventricular septal rupture and cardiogenic shock [13,14]. Once the patient survives the initial phase after surgery, survival rates are good.

For percutaneous interventional ventricular septal closure, a meta-analysis reported a mortality of 32 percent [15]. However, a direct comparison to surgery is not possible, owing to the nonrandomized design and an inherent selection bias with all case series of either surgical or interventional closure.

●In a study of 54 patients undergoing surgery for papillary muscle rupture between 1980 and 2000, 10-year survival was only 35 percent, and 10-year survival free of heart failure was only 23 percent [16]. These patients had a mean age of 70, were predominantly male (74 percent), and 91 percent presented with cardiogenic shock, pulmonary edema, or cardiac arrest. Operative mortality (overall 18.9 percent) was high but decreased over time, with an operative mortality of 8.7 percent in patients operated on after 1990 with coronary artery bypass grafting.

In addition to the significant mortality, rates of cardiogenic shock, acute kidney injury, hemodialysis, and respiratory complications are higher in those with mechanical complications than in those without [1].

RUPTURE OF THE LEFT VENTRICULAR FREE WALL — Myocardial rupture more frequently involves the left than the right ventricle [8,17,18].

A number of different pathologic patterns can be seen, depending in part on the time of occurrence (figure 1) [19]. This was illustrated by a study of 1450 consecutive patients with acute MI, 27 (1.9 percent) of whom developed free wall myocardial rupture [20]. The findings were different in the early (<72 hours) and late phase (>4 days) of ruptures. Early rupture was characterized by an abrupt slit-like tear in the infarcted myocardium, with a preference for anterior infarction sites. There was no difference in incidence between patients treated with conventional and reperfusion therapy. Late rupture was characterized by the presence of infarct expansion, with no preferential infarction site. There was a very low incidence in patients with successful reperfusion.

Risk factors — Risk factors for left ventricular free wall (and septal) myocardial rupture were identified in observational studies during the fibrinolytic era. One study found that myocardial rupture was 9.2 times more likely to occur in patients with all of the following characteristics [21]:

●No history of previous angina or MI

●ST-segment elevation or Q wave development on the initial electrocardiogram

●Peak MB-creatine kinase above 150 international units/L

Other studies identified risk factors: first infarction, large transmural infarctions, anterior MI locations, age >70 years, and female sex [22-24]. Rupture was rarely seen in a hypertrophied ventricle or in an area of extensive collateral circulation.

Due to the very low incidence of free wall rupture in the percutaneous coronary intervention era, there are limited reports on risk factors. Women, White patients, valvular heart disease, and chronic kidney disease have been identified as risk factors [1].

Clinical presentation — The clinical presentation of myocardial rupture is variable. Left ventricular free wall rupture (picture 1) often occurs within the first five days after MI in about one-half of cases and within two weeks in over 90 percent [8,19,25,26].

Rupture can present as sudden death in an undetected or silent MI. In patients with known MI, complete or incomplete/subacute rupture can occur [27]:

●Complete rupture of the left ventricular free wall usually leads to hemopericardium and death from cardiac tamponade. The presence of rupture is first suggested by the development of sudden profound right heart failure and shock, often progressing rapidly to pulseless electrical activity (electromechanical dissociation) and death. Pulseless electrical activity in a patient with a first MI and without overt heart failure had, in one report, a high predictive accuracy (95 percent) for the diagnosis of left ventricular free wall rupture [28]. In contrast, the predictive accuracy of rupture was low (17 percent) in those with heart failure.

●Incomplete/subacute rupture of the left ventricular free wall can occur when organized thrombus and the pericardium seal the ventricular perforation. This condition can progress to one of four outcomes: frank rupture with cardiac tamponade and hemodynamic compromise, formation of a false aneurysm walled off by pericardial tissue, communication with the left ventricle through the perforation, or formation of a left ventricular diverticulum [8,25,26,29]. (See "Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction".)

Incomplete/subacute rupture may be manifested clinically by persistent or recurrent chest pain, particularly pericardial pain, nausea, restlessness and agitation, abrupt, transient hypotension, and/or electrocardiographic features of localized or regional pericarditis [8,25,26].

Diagnosis — The diagnosis of free wall rupture is based on clinical and echocardiographic signs of pericardial tamponade [8] (see "Cardiac tamponade", section on 'Diagnosis'). The echocardiogram typically shows pericardial effusion with evidence of chamber compression and may also be able to show the rupture itself (movie 1) [27].

Emergency pericardiocentesis, when performed in a patient with acute cardiogenic shock and suspected free wall rupture, may confirm the diagnosis.

In selected stable patients with subacute or covered rupture, cardiac magnetic resonance imaging may be used for differential diagnosis and preoperative planning [30].

Management — Survival depends primarily upon the early recognition of myocardial rupture and provision of immediate therapy. In patients with suspected or diagnosed free wall rupture, emergency pericardiocentesis is indicated if fluid is visualized (see "Emergency pericardiocentesis" and "Pericardial effusion: Approach to diagnosis" and "Cardiac tamponade"). If the patient stabilizes and bleeding stops, a conservative approach might be justified in selected cases; however, immediate cardiac surgery should be considered. Many patients do not survive the acute phase because of the development of immediate cardiogenic shock and pulseless electrical activity.

Initial medical therapy aimed at hemodynamic stabilization should be instituted. This usually includes fluids, inotropic support, and vasopressors [8,20,25,26,31-33]. (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction", section on 'Our approach'.)

RUPTURE OF THE INTERVENTRICULAR SEPTUM — In patients with ventricular septal rupture (movie 2), the median time from infarction to rupture is usually 24 hours but may be up to two weeks.

Septal rupture is seen with equal frequency in anterior and nonanterior infarctions [25]. The size of the defect determines the magnitude of left-to-right shunting, which, in turn, together with the impairment of left and right ventricular function, usually affects the likelihood of survival.

Rupture develops at the margin of the necrotic and non-necrotic myocardium. The perforation is usually single and ranges from one to several centimeters in size. It may be a direct through-and-through hole or more irregular and serpiginous [34,35]. The size of the defect determines the magnitude of left-to-right shunting, which in turn affects the likelihood of survival.

Risk factors — Risk factors for septal rupture include single-vessel disease (especially the left anterior descending artery), extensive myocardial damage, poor septal collateral circulation, and late presentation in some studies [36-39]. Others describe septal rupture in patients with multivessel coronary artery disease [34,37] and a higher incidence in first infarctions. The risk of septal rupture may be increased in patients with right ventricular infarction [35,40].

Clinical manifestations — Patients with a ruptured septum may present with a wide range of symptoms and signs, from mild compromise with dyspnea at exertion to severe cardiogenic shock. When the onset of hemodynamic compromise is immediate, hypotension and tachycardia are present. Biventricular heart failure with predominant right-sided failure may be present.

A new cardiac murmur is nearly always present. The new murmur is typically harsh, loud, and holosystolic, and is heard best at the lower left and usually right sternal borders, with occasionally widespread radiation [34,41,42]. In some cases, the murmur is heard best at the apex and may be mistaken for acute mitral regurgitation. A thrill can be detected in up to 50 percent of patients; right ventricular lift and a hyperdynamic precordium may also be noted [34,42]. (See "Auscultation of cardiac murmurs in adults".)

Diagnosis — Initial diagnosis is usually made by auscultation of a new cardiac murmur. The next step is usually echocardiography, which in the majority of cases will lead to the definitive diagnosis (picture 2 and image 1). The defect can be diagnosed by transthoracic echocardiography (movie 3 and movie 4 and movie 5 and movie 6 and movie 7) [34,41,43-45]. Transesophageal echocardiography may occasionally be necessary to delineate the complete extent of the abnormality [45].

In patients undergoing coronary angiography, a left ventricular angiogram also can easily lead to the diagnosis by showing the shunting of contrast dye from the left to the right ventricle (movie 8).

In uncommon cases where the suspicion is still high, and transthoracic or transesophageal echocardiogram may reveal no definitive diagnosis, confirmation of the diagnosis may require insertion of a pulmonary artery balloon catheter to document the left-to-right shunt [34,41]. (See "Pathophysiology of left-to-right shunts", section on 'Ventricular level shunts'.)

In hemodynamically stable patients, cardiac magnetic resonance is able to show the delineation of the infarcted tissue and also the ruptured septum. However, this is not a standard diagnostic tool. Also, computed tomography with three-dimensional reconstruction can show the extent of the ventricular septal rupture. This may be beneficial for planning of surgical or interventional ventricular septal rupture closure.

Management — Survival after ventricular septal rupture may occur only after surgical repair. Thus, the diagnosis of ventricular septal rupture should prompt a heart team discussion of options. This discussion should take into account that, for some patients, surgery is futile as mortality approaches 100 percent. Older patients and those with poor right ventricular function often fall into this group.

The timing of ventricular septal rupture repair is controversial. Many surgical studies noted lower operative mortality rates in patients who underwent surgery a few weeks after infarction than in those who underwent earlier operation [11,12,46,47]. However, these observations likely reflect selection bias, in which patients with relatively well-preserved left ventricular function and smaller defects survived to become low-risk surgical candidates. Surgery should not be delayed to allow fibrosis of the septum, as most patients will not survive the delay due to progressive heart failure and/or multiorgan failure and infection.

In patients undergoing surgery, coronary angiography should be performed if not already performed before the diagnosis of the mechanical complication. In case of severe coronary artery disease, additional coronary artery bypass grafting for surgical closure of the rupture should be performed.

As a bridge to surgery in patients with cardiogenic shock, patient stabilization may be attempted with inotropic agents and vasopressors. Although there is no supportive evidence, some experts place mechanical support devices such as an intraaortic balloon pump [48,49] (see "Intraaortic balloon pump counterpulsation", section on 'Other potential uses'). However, in a registry, the use of mechanical circulatory support did not have an impact on outcome [1].

Surgical repair of ventricular septal rupture is associated with a relatively high mortality and suboptimal results with a postoperative residual shunt in up to 20 percent [13,50]. Given these poor results, the technique of percutaneous ventricular septal rupture device closure has been developed [51]. Such a less invasive approach with a catheter-based intervention may offer improved survival or provide hemodynamic stabilization as a bridge to surgery. It might be used as an adjunctive therapy for residual postsurgical shunts. Data are limited for ventricular septal rupture interventional closure. The largest single-center experience in 29 patients reported a survival rate at 30 days of 35 percent, with much higher mortality in cardiogenic shock, as opposed to non-shock patients (88 versus 38 percent, p<0.001) [51]. Procedure-related complications were frequent, which further demonstrates the requirement of technical improvement. An overview of potential technical improvements has been reported [52]. Furthermore, a meta-analysis on all published reports with percutaneous ventricular septal rupture closure has been published, reporting acceptable mortality rates similar to the surgical literature [15].

PAPILLARY MUSCLE RUPTURE — Acute mitral regurgitation (MR) due to papillary muscle rupture occurs in both STEMI and NSTEMI. Other causes of acute MR include left ventricular dilatation or chordal rupture [34,41,53-55].

Papillary muscle rupture is a life-threatening complication that accounts for approximately 5 percent of deaths in these patients. It usually occurs two to seven days after the infarct [53,56]. The rupture may be partial (occurring at one of the muscle heads) or complete.

Most patients have relatively small areas of necrosis with poor collaterals, and up to 50 percent have single-vessel disease (picture 3) [41,53]. Because of differences in blood supply, rupture of the posteromedial papillary muscle occurs 6 to 12 times more frequently than rupture of the anterolateral papillary muscle. The posteromedial papillary muscle is supplied with blood from the posterior descending artery, while the anterolateral papillary muscle has a dual blood supply from the left anterior descending and left circumflex arteries [34,41,53,57].

Risk factors — Risk factors for papillary muscle rupture include poor collateral circulation to the affected muscle, single-vessel disease, first MI, and infarct extension [41,53,58,59].

Clinical manifestations — The clinical manifestations of hemodynamically significant papillary muscle rupture include the acute onset of hypotension and severe pulmonary edema. On physical examination, the precordium may be hyperactive, and systolic murmur may be present. Typically a mid-, late-, or holosystolic murmur is present that may have widespread radiation. Although the murmur may be loud, a thrill is generally not present. Furthermore, many patients have no or only a soft murmur. In addition, pulmonary edema and mechanical ventilation may mask the murmur.

Diagnosis — The diagnosis of papillary muscle rupture is typically confirmed by echocardiography, which usually demonstrates a flail segment of the mitral valve; a severed papillary muscle or chordae can frequently be seen moving freely within the left ventricular cavity. In some cases, however, transthoracic echocardiography is not informative, and transesophageal echocardiography is required to establish the diagnosis. This is most likely to occur in those patients in whom the ruptured head does not prolapse into the left atrium (which may occur in up to 35 percent of cases) [45]. Left ventricular function is usually hyperdynamic as a result of ventricular contraction against the low-impedance left atrium [41,53,58].

Cardiac catheterization is performed to define the coronary anatomy and can also show acute MR by a left ventricular angiogram (movie 9). Pulmonary capillary pressure in right-heart catheterization (if a pulmonary artery catheter is used) usually shows giant V waves. However, this finding is nonspecific since it may also be associated with an acute ventricular septal defect and severe left-sided heart failure [53,60].

Management — Prompt initiation of medical therapy and emergent surgery are necessary for a favorable outcome in patients with papillary muscle rupture. Initial medical therapy may include afterload reduction using nitrates, sodium nitroprusside, and diuretics in case of adequate blood pressure. However, patients often present in cardiogenic shock, which will mandate the use of inotropes and vasopressors for stabilization. Intraaortic balloon pump counterpulsation is considered useful based on theoretical assumptions (afterload reduction decreases the regurgitant fraction, thereby increasing forward flow). (See "Intraaortic balloon pump counterpulsation", section on 'Other potential uses'.)

Emergency surgical intervention remains the treatment of choice for papillary muscle rupture. In contrast to ventricular septal rupture repair, surgery of papillary muscle rupture does not involve necrotic myocardium in suture lines. Therefore, mortality associated with this repair is lower [61]. In general, the unpredictability of rapid deterioration and death with papillary muscle rupture makes early surgery necessary [62]. Even though there is a high operative mortality, survival in medically treated patients is very low [63]. Mitral valve repair rather than replacement should be attempted in centers experienced in performing this procedure [53,56]. Valve repair can be performed only when there is no papillary muscle necrosis.

Small case series and case reports have been published with successful interventional repair of acute ischemic MR by edge-to-edge repair [64]. However, experience is limited, and this should be reserved only for very-high-risk patients after heart team discussion.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)".)

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Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

●Basics topics (see "Patient education: What can go wrong after a heart attack? (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Three potentially life-threatening mechanical complications of acute myocardial infarction (MI) include rupture of the left ventricular free wall, rupture of the interventricular septum, and development of severe mitral regurgitation. (See 'General comments' above.)

●The incidence of a mechanical complication is estimated to be about 3 per 1000 patients with acute MI, and most of these events occur in patients with ST-elevation MI. (See 'Incidence' above.)

●The diagnosis of these complications is markedly facilitated by a heightened index of suspicion and should be considered in any acute MI patient with a new murmur, evidence of hypoperfusion, severe acute decompensated heart failure, or the development of cardiogenic shock. Transthoracic or transesophageal echocardiography are usually diagnostic. (See 'Diagnosis' above and 'Diagnosis' above and 'Diagnosis' above.)

●Since a mechanical complication often leads directly to cardiogenic shock and subsequent death, therapy must be initiated emergently. (See 'Management' above and 'Management' above and 'Management' above.)

●Early surgical intervention is usually the definitive treatment and should be considered when there is a reasonable likelihood of survival. Standard practice is to support the patient with the modalities described below until surgery is performed.

•For patients with rupture of the left ventricular free wall, early intervention includes fluids, inotropic support, and vasopressors. Pericardiocentesis should be attempted. (See 'Management' above.)

•For patients with rupture of the left ventricular septum, inotropic agents and vasopressors should be tried in patients with cardiogenic shock. (See 'Management' above.)

•For patients with papillary muscle rupture, initial medical therapy may include afterload reduction using nitrates, sodium nitroprusside, and diuretics in patients with adequate blood pressure. Intraaortic balloon pumping may be attempted. (See 'Management' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Roger Laham, MD, Michael Simons, MD, and Rakesh Suri, MD, DPhil, who contributed to earlier versions of this topic review.