What is the most common cause of death immediately following a myocardial infarction?

Mechanical complications of acute myocardial infarction (AMI) are ventricular septal defect (VSD), papillary muscle rupture or dysfunction, cardiac free wall rupture, ventricular aneurysm, dynamic left ventricular (LV) outflow tract (OT) obstruction, and right ventricular (RV) failure. All of these conditions could potentially lead to LV failure with cardiogenic shock.

A thorough understanding of the mechanical complications of AMI and their risk factors can help clinicians make an early diagnosis. For favorable patient outcomes, prompt diagnosis with appropriate medical therapy and timely surgical intervention are required. [11, 12]  Important factors for in-hospital mortality from mechanical complications of MI include advanced age, cardiogenic shock, and cardiorespiratory failure. [13] ​

Ventricular free wall rupture

VFWR is the most serious complication of AMI. VFWR is usually associated with large transmural infarctions and antecedent infarct expansion. It is the most common cause of death, second only to LV failure, and it accounts for 15-30% of the deaths associated with AMI. Incontrovertibly the most catastrophic of mechanical complications, VFWR leads to acute hemopericardium and death from cardiac tamponade.

The overall incidence of VFWR ranges from 0.8-6.2%. The incidence of this complication has declined over the years with better 24 hour systolic blood pressure control; increased use of reperfusion therapy, beta blockers, and ACE inhibitors; and decreased use of heparin. [14]

Data from the National Registry of Myocardial Infarction (NRMI) showed an elevated incidence of in-hospital mortality among patients who received thrombolytic therapy (12.1%) than among patients who did not (6.1%). [15] In the Thrombolysis in Myocardial Infarction Phase II (TIMI II) trial, 16% of patients died from cardiac rupture within 18 hours of therapy. [16] Patients who underwent percutaneous transluminal coronary angioplasty (PTCA) had an incidence of free wall rupture lower than that of patients receiving thrombolytic therapy.

Risk factors for VFWR include advanced age greater than 70 years, female sex, no previous MIs, Q waves on ECG, hypertension during the initial phase of STEMI, corticosteroid or NSAID use, and fibrinolytic therapy more than 14 hours after STEMI onset. Patients with a history of angina pectoris, previous AMI, multivessel coronary disease, and chronic heart failure are less likely than others to develop VFWR of the LV because they develop collaterals and ischemic preconditioning. [15, 17, 18]

Clinical presentation of VFWR

VFWRs are dramatic; they present acutely or occasionally subacutely as pseudoaneurysms; and they most often involve the anterior or lateral wall of the LV. Most VFWRs occur within the first week after AMI.

Becker et al classified the following three types of VFWRs [19] :

• Type I - an abrupt slitlike tear that is frequently associated with anterior infarcts and that occurs early (within 24 h)

• Type II - an erosion of infarcted myocardium at the border between the infarcted and viable myocardium

• Type III - an early aneurysm formation correlated with older and severely expanded infarcts

Type III usually occurs later than type I or type II ruptures. Thrombolytic therapy accelerates the occurrence of cardiac rupture in Becker type I and type II VFWRs. In severely expanded infarctions (type III), thrombolytic therapy decreases the incidence of cardiac rupture.

A pseudoaneurysm is formed when adjacent pericardium and hematoma seals off a myocardial rupture or perforation. The wall of a pseudoaneurysm is most often visualized as an aneurysmal outpouching that communicates with the LV cavity by means of a narrow neck. This wall is composed of pericardium and organized thrombus and/or hematoma. It is devoid of myocardial elements, whereas a true aneurysm has all the elements of the original myocardial wall and a relatively wide base. The pseudoaneurysm may vary in size and is at high risk of rupturing.

Clinical presentations of VFWR vary depending on the acuity, location, and size of the rupture. Patients with acute VFWR present with severe chest pain, abrupt electromechanical dissociation or asystole, hemodynamic collapse, and possibly death. In about one third of the patients, the course is subacute, and they present with symptoms such as syncope, hypotension, shock, arrhythmia, and prolonged and recurrent chest pain.

Diagnosis of VFWR

Early diagnosis of VFWRs and intervention are critical to patient survival. A high index of suspicion is required when patients with AMI present with severe chest pain, shock or arrhythmias, and abrupt development of electromechanical dissociation. [20] ECG signs of impending VFWR have limited specificity but include sinus tachycardia, intraventricular conduction defect, and persistent or recurrent ST-segment elevation.

Echocardiography is the diagnostic tool of choice. The key diagnostic finding is a moderate-to-large pericardial effusion with clinical and echocardiographic signs of impending pericardial tamponade. In patients with cardiac tamponade and electromechanical dissociation, moderate-to-severe pericardial effusion increases the mortality risk. Those patients without initial cardiac tamponade, while at a lower rate of mortality, should still be followed, as late rupture may still occur. [21] The absence of pericardial effusion on echocardiography has high negative predictive value. If the ability to obtain transthoracic echocardiograms is limited in patients receiving mechanical ventilation, transesophageal echocardiography can assist in confirming VFWR.

MRI provides superior image quality and permits identification of the site and anatomy of a ventricular pseudoaneurysm (ie, ruptured LV restrained by the pericardium with enclosed clot). However, MRI is of limited use in the acute setting because of the time involved and nonportability of imaging units.

Treatment of VFWR

The most important prevention strategy is early reperfusion therapy, with percutaneous coronary intervention (PCI) being the preferred modality. Fibrinolytic therapy is associated with overall decreased risk of VFWR; however, its use more than 14 hours after STEMI onset can increase the risk of early rupture. [22, 23]

The standard treatment for VFWR is emergency surgical repair after hemodynamic stability is achieved. Patients may first need intravenous fluids, inotropic agents, and emergency pericardiocentesis.

Pifarré and associates recommended the deployment of an intra-aortic balloon pump to decrease systolic afterload and improve diastolic myocardial perfusion. [24]

Several surgical techniques have been applied, including infarctectomy, adhering with biologic glue patches made of polyethylene terephthalate polyester fiber (Dacron; DuPont, Wilmington, DE) or polytetrafluoroethylene fluoropolymer resin (Teflon; DuPont); and use of pledgeted sutures without infarctectomy.

The mortality rate is significantly high and largely depends on the patient's preoperative hemodynamic status. Early diagnosis, rapid institution of the measures described above to achieve hemodynamic stability, and prompt surgical repair can improve survival rates. A follow-up to the Acorn randomized trial demonstrated long-term improvement in left ventricular structure and function after mitral valve surgery for as long as 5 years. These data provide evidence supporting mitral valve repair in combination with the Acorn CorCap device for patients with nonischemic heart failure with severe left ventricular dysfunction who have been medically optimized yet remain symptomatic with significant mitral regurgitation. [25]

Ventricular septal rupture

VSR is an infrequent but life-threatening complication of AMI. Despite optimal medical and surgical treatment, patients with VSR have a high in-hospital mortality rate. During the prethrombolytic era, VSRs occurred in 1-3% of individuals with MIs. The incidence declined with thrombolytic therapy (to 0.2-0.34%) because of improvements in reperfusion and myocardial salvage. The bimodal distribution of VSR is characterized by a high incidence in the first 24 hours, with another peak on days 3-5 and rarely more than 2 weeks after AMI.

In patients receiving thrombolytics, the median time from the onset of symptoms of AMI to septal rupture was 1 day in the Global Utilization of Streptokinase and TPA [tissue plasminogen activator] for Occluded Coronary Arteries (GUSTO-I) trial [26] and 16 hours in the Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock? (SHOCK) trial. [27]

Risk factors for septal rupture include advanced age (>65 y), female sex, single-vessel disease, extensive MI, and poor septal collateral circulation. [28, 29] Before the advent of thrombolytics, hypertension and absence of a history of angina were risk factors for VSR. Extensive infarct size and RV involvement are other known risk factors for septal rupture.

In patients with AMI without reperfusion, coagulation necrosis develops within 3-5 days after infarction. Neutrophils migrate to the necrotic zone and undergo apoptosis, release lytic enzymes, and hasten the disintegration of necrotic myocardium. Some patients have infarcts with large intramural hematomas, which dissect into the tissue and result in early septal rupture. The size of the septal rupture ranges from a few millimeters to several centimeters.

VSR is categorized as simple or complex depending on its length, course, and location. In simple septal rupture, the perforation is at the same level on both sides of the septum, and a direct through-and-through communication is present across the septum. A complex septal rupture is characterized by extensive hemorrhage with irregular, serpiginous tracts in the necrotic tissue.

Septal ruptures are most common in patients with large anterior MIs due to occlusion of the LAD artery causing extensive septal infarcts. These infarcts are associated with ST-segment elevations and Q waves in inferior leads (II, III, aVF) and these ECG changes are therefore more commonly seen in septal ruptures. [30] These ruptures are generally apical and simple.

Septal ruptures in patients with inferior MI occur relatively infrequently. These ruptures involve the basal inferoposterior septum and are often complex.

Clinical presentation of VSR

Symptoms of VSR complicating AMI include chest pain, shortness of breath, hypotension, biventricular failure, and shock within hours to days. Patients often present with a new, loud, and harsh holosystolic murmur. This murmur is loudest along the lower left sternal border and is associated with a palpable parasternal systolic thrill. RV and LV S3 gallops are common.

In patients with cardiogenic shock complicating septal rupture, the murmur and thrill may be difficult to identify. In contrast, patients with acute MR often have a soft systolic murmur at the apex without a thrill.

Diagnosis of VSR

Echocardiography with color flow Doppler imaging is the diagnostic tool of choice for identifying a VSR. (See the image below.) Its sensitivity and specificity have been reported to be as high as 100%. In addition, it can be used for the following:

• Define the site and size of septal rupture

• Assess the LV and RV function

• Estimate the RV systolic pressure

• Quantify the left-to-right shunt

Cardiac catheterization is usually required to confirm the diagnosis, quantitate the degree of left-to-right shunt, differentiate VSR from other conditions (eg, mitral regurgitation), plus visualize the coronary arteries.

In patients with VSR, right-heart catheterization shows a step-up in oxygen saturation from the right atrium to the RV; in contrast, no step-up in oxygen saturation occurs among patients with MR. The presence of large V waves in the pulmonary capillary wedge tracing supports the diagnosis of severe acute MR.

Left ventriculography can also be used to identify the site of ventricular rupture (see Cardiac Catheterization [Left Heart]). However, this study is usually unnecessary after a good-quality echocardiographic and Doppler examination is conducted.

Treatment of VSR

The key to management of VSR is prompt diagnosis and an aggressive approach to hemodynamic stabilization, angiography, and surgery. The optimal approach includes hemodynamic stabilization with the administration of oxygen and mechanical support with use of an intra-aortic balloon pump, as well as the administration of vasodilators (to reduce afterload and thus LV pressure and the left-to-right shunt), diuretics, and inotropic agents.

Cardiac catheterization is needed to define the coronary anatomy; this is followed by urgent surgical repair.

In a study of 52 consecutive patients with postinfarction ventricular septal rupture that was surgically repaired, investigators found that the 30-day mortality rate was 36% (n = 19). Most patients who survived for less than 30 days had a preoperative shock status. The investigators conclude that for patients with ventricular septal rupture, preoperative improvement in shock status and aggressive coronary revascularization are necessary. [31]

Medical therapy is intended only for temporary stabilization before surgery, as most patients' conditions deteriorate rapidly and they die in the absence of surgical intervention. In the GUSTO-I trial, the 30-day mortality rate was lower in patients with VSR who underwent surgical repair than in patients treated medically (47% vs 94%), as was the 1-year mortality rate (53% vs 97%). [26] Lemery et al reported a 30-day survival rate of 24% in patients treated medically compared with 47% in those treated surgically. [32]

Guidelines from the American College of Cardiology/American Heart Association (ACC/AHA) for the treatment of patients with septal rupture complicating AMI highlight urgent surgical intervention, regardless of their clinical status. [33] Surgical management of septal rupture includes the following elements:

• Prompt establishment of hypothermic cardiopulmonary bypass

• An approach to the septal rupture through the infarct area and the excision of all necrotic, friable margins of the septum and ventricular walls to avoid postoperative hemorrhage, residual septal defect, or both

• Reconstruction of the septum and ventricular walls by using prosthetic material and preservation of the geometric configuration of the ventricles and heart function

Percutaneous closure of septal rupture is a relatively new approach, one used in select patients as an alternative to surgical repair or for the acute stabilization of critically ill patients. However, percutaneous closure is currently unavailable in many institutions, and no long-term outcome data are available.

Several studies failed to show a relationship between perioperative mortality and concomitant coronary revascularization (coronary artery bypass grafting). Patients with cardiogenic shock due to septal rupture have the poorest outcome. In the SHOCK trial, the in-hospital mortality rate was higher in patients with cardiogenic shock due to septal rupture (87.3%) than in patients with cardiogenic shock from all other causes (59.2% with pure LV failure and 55.1% with acute MR). [27, 34]

In patients who survive surgical repair, the rate of recurrent or residual septal defect is reported to be about 28%, and the associated mortality rate is high.

Repeat surgical intervention is indicated in patients who have clinical heart failure or a pulmonary-systemic fraction greater than 2.

Acute mitral regurgitation

MR is a common complication of AMI that results from local and global LV remodeling and that is an independent predictor of heart failure and death. MR typically occurs 7-10 days after an AMI, though this onset may vary according to the mechanism of MR. Papillary muscle rupture resulting in MR occurs within 1-14 days (median, 1 d).

Mild-to-moderate MR is often clinically silent and detected on Doppler echocardiography performed during the early phase of AMI. In such cases, MR rarely causes hemodynamic compromise.

Speckle tracking and 3-dimensional echocardiography proved to be important imaging tools in assessing reverse LV remodeling after degenerative mitral valve regurgitation surgery. Subtle regional preoperative changes in diastolic function of the septal and lateral wall could be preoperatively identified, aiding in optimizing the referral timing and recognizing potential culprits as indicators of disease recurrence after mitral repair. [35]

Severe acute MR that results from the rupture of papillary muscles or chordae tendineae results in abrupt hemodynamic deterioration with cardiogenic shock. Rapid diagnosis, hemodynamic stabilization, and prompt surgical intervention are needed because acute severe MR is associated with a high mortality rate.

The reported incidence of MR may vary because of several factors, including the diagnostic methods used, the presence or absence of heart failure, the degree of MR reported, the type of therapy rendered, and the time from infarct onset to testing.

During the GUSTO-I trial, the incidence of MR in patients receiving thrombolytic therapy was 1.73%. [26] The SHOCK trial, which included MI patients presenting with cardiogenic shock, noted a 39.1% incidence of moderate to severe MR. [36] Kinn et al reported that reperfusion with angioplasty resulted in an 82% decrease in the rate of acute MR, as compared with thrombolytic therapy (0.31% vs 1.73%). [37]

Risk factors for MR are advanced age, female sex, large infarct, previous AMI, recurrent ischemia, multivessel coronary artery disease, and heart failure.

Several mechanisms can cause MR after AMI. Rupture of the papillary muscle is the most commonly reported mechanism.

Such rupture occurs in 1% of patients with AMI and frequently involves the posteromedial papillary muscle rather than the anterolateral papillary muscle, as the former has a single blood supply versus the dual supply for the latter. Papillary muscle rupture may lead to flailing or prolapse of the leaflets, resulting in severe MR. Papillary muscle dysfunction due to scarring or recurrent ischemia may also lead to MR in the subacute and chronic phases after MI; this condition can resolve spontaneously.

Large posterior infarctions produce acute MR due to asymmetric annular dilation and altered function and geometry of the papillary muscle.

Clinical presentation of MR

Patients with functional mild or moderate MR are often asymptomatic. The severity of symptoms varies depending on ventricular function. Clinical features of acute severe MR include shortness of breath, fatigue, a new apical holosystolic murmur, flash pulmonary edema, and shock.

The new systolic murmur may be only early-to-mid systolic, not holosystolic. It may be soft or even absent because of the abrupt rise in left atrial pressure, which lessens the pressure gradient between the left atrium and the LV, as compared with chronic MR. The murmur is best heard at the apex rather than the lower left sternal border, and it is uncommonly associated with a thrill. S3 and S4 gallops are expected.

Diagnosis of MR

The clinician cannot rely on a new holosystolic murmur to diagnose MR or assess its severity because of the variable hemodynamic status. In a patient with AMI who presents with a new apical systolic murmur, acute pulmonary edema, and cardiogenic shock, a high index of clinical suspicion for severe MR is the key to diagnosis.

Chest radiography may show evidence of pulmonary edema in the acute setting without clinically significant cardiac enlargement.

Echocardiography with color flow Doppler imaging is the standard diagnostic tool for detecting MR. Transthoracic echocardiography is the preferred initial screening tool, but transesophageal echocardiography is invaluable in defining the severity and exact mechanism of acute MR, especially when suspicion for papillary muscle rupture is high. Cardiac catheterization should be performed in all patients to determine the extent and severity of coronary artery disease.

Treatment of MR

Determination of hemodynamic stability, elucidation of the exact mechanism of acute MR, and expedient therapy are all necessary for a favorable outcome. Medical management includes afterload reduction with the use of diuretics, sodium nitroprusside, and nitrates in patients who are not hypotensive.

In patients who have hemodynamic compromise, intra-aortic balloon counterpulsation should be deployed rapidly. This intervention usually substantially reduces afterload and regurgitant volume, improving cardiac output in preparation for surgical repair. Without surgical repair, medical therapy alone in patients with papillary muscle rupture results in inadequate hemodynamic improvement and a poor short-term prognosis.

Emergency surgical intervention is the treatment of choice for papillary muscle rupture. Surgical approaches may include mitral valve repair or replacement. In the absence of papillary muscle necrosis, mitral valve repair improves the survival rate more than mitral valve replacement does. This difference is because the subvalvular apparatus is usually preserved. Mitral valve repair also eliminates complications related to malfunction of the prosthesis.

In patients with extensive necrosis of papillary muscle and/or ventricular free wall, mitral valve replacement is the preferred modality. Coronary artery bypass grafting (CABG) performed at the time of surgery was shown in one study to improve short- and long-term survival. [38]

The only situation in which emergency surgery can safely be avoided is in the case of intermittent MR due to recurrent ischemia. In these patients, successful myocardial revascularization may be effective. This procedure is accomplished by means of either angioplasty or coronary artery bypass grafting.

Dynamic LVOTO

Originally thought to be present only in hypertrophic cardiomyopathy, various investigators have reported the presence of dynamic LVOTO as a complication of acute anterior MI. [39, 40] The presence of dynamic LVOTO has also been postulated to be one of the etiologies for myocardial rupture. [41]

Dynamic LVOTO is mechanically caused by compensatory hyperkinesis of the basal and midsegments of the LV in patients with distal LAD infarcts. Predictors of enhanced regional wall motion in noninfarct zones are the absence of multivessel disease, female sex, and higher flow in the infarct-related vessel. The increased contractile force of the basal myocardium causes mitral regurgitation via the Venturi effect. This results in enhanced OTO, leading to further reduction in LV output in the setting of already present systemic hypoperfusion.

This increased LVOTO in the setting of damaged transmural myocardium forms a perfect setting in which there is increased end-systolic intraventricular pressure, which induces increased wall stress of the weakened, necrotic infarct zone. This frequently fatal complication occurs most often in women, older patients (>70 years), and those without prior MI.

Clinical presentation of LVOTO

Affected patients may have the usual symptoms of a heightened autonomic symptom complex such as respiratory distress, diaphoresis, and cool, clammy extremities, in addition to the typical signs and symptoms of AMI.

These patients may rapidly progress to cardiogenic shock with severe orthopnea, dyspnea, and oliguria, and they may have altered mental status from cerebral hypoperfusion. Patients may present with a new systolic ejection murmur, a new holosystolic murmur radiating to the axilla as a result of systolic anterior motion (SAM) of the mitral leaflet. An S3 gallop, pulmonary rales, hypotension, and tachycardia can also be present; these latter physical signs may be entirely absent in the acute setting.

Either transthoracic or transesophageal echocardiography (TTE/TEE) is the diagnostic test of choice and can accurately characterize the hyperkinetic segment, LVOTO, and mitral leaflet SAM.

Treatment of LVOTO

Consider reducing the hypercontractility of the myocardium by employing careful addition of beta blockade. Also slow volume resuscitation by afterload augmentation (phenylephrine) can increase preload and decrease LVOTO and SAM. It would be best to avoid afterload-augmenting medications. Vasodilators, inotropes, and balloon pumps should also be avoided because they can increase LVOTO.

RV failure

Often seen in the setting of inferior MI, post-MI mild RV dysfunction is common; however, in most cases the effect on the LV is minimal.

Significant RV hypokinesis occurs when there is proximal right coronary artery occlusion with little collateral from the left-sided circulation. It is postulated that because the RV is thin-walled and has a lower oxygen demand, there is coronary perfusion during the entire cardiac cycle; therefore, widespread irreversible infarction is rare.

Typical RV failure can present with hypotension (due to the lack of LV preload) and jugular venous distention with a clear lung field. Though classically described in the setting of RV failure, this triad is rarely seen in its pure form in the clinical setting. Most patients present with low-output cardiogenic shock or LV failure with associated autonomic symptoms.

The presence of jugular venous pressure above 8 cm H2O and Kussmaul sign is highly sensitive and specific for severe RV failure. [42]

Occasionally, right-to-left shunting via a patent foramen ovale causes persistent hypoxemia. Keep this peculiar complication in mind.

Electrocardiographically, patients present with inferior ST elevation in conjunction with ST elevation in the V4R lead. The chest radiograph usually appears bland, with no upper lobe venous distention. [43, 44]

Diagnosis of RV failure

Two-dimensional (2D) echocardiography and magnetic resonance imaging (MRI) are very useful. Most often, echocardiography will help to clinch the diagnosis.

Swan-Ganz catheterization findings are usually suggestive of high RA pressures with a low PCWP.

Treatment of RV failure

Volume resuscitation to keep the PCWP at or around 15 mmHg could help temporize by transiently increasing the RV preload. Though the definitive treatment involves re-establishing the coronary circulation. In rare cases of severe RV failure, consideration should be given for mechanical circulatory support using RV assist devices (AD) either temporarily or as bridge therapy in the setting of extensive biventricular involvement. [45, 46, 47]

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