Complications of Acute Coronary Syndromes

Ventricular arrhythmias are common and may result from hypoxia, electrolyte imbalance (hypokalemia, possibly hypomagnesemia), or sympathetic overactivity in ischemic cells adjacent to infarcted tissue (which is not electrically active). Treatable causes of ventricular arrhythmias are sought and corrected.

Serum potassium should be kept above 4.0 mEq/L (4.0 mmol/L). IV potassium chloride is recommended; usually 10 mEq/hour (10 mmol/hour) can be infused, but for severe hypokalemia (potassium level < 2.5 mEq/L [2.5 mmol/L]), 20 to 40 mEq/hour (20 to 40 mmol/hour) can be infused through a central venous line.

During the first 40 days after MI, beta-blockers and sometimes other antiarrhythmic therapy are used to prevent and treat ventricular arrhythmias (5). Early use of oral beta-blockers reduces the incidence of ventricular arrhythmias (including ventricular fibrillation) and mortality in patients who do not have heart failure or hypotension (6), although IV beta-blockade has been associated with an increased risk of cardiogenic shock (7). Prophylaxis with other medications (eg, lidocaine) may increase mortality risk and is not recommended (8). The role of implantable cardioverter-defibrillators (ICD) placed between 6 and 40 days after MI in patients with significant ventricular arrhythmias is unclear.

After the acute phase (≥ 40 days after MI and 90 days after revascularization), the presence of complex ventricular arrhythmias or nonsustained ventricular tachycardia, especially with significant left ventricular systolic dysfunction, increases mortality risk. Programmed endocardial stimulation can help select the most effective antiarrhythmics or determine the need for an implantable cardioverter-defibrillator (ICD). An ICD should be considered and is indicated for the following groups of patients when life expectancy is at least 1 year:

• All patients with left ventricular ejection fraction (LVEF) ≤ 40% with inducible ventricular tachycardia

• Patents with LVEF 31 to 35% and New York Heart Association class II or class III heart failure

• Patients with LVEF ≤ 30% and New York Heart Association class I, II, or III heart failure

Before treatment with an antiarrhythmic or ICD, coronary angiography and other tests are performed to look for recurrent myocardial ischemia, which may require PCI or coronary artery bypass grafting (CABG).

Ventricular ectopic beats, which are common after myocardial infarction, do not warrant specific treatment.

Ventricular tachycardia

Nonsustained ventricular tachycardia (ie, < 30 seconds) and even sustained slow ventricular tachycardia (accelerated idioventricular rhythm) without hemodynamic instability do not usually require treatment in the first 24 to 48 hours (see figure Broad QRS Ventricular Tachycardia).

Synchronized cardioversion is performed for:

• Polymorphic ventricular tachycardia

• Sustained (≥ 30 seconds) monomorphic ventricular tachycardia

• Any ventricular tachycardia with symptoms of instability (eg, heart failure, hypotension, chest pain)

Ventricular tachycardia without hemodynamic instability may be treated with IV lidocaine, procainamide, or amiodarone. Some clinicians also treat complex ventricular arrhythmias with magnesium sulfate 2 g IV over 5 minutes whether or not serum magnesium level is low.

Ventricular tachycardia may occur months after myocardial infarction. Late ventricular tachycardia is more likely to occur in patients with transmural infarction and to be sustained.

Broad QRS Ventricular Tachycardia

The QRS duration is 160 millisecond. An independent P wave can be seen in II (arrows). There is a leftward mean frontal axis shift.

Ventricular fibrillation

Ventricular Fibrillation

Image

These rhythm strips show the ultrarapid baseline undulations, irregular in timing and morphology, that characterize ventricular fibrillation. The asterisks indicate close-coupled premature ventricular beats.

© Springer Science+Business Media

Ventricular fibrillation occurs in some patients during the first 24 hours after myocardial infarction, usually within 6 hours (2). Late ventricular fibrillation usually indicates continued or recurrent myocardial ischemia and, when accompanied by hemodynamic deterioration, is a poor prognostic sign. Ventricular fibrillation is treated with immediate unsynchronized cardioversion (defibrillation).

If the artery supplying the sinus node is affected by an acute coronary syndrome, sinus node disturbances can occur; they are more likely if there is a preexisting sinus node disorder (common among older patients).

Atrial arrhythmias (atrial ectopic beats, atrial fibrillation, and, less commonly, atrial flutter) occur in approximately 10 to 20% of patients who have had a myocardial infarction and may reflect left ventricular failure or right atrial infarction (3, 10). Atrial fibrillation is more common after non–ST-segment elevation myocardial infarction (NSTEMI) than STEMI.

Paroxysmal atrial tachycardia usually occurs in patients who have had previous episodes of it.

Atrial ectopy is usually benign, but if frequency increases, causes, particularly heart failure, are sought. Frequent atrial ectopic beats may respond to a beta-blocker.

Atrial fibrillation

Atrial fibrillation is usually transient if it occurs within the first 24 hours (see figure Atrial Fibrillation). Risk factors for developing atrial fibrillation after MI include female gender, older age, increased heart rate on admission, and decreased LVEF (11, 12, 13).

Atrial Fibrillation

Recurrent paroxysmal atrial fibrillation is a poor prognostic sign and increases risk of systemic emboli (4, 14).

For atrial fibrillation, an anticoagulant is usually given because of the risk of systemic emboli. Patients are given an oral anticoagulant, along with aspirin and a P2Y12 inhibitor ("triple therapy"). These medications are continued for 1 to 4 weeks before the patient is transitioned to the oral anticoagulant and P2Y12 inhibitor for 12 months (5, 15).

Intravenous beta-blockers (eg, atenolol 2.5 to 5.0 mg over 2 minutes to total dose of 10 mg in 10 to 15 minutes, metoprolol 2 to 5 mg every 2 to 5 minutes to a total dose of 15 mg in 10 to 15 minutes) rapidly slow the ventricular rate and are typically given when heart rate is > 100 beats per minute. Heart rate and blood pressure are closely monitored. Treatment is withheld when ventricular rate decreases satisfactorily, systolic blood pressure is < 100 mm Hg, or significant bronchospasm occurs (10).

Other options for rate control include digoxin, non-dihydropyridine calcium channel blockers, and amiodarone (10).

Intravenous digoxin, which is not as effective as beta-blockers, is used cautiously and only in patients with atrial fibrillation and left ventricular systolic dysfunction. Usually, digoxin takes at least 2 hours to effectively slow heart rate and may rarely aggravate ischemia in patients with recent acute coronary syndrome.

For patients without evident left ventricular systolic dysfunction or conduction delay manifested by a wide QRS complex, the non-dihydropyridine IV calcium channel blockers verapamil or diltiazem may be used for rate control when beta-blockers are contraindicated or if adequate ventricular rate control is not achieved with other agents. Diltiazem may be given as a continuous IV infusion to control heart rate for long periods.

Intravenous amiodarone may also be used for treatment of acute atrial fibrillation, especially when IV beta-blockade or calcium channel blockade is not appropriate or contraindicated (such as in patients with low blood pressure or active asthma).

Due to a high risk of recurrent atrial fibrillation in patients with acute MI, an initial cardioversion strategy may not be preferred. However, if atrial fibrillation compromises circulatory status (eg, causing left ventricular failure, hypotension, or chest pain), urgent electrical synchronized cardioversion is performed (10). If atrial fibrillation returns after cardioversion, IV amiodarone should be considered for patients who continue to experience symptoms (eg, chest pain) or remain hemodynamically compromised.

Atrial flutter

For atrial flutter (see also figure Atrial Flutter), rate is controlled as for atrial fibrillation; anticoagulation along with antiplatelet therapy is required because the risk of thromboembolism is similar to that with atrial fibrillation. Rate control for atrial flutter in patients with acute MI is usually unsatisfactory. Low-energy direct current (DC) synchronized cardioversion will usually terminate atrial flutter.

Atrial Flutter

(Note: Conducted with right bundle branch block.)

Mobitz type I block (Wenckebach block, progressive prolongation of the PR interval with eventual dropped beats) is relatively common with an inferior-diaphragmatic infarction (see figure Mobitz Type I Second-Degree Atrioventricular Block); it is usually self-limited and rarely progresses to higher grade block.

Classic Mobitz Type I Second-Degree Atrioventricular Block

The PR interval progressively lengthens with each beat until the atrial impulse is not conducted and the QRS complex is dropped (Wenckebach phenomenon); atrioventricular nodal conduction resumes with the next beat, which has the shortest PR interval, and the sequence is repeated.

Mobitz type II block (dropped beats without progressive lengthening of the PR interval) usually indicates massive anterior myocardial infarction and is associated with an increased mortality risk, as does complete heart block with wide QRS complexes (atrial impulses do not reach the ventricle); both are uncommon (5, 16, 17). Complete AV block (see figure Third-Degree Atrioventricular Block) occurs in 2 to 10% of patients with after myocardial infarction (higher in non-anterior locations).

Frequency of third-degree atrioventricular block (complete block) depends on site of infarction, and its presence confers an increased risk of mortality (16, 17).

Third-Degree Atrioventricular Block

Hypotension may be due to:

• Decreased ventricular filling

• Loss of contractile force secondary to massive myocardial infarction

Decreased left ventricular filling is most often caused by reduced venous return secondary to hypovolemia, especially in patients receiving intensive loop diuretic therapy, but it may reflect right ventricular infarction. Marked pulmonary congestion suggests loss of left ventricular contractile force (left ventricular failure) as the cause.

Treatment depends on the cause. In some patients, determining the cause requires use of a pulmonary artery catheter to measure intracardiac pressures.

For hypotension due to hypovolemia, cautious fluid replacement with 0.9% saline is usually possible without left heart overload (excessive rise in left atrial pressure). However, sometimes left ventricular function is so compromised that adequate fluid replacement sharply increases pulmonary artery occlusion pressure to levels associated with pulmonary edema (> 25 mm Hg). If left atrial pressure is high, hypotension is probably due to left ventricular failure, and if diuretics are ineffective, inotropic therapy or mechanical circulatory support may be required.

Right ventricular infarction rarely occurs in isolation; it usually accompanies inferior left ventricular infarction. The first sign may be hypotension developing in a patient whose condition had been previously stable.

Right-sided ECG leads may show ST-segment changes. Volume loading with 1 to 2 L of 0.9% saline is often effective. Dobutamine or milrinone (which has better dilating effects on the pulmonary circulation) may help. Nitrates and diuretics are not used; they reduce preload (and hence cardiac output), causing severe hypotension. Increased right-sided filling pressure should be maintained by IV fluid infusion, but excessive volume overload may compromise left ventricular filling and cardiac output.

Approximately 5 to 10% of patients with acute myocardial infarction have cardiogenic shock (1).

Marked hypotension (eg, systolic blood pressure < 90 mm Hg) with tachycardia and symptoms of end-organ hypoperfusion (reduced urine output, mental confusion, diaphoresis, cold extremities) is termed cardiogenic shock. Pulmonary congestion develops rapidly in cardiogenic shock.

Definitive treatment for cardiogenic shock caused by acute MI is revascularization of the specific vessel involved by percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) if PCI is not feasible (2). Revascularization usually greatly improves ventricular function. Treatment with PCI of stenotic arteries not related to the infarct causing cardiogenic shock is deferred.

Supportive care often involves inotropic support (eg, dobutamine, milrinone, epinephrine, norepinephrine, levosimendan), with the inotropic effects of any agent balanced carefully against chronotropic effects, which can affect myocardial oxygen demand, and vasoconstrictor effects, which can affect systemic afterload.

Temporary mechanical circulatory support can be provided with a microvascular intra-axial flow pump, which unloads the left ventricle by pumping blood directly into the aorta and can be placed percutaneously or surgically (2). Other technologies, such as an intraortic balloon pump or veno-arterial extracorporeal membrane oxygenation, are not recommended. Temporary mechanical circulatory support can allow the myocardium to recover or serve as a bridge toward long-term mechanical support or heart transplantation.

Heart failure occurs in 14 to 36% of patients hospitalized with MI (3). Heart failure following MI is more likely in patients with (4):

• Chronic kidney disease

• Recurrent MI

• African American ancestry

• Diabetes

The extent of myocardial dysfunction, overall hemodynamic status, and clinical findings depend on infarct size, elevation of left ventricular filling pressure, and degree of reduction in cardiac output. Dyspnea, inspiratory crackles at the lung bases, and hypoxemia are common.

Initial treatment depends on severity.

For mild cases, a loop diuretic (eg, furosemide 20 to 40 mg IV once or twice a day) to reduce ventricular filling pressure is often sufficient. For severe cases, vasodilators (eg, IV nitroglycerin, nitroprusside) are often used to reduce preload and afterload; these agents are effective acutely (eg, in acute pulmonary edema) and may be continued over 24 to 72 hours as necessary. During treatment, pulmonary artery occlusion pressure may be measured via right heart (pulmonary artery) catheterization, especially if the response to therapy is not as desired.

Longer term heart failure therapy is added as indicated, which can include renin-angiotensin system inhibitors (or angiotensin receptor/neprilysin inhibitor), beta-blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors. (See Treatment of Chronic Heart Failure.) Note that in the post-MI setting, the benefit of universal beta-blockade in patients with LVEF ≥ 40% is equivocal (5, 6).

For severe heart failure, a microvascular intra-axial flow pump may provide temporary hemodynamic support until the patient's condition stabilizes or the decision is made to provide more advanced support (2). When revascularization or surgical repair is not feasible, heart transplantation is considered. Long-term left ventricular or biventricular implantable assist devices may be used as a bridge to transplantation. If transplantation is not possible, the left ventricular assist device may be used as permanent treatment (destination therapy). Occasionally, use of such a device results in recovery, and the device can be removed in 3 to 6 months.

Functional papillary muscle insufficiency, as detected by late gadolinium enhancement on cardiac MRI, occurs in up to 40% of patients during the first few hours of infarction (2). Papillary muscle ischemic dysfunction causes incomplete coaptation of the mitral valve leaflets, which is transient in most patients. But in some patients, papillary muscle or free wall scarring causes permanent mitral regurgitation. Functional papillary muscle insufficiency is characterized by an apical late systolic murmur and typically resolves without treatment.

Papillary muscle rupture occurs most often after an inferoposterior infarct due to right or circumflex coronary artery occlusion that affects the posteromedial papillary muscle, which has a single blood supply (unlike the anterolateral papillary muscle, which has a dual blood supply) (3). It causes acute, severe mitral regurgitation. Papillary muscle rupture is characterized by the sudden appearance of a loud apical holosystolic murmur and thrill, usually with pulmonary edema. Occasionally, severe regurgitation is silent. An abrupt hemodynamic deterioration raises clinical suspicion of papillary muscle rupture; echocardiography should be performed to make the diagnosis. Urgent mitral valve repair or replacement is necessary and effective.

Interventricular septum or free wall rupture occurs in 1% of patients with acute myocardial infarction. It causes 15% of in-hospital mortality.

Interventricular septum rupture occurs in approximately 0.3% of patients; is more common in females, older patients, and those who have had delayed reperfusion; and confers an in-hospital mortality of approximately 40% even with surgery (3). Interventricular septum rupture is characterized by the sudden appearance of a loud systolic murmur and thrill medial to the apex along the left sternal border in the third or fourth intercostal space, which is accompanied by hypotension with or without signs of left ventricular failure. Diagnosis may be confirmed using a balloon-tipped catheter and comparing blood oxygen saturation or partial pressure of oxygen (PO₂) of right atrial, right ventricular, and pulmonary artery samples. A significant increase in right ventricular PO₂ is diagnostic, as is Doppler echocardiography, which may demonstrate the actual shunt of blood across the ventricular septum.

Treatment is surgery, which should be delayed if possible for up to 6 weeks after MI so that infarcted myocardium can heal maximally; if hemodynamic instability persists, earlier surgery is indicated despite a high mortality risk. Patients with high surgical risk may undergo transcatheter closure.

Free wall rupture is thought to be an important cause of out-of-hospital sudden cardiac death; its incidence is not known (3). It is characterized by sudden loss of arterial pressure with momentary persistence of sinus rhythm and often by signs of cardiac tamponade. Rupture of a free wall is almost always fatal. When discovered in time, surgery can be successful, but mortality after surgery is approximately 35%.

A localized bulge in the ventricular wall, usually the left ventricular anterior or apical wall, can occur at the site of a large infarction (3). Ventricular aneurysms are common, especially with a large transmural infarct (usually anterior). Aneurysms may develop in a few days, weeks, or months. They are unlikely to rupture but may lead to recurrent ventricular arrhythmias, low cardiac output, and mural thrombosis with systemic embolism.

A ventricular aneurysm may be suspected when paradoxical precordial movements are seen or felt, ECG shows persistent ST-segment elevation, and chest radiograph shows a characteristic bulge of the cardiac shadow. Because these findings are not diagnostic of an aneurysm, echocardiography is performed to confirm the diagnosis and determine whether a thrombus is present.

Surgical excision may be indicated when left ventricular failure or arrhythmia persists. Early revascularization and probably the use of angiotensin-converting enzyme (ACE) inhibitors during acute myocardial infarction modify left ventricular remodeling and have reduced the incidence of aneurysm.

Pseudoaneurysm is incomplete rupture of the free left ventricular wall (often inferior or lateral); it is limited by the pericardium (3). Pseudoaneurysms may be large, contributing to heart failure, almost always contain a thrombus, and often rupture completely. They are repaired surgically.

Any chest pain that remains or recurs 12 to 24 hours after myocardial infarction may represent recurrent ischemia. Post-MI ischemic pain indicates that more myocardium is at risk of infarction. Usually, recurrent ischemia can be identified by reversible ST-T changes on the ECG; blood pressure may be elevated.

Recurrent ischemia is often silent (ECG changes without pain) (1), so serial ECGs are routinely performed every 8 hours for 1 day and then daily. Recurrent ischemia is treated similarly to unstable angina. Sublingual or IV nitroglycerin is usually effective. Coronary angiography and revascularization with percutaneous coronary intervention or coronary artery bypass grafting should be considered to salvage ischemic myocardium.

A study of patients with acute anterior MI treated with PCI found that 3.9% developed a left ventricular mural thrombosis during the hospitalization (2). Because risk is low, prophylaxis with anticoagulation is not always indicated (3).

Anticoagulant therapy may be considered for patients with STEMI and anterior wall akinesis or dyskinesis, but the patient's risk of bleeding must also be evaluated in light of dual antiplatelet therapy and resultant triple therapy should anticoagulation be chosen. Anticoagulants are recommended for patients after ACS with concomitant:

• Atrial fibrillation and high thromboembolic risk (eg, see table CHA2DS2-VASc score of ≥ 2)

• Mechanical heart valves

• Venous thromboembolism

• Hypercoagulable disorders

It also is considered reasonable to give anticoagulants to patients with STEMI and asymptomatic confirmed left ventricular mural thrombi, along with a P2Y12 inhibitor (4).

 Pericarditis results from extension of myocardial necrosis through the wall to the epicardium; it is rare in the current era of reperfusion therapy (< 1%) (1).

A friction rub usually begins 24 to 96 hours after myocardial infarction onset. Earlier onset of the friction rub is unusual, although hemorrhagic pericarditis occasionally complicates the early phase of myocardial infarction. Acute tamponade is rare.

In addition to the friction rub, ECG shows diffuse ST-segment elevation and sometimes PR-interval depression. Echocardiography is frequently performed but is usually normal. Occasionally, small pericardial effusions and even unsuspected tamponade are detected.

Aspirin or another nonsteroidal anti-inflammatory drug (NSAID) usually relieves symptoms. Colchicine 0.5 to 1 mg orally once a day, alone, and especially added to conventional treatment, speeds recovery and helps prevent recurrences. High doses or prolonged use of NSAIDs or glucocorticoids may impair infarct healing and should be avoided; glucocorticoids may also increase the likelihood of recurrence (1). Anticoagulation is not contraindicated in early peri-infarction pericarditis but is contraindicated in later post-MI (Dressler) syndrome.

Post-MI syndrome develops rarely in patients several days to weeks or even months after acute myocardial infarction; incidence appears to have decreased in recent years (2, 3, 4). It is characterized by fever, pericarditis with a friction rub, pericardial effusion, pleuritis, pleural effusions, pulmonary infiltrates, and joint pain. This syndrome is caused by an autoimmune reaction to material from necrotic myocytes. It may recur.

Differentiating post-MI syndrome from extension or recurrence of infarction may be difficult. However, in post-MI syndrome, cardiac troponin does not increase significantly, and ECG changes are nonspecific.

NSAIDs (eg, aspirin 500 to 1000 mg orally every 6 to 8 hours until symptoms are relieved) are usually effective, but the syndrome can recur several times. Colchicine is effective for treatment and to prevent recurrences. In severe cases, a short, intensive course of another NSAID or a glucocorticoid may be necessary. High doses of an NSAID or a glucocorticoid are not used for more than a few days because they may interfere with early ventricular healing after an acute myocardial infarction.