Complications of Acute Coronary Syndromes

If the artery supplying the sinus node is affected by an acute coronary syndrome, sinus node disturbances Sinus Node Dysfunction Sinus node dysfunction refers to a number of conditions causing physiologically inappropriate atrial rates. Symptoms may be minimal or include weakness, effort intolerance, palpitations, and... read more can occur; they are more likely if there is a preexisting sinus node disorder (common among older patients).

Atrial arrhythmias (atrial ectopic beats Atrial premature beats Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment. (See also Overview of Arrhythmias... read more , atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more , and, less commonly, atrial flutter Atrial Flutter Atrial flutter is a rapid regular atrial rhythm due to an atrial macroreentrant circuit. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial... read more ) occur in about 10% of patients who have had a myocardial infarction and may reflect left ventricular failure or right atrial infarction.

Paroxysmal atrial tachycardia Atrial tachycardia Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment. (See also Overview of Arrhythmias... read more is uncommon and usually occurs in patients who have had previous episodes of it.

Atrial ectopy is usually benign, but if frequency increases, causes, particularly heart failure Heart Failure (HF) Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular (LV) failure causes shortness of breath and fatigue, and right ventricular (RV) failure causes peripheral and abdominal... read more , are sought. Frequent atrial ectopic beats may respond to a beta-blocker.

Mobitz type I block Second-degree AV block Atrioventricular (AV) block is partial or complete interruption of impulse transmission from the atria to the ventricles. The most common cause is idiopathic fibrosis and sclerosis of the conduction... read more (Wenckebach block, progressive prolongation of PR interval with eventual dropped beats) is relatively common with an inferior-diaphragmatic infarction (see figure Mobitz type I 2nd-degree atrioventricular block ); it is usually self-limited and rarely progresses to higher grade block.

Mobitz type II block Second-degree AV block Atrioventricular (AV) block is partial or complete interruption of impulse transmission from the atria to the ventricles. The most common cause is idiopathic fibrosis and sclerosis of the conduction... read more (dropped beats) usually indicates massive anterior myocardial infarction, as does complete heart block with wide QRS complexes (atrial impulses do not reach the ventricle); both are uncommon.

Frequency of 3rd degree atrioventricular Third-degree AV block Atrioventricular (AV) block is partial or complete interruption of impulse transmission from the atria to the ventricles. The most common cause is idiopathic fibrosis and sclerosis of the conduction... read more (complete) block depends on site of infarction (see figure Third-degree atrioventricular block Third-degree atrioventricular block ). Complete AV block occurs in 5 to 10% of patients with inferior infarction and is usually transient. It occurs in < 5% with uncomplicated anterior infarction but in up to 26% of those with right bundle branch block and left posterior hemiblock. Even transient complete AV block with an anterior myocardial infarction is an indication for permanent pacemaker insertion because the risk of sudden death without pacing is significant.

Ventricular arrhythmias are common and may result from hypoxia, electrolyte imbalance (hypokalemia Hypokalemia Hypokalemia is serum potassium concentration < 3.5 mEq/L (< 3.5 mmol/L) caused by a deficit in total body potassium stores or abnormal movement of potassium into cells. The most common... read more , possibly hypomagnesemia Hypomagnesemia Hypomagnesemia is serum magnesium concentration < 1.8 mg/dL (< 0.70 mmol/L). Causes include inadequate magnesium intake and absorption or increased excretion due to hypercalcemia or drugs... read more ), 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.

Ventricular ectopic beats Ventricular Premature Beats (VPB) Ventricular premature beats (VPB) are single ventricular impulses caused by reentry within the ventricle or abnormal automaticity of ventricular cells. They are extremely common in both healthy... read more , which are common after myocardial infarction, do not warrant specific treatment.

An IV beta-blocker early in myocardial infarction followed by continued oral beta-blockers reduces the incidence of ventricular arrhythmias (including ventricular fibrillation Ventricular Fibrillation (VF) Ventricular fibrillation causes uncoordinated quivering of the ventricle with no useful contractions. It causes immediate syncope and death within minutes. Treatment is with cardiopulmonary... read more ) and mortality in patients who do not have heart failure or hypotension. Prophylaxis with other drugs (eg, lidocaine) increases mortality risk and is not recommended.

After the acute phase, the presence of complex ventricular arrhythmias or nonsustained ventricular tachycardia, especially with significant left ventricular systolic dysfunction, increases mortality risk. An implantable cardioverter-defibrillator Implantable Cardioverter-Defibrillators (ICD) The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more (ICD) should be considered and is indicated when the left ventricular ejection fraction is < 35%. Programmed endocardial stimulation can help select the most effective antiarrhythmics or determine the need for an ICD. Before treatment with an antiarrhythmic or ICD, coronary angiography and other tests are done to look for recurrent myocardial ischemia, which may require percutaneous coronary intervention or coronary artery bypass grafting.

Heart failure Heart Failure (HF) Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular (LV) failure causes shortness of breath and fatigue, and right ventricular (RV) failure causes peripheral and abdominal... read more is more likely in patients with

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.

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 drugs are effective acutely (eg, in acute pulmonary edema Pulmonary Edema Pulmonary edema is acute, severe left ventricular failure with pulmonary venous hypertension and alveolar flooding. Findings are severe dyspnea, diaphoresis, wheezing, and sometimes blood-tinged... read more ) 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.

ACE inhibitors are used as long as systolic blood pressure remains > 100 mm Hg. A short-acting ACE inhibitor given in low doses (eg, captopril 3.125 to 6.25 mg orally every 4 to 6 hours, increasing doses as tolerated) is best for initial treatment. Once the maximum dose is reached (maximum for captopril, 50 mg 3 times a day), a longer-acting ACE inhibitor (eg, fosinopril, lisinopril, perindopril, ramipril) is substituted for the long-term. If the patient remains in New York Heart Association class II or worse (see table Classification of Heart Failure Overview of Coronary Artery Disease Coronary artery disease (CAD) involves impairment of blood flow through the coronary arteries, most commonly by atheromas. Clinical presentations include silent ischemia, angina pectoris, acute... read more ), an aldosterone inhibitor (eg, eplerenone, spironolactone) should be added.

For severe heart failure, an intraarterial counterpulsation balloon pump or an implantable intravascular ventricular assist pump may provide temporary hemodynamic support until the patient stabilizes or the decision is made to provide more advanced support. When revascularization or surgical repair is not feasible, heart transplantation Heart Transplantation Heart transplantation is an option for patients who have any of the following and who remain at risk of death and have intolerable symptoms despite optimal use of drugs and medical devices:... read more is considered. Long-term left ventricular or biventricular implantable assist devices may be used as a bridge to transplantation. If transplantation is impossible, the left ventricular assist device is increasingly used as permanent treatment (destination therapy). Occasionally, use of such a device results in recovery and can be removed in 3 to 6 months.

Functional papillary muscle insufficiency occurs in about 35% of patients during the first few hours of infarction. 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 Mitral Regurgitation Mitral regurgitation (MR) is incompetency of the mitral valve causing flow from the left ventricle (LV) into the left atrium during ventricular systole. MR can be primary (common causes are... read more . 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 coronary artery occlusion. 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 Pulmonary Edema Pulmonary edema is acute, severe left ventricular failure with pulmonary venous hypertension and alveolar flooding. Findings are severe dyspnea, diaphoresis, wheezing, and sometimes blood-tinged... read more . Occasionally, severe regurgitation is silent. An abrupt hemodynamic deterioration raises clinical suspicion of papillary muscle rupture; echocardiography should always be done 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 hospital mortality.

Interventricular septum rupture, although rare, is 8 to 10 times more common than papillary muscle rupture. 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 3rd or 4th intercostal space, 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 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.

Free wall rupture increases in incidence with age and is more common among women. It is characterized by sudden loss of arterial pressure with momentary persistence of sinus rhythm and often by signs of cardiac tamponade. Surgery is rarely successful. Rupture of a free wall is almost always fatal.

A localized bulge in the ventricular wall, usually the left ventricular wall, can occur at the site of a large infarction. 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 x-ray shows a characteristic bulge of the cardiac shadow. Because these findings are not diagnostic of an aneurysm, echocardiography is done 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; it is limited by the pericardium. Pseudoaneurysms may be large, contributing to heart failure, almost always contain a thrombus, and often rupture completely. They are repaired surgically.

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

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.

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 silent (ECG changes without pain) in up to one third of patients, so serial ECGs are routinely done every 8 hours for 1 day and then daily. Recurrent ischemia (which is actually classified as unstable angina class lllC—see table ) is treated similarly to unstable angina. Sublingual or IV nitroglycerin is usually effective. Coronary angiography and revascularization Revascularization for Acute Coronary Syndromes Revascularization is the restoration of blood supply to ischemic myocardium in an effort to limit ongoing damage, reduce ventricular irritability, and improve short-term and long-term outcomes... read more with percutaneous coronary intervention or coronary artery bypass grafting should be considered to salvage ischemic myocardium.

Prior to the modern era of reperfusion therapy, mural thrombosis occurred in about 20% of patients with acute myocardial infarction. Systemic embolism occurs in about 10% of patients with left ventricular thrombosis; risk is highest in the first 10 days but persists at least 3 months. Risk is highest (about 60%) for patients with large anterior infarctions (especially involving the distal septum and apex), a dilated and diffusely hypokinetic left ventricle, or chronic atrial fibrillation. With modern therapy, risk of mural thrombosis is much lower.

Anticoagulants are no longer given routinely for primary prevention of mural thrombosis after acute coronary syndrome. 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:

It also is reasonable to give anticoagulants to patients with STEMI and asymptomatic confirmed LV mural thrombi.

Pericarditis Pericarditis Pericarditis is inflammation of the pericardium, often with fluid accumulation in the pericardial space. Pericarditis may be caused by many disorders (eg, infection, myocardial infarction, trauma... read more results from extension of myocardial necrosis through the wall to the epicardium; it develops in about one third of patients with acute transmural myocardial infarction, although the rate appears to be much less in patients who have early reperfusion done.

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.

Pericarditis is diagnosed by ECG, which shows diffuse ST-segment elevation and sometimes PR-interval depression. Echocardiography is frequently done, but results are 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 corticosteroids may impair infarct healing and should be avoided; corticosteroids may also increase the likelihood of recurrence. Anticoagulation is not contraindicated in early peri-infarction pericarditis but is contraindicated in later post-MI (Dressler) syndrome.

Post-MI syndrome develops in a few patients several days to weeks or even months after acute myocardial infarction; incidence also appears to have decreased in recent years. It is characterized by fever, pericarditis with a friction rub, pericardial effusion, pleurisy, 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 markers do not increase significantly, and ECG changes are nonspecific.

NSAIDs 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 corticosteroid may be necessary. High doses of an NSAID or a corticosteroid are not used for more than a few days because they may interfere with early ventricular healing after an acute myocardial infarction.