eMedicine Specialties > Neurology > Neuro-vascular Diseases

Cardioembolic Stroke

Author: Michael J Schneck, MD, Associate Professor, Departments of Neurology and Neurosurgery, Stritch School of Medicine, Loyola University; Associate Director, Stroke Program, Director, Neurology Intensive Care Program, Medical Director, Neurosciences ICU, Loyola University Medical Center
Coauthor(s): Lei Xu, MD, PhD, Resident Physician, Department of Neurology, Loyola University Chicago, Stritch School of Medicine; Santiago Palacio, MD, Neurology Fellow, Department of Medicine (Division of Neurology)
Contributor Information and Disclosures

Updated: Feb 13, 2008

Introduction

Background

The heart was established as an important source for the development of emboli when Gowers, in 1875, described a case of left middle cerebral artery and retinal artery emboli. Cardiogenic embolism accounts for approximately 20% of ischemic strokes each year. New diagnostic techniques (transesophageal echocardiography, cardiac magnetic resonance) have allowed clinicians to better characterize well-established sources of embolism and to discover other potential etiologies of cardioembolic stroke. Cardioembolic stroke is largely preventable, warranting efforts at primary prevention for major-risk cardioembolic sources. Once stroke due to cardiac embolism has occurred, the likelihood of recurrence is relatively high for most cardioembolic sources, and consequently, secondary prevention is also important.

Pathophysiology

The underlying mechanism of cardioembolic stroke is occlusion of cerebral vessels with debris from a cardiac source. An embolus may consist of platelet aggregates, thrombus, platelet-thrombi, cholesterol, calcium, bacteria, etc. Most embolic debris contains platelet aggregates.

However, no single mechanism is responsible for the development of cardiac emboli. The specific underlying cardiac disease determines the pathophysiology and natural history, and hence each cardioembolic source must be considered individually. Emboli secondary to chamber abnormalities (eg, atrial fibrillation, acute myocardial infarction) are induced mainly by stasis, while those secondary to valve involvement are the result of endothelial abnormalities with attachment of material (eg, platelets, bacteria) to their free borders. The nature of the embolus differs depending on the source (eg, calcified particles from calcific valves, neoplastic cells from myxomas). This must be considered when choosing specific therapies; no single treatment covers the wide variety of heart disease that can cause embolism to the brain.

Emboli from the heart are distributed evenly throughout the body according to cardiac output, but more than 80% of symptomatic or clinically recognized emboli involve the brain. Of emboli to the brain, approximately 80% involve the anterior circulation (ie, carotid artery territory) while 20% involve the vertebrobasilar distribution, proportional to the distribution of cerebral blood flow.

Once emboli have reached the cerebral circulation, they obstruct brain-supplying arteries, causing ischemia to the neurons and to the blood vessels within the area of ischemia. In contrast to thrombi, emboli are attached loosely to the vascular walls and thus commonly migrate distally. When this occurs, reperfusion of the damaged capillaries and arterioles allows blood to leak into the surrounding infarcted tissue. This explains the more frequent association of hemorrhagic infarction with cardiogenic embolism than with other causes of ischemic stroke. In the great majority of patients with hemorrhagic infarcts, the hemorrhagic transformation does not cause clinical worsening because the bleeding involves necrotic tissue.

In short, cardioembolic stroke is not one disease with a single natural history. Many different types of cardiac disorders lead to cardioembolic stroke, each with unique clinical features, risks of initial and recurrent stroke, and optimal therapy.

Frequency

United States

Approximately 20% of ischemic strokes are considered cardioembolic. The annual incidence is estimated at approximately 146,000 cases.

International

Estimated frequency varies from 12-31% of ischemic strokes depending on criteria applied for definition, extent of evaluation, and study design (see Table 1). Consistent geographic variation is not evident, and the frequency is likely similar throughout the world if adjusted for mean population age. The risk of a cardioembolic event rises with age. The older the cohort, the higher the estimated frequency of cardioembolic stroke because of the rapidly increasing prevalence of atrial fibrillation in elderly persons.

Table 1. Frequency of Cardioembolic Stroke/All Ischemic Stroke

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*Frequency of presumed cardioembolic stroke is a percentage of consecutive ischemic strokes, using each author's criteria. Criteria, design, and extent of evaluation varied substantially among studies.

† 20% had a major embolic source.

†† This study included transient ischemic attacks (TIAs).

Mortality/Morbidity

In general, cardioembolic strokes have a worse prognosis and produce larger and more disabling strokes than other ischemic stroke subtypes. This general observation is derived from emboli originating in cardiac chambers, which are on average of large size (eg, atrial appendage, ventricular thrombi).

Race

Blacks and Hispanics reportedly have a lower frequency of cardioembolic strokes than whites, possibly reflecting a lower prevalence of atrial fibrillation in these racial groups, who tend to experience stroke at younger mean ages.

Sex

The female-to-male ratio of cardioembolic stroke increases with age, reflecting the increased prevalence of atrial fibrillation among elderly women.

Age

The relative frequency of cardioembolic stroke as a proportion of all strokes is bimodal, higher in young (<50 y) and very old (>75 y) individuals. The incidence steadily increases with age because of the escalating frequency of atrial fibrillation.

Clinical

History

Although not sufficiently sensitive or specific to establish the diagnosis, several clinical features help to distinguish cardiogenic embolism from other mechanisms of cerebral ischemia and are useful to consider in patient management.

• Clinical features of cardioembolic stroke include the following:
  • Decreased level of consciousness at onset of stroke
  • Neurologic symptoms of abrupt onset with maximal severity at onset
  • Rapid recovery from major hemispheric deficits ("spectacular shrinking deficit") due to reperfusion of brain with early lysis of the embolus
  • Onset of symptoms after a Valsalva-provoking activity (enhancing right-to-left shunting in patients with a patent foramen ovale [PFO])
  • Symptoms reflecting involvement of different vascular territories of the brain
• Neither seizures nor headache at the onset is a useful predictor of cardiogenic embolism.
• Cardiogenic emboli (especially from chamber sources) do not often affect the deep penetrating arteries or manifest as a lacunar syndrome. Small cardiogenic emboli from valvular sources (eg, calcific aortic stenosis, infective endocarditis) can obstruct the small penetrating arteries, causing subcortical lacunar infarcts.

Physical

• Evidence of cardiac atrial dysrhythmias (eg, atrial fibrillation, sick sinus syndrome)
• Presence of cardiac murmurs (eg, mitral stenosis, calcific aortic stenosis)
• Signs of congestive heart failure (eg, after acute myocardial infarction, nonischemic cardiomyopathies)
• Recent myocardial infarction (highest cerebral embolism in the first 4 weeks of acute myocardial infarction)
• Concomitant diseases (eg, systemic lupus erythematosus and Libman-Sacks endocarditis, neoplasia, marantic endocarditis)
• Concomitant signs of systemic embolism
  • The probability of finding such signs in patients with suspected cardioembolic stroke is low (approximately 1%) for most cardioembolic sources.
  • The diagnosis of cardioembolic stroke is based on the triad of (1) identification of a potential cardioembolic source, (2) absence of other likely causes of stroke, and (3) supportive clinical features described above.

Causes

More than 20 specific cardiac disorders have been implicated in leading to brain embolism. Dividing cardiac sources of emboli into major- and minor-risk categories is clinically useful (see below). Major-risk sources carry a relatively high risk of initial and recurrent stroke convincingly linked to a cardioembolic mechanism. When a major-risk cardioembolic source is present, efforts at primary prevention of stroke usually are indicated; stroke in patients with any of these causes is most often cardioembolic. Minor-risk sources are frequent in the general population, and the associated risk of initial and recurrent stroke with any of these conditions is either low or uncertain. When a minor-risk cardioembolic source is present in a patient with cerebral ischemia, the etiologic role must be viewed with skepticism and considered in the context of other diagnostic information.

Sources of cardioembolic embolism include the following: Asterisk (*) indicates a major-risk source; dagger (†) indicates emboli originating in the venous circulation or right heart that cause ischemic stroke via abnormal cardiac or pulmonary shunting around the pulmonary capillary bed.

• Valvular diseases
  • Rheumatic mitral stenosis*
  • Prosthetic valves*
  • Infective endocarditis*
  • Nonbacterial thrombotic (marantic) endocarditis* associated with malignancies and prothrombic states
  • Calcific aortic stenosis
  • Bicuspid aortic valves
  • Mitral annulus calcification
  • Myxomatous mitral valvulopathy with prolapse
  • Inflammatory valvulitis (ie, Libman-Sacks endocarditis, Behçet disease, syphilis)
  • Lambl excrescences and/or strands
• Left ventricular thrombi
  • Ischemic heart disease*
  • Acute myocardial infarction*
  • Left ventricular akinesis or aneurysm*
  • Nonischemic cardiomyopathies* (eg, idiopathic dilating, viral myocarditis–associated, echinococcal, peripartum, amyloid-associated, hypereosinophilia syndrome–associated, rheumatic myocarditis–associated, sarcoidosis-related, neuromuscular disorder–associated, alcoholism-related, catecholamine-induced, Chagas disease–associated, doxorubicin-induced, mitoxantrone-related, crack cocaine–related, cardiac oxalosis–associated)
  • Idiopathic hypertrophic subaortic stenosis
  • Trauma (myocardial contusion
  • Ventricular noncompaction
• Left ventricular thrombi associated with prothrombotic states*
• Antiphospholipid antibodies
• Diffuse intravascular coagulation
• Essential thrombocythemia and myeloproliferative diseases
• Left atrial thrombi
  • Atrial fibrillation*
  • Atrial flutter*
  • Sick sinus syndrome/atrial asystole
  • Arrhythmias
  • Atrial septal aneurysms
  • Chiari network
• Cardiac tumors
  • Atrial myxoma*
  • Cardiac sarcoma
  • Endocardial fibroelastoma
  • Metastatic disease
• Paradoxical emboli†
  • Atrial septal defects
  • Patent foramen ovale (PFO)
  • Ventricular septal defects
  • Pulmonary arteriovenous fistulas
• Miscellaneous
  • Postcardiac catheterization
  • Postvalvuloplasty
  • Esophageal-atrial fistula

Major-risk sources

• Atrial fibrillation: The leading cause of cardioembolic stroke (see Media file 1), especially in elderly individuals. Atrial fibrillation is present in approximately 1% of the US population and in approximately 5% of those older than 70 years.
  • Formerly associated with rheumatic valvular disease, it now is related most frequently to hypertension and ischemic heart disease (ie, nonvalvular atrial fibrillation).
  • Atrial fibrillation is found in up to 50% of all cardioembolic strokes. Both paroxysmal and chronic atrial fibrillation are associated with increased risk of stroke.
  • Stasis secondary to decreased contractility of the left atrium leading to thrombus formation in its appendage is the postulated mechanism (see Media file 2).
  • Transesophageal echocardiography is more sensitive than transthoracic echocardiography for the visualization of the left atrium and its appendage (see Media file 3).
  • Not all atrial fibrillation–associated strokes are cardioembolic; in individual cases, excluding other potential causes of stroke such as intrinsic cerebrovascular disease or aortic atheroma is important.
  • The annual rate of stroke in atrial fibrillation varies widely from 0.5-12% per year depending on prevalence and combination of risk factors; thus, risk stratification is the first necessary step in choosing the best preventive therapy. Several clinical risk stratification schemes have been proposed to identify atrial fibrillation at high, moderate, or low risk; this is crucial for selecting which patients would benefit most and least from anticoagulation. The CHADS2 (ie, CHF, hypertension, age >75 y, diabetes, stroke or TIA) classification scheme (see Table 2 below) is the most validated and accurately stratifies stroke risk.^1,2,3
  • Two randomized controlled trials have demonstrated that a strategy aimed at restoring (and maintaining) sinus rhythm neither improves the survival rate nor reduces the risk of stroke. In the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study⁴ , 4060 patients aged 65 years or older whose atrial fibrillation was likely to be recurrent and who were at risk for stroke were randomized to a strategy of rhythm control (cardioversion to sinus rhythm, plus a drug[s] to maintain sinus rhythm) versus a strategy of rate control (in which no attempt was made to restore or maintain normal sinus rhythm). No evidence suggested that the rhythm control strategy protected patients from stroke.
  • The AFFIRM study (and similar findings from the smaller Rate Control Versus Electrical Cardioversion [RACE] trial⁵ ) has led to the development of consensus guidelines advocating a rate-control strategy for most patients with atrial fibrillation.
  • Adjusted-dose warfarin (international normalized ratio [INR] 2-3) is associated with a 60% reduction in stroke incidence, while the efficacy of aspirin is modest (20%). Low-dose warfarin (INR <1.5), either alone or combined with aspirin, is not effective, highlighting the marginal benefit of warfarin when anticoagulation is not carefully regulated. Incidence of intracerebral hemorrhage, the most dreaded complication of warfarin therapy, is estimated to be 0.5% per year among elderly patients with atrial fibrillation and is sensitive to blood pressure control. When warfarin is given to elderly patients with atrial fibrillation, hypertension must be managed aggressively.⁶
  • Recommendations for primary and secondary prevention based on risk factor stratification are presented in Table 3 below.
  • In the setting of acute stroke secondary to atrial fibrillation, anticoagulation with heparin has not demonstrated more benefit than early treatment with aspirin. Initiate aspirin early, followed by warfarin as soon as the patient is medically stable; discontinue aspirin after therapeutic anticoagulation is achieved.⁷
  • In short, warfarin has demonstrated high efficacy in stroke prevention in patients with this common arrhythmia. Disadvantages include the increased risk of hemorrhagic complications and the need for close INR monitoring in these patients; thus, consider patient preferences along with risk stratification and absolute risk reduction offered by this therapy. Alternative approaches (eg, surgical ablation of atrial appendage) are the subjects of ongoing clinical investigation.
  • Ximelagatran, an oral thrombin inhibitor, is comparable to adjusted-dose warfarin for stroke prevention in patients with atrial fibrillation. The Stroke Prevention Using an Oral Direct Thrombin Inhibitor in Patients with Atrial Fibrillation (SPORTIF) III and V clinical trials recently demonstrated that treatment of atrial fibrillation with ximelagatran twice daily is equivalent to adjusted-dose warfarin when considering stroke and major hemorrhage, but INR monitoring and dosage adjustments are unnecessary.⁸ However, potential liver toxicity led to disapproval by the US Food and Drug Administration (FDA) in late 2004.
  • Table 2. CHADS2 Stratification Schemes for Prevention of Stroke in Nonvalvular Atrial Fibrillation³ *
    
    

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    Table

    Stroke Rates by CHADS2 Score*
    CHADS2 Score	Risk	Stroke Rate Per Year
    0	Low	1.9%
    1	Low	2.8%
    2	Moderate	4%
    3	High	5.9%
    >3	Very high	>8.5%

    Stroke Rates by CHADS2 Score*
    CHADS2 Score	Risk	Stroke Rate Per Year
    0	Low	1.9%
    1	Low	2.8%
    2	Moderate	4%
    3	High	5.9%
    >3	Very high	>8.5%

  • Table 3. Risk-Based Approach to Antithrombotic Therapy in Patients With Atrial Fibrillation⁹
    

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    Table

    Patient Features	Antithrombotic Therapy	Class of Recommendation
    Age <60 y, no heart disease (lone AF)	Aspirin (81-325 mg/d) or no therapy	I
    Age <60 y, heart disease but no risk factors*	Aspirin (81-325 mg/d)	I
    Age 60-74 y, no risk factors*	Aspirin (81-325 mg/d)	I
    Age 65-74 y with diabetes mellitus or CAD	Oral anticoagulation (INR 2.0-3.0)	I
    Age ≥75 y, women	Oral anticoagulation (INR 2.0-3.0)	I
    Age ≥75 y, men, no other risk factors	Oral anticoagulation (INR 2.0-3.0) or aspirin (81-325 mg/d)	I
    Age ≥65, heart failure	Oral anticoagulation (INR 2.0-3.0)	I
    LV EF <35% or fractional shortening <25%, and hypertension	Oral anticoagulation (INR 2.0-3.0)	I
    Rheumatic heart disease (mitral stenosis)	Oral anticoagulation (INR 2.0-3.0)	I
    Prosthetic heart valves	Oral anticoagulation (INR 2.0-3.0 or higher)	I
    Prior thromboembolism	Oral anticoagulation (INR 2.0-3.0 or higher)	I
    Persistent atrial thrombus on Tee	Oral anticoagulation (INR 2.0-3.0 or higher)	IIA

    Patient Features	Antithrombotic Therapy	Class of Recommendation
    Age <60 y, no heart disease (lone AF)	Aspirin (81-325 mg/d) or no therapy	I
    Age <60 y, heart disease but no risk factors*	Aspirin (81-325 mg/d)	I
    Age 60-74 y, no risk factors*	Aspirin (81-325 mg/d)	I
    Age 65-74 y with diabetes mellitus or CAD	Oral anticoagulation (INR 2.0-3.0)	I
    Age ≥75 y, women	Oral anticoagulation (INR 2.0-3.0)	I
    Age ≥75 y, men, no other risk factors	Oral anticoagulation (INR 2.0-3.0) or aspirin (81-325 mg/d)	I
    Age ≥65, heart failure	Oral anticoagulation (INR 2.0-3.0)	I
    LV EF <35% or fractional shortening <25%, and hypertension	Oral anticoagulation (INR 2.0-3.0)	I
    Rheumatic heart disease (mitral stenosis)	Oral anticoagulation (INR 2.0-3.0)	I
    Prosthetic heart valves	Oral anticoagulation (INR 2.0-3.0 or higher)	I
    Prior thromboembolism	Oral anticoagulation (INR 2.0-3.0 or higher)	I
    Persistent atrial thrombus on Tee	Oral anticoagulation (INR 2.0-3.0 or higher)	IIA

    *Risk factors for thromboembolism include heart failure (HF), left ventricular (LV) ejection fraction less than 35%, and history of hypertension. AF=atrial fibrillation; CAD=coronary artery disease; INR=international normalized ratio; TEE=transesophageal echocardiography; EF=ejection fraction.
• Rheumatic mitral stenosis: The incidence of this valvulopathy has decreased dramatically in recent decades in the United States, but it remains an important problem in developing countries. Few estimates of absolute stroke rates or randomized comparison of different therapies are available, but because it generally is associated closely with atrial fibrillation, anticoagulation with warfarin (INR 2-3) usually is recommended.
• Sick sinus syndrome: Also known as brady-tachy syndrome, this arrhythmia usually occurs in elderly (>70 y) individuals. Annual risk of stroke is 5-10%. Atrial and dual chamber pacing may reduce the stroke rate somewhat, but anticoagulation (INR 2-3) is still recommended for select patients, such as those with associated atrial fibrillation; a lower target INR (eg, 1.6-2.5) may be tolerated better in these elderly patients.
• Atrial flutter (sustained): This is an uncommon arrhythmia. Because of the close association of atrial fibrillation with appendage stasis, anticoagulation (INR 2-3) is advocated.
• Prosthetic valves: Mechanical prosthetic valves carry an annual risk of stroke of 2-4% even in patients receiving anticoagulation. Permanent anticoagulation (INR 2.5-3.5) is mandatory. Bioprosthetic valves carry a lower annual risk rate (0.2-2.9%), and aspirin usually is recommended unless the patient has atrial fibrillation or evidence of atrial stasis.
• Infective endocarditis: Of patients with infective endocarditis, 20% experience an embolic stroke but accounted for less than 1% of all causes of cerebral embolism in the Cerebral Embolism Stroke Registry¹⁰ . Staphylococcus aureus is the agent producing the highest stroke rate. Mitral valve endocarditis is the most common source of emboli. Antibiotic therapy reduces the embolic potential when administrated in the acute phase. Anticoagulation is contraindicated because of unacceptable rates of hemorrhagic stroke due to either mycotic aneurysm rupture or septic arteritis. In patients with prosthetic valve endocarditis, the risk of thromboembolism is greater than the risk of intracranial hemorrhage, thus anticoagulation usually is recommended if no evidence of hemorrhage is found on CT scanning 24-48 hours after the stroke. Consensus is to start anticoagulation 7 days after the stroke. The role of antiplatelet therapy has not been established.
• Nonbacterial thrombotic endocarditis: Associated with a variety of malignancies, nonbacterial thrombotic endocarditis also has been reported in patients with severe diseases such as septicemia and extensive burns. Mitral and aortic valves are affected most commonly, and embolic stroke is frequent. A prothrombotic state has been postulated as the precursor of emboli development. Treatment is directed toward control of the underlying disease, and heparin (intravenous in the acute stage, subcutaneous in the outpatient setting) is advocated for stroke prevention. Warfarin failed to show any benefit.
• Atrial myxomas: This is the most common cardiac tumor, and it usually is located on the fossa ovalis. It is believed to cause 1% of strokes in young individuals. Surgical excision is the treatment of choice. Most can be detected by transthoracic echocardiography; rarely, they are detected only by transesophageal echocardiography.
• Acute myocardial infarction: The incidence of stroke after acute myocardial infarction is approximately 2% in the first 3 months. Anterior myocardial infarctions with mural thrombus on transthoracic echocardiography have been recognized as predictive of stroke. Anticoagulation (INR 2-3) is recommended in these patients in the first 3 months, while antiplatelet therapy is advocated long term. The presence of congestive heart failure after myocardial infarction usually dictates treatment with warfarin indefinitely, although randomized comparisons with other therapies are ongoing. Low-output cardiac failure (ejection fraction <30%) also is considered a high-risk situation, as is the presence of a large ventricular aneurysm on echocardiography.

Minor-risk sources

• Patent foramen ovale: Persistent connection between the right and left atrium has a prevalence of about 20% in the general population (see Media file 4). Screening for PFOs can be done reliably with contrast precordial echocardiography, which detects interatrial shunting, but transesophageal echocardiography is required to document the PFO and more accurately determine its size, associated atrial septal aneurysm, and amount of shunting.
  • While case-control studies have documented a higher frequency of PFO in young adults with cryptogenic ischemic stroke, it is present by chance association in patients with stroke in at least 50% of cases. The rate of stroke recurrence is 1-2% per year. Larger size, spontaneous right-to-left shunting, and associated atrial septal aneurysm are postulated to identify subgroups at high risk for recurrence.
  • PFO is not associated with increased risk of subsequent stroke or death among medically treated patients with cryptogenic stroke. However, both PFO and ASA possibly increase the risk of subsequent stroke (but not death) in medically treated patients younger than 55 years. In patients with a cryptogenic stroke and an atrial septal abnormality, the evidence is insufficient to determine if warfarin or aspirin is superior in preventing recurrent stroke or death, but minor bleeding is more frequent with warfarin. Evidence evaluating the efficacy of surgical or endovascular closure is insufficient.¹¹
  • Elucidation of the role of other therapeutic approaches such as surgical closure (eg, transthoracic, percutaneous) awaits the results of clinical trials and better characterization of the natural history. At present, PFO should not be considered the cause of stroke until other etiologies have been excluded thoroughly.
• Atrial septal aneurysms: These aneurysms are areas of redundant atrial septal tissue that bulge alternatively into the right or left atrium. They have a high degree of association with other sources of embolism (mainly atrial fibrillation and PFO). Insufficient data are available at present to consider atrial septal aneurysm as an independent risk factor for stroke. When atrial septal aneurysms coexist with a PFO or other sources of embolism, anticoagulation usually is recommended (Mas, 2002), but there are no randomized trials supporting this policy.
• Mitral valve prolapse: Mitral valve prolapse is the most common valve disease in adults. The role of mitral valve prolapse as an independent risk factor for stroke is a controversial and evolving issue. The estimated prevalence is not greater in patients who have had a stroke than in the general population in recent population-based studies. Long-term aspirin therapy is recommended, although its value has not been confirmed by randomized trials. Anticoagulation is reserved for failure of antiplatelet therapy.
• Calcific aortic stenosis and bicuspid aortic valves: Systemic embolism is uncommon in isolated aortic valve disease. Calcific microemboli can be detected in the retinal artery in asymptomatic patients, possibly reflecting the fact that most cerebral emboli are asymptomatic. Clinical embolism often follows invasive cardiac procedures (ie, catheterization). Because of the calcific nature of the emboli, anticoagulation is not recommended, and antiplatelet therapy remains an empiric approach.
• Fibroelastomas and Lambl excrescences: Fibroelastomas are rare benign tumors located on the valves. Antiplatelet therapy is indicated, and surgical repair is reserved for patients who have stroke recurrence. Lambl excrescences are filiform outgrowths from the free borders of the cardiac valves and have been implicated as sources of embolism when they attain large size. Antiplatelet therapy is initiated followed by surgery if aspirin fails.
• Mitral annular calcification: This is associated with advancing age, hypertension, and atherosclerosis, and it is rarely an embolic source.

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