Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Cardioembolic stroke |CT Basics for Stroke |Endocarditis and Stroke |Haemorrhagic Stroke |Stroke Thrombolysis |Hyperacute Stroke Care

Introduction

Cardioembolic stroke refers to cerebral ischaemia resulting from emboli that originate in the heart and occlude cerebral arteries. These emboli can arise from various cardiac sources such as the left atrium, left ventricle, or heart valves. Additionally, paradoxical emboli can occur via intracardiac shunts like a patent foramen ovale (PFO) or atrial septal defect (ASD). Cardioembolic strokes account for approximately 15-30% of all ischemic strokes and are associated with a high in-hospital mortality rate of 25-30%. Notably, over 20% of strokes in individuals over 80 years old are due to atrial fibrillation (AF), highlighting the potential for prevention through appropriate management.

Causes and Sources of Cardioembolism

Cardioembolic strokes can arise from various cardiac conditions, which can be stratified based on the risk of embolism:

• High-Risk Sources:
  • Atrial Fibrillation: Both valvular and non-valvular AF increase stroke risk, with risk stratified using the CHA₂DS₂-VASc score.
  • Recent Myocardial Infarction (MI): Particularly with left ventricular (LV) aneurysm or areas of hypokinesia/akinesia.
  • Mechanical Heart Valves: Prosthetic valves, especially mechanical ones, have a high thrombogenic potential.
  • Dilated Cardiomyopathy: Enlarged and weakened heart chambers increase the risk of thrombus formation.
  • Rheumatic Mitral Stenosis: Stenotic valves promote atrial enlargement and stasis, leading to thrombus formation.
• Other Sources:
  • Infective Endocarditis: Vegetations on valves can embolize.
  • Atrial Myxoma: Cardiac tumors that can fragment and embolize.
  • Patent Foramen Ovale (PFO): Allows paradoxical emboli from venous to arterial circulation.
  • Left Atrial Appendage Thrombus: Common in AF due to blood stasis.
  • Mitral Valve Prolapse and Calcification: Structural abnormalities increasing thrombotic risk.
  • Nonbacterial Thrombotic (Marantic) Endocarditis: Associated with malignancy and hypercoagulable states.

Classification

Cardioembolic sources can be categorized based on the underlying cardiac pathology:

• Cardiac Wall and Chamber Abnormalities:
  • Cardiomyopathies (dilated, hypertrophic, restrictive)
  • Left ventricular aneurysms post-MI
  • Atrial septal aneurysms
  • Atrial myxomas and other cardiac tumors
  • Papillary fibroelastomas
  • Intracardiac thrombi due to stasis or hypokinesia
  • Septal defects (PFO, ASD) allowing paradoxical emboli
• Valvular Disorders:
  • Rheumatic heart disease affecting mitral and aortic valves
  • Prosthetic heart valves (mechanical & bioprosthetic)
  • Infective endocarditis with valvular vegetations
  • Libman-Sacks endocarditis (nonbacterial thrombotic endocarditis)
  • Mitral valve prolapse and annular calcification
• Arrhythmias:
  • Atrial fibrillation (paroxysmal, persistent, or permanent)
  • Sick sinus syndrome
  • Atrial flutter

Clinical Features

Cardioembolic strokes typically present with sudden onset of neurological deficits that are maximal at onset. Key characteristics include:

• Acute Onset: Symptoms develop abruptly without a progressive phase.
• Maximum Deficit at Onset: Neurological deficits are severe from the beginning.
• Multiple Vascular Territories: Infarcts may occur in different arterial territories simultaneously.
• Fluctuating Symptoms: Transient improvement can occur if the embolus fragments or moves distally.
• Large Vessel Occlusion: Often involves major cerebral arteries, making reperfusion therapies viable.
• Higher Risk of Hemorrhagic Transformation: Due to reperfusion injury and fragile vasculature.
• Decreased Level of Consciousness: May occur at onset due to extensive cerebral involvement.

Physical examination may reveal signs of underlying cardiac conditions such as atrial fibrillation, murmurs, signs of infective endocarditis, or features of heart failure.

Causes and Frequency

The table below summarizes common cardiac sources of embolism and their relative frequencies:

Structural Cardiac Disease and Stroke

Structural abnormalities of the heart can predispose to thrombus formation and subsequent embolization. A thorough history and examination are crucial in identifying potential cardiac sources:

• Cardiomyopathy: Dilated, hypertrophic, or restrictive cardiomyopathies can cause stasis and thrombus formation.
• Infective Endocarditis: Vegetations on valves can embolize; consider in patients with fever, murmurs, and embolic events.
• Atrial Myxoma: Benign cardiac tumors presenting with constitutional symptoms and embolic phenomena.
• Left Ventricular Aneurysm: Post-MI scar formation can lead to aneurysm and thrombus formation.
• Mitral Valve Prolapse and Calcification: Associated with endothelial damage and thrombus formation on valve leaflets.
• Patent Foramen Ovale: Allows paradoxical emboli; often identified in cryptogenic strokes in younger patients.

Clinical Presentation

Patients with cardioembolic stroke may present with:

• Sudden focal neurological deficits (e.g., hemiparesis, aphasia, visual field defects)
• Symptoms involving multiple vascular territories
• Decreased level of consciousness or syncope
• Seizures at onset (more common in embolic strokes)
• Cardiac symptoms such as palpitations, chest pain, or dyspnea
• Signs of systemic emboli (e.g., limb ischaemia)
• Physical findings like irregular pulse (AF), murmurs, or signs of heart failure

Investigations

A comprehensive workup is essential to identify the source of embolism and guide management:

• Laboratory Tests: Complete blood count, ESR (may be elevated in endocarditis or myxoma), coagulation profile.
• Electrocardiogram (ECG): Detects arrhythmias such as AF, evidence of recent MI, or conduction abnormalities.
• Cardiac Monitoring: Holter monitoring (24-48 hours) or extended event monitors to detect paroxysmal AF.
• Imaging Studies:
  • CT Scan: May show multiple infarcts in different vascular territories.
  • MRI with Diffusion-Weighted Imaging (DWI): More sensitive for detecting acute ischaemia and small embolic infarcts.
  • CT Angiography (CTA) or MR Angiography (MRA): To assess intracranial and extracranial vessels for occlusions.
• Echocardiography:
  • Transthoracic Echocardiogram (TTE): Initial assessment of cardiac structure and function.
  • Transesophageal Echocardiogram (TEE): More sensitive for detecting left atrial appendage thrombus, valvular vegetations, PFO, and aortic arch atheroma.
  • Bubble Study: Uses agitated saline to detect right-to-left shunts such as PFO.
• Transcranial Doppler Ultrasound: Can detect microembolic signals and assess for intracranial stenosis.
• Blood Cultures: If infective endocarditis is suspected.
• Additional Tests: Troponin levels if recent MI is suspected; consider hypercoagulable workup in younger patients or those with recurrent events.

Management

Management of cardioembolic stroke involves acute treatment and secondary prevention:

• Acute Stroke Management:
  • Adhere to standard protocols for acute ischemic stroke, including reperfusion therapies if within the therapeutic window.
  • Monitor for hemorrhagic transformation, especially after thrombolysis.
  • Supportive care with attention to airway, breathing, and circulation.
• Secondary Prevention:
  • Anticoagulation:
    • Initiate anticoagulation with warfarin (target INR 2-3) or direct oral anticoagulants (DOACs) in non-valvular AF.
    • Warfarin is preferred in mechanical heart valves and rheumatic mitral stenosis; DOACs are not indicated in these conditions.
    • Timing of initiation depends on stroke severity and risk of hemorrhagic transformation; typically between 4-14 days after the event.
  • Management of Underlying Cardiac Conditions:
    • Treat heart failure, arrhythmias, and valvular diseases appropriately.
    • Consider surgical interventions for cardiac tumors or significant valvular lesions.
  • Risk Factor Modification:
    • Control hypertension, diabetes, and hyperlipidemia.
    • Encourage smoking cessation and lifestyle modifications.
• Multidisciplinary Approach: Collaboration between neurologists, cardiologists, and other specialists is essential for optimal care.

Prognosis

Cardioembolic strokes are generally associated with:

• Higher Initial Stroke Severity: Due to occlusion of large cerebral vessels.
• Increased Mortality: Both short-term and long-term mortality rates are higher compared to other stroke subtypes.
• Risk of Recurrence: High risk of early and late recurrent strokes if underlying cardiac sources are not addressed.
• Functional Outcomes: Lower likelihood of being symptom-free at discharge; rehabilitation is often necessary.

References

• Hart RG, Diener HC, Coutts SB, et al. Embolic strokes of undetermined source: the case for a new clinical construct. Lancet Neurol. 2014;13(4):429-438.
• Adams HP Jr, Bendixen BH, Kappelle LJ, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. Stroke. 1993;24(1):35-41.
• January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation. Circulation. 2019;140(2):e125-e151.
• American Heart Association/American Stroke Association. Guidelines for the Early Management of Patients with Acute Ischemic Stroke. Stroke. 2019;50:e344–e418.
• Arboix A, Alió J. Cardioembolic Stroke: Clinical Features, Specific Cardiac Disorders and Prognosis. Curr Cardiol Rev. 2010;6(3):150-161.
• Yaghi S, Amarenco P, Bogousslavsky J, et al. Mechanical Heart Valves and Stroke: A Transatlantic Alliance (MHaSTA) Consensus Statement. Am J Med. 2017;130(8):932.e1-932.e7.