Cardioembolic Strokes

From Stroke Education
Jump to: navigation, search

Learning objectives

  • Understand the cardiac causes of embolic stroke
  • Be able to recognise these clinically and with investigations
  • Manage ongoing risks

Introduction

Brain is 1-2% of body mass but gets 10% of the resting blood flow. Cardioembolism refers to strokes due to emboli emanating from the heart. There are several underlying reasons why this can happen. The high flow rate of blood to the brain per unit volume means that it is inherently susceptible to cardioembolism. Cardioembolic strokes related to AF and PAF are very preventable with anticoagulation and so detecting AF/PAF is incredibly important. There are other less common aetiologies. Please also see <a href="paradoxicalembolism.php" title="Paradoxical Embolism">Paradoxical Embolism</a> as another cause dealt with separately

Mechanisms

Cardioembolism accounts for 20% of ischaemic strokes. Cardioembolic strokes are generally more severe and are more prone to recurrence than other stroke types. The risk of long-term recurrence and mortality are high after a cardioembolic stroke. By far the most common cause of cardioembolic stroke disease is non-valvular Atrial fibrillation. Cardiac emboli tend to flow to the intracranial vessels. Over two-thirds of blood goes via the anterior circulation and most of the time thrombi occlude the proximal MCA often causing massive, superficial or single large striatocapsular or multiple MCA territory infarcts. Be aware that a large clot or a pre-existing carotid stenosis can cause thrombus to cause acute internal carotid artery subacute or total occlusion. Posterior circulation emboli can occlude vertebral and basilar arteries as well as reaching distal posterior cerebral artery. Brainstem, cerebellar and occipital lesions can be seen which may be multiple.

Causes and Risk of Cardioembolic stroke [Tudor G. et al. 2008]

High Risk Lesions
Atrial Fibrillation (x5 risk) and Sustained Atrial Flutter
Sick Sinus Syndrome
Left Atrial Thrombus and Left Atrial Appendage Thrombus
Left Atrial Myxoma and Mitral Stenosis
Mechanical Valve, Infective Endocarditis
Non Infective Endocarditis
Left Ventricular Myxoma
Recent Anterior MI, Dilated Cardiomyopathy
Low Risk Lesions
Patient Foramen Ovale, Atrial septal aneurysm
Spontaneous atrial contrast, Mitral Valve prolapse
Calcific aortic stenosis, Fibroelastoma
Giant Lambel Excrescence
Akinetic Ventricular wall segment
Subaortic hypertrophic cardiomyopathy
Congestive cardiac failure

Clinical

  • Clinical effects will depend on the proximity of occlusion in the MCA
  • Also depend on existing collateralisation, rapidly or reperfusion of the vessel
  • Pulse and exam may detect AF
  • Murmurs can suggest mitral stenosis or atrial myxoma or ASD
  • Embolic Strokes usually instant onset large vessel syndromes
  • Embolic strokes reputed to also suddenly improve as emboli break up
  • May be due to thrombus break up and distal embolisation with thrombolysis.
  • Sequential Embolic strokes go to different vascular beds - right left/ant post
  • Recanalisation and haemorrhagic transformation commoner with an embolism
  • Look for stigmata of endocarditis
  • Recent cardiac surgery is a red flag

Structural Heart Disease as a source of Cardioembolism

Structural Heart Disease as a source of Cardioembolism
  • Various Cardiac structural defects can lead to the formation of intracardiac thrombi and cardioembolism. If suspected the first investigations include a clinical history and a search for any determinants that will give a clue. Cardiac symptoms suggestive of Ischaemic heart disease, chest pain, breathlessness and palpitations which could suggest an Ischaemic cardiomyopathy. A history of rheumatic fever could suggest valvular disease and Temperature and stigmata for endocarditis must always be considered.
  • Cardiac conditions These include any condition that allows stasis and the formation of thrombi. Severely Impaired LV function, LV aneurysm formation. Atrial or Ventricular myxomas. There may be coexisting AF. Others include Cardiomyopathy, Mitral valve prolapse and prosthetic heart valves.
  • Cardiomyopathy Risks of cardioembolism may be seen in those with very poor LV function and those with underlying Chronic AF with enlarged LA. A history of excess alcohol might suggest an alcoholic cardiomyopathy. Cardiomyopathy may also be seen with HIV. The examination may reveal heart failure, rashes, AF, sighs of chronic liver disease, nicotine staining, hypertension and murmurs. An ECG and CXR and then Echo will be useful. A Troponin may be useful acutely if recent myocardial infarction is suspected.
  • Mitral Valve Prolapse Studies have shown that mitral valve prolapse (MVP) is associated with fibrinous deposits on the valve, endothelial denudation and annular thrombus at the junction with the atrial wall. The myxomatous redundant valve leaflets appear to increase the predisposition to thromboembolic events. There is no evidence for anti thrombotic treatment other than antiplatelets in those who have experienced stroke. There should be a search for undetected PAF.
  • Mitral annulus calcification Is seen with mitral stenosis, mitral regurgitation and may be increased in those with cardiogenic brain embolism. Detected on echocardiography it suggests a twofold increase in risk for stroke. Embolism of fibrinated cell clot or calcium spicules has been reported.
  • Prosthetic Heart Valves Diseased and damaged heart valves are often replaced with either mechanical or bioprosthetic (tissue) valves. Tissue prosthetic valves are believed to be associated with a smaller risk of thromboembolism than mechanical valves. Mitral valve prostheses are associated with a greater risk of thromboembolism than Aortic, possibly because of the higher incidence of atrial fibrillation and other thromboembolic risk factors in these patients.
  • Endocarditis Emboli can also arise from valvular vegetations in nonbacterial thrombotic endocarditis or infective endocarditis.
  • Aortic emboli It is possible that emboli can be dislodged from the proximal aorta spontaneously or due to coronary intervention e.g. trying to cannulate the coronary vessels. Another important cause is thrombus forming over areas of arterial dissection. Aortic atheroma is detectable by TOE is significantly more common in stroke patients than healthy controls. Atheromatous plaques may be a source of embolic material through rupture and thrombus formation and are themselves associated with increased stroke risk. There is no known specific management. Lipid-lowering and management of vascular risk factors is advocated.

Investigations

  • Bloods: FBC, U&E, LFTs, Troponin if MI considered (e.g. ECG changes)
  • Dimer and USS legs if VTE and Paradoxical embolism considered
  • ESR and CRP: elevated with atrial myxoma and endocarditis
  • ECGAF, AFl, recent MI, ST elevation with MI or LV aneurysm
  • Holter ECG Difficulties arise when AF is paroxysmal but in acute stroke it should be detectable acutely and if not present then Holter monitoring should really be considered for at least 48 hours. There should be a very low threshold for looking for PAF or sick sinus syndrome both of which are associated with embolism.
  • Echocardiography in the first hours after the onset of stroke is necessary only in rare cases, such as if infective endocarditis is suspected. In the days thereafter, transthoracic echocardiography or, preferably, transoesophageal echocardiography can be undertaken to support or refute a possibility of cardioembolism. Transthoracic echocardiogram can detect the typical findings of mitral stenosis or dilated cardiomyopathy and other structural ventricular diseases. Left ventricular thrombus, valve vegetations, or atrial myxomas can also be detected. Left atrial size and left ventricular systolic function can be assessed. In younger patients or when valve or other structural lesions need better defined then Transoesophageal echocardiogram is used. Diagnostic views of aortic arch, ascending aorta, left atrium and left atrial appendages, intra-atrial septum, pulmonary veins, and valve vegetations can be seen. Any PFO or atrial septal aneurysm can be detected and bubble contrast may be given to look for shunting.
  • Brain Imaging useful but until there are bilateral or anterior and posterior circulation large vessel stroke lesions the CT does not help greatly with aetiology. MRI in this respect can show more detail, can identify older lesions not seen on CT and show that subcortical strokes extend to cortex and more likely to be large vessel. CT may show Haemorrhagic transformation seen in up to 71% of cardioembolic strokes [Jorgensen L et al. 1969]. Haemorrhagic infarcts are predominately cardioembolic [Fisher CM et al. 1951].

Management

  • Making a diagnosis of Cardioembolism is usually supported by finding of either AF or a structural cardiac lesion. The history of examination findings of AF or rheumatic valve disease or prosthetic valves makes the diagnosis straightforward.
  • Anticoagulation. To be continued if safe after formal risk benefit analysis
  • Left atrial appendage closure if anticoagulation not possible with AF
  • Cardiac surgery for some e.g.atrial myxoma