Endomyocardial fibrosis is a rare disease in European countries and is more prevalent in sub-Saharan Africa [75]. The etiology of endomyocardial fibrosis is unknown. Immunological, infectious, and toxico-logical etiologies are assumed [75]. Clinically, endo-myocardial fibrosis is characterized by severe congestive heart failure with only moderately increased heart size. Systolic performance is normal or only slightly depressed despite severe restriction of filling, atrioventricular valve regurgitation, or both. Echocardiography may reveal partial obliter-ation of the right or left ventricle [75]. Endocardial resection with atrioventricular valve replacement is the treatment of choice, with appreciable postopera-tive improvement and a 10-year survival of approxi-mately 70% [75]. Whether there is a generally increased risk of stroke in patients with endomyocar-dial fibrosis is unknown, but single patients have been reported who developed an ischemic stroke.
Among these is one who developed multiple ische-mic strokes in association with endomyocardial fibro-sis from schistosomiafibro-sis and one with multiple cerebellar and cerebral infarctions from endomyocar-dial fibrosis associated with hypereosinophilic syndrome [76].
Chapter summary
Rhythm disturbances
Atrial fibrillation (AF) may lead to embolic stroke or peripheral or mesenteric embolism. Patients with AF have a 5-fold (non-rheumatic AF) to 17-fold increased risk of stroke (embolism due to rheumatic heart disease). Diagnosis of permanent AF is feasible from the 12-lead electrocardiogram, and paroxysmal AF can be diagnosed with 24–72-hour Holter moni-toring or 7-day event loop recorders. Implantable loop recorders may facilitate the detection of AF.
Brady- or tachycardia causes symptoms such as dizziness, light-headedness, fainting spells. These symptoms may erroneously be interpreted as epilep-tic seizures.
QT prolongation: stroke is associated with QT prolongation in 30–40% of patients. QT prolongation in stroke may be due to cardiovascular comorbidity, concomitant drug intake, and metabolic disturb-ances, but may also be due to the affected brain region, especially the insular region. QT prolongation may be associated with torsades de pointes tachy-cardia, which manifests as palpitations, dizziness, or syncope. Degeneration into ventricular fibrillation and sudden cardiac death can occur.
Coronary heart disease
There is a frequent coexistence of coronary heart disease and stroke, most probably due to common atherosclerotic risk factors. Suspected coronary heart disease should lead to cardiological consultation for further therapeutic and diagnostic measures, includ-ing coronary angiography and percutaneous coron-ary intervention. Acute or subacute myocardial infarction and ventricular aneurysms can also be a cause of embolic stroke.
Valvular heart disease
Ischemic and hemorrhagic strokes occur in 10–23%
of patients with endocarditis, especially of the mitral valve. Diagnosis of infective endocarditis is difficult.
Thus, endocarditis has to be considered as a differen-tial diagnosis in all stroke patients if laboratory signs of inflammation are present.
After heart valve surgery patients are at increased risk of thromboembolism. The embolic risk varies according to the type of surgery (repair versus replacement), the type of replaced valve (bioprosth-esis versus mechanical prosth(bioprosth-esis), and the affected valve (mitral versus aortic valve).
Patent foramen ovale (PFO)
In about 25% of humans the foramen ovale remains open, permitting right-to-left shunting when the right atrial pressure exceeds the left atrial pressure.
In patients with cryptogenic stroke the prevalence of PFO is 30–46% (paradoxical embolism from venous thrombosis), but it has not been demonstrated that patients with PFO are at increased risk of recurrent stroke. Randomized trials have shown that percutan-eous PFO closure offers no benefit after ischemic stroke compared with medical therapy.
Atrial septal aneurysms (ASM)
An ASM is diagnosed echocardiographically if the atrial septum appears abnormally redundant and mobile. Similarly to PFO, ASM has been found to be closely associated with cryptogenic stroke in
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retrospective and case–control studies, but failed to be identified as a risk factor for future stroke in prospective randomized or population-based studies.
It is unknown whether conditions such as dilated cardiomyopathy, restrictive cardiomyop-athy, Takotsubo cardiomyopathy (a reversible
neuromyocardial failure, which resembles acute myocardial infarction clinically and electrophysiolo-gically in patients with normal coronary arteries), left ventricular hypertrabeculation /non-compaction, or endomyocardial fibrosis raise the risk of stroke inde-pendently of the presence of atrial fibrillation.
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