Why the study?
Can cardiogenic microembolic signals (MES) detected by transcranial Doppler serve as a surrogate parameter for future thromboembolic risk in patients with chronic cardiac diseases?
Can cardiogenic microembolic signals (MES) detected by transcranial Doppler serve as a surrogate parameter for future thromboembolic risk in patients with chronic cardiac diseases?
Current evidence on cardiogenic microembolic signals as a surrogate for thromboembolic risk is sparse and based on small cohorts, highlighting the need for large prospective studies to establish clinical utility.
MES should not guide thromboembolic risk stratification in cardiac disease; leaves open validation as a surrogate in large prospective studies.
BACKGROUND: In various cardiac diseases, thrombembolism constitutes a major risk, and in these patients clinically silent microembolic signals (MES) are detectable within the transcranial Doppler frequency spectrum (TCD) of the major brain arteries. MES are already an accepted surrogate parameter of the future risk of stroke in patients with carotid artery stenosis. The aim of this review is to summarize and evaluate the data about occurence and clinical impact of MES in patients with chronic cardiac diseases and to clarify whether cardiogenic MES can serve as a surrogate parameter of the heart's future thrombembolic risk as well. METHODS: We performed a systematic MEDLINE search and reviewed the currently available literature about chronic cardiac diseases and atheroaortic plaques leading to MES apart from cardiosurgical procedures. CONCLUSION: The cardiac conditions producing MES are heterogenous and therefore the prevalence of MES is highly variable. The data in patients with acute or after myocardial infarction, endocarditis, patent foramen ovale, mitral valve prolapse, dilatative cardiomyopathy and intracardiac thrombus is promising but only small patient cohorts have been investigated by means of TCD in these categories. MES in atrial fibrillation, or derived from atheroaortic plaques, have been investigated more intensively, but again larger cohorts need to be explored to draw firm conclusions. In all cardiac diseases there is a lack of large prospective studies allowing to reliably correlating MES with clinical events. Compared to carotid artery disease, the current knowledge about the impact of cardiogenic MES on the patient's risk is sparse. This should encourage the clinical research in this promising field.
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Dittrich et al. (2008) studied this question.
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