Why the study?
What is the prevalence of microemboli and its association with hemorheological parameters in asymptomatic patients with cardiac aneurysm, severe ventricular dysfunction, or atrial fibrillation?
What is the prevalence of microemboli and its association with hemorheological parameters in asymptomatic patients with cardiac aneurysm, severe ventricular dysfunction, or atrial fibrillation?
Asymptomatic patients with left ventricular aneurysm, severe ventricular dysfunction, or atrial fibrillation have ongoing microembolic activity that is exacerbated by ineffective anticoagulation and increased platelet aggregation.
Microemboli occur in 31% of asymptomatic high-risk patients; cross-sectional association with ineffective anticoagulation plus platelet aggregation is hypothesis-generating.
Transcranial Doppler sonography has become a widely used method for detecting cerebral circulating microemboli (ME) arising from the carotid arteries or the heart. Yet, studies on subgroups of patients with distinct cardiac sources of embolism are still limited. The same holds true for investigation on the relationship between microembolization and hemorheological parameters. A total of 142 patients suffering from left ventricular aneurysm (LVA, n = 52), severe left ventricular dysfunction (LVD, n = 43), or chronic atrial fibrillation (AF, n = 47) were enrolled in this study. All patients had been neurologically asymptomatic for at least 1 month. Further relevant embolic disorders of the carotid arteries and the heart had been excluded. Unilateral monitoring for ME over the middle cerebral artery was performed for 30 min. Blood was drawn after each monitoring for determination of plasmatic coagulation parameters, as well as plasma viscosity, and platelet reactivity. The overall prevalence of ME was 31%, with a slightly higher prevalence in patients with LVA (37%) compared to patients suffering from AF (30%) or LVD (26%). With single-factor analysis, a trend towards higher ME prevalences was found with (a) a history of remote embolic events, (b) ineffective anticoagulation, (c) increased platelet aggregation, or (d) increased plasma viscosity (all p > 0.1). The combination of ineffective anticoagulation in conjunction with increased platelet aggregation, however, was significantly associated with higher ME rates even after adjustment for other factors by logistic regression analysis. Our results demonstrate a low ongoing microembolic activity in asymptomatic patients suffering from LVA, LVD and AF. An activated plasmatic coagulation system together with increased platelet aggregation contributes to ME generation.
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Nabavi et al. (1998) studied this question.
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