Related Experiment Videos
Atrial fibrillation as a cause of myocardial and cerebral infarctions
Insights
Atrial fibrillation (AF) significantly increases the risk of myocardial and cerebral infarctions, primarily through the formation of intracardiac mural thrombus. This study highlights AF
Area of Science:
- Cardiovascular Pathology
- Neuropathology
- Geriatric Medicine
Background:
- Atrial fibrillation (AF) is a common cardiac arrhythmia in the elderly.
- The relationship between AF and the pathogenesis of myocardial and cerebral infarctions requires further elucidation.
Purpose of the Study:
- To investigate the pathogenetic role of atrial fibrillation (AF) in myocardial and cerebral infarctions.
- To determine the association between AF, intracardiac mural thrombus, and infarction size.
Main Methods:
- Retrospective autopsy study of 2340 elderly individuals.
- Analysis of myocardial infarction, cerebral infarction, and intracardiac mural thrombus prevalence in relation to AF.
- Comparison of infarction characteristics between AF and non-AF groups.
Main Results:
- AF prevalence was 17.3% and increased with age.
- Myocardial infarction and scar were significantly more prevalent in AF patients (56.8% vs. 36.4%).
- AF was associated with a higher incidence of small myocardial infarctions and large/medium cerebral infarctions, linked to intracardiac mural thrombus.
Conclusions:
- Atrial fibrillation plays a significant pathogenetic role in both myocardial and cerebral infarctions.
- Intracardiac mural thrombus formation in AF is a key mechanism for embolic infarctions.
- AF-related infarctions, particularly cerebral ones, may differ in size and prevalence compared to non-AF cases.
Abstract:
Pathogenetic role of atrial fibrillation (AF) on myocardial and cerebral infarctions was studied in 2340 consecutive autopsies of the aged. AF was found in 405 cases or 17.3%, and the incidence of AF increased with age. Myocardial infarction and scar were found in 56.8% in AF, but in 36.4% in non-AF (p less than 0.001). Small myocardial infarction was 2.9 times (12.6% vs. 4.3%), and the scar was 1.5 times (27.2% vs. 18.7%) as prevalent in AF as in non-AF. Intracardiac mural thrombus was found in 14.8% in AF and in 4.8% in non-AF, 8 to 10 times as prevalent in small myocardial infarction (29.4% vs. 3.7%) and scar (17.4% vs. 1.7%) in AF as in non-AF. Coronary stenotic index revealed no difference between AF and non-AF. Large cerebral infarction was observed in 21.9% in AF and 7.3% in non-AF, and this difference was prominent in cases with myocardial infarction or myocardial scar indicating the common pathogenetic role of AF. In cases with large cerebral infarction severe cerebral atherosclerosis was less frequent in AF than in non-AF. Medium sized cortical infarction was also prevalent in AF. The prevalences of myocardial and cerebral infarctions were not different in AF complicated with valvular heart disease from those without it, but increased in the permanent AF in comparison to the transient AF. AF induced small myocardial infarction and large or medium sized cerebral infarctions by embolism from mural thrombus. The mechanism for the difference in size is discussed.