Stroke in Dilated Cardiomyopathy: An Autopsy-Based Study of Mechanisms, Topography, and Clinical Implications

Abstract

Background: Dilated cardiomyopathy (DCM) is a major cause of heart failure and arrhythmic mortality; yet, its association with cerebrovascular events, particularly in the absence of atrial fibrillation (AF), remains insufficiently explored. Purpose: This study aimed to determine the prevalence, mechanisms, and anatomical distribution of stroke in patients with DCM and to assess the role of AF and structural remodeling in stroke risk. Methods: We retrospectively analyzed 471 patients who died with DCM at the Emergency County Clinical Hospital of Bihor between 1 January 2022 and 31 December 2024. Clinical records, neuroimaging, autopsy reports, and histopathological data were reviewed. Stroke subtypes were classified according to TOAST criteria (large artery atherosclerosis, cardioembolic, small vessel disease, other determined, undetermined) and hemorrhagic categories (intracerebral, subarachnoid). Demographic, echocardiographic, and comorbidity data were compared between patients with and without cerebrovascular events. Results: Of 471 patients with DCM, 45 (9.6%) had concomitant stroke: pure ischemic in 32 (71.1%), 7 (15.6%) showed ischemic with hemorrhagic transformation, and primary hemorrhagic in 6 (13.3%). The parietal lobe was most frequently affected. AF was present in 26 patients (57.8%) and was significantly associated with ischemic stroke (p = 0.004), though embolic strokes also occurred in sinus rhythm. Patients with stroke had significantly lower left ventricular ejection fraction (28.0 ± 13.7% vs. 34.0 ± 11.2%, p = 0.007) and larger atrial dimensions. Histopathological findings confirmed acute and chronic ischemic injury patterns, including "red neurons," white matter vacuolization, and gliotic scarring. Conclusions: Stroke is a frequent and often underdiagnosed complication in DCM, predominantly ischemic and embolic in nature. Importantly, embolic events were observed even in patients without AF, suggesting that atrial remodeling in DCM may independently predispose to cerebrovascular risk. These results underscore the need for refined preventive strategies, including careful atrial assessment and exploration of whether anticoagulation may benefit selected high-risk DCM patients without AF, a question that requires confirmation in prospective trials. Potential embolic sources in DCM include atrial cardiopathy and left ventricular thrombus in the setting of severe systolic dysfunction; therefore, careful ventricular as well as atrial assessment is warranted in high-risk DCM.

Keywords: atrial fibrillation; autopsy; dilated cardiomyopathy; heart failure; histopathology; ischemic stroke; stroke; thromboembolic risk.

Figure 1

Mechanisms of cerebrovascular events in patients with dilated cardiomyopathy (DCM). The pie chart illustrates the proportions of ischemic stroke (32/45, 71.1%), ischemic stroke with haemorrhagic transformation (7/45, 15.6%), and primary haemorrhagic stroke (6/45, 13.3%).

Figure 2

Anatomical distribution of stroke lesions in patients with dilated cardiomyopathy (DCM). The figure shows the frequency of stroke locations by cerebral region, including parietal, frontal, temporal, occipital lobes, and posterior fossa (cerebellum and brainstem). Abbreviations: DCM, dilated cardiomyopathy. A statistically significant association was identified between stroke subtype (ischemic, ischemic with haemorrhagic transformation, haemorrhagic) and anatomical localization (p = 0.004; likelihood ratio = 0.003). This relationship was further validated in autopsied patients via linear regression analysis, which demonstrated a significant correlation between stroke subtype and cerebral region (p = 0.031).

Figure 3

Stroke mechanism versus anatomical location in patients with dilated cardiomyopathy (DCM). Grouped bar chart illustrating the number of cases by stroke mechanism (ischemic, ischemic with haemorrhagic transformation, and primary haemorrhagic) and by brain region (parietal, frontal, temporal, occipital, posterior fossa). Ischemic strokes (n = 32) most frequently involved the parietal lobe (21 cases) but were present across all regions. Haemorrhagic transformations (n = 7) were observed in parietal, temporal, and occipital lobes. Primary haemorrhagic strokes (n = 6) were localized predominantly to the posterior fossa.

Figure 4

Histopathological features of acute cerebral infarction in a patient with dilated cardiomyopathy (DCM). Hematoxylin and eosin (H&E) stain, 40× magnification, showing eosinophilic degeneration of pyramidal neurons (‘red neurons’) with pyknotic nuclei and condensed chromatin, consistent with acute ischemic injury. Abbreviations: DCM, dilated cardiomyopathy; H&E, hematoxylin and eosin.

Figure 5

Histopathological features of evolving cerebral infarction in a patient with dilated cardiomyopathy (DCM). Hematoxylin and eosin (H&E) stain, 10× magnification, showing disruption of axons and dendrites, vacuolization of the white matter, and early endothelial proliferation indicative of neovascularization during infarct evolution. Abbreviations: DCM, dilated cardiomyopathy; H&E, hematoxylin and eosin.