Prevalence of neurogenic stress cardiomyopathy in acute ischemic stroke and relationship with leukocytosis

Objective

Describe the prevalence and features of neurogenic stress cardiomyopathy in acute ischemic stroke. Describe leukocytosis as an inflammatory marker in neurogenic stress cardiomyopathy.

Materials/Methods

Retrospective review of 688 adult ischemic stroke patients at a tertiary care center (1/2018 – 12/2021). Neurogenic stress cardiomyopathy was identified by one of: low left ventricular ejection fraction, ventricular wall motion abnormalities, elevated Troponin-I, or elevated brain natriuretic peptide. Leukocytosis defined as white blood cell count ≥12.0 × 10^9/L. Clinical and demographic data were collected.

Results

Neurogenic stress cardiomyopathy was observed in 147 (21 %) patients. In this group, mean age was 68, 44 % were female, mean National Institutes of Health Stroke Scale was 10 and mean hospital stay was 8 days. Low left ventricular ejection fraction (median 40 %) was observed in 64 % of these patients, elevated Troponin-I (median 0.252 ng/mL) in 40 %, and ventricular wall motion abnormalities in 55 %. Stroke mechanisms were cryptogenic (43 %), cardioembolic (24 %), small vessel disease (13 %), large artery atherosclerosis (12 %), and other (8 %). Mean white blood cell count was 8.63 × 10^9/L. Leukocytosis occurred in 12 % of patients with cardiomyopathy and 8 % without, with no significant difference (p=0.9).

Conclusion

We propose defining neurogenic stress cardiomyopathy by one of four cardiac biomarkers. The prevalence aligns with prior reports, most frequently identified by low left ventricular ejection fraction or ventricular wall motion abnormalities. Unlike Takotsubo Cardiomyopathy, abnormal wall motion patterns were predominantly diffuse. No significant difference in leukocytosis was found between groups. Further research is needed to identify neurogenic stress cardiomyopathy risk factors.