P895Apical sparing in patients without cardiac amyloidosis

Abstract

Abstract Background Apical sparing describes a reduced longitudinal strain in the basal segments and preserved or supranormal longitudinal strain in the apical segments of the left ventricular (LV) myocardium. This pattern has been described as a typical finding in patients with cardiac amyloidosis (CA) and restrictive cardiomyopathy. However, apical sparing is not a quantitative parameter and is fairly subjective to the echocardiographer's judgement. It is not known, if a certain degree of apical sparing is also present in patients with only mild LV hypertrophy and diastolic dysfunction such as it is present in heart failure with preserved ejection fraction (HFpEF). Methods Patients with cardiac transthyretin and light chain amyloidosis and patients with HFpEF were included in a clinical registry at our outpatient clinic. CA was diagnosed according to current guidelines. All patients underwent a comprehensive transthoracic echocardiography (TTE) exam at the time of study inclusion. The TTE protocol included standard and speckle-tracking imaging to assess the presence of apical sparing as well as the basal to apical strain gradient. Patients with known coronary artery disease were excluded. Results In total 115 patients were included in this study. Of these, 87 (75.7%) were diagnosed with CA and 28 (24.3%) with HFpEF. Not surprisingly, apical sparing was found in a majority (86.2%) of patients with CA, however mild forms of this phenomenon were also present in 67.9% of patients with HFpEF (p=0.029, Figure 1). Median basal longitudinal strain was significantly more impaired in patients with CA (p<0.001) but there was no difference between longitudinal strain in the apical segments when comparing CA to HFpEF (p=0.443). This resulted in a higher median apical to basal strain gradient in patients with CA (2.3 (IQR 1.7–3.83) versus 1.13 (IQR 1.5–1.8), p<0.001). Figure 1 Conclusion Mild forms of apical sparing can be found in patients without CA. Gradual reduction in strain from base to apex could be an unspecific pathophysiologic mechanism which is remarkably pronounced in patients with CA.