Federico Guerra1,2, Chiara Gelardi1,2, Alessandro Capucci1,2, Armando Gabrielli1,2, Maria Giovanna Danieli3,4. 1. From the Cardiology and Arrhythmology Clinic, and the Clinical Medicine, Clinical and Molecular Sciences Department, Marche Polytechnic University, University Hospital "Ospedali Riuniti," Ancona, Italy. 2. F. Guerra, MD, Cardiology and Arrhythmology Clinic, Marche Polytechnic University, University Hospital Ospedali Riuniti; C. Gelardi, MD, Clinical Medicine, Clinical and Molecular Sciences Department, Marche Polytechnic University, University Hospital Ospedali Riuniti; A. Capucci, MD, Professor, Cardiology and Arrhythmology Clinic, Marche Polytechnic University, University Hospital Ospedali Riuniti; A. Gabrielli, MD, Professor, Clinical Medicine, Clinical and Molecular Sciences Department, Marche Polytechnic University, University Hospital Ospedali Riuniti; M.G. Danieli, MD, PhD, Associate Professor, Clinical Medicine, Clinical and Molecular Sciences Department, Marche Polytechnic University, University Hospital Ospedali Riuniti. 3. From the Cardiology and Arrhythmology Clinic, and the Clinical Medicine, Clinical and Molecular Sciences Department, Marche Polytechnic University, University Hospital "Ospedali Riuniti," Ancona, Italy. m.g.danieli@univpm.it. 4. F. Guerra, MD, Cardiology and Arrhythmology Clinic, Marche Polytechnic University, University Hospital Ospedali Riuniti; C. Gelardi, MD, Clinical Medicine, Clinical and Molecular Sciences Department, Marche Polytechnic University, University Hospital Ospedali Riuniti; A. Capucci, MD, Professor, Cardiology and Arrhythmology Clinic, Marche Polytechnic University, University Hospital Ospedali Riuniti; A. Gabrielli, MD, Professor, Clinical Medicine, Clinical and Molecular Sciences Department, Marche Polytechnic University, University Hospital Ospedali Riuniti; M.G. Danieli, MD, PhD, Associate Professor, Clinical Medicine, Clinical and Molecular Sciences Department, Marche Polytechnic University, University Hospital Ospedali Riuniti. m.g.danieli@univpm.it.
Abstract
OBJECTIVE: Subclinical heart disease occurs in up to 50% of patients with idiopathic inflammatory myopathies (IIM) and is difficult to detect through conventional imaging. We investigated the usefulness of global longitudinal strain (GLS) measurement to detect a subclinical systolic ventricular dysfunction in patients with IIM. METHODS: We enrolled 28 patients with IIM and 28 matched controls in a 1:1 fashion. Standard variables for the left ventricle (LV) and right ventricle (RV) systolic and diastolic function were measured and compared between cases and controls, along with speckle-tracking GLS of the LV and RV. A possible correlation between GLS and muscle strength, disease activity, cardiovascular risk factors, and other organ systems involvement was searched. RESULTS: Standard variables of systolic and diastolic dysfunction were similar between patients and controls. GLS was significantly lower in patients when compared with controls for both LV (-18.7 ± 4.2% vs -21.2 ± 2.1%, p = 0.006) and RV (-19.3 ± 6.3% vs -22.5 ± 3.8%, p = 0.033). Patients with IIM had a 4.9-fold increased risk for impaired left GLS [relative risk (RR) 4.9, 95% CI 1.5-15.8, p = 0.006], which involved usually basal and mid-segments of the anterior, anterior-septal, and lateral wall. Patients with IIM had a 3.4-fold increased risk for impaired right GLS (RR 3.4, 95% CI 1.1-11.7, p = 0.04) with the basal segment of the free RV wall most frequently involved. Muscle strength, disease activity, damage and duration, other organ system involvement, and previous treatment were not associated with reduced GLS. CONCLUSION: Subclinical systolic impairment is common in patients with IIM without overt LV dysfunction. In this context, GLS is a potentially useful variable.
OBJECTIVE: Subclinical heart disease occurs in up to 50% of patients with idiopathic inflammatory myopathies (IIM) and is difficult to detect through conventional imaging. We investigated the usefulness of global longitudinal strain (GLS) measurement to detect a subclinical systolic ventricular dysfunction in patients with IIM. METHODS: We enrolled 28 patients with IIM and 28 matched controls in a 1:1 fashion. Standard variables for the left ventricle (LV) and right ventricle (RV) systolic and diastolic function were measured and compared between cases and controls, along with speckle-tracking GLS of the LV and RV. A possible correlation between GLS and muscle strength, disease activity, cardiovascular risk factors, and other organ systems involvement was searched. RESULTS: Standard variables of systolic and diastolic dysfunction were similar between patients and controls. GLS was significantly lower in patients when compared with controls for both LV (-18.7 ± 4.2% vs -21.2 ± 2.1%, p = 0.006) and RV (-19.3 ± 6.3% vs -22.5 ± 3.8%, p = 0.033). Patients with IIM had a 4.9-fold increased risk for impaired left GLS [relative risk (RR) 4.9, 95% CI 1.5-15.8, p = 0.006], which involved usually basal and mid-segments of the anterior, anterior-septal, and lateral wall. Patients with IIM had a 3.4-fold increased risk for impaired right GLS (RR 3.4, 95% CI 1.1-11.7, p = 0.04) with the basal segment of the free RV wall most frequently involved. Muscle strength, disease activity, damage and duration, other organ system involvement, and previous treatment were not associated with reduced GLS. CONCLUSION: Subclinical systolic impairment is common in patients with IIM without overt LV dysfunction. In this context, GLS is a potentially useful variable.