CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 3, July/August 2023 AFRICA 169 Assessment of papillary muscle free strain in hypertrophic cardiomyopathy and hypertension-induced left ventricular hypertrophy Cennet Yildiz, Atilla Koyuncu, Lutfi Ocal, Mustafa Ozan Gursoy, Ersan Oflar, Gokhan Kahveci Abstract Objectives: We aimed to evaluate and compare papillary muscle free strain in hypertrophic cardiomyopathy (HCMP) and hypertensive (HT) patients. Methods: Global longitudinal strain (GLS), and longitudinal myocardial strain of the anterolateral (ALPM) and posteromedial papillary muscles (PMPM) were obtained in 46 HCMP and 50 HT patients. Results: Interventricular septum (IVS)/posterior wall (PW) thickness ratio, left ventricular mass index (LVMI), left atrial anteroposterior diameter (LAAP) and mitral E/E′ were found to be increased in patients with HCMP compared to HT patients. Left ventricular cavity dimensions were smaller in HCMP patients. GLS of HCMP and HT patients were –14.52 ± 3.01 and –16.85 ± 1.36%, respectively (p < 0.001). Likewise, ALPM and PMPM free strain values were significantly reduced in HCMP patients over HT patients [–14.00% (–22 to –11%) and –15.5% (–24.02 to –10.16%) vs –23.00% (–24.99 to –19.01%) and –22.30% (–26.48 to –15.95%) (p = 0.016 and p = 0.010)], respectively. ALPM free strain showed a statistically significant correlation with GLS, maximal wall thickness, IVS thickness and LVMI. PMPM free strain showed a significant correlation with GLS, IVS thickness and LAAP. The GLS value of –13.05 had a sensitivity of 61.9% and a specificity of 97.4% for predicting HCMP. ALPM and PMPM free strain values of –15.31 and –17.17% had 63 and 76.9% sensitivity and 85.7 and 76.9% specificity for prediction of HCMP. Conclusions: Besides other echocardiographic variables, which were investigated in earlier studies, papillary muscle free strain also could be used in HCMP to distinguish HCMP- from HT-associated hypertrophy. Keywords: hypertrophic cardiomyopathy, hypertension, papillary muscle, strain Submitted 26/7/22; accepted 12/12/22 Published online 27/2/23 Cardiovasc J Afr 2023; 34: 169–174 www.cvja.co.za DOI: 10.5830/CVJA-2022-070 Hypertrophic cardiomyopathy (HCMP) is an autosomal dominantly inherited disease with a wide spectrum of clinical phenotypes. Its estimated prevalence has been reported to be one in 500 persons in the general population.1 With the advancements in understanding the molecular and genetic bases of the disease and technological improvements in cardiac imaging modalities, it seems that the prevalence of HCMP has been underestimated. In addition, prevalence estimates have not included genotypepositive and phenotype-negative patients who are clinically normal but at risk of developing the disease in the future.2 Diagnosis of HCMP has the utmost importance in terms of bothmanagement of the disorder and screeningof patients’ family members. The histopathological features of the disease include myocyte disarray and interstitial fibrosis with heterogeneous involvement of the heart.3 The current guidelines recommend that if one of the myocardial segments has an end-diastolic wall thickness greater than 15 mm, then HCMP must be considered.4 Transthoracic echocardiography (TTE) is usually the first-line imaging modality used to assess patients with left ventricular hypertrophy (LVH). Cardiac anatomy and function can be delineated via two- (2D) or three-dimensional echocardiography, tissue Doppler imaging (TDI) and speckle-tracking echocardiography (STE). In addition to HCMP, LVH constitutes an adaptation response to exercise or hypertension. Clinicians frequently encounter it in clinical practice. Differentiation of the aetiology of LVH may be challenging in some cases. It has been suggested that the pattern and degree of LVH help distinguish HCMP from HT hypertrophy. Hypertrophy associated withHCMP tends to be more severe than HT hypertrophy.5 Although concentric LVH has been thought to be associated with hypertension, asymmetric involvement of the left ventricle has also been reported.5 Myocardial strain analysis of the left ventricle has shown that increased endocardial to epicardial myocardial strain values can be used to distinguish HCMP from HT LVH.6 In most HCMP patients, the predominant phenotypic expression of the disease is characterised by LVH. However, in one study, the papillary muscles of four to 13% of the patients had morphological abnormalities, such as papillary muscle hypertrophy, anomalous insertion of papillary muscles, and hypermobile or bifid papillary muscles.7,8 It has been found that antero-apical displacement of the anterolateral papillary muscles (ALPM) was associated with a higher incidence of Department of Cardiology, Bakırköy Dr Sadi Konuk Education and Research Hospital, Istanbul, Turkey Cennet Yildiz, MD, cennet_yildiz@live.com Atilla Koyuncu, MD Ersan Oflar, MD Department of Cardiology, Kosuyolu Education and Research Hospital, Istanbul, Turkey Lutfi Ocal, MD Department of Cardiology, Izmir Ataturk Education and Research Hospital, Izmir, Turkey Mustafa Ozan Gursoy, MD Department of Cardiology, Istinye University, Liv Hospital, Istanbul, Turkey Gokhan Kahveci, MD
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