CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 3, July/August 2023 AFRICA 173 is associated with hypertension but about 4–47% of patients with hypertension have asymmetrical hypertrophy, whereas 13–31% of patients with HCMP have concentric hypertrophy.15 Several studies have been conducted to differentiate HT hypertrophy from HCMP-associated hypertrophy. Kator et al. studied conventional echocardiographic and TDI strain parameters in HCMP and HT patients. Their study showed that septum-to-posterior wall thickness ratio and mean systolic strain were independently associated with HCMP, with a cut-off systolic strain value of –10.6%.15 Ozer et al. investigated the prognostic utility of left ventricular GLS in HCMP, HT and athlete’s heart. The HCMP patients had the worst left ventricular GLS values, and a cut-off value of –12.5% predicted mortality in HCMP patients with 64% sensitivity and 70% specificity.16 Other studies also confirmed the diagnostic value of strain measurements in differentiating pathological from physiological LVH.17-19 In a study by Yang et al., the degree of reduction in strain value was greater in the hypertrophied cardiac segments and correlated with the amount of histopathological abnormalities.20 Our findings with regard to GLS values were in concordance with previous data. The HCMP patients in our study had a greater GLS reduction than the HT patients. In the last few decades, improvements in imaging techniques have shed light on papillary muscle anatomy and function in HCMP patients. It has been suggested that papillary muscle abnormalities are among the causal factors underlying the mechanism of left ventricular outflow obstruction, which was traditionally attributed to septal hypertrophy and the Venturi effect.21-25 Studies have shown that left ventricular obstruction and systolic anterior motion of the mitral valve are independent from interventricular septal hypertrophy, which persisted in almost 25% of the patients after septal myectomy.8 Cardiac MRI studies revealed papillary muscle hypertrophy that was in correlation with LVH, and abnormal insertion of papillary and accessory papillary muscles in HCMP.10 In one study, delayed gadolinium-enhanced areas were reported in up to 6% of the HCMP patients and increased papillary muscle mass was found to be associated with greater LVMI.26 In the present study, the papillary muscle free strain of both papillary muscles in HCMP patients was reduced compared to the HT patients. Our results confirm that pathological hypertrophy is associated with a more severe impairment of left ventricular function, including papillary muscles. In addition, both papillary muscle strains predicted the presence of HCMP over HT. Whether this impairment was due to fibrosis, perfusion abnormalities or myocyte dysfunction needs to be clarified. Other findings of our study merit some comments. In addition to the 2D-STE strain parameters, the IVS thickness, LVEDD, LVESD, LVMI, IVS/PW, LAAP diameter and mitral E/E′ ratio were significantly different between the two groups. Previous reports have shown that left ventricular cavity dimensions are good predictors of pathological hypertrophy, characterised by unproportioned hypertrophy compared to left ventricular cavity size.27 We found smaller LVEDD and LVESD in patients with HCMP. A high IVS/PW ratio, although not specific for HCMP, was suggested as a criterion for the diagnosis of HCMP.28 Similarly, IVS/PW ratio was found to be significantly higher in HCMP patients than in HT patients (1.85 ± 0.50 vs 1.18 ± 0.24, p < 0.001). In our study, mitral E/E′ ratio and LAAP diameter were higher in HCMP patients compared to HT patients. These findings support earlier reports that stated HCMP was associated with increased left atrial filling pressures.14 Limitations of the study are as follows. It was a single-centre study and the sample size was relatively small. Long-term follow up of patients was not done and the prognostic value of papillary free strain was not evaluated. Since coronary angiograms of the patients were not done, asymptomatic coronary artery disease was not excluded. Conclusions The novelty of our study lies in assessing the papillary muscle free strain in HCMP and HT patients and exploring whether it had a value in differentiation between LVH associated with HCMP and HT. Besides other echocardiographic variables, which have been investigated in earlier studies, papillary muscle free strain also could be used in HCMP patients to distinguish HCMP-associated from HT-associated hypertrophy. Further studies are needed to explore the prognostic use of papillary muscle free strain in this group of subjects. Table 4. ROC curve analysis of strain values for predicting HCMP Strain AUC p- value 95% CI Value Sensi- tivity Specificity GLS 0.789 0.003 0.647–0.931 –13.05 61.9 97.4 ALPM strain 0.751 0.010 0.598–0.905 –15.31 63 85.7 PMPM strain 0.749 0.011 0.590–0.908 –17.17 76.9 71.4 GLS, global longitudinal strain; ROC, receiver operating characteristic; AUC, area under the curve; CI, confidence interval. Sensitivity 1 – Specificity 0.0 0.2 0.4 0.6 0.8 1.0 Diagonal segments are produced by ties. 1.0 0.8 0.6 0.4 0.2 0.0 Source of the curve GLS ALPM strain PMPM strain Reference line Fig. 5. ROC curve of GLS, and ALPM and PMPM free strain for prediction of HCMP.
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