CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 3, July/August 2023 170 AFRICA systolic anterior motion of the mitral valve. Moreover, increased papillary muscle thickness resulted in reduced distance between the ALPM and the interventricular septum (IVS) and smaller left ventricular cavity volume.8 Cardiac magnetic resonance imaging (MRI) studies have shown that the severity of symptoms, cardiac dysfunction and arrhythmias tend to increase in cases of co-existing papillary muscle abnormalities.9 Papillary muscle hypertrophy and fibrosis could also be seen in hypertension, which is proportional to LVH.10 Therefore, we aimed to evaluate papillary muscle function by measuring papillary muscle free strain in HCMP and HT patients to find any differences that might exist. In addition, we investigated the predictive value of papillary muscle free strain for the diagnosis of HT hypertrophy and HCMPassociated hypertrophy. Methods We enrolled 46 HCMP patients and 50 HT patients in this retrospective, comparative study. Echocardiographic recordings, and clinical and demographical characteristics of the patients were obtained from the hospital database system. Echocardiographic images of the patients were re-evaluated and the strain analysis was performed on stored images. Participants with systemic diseases, ischaemic heart disease, primary valvular disease, malignancy, thyroid abnormalities, hepatic and/or renal failure, poor image quality, Fabry disease, amyloidosis, or Noonan’s syndrome were excluded. Conventional echocardiography, TDI and 2D speckletracking imaging (2D-STI) of each patient were evaluated. The local ethics committee approved the study, which was compiled in accordance with the Declaration of Helsinki. All patients’ written informed consents were acquired before study enrollment. Diagnosis of HCMP was done according to the current guidelines, which state that HCMP diagnosis can be done in the presence of left ventricular maximum wall thickness greater than or equal to 15 mmwithout underlying secondary causes.4 Diagnosis of HT was done if a patient used antihypertensive medication or her/his blood pressure was greater than 140/90 mmHg. All echocardiographic examinations were performed by iE33 and Q-lab version 8.1 (CMQ, Philips Inc) according to current guidelines.11 Conventional cardiac structural and functional assessment was done by 2D echocardiography. IVS and posterior wall (PW) thickness, maximal wall thickness, left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), left atrial anteroposterior diameter (LAAP), left ventricular mass index (LVMI), aortic annulus, and tricuspid annular systolic excursion (TAPSE) were measured. Left ventricular ejection fraction (LVEF) was measured using the modified Simpson method. Early (E) and late (A) mitral diastolic inflow velocities and deceleration time (DT) were obtained by pulsed-wave Doppler sample volume, which was placed at the tips of the mitral and tricuspid valves. Mitral annular septal velocities were taken by TDI. Besides 2D echocardiographic parameters, 2D-STI was also used in order to measure longitudinal systolic strain from the apical four-, two- and three-chamber views with an increased frame rate of 50 to 70 frames per second. Three to four cardiac cycles from acceptable images were digitally stored for offline analysis in the Q-lab software package. Two basal and one apical anchor point was identified manually, after which the program traced the endocardial border automatically. In the case of inappropriate endocardial tracking, endocardial surfaces were manually corrected by the operator. Apical four-chamber (4C), three-chamber (3C) and two-chamber (2C) longitudinal strain analyses of each patient were performed. The 17-segment left ventricular model was used for calculation of segmental longitudinal strain values that were obtained from three views. Global longitudinal strain (GLS) was the average strain value measured by STI, with more negative values indicating higher contractility. Longitudinal myocardial strain of the ALPM and posteromedial papillary muscles (PMPM) were obtained with the free-strain method, which evaluates strain values within a myocardial region. This method enables us to measure myocardial deformation in a quick and practical way. In order to calculate papillary muscle strain, the base and tip of the papillary muscle were selected manually. The first point was the base of the papillary muscle where it attaches to the left ventricular wall. The second point was the tip of the papillary muscle where it attaches to the chorda tendinea. ALPM and PMPM free strains were measured in the apical 4C and 3C views, respectively. Fig. 1 depicts the measurement of ALPM and PMPM free strain. Patients who did not have adequate echocardiographic images for assessment of systolic and diastolic papillary muscle free strain were excluded from the study. All echocardiographic examinations were performed by the same cardiologist who was experienced in echocardiographic imaging. In order to evaluate intra-observer reliability, recordings of the 15 patients were re-evaluated one week later. Statistical analysis Normality of data was examined with the Kolmogorov–Smirnov test. Data with Gaussian and non-Gaussian distribution are expressed as mean ± standard deviation (SD) or median and Fig. 1. Measurement of ALPM and PMPM free strain.
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