Assessment of left ventricular global longitudinal strain in patients with hypertrophic cardiomyopathy and coronary artery disease

Gjergjindreaj, Medeona; Escolar, Esteban; Papadopoulos, Konstantinos; Mihos, Christos G.

doi:10.1007/s10554-023-02994-9

Cited by 1 publication

(1 citation statement)

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“…Apical hypertrophic cardiomyopathy (ApHCM) is characterized by increased apical left ventricular (LV) wall thickness ≥ 15 mm with an ‘ace of spades’ morphology in the absence of abnormal loading conditions or identifiable causes [ 1 ]. It accounts for approximately 20% of all hypertrophic cardiomyopathy cases, may be sporadic or inherited due to myofilament gene mutations, and has contemporaneously been shown to confer important cardiovascular morbidity [ 2 , 3 , 4 , 5 , 6 ]. Speckle-tracking strain mechanics reveal that despite a generally preserved or even hyperdynamic LV ejection fraction, patients with ApHCM have a progressive impairment of LV global longitudinal strain (GLS) and myocardial energetics, which most commonly manifests as heart failure with a preserved ejection fraction [ 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Interventricular Septal Involvement Is Associated with More Impaired Ventricular Function and Mechanics in Apical Hypertrophic Cardiomyopathy

Mihos,

Elajami,

Misra

et al. 2024

JCDD

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Background: The interventricular septum has an important role in bi-ventricular performance. We hypothesized that septal involvement in apical hypertrophic cardiomyopathy (ApHCM-Mixed) adversely impacts ventricular structure and function when compared with isolated apical hypertrophy (ApHCM-Pure). Methods: A total of 72 patients (ApHCM-Mixed = 36, ApHCM-Pure = 36) with serial 2D and speckle-tracking echocardiographic analyses were identified. Ventricular function and mechanics were characterized by left (LV) and right (RV) ventricular global longitudinal strain (GLS), RV free wall strain, and LV myocardial work indices, and clinical events were adjudicated. Results: Clinical characteristics were similar between groups (mean age, 66 ± 15 years; 49% female; LV ejection fraction, 68 ± 11%). The ApHCM-Mixed group had larger LV mass indexes (141 ± 39 vs. 111 ± 30 g/m2, p < 0.001), worse LV (−9.6 ± 3.1 vs. −14.4 ± 3.4%, p < 0.001) and RV GLS (−14.3 ± 6.7 vs. −19.2 ± 5.2%, p = 0.001), impaired RV free wall strain (−18.5 ± 7.4 vs. −22.4 ± 6.3%, p = 0.02), and lower LV myocardial work indices including global work index (938 ± 306 vs. 1272 ± 339 mmHg%, p < 0.001), when compared with the ApHCM-Pure group. At a mean follow-up of 3.9 years, these differences all persisted. Five deaths were observed, all occurring in the ApHCM-Mixed group (14% vs. 0, p = 0.05), and with four being cardiac-related. This subgroup had a mean LV ejection fraction of 63%, LV GLS of −8.7%, an LV global work index of 875 mmHg%, and RV free wall strain of −15.9%, indicating significant subclinical bi-ventricular dysfunction. Conclusions: ApHCM-Mixed represents a distinct morphology in hypertrophic cardiomyopathy associated with more impaired ventricular function and mechanics when compared with ApHCM-Pure.

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