Key result
Systemic amyloidosis and hypertension enhanced LV twist and untwist rates before LV hypertrophy developed compared to controls, with amyloidosis causing a significant untwisting rate peak delay.
Why the study?
Does 2D speckle-tracking echocardiography detect subclinical alterations in LV twist and untwist in early-stage hypertension and systemic amyloidosis before LV hypertrophy develops?
Cross-Sectional (n=95)
Does 2D speckle-tracking echocardiography detect subclinical alterations in LV twist and untwist in early-stage hypertension and systemic amyloidosis before LV hypertrophy develops?
Systemic amyloidosis and hypertension both enhance LV twist and untwist rates before hypertrophy develops, but amyloidosis uniquely delays the untwisting rate peak regardless of infiltration degree.
Speckle-tracking may detect early LV mechanical changes in hypertension and amyloidosis; leaves open prognostic value and need for longitudinal validation.
INTRODUCTION: Recently, two-dimensional (2D) speckle-tracking echocardiography has enabled assessment of a particular behaviour of left ventricular (LV) motion defined as twisting/untwisting. The aim of our study is to evaluate whether in early stage of hypertension and systemic amyloidosis, subclinical alteration of LV twist and untwist is already present even if no LV hypertrophy is evidenced. METHODS: Forty-seven patients with light chain immunoglobulin amyloidosis (AL) entered the study and were classified having cardiac amyloidosis (CA) or not (NCA) if the mean value of LV wall thickness was ≥12 mm or not. Twenty-two consecutive patients with history of arterial essential hypertension (Hyp Group) and no sign of LV hypertrophy were enrolled. A total of 26 asymptomatic healthy subjects, age-matched, were analysed as control group. All three groups of patients and healthy subjects underwent traditional and 2D speckle-tracking echocardiography evaluation. LV diameters, volumes, wall thickness, mass, ejection fraction, E/A and E/E' ratio were evaluated. RESULTS: Twisting and untwisting rates were significantly increased in NCA and Hyp group when compared with CA and control group. Moreover, despite similar LV mass and diastolic dysfunction degree, untwisting rate peak was significantly delayed in NCA when compared with Hyp group. In patients with CA, untwisting rate delay was similar to patients with NCA. CONCLUSION: Our results show that amyloidosis and systemic hypertension produce both LV twist and untwist rate enhancement before LV hypertrophy is developed. In patients with amyloidosis irrespectively of LV infiltration degree, a significant LV untwisting rate peak delay occurs suggesting that different aetiology of cardiac involvement could differently affect LV untwisting rate.
No takes yet. Share an insight, caveat, or question.
Cappelli et al. (2010) conducted a cross-sectional in Systemic amyloidosis, systemic hypertension (n=95). Systemic amyloidosis and systemic hypertension vs. Healthy controls was evaluated on LV twisting and untwisting rates. Systemic amyloidosis and hypertension enhanced LV twist and untwist rates before LV hypertrophy developed compared to controls, with amyloidosis causing a significant untwisting rate peak delay.
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: