Left Ventricular Basal Strain Research Articles

Left ventricular longitudinal shortening at cardiac base as a determinant of left atrial reservoir function in cardiac amyloidosis

Abstract Objective To investigate a mechanistic determinant of left atrial (LA) reservoir function in patients presenting left ventricular (LV) hypertrophy, and clarify diagnostic and prognostic values of LA reservoir strain in patients with cardiac amyloidosis (CA). Methods Three-hundred sixty patients (median age: 68 years, male gender: 65%) with left ventricular hypertrophy (LVH) assessed by echocardiography were retrospectively included. The LVH etiologies were diagnosed by any of biopsy, cardiac magnetic resonance imaging or 99mTc-PYP scintigraphy. LV segmental longitudinal strain was estimated from apical three views, and LA reservoir strain was measured from an apical 4-chamber view. Results The LVH etiologies were confirmed with CA in 81 patients, hypertensive heart disease in 87 patients, hypertrophic cardiomyopathy in 143 patients, and miscellaneous disorders in 49 patients. The median (25th, 75th percentile) value of LV ejection fraction was 59% (48–67). LV basal longitudinal strain and LA reservoir strain were significantly reduced in patients with CA compared with those with other etiologies; LV basal strain: 5.4% (3.9–8.7) vs. 11.9% (9.3–14.6), LA reservoir strain: 9.2% (6.3–12.3) vs. 17.5% (11.3–24.1), p<0.01 respectively. LV basal strain was significantly correlated with LA reservoir strain in patients with CA (r=0.57, p<0.01) and in those with other etiologies (r=0.45, p<0.01). The area under the receiver-operating characteristic curves of LA reservoir strain and E/e' (0.78 and 0.74) to identify CA etiology were significantly larger than that of LA volume index (0.62) (p<0.01). During the follow-up period (median 2.9 years), 53 patients experienced heart failure hospitalization. The Cox regression model including age, gender, LV ejection fraction, E/e' and LA reservoir strain showed that male gender (hazard ratio: 0.46, p=0.03), E/e' (hazard ratio: 1.04, p<0.01) and LA reservoir strain (hazard ratio: 0.94, p<0.01) independently predicted heart failure hospitalization. Conclusions The decrease of LV longitudinal shortening at cardiac base could worsen LA reservoir function especially in patients with CA. LA reservoir strain might be an alternative measure to identify CA etiology and have a predictive value of heart failure hospitalization in patients with LV hypertrophy. Funding Acknowledgement Type of funding sources: None.

Can Marathon Running Induce Myocardial Microdamage?

An acute bout of high-volume high-intensity exercise, such as marathon running, can increase cardiac biomarker concentrations. It is unknown whether these biomarker elevations are related to myocardial micro-damage. PURPOSE: To assess cardiomyocyte damage following a marathon run using troponin I and novel magnetic resonance imaging (MRI) techniques including T1, T2 mapping and diffusion tensor imaging (DTI), and subsequently relate troponin I to MRI parameters of cardiomyocyte damage. METHODS: Cardiac MRI was performed at 3T in 12 male participants of the 2017 Amsterdam Marathon. MR data and blood samples were collected during 3 study visits: I) 1 week before, II) 4±2 hrs post-marathon and III) 2 weeks post-marathon. We measured troponin I, cardiac function (ejection fraction, strain, torsion) and morphology (volumes, T1 and T2 maps, and DTI). RESULTS: 11 men (51 [50-56] years) finished the race (42.195km) in 236±35 min at 89±5% of their predicted maximum heart rate. Troponin I increased post-exercise (from 0 [0-0] at baseline to 57 [16-82] ng/L), but returned to baseline values after 2 weeks recovery (0 [0-0] ng/L). Cardiac ejection fraction and morphology (volumes, T1, T2 maps) did not change following the marathon run (native T1:1214±23 at baseline, 1221±26 4hrs post-marathon and 1206±24 ms 2 weeks post-marathon, p=.15; T2: 50 [48-51] vs. 50 [48-52] vs. 50 [48-52] ms, p=.44). Left ventricular basal strain became less negative from baseline (-25±2%) to post-marathon (-22±2%) and did not completely recover after 2 weeks (-23±3%, p=.003). Extracellular volume fraction (24.6±2.9 vs 26.5±2.6 vs 25.0±3.4 %, p=.37), mean diffusivity (1.49±.09 vs.1.60±.16 vs. 1.48±.08 mm2/s, p=.09) and fractional anisotropy (.37 [.33-.39] vs .38 [.37-.40] vs .38 [.34-.40], p=.76) did not significantly change post-marathon. Post-exercise troponin was positively associated with changes in mean diffusivity (r=.62, p=.04). CONCLUSION: We observed elevations in cardiac troponin I after marathon running, which were significantly associated with higher mean diffusivity of myocardial tissue water. These findings suggest that cardiac biomarker elevations may result from exercise-induced myocardial micro-damage such as disruption of cardiomyocyte integrity and associated edema. Recovery largely occurred within 2 weeks.