Septal ablation in hypertrophic obstructive cardiomyopathy improves systolic myocardial function in the lateral (free wall): a follow-up study using CMR tissue tagging and 3D strain analysis

Aims: Alcohol septal ablation (ASA) has been successful in the treatment of symptomatic hypertrophic obstructive cardiomyopathy (HOCM). The aim of this study is to evaluate the effects of ethanol-induced myocardial infarcts on regional myocardial function using cardiac magnetic resonance (CMR) tissue tagging and 3-dimensional (3D) strain analysis. Methods and results: In nine patients (age 52±15 years) who underwent ASA, CMR was performed prior to and 6 months after the procedure. Regional myocardial mass was evaluated using cine imaging. Myocardial tagging was used to calculate systolic 3D myocardial strain values. These strain values were used to calculate the shortening index (SI), a robust parameter for myocardial contraction. Maximum end-systolic (ES) SI and systolic SI rate were quantified in three circumferential segments: septum, adjacent, and remote (lateral) myocardium. Compared with baseline, septal and non-septal mass decreased at follow-up (from 72±27 to 59±21 g; P=0.008 and from 131±34 to 109±30 g; P=0.008, respectively). In the septum, maximum ES SI and SI rate remained unchanged after ASA. In adjacent myocardium, ES SI remained unchanged, whereas SI rate improved (from -56.5±21.1 to -70.0±16.7%/s; P=0.02). Both ES SI and SI rate improved significantly in remote myocardium (from -16.9±2.8 to -18.8±3.2%; P=0.02 and from -70.3±9.2 to -86.1±15.0%/s; P=0.01, respectively). Conclusion: Reduction of left ventricular (LV) outflow tract obstruction in symptomatic HOCM is associated with a significant reduction in myocardial mass and improvement of intramural systolic function in the lateral (remote) wall, indicating reversed LV remodelling. © The European Society of Cardiology 2006. All rights reserved

Altered left atrial 4D flow characteristics in patients with paroxysmal atrial fibrillation in the absence of apparent remodeling

The pathophysiology behind thrombus formation in paroxysmal atrial fibrillation (AF) patients is very complex. This can be due to left atrial (LA) flow changes, remodeling, or both. We investigated differences for cardiovascular magnetic resonance (CMR)-derived LA 4D flow and remodeling characteristics between paroxysmal AF patients and patients without cardiac disease. In this proof-of-concept study, the 4D flow data were acquired in 10 patients with paroxysmal AF (age=61 +/- 8 years) and 5 age/gender matched controls (age=56 +/- 1 years) during sinus rhythm. The following LA and LA appendage flow parameters were obtained: flow velocity (mean, peak), stasis defined as the relative volume with velocities<10 cm/s, and kinetic energy (KE). Furthermore, LA global strain values were derived from b-SSFP cine images using dedicated CMR feature-tracking software. Even in sinus rhythm, LA mean and peak flow velocities over the entire cardiac cycle were significantly lower in paroxysmal AF patients compared to controls [(13.12.4 cm/s vs. 16.7 +/- 2.1 cm/s, p=0.01) and (19.3 +/- 4.7 cm/s vs. 26.8 +/- 5.5 cm/s, p=0.02), respectively]. Moreover, paroxysmal AF patients expressed more stasis of blood than controls both in the LA (43.2 +/- 10.8% vs. 27.8 +/- 7.9%, p=0.01) and in the LA appendage (73.3 +/- 5.7% vs. 52.8 +/- 16.2%, p=0.04). With respect to energetics, paroxysmal AF patients demonstrated lower mean and peak KE values (indexed to maximum LA volume) than controls. No significant differences were observed for LA volume, function, and strain parameters between the groups. Global LA flow dynamics in paroxysmal AF patients appear to be impaired including mean/peak flow velocity, stasis fraction, and KE, partly independent of LA remodeling. This pathophysiological flow pattern may be of clinical value to explain the increased incidence of thromboembolic events in paroxysmal AF patients, in the absence of actual AF or LA remodeling.Cardiovascular Aspects of Radiolog

Interventricular mechanical asynchrony in pulmonary arterial hypertension: left-to-right delay in peak shortening is related to right ventricular overload and left ventricular underfilling

ObjectivesThe purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening.BackgroundIn PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening.MethodsIn 21 PAH patients (mean pulmonary arterial pressure 55 ± 13 mm Hg and electrocardiogram–QRS width 100 ± 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (Tonset) and peak time (Tpeak) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law.ResultsThe Tonset was 51 ± 23 ms, 65 ± 4 ms, and 52 ± 22 ms for LV, septum, and RV, respectively. The Tpeak was 293 ± 58 ms, 267 ± 22 ms, and 387 ± 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 ± 45 ms, coinciding with septal overstretch and RV Tpeak. The L-R delay in Tonset was −1 ± 16 ms (p = 0.84), and the L-R delay in Tpeak was 94 ± 41 ms (p < 0.001). The L-R delay in Tpeak was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in Tpeak correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05).ConclusionsIn PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume