Nonselective versus selective His bundle pacing: An acute intrapatient speckle-tracking strain echocardiographic study.

INTRODUCTION: We aimed to compare the acute differences in left ventricular (LV) function and mechanical synchrony during nonselective His bundle pacing (ns-HBP) versus selective His bundle pacing (s-HBP) using strain echocardiography. METHODS AND RESULTS: Consecutive patients with permanent His bundle pacing, in whom it was possible to obtain both s-HBP and ns-HBP, were studied in two centers. In each patient, echocardiography was performed sequentially during s-HBP and ns-HBP. Speckle-tracking echocardiography parameters were analyzed: Global longitudinal strain (GLS), the time delay between peak systolic strain in the basal septal and basal lateral segments (BS-BL delay), peak strain dispersion (PSD) and strain delay index. Right ventricle function was assessed using tricuspid annular plane systolic excursion (TAPSE) and tissue Doppler velocity of the lateral tricuspid annulus (S'). A total of 69 patients (age: 75.6 ± 10.5 years; males: 75%) were enrolled. There were no differences in LV ejection fraction and GLS between s-HBP and ns-HBP modes: 59% versus 60%, and -15.6% versus -15.7%, respectively; as well as no difference in BS-BL delay and strain delay index. The PSD value was higher in the ns-HBP group than in the s-HBP group with the most pronounced difference in the basal LV segments. No differences in right ventricular function parameters (TAPSE and S') were found. CONCLUSION: The ns-HBP and s-HBP modes seem comparable regarding ventricular function. The dyssynchrony parameters were significantly higher during ns-HBP, however, the difference seems modest and clarification of its impact on LV function requires a larger long-term study.

Left ventricular adaptation following orthotopic heart transplantation in children: A speckle tracking echocardiographic imaging study.

BACKGROUND: Evolution of left ventricle (LV) function in the pediatric OHT population has not been well described. Our hypothesis was that, in children following OHT without any rejection, there would be progressive normalization of LV size and function over 2 years. METHODS: LV function was evaluated using STE and conventional echo parameters at five time points in pediatric OHT patients without any rejection in the first 2 years following OHT and normal controls. LV global peak systolic longitudinal strain (LVPLS) and strain rate, LV peak systolic radial and circumferential strain (LVRS and LVCS), and strain rate were analyzed. RESULTS: We had twenty two patients with median age at OHT of 1.27 years ( IQR 0.19, 5.6 years). The LVPLS (mean ± SD) was abnormal in the post-OHT echocardiograms at 1 week (-12.4 ± 3.7) and 1 month (-13.9 ± 3.7) and significantly improved at 6 months (-15.8 ± 3.2), 1 year (-15.7 ± 3.1), and 2 years (-17.8 ± 2.8). However, LVPLS remained below the normal group even at 2 years following OHT (-21.3 ± 1.76). CONCLUSION: In children following OHT, despite the absence of rejection, strain values are significantly impaired in the initial months, improve progressively over the first 2 years but remain abnormal compared with healthy controls.

Vector velocity imaging echocardiography to study the effects of submassive pulmonary embolism on the right atrium.

OBJECTIVES: To assess the effects of submassive pulmonary embolism (SMPE) on right atrial (RA) anatomy and function. BACKGROUND: Right ventricular dysfunction (RVD) is associated with adverse outcomes in SMPE. However, the effects of SMPE on the structure and function of the RA have received much less attention. METHODS: Fifty patients with SMPE documented by CT angiography (SMPE group) and evidence of RVD on two-dimensional echocardiography were retrospectively identified and compared to 50 controls (control group). Both RA and RV areas, volumes and fractional area change (FAC) were measured. Pulmonary artery systolic pressures were estimated. RA and RV longitudinal strains were obtained using vector velocity imaging (VVI). RESULTS: Compared with controls, RA and RV FACs were significantly reduced and associated with higher chamber volumes in the SMPE group. Global longitudinal RA strain was reduced in the SMPE group (29% + 11% vs 55% + 16%; P < .01), as was global RV longitudinal strain (-12% + 5% vs -20% + 5%, P < .01), when compared to the controls. A linear relationship existed between RV and RA strain in both groups; however, the curve was shifted downward among those with SMPE. Furthermore, ROC curve analysis suggests RA area performs better than RV area as a marker of SMPE. CONCLUSIONS: RA structure and function are adversely affected in SMPE, similar to the effects observed in RV. Lower RA strain appears to be a novel quantitative indicator of SMPE, and RA area may be a more sensitive marker of this condition and may provide additional prognostic information in this condition.

Left atrial and ventricular systolic and diastolic myocardial mechanics in patients with end-stage renal disease.

BACKGROUND: Diastolic cardiac dysfunction is an important complication of end-stage renal disease (ESRD), but quantification remains a challenge. Given that diastolic dysfunction is reflected in both left atrial (LA) and ventricular (LV) function, we aimed to identify abnormalities in LV and LA volume and function using measures of myocardial mechanics. METHODS: We retrospectively studied 53 incident ESRD patients (46±16 y/o 44% male) and compared them to 85 normal controls. LA phasic volumes and functional parameters were obtained from the apical 4CH view. Global ventricular peak longitudinal and circumferential strain, strain rate (GLS, GL-SR, CS), and rotation were obtained from apical and short-axis views. LA and LV measurements were taken off line using dedicated software (eSie VVI). RESULTS: ESRD patients had abnormal systolic function with lower LV ejection fraction and peak endocardial strain parameters (mean: GLS -16.6% vs -19.9%, GL-SR -0.91 vs -1.04, and CS -25.6% vs 27.9%, P≤.01 for all). Traditional Doppler parameters remained similar between groups, while diastolic mechanics were abnormal in ESRD. Reduced LV-derived diastolic parameters, fractional early reverse rotation, a marker of ventricular relaxation (P<.006), and ratio of early diastolic SR to systolic SR (P<.04) denote significant diastolic dysfunction. Increased LA volumes (P<.001), decreased LA reservoir (P<.001), conduit (P<.0004), and contractile (P<.02) function reflect diastolic dysfunction. CONCLUSION: Myocardial strain measurements quantitated the abnormalities in both LV diastolic and LA function associated with the uremic state. The distinct abnormal diastolic parameters were suggestive of abnormal relaxation and increased filling pressures. Early and accurate assessment of diastolic function may help tailor patient management ESRD.

Immune Checkpoint Inhibitor-Induced Myocarditis vs. COVID-19 Vaccine-Induced Myocarditis-Same or Different?

Immune checkpoint inhibitor (ICI) and coronavirus disease 2019 (COVID-19) vaccine-induced myocarditis possibly share common mechanisms secondary to overactivation of the immune system. We aimed to compare the presenting characteristics of ICIs and COVID-19 vaccine-induced myocarditis. We performed a retrospective analysis of characteristics of patients diagnosed with either ICIs or COVID-19 vaccine-induced myocarditis and compared the results to a control group of patients diagnosed with acute viral myocarditis. Eighteen patients diagnosed with ICIs (ICI group) or COVID-19 vaccine (COVID-19 vaccine group)-induced myocarditis, and 20 patients with acute viral myocarditis (Viral group) were included. The ICI group presented mainly with dyspnea vs. chest pain and fever among the COVID-19 vaccine and Viral groups. Peak median high sensitivity Troponin I was markedly lower in the ICI group (median 619 vs. 15,527 and 7388 ng/L, p = 0.004). While the median left ventricular (LV) ejection fraction was 60% among all groups, the ICI group had a lower absolute mean LV global longitudinal strain (13%) and left atrial conduit strain (17%), compared to the COVID-19 vaccine (17% and 30%) and Viral groups (18% and 37%), p = 0.016 and p = 0.001, respectively. Despite a probable similar mechanism, ICI-induced myocarditis's presenting characteristics differed from COVID-19 vaccine-induced myocarditis.

Modifications of Sarcoplasmic Reticulum Function Prevent Progression of Sarcomere-Linked Hypertrophic Cardiomyopathy Despite a Persistent Increase in Myofilament Calcium Response.

Hypertrophic cardiomyopathy (HCM) is a genetic disorder caused by mutations in different genes mainly encoding myofilament proteins and therefore called a "disease of the sarcomere." Despite the discovery of sarcomere protein mutations linked to HCM almost 30 years ago, the cellular mechanisms responsible for the development of this disease are not completely understood and likely vary among different mutations. Moreover, despite many efforts to develop effective treatments for HCM, these have largely been unsuccessful, and more studies are needed to better understand the cellular mechanisms of the disease. In experiments reported here, we investigated a mouse model expressing the mutant cTnT-R92Q, which is linked to HCM and induces an increase in myofilament Ca2+ sensitivity and diastolic dysfunction. We found that early correction of the diastolic dysfunction by phospholamban knockout (PLNKO) was able to prevent the development of the HCM phenotype in troponin T (TnT)-R92Q transgenic (TG) mice. Four groups of mice in FVB/N background were generated and used for the experiments: (1) non-transgenic (NTG)/PLN mice, which express wild-type TnT and normal level of PLN; (2) NTG/PLNKO mice, which express wild-type TnT and no PLN; (3) TG/PLN mice, which express TnT-R92Q and normal level of PLN; (4) TG/PLNKO mice, which express TnT-R92Q and no PLN. Cardiac function was determined using both standard echocardiographic parameters and speckle tracking strain measurements. We found that both atrial morphology and diastolic function were altered in TG/PLN mice but normal in TG/PLNKO mice. Histological analysis showed a disarray of myocytes and increased collagen deposition only in TG/PLN hearts. We also observed increased Ca2+/calmodulin-dependent protein kinase II (CaMKII) phosphorylation only in TG/PLN hearts but not in TG/PLNKO hearts. The rescue of the HCM phenotype was not associated with differences in myofilament Ca2+ sensitivity between TG/PLN and TG/PLNKO mice. Moreover, compared to standard systolic echo parameters, such as ejection fraction (EF), speckle strain measurements provided a more sensitive approach to detect early systolic dysfunction in TG/PLN mice. In summary, our results indicate that targeting diastolic dysfunction through altering Ca2+ fluxes with no change in myofilament response to Ca2+ was able to prevent the development of the HCM phenotype and should be considered as a potential additional treatment for HCM patients.

Mitral chordal-leaflet-myocardial interactions in mitral valve prolapse.

BACKGROUND: The submitral apparatus maintains annular-papillary continuity and myocardial geometry. In mitral valve prolapse (MVP), elongated chords and redundant leaflets can interact at the region of myocardial attachment, leading to apparent discordant motion of the basal inferolateral wall. The aim of this study was to test the hypothesis that basal inferolateral wall inward motion would occur later in MVP and that this delay is associated with MVP severity. METHODS: Thirty consecutive patients with MVP and matched controls underwent stress echocardiography. Time to peak transverse displacement (TPD) of the inferolateral wall compared with the anteroseptal wall was measured using speckle-tracking echocardiography. The time difference was analyzed as raw data, normalized to the RR interval, and as a percentage of the time to maximal displacement of the anteroseptal segment(s). RESULTS: Compared with controls, TPD was delayed in patients with MVP both at rest and at peak stress, when evaluating basal segments or basal-mid segments as a unit, both in real time and, more importantly, when correcting for anteroseptal TPD. In patients compared with controls, observed delay at rest and at peak stress was 50 ± 90 versus -30 ± 90 msec (P = .006) and 70 ± 80 versus -30 ± 60 msec (P < .0001), respectively; relative to TPD of the anteroseptal segment, the observed delay at rest and at peak stress was 117 ± 24% versus 97 ± 22% (P = .007) and 144 ± 68% versus 95 ± 21% (P = .003), respectively. Similar significant findings were observed in basal-mid segments. TPD results were not statistically significant when stratified by prolapse severity. Intraclass correlation coefficients were 0.88 and 0.93, and two-tailed t tests indicated good interobserver and intraobserver variability. CONCLUSIONS: Inferolateral wall TPD is delayed in MVP. TPD is a novel method to characterize chordal-leaflet-myocardial interactions in patients with MVP. Prolapse severity does not predict TPD, likely because of the timing of prolapse and dynamic loading conditions. Implications of this observation include attribution of a perceived wall motion abnormality in MVP during stress echocardiography to a physiologic state and new mechanistic insights into mitral valve physiology.