Øyvind Lie

BrochAtherosclerosis

Plasma Lp(a) levels rose slightly from baseline (17 nmol/L) to a peak of 25 nmol/L at 3-7 days (p < 0.001), and tocilizumab did not affect Lp(a) levels.

Heart failure treatment recommendations are currently lacking for genotype-positive early dilated and non-dilated LV cardiomyopathy.

In patients with mitral annulus disjunction, severe arrhythmic events occurred in 12% and were associated with younger age, lower ejection fraction, and papillary muscle fibrosis, but not MVP.

Right ventricular structure and function remained stable in EiAC patients while deteriorating in ARVC patients, but the 5-year and 10-year cumulative incidences of ventricular arrhythmias were similar between both groups.

Self-reported symptoms or elevated cardiovascular risk scores identified cardiovascular disease in 30.8% of master athletes compared to 9.5% of asymptomatic controls (p=0.024).

Indexed left atrial volume independently predicted all-cause mortality and major adverse cardiac events after acute myocardial infarction, with a 21% higher risk per 10 mL/m2 increase.

CPAP treatment did not improve left atrial or ventricular remodelling over 12 months in patients with paroxysmal atrial fibrillation and OSA, although PVI reduced AF burden (P≤0.001).

The Prognostic Value of Left Atrial Function in Patients with Acute Myocardial Infarction

The prognostic value of left atrial (LA) volume is well-established in acute myocardial infarction (AMI) patients. LA strain provides further patophysological insights. In the present study, we evaluated LA volume and LA strain in AMI patients including those with atrial fibrillation (AF). The aim of the study was to determine if LA strain provide additional prognostic value. Patients with AMI underwent two-dimensional echocardiography within 72 h of admission. The primary outcome was a composite of all-cause mortality and major adverse cardiovascular events. Cox regression analyses were performed. We included 501 patients and during follow-up, 132 patients (26.4%) met the primary outcome. Left ventricular (LV) global longitudinal strain (GLS) (HR 0.94 [95% CI 0.88-0.99],

Subtle deterioration of right ventricular function by free wall longitudinal strain was strongly associated with subsequent first-time VA (OR 1.12, 95% CI 1.01–1.25, P = .031, per 1% deterioration).

Changes in electrical delay is associated with the hemodynamic response to cardiac pacing

Landmark studies on heart failure patients with prolonged QRS duration on the electrocardiogram (ECG) demonstrated that biventricular pacing (BIVP) was superior to right ventricular pacing (RVP).1Kass D.A. Chen C.-H. Curry C. et al.Improved left ventricular mechanics from acute vdd pacing in patients with dilated cardiomyopathy and ventricular conduction delay.Circulation. 1999; 99: 1567-1573Crossref PubMed Google Scholar Detrimental long-term effects and unpredictable acute hemodynamic effect to RVP led to the existing RVP skepticism, and BIVP was favored as the standard of care implementing cardiac resynchronization therapy (CRT).2Wilkoff B.L. Cook J.R. Epstein A.E. et al.Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator -The dual chamber and VVI implantable defibrillator (DAVID) trial.JAMA. 2002; 288: 3115-3123Crossref PubMed Scopus (0) Google Scholar However, despite reduction in mortality and morbidity, one third of eligible patients do not benefit from BIVP demonstrating the shortcoming of QRS duration and morphology to predict CRT response. Patients with left bundle branch block (LBBB) typically have deep S-waves in ECG electrode V1 and large R-waves in V5 representing a septal-to-lateral activation sequence. Plesinger et al. reported that ventricular electrical delay may be assessed as the dispersion of peak septal and lateral ECG amplitudes, and that a high ventricular electrical delay at sinus rhythm was associated with greater CRT benefit.3Plesinger J.F. Jurak J.P. Halamek J.J. et al.Ventricular electrical delay measured from body surface ECGs is associated with cardiac resynchronization therapy response in left bundle branch block patients from the MADIT-CRT trial (Multicenter automatic defibrillator implantation-cardiac resynchronization therapy).Circ Arrhythm Electrophysiol. 2018; 11e005719PubMed Google Scholar Conduction system pacing (CSP) have recently gained great interest and specifically left bundle branch area pacing (LBBAP) appears to be an attractive pacing option. Rapid activation is the overall aim of cardiac pacing and is measured continuously during the LBBAP procedure. Jastrzebski et al recently showed that the V6-V1 interpeak interval is a novel criterion for LBB capture confirmation.4Jastrzebski M. Burri H. Kielbasa G. et al.The V6-V1 interpeak interval: a novel criterion for the diagnosis of left bundle branch capture.Europace. 2022; 24: 40-47Crossref PubMed Scopus (86) Google Scholar The intrinsic conduction system is not utilized with RVP and BIVP. Still, we hypothesized that measurements of cardiac activation times would provide valuable information also in conventional pacing. In the present acute experimental study, we aimed to investigate the association between the electrical and hemodynamic changes induced by cardiac pacing and hypothesized that modification of the ventricular electrical delay caused by RVP and BIVP would influence on the acute hemodynamic response in patients undergoing CRT implantation. The Regional Ethical Committee for Medical Research (REK South East, Oslo, Norway) approved the research protocol and the study complied with the Declaration of Helsinki. All patients gave written informed consent. Statistical analysis was performed by linear mixed model regression (STATA SE 15.1) Values are reported as mean with 95% confidence interval. Thirty-eight patients (63±10 years, 31% women, 40% ischemic) with LBBB and a mean ejection fraction of 29±5% were included. Atrial pacing was followed by sequential RVP and BIVP with a patient specific paced AV delay (142±30 ms). Acute hemodynamic response was defined as the maximum rate of invasive LV pressure change (LV dP/dtmax). ECG analyses were performed using digital software (LabChart Pro 8.0, ADInstruments Ltd, Oxford, UK) and averaged over three consecutive heart beats. Ventricular electrical delay was assessed using ECG electrode V1 and V5. We measured time from intrinsic QRS onset or pacing spike to the point of steepest deflection at or after the peak amplitude of the S-wave or R-wave (Figure, left panel). Ventricular electrical delay was defined as the absolute time difference between these two points. We observed improved LV dP/dtmax with decreasing ventricular electrical delay independent of pacing site (10 [4,16] mmHg/s increase in LV dP/dtmax per 10 ms reduction of ventricular electrical delay, p=0.002). Compared to baseline, the increase in LV dP/dtmax during RVP was 32 (10,54) mmHg/s (p=0.004) but this effect was confounded by a reduction of ventricular electrical delay (Adjusted beta LV dP/dtmax 17 [-5,39], p=0.14). LV dP/dtmax increased 74 (46,101) mmHg/s with BIVP (p<0.001), plus an additional 10 mmHg/s per 10 ms reduction in ventricular electrical delay. Our results were independent of paced QRS duration. (Figure). This indicate that alignment of V1 and V5 reflect reduced LV electrical dyssynchrony regardless of paced QRS duration and translates into beneficial hemodynamics. In line with previous data, we found a great variation in acute hemodynamic response to RVP ranging from -21% to +20% change in LV dP/dtmax when compared to atrial pacing. Ventricular electrical delay identified the patients with LV dP/dtmax increase during RVP (AUC=0.78, p=0.009). However, whether a reduction in ventricular electrical delay is indicative of ability to withstand pacing induced heart failure remains to be explored. Time to onset of the steepest deflection measured in two precordial ECG electrodes is a simple method for assessment of LV electrical dyssynchrony in heart failure patients with LBBB. Reduction of ventricular electrical delay was a marker of favorable hemodynamic response to both RVP and BIVP and should be validated in a larger cohort including long-term response and clinical outcome.

No adverse association between exercise exposure and diffuse myocardial fibrosis in male endurance athletes

The potential association between endurance exercise and myocardial fibrosis is controversial. Data on exercise exposure and diffuse myocardial fibrosis in endurance athletes are scarce and conflicting. We aimed to investigate the association between exercise exposure and markers of diffuse myocardial fibrosis by cardiovascular magnetic resonance imaging (CMR) in endurance athletes. We examined 27 healthy adult male competitive endurance athletes aged 41 ± 9 years and 16 healthy controls in a cross sectional study using 3 Tesla CMR including late gadolinium enhancement and T1 mapping. Athletes reported detailed exercise history from 12 years of age. Left ventricular total mass, cellular mass and extracellular mass were higher in athletes than controls (86 vs. 58 g/m 2 , 67 vs. 44 g/m 2 and 19 vs. 13 g/m 2 , all p < 0.01). Extracellular volume (ECV) was lower (21.5% vs. 23.8%, p = 0.03) and native T1 time was shorter (1214 ms vs. 1268 ms, p < 0.01) in the athletes. Increasing exercise dose was independently associated with shorter native T1 time (regression coefficient − 24.1, p < 0.05), but expressed no association with ECV. Our results indicate that diffuse myocardial fibrosis has a low prevalence in healthy male endurance athletes and do not indicate an adverse dose–response relationship between exercise and diffuse myocardial fibrosis in healthy athletes.

Differentiation of Myocardial Properties in Physiological Athletic Cardiac Remodeling and Mild Hypertrophic Cardiomyopathy

Clinical differentiation between athletes’ hearts and those with hypertrophic cardiomyopathy (HCM) can be challenging. We aimed to explore the role of speckle tracking echocardiography (STE) and cardiac magnetic resonance imaging (CMR) in the differentiation between athletes’ hearts and those with mild HCM. We compared 30 competitive endurance elite athletes (7% female, age 41 ± 9 years) and 20 mild phenotypic mutation-positive HCM carriers (15% female, age 51 ± 12 years) with left ventricular wall thickness 13 ± 1 mm. Mechanical dispersion (MD) was assessed by means of STE. Native T1-time and extracellular volume (ECV) were assessed by means of CMR. MD was higher in HCM mutation carriers than in athletes (54 ± 16 ms vs. 40 ± 11 ms, p = 0.001). Athletes had a lower native T1-time (1204 (IQR 1191, 1234) ms vs. 1265 (IQR 1255, 1312) ms, p < 0.001) and lower ECV (22.7 ± 3.2% vs. 25.6 ± 4.1%, p = 0.01). MD > 44 ms optimally discriminated between athletes and HCM mutation carriers (AUC 0.78, 95% CI 0.65–0.91). Among the CMR parameters, the native T1-time had the best discriminatory ability, identifying all HCM mutation carriers (100% sensitivity) with a specificity of 75% (AUC 0.83, 95% CI 0.71–0.96) using a native T1-time > 1230 ms as the cutoff. STE and CMR tissue characterization may be tools that can differentiate athletes’ hearts from those with mild HCM.

Contemporary STEMI care linked to ~68% lower 5-year mortality over a decade, but NSTEMI mortality unchanged.

Lifetime exercise dose did not differ in patients with and without severe VA (17 vs. 14 MET h/week, P = 0.34), and exercise > 9.6 MET h/week was not significantly associated with severe VA after age adjustment (OR 2.63, 95% CI 0.66-10.56, P = 0.17).

The ACASA-TAVI trial is designed to compare anti-factor Xa NOAC monotherapy versus single antiplatelet therapy for 12 months in 360 patients after successful TAVI.

Early ARVC shows progressive RV strain worsening of ~0.6 percentage points per year across all ages.

Regional functional abnormalities measured by echocardiographic deformation imaging refine personalized arrhythmic risk prediction, with normal RV deformation demonstrating excellent negative predictive value.

The LMNA-risk VTA calculator predicted 5-year ventricular tachyarrhythmias with 83% sensitivity and a Harrell's C-statistic of 0.85, but overestimated risk at a ≥7% threshold.