Heart rhythm最新文献

Background: Atrial fibrillation (AF) occurs after heart transplantation (HT) and may increase morbidity and mortality; however, data on its incidence, predictors, and outcomes remain limited.

Objective: To evaluate the incidence of AF and stroke after HT and identify predictors and outcomes of post-HT AF.

Methods: We conducted a retrospective study of adult patients who underwent HT at a high-volume center between January 1, 2005, and September 30, 2024. AF was classified as early (<30 days post-HT) or late (≥30 days). Clinical variables for both recipient and donor were collected. Separate CHA₂DS₂-VASc scores were calculated using recipient and donor age. Predictors of early and late AF were assessed using univariate and multivariable logistic regression.

Results: Among 1,072 patients (median age 55 [IQR 45-63] years; 75% male), AF occurred in 11% (n=111), most commonly as late or combined early and late AF. Donor age, post-HT extracorporeal membrane oxygenation, and pericardial effusion predicted early AF, while rejection, cardiac allograft vasculopathy, and early AF predicted late AF. Stroke occurred in 9% of patients and was independently associated with pre-HT mechanical circulatory support and ischemic time but not AF. CHA₂DS₂-VASc scores incorporating recipient and donor factors predicted post-HT stroke; the donor-derived score also predicted AF. Survival was similar through three years post-HT but was lower in patients with AF at five years (72% vs. 86%, p<0.01).

Conclusions: AF after HT is associated with reduced long-term survival. Both donor and recipient factors contribute, and donor-derived CHA₂DS₂-VASc scoring may aid risk stratification and surveillance.

Background: Tachycardia upon standing implicates a cardiovascular dysreflexia, potentially resulting from impaired autonomic regulation. However, the pathophysiology of POTS remains unclear. Here we evaluated the central nervous system in POTS.

Objectives: To evaluate brain tissue changes, functional networks (central autonomic network), and cerebral hemodynamic status in patients with postural orthostatic syndrome (POTS) using magnetic resonance imaging and autonomic reflex challenges.

Methods: Individuals with POTS and age and sex-matched healthy controls were enrolled. Brain MRI data were collected using a 3.0-Tesla scanner at rest and during functional MRI using three autonomic reflex challenges: passive leg raise (PLR), mental arithmetic (MA), and isometric handgrip reflex (IHR).

Results: 38 participants were enrolled (18 POTS and 20 controls). No significant differences emerged in age, sex, or BMI between POTS and controls (P>0.05). POTS patients had higher anxiety and depression symptoms. Although global screening indicators of cognitive function were preserved (MoCA test; POTS vs controls, 28±1 vs. 29±1, P=0.2), executive function was slowed in POTS (Trail-making test-B; POTS vs controls, 44±12 vs 67±34, P=0.008). Brain tissue structural changes (P<0.005) and reduced cerebral blood flow appeared in POTS compared to controls (P<0.005). Further, impaired neural responses were seen in POTS during PLR, MA and IHR (P<0.005), despite preserved peripheral reflex function (P>0.05).

Conclusions: POTS patients show evidence of brain tissue structural changes, impaired central neural responses, and reduced cerebral blood flow in autonomic regulatory sites during cardiovascular reflex testing. These findings indicate that central autonomic control deficits may help explain the cardiovascular dysreflexia in POTS.

Background: Myotonic dystrophy type 1 (DM1) is a multisystemic disorder characterized by conduction defects and arrhythmias that contribute significantly to cardiac morbidity and sudden death. Human induced pluripotent stem cell (hiPSC)-derived cardiomyocytes provide a powerful platform to model disease-specific cardiac dysfunction; however, immature 2D cultures may not fully capture late-stage pathological mechanisms.

Objective: To investigate the temporal evolution of cardiac dysfunction in DM1 using developmentally mature 3D cardioids derived from patient-specific hiPSCs.

Methods: Control and DM1 hiPSC lines were differentiated into left ventricular and atrial cardioids following chamber-specific protocols and characterized at multiple developmental stages. Electrophysiological properties were assessed using optical mapping and multi-electrode arrays (MEA), while contractile performance was quantified via motion analysis (MUSCLEMOTION). Gene expression and immunofluorescence analyses were performed to evaluate molecular and structural maturation.

Results: DM1 cardioids displayed a stage-dependent trajectory of dysfunction. Early-stage cardioids showed electrical hyperexcitability with shortened action potential duration and increased spontaneous activity. As differentiation progressed, DM1 cardioids exhibited significant conduction slowing, impaired calcium handling, and reduced contractile amplitude compared to controls. These progressive alterations were accompanied by dysregulation of ion channel and gap junction gene expression.

Conclusion: Our findings demonstrate that DM1 cardiac pathology evolves dynamically during maturation, transitioning from early hyperexcitability to late-stage conduction and contractile defects. This study underscores the necessity of using developmentally mature 3D cardiac models to capture the full spectrum of DM1 pathophysiology and to improve translational modeling for therapeutic discovery.