Enhancing cardiac postoperative care: a smartwatch-integrated remote telemonitoring platform for health screening with ECG analysis.

Aims: The integration of smartwatches into postoperative cardiac care transforms patient monitoring, systematically tracking vital signs and delivering real-time data to a centralized platform. This study focuses on developing a platform for seamless integration, assessing reliability, and evaluating the impact on post-cardiac surgery. The goal is to establish a robust foundation for understanding the efficacy and dependability of smartwatch-based telemonitoring, enhancing care for this population. Methods and results: A total of 108 cardiac surgery patients were divided into telemonitoring (TLM) and control (CTL) groups. The TLM group utilized smartwatches for continuous monitoring of vital parameters (SpO2, HR, BP, ECG) over 30 ± 3 days. Statistical analyses (Pearson, Intraclass Correlation, Bland-Altman, Tost Test) were employed to compare smartwatch measurements with traditional methods. Significant correlations and concordance were observed, particularly in HR and BP measurements. Challenges were noted in SpO2 measurement. The ECG algorithm exhibited substantial agreement with cardiologists (Kappa: 0.794; p > 0.001), highlighting its reliability. The telemonitoring platform played a crucial role in early detection of clinical changes, including prompt Emergency Department (ED) visits, contributing significantly to preventing outcomes that could lead to mortality, such as asymptomatic Atrioventricular block. Positive patient responses affirmed technological efficacy, especially in identifying cardiac arrhythmias like atrial fibrillation. Conclusion: The integration of smartwatches into remote telemonitoring for postoperative cardiac care demonstrates substantial potential, improving monitoring and early complication detection, thereby enhancing patient outcomes. The FAPO-X Study (Assisted Digital Telemonitoring with Wearables in Patients After Cardiovascular Surgery; NCT05966857) underscores the promising role of telemonitoring in postoperative cardiac care.

Andersen-Tawil Syndrome: A Comprehensive Review.

Andersen-Tawil syndrome (ATS) is a very rare orphan genetic multisystem channelopathy without structural heart disease (with rare exceptions). ATS type 1 is inherited in an autosomal dominant fashion and is caused by mutations in the KCNJ2 gene, which encodes the α subunit of the K+ channel protein Kir2.1 (in ≈ 50-60% of cases). ATS type 2 is in turn linked to a rare mutation in the KCNJ5-GIRK4 gene that encodes the G protein-sensitive-activated inwardly rectifying K+ channel Kir3.4 (15%), which carries the acetylcholine-induced potassium current. About 30% of cases are de novo/sporadic, suggesting that additional as-yet unidentified genes also cause the disorder. A triad of periodic muscle paralysis, repolarization changes in the electrocardiogram, and structural body changes characterize ATS. The typical muscular change is episodic flaccid muscle weakness. Prolongation of the QU/QUc intervals and normal or minimally prolonged QT/QTc intervals with a tendency to ventricular arrhythmias are typical repolarization changes. Bidirectional ventricular tachycardia is the hallmark ventricular arrhythmia, but also premature ventricular contractions, and rarely, polymorphic ventricular tachycardia of torsade de pointes type may be present. Patients with ATS have characteristic physical developmental dysmorphisms that affect the face, skull, limbs, thorax, and stature. Mild learning difficulties and a distinct neurocognitive phenotype (deficits in executive function and abstract reasoning) have been described. About 60% of affected individuals have all features of the major triad. The purpose of this review is to present historical aspects, nomenclature (observations/criticisms), epidemiology, genetics, electrocardiography, arrhythmias, electrophysiological mechanisms, diagnostic criteria/clues of periodic paralysis, prognosis, and management of ATS.

Left atrium reverse remodeling in patients with mitral valve stenosis after percutaneous valvuloplasty: a 2- and 3-dimensional echocardiographic study.

INTRODUCTION AND OBJECTIVES: The left atrium is clinically relevant in patients with mitral valve stenosis. The objective of this study was to analyze the effects of percutaneous balloon valvuloplasty on left atrium volumes and the left atrium emptying fraction in symptomatic mitral valve stenosis patients using 2-dimensional and real-time 3 -dimensional transthoracic echocardiography. METHODS: We carried out a prospective study of 28 consecutive symptomatic mitral valve stenosis patients, aged 22-72 (39 [11.5]) years, 24/28 (85.6%) women, who underwent to percutaneous balloon valvuloplasty between March 2009 and May 2011. Patients underwent 2- and 3-dimensional transthoracic and transesophageal echocardiography (atrial fibrillation) and invasive mitral valve area measurement. Echocardiographic analysis was performed before, 72 h after and 12 months after percutaneous balloon valvuloplasty. The following parameters were analyzed: a) mitral valve area (2-dimensional planimetry, pressure half-time, 3-dimensional echocardiography, invasive hemodynamic measurement); b) indexed left atrium maximum and indexed minimum volumes, and c) left atrium emptying fraction. RESULTS: The 3-dimensional parameters of the mitral valve stenosis patients before and 72 h and 12 months after percutaneous balloon valvuloplasty were as follows: a) mitral valve area: 0.9 (0.1) cm(2); 1.8 (0.2) cm(2) (P<.001); 1.7 (0.2) cm(2) (P<.001); b) left atrium maximum volumes: 49.9 (12) mL/m(2); 42 (11.4) mL/m(2) (P<.001); 40.3 (10.2) mL/m(2) (P<.001), and c) left atrium emptying fraction: 30.1 (9.4%); 40.6 (7.4%) (P<.001); 44.1 (8%) (P<.001), respectively. CONCLUSIONS: In symptomatic mitral valve stenosis patients who underwent percutaneous balloon valvuloplasty analysis by 2- and 3-dimensional echocardiography, improvements in left atrium reverse remodeling and left atrium emptying fraction were observed 72 h and 12 months after the procedure.

Eletrocardiografia dos marcapassos, desfibriladores e ressincronizadores / Pacemaker, cardioverter-defibrillator and resynchronizator electrocardiography

Os sistemas de estimulação artificial que inicialmente eram indicados somente para as bradicardias sintomáticas expandiram sua indicação e atualmente são utilizados, entre outras, para a interrupção de taquiarritmias graves e para a ressincronização ventricular.O eletrocardiograma convencional constitui a ferramenta mais útil e simples para a avaliação desses sistemas. Existem também o Holter e o monitor de eventos(Looper), para identificar os eventos transitórios e raros. O elemento que caracteriza o eletrocardiograma de uma paciente com marcapasso artificial é a espícula emitida por este. A relação dos tempos das espículas entre si com a atividade elétrica das câmaras cardíacas, seja estimulada ou espontânea, vai permitir o entendimento do funcionamento do sistema de estimulação e a identificação de seus defeitos.Para a interrupção de taquiarritmias graves são utilizados os cardioversores desfibriladores implantáveis, que, além da função de marcapasso, são capazes de revertê-las por sobreestimulação ou por uma descarga elétrica simples. Estes estão equipados com sistemas de monitorização do eletrograma intracavitário, porém nem sempre apresentam informações totalmente confiáveis, sendo necessária a utilização do eletrocardiograma para a melhor decisão clínicaA possibilidade de estimular simultaneamente os ventrículos direito e esquerdo permte melhorar o desempenho ventricular; entretanto, cria a necessidade de avaliação da perfeita estimulação dos dois ventrículos, que pode ser feita analisando-se a posição do eixo do QRS estimulado no eletrocardiograma convencional

Hipertrofia ventricular esquerda / Left ventricular hypertrofy

Com o desenvolvimento tecnológico, principalmente na área da biologia molecular, pode-se entender melhor os intrincados mecanismos responsáveis pelo desenvolvimento da HVE em hipertensão arterial. O coração é constituído basicamente de células musculares, fibras elásticas e uma quantidade variável de colágeno duro e colágeno mole. A proporcionalidade desses elementos no coração normal é determinada geneticamente. A hipertrofia das células cardíacas acontece por modificações no processo de síntese protéica através de vários estímulos hemodinâmicos e neuro-humorais. Os estímulos hemodinâmicos determinam estiramento mecânico das fibras miocárdicas, enquanto os fatores neuro-humorais (fatores ativadores de receptores alfa-I-adrenérgicos, da angiotensina II, da endotelina, dos receptores hormonais tireoideanos e insulínicos) determinam um aumento do influxo de íons sódio, cálcio e hidrogênio para dentro da célula. Além disso, há uma ativação da síntese de proteínas G, AMPc, e desencadeamento de uma série de cascatas de eventos bioquímicos que, através de modificações nos mecanismos de transdução celular, determinam uma mensagem errada na formação de novas proteínas que determinarão a formação de um tecido miocárdico com proporcionalidade de fibras diferentes do tecido normal no que concerne a fibras elásticas, colágenos e células musculares cardíacas. Através de estudos epidemiológicos, principalmente aqueles realizados na cidade de Framingham, EUA, sabe-se que a hipertrofia ventricular esquerda é considerada um fator de risco independente para arritmias e morte súbita. Este artigo tem como finalidade fazer uma atualização sobre hipertrofia ventricular esquerda, abordando aspectos epidemiológicos, fisiopatológicos, seu diagnósticos e de tratamento.