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1.
Int J Cardiol ; 325: 62-68, 2021 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-32987050

RESUMO

BACKGROUND: VDD pacemakers are regarded as a second choice in patients with atrio-ventricular blocks mainly due to the potential failure of atrial sensing, leading to a loss of atrio-ventricular synchrony. This single-centre study aimed to evaluate the prevalence of loss of atrial sensing and its potential determinants in patients with VDD pacemakers. METHOD: 142 patients with an implanted VDD device underwent long-term follow-up with clinical evaluation, electrocardiogram, device interrogation and echocardiogram. RESULTS: Over a long follow-up period [median 110 (68-156) months], 17 patients (12%) in sinus rhythm presented loss of atrial sensing. This was most often intermittent, but three patients required a permanent switch to VVI mode. ECG showed higher prevalence of interatrial blocks (50% vs 26.6%, p = 0.057) and longer P wave duration (116 ± 19 vs 105 ± 15 ms, p = 0.019) in patients with loss of atrial sensing. Echocardiography revealed larger left atrial (LA) volumes (p < 0.05) in patients with loss of atrial sensing, and lower LA ejection fraction (0.40 vs 0.47, p = 0.0037) and expansion index (0.63 ± 0.26 vs 0.90 ± 0.31, p = 0.003). P wave duration on ECG proved to be independently associated with loss of atrial sensing on multivariable analysis (OR 1.062, 95% CI 1.015-1.110; p = 0.008). The prevalence of atrial fibrillation and subsequent switch to VVI mode was high (16%). CONCLUSIONS: In the long-term follow-up, the loss of atrial sensing is present in 12% of patients with implanted VDD pacemakers. ECG and echocardiographic parameters may serve as screening tools for the detection of atrial myopathy which is associated with the loss of atrial sensing.


Assuntos
Fibrilação Atrial , Bloqueio Atrioventricular , Marca-Passo Artificial , Bloqueio Atrioventricular/diagnóstico por imagem , Bloqueio Atrioventricular/epidemiologia , Estimulação Cardíaca Artificial , Átrios do Coração , Humanos
2.
JACC Heart Fail ; 7(2): 121-128, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30704603

RESUMO

OBJECTIVES: This case control study sought to assess the presence and characteristics of cardiac abnormalities in patients with Alzheimer disease (AD). BACKGROUND: Protein misfolding is involved in the pathophysiology of neurodegenerative disorders such as AD. Recently, amyloid-beta (Aß) aggregates were identified within the cardiomyocytes and interstitium of patients with AD, suggesting that Aß oligomers may reach and damage the heart. METHODS: The authors studied 32 patients with AD and 34 controls matched by age and sex, all of whom were free from cardiac or systemic diseases. A clinical evaluation, an electrocardiogram, and an echocardiogram were performed in all subjects. Furthermore, patients with AD underwent genetic analyses (of the PSEN1, PSEN2, APP, and APOE genes). RESULTS: Compared to the control group, patients with AD had a higher prevalence of low-voltage electrocardiographic QRS complexes (28% vs. 3%, respectively; p = 0.004), a lower voltage/mass ratio (p = 0.05), a greater echocardiographic interventricular septum (10.1 ± 1.3 mm vs. 9.3 ± 1.1 mm, respectively; p = 0.01), a greater maximum wall thickness (10.8 ± 1.7 mm vs. 9.3 ± 1.1 mm, respectively; p = 0.0001), and a 2-fold higher prevalence of diastolic dysfunction (70% vs. 35%, respectively; p = 0.007). Symptoms and signs of heart failure were absent in all patients with AD. CONCLUSIONS: This study shows that electrocardiographic and echocardiographic abnormalities, including diastolic dysfunction, are present in patients with AD and that these studies reproduce the pattern of cardiac amyloidosis. These findings suggest that, in AD, there may be subclinical cardiac involvement likely associated with Aß amyloid deposition. The clinical relevance of these cardiac abnormalities should be evaluated in larger prospective studies.


Assuntos
Doença de Alzheimer/complicações , Cardiomiopatias/etiologia , Ecocardiografia Tridimensional/métodos , Eletrocardiografia , Ventrículos do Coração/fisiopatologia , Tomografia Computadorizada de Emissão de Fóton Único/métodos , Função Ventricular Esquerda/fisiologia , Idoso , Cardiomiopatias/diagnóstico , Cardiomiopatias/fisiopatologia , Estudos de Casos e Controles , Diástole , Feminino , Seguimentos , Ventrículos do Coração/diagnóstico por imagem , Humanos , Masculino , Estudos Prospectivos
5.
J Cardiol ; 72(4): 269-276, 2018 10.
Artigo em Inglês | MEDLINE | ID: mdl-29853275

RESUMO

It has been documented that physical activity may increase the risk of atrial fibrillation (AF) in active or former competitive athletes. Different mechanisms are involved and responsible for the development of the arrhythmia, such as structural changes of the left atrium, influences of autonomic nervous system with enhanced vagal tone, and the use of prohibited substances with arrhythmogenic effects. Difficulties in the management of AF in athletes may derive from the low compliance to antiarrhythmic therapy and the selection of the most appropriate strategy for thromboembolic risk prevention. In fact, the majority of athletes are young, healthy, without any particular risk factor, except for arterial hypertension which can be the only risk factor in the evaluation of antithrombotic therapy with the CHA2DS2-VASc score. The integration of actual score with serum biomarkers and other clinical factors may be useful to identify patients who will benefit the most from anticoagulation. Nowadays the non-vitamin K antagonist oral anticoagulants (NOACs) may represent a valid alternative to vitamin K antagonists (VKA) in the prevention of ischemic stroke due to AF with a better safety profile.


Assuntos
Anticoagulantes/uso terapêutico , Atletas , Fibrilação Atrial/tratamento farmacológico , Fibrilação Atrial/epidemiologia , Administração Oral , Adulto , Idoso , Fibrilação Atrial/etiologia , Coagulação Sanguínea , Feminino , Humanos , Hipertensão/complicações , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/prevenção & controle , Tromboembolia/etiologia , Tromboembolia/prevenção & controle , Vitamina K/antagonistas & inibidores
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