RESUMO
Current solutions for the monitoring of pulmonary artery pressure (PAP) in patients suffering from pulmonary hypertension are limited to invasive means. Non-invasive alternatives, such as Doppler echocardiography, are incompatible with continuous monitoring due to their dependency on qualified personnel to perform the measurements. In the present study, a novel non-invasive and unsupervised approach based on the use of electrical impedance tomography (EIT) is presented. The approach was evaluated in three healthy subjects undergoing hypoxia-induced variations in PAP. A timing parameter - physiologically linked to the PAP via the so-called pulse wave velocity principle - was automatically extracted from the EIT data. Reference systolic PAP estimates were obtained by echocardiography. Strong correlation scores (r e [0.844, 0.990]) were found between the EIT-derived parameter and the reference PAP, thereby suggesting the validity of the proposed approach. If confirmed in larger datasets, these findings could open the way for a new branch of fully non-invasive hemodynamic monitors for patients with pulmonary hypertension.
Assuntos
Artéria Pulmonar/fisiologia , Tomografia , Adulto , Ecocardiografia Doppler , Impedância Elétrica , Voluntários Saudáveis , Hemodinâmica , Humanos , Hipertensão Pulmonar/diagnóstico por imagem , Masculino , Análise de Onda de PulsoRESUMO
Endurance athletes have an increased risk of atrial fibrillation. We performed a longitudinal study on elite runners of the 2010 Jungfrau Marathon, a Swiss mountain marathon, to determine acute effects of long-distance running on the atrial myocardium. Ten healthy male athletes were included and examined 9 to 1 week prior to the race, immediately after, and 1, 5, and 8 days after the race. Mean age was 34.9 ± 4.2 years, and maximum oxygen consumption was 66.8 ± 5.8 mL/kg*min. Mean race time was 243.9 ± 17.7 min. Electrocardiographic-determined signal-averaged P-wave duration (SAPWD) increased significantly after the race and returned to baseline levels during follow-up (128.7 ± 10.9 vs. 137.6 ± 9.8 vs. 131.5 ± 8.6 ms; P < 0.001). Left and right atrial volumes showed no significant differences over time, and there were no correlations of atrial volumes and SAPWD. Prolongation of the SAPWD was accompanied by a transient increase in levels of high-sensitivity C-reactive protein, proinflammatory cytokines, total leucocytes, neutrophil granulocytes, pro atrial natriuretic peptide and high-sensitivity troponin. In conclusion, marathon running was associated with a transient conduction delay in the atria, acute inflammation and increased atrial wall tension. This may reflect exercise-induced atrial myocardial edema and may contribute to atrial remodeling over time, generating a substrate for atrial arrhythmias.
Assuntos
Remodelamento Atrial/fisiologia , Inflamação/sangue , Neutrófilos , Corrida/fisiologia , Adulto , Fator Natriurético Atrial/sangue , Proteína C-Reativa/metabolismo , Eletrocardiografia , Átrios do Coração/diagnóstico por imagem , Átrios do Coração/fisiopatologia , Humanos , Interleucina-6/sangue , Contagem de Leucócitos , Estudos Longitudinais , Masculino , Estudos Prospectivos , Troponina/sangue , Fator de Necrose Tumoral alfa/sangue , UltrassonografiaRESUMO
There exists an association between pathologic events occurring during early life and the development of cardiovascular disease in adulthood. For example, transient perinatal hypoxemia predisposes to exaggerated hypoxic pulmonary hypertension and preeclampsia predisposes the offspring to pulmonary and systemic endothelial dysfunction later in life. The latter finding offers a scientific basis for observations demonstrating an increased risk for premature cardiovascular morbidity in this population. Very recently, we showed that offspring of assisted reproductive technologies also display generalized vascular dysfunction and early arteriosclerosis. Studies in animal models have provided evidence that oxidative stress and/or epigenetic alterations play an important pathophysiological role in the fetal programming of cardiovascular disease.