CHA2DS2-VASc score, P-wave indexes, and echocardiographic parameters in sinus rhythm patients without valvular heart disease.

OBJECTIVE: The aim of this study was to evaluate the correlation between P-wave indexes, echocardiographic parameters, and CHA2DS2-VASc score in patients without atrial fibrillation and valvular disease. METHODS: This retrospective cross-sectional study included patients of a tertiary hospital with no history of atrial fibrillation, atrial flutter, or valve disease and collected data from June 2021 to May 2022. The exclusion criteria were as follows: unavailable medical records, pacemaker carriers, absence of echocardiogram report, or uninterpretable ECG. Clinical, electrocardiographic [i.e., P-wave duration, amplitude, dispersion, variability, maximum, minimum, and P-wave voltage in lead I, Morris index, PR interval, P/PR ratio, and P-wave peak time], and echocardiographic data [i.e., left atrium and left ventricle size, left ventricle ejection fraction, left ventricle mass, and left ventricle indexed mass] from 272 patients were analyzed. RESULTS: PR interval (RHO=0.13, p=0.032), left atrium (RHO=0.301, p<0.001) and left ventricle diameter (RHO=0.197, p=0.001), left ventricle mass (RHO=0.261, p<0.001), and left ventricle indexed mass (RHO=0.340, p<0.001) were positively associated with CHA2DS2-VASc score, whereas P-wave amplitude (RHO=-0.141, p=0.02), P-wave voltage in lead I (RHO=-0.191, p=0.002), and left ventricle ejection fraction (RHO=-0.344, p<0.001) were negatively associated with the same score. The presence of the Morris index was associated with high CHA2DS2-VASc (p=0.022). CONCLUSION: Prolonged PR interval, Morris index, increased left atrium diameter, left ventricle diameter, left ventricle mass, and left ventricle indexed mass values as well as lower P-wave amplitude, P-wave voltage in lead I, and left ventricle ejection fraction values were correlated with higher CHA2DS2-VASc scores.

Relationship between ventricular repolarization parameters and the inducibility of ventricular arrhythmias during electrophysiological study in patients with coronary artery disease.

OBJECTIVE: Risk stratification of sudden cardiac death in patients with coronary artery disease is of great importance. We evaluated the association between ventricular repolarization and induction of malignant ventricular arrhythmias on electrophysiological study of patients with coronary artery disease. METHODS AND RESULTS: A total of 177 patients (65±10.1 years, 83.6% male, mean left ventricular ejection fraction [LVEF] 37.5±13.6%) were analyzed. For each 10 ms increment in the QT interval, there was a 7% increase in malignant ventricular arrhythmias inducibility; QT cutoff point of 452 ms had an accuracy of 0.611 for predicting malignant ventricular arrhythmias (p=0.011). Male gender (odds ratio [OR]=4.18, p=0.012), LVEF <35% (OR=2.32, p=0.013), amiodarone use (OR=2.01, p=0.038), and prolonged QT (OR=1.07, p=0.023) were associated with malignant ventricular arrhythmias. In patients with ventricular dysfunction, QT >452 ms was associated with significantly increased risk of malignant ventricular arrhythmias (OR=5.44, p=0.0004). In those with LVEF ³35%, QT dispersion (QTd) was significantly higher in patients with inducible malignant ventricular arrhythmias. QTd >20 ms had 0.638 accuracy and 81.3% negative predictive value in predicting malignant ventricular arrhythmias. CONCLUSION: QT interval is an independent factor associated with malignant ventricular arrhythmias in patients with coronary artery disease. The combination of ventricular dysfunction and prolonged QT interval is associated with a 5.44-fold increase of malignant ventricular arrhythmias induction. Male gender, amiodarone use, and decreased left ventricular ejection fraction are also associated with increased risk of inducibility of malignant ventricular arrhythmias on the electrophysiological study.

Continuum Cardiovascular 25 anos - Evolução de um Modelo Etiofisiopatológico / Cardiovascular Continuum 25 years – The Evolution of an Etiopathophysiology Model

O conceito de continuum cardiovascular foi elaborado por Dzau e Braunwald e difundido entre cardiologistas como modelo etiofisiopatológico que direciona o desenvolvimento de medidas intervencionistas na prevenção das doenças cardiovasculares. Após workshop realizado em 1989, foi possível reunir questões resolvidas e não resolvidas sobre fatores relacionados à terapia e proteção cardiovascular, resultando na primeira publicação por Dzau e Braunwald, em 1991. O avanço nos estudos da biologia molecular e celular permitiu entendimento do papel da disfunção endotelial no estresse oxidativo e do óxido nítrico na doença aterosclerótica coronariana (DAC),concedendo prêmio Nobel aos autores Ferid Murad, Robert Furchgott e Louis Ignarro. Em 2006, uma segunda publicação, também liderada por Dzau, consolidou o modelo clássico do continuum cardiovascular, no qual fatores de risco para DAC se associam e desencadeiam cascata progressiva de eventos levando aos estágios finais da doença cardiovascular. A partir da observação da existência de doenças isquêmicas do miocárdio em populações com baixa incidência de aterosclerose coronariana, estudos comprovaram que a doença isquêmica não está apenas associada à aterosclerose, mas também ao envelhecimento vascular. Este achado levou à publicação do terceiro artigo de O’Rourke em 2010, que apresentou um modelo adicional: continuum do envelhecimento vascular. Aevolução desse modelo possibilitou o enfoque não apenas em tratamentos preventivos dos fatores de risco da DAC, mas também na busca de terapias capazes de prevenir dano endotelial causado pelo envelhecimento vascular e de modular o estresse oxidativo. Esta revisão tem por objetivo reunir os principais estudos que embasam a evolução do modelo continuum cadiovascular em 25 anos...

The concept of cardiovascular continuum was devised by Dzau and Braunwald and spread among cardiologists as na etiopathophysiology model that directs the development of interventionist measures in the prevention of cardiovascular diseases. After a workshop held in 1989, it was possible to gather resolved and unresolved issues about factors related to cardiovascular therapy and protection, resulting in the first publication by Dzau and Braunwald, in 1991. Progress in the studies of molecular and cellular biology allowed understanding the role of endothelial dysfunction in oxidative stress and nitric oxide in coronary artery atherosclerosis (CAA), awarding Nobel Prize to authors Ferid Murad, Robert Furchgott and Louis Ignarro. In 2006, a second publication, also ledby Dzau, consolidated the classic model of cardiovascular continuum, in which risk factors for CAA are associated and trigger a progressive cascade of events leading to the final stages of cardiovascular disease. By observing the existence of ischemic myocardial diseases in populations with low incidence of coronary artery atherosclerosis, studies have shown that ischemic heart disease is not only associated with atherosclerosis, but also to vascular aging. This finding led to the publication of O’Rourke’s third manuscriptin 2010, which presented an additional model: vascular aging continuum. The evolution of this model allowed focusing on preventive treatments for the risk factors of CAA and the search for therapies capable of preventing endothelial damage caused by vascular aging and modulating oxidative stress. This review aims to bring together the leading studies that support the evolution of the cardiovascular continuum model over 25 years...