ABSTRACT Coordinated and harmonic (synchronous) ventricular electrical activation is essential for better left ventricular systolic function. Intraventricular conduction abnormalities, such as left bundle branch block due to artificial cardiac pacing, lead to electromechanical “dyssynchronopathy” with deleterious structural and clinical consequences. The aim of this review was to describe and improve the understanding of all the processes connecting the several mechanisms involved in the development of artificially induced ventricular dyssynchrony by cardiac pacing, most known as pacing-induced cardiomyopathy (PiCM). The chronic effect of abnormal impulse conduction and nonphysiological ectopic activation by artificial cardiac pacing is suspected to affect metabolism and myocardial perfusion, triggering regional differences in the activation/contraction processes that cause electrical and structural remodeling due to damage, inflammation, and fibrosis of the cardiac tissue. The effect of artificial cardiac pacing on ventricular function and structure can be multifactorial, and biological factors underlying PiCM could affect the time and probability of developing the condition. PiCM has not been included in the traditional classification of cardiomyopathies, which can hinder detection. This article reviews the available evidence for pacing-induced cardiovascular disease, the current understanding of its pathophysiology, and reinforces the adverse effects of right ventricular pacing, especially right ventricular pacing burden (commonly measured in percentage) and its repercussion on ventricular contraction (reflected by the impact on left ventricular systolic function). These effects might be the main defining criteria and determining mechanisms of the pathophysiology and the clinical repercussion seen on patients.

ABSTRACT Coordinated and harmonic (synchronous) ventricular electrical activation is essential for better left ventricular systolic function. Intraventricular conduction abnormalities, such as left bundle branch block due to artificial cardiac pacing, lead to electromechanical “dyssynchronopathy” with deleterious structural and clinical consequences. The aim of this review was to describe and improve the understanding of all the processes connecting the several mechanisms involved in the development of artificially induced ventricular dyssynchrony by cardiac pacing, most known as pacing-induced cardiomyopathy (PiCM). The chronic effect of abnormal impulse conduction and nonphysiological ectopic activation by artificial cardiac pacing is suspected to affect metabolism and myocardial perfusion, triggering regional differences in the activation/contraction processes that cause electrical and structural remodeling due to damage, inflammation, and fibrosis of the cardiac tissue. The effect of artificial cardiac pacing on ventricular function and structure can be multifactorial, and biological factors underlying PiCM could affect the time and probability of developing the condition. PiCM has not been included in the traditional classification of cardiomyopathies, which can hinder detection. This article reviews the available evidence for pacing-induced cardiovascular disease, the current understanding of its pathophysiology, and reinforces the adverse effects of right ventricular pacing, especially right ventricular pacing burden (commonly measured in percentage) and its repercussion on ventricular contraction (reflected by the impact on left ventricular systolic function). These effects might be the main defining criteria and determining mechanisms of the pathophysiology and the clinical repercussion seen on patients.

Resumo Fundamento: A estratificação de risco continua sendo clinicamente desafiadora em pacientes com insuficiência cardíaca (IC) de etiologia não isquêmica. A galectina-3 é um marcador sérico de fibrose que pode ajudar no prognóstico. Objetivo: Determinar o papel da galectina-3 como preditora de eventos arrítmicos graves e mortalidade total. Métodos: Este é um estudo de coorte prospectivo que incluiu 148 pacientes com IC não isquêmica. Todos os pacientes foram submetidos a uma avaliação clínica e laboratorial abrangente para coleta de dados de referência, incluindo níveis de galectina-3 sérica. O desfecho primário foi a ocorrência de síncope arrítmica, intervenções apropriadas do cardioversor desfibrilador implantável, taquicardia ventricular sustentada ou morte súbita cardíaca. O desfecho secundário foi a morte por todas as causas. Para todos os testes estatísticos, considerou-se significativo o valor p<0,05 (bicaudal). Resultados: Em seguimento mediano de 941 dias, os desfechos primário e secundário ocorreram em 26 (17,5%) e 30 (20%) pacientes, respectivamente. A galectina-3 sérica>22,5 ng/mL (quartil mais alto) não foi preditora de eventos arrítmicos graves (HR: 1,98; p=0,152). Os preditores independentes do desfecho primário foram diâmetro diastólico final do ventrículo esquerdo (DDFVE)>73 mm (HR: 3,70; p=0,001), ventilação periódica durante o exercício (VPE) no teste de esforço cardiopulmonar (HR: 2,67; p=0,01) e taquicardia ventricular não sustentada (TVNS)>8 batimentos na monitorização por Holter (HR: 3,47; p=0,027). Os preditores de morte por todas as causas foram: galectina-3>22,5 ng/mL (HR: 3,69; p=0,001), DDFVE>73 mm (HR: 3,35; p=0,003), VPE (HR: 3,06; p=0,006) e TVNS>8 batimentos (HR: 3,95; p=0,007). A ausência de todos os preditores de risco foi associada a um valor preditivo negativo de 91,1% para o desfecho primário e 96,6% para a mortalidade total. Conclusões: Em pacientes com IC não isquêmica, níveis elevados de galectina-3 não foram preditores de eventos arrítmicos graves, mas foram associados à mortalidade total. A ausência de preditores de risco revelou um subgrupo prevalente de pacientes com IC com excelente prognóstico.

Abstract Background: Risk stratification remains clinically challenging in patients with heart failure (HF) of non-ischemic etiology. Galectin-3 is a serum marker of fibrosis that might help in prognostication. Objective: To determine the role of galectin-3 as a predictor of major arrhythmic events and overall mortality. Methods: We conducted a prospective cohort study that enrolled 148 non-ischemic HF patients. All patients underwent a comprehensive baseline clinical and laboratory assessment, including levels of serum galectin-3. The primary outcome was the occurrence of arrhythmic syncope, appropriate implantable cardioverter defibrillator therapy, sustained ventricular tachycardia, or sudden cardiac death. The secondary outcome was all-cause death. For all statistical tests, a two-tailed p-value<0.05 was considered significant. Results: In a median follow-up of 941 days, the primary and secondary outcomes occurred in 26 (17.5%) and 30 (20%) patients, respectively. Serum galectin-3>22.5 ng/mL (highest quartile) did not predict serious arrhythmic events (HR: 1.98, p=0.152). Independent predictors of the primary outcome were left ventricular end-diastolic diameter (LVEDD)>73mm (HR: 3.70, p=0.001), exercise periodic breathing (EPB) on cardiopulmonary exercise testing (HR: 2.67, p=0.01), and non-sustained ventricular tachycardia (NSVT)>8 beats on Holter monitoring (HR: 3.47, p=0.027). Predictors of all-cause death were galectin-3>22.5 ng/mL (HR: 3.69, p=0.001), LVEDD>73mm (HR: 3.35, p=0.003), EPB (HR: 3.06, p=0.006), and NSVT>8 beats (HR: 3.95, p=0.007). The absence of all risk predictors was associated with a 91.1% negative predictive value for the primary outcome and 96.6% for total mortality. Conclusions: In non-ischemic HF patients, elevated galectin-3 levels did not predict major arrhythmic events but were associated with total mortality. Absence of risk predictors revealed a prevalent subgroup of HF patients with an excellent prognosis.

Abstract Background: Hemodilution, transoperative bleeding and cardiopulmonary bypass (CPB) are some of the factors associated with high transfusion rates in cardiac surgery. Objective: To analyze the incidence of blood transfusion and early postoperative outcomes in cardiac surgery patients. Methods: Cohort study of patients undergoing cardiac surgery in a university hospital, consecutively enrolled from May 2015 to February 2017. Data were prospectively collected and comparisons were made between two patients’ groups: transfused and not transfused. Student's t-test, chi-square test, and logistic regression were used, and a p-value < 0.05 was considered significant. Results: Among the 271 patients evaluated, 100 (37%) required transfusion in the transoperative (32.1%) and/or postoperative periods (19.5%). The following predictors of transfusion were identified by multivariate analysis: EuroScore II (OR 1.2); chronic kidney disease (CKD) (OR 3.2); transoperative bleeding ≥ 500 mL (OR 6.7); baseline hemoglobin (Hb) ≤ 10 g/dL (OR 11.5); activated partial thromboplastin time (aPTT) (OR 1.1) and CPB duration (OR 1.03). Transfusion was associated with prolonged mechanical ventilation (≥ 24h) (2.4% vs. 23%), delirium (5.9% vs. 18%), bronchopneumonia (1.2% vs. 16%), acute renal failure (3.5% vs. 25%), acute on CKD (0.6% vs. 8%), stroke or transient ischemic attack (1.8% vs. 8%), intensive care unit stay ≥ 72 h (36% vs. 57%), longer hospital stay (8 ± 4 days vs. 16 ± 15 days), as well as increased early mortality (1.75% vs. 15%). Conclusion: EuroScore II, CKD, major transoperative bleeding, preoperative Hb and aPTT values and CPB time were independent predictors of transfusion, which was associated with a higher rate of adverse outcomes, including early mortality.

Abstract Objective: Rhythm abnormalities following transcatheter aortic valve implantation (TAVI) and indications for permanent pacemaker implantation (PPI) were reviewed, which aren't well established in the current guidelines. New left bundle branch block and atrioventricular block are the most common electrocardiographic changes after TAVI. PPI incidence ranges from 9-42% for self-expandable and 2.5-11.5% for balloon expandable devices. Not only anatomical variations in conduction system have an important role in conduction disorders, but different valve characteristics and their relationship with cardiac structures as well. Previous right bundle branch block has been confirmed as one of the most significant predictors for PPI.

Abstract Introduction: Spontaneous coronary artery dissection is a sudden separation between the layers of a coronary artery wall, non-iatrogenic or trauma related, that has been recognized as an important cause of myocardial infarction. Objective: To report an emblematic case, in terms of angiographic images, clinical presentation and predisposing factors, whose clinical management failure led to surgical intervention. Methods: A previously healthy 48-year-old male farmer was admitted to the emergency room complaining of anterior chest pain described as "tearing", which started after physical exertion. Anterior wall ST-segment depression was observed in the electrocardiogram and troponin levels were increased. The patient then underwent coronary catheterization. Angiography showed a tortuous left anterior descending coronary artery with a dissection line involving proximal and middle segments, resulting in mild to moderate luminal stenosis. At first, a conservative approach was chosen. Control cardiac catheterization, 3 months later, showed dissection progression to the distal segment. Results: The patient was referred to surgical treatment. Internal thoracic artery and a great saphenous vein graft were used to revascularize the target vessels. He had an uneventful postoperative course. Conclusion: In this report, we describe a typical clinical manifestation of an uncommon cause of acute myocardial infarction. The dissection was started by an extreme physical effort, which is a known triggering factor. Management of these cases is always challenging because there are no evidence-based therapies or guideline-based recomendations.