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Aims: In this multicentre study, we compared cardio‐pulmonary exercise test (CPET) parameters between heart failure (HF) patients classified as New York Heart Association (NYHA) class I and II to assess NYHA performance and prognostic role in mild HF. Methods and results: We included consecutive HF patients in NYHA class I or II who underwent CPET in three Brazilian centres. We analysed the overlap between kernel density estimations for the per cent‐predicted peak oxygen consumption (VO2), minute ventilation/carbon dioxide production (VE/VCO2) slope, and oxygen uptake efficiency slope (OUES) by NYHA class. Area under the receiver‐operating characteristic curve (AUC) was used to assess the capacity of per cent‐predicted peak VO2 to discriminate between NYHA class I and II. For prognostication, time to all‐cause death was used to produce Kaplan–Meier estimates. Of 688 patients included in this study, 42% were classified as NYHA I and 58% as NYHA II, 55% were men, and mean age was 56 years. Median global per cent‐predicted peak VO2 was 66.8% (IQR 56–80), VE/VCO2 slope was 36.9 (31.6–43.3), and mean OUES was 1.51 (±0.59). Kernel density overlap between NYHA class I and II was 86% for per cent‐predicted peak VO2, 89% for VE/VCO2 slope, and 84% for OUES. Receiving‐operating curve analysis showed a significant, albeit limited performance of per cent‐predicted peak VO2 alone to discriminate between NYHA class I vs. II (AUC 0.55, 95% CI 0.51–0.59, P = 0.005). Model accuracy for probability of being classified as NYHA class I (vs. NYHA class II) across the spectrum of the per cent‐predicted peak VO2 was limited, with an absolute probability increment of 13% when per cent‐predicted peak VO2 increased from 50% to 100%. Overall mortality in NYHA class I and II was not significantly different (P = 0.41), whereas NYHA class III patients displayed a distinctively higher death rate (P < 0.001). Conclusions: Patients with chronic HF classified as NYHA I overlapped substantially with those classified as NYHA II in objective physiological measures and prognosis. NYHA classification may represent a poor discriminator of cardiopulmonary capacity in patients with mild HF. [ABSTRACT FROM AUTHOR]

Sudden cardiac death (SCD) is an unpredictable and common mode of death in patients with heart failure (HF). Alterations in calcium handling may lead to malignant arrhythmias, resulting in SCD, and variants in calcium signaling-related genes have a significant association with SCD. Therefore, the aim of the present retrospective cohort study was to investigate the association of Ser96Ala [histidine-rich calcium-binding protein (HRC)], Ser49Gly [β1-adrenergic receptor (ADRB1)], Arg389Gly (ADRB1) and Gly1886Ser [ryanodine receptor 2 (RYR2)] polymorphisms with serious arrhythmic events and overall mortality in patients with HF with reduced left ventricular ejection fraction of non-ischemic etiology. In total, 136 patients with HF underwent physical examination, routine laboratory tests, non-invasive assessment of cardiac function and an invasive electrophysiological study. The primary outcome was the occurrence of serious arrhythmic events, set as either SCD or appropriate implantable cardioverter-defibrillator (ICD) therapy, and the secondary outcome was all-cause death. During a median follow-up of 37 months, arrhythmic events occurred in 26 patients (19%) and 41 patients (30%) died. Patients carrying the Ser allele of the Ser96Ala polymorphism in HRC had worse survival than those with the Ala/Ala genotype (log-rank P=0.043). Despite the difference in survival time, the Ala/Ala genotype was not associated with all-cause death in the regression analysis [unadjusted hazard ratio (HR)=0.17; 95% CI, 0.02-1.21]. Regarding the Ser49Gly and Arg389Gly polymorphisms in ADRB1, homozygosity for the major alleles at both sites (Ser49Ser and Arg389Arg) was associated with a two-fold increased risk of all-cause death compared with the other genotype combinations (unadjusted HR=1.98; 95% CI, 1.02-3.82). However, this association was lost after controlling for clinical covariates. No association was observed for the Gly1886Ser polymorphism in RYR2. Overall, the present findings are concurrent with the hypothesis that the Ser96Ala (HRC), Ser49Gly (ADRB1) and Arg389Gly (ADRB1) polymorphisms may be associated with HF prognosis. In particular, the Ser96Ala polymorphism might aid in risk stratification and patient selection for ICD implantation. [ABSTRACT FROM AUTHOR]

Circulating advanced glycation end products (AGE) and their receptor, RAGE, are increased after a myocardial infarction (MI) episode and seem to be associated with worse prognosis in patients. Despite the increasing importance of these molecules in the course of cardiac diseases, they have never been characterized in an animal model of MI. Thus, the aim of this study was to characterize AGE formation and RAGE expression in plasma and cardiac tissue during cardiac remodeling after MI in rats. Adult male Wistar rats were randomized to receive sham surgery (n = 15) or MI induction (n = 14) by left anterior descending coronary artery ligation. The MI group was stratified into two subgroups based on postoperative left ventricular ejection fraction: low (MIlowEF) and intermediate (MIintermEF). Echocardiography findings and plasma levels of AGEs, protein carbonyl, and free amines were assessed at baseline and 2, 30, and 120 days postoperatively. At the end of follow-up, the heart was harvested for AGE and RAGE evaluation. No differences were observed in AGE formation in plasma, except for a decrease in absorbance in MIlowEF at the end of follow-up. A decrease in yellowish-brown AGEs in heart homogenate was found, which was confirmed by immunodetection of N-ε-carboxymethyl-lysine. No differences could be seen in plasma RAGE levels among the groups, despite an increase in MI groups over the time. However, MI animals presented an increase of 50% in heart RAGE at the end of the follow-up. Despite the inflammatory and oxidative profile of experimental MI in rats, there was no increase in plasma AGE or RAGE levels. However, AGE levels in cardiac tissue declined. Thus, we suggest that the rat MI model should be employed with caution when studying the AGE-RAGE signaling axis or anti-AGE drugs for not reflecting previous clinical findings. [ABSTRACT FROM AUTHOR]

Heart failure is an increasingly prevalent disease associated with high morbidity and mortality. In 30-40% of patients, the etiology is non-ischemic. In this group of patients, the implantable cardioverter-defibrillator (ICD) prevents sudden death and decreases total mortality. However, due to burden of cost, the fact that many ICD patients will never need any therapy, and possible complications involved in implant and follow-up, the device should not be implanted in every patient with non-ischemic heart failure. There is an urgent need to adequately identify patients with highest sudden death risk, in whom the implant is most cost-effective. In the present paper, the authors discuss current available tests for risk stratification of sudden cardiac death in patients with non-ischemic heart failure. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

There is a very well known correlation between diabetes and cardiovascular disease but many health care professionals are just concerned with glycemic control, ignoring the paramount importance of controlling other risk factors involved in the pathogenesis of serious cardiovascular diseases. This Position Statement from the Brazilian Diabetes Society was developed to promote increased awareness in relation to six crucial topics dealing with diabetes and cardiovascular disease: Glicemic Control, Cardiovascular Risk Stratification and Screening Coronary Artery Disease, Treatment of Dyslipidemia, Hypertension, Antiplatelet Therapy and Myocardial Revascularization. The issue of what would be the best algorithm for the use of statins in diabetic patients received a special attention and a new Brazilian algorithm was developed by our editorial committee. This document contains 38 recommendations which were classified by their levels of evidence (A, B, C and D). The Editorial Committee included 22 specialists with recognized expertise in diabetes and cardiology. [ABSTRACT FROM AUTHOR]

Context: Matrix metalloproteinases are involved in atherosclerosis and plaque vulnerability. Objective: To investigate serum levels and genetic polymorphisms of matrix metalloproteinases (MMPs) -1, -3 and -9 in patients submitted to carotid endarterectomy. Methods: Genetic polymorphisms were evaluated using polymerase chain reaction (PCR-RFLP); serum levels were measured using ELISA; histological sections were stained with Picrosirius Red to analyze the fibrous cap thickness, lipid core and collagen content and with hematoxylin--eosin to detect the presence of intraplaque hemorrhage. Results: MMP-9 serum levels were significantly higher in patients with a thinner fibrous cap ( p = 0.033) or acute or recent intraplaque hemorrhage ( p = 0.008) on histology, as well as in patients with previous stroke ( p = 0.009) or peripheral vascular disease ( p = 0.049). No consistent associations were observed between different MMP genotypes and fibrous cap thickness, lipid core, collagen content or intraplaque hemorrhage. Conclusions: MMP-9 serum levels were consistently associated with markers of carotid atherosclerosis and lesion vulnerability, whereas specific MMP genotypes were not. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 38 year-old male who was admitted to the emergency room with fever and hemoptysis in the last 3 weeks.

• Patients vaccinated against COVID-19 may become infected with SARS-CoV-2. • Severe heart failure can be identified after myocarditis caused by SARS-CoV-2. • Severe cardiac sequelae may be associated with reinfection and COVID-19 vaccination. Cardiac involvement in COVID-19 can range from mild damage to severe myocarditis. The precise mechanism by which COVID-19 causes myocardial injury is still unknown. Myocarditis following administration of COVID-19 vaccines, especially those based on mRNA, has also been described. However, no reports of heart failure following reinfection with SARS-CoV-2 in patients immunized with an inactivated vaccine have been identified. The patient was a 47-year-old male construction worker of African descent, with type II diabetes and a history of infection by SARS-CoV-2 in December 2020 and May 2021, confirmed by RT-PCR. He received two doses of an inactivated vaccine against COVID-19. Between the two COVID-19 episodes with positive RT-PCR, he had two episodes of bacterial lung infection. After the second episode of SARS-CoV-2 infection, he was diagnosed with severe heart failure as a sequela of myocarditis. It is essential to perform a thorough follow-up after infection with SARS-CoV-2 since, even with proper immunization, it is possible that the patient was reinfected and suffered severe cardiac sequelae as a consequence. The hypothesis of an etiology associated with the use of an inactivated vaccine against COVID-19, with a potential immune enhancement mechanism following reinfection with SARS-CoV-2, cannot be rejected. [ABSTRACT FROM AUTHOR]

Aims MicroRNAs (miRs) regulate processes involved in both cardiac remodeling and obesity. We investigated if the expression of selected miRs in patients with heart failure (HF) is influenced by the presence of obesity. Methods In this case–control study, we compared plasma levels of miR-21, -130b, -221, -423-5p, and the -221/-130b ratio in 57 age- and gender-matched subjects: 40 HF patients (20 obese HF and 20 lean HF) and 17 lean healthy controls. Body composition was estimated by bioelectrical impedance analysis. MiRs were measured by quantitative reverse transcription-PCR. Bioinformatics analysis was performed based on miRs findings to predict their putative targets and investigate their biological function. Results HF was associated with increased miR-423-5p levels in both lean and obese patients ( P < 0.05 vs. controls) without differences between HF groups. MiR-130b levels were reduced in obese HF patients compared with HF lean ( P = 0.036) and controls ( P = 0.025). MiR-221 levels were non-significantly increased in obese HF patients. MiR-21 levels were not different among the groups. MiR-221/-130b ratio was increased in obese HF patients, and was positively associated with body fat percentage ( r = 0.43; P = 0.002), body mass index ( r = 0.44; P = 0.002), and waist circumference ( r = 0.40; P = 0.020). Computational prediction of target genes followed by functional enrichment analysis indicated a relevant role of miR-130b and miR-221 in modulating the expression of genes associated to cardiovascular and endocrine diseases, and suggested their influence in important signaling mechanisms and in numerous processes related to the circulatory and endocrine systems. Conclusions In HF patients, the presence of obesity is associated with a differential expression of selected miRs and the miR-221/-130b ratio had significant correlations with adiposity parameters. Computational target prediction analysis identified several interrelated pathways targeted by miR-130b and miR-221 with a known relationship with endocrine and cardiovascular diseases, representing potential mechanisms to be further validated. [ABSTRACT FROM AUTHOR]

Abstract: Background and purpose: To investigate early vascular changes related to carotid atherosclerotic injury post-radiation therapy (RT), we studied carotid intima–media thickness (IMT) and vascular cellular adhesion molecule (VCAM)-1 at two time-points after RT and compared local and remote irradiation effects in patients with head and neck (HNC) and prostate cancer (PC), respectively. Material and methods: We prospectively studied patients beginning RT for HNC or PC, performing carotid ultrasound before RT, early after and six months after treatment to measure carotid IMT. Blood samples were simultaneously collected to study VCAM-1 by ELISA. Results: We studied 19 patients with HNC and 24 with PC. Patients with HNC were younger (55±10years) than PC patients (68±8years). Early post-RT only HNC patients had an increase in IMT compared to baseline measurements (0.73±0.04mm vs. 0.80±0.05mm, p =0.029). On the other hand, VCAM-1 levels decreased in PC patients, remaining unchanged in HNC patients. Late post-RT (six months from previous assessment), neither IMT nor VCAM-1 values changed in both groups. Conclusion: Local and remote RT seem to exert differential early effects regarding vascular-related changes: (1) local RT seems to affect vascular structure and increase IMT and (2) RT for PC is associated with reduction in VCAM levels, suggesting systemic modulation of cancer-related factors. [Copyright &y& Elsevier]

Abstract: Objective: To identify factors related to NT-proBNP levels in systemic sclerosis (SSc). Design and methods: NT-proBNP was measured in 119 patients with SSc and 20 controls. Patients with transtricuspid gradient (TG) ≥36mmHg or ≥31mmHg plus dyspnea were considered to have suspected systemic sclerosis-associated pulmonary arterial hypertension (SScPAH). Results: Increasing age, NYHA functional class, skin score, history of systemic arterial hypertension (SAH), anticentromere antibodies, diastolic dysfunction, reduced pulmonary diffusing capacity, and TG were positively associated with NT-proBNP. In multivariable linear regression, TG, age, and SAH were independently associated to NT-proBNP levels. An ROC curve analysis (with an area under the curve of 0.89, 95% CI: 0.83–0.95) suggested a cutoff of 157.8pg/mL to identify patients with suspected SScPAH, presenting a sensitivity of 100% (78.1–100) and specificity of 72.3% (62.3–80.5). Conclusions: NT-proBNP levels are related to clinical and laboratory abnormalities in SSc. The results indicate that NT-proBNP may be a useful tool in the evaluation of SScPAH. [Copyright &y& Elsevier]