Patrícia Rodrigues

Scenarios for Global Biodiversity in the 21st Century

Assessing Biodiversity Declines Understanding human impact on biodiversity depends on sound quantitative projection. Pereira et al. (p. 1496, published online 26 October) review quantitative scenarios that have been developed for four main areas of concern: species extinctions, species abundances and community structure, habitat loss and degradation, and shifts in the distribution of species and biomes. Declines in biodiversity are projected for the whole of the 21st century in all scenarios, but with a wide range of variation. Hoffmann et al. (p. 1503, published online 26 October) draw on the results of five decades worth of data collection, managed by the International Union for Conservation of Nature Species Survival Commission. A comprehensive synthesis of the conservation status of the worlds vertebrates, based on an analysis of 25,780 species (approximately half of total vertebrate diversity), is presented: Approximately 20% of all vertebrate species are at risk of extinction in the wild, and 11% of threatened birds and 17% of threatened mammals have moved closer to extinction over time. Despite these trends, overall declines would have been significantly worse in the absence of conservation actions. Quantitative scenarios are coming of age as a tool for evaluating the impact of future socioeconomic development pathways on biodiversity and ecosystem services. We analyze global terrestrial, freshwater, and marine biodiversity scenarios using a range of measures including extinctions, changes in species abundance, habitat loss, and distribution shifts, as well as comparing model projections to observations. Scenarios consistently indicate that biodiversity will continue to decline over the 21st century. However, the range of projected changes is much broader than most studies suggest, partly because there are major opportunities to intervene through better policies, but also because of large uncertainties in projections.

Myocardial reverse remodeling: how far can we rewind?

Heart failure (HF) is a systemic disease that can be divided into HF with reduced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF). HFpEF accounts for over 50% of all HF patients and is typically associated with high prevalence of several comorbidities, including hypertension, diabetes mellitus, pulmonary hypertension, obesity, and atrial fibrillation. Myocardial remodeling occurs both in HFrEF and HFpEF and it involves changes in cardiac structure, myocardial composition, and myocyte deformation and multiple biochemical and molecular alterations that impact heart function and its reserve capacity. Understanding the features of myocardial remodeling has become a major objective for limiting or reversing its progression, the latter known as reverse remodeling (RR). Research on HFrEF RR process is broader and has delivered effective therapeutic strategies, which have been employed for some decades. However, the RR process in HFpEF is less clear partly due to the lack of information on HFpEF pathophysiology and to the long list of failed standard HF therapeutics strategies in these patients outcomes. Nevertheless, new proteins, protein-protein interactions, and signaling pathways are being explored as potential new targets for HFpEF remodeling and RR. Here, we review recent translational and clinical research in HFpEF myocardial remodeling to provide an overview on the most important features of RR, comparing HFpEF with HFrEF conditions.

Early cardiac changes induced by a hypercaloric Western-type diet in “subclinical” obesity

Obesity cardiomyopathy effects have been widely described; however, the specific contribution of metabolic changes and altered adipokine secretion are still uncharacterized. Moreover, a diagnosis based on body mass index might not be the most accurate to identify increased adiposity and its outcomes. In this study, we aimed to determine the impact of a Western-type diet [hypercaloric diet (HCD)] ingestion on biventricular structure and function, as well as the metabolic and endocrine changes that occur before the establishment of overt obesity. Wistar rats were fed for 6 wk with a regular diet or HCD. At the end of the protocol, metabolic tests, cardiac structure, and functional evaluation were performed, and blood and tissue samples collected to perform histological, molecular biology, and functional studies. The animals that ingested the HCD presented increased adiposity and larger adipocyte cross-sectional area, but similar body weight compared with the regular diet group. At the cardiac level, HCD induced biventricular cardiomyocyte hypertrophy, fibrosis, increased stiffness, and impaired relaxation. Galectin-3 plasma expression was likewise elevated in the same animals. The nutritional modulation also altered the secretory pattern of the adipose tissue, originating a proinflammatory systemic environment. In this study, we observed that before clinical overweight or frank obesity is established, the ingestion of a HCD-induced cardiac remodeling manifests by increased biventricular stiffness and diastolic dysfunction. The mechanism triggering the cardiac alterations appears to be the proinflammatory environment promoted by the adipose tissue dysfunction. Furthermore, galectin-3, a profibrotic molecule, might be a potential biomarker for the myocardial alterations promoted by the HCD before overweight or obesity.

Apocynin influence on oxidative stress and cardiac remodeling of spontaneously hypertensive rats with diabetes mellitus

PurposeAlthough increased oxidative stress is a major component of diabetic hypertensive cardiomyopathy, research into the effects of antioxidants on cardiac remodeling remains scarce. The actions of antioxidant apocynin include inhibiting reactive oxygen species (ROS) generation by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases and ROS scavenging. We evaluated the effects of apocynin on cardiac remodeling in spontaneously hypertensive rats (SHR) with diabetes mellitus (DM).MethodsMale SHR were divided into four groups: control (SHR, nxa0=xa016); SHR treated with apocynin (SHR-APO; 16xa0mg/kg/day, added to drinking water; nxa0=xa016); diabetic SHR (SHR-DM, nxa0=xa013); and SHR-DM treated with apocynin (SHR-DM-APO, nxa0=xa014), for eight weeks. DM was induced by streptozotocin (40xa0mg/kg, single dose). Statistical analyzes: ANOVA and Tukey or Mann–Whitney.ResultsEchocardiogram in diabetic groups showed higher left ventricular and left atrium diameters indexed for body weight, and higher isovolumetric relaxation time than normoglycemic rats; systolic function did not differ between groups. Isolated papillary muscle showed impaired contractile and relaxation function in diabetic groups. Developed tension was lower in SHR-APO than SHR. Myocardial hydroxyproline concentration was higher in SHR-DM than SHR, interstitial collagen fraction was higher in SHR-DM-APO than SHR-APO, and type III collagen protein expression was lower in SHR-DM and SHR-DM-APO than their controls. Type I collagen and lysyl oxidase expression did not differ between groups. Apocynin did not change collagen tissue. Myocardial lipid hydroperoxide concentration was higher in SHR-DM than SHR and SHR-DM-APO. Glutathione peroxidase activity was lower and catalase higher in SHR-DM than SHR. Apocynin attenuated antioxidant enzyme activity changes in SHR-DM-APO. Advanced glycation end-products and NADPH oxidase activity did not differ between groups.ConclusionApocynin reduces oxidative stress independently of NADPH oxidase activity and does not change ventricular or myocardial function in spontaneously hypertensive rats with diabetes mellitus. The apocynin-induced myocardial functional impairment in SHR shows that apocynin actions need to be clarified during sustained chronic pressure overload.

Cardiac Rehabilitation after an Acute Coronary Syndrome: The Impact in Elderly Patients

Introduction: Cardiac rehabilitation (CR) has been shown to decrease mortality and morbidity, improve the control of risk factors and the quality of life of patients with coronary artery disease. However, the elderly are underrepresented in most studies and in real-life CR programs. Our goal was to evaluate the impact of CR after an acute coronary syndrome in the elderly population. Methods: A cutoff of 65 years was used to dichotomize age. Our main focus was on the effects of ambulatory supervised exercise training on several surrogate markers, namely total cholesterol, low- and high-density lipoprotein cholesterol, triglycerides, body mass index, fasting glucose, glycated hemoglobin, probrain natriuretic peptide, International Physical Activity Questionnaire score, maximal exercise capacity, chronotropic response index and heart rate recovery. We evaluated those variables at the beginning and at the end of phase II of the CR program (after 3 months) and repeated the treadmill test at 12 months. Results: A total of 548 patients with a recent acute coronary syndrome were enrolled; 37% were 65 years old or older. Both age groups had a statistically significant improvement in all the evaluated parameters. Interestingly, at 12 months both groups maintained the improvement in functional capacity seen immediately after 3 months. Conclusions: The benefits of CR in terms of functional capacity, metabolic profile and other prognostic parameters were significant in both younger and older patients. Therefore, all eligible patients should be referred to CR programs, irrespective of age.

Preinfarction angina: clinical significance and relationship with total ischemic time in patients with ST-elevation myocardial infarction.

ObjectivesPreinfarction angina (PIA) may play a protective role in patients with ST-elevation myocardial infarction. Data on the relationship between PIA and time to reperfusion are scarce. We aimed to assess infarct size by peak troponin-T (TnT) in patients with or without PIA in three different time intervals to a primary percutaneous coronary intervention (PPCI), the relationship between PIA and left ventricular ejection fraction, and its impact on midterm survival. Patients and methodsSingle-center, retrospective analyses were carried out of 575 consecutive PPCI-treated patients, divided into three groups from symptom onset to reperfusion: less than 3, 3–6, and greater than 6u2009h. ResultsPatients with PIA had smaller infarct size [TnT=3.76 (5.07) vs. 5 (6.12)u2009ng/ml, P=0.024]. Infarct size of patients with PIA versus no-PIA was lower for patients presenting within 3–6u2009h from onset of symptoms [3.73 (5.38) vs. 5.53 (6.9)u2009ng/ml, P=0.028], but not different for those who presented less than 3u2009h [4.15 (5.53) vs. 4.0 (3.96)u2009ng/ml, P=0.702] nor for those who presented greater than 6u2009h [3.65 (4.24) vs. 5.0 (5.9)u2009ng/ml, P=0.141]. On multivariate analyses, only PIA protected from moderate to severe left ventricle dysfunction (odds ratio=0.557, 95% confidence interval: 0.352–0.881, P=0.012), but failed to reduce overall mortality [hazard ratio=0.784, 95% confidence interval: 0.356–1.724, P=0.545; median follow-up time=23 (20) months]. ConclusionPPCI-treated patients within 3–6u2009h from symptom onset had smaller infarcts if they had experienced PIA, with no benefit for those who presented less than 3u2009h nor for those who presented greater than 6u2009h from symptom onset. Moderate to severe left ventricle dysfunction was less prevalent in PIA patients. However, PIA failed to have an independent impact on midterm survival.

A trombectomia aspirativa na reperfusão do enfarte agudo de miocárdio: preditores e impacto clínico da sua ineficácia

INTRODUCTION AND OBJECTIVESnThe benefit of manual thrombus aspiration (TA) in the reperfusion of patients with ST-elevation myocardial infarction (STEMI) has been hotly debated. In most series, failure of TA has been largely unreported. Our objectives were to assess the rate, predictors, and impact on cumulative mortality of failed TA during primary percutaneous coronary intervention (PPCI).nnnMETHODSnThis was a single-center, retrospective study of consecutive STEMI patients undergoing PPCI with TA. TA was considered ineffective if, before angioplasty, coronary flow was TIMI <2. Independent predictors of TA failure were assessed by logistic regression, and predictors of cumulative mortality were assessed by Cox regression analysis.nnnRESULTSnOf 574 patients, TA was used in 417 (72.6%), and was effective in 365 (87.5%) and ineffective in 52 (12.5%). On multivariate analysis, SYNTAX score (OR=1.049, 95% CI: 1.015-1.084, p=0.005) and total ischemic time (OR=1.001, 95% CI: 1.000-1.003, p=0.02) were independent predictors of TA failure. Moderate or severe left ventricular dysfunction (HR=6.256, 95% CI: 1.896-20.644, p=0.003), APPROACH score (HR=1.094, 95% CI: 1.016-1.177, p=0.017), Killip class III/IV (HR=2.953, 95% CI: 1.122-7.770, p=0.028) and creatinine clearance on admission (HR=0.973, 95% CI: 0.953-0.994, p=0.011) were independently related to cumulative mortality at 24 ± 0.82 months.nnnCONCLUSIONSnTotal ischemic time and SYNTAX score were independent predictors of TA failure. However, in medium-term follow-up, ineffective manual TA was not independently related to cumulative mortality.

Aortocoronary dissection complicating percutaneous angioplasty

A 56-year-old man was admitted to our hospital for elective coronary angioplasty of a chronic total occlusion (CTO) of the right coronary artery (RCA). After insertion of a right femoral sheath, the RCA was engaged with a 6 French Amplatz AL-2 (Cordis, Miami, Fl, USA) guiding catheter. Recanalization was begun using a 0.014-inch Miracle 3 guidewire (Asahi Intecc, Japan). At this stage, an ostial dissection flap of the RCA with immediate retrograde extension to the ascending aorta was noticed (Figure 1). Stenting of the RCA ostium with a Xience Prime 3.0 × 15 mm stent (Abbott Vascular, Santa Clara, California, USA) was performed, followed by a PTFE-covered 3.0 × 19 mm Jostent graft

Stretch-induced compliance: a novel adaptive biological mechanism following acute cardiac load

AimsnThe heart is constantly challenged with acute bouts of stretching or overload. Systolic adaptations to these challenges are known but adaptations in diastolic stiffness remain unknown. We evaluated adaptations in myocardial stiffness due to acute stretching and characterized the underlying mechanisms.nnnMethods and resultsnLeft ventricles (LVs) of intact rat hearts, rabbit papillary muscles and myocardial strips from cardiac surgery patients were stretched. After stretching, there was a sustained >40% decrease in end-diastolic pressure (EDP) or passive tension (PT) for 15 min in all species and experimental preparations. Stretching by volume loading in volunteers and cardiac surgery patients resulted in E/E and EDP decreases, respectively, after sustained stretching. Stretched samples had increased myocardial cGMP levels, increased phosphorylated vasodilator-stimulated phosphoprotein phosphorylation, as well as, increased titin phosphorylation, which was reduced by prior protein kinase G (PKG) inhibition (PKGi). Skinned cardiomyocytes from stretched and non-stretched myocardia were studied. Skinned cardiomyocytes from stretched hearts showed decreased PT, which was abrogated by protein phosphatase incubation; whereas those from non-stretched hearts decreased PT after PKG incubation. Pharmacological studies assessed the role of nitric oxide (NO) and natriuretic peptides (NPs). PT decay after stretching was significantly reduced by combined NP antagonism, NO synthase inhibition and NO scavenging, or by PKGi. Response to stretching was remarkably reduced in a rat model of LV hypertrophy, which also failed to increase titin phosphorylation.nnnConclusionsnWe describe and translate to human physiology a novel adaptive mechanism, partly mediated by titin phosphorylation through cGMP-PKG signalling, whereby myocardial compliance increases in response to acute stretching. This mechanism may not function in the hypertrophic heart.

Manual thrombectomy efficiency in relationship to the area at risk in patients with myocardial infarction with TIMI 0-1 coronary flow: Insights from an all comers registry

To review the effectiveness of manual thrombectomy (MT) in a series of patients with ST‐elevation myocardial infarction (STEMI) exclusively presenting with TIMI 0‐1 flow undergoing percutaneous coronary intervention (PCI), in accordance to the angiographically estimated area at risk (AAR). Second, to assess major in‐hospital clinical events, emphasizing neurological outcomes.