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"Ferrari, Roberto"
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Liquidity risk management in banks : economic and regulatory issues
Turmoil on financial markets has made evident the importance of efficient liquidity risk management for the stability of banks. This book analyses the economic impact of a new regulation on profitability, on assets composition and business mix, on liabilities structure and replacement effects on banking and financial products.
Book
Heart rate reduction in coronary artery disease and heart failure
Key Points
The role of heart rate in coronary artery disease and heart failure has been explored using ivabradine, a drug that selectively targets heart rate
Increased heart rate can provoke myocardial ischaemia
Heart rate reduction can reduce the symptoms of angina
Increased heart rate is a risk marker in patients with coronary artery disease, but heart rate reduction does not improve prognosis in this clinical setting
In the setting of heart failure, elevated heart rate is a modifiable risk factor — reducing heart rate improves prognosis in these patients
Excessive bradycardia can cause dispersion of atrial fibrillation
Elevated heart rate can induce myocardial ischaemia in patients with coronary artery disease, and is a risk factor for cardiovascular events in those with heart failure. In this Review, Ferrari and Fox discuss the evidence for therapeutic heart rate reduction, drawing particularly on data from the BEAUTIFUL, SHIFT, and SIGNIFY trials.
Elevated heart rate is known to induce myocardial ischaemia in patients with coronary artery disease (CAD), and heart rate reduction is a recognized strategy to prevent ischaemic episodes. In addition, clinical evidence shows that slowing the heart rate reduces the symptoms of angina by improving microcirculation and coronary flow. Elevated heart rate is an established risk factor for cardiovascular events in patients with CAD and in those with chronic heart failure (HF). Accordingly, reducing heart rate improves prognosis in patients with HF, as demonstrated in SHIFT. By contrast, data from SIGNIFY indicate that heart rate is not a modifiable risk factor in patients with CAD who do not also have HF. Heart rate is also an important determinant of cardiac arrhythmias; low heart rate can be associated with atrial fibrillation, and high heart rate after exercise can be associated with sudden cardiac death. In this Review, we critically assess these clinical findings, and propose hypotheses for the variable effect of heart rate reduction in cardiovascular disease.
Journal Article
Ivabradine in Stable Coronary Artery Disease without Clinical Heart Failure
In this trial, over 19,000 patients with stable coronary artery disease were assigned to ivabradine (adjusted to achieve a target heart rate) or placebo. At 27 months, there was no between-group difference in the rate of death from cardiovascular causes or nonfatal MI.
An elevated heart rate is established as a marker of cardiovascular risk in the general population and among patients with cardiovascular disease.
1
–
5
Ivabradine inhibits the
I
f
(pacemaker) current in the sinoatrial node
6
and reduces the heart rate without affecting blood pressure or left ventricular systolic function. It has been shown to lessen symptoms and reduce ischemia in patients with stable angina pectoris.
7
,
8
Ivabradine is known to improve outcomes in patients with systolic heart failure.
9
A trial of ivabradine involving patients with coronary artery disease and left ventricular systolic dysfunction did not show clinical benefit,
10
but post hoc . . .
Journal Article
Cardiovascular event rates and mortality according to achieved systolic and diastolic blood pressure in patients with stable coronary artery disease: an international cohort study
The optimum blood pressure target in hypertension remains debated, especially in coronary artery disease, given concerns for reduced myocardial perfusion if diastolic blood pressure is too low. We aimed to study the association between achieved blood pressure and cardiovascular outcomes in patients with coronary artery disease and hypertension.
We analysed data from 22 672 patients with stable coronary artery disease enrolled (from Nov 26, 2009, to June 30, 2010) in the CLARIFY registry (including patients from 45 countries) and treated for hypertension. Systolic and diastolic blood pressures before each event were averaged and categorised into 10 mm Hg increments. The primary outcome was the composite of cardiovascular death, myocardial infarction, or stroke. Hazard ratios (HRs) were estimated with multivariable adjusted Cox proportional hazards models, using the 120–129 mm Hg systolic blood pressure and 70–79 mm Hg diastolic blood pressure subgroups as reference.
After a median follow-up of 5·0 years, increased systolic blood pressure of 140 mm Hg or more and diastolic blood pressure of 80 mm Hg or more were each associated with increased risk of cardiovascular events. Systolic blood pressure of less than 120 mm Hg was also associated with increased risk for the primary outcome (adjusted HR 1·56, 95% CI 1·36–1·81). Likewise, diastolic blood pressure of less than 70 mm Hg was associated with an increase in the primary outcome (adjusted HR 1·41 [1·24–1·61] for diastolic blood pressure of 60–69 mm Hg and 2·01 [1·50–2·70] for diastolic blood pressure of less than 60 mm Hg).
In patients with hypertension and coronary artery disease from routine clinical practice, systolic blood pressure of less than 120 mm Hg and diastolic blood pressure of less than 70 mm Hg were each associated with adverse cardiovascular outcomes, including mortality, supporting the existence of a J-curve phenomenon. This finding suggests that caution should be taken in the use of blood pressure-lowering treatment in patients with coronary artery disease.
Servier.
Journal Article
Myocarditis in COVID-19 patients: current problems
Myocarditis has been reported as a possible clinical presentation or complication in patients with coronavirus disease (COVID)-19 due to SARS-CoV-2. Despite the alarm that this possibility generated among physicians, there is paucity of information about mechanisms, prevalence, prognosis, diagnosis and therapy of myocarditis in the context of COVID-19. This brief review has the goal to revise and summarize current knowledge on myocarditis in COVID-19 patients and underline problems especially related to diagnosis and treatment.
Journal Article
“Far too black”: Fanny Eaton, Simeon Solomon, and The Mother of Moses
In 1860 the Jewish artist Simeon Solomon exhibited at the Royal Academy in London a painting with a biblical theme entitled The Mother of Moses, for which his model was Fanny Eaton, a Jamaican-born, multiracial woman whose mother had been formerly enslaved. This article considers the creation, display, and reception of this early painting in Solomon’s oeuvre, with an emphasis on the racial, cultural, and sociopolitical implications of the painting’s subject vis-à-vis its model and a focus on historical and contemporaneous issues of slavery and emancipation for both Jewish and Black people at the time.
Journal Article
COVID-19 in the heart and the lungs: could we “Notch” the inflammatory storm?
From January 2020, coronavirus disease (COVID-19) originated in China has spread around the world. The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The presence of myocarditis, cardiac arrest, and acute heart failure in COVID-19 patients suggests the existence of a relationship between SARS-CoV-2 infection and cardiac disease. The Notch signalling is a major regulator of cardiovascular function and it is also implicated in several biological processes mediating viral infections. In this report we discuss the possibility to target Notch signalling to prevent SARS-CoV-2 infection and interfere with the progression of COVID-19- associated heart and lungs disease.
Journal Article
Markers of endothelial and epithelial pulmonary injury in mechanically ventilated COVID-19 ICU patients
Background
Biomarkers can be used to detect the presence of endothelial and/or alveolar epithelial injuries in case of ARDS. Angiopoietin-2 (Ang-2), soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion protein-1 (VCAM-1), P-selectin and E-selectin are biomarkers of endothelial injury, whereas the receptor for advanced glycation end-products (RAGE) reflects alveolar epithelial injury. The aims of this study were to evaluate whether the plasma concentration of the above-mentioned biomarkers was different 1) in survivors and non-survivors of COVID-19-related ARDS and 2) in COVID-19-related and classical ARDS.
Methods
This prospective study was performed in two COVID-19-dedicated Intensive Care Units (ICU) and one non-COVID-19 ICU at Ferrara University Hospital. A cohort of 31 mechanically ventilated patients with COVID-19 ARDS and a cohort of 11 patients with classical ARDS were enrolled. Ang-2, ICAM-1, VCAM-1, P-selectin, E-selectin and RAGE were determined with a bead-based multiplex immunoassay at three time points: inclusion in the study (T1), after 7 ± 2 days (T2) and 14 ± 2 days (T3). The primary outcome was to evaluate the plasma trend of the biomarker levels in survivors and non-survivors. The secondary outcome was to evaluate the differences in respiratory mechanics variables and gas exchanges between survivors and non-survivors. Furthermore, we compared the plasma levels of the biomarkers at T1 in patients with COVID-19-related ARDS and classical ARDS.
Results
In COVID-19-related ARDS, the plasma levels of Ang-2 and ICAM-1 at T1 were statistically higher in non-survivors than survivors, (p = 0.04 and p = 0.03, respectively), whereas those of P-selectin, E-selectin and RAGE did not differ. Ang-2 and ICAM-1 at T1 were predictors of mortality (AUROC 0.650 and 0.717, respectively). At T1, RAGE and P-selectin levels were higher in classical ARDS than in COVID-19-related ARDS. Ang-2, ICAM-1 and E-selectin were lower in classical ARDS than in COVID-19-related ARDS (all p < 0.001).
Conclusions
COVID-19 ARDS is characterized by an early pulmonary endothelial injury, as detected by Ang-2 and ICAM-1. COVID-19 ARDS and classical ARDS exhibited a different expression of biomarkers, suggesting different pathological pathways.
Trial registration
NCT04343053
, Date of registration:
April 13, 2020
Journal Article
Short Physical Performance Battery and all-cause mortality: systematic review and meta-analysis
Background
The Short Physical Performance Battery (SPPB) is a well-established tool to assess lower extremity physical performance status. Its predictive ability for all-cause mortality has been sparsely reported, but with conflicting results in different subsets of participants. The aim of this study was to perform a meta-analysis investigating the relationship between SPPB score and all-cause mortality.
Methods
Articles were searched in MEDLINE, the Cochrane Library, Google Scholar, and BioMed Central between July and September 2015 and updated in January 2016. Inclusion criteria were observational studies; >50 participants; stratification of population according to SPPB value; data on all-cause mortality; English language publications. Twenty-four articles were selected from available evidence. Data of interest (i.e., clinical characteristics, information after stratification of the sample into four SPPB groups [0–3, 4–6, 7–9, 10–12]) were retrieved from the articles and/or obtained by the study authors. The odds ratio (OR) and/or hazard ratio (HR) was obtained for all-cause mortality according to SPPB category (with SPPB scores 10–12 considered as reference) with adjustment for age, sex, and body mass index.
Results
Standardized data were obtained for 17 studies (
n
= 16,534, mean age 76 ± 3 years). As compared to SPPB scores 10–12, values of 0–3 (OR 3.25, 95%CI 2.86–3.79), 4–6 (OR 2.14, 95%CI 1.92–2.39), and 7–9 (OR 1.50, 95%CI 1.32–1.71) were each associated with an increased risk of all-cause mortality. The association between poor performance on SPPB and all-cause mortality remained highly consistent independent of follow-up length, subsets of participants, geographic area, and age of the population. Random effects meta-regression showed that OR for all-cause mortality with SPPB values 7–9 was higher in the younger population, diabetics, and men.
Conclusions
An SPPB score lower than 10 is predictive of all-cause mortality. The systematic implementation of the SPPB in clinical practice settings may provide useful prognostic information about the risk of all-cause mortality. Moreover, the SPPB could be used as a surrogate endpoint of all-cause mortality in trials needing to quantify benefit and health improvements of specific treatments or rehabilitation programs.
The study protocol was published on PROSPERO (CRD42015024916).
Journal Article
Heart rate as a prognostic risk factor in patients with coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a subgroup analysis of a randomised controlled trial
The BEAUTIFUL study assessed the morbidity and mortality benefits of the heart rate-lowering agent ivabradine. The placebo arm of the BEAUTIFUL trial was a large cohort of patients with stable coronary artery disease and left-ventricular dysfunction. We did a subanalysis of this placebo group to test the hypothesis that elevated resting heart rate at baseline is a marker for subsequent cardiovascular death and morbidity.
The association of baseline resting heart rate with cardiovascular outcomes was analysed using Cox proportional hazard models for groups with a heart rate of 70 beats per min (bpm) or greater (2693 patients) versus less than 70 bpm (2745 patients). Additional analyses were done with finer categorisation of heart rate, and with heart rate as a continuous variable.
After adjustment for baseline characteristics, patients with heart rates of 70 bpm or greater had increased risk for cardiovascular death (34%, p=0·0041), admission to hospital for heart failure (53%, p<0·0001), admission to hospital for myocardial infarction (46%, p=0·0066), and coronary revascularisation (38%, p=0·037). For every increase of 5 bpm, there were increases in cardiovascular death (8%, p=0·0005), admission to hospital for heart failure (16%, p<0·0001), admission to hospital for myocardial infarction (7%, p=0·052), and coronary revascularisation (8%, p=0·034). The analysis of fine-groupings of heart rate suggests that the increase in mortality and heart failure outcomes rises continuously above 70 bpm, whereas the relation is less pronounced for coronary outcomes. For heart failure outcomes, the predictive value of resting heart rate was stronger for earlier events than for later events.
In patients with coronary artery disease and left-ventricular systolic dysfunction, elevated heart rate (70 bpm or greater) identifies those at increased risk of cardiovascular outcomes, with a differential effect on outcomes associated with heart failure and outcomes associated with coronary events.
Servier, France.
Journal Article