Has natural variability a lagged influence on global temperature? A multi-horizon Granger causality analysis

At present, the role of natural variability in influencing climate behaviour is widely discussed. The generally accepted view is that atmosphere-ocean coupled circulation patterns are able to amplify or reduce temperature increase from interannual to multidecadal time ranges, leaving the principal driving role to anthropogenic forcings. In this framework, the influence of these circulation patterns is considered synchronous with global temperature changes. Here, we would like to investigate if there exists a lagged influence of these indices on temperature. In doing so, an extension of the Granger causality technique, which permits to test both direct and indirect causal influences, is applied. A lagged influence of natural variability is not evident in our analysis, if we except weak influences of some peculiar circulation indices in specific periods

Clarifying the Roles of Greenhouse Gases and ENSO in Recent Global Warming through Their Prediction Performance

Abstract It is well known that natural external forcings and decadal-to-millennial variability drove changes in the climate system throughout the Holocene. Regarding recent times, attribution studies have shown that greenhouse gases (GHGs) determined the trend of temperature (T) in the last half century, while circulation patterns contributed to modify its interannual, decadal, or multidecadal behavior over this period. Here temperature predictions based on vector autoregressive models (VARs) have been used to study the influence of GHGs and El Niño–Southern Oscillation (ENSO) on recent temperature behavior. It is found that in the last decades of steep temperature increase, ENSO shows just a very short-range influence on T, while GHGs are dominant for each forecast horizon. Conversely and quite surprisingly, in the previous quasi-stationary period the influences of GHGs and ENSO are comparable, even at longer range. Therefore, if the recent hiatus in global temperatures should persist into the near future, an enhancement of the role of ENSO can be expected. Finally, the predictive ability of GHGs is more evident in the Southern Hemisphere, where the temperature series is smoother

Right ventricular failure in left heart disease: from pathophysiology to clinical manifestations and prognosis

Right heart failure (RHF) is a clinical syndrome in which symptoms and signs are caused by dysfunction and/or overload of the right heart structures, predominantly the right ventricle (RV), resulting in systemic venous hypertension, peripheral oedema and finally, the impaired ability of the right heart to provide tissue perfusion. Pathogenesis of RHF includes the incompetence of the right heart to maintain systemic venous pressure sufficiently low to guarantee an optimal venous return and to preserve renal function. Virtually, all myocardial diseases involving the left heart may be responsible for RHF. This may result from coronary artery disease, hypertension, valvular heart disease, cardiomyopathies and myocarditis. The most prominent clinical signs of RHF comprise swelling of the neck veins with an elevation of jugular venous pressure and ankle oedema. As the situation worsens, fluid accumulation becomes generalised with extensive oedema of the legs, congestive hepatomegaly and eventually ascites. Diagnosis of RHF requires the presence of signs of elevated right atrial and venous pressures, including dilation of neck veins, with at least one of the following criteria: (1) compromised RV function; (2) pulmonary hypertension; (3) peripheral oedema and congestive hepatomegaly. Early recognition of RHF and identifying the underlying aetiology as well as triggering factors are crucial to treating patients and possibly reversing the clinical manifestations effectively and improving prognosis

Heart Failure and Cancer: Mechanisms of Old and New Cardiotoxic Drugs in Cancer Patients

Although there have been many improvements in prognosis for patients with cancer, anticancer therapies are burdened by the risk of cardiovascular toxicity. Heart failure is one of the most dramatic clinical expressions of cardiotoxicity, and it may occur acutely or appear years after treatment. This article reviews the main mechanisms and clinical presentations of left ventricular dysfunction induced by some old and new cardiotoxic drugs in cancer patients, referring to the most recent advances in the field. The authors describe the mechanisms of cardiotoxicity induced by anthracyclines, which can lead to cardiovascular problems in up to 48% of patients who take them. The authors also describe mechanisms of cardiotoxicity induced by biological drugs that produce left ventricular dysfunction through secondary mechanisms. They outline the recent advances in immunotherapies, which have revolutionised anticancer therapies

Impact of COVID-19 on cardiovascular testing in the United States versus the rest of the world

Objectives: This study sought to quantify and compare the decline in volumes of cardiovascular procedures between the United States and non-US institutions during the early phase of the coronavirus disease-2019 (COVID-19) pandemic. Background: The COVID-19 pandemic has disrupted the care of many non-COVID-19 illnesses. Reductions in diagnostic cardiovascular testing around the world have led to concerns over the implications of reduced testing for cardiovascular disease (CVD) morbidity and mortality. Methods: Data were submitted to the INCAPS-COVID (International Atomic Energy Agency Non-Invasive Cardiology Protocols Study of COVID-19), a multinational registry comprising 909 institutions in 108 countries (including 155 facilities in 40 U.S. states), assessing the impact of the COVID-19 pandemic on volumes of diagnostic cardiovascular procedures. Data were obtained for April 2020 and compared with volumes of baseline procedures from March 2019. We compared laboratory characteristics, practices, and procedure volumes between U.S. and non-U.S. facilities and between U.S. geographic regions and identified factors associated with volume reduction in the United States. Results: Reductions in the volumes of procedures in the United States were similar to those in non-U.S. facilities (68% vs. 63%, respectively; p = 0.237), although U.S. facilities reported greater reductions in invasive coronary angiography (69% vs. 53%, respectively; p < 0.001). Significantly more U.S. facilities reported increased use of telehealth and patient screening measures than non-U.S. facilities, such as temperature checks, symptom screenings, and COVID-19 testing. Reductions in volumes of procedures differed between U.S. regions, with larger declines observed in the Northeast (76%) and Midwest (74%) than in the South (62%) and West (44%). Prevalence of COVID-19, staff redeployments, outpatient centers, and urban centers were associated with greater reductions in volume in U.S. facilities in a multivariable analysis. Conclusions: We observed marked reductions in U.S. cardiovascular testing in the early phase of the pandemic and significant variability between U.S. regions. The association between reductions of volumes and COVID-19 prevalence in the United States highlighted the need for proactive efforts to maintain access to cardiovascular testing in areas most affected by outbreaks of COVID-19 infection

Pulmonary Hypertension Phenotypes in Systemic Sclerosis: The Right Diagnosis for the Right Treatment

Systemic sclerosis is an auto-immune disease characterized by skin involvement that often affects multiple organ systems. Pulmonary hypertension is a common finding that can significantly impact prognosis. Molecular pathophysiological mechanisms underlying pulmonary hypertension in systemic sclerosis can be extremely heterogeneous, leading to distinct clinical phenotypes. In addition, different causes of pulmonary hypertension may overlap within the same patient. Since pulmonary hypertension treatment is very different for each phenotype, it is fundamental to perform an adequate diagnostic work-up to properly and promptly identify the prevalent mechanism underlying pulmonary hypertension in order to start the right therapies. When pulmonary hypertension is caused by a primary vasculopathy of the small pulmonary arteries, treatment with pulmonary vasodilators, often in an initial double-combination regimen, is indicated, aimed at reducing the mortality risk profile. In this review, we describe the different clinical phenotypes of pulmonary hypertension in the scleroderma population and discuss the utility of clinical tools to identify the presence of pulmonary vascular disease. Furthermore, we focus on systemic sclerosis-associated pulmonary arterial hypertension, highlighting the advances in the knowledge of right ventricular dysfunction in this setting and the latest updates in terms of treatment with pulmonary vasodilator drugs

Has natural variability a lagged influence on global temperature? A multi-horizon Granger causality analysis

At present, the role of natural variability in influencing climate behaviour is widely discussed. The generally accepted view is that atmosphere-ocean coupled circulation patterns are able to amplify or reduce temperature increase from interannual to multidecadal time ranges, leaving the principal driving role to anthropogenic forcings. In this framework, the influence of these circulation patterns is considered synchronous with global temperature changes. Here, we would like to investigate if there exists a lagged influence of these indices on temperature. In doing so, an extension of the Granger causality technique, which permits to test both direct and indirect causal influences, is applied. A lagged influence of natural variability is not evident in our analysis, if we except weak influences of some peculiar circulation indices in specific periods

Evidence of recent causal decoupling between solar radiation and global temperature

The Sun has surely been a major external forcing to the climate system throughout the Holocene. Nevertheless, opposite trends in solar radiation and temperatures have been empirically identified in the last few decades. Here, by means of an inferential method—the Granger causality analysis—we analyze this situation and, for the first time, show that an evident causal decoupling between total solar irradiance and global temperature has appeared since the 1960s

Janus, or the inevitable battle between too much and too little oxygen

: Oxygen levels are key regulators of virtually every living mammalian cell, both under physiological and pathological conditions. Starting from embryonic and fetal development, through growth, onset and progression of diseases, oxygen is a subtle, although pivotal, mediator of key processes such as differentiation, proliferation, autophagy, necrosis and apoptosis. Hypoxia-driven modifications of cellular physiology are deeply investigated for the clinical and translational relevance, especially in the ischemic scenario. The mild or severe lack of oxygen is undoubtedly related to cell death although abundant evidence points at oscillating oxygen levels, instead of permanent low pO2, as the most detrimental factor. Different cell types can consume oxygen at different rates and, most interestingly, some cells can shift from low to high consumption according to the metabolic demand. Hence, we can assume that, in the intracellular compartment, oxygen tension varies from low to high levels depending on both supply and consumption. The positive balance between supply and consumption leads to a pro-oxidative environment, with some cell types facing hypoxia/hyperoxia cycles, while some others are under fairly constant oxygen tension. Within this frame, the alterations of oxygen levels (dysoxia) are critical in two paradigmatic organs, heart the brain, under physiological and pathological conditions and the interactions of oxygen with other physiologically relevant gases, such as nitric oxide, can alternatively contribute to the worsening or protection of ischemic organs. Furthermore, the effects of dysoxia is of pivotal importance for iron metabolism