Climate change is widely recognized as one of the most significant challenges facing our planet and human civilization. Human activities such as the burning of fossil fuels, deforestation, and industrial processes release greenhouse gases into the atmosphere, leading to a warming of the Earth’s climate. The relationship between climate change and cardiovascular (CV) health, mediated by air pollution and increased ambient temperatures, is complex and very heterogeneous. The main mechanisms underlying the pathogenesis of CV disease at extreme temperatures involve several regulatory pathways, including temperature-sympathetic reactivity, the cold-activated renin-angiotensin system, dehydration, extreme temperature-induced electrolyte imbalances, and heat stroke-induced systemic inflammatory responses. The interplay of these mechanisms may vary based on individual factors, environmental conditions, and an overall health background. The net outcome is a significant increase in CV mortality and a higher incidence of hypertension, type II diabetes mellitus, acute myocardial infarction (AMI), heart failure, and cardiac arrhythmias. Patients with pre-existing CV disorders may be more vulnerable to the effects of global warming and extreme temperatures. There is an urgent need for a comprehensive intervention that spans from the individual level to a systemic or global approach to effectively address this existential problem. Future programs aimed at reducing CV and environmental burdens should require cross-disciplinary collaboration involving physicians, researchers, public health workers, political scientists, legislators, and national leaders to mitigate the effects of climate change.

Background: An extensive use of transesophageal echocardiography (TEE) has recently been suggested for the diagnosis of infective endocarditis (IE). In this study, we investigated whether among patients with negative transthoracic echocardiography (TTE), subgroups can be identified among whom TEE can be avoided/delayed. Methods: We conducted a retrospective study of 637 consecutive patients who underwent TEE for suspected IE. We selected 375 patients with negative TTE. For each patient, we obtained age, sex, blood culture (BC), blood exams, evidence of embolism, presence of moderate/severe heart valve disease, valve prostheses, and intracardiac devices. Results: IE was eventually diagnosed in 56 patients. Variables independently associated with IE at multivariate analysis included positive BC (OR 3.45; p = 0.006), evidence of embolism (OR 13.0; p < 0.001), bioprosthetic heart valves (OR 4.31; p < 0.001) and platelet count < 150,000/mL (OR 2.47; p = 0.014). In patients without any of these predictors for IE (n = 81), only 1 had a diagnosis of IE and no in-hospital IE-related deaths occurred. Among patients with negative BC (n = 127), IE prevalence increased with the number of other predictors, but IE-related mortality was 0%. IE prevalence (10.8%) and IE related in-hospital mortality (2.7%) were also rather low in patients with a positive blood culture without any other independent predictors for IE but were 20% (IE-related mortality 3.8%) and 71% (IE-related mortality 28.6%) in those with only one or 2–3 other IE predictors, respectively. Conclusions: Our data suggest that, among patients with suspected IE and negative TTE, subgroups can be identified in whom TEE might be safely avoided or delayed.

Background: Pharmacologic therapy guided by invasive coronary function tests (CFTs) may improve symptomatic outcomes in patients with angina and non-obstructive coronary artery disease (ANOCA). In this study, we specifically aimed to investigate whether the induction of coronary microvascular spasm (CMVS) by the acetylcholine (Ach) test predicts a better therapeutic effect of calcium-channel blocker therapy compared to beta-blocker therapy. Methods: We enrolled 31 ANOCA patients, who were divided into two groups according to the result of Ach testing: 16 patients with CMVS (CMVS group) and 15 patients with a negative test (NEG group). Patients with Ach-induced epicardial spasm were excluded. In an open-label crossover trial, patients were randomly assigned to each receive, for a period of 4 weeks, either metoprolol (50 mg twice daily) or diltiazem (120 mg twice daily). At the end of each 4-week period, patients underwent an ECG–exercise stress test (EST) and were invited to fill out the Seattle Angina Questionnaire (SAQ). Results: No significant differences were found between metoprolol and diltiazem in terms of SAQ scores, and ECG-EST results were also largely comparable with the two drug treatments, both in the CMVS group and the NEG group. In particular, the SAQ summary score was 63.1 ± 24 and 66.0 ± 25 (p = 0.59) for metoprolol and diltiazem, respectively, in the CMVS group, and 70.9 ± 17 and 74.3 ± 16 (p = 0.37) with the two drugs, respectively, in the NEG group. Conclusions: Our small open-label study shows that patients with ANOCA with negative Ach test or Ach-induced CMVS show largely comparable short-term symptomatic outcomes and ECG-EST results when treated with either metoprolol or diltiazem.