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.

Coronary artery disease (CAD) has traditionally been diagnosed and managed based on anatomical assessments of the epicardial coronary arteries. However, a growing body of evidence highlights the limitations of coronary angiography in evaluating the ischemic burden of atherosclerotic plaques. The coronary microcirculation is increasingly recognized for its pivotal role in myocardial ischemia. Coronary microvascular dysfunction (CMD) contributes significantly to both acute and chronic coronary syndromes, even in the absence of obstructive epicardial disease. Despite its clinical significance, CMD remains underdiagnosed due to the lack of routine assessment in contemporary cardiac catheterization practices. Emerging invasive and noninvasive techniques now enable comprehensive evaluation of coronary microvascular dysfunction (CMD) by assessing microvascular resistance, coronary flow reserve, and tissue-level perfusion. Advances in thermodilution-based indices, intracoronary Doppler, and functional coronary angiography continue to provide quantitative insights into microvascular physiology, whereas noninvasive modalities—including cardiac magnetic resonance (MRI), positron-emitted tomography (PET), transthoracic Doppler echocardiography, and computed tomography-based perfusion imaging—offer powerful tools for diagnosing CMD without the need for catheter-based assessment. Integrating these complementary approaches into clinical practice enhances risk stratification and supports personalized management strategies, particularly in patients with ischemia and nonobstructive coronary arteries (INOCA). This review explores in-depth the diagnostic tools and the quantitative metrics used or the invasive assessment of CMD, emphasizing their clinical utility and impact on patient management.

Background: Invasive coronary functional tests (I-CFTs) can identify the mechanism(s) of angina in patients with non-obstructed coronary arteries (ANOCA). In this study, we assessed whether non-invasive coronary functional tests (NI-CFTs) can also produce reliable results when assessing these mechanisms. Methods: We performed NI-CFTs by recording coronary blood flow velocity (CBFV) in the left anterior descending coronary artery by transthoracic Doppler echocardiography in 18 patients with ANOCA who had undergone I-CFTs (an acetylcholine provocation test and an adenosine stress test) and 13 healthy controls. The NI-CFTs included hyperventilation, a dipyridamole stress test and a cold pressor test. Results: Acetylcholine induced epicardial or coronary microvascular spasm in 11 patients (61.1%), whereas adenosine coronary flow reserve (CFR) was reduced (10% compared to baseline in eight patients (44.4%) and none in the control group (p=0.005). Dipyridamole-CFR was lower in the patient group than in the control group (2.25 ± 0.49 versus 2.76±0.49; p=0.01) and correlated with adenosine-CFR (r=0.75; p<0.001). Full agreement in coronary abnormalities detected during I-CFTs and NI-CFTs (hyperventilation/dipyridamole stress test) was found in 14 patients (77.8%). Furthermore, cold pressor test-CFR was lower in patients than in the control group (1.33 ± 0.18 versus 1.52 ± 0.22; p=0.019); cold pressor test-CFR <1.35 identified three patients who showed both normal I-CFTs and a normal response to hyperventilation and dipyridamole at NI-CFTs. Conclusion: In ANOCA patients, the results of NI-CFTs performed with transthoracic Doppler echocardiography of the left anterior descending coronary artery showed a high correlation with coronary function abnormalities detected using I-CFTs. Our data suggest that NI-CFTs deserve investigation in larger multicentre studies to assess their usefulness in guiding clinical management of ANOCA patients.

Background: Detection of myocardial bridge (MB) at angiography suggests it has a role in ischaemic-related symptoms in patients with angina without obstructive coronary artery disease. However, evidence that MB may cause myocardial ischaemia is limited. Methods: We studied 41 patients with MB of the left anterior descending coronary artery and otherwise normal coronary arteries. Fourteen patients with normal coronary arteries and without MB served as controls. All subjects underwent a maximal treadmill exercise stress test (EST) under ECG monitoring. Standard and speckle-tracking echocardiography were performed at baseline and immediately after peak EST. Results: EST duration and peak heart rate and systolic pressure were similar in the two groups. A positive EST (ST-segment depression ≥1 mm) was found in 18 patients in the MB group (43.9%) and none in the control group (p=0.001). No abnormalities in both left ventricle systolic and diastolic function were found between the two groups in the standard echocardiographic evaluation. Global and segmental (anterior, inferior) longitudinal strain (LS) did not differ at baseline between the groups. There was a small increase in global LS during EST in MB patients but not in the control group (p=0.01). Similar trends were found for regional LSs, with differences being significant for the medium (p=0.028) and apical (p=0.032) anterior segments. No differences in echocardiographic parameters and both global and segmental LSs were observed between MB patients with ischaemic ECG changes during EST versus those without. Conclusion: Our findings do not support the notion that MB results in significant degrees of myocardial ischaemia during maximal myocardial work.

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.