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Objectives We assessed the relationship between exposure to air pollutants and mechanisms of coronary instability evaluated by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). Background Air pollution is an emerging key player in determining the residual risk of coronary events. However, pathophysiological mechanisms linking air pollution and coronary events have been not adequately investigated. Methods Patients with ACS undergoing OCT imaging were retrospectively selected. Mechanism of culprit lesion instability was classified as plaque rupture (PR) or intact fibrous cap (IFC) by OCT, and the presence of macrophage infiltrates (MOI) and thin-cap fibroatheroma (TCFA) at the culprit site was also assessed. Based on each case’s home address, exposure to several pollutants was evaluated, including particulate matter 2.5 (PM2.5), PM10, and carbon monoxide (CO). Only patients with >2 years of available data on air pollution exposure prior to ACS were enrolled. Results We included 126 patients (median age: 67.0 years of age; interquartile range: 55.5-76.0; 97 male patients [77.0%]). Sixty-six patients (52.4%) had PR as the mechanism of plaque instability. Patients with PR were exposed to significantly higher PM2.5 levels than to IFC, and PM2.5 was independently associated with PR (odds ratio: 1.194; 95% CI: 1.036 to 1.377; P = 0.015). Moreover, exposure to higher levels of PM2.5 was independently associated with the presence of TCFA and of MOI at the culprit site. Interestingly, PM2.5, PM10, and C o levels were positively and significantly correlated with serum levels of C-reactive protein. Conclusions We provide novel insights into the missing link between air pollution and increased risk of coronary events. In particular, exposure to higher concentrations of air pollutants is associated with the presence of vulnerable plaque features and with plaque rupture as a mechanism of coronary instability. An enhanced systemic and plaque inflammatory activation may explain these findings.

Takotsubo syndrome (TS) is an acute and reversible form of myocardial stunning preceded by emotional or physical stress, not explained by an obstruction of an epicardial coronary artery as in acute coronary syndrome. Over the last decades, TS is receiving growing attention, leading to an increase in awareness and diagnostic rate. Chest pain and dyspnea are the most common presenting symptoms; however, nonspecific presentations make the diagnosis challenging for clinicians. Here, we present the case of a 76-year-old female who experienced two completely asymptomatic episodes of TS 20 years apart.

Over the last decades, inflammation proved to play a pivotal role in atherosclerotic plaque formation, progression and destabilization. Several studies showed that the patients presenting with acute coronary syndrome are at increased risk of adverse cardiovascular events at both short- and long-term follow-up. Results from different clinical trials highlighted that a residual inflammatory risk exist and targeting inflammation is a successful strategy in selected cases associated to an increased inflammatory burden. Recently, the optimization of intracoronary and multimodality imaging allowed to also assess the entity of local inflammation, thus encouraging the individuation of plaque characteristics that portend a higher risk of future cardiovascular events. In this short review, we aim to highlight the role of systemic and local inflammation in acute coronary syndromes, to provide a summarized overview of the possible medical strategies applicable in selected cases and to underline the diagnostic and prognostic potential of multimodality imaging.

Takotsubo syndrome (TS) is a condition of transient regional ventricular systolic dysfunction, usually presenting with acute chest pain and/or dyspnea, that is increasingly recognized especially in post-menopausal women following a psychological or physical stress. Initially considered as a benign condition with an isolated and self-limiting episode, it is now recognized that it is associated with a significant risk of in-hospital mortality and of recurrence. We herein describe a case of a 61-year-old female with left ventricular non-compaction cardiomyopathy (LVNC) who experienced a recurrence of TS, highlighting the potential pathophysiological role for LVNC in predisposing this syndrome and its recurrence. Moreover, we underscored possible therapeutic implications deriving from this case.

AIMS Killip classification is a simple and fast clinical tool for risk stratification of patients presenting with acute coronary syndrome (ACS). However, the clinical features and predictors of high Killip class at admission, and its prognostic impact in patients presenting with anterior ST elevation MI (STEMI) as first clinical cardiovascular event are still poorly known. The aim of this study was to identify the predictors of high Killip class and its impact on in-hospital and follow-up outcomes. METHODS We prospectively enrolled patients with unheralded anterior STEMI because of proximal or mid left anterior descending (LAD) artery categorized according to Killip classification. Patients' characteristics, in-hospital complications and major adverse cardiovascular events (MACEs; composite of all-cause death, heart failure hospitalization and new-onset ACS) at follow-up were collected. RESULTS We enrolled 147 patients [age 66.16±13.33, 113 male patients (76.9%)]. Killip class III--IV occurred in 22 (15%) patients. The median duration of follow-up was 12 [6--15.1] months. At multivariate analysis age [hazard ratio 1.137, 95% CI (1.068--1.209), P < 0.001], prehospital cardiac arrest [hazard ratio 12.145, 95% CI (1.710--86.254), P = 0.013] and proximal LAD lesion [hazard ratio 5.066, 95% CI (1.400--18.334), P = 0.013] were predictive of Killip class III--IV at admission. At multivariate analysis, Killip class III--IV was an independent predictor of in-hospital mortality [hazard ratio 7.790, 95% CI (1.024--59.276], P = 0.047 and of MACEs [hazard ratio 4.155 (1.558--11.082), P = 0.004) at follow-up. CONCLUSION Killip classification performed at the time of admission is a simple and useful clinical marker of a high risk of early and late adverse cardiovascular events.

BackgroundMyocardial bridging (MB) may represent a cause of myocardial ischemia in patients with non‐obstructive coronary artery disease (NOCAD). Herein, we assessed the interplay between MB and coronary vasomotor disorders, also evaluating their prognostic relevance in patients with myocardial infarction and non‐obstructive coronary arteries (MINOCA) or stable NOCAD.Methods and ResultsWe prospectively enrolled patients with NOCAD undergoing intracoronary acetylcholine provocative test. The incidence of major adverse cardiac events, defined as the composite of cardiac death, non‐fatal myocardial infarction, and rehospitalization for unstable angina, was assessed at follow‐up. We also assessed angina status using Seattle Angina Questionnaires summary score. We enrolled 310 patients (mean age, 60.6±11.9; 136 [43.9%] men; 169 [54.5%] stable NOCAD and 141 [45.5%] MINOCA). MB was found in 53 (17.1%) patients. MB and a positive acetylcholine test coexisted more frequently in patients with MINOCA versus stable NOCAD. MB was an independent predictor of positive acetylcholine test and MINOCA. At follow‐up (median, 22 months; interquartile range, 13–32), patients with MB had a higher rate of major adverse cardiac events, mainly driven by a higher rate of hospitalization attributable to angina, and a lower Seattle Angina Questionnaires summary score (allPConclusionsAmong patients with NOCAD, coronary spasm associated with MB may predict a worse clinical presentation with MINOCA and a higher rate of hospitalization attributable to angina at long‐term follow‐up with a low rate of hard events.

Background Coronary microvascular obstruction (MVO) is a noxious condition frequently occurring in patients with ST-elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI). However, multiple mechanisms are involved in the pathogenesis of MVO and not yet fully understood. Recent studies suggested that perilipin 2 (PLIN2) may play an important role in lipid metabolism of macrophages resident in atherosclerotic plaques along with a role in enhancing oxidative stress. Purpose To study the association between PLIN2 and MVO in STEMI patients undergoing primary PCI. We also assessed the role of PLIN2 to predict future major cardiovascular events (MACEs). Methods STEMI patients undergoing primary PCI were enrolled. PLIN2 was dosed within 24 hours from admission in peripheral blood monocytes. MVO was assessed using TIMI flow grade and myocardial blush grade on coronary angiogram after PCI, and patients were stratified accordingly (MVO or noMVO). Major adverse cardiac events (defined as a composite of cardiac death, non-fatal myocardial infarction, re-admission for heart failure and target vessel revascularization) were assessed at clinical follow-up. Results Among 100 STEMI patients (mean age, 65.2±12.0 years, 81 males), 33 (33.0%) had MVO. Patients with MVO were older, had higher troponin I peak, C-reactive protein and lower left ventricular ejection fraction on admission. Patients with MVO had significantly higher levels of PLIN2 (1.03±0.28 vs. 0.90±0.16, p=0.019) compared to noMVO patients. Age [OR (95% CI) per year, 1.045 (1.005–1.087), p=0.026] and PLIN2 [OR (95% CI) per unit, 16.606 (2.027–136.030), p=0.009] were associated with MVO at univariate logistic regression analysis. However, only PLIN2 levels [OR (95% CI) per unit, 12.325 (1.446–105.039), p=0.033] were independently associated with MVO at multivariate analysis. Follow up data were available for 76 patients (76%). After a mean follow up of 182.2±126.6 days, 13 MACEs occurred. Patients with MVO had more MACEs [9 (37.5%) vs. 4 (7.7%), p Conclusions In STEMI patients undergoing primary PCI, PLIN2 was independently associated with MVO. PLIN2 was an independent predictor of MACEs at clinical follow-up. These findings suggest that PLIN2 may represent a promising therapeutic target, opening the avenue towards novel therapeutic approaches for MVO. Funding Acknowledgement Type of funding source: None

Over the past few months, health systems worldwide have been put to the test with the coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Even though the leading clinical manifestations of the SARS-CoV-2 infection involve the respiratory tract, there is a non-negligible risk of systemic involvement leading to the onset of multi-organ failure with fatal consequences. Since the onset of COVID-19, patients with underlying cardiovascular disease have been at increased risk of poor clinical outcomes with higher death rates. Moreover, the occurrence of new-onset cardiac complications is not uncommon among patients hospitalised for COVID-19. Of importance, a significant portion of COVID-19 patients present with myocardial injury. Herein, the authors discuss the mechanisms leading to myocardial and microvascular injury in SARS-CoV-2 infection and their clinical implications.

Aims Functional alterations of epicardial coronary arteries or coronary microcirculation represent a frequent cause of myocardial infarction and non-obstructive coronary arteries (MINOCA). We aimed at assessing the prognostic value of intracoronary provocative tests in patients presenting with MINOCA and in which other causes of MINOCA have been excluded. Methods and results We prospectively evaluated patients with a diagnosis of MINOCA, excluding patients with aetiologies other than suspected coronary vasomotor abnormalities. Immediately after coronary angiography, an invasive provocative test using acetylcholine or ergonovine was performed. The incidence of death from any cause, cardiac death, and recurrence of acute coronary syndrome (ACS) was assessed at follow-up. We also assessed angina status using Seattle Angina Questionnaires (SAQ). We enrolled 80 consecutive patients [mean age 63.0 ± 10.7 years, 40 (50%) male]. Provocative test was positive in 37 (46.2%) patients without any complication. Among patients with a positive test, epicardial spasm was detected in 24 (64.9%) patients and microvascular spasm in 13 (35.1%) patients. After a median follow-up of 36.0 (range 12.0-60.0) months, patients with a positive test had a significantly higher occurrence of death from any cause [12 (32.4%) vs. 2 (4.7%); P = 0.002], cardiac death [7 (18.9%) vs. 0 (0.0%); P = 0.005], and readmission for ACS [10 (27.0%) vs. 3 (7.0%); P = 0.015] as well as a worse angina status as assessed by SAQ [Seattle score: 88.0 (33.0-100.0) vs. 100.0 (44.0-100.0); P = 0.001] when compared with patients with a negative test. Conclusions We demonstrate that in patients presenting with MINOCA and suspected coronary vasomotor abnormalities, a positive provocative test for spasm is safe and identifies a high-risk subset of patients.