Myocardial and microvascular injury due to Coronavirus disease 2019

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

Interplay between myocardial bridging and coronary spasm in patients with myocardial ischemia and non-obstructive coronary arteries: Pathogenic and prognostic implications

BACKGROUND: Myocardial 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 evalu-ating their prognostic relevance in patients with myocardial infarction and non-obstructive coronary arteries (MINOCA) or stable NOCAD. METHODS AND RESULTS: We 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 infarc-tion, 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 (all P<0.001) compared with patients without MB. In particular, the group of patients with MB and a positive acetylcholine test had the worst prognosis. CONCLUSIONS: Among 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

Microvascular complications identify a specific coronary atherosclerotic phenotype in patients with type 2 diabetes mellitus

Background: Patients with type 2 diabetes mellitus (T2DM) are considered as a homogeneous cohort of patients. However, the specific role of diabetic microvascular complications (DMC), in determining the features of coronary plaques is poorly known. We investigated whether the presence of DMC may identify a different phenotype of patients associated to specific clinical, angiographic, optical coherence tomography (OCT) features and different prognosis. Methods: We prospectively enrolled consecutive T2DM patients with obstructive coronary artery disease (CAD) at their first coronary event. Patients were stratified according to the presence or absence of DMC, including diabetic retinopathy, diabetic neuropathy, and diabetic nephropathy. OCT assessment of the culprit vessel was performed in a subgroup of patients. The incidence of major adverse cardiac events (MACEs) was assessed at follow-up. Results: We enrolled 320 T2DM patients (mean age 70.3 ± 8.8 years; 234 [73.1%] men, 40% acute coronary syndrome, 60% chronic coronary syndrome). Patients with DMC (172 [53.75%]) presented a different clinical and biochemical profile and, of importance, a higher prevalence of multivessel CAD (109 [63.4%] vs. 68 [45.9%], p = 0.002). At OCT analysis, DMC was associated to a higher prevalence of large calcifications and healed plaques and to a lower prevalence of lipid plaques. Finally, MACEs rate was significantly higher (25 [14.5%] vs. 12 [8.1%], p = 0.007) in DMC patients, mainly driven by a higher rate of planned revascularizations, and DMC predicted the occurrence of MACEs (mean follow-up 33.4 ± 15.6 months). Conclusions: The presence of DMC identifies a distinct diabetic population with more severe CAD but with a more stable pattern of coronary atherosclerosis

Looking for optimal antithrombotic strategy after transcatheter left atrial appendage occlusion: a real-world comparison of different antiplatelet regimens

Background: Transcatheter left atrial appendage occlusion (LAAO) has emerged as an effective procedure for the prevention of thromboembolic events in non-valvular atrial fibrillation (AF) patients with contraindications to oral anticoagulation. After the procedure, different antithrombotic regimens have been used, in order to prevent device-related thrombus and trying to minimize bleedings. The search for the optimal antithrombotic strategy is still ongoing. We sought to assess efficacy and safety of different antiplatelet therapy (APT) regimens. Methods: We enrolled non-randomized consecutive patients who underwent LAAO at the University Hospital of Parma between 2010 and 2021. Three study groups were identified according to post-procedural APT: long (>1, ≤12 months)-dual APT (DAPT), short (≤ 1 month)-DAPT, lifelong single APT (SAPT). The choice of the APT was left to multidisciplinary team evaluation. The incidence of the primary outcome, a composite of any ischemic or hemorrhagic event, was assessed at follow-up. Results: We enrolled a total of 130 patients. Technical success was achieved in 123 (94.6%) patients. After LAAO, 39 [31.7%] patients were discharged on short-DAPT, 35 [28.5%] on long-DAPT and 49 [39.8%] on SAPT. After a median follow-up of 32 months, short-DAPT group had a significantly lower occurrence of the primary outcome (3 [7.7%] vs. 7 [20.0%] in long-DAPT vs. 14 [28.6%] in SAPT, p = 0.049], mainly driven by a lower occurrence of the bleeding endpoint (0 vs. 4 [11.4%] in long-DAPT vs. 9 [18.4%] in SAPT, p = 0.020). Finally, comparison of the Kaplan-Meier curves showed that short-DAPT group had a higher primary endpoint-free survival [p = 0.015] compared to the other groups. Conclusion: Post-procedural short-DAPT strategy was associated with better outcomes, mainly driven by reduction of major bleedings

"No-reflow": Update on diagnosis, pathophysiology and therapeutic strategies

Primary percutaneous coronary intervention (PCI) represents the reperfusion strategy of choice for patients presenting with ST-segment elevation myocardial infarction. However, despite the restoration of epicardial flow, primary PCI may not determine an effective reperfusion of myocardial tissue due to the occurrence of microvascular obstruction. This phenomenon also known as \u201cno-reflow\u201d may occur in 30-60% of patients treated with primary PCI. Of importance, no-reflow attenuates the benefit of reperfusion therapy and is associated with a poor clinical outcome in terms of adverse ventricular remodeling, heart failure and mortality. The pathophysiology of no-reflow is complex and multiple players may be involved. Indeed, distal embolization, ischemia-reperfusion injury and an individual predisposition to microvascular dysfunction synergically interact to determine the occurrence of no-reflow. In this review, we will analyze the pathophysiological mechanisms, the diagnostic tools and the main therapeutic targets of no-reflow, with particular attention to the most recent acquisitions in this field

Redefining residual inflammatory risk after acute coronary syndrome

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