Coronary microvascular obstruction and dysfunction (CMVO) frequently arise following primary percutaneous coronary intervention (PCI), particularly in individuals with myocardial infarction. Despite the restoration of epicardial blood flow, microvascular perfusion might still be compromised, resulting in negative clinical outcomes. CMVO is a complex condition resulting from a combination of ischemia, distal thrombotic embolization, reperfusion injury, and individual susceptibilities such as inflammation and endothelial dysfunction. The pathophysiological features of this condition include microvascular spasm, endothelial swelling, capillary plugging by leukocytes and platelets, and oxidative stress. Traditional angiographic assessments, such as Thrombolysis in Myocardial Infarction (TIMI) flow grade and myocardial blush grade, have limited sensitivity. Cardiac magnetic resonance imaging (CMR) stands as the gold standard for identifying CMVO, while the index of microvascular resistance (IMR) is a promising invasive option. Treatment approaches involve powerful antiplatelet drugs, anticoagulants, and supersaturated oxygen, yet no treatment has been definitively shown to reverse established CMVO. CMVO remains a significant therapeutic challenge in coronary artery disease management. Enhancing the comprehension of its core mechanisms is vital for the development of more effective and personalized treatment strategies.

Non-vitamin K antagonist oral anticoagulants represent a new option for prevention of embolic events in patients with atrial fibrillation (AF). However, little is known about the impact of non-cardiac comorbidities on the efficacy and safety profile of these drugs. In a post hoc analysis of the ENGAGE AF-TIMI 48 trial, we analysed 21 105 patients with AF followed for an average of 2.8 years and randomized to either a higher-dose edoxaban regimen (HDER), a lower-dose edoxaban regimen, or warfarin. We used the updated Charlson Comorbidity Index (CCI) to stratify the patients according to the burden of concomitant disease (CCI = 0, 1, 2, 3, and ≥4). The treatment groups were then compared for safety, efficacy, and net clinical outcomes across CCI categories. There were 32.0%, 7.3%, 42.1%, 12.7%, and 6.0% of patients with CCI scores of 0, 1, 2, 3, and ≥4, respectively. A CCI score ≥4 was associated with significantly higher rates of thromboembolic events, bleeding, and death compared to CCI = 0 (P < 0.05 for each). The annualized rates of the primary net clinical outcome (stroke/systemic embolism, major bleeding, or death) for CCI = 0, 1, 2, 3, or ≥4 were 5.9%, 8.7%, 6.6%, 10.3%, and 13.6% (P_trend < 0.001). There were no significant interactions between treatment with HDER vs. warfarin and efficacy, safety, and net outcomes across the CCI groups (P-interaction > 0.10 for each). Although increasing CCI scores are associated with worse outcomes, the efficacy, safety, and net clinical outcomes of edoxaban vs. warfarin were independent of the degree of comorbidity present.

High-density lipoprotein (HDL) is associated with decreased incidence of cardiovascular events, and its functionality also influences prognosis. Exercise is an important tool to improve prognosis in the post-infarction (MI) population, but the role of exercise on HDL functionality is poorly understood. Sixty-two patients with acute MI were randomized in a supervised exercise program for 12–14 weeks (exercise group—EG) or a control group (CG). The main objective of the study was to analyze the role of exercise on esterified cholesterol (EC) and unesterified cholesterol (UC) transfer to HDL. For the total population, the baseline mean rate of EC transfer to HDL was 2.53 ± 0.83 and at the end of follow-up, it was 2.74 ± 0.64 (p = 0.03). The figures for UC were, respectively, 4.08 ± 1.2 and 4.4 ± 1.06 (p = 0.02). The difference (follow-up minus baseline) for EC was 0.15 ± 0.84 for the control group and 0.27 ± 0.69 for the exercise group (p = 0.53); for UC, the figures were 0.28 ± 1.14 and 0.35 ± 0.96 (p = 0.80), respectively, for the control and exercise groups. In post-MI patients, 12–14 weeks of supervised exercise did not improve HDL functionality.

Percutaneous coronary intervention (PCI) is the most widely used coronary revascularization method worldwide, even in cases of high anatomical complexity. However, this increasing complexity has increased the risks associated with the procedure. Mechanical circulatory assist devices (MCADs), such as the iVAC 2L, have been used for hemodynamic support in high-risk PCIs. We describe the first case in Brazil of PCI performed with the support of the iVAC 2L, a pulsatile MCAD. The patient, an 81-year-old man, had functional class III angina and severe lesions in the left main coronary artery (LMCA), left anterior descending artery (LAD), and circumflex artery (CX), associated with extensive calcification. The procedure was performed with the support of the iVAC 2L, and PCI was performed with stenting of the LMCA, LAD, and CX. The entire procedure was performed without the need for vasoactive drugs, and the device was removed without vascular complications. High-risk PCI has become increasingly common, often requiring ventricular mechanical support. The iVAC 2L offers advantages such as pulsatile flow and ease of implantation, making it an alternative to the intra-aortic balloon pump and Impella. This report highlights the potential use of the iVAC 2L in Brazil, expanding therapeutic options for high-risk patients.

Neoplastic infiltration of the coronary arteries is an exceptionally rare cause of ST-segment elevation myocardial infarction and may closely mimic atherosclerotic acute coronary occlusion on clinical presentation and angiography. A 69-year-old woman presented with new-onset angina and worsening chest pain. Electrocardiography demonstrated ST-segment elevation in the anterior leads. Coronary angiography revealed long, smooth severe narrowing of the distal left anterior descending coronary artery, raising suspicion for type 2 spontaneous coronary artery dissection. Given hemodynamic stability and distal vessel involvement, a conservative strategy was pursued. Subsequent computed tomography angiography identified an anterior mediastinal mass infiltrating the anterior left ventricular wall, the left anterior descending coronary artery, 2 diagonal branches, and adjacent costal arches. Transthoracic biopsy confirmed squamous cell carcinoma of unknown primary origin. Care was redirected toward symptom-directed (palliative) management. This case highlights that anterior ST-segment elevation does not invariably reflect acute atherothrombotic coronary occlusion. Alternative mechanisms, including malignant coronary invasion, should be considered, particularly when angiographic findings are atypical. Even in the presence of classic ST-segment elevation, nonatherosclerotic mechanisms must be considered. Multimodality imaging plays a critical role in identifying uncommon etiologies such as extrinsic compression or infiltrative malignancy.