Search Results (34)

Background: Kounis syndrome is an acute coronary syndrome triggered by hypersensitivity reactions, which may result in coronary vasospasm, thrombosis, or stent-related complications. Case Summary: A 64-year-old male smoker with dyslipidemia and recently diagnosed urothelial carcinoma presented with exertional angina and underwent coronary angiography. Percutaneous coronary intervention was performed for a critical proximal–mid left anterior descending artery lesion using a drug-eluting stent. Immediately after stent deployment, the patient developed diffuse multivessel coronary vasospasm involving the left main stem, left anterior descending, and left circumflex arteries, accompanied by slow-flow/no-reflow phenomena and subsequent acute in-stent thrombosis. The clinical course rapidly progressed to ventricular arrhythmias and cardiogenic collapse. Despite transient return of spontaneous circulation after cardiopulmonary resuscitation, the patient developed fatal asystole during a repeat angiographic attempt. No cutaneous or respiratory allergic manifestations were observed. The abrupt onset of diffuse coronary dysfunction immediately following contrast exposure was suggestive of suspected Kounis syndrome, although mechanical causes and chemotherapy-related vasospasm could not be entirely excluded. Conclusions: Diffuse coronary vasospasm with multivessel dysfunction occurring abruptly after contrast exposure should raise suspicion for Kounis syndrome, even in the absence of overt allergic manifestations. Early recognition is essential to avoid misattribution to procedural complications and may be particularly important in patients with malignancy undergoing invasive coronary procedures. Full article

Angina or objective myocardial ischaemia in the absence of obstructive coronary artery disease, referred to as ANOCA/INOCA, represents a prevalent and clinically significant condition associated with persistent symptoms, impaired quality of life, and increased healthcare utilisation. Contemporary evidence has reframed these syndromes as manifestations of coronary vascular dysfunction, encompassing structural and functional coronary microvascular dysfunction, epicardial vasospasm, microvascular spasm, and mixed phenotypes. In this context, multimodality imaging should not be conceptualised as sequential test accumulation, but rather as a structured, mechanism-based diagnostic strategy aimed at defining the underlying coronary endotype. The 2024 ESC Guidelines for chronic coronary syndromes endorse dedicated diagnostic pathways beyond a stenosis-centred paradigm and support the use of invasive coronary function testing (ICFT) in selected patients with persistent symptoms or inconclusive non-invasive findings. An integrated approach combining anatomical assessment (coronary computed tomography angiography or invasive angiography ± pressure-based indices), quantitative perfusion imaging (positron emission tomography or stress cardiovascular magnetic resonance), and ICFT (including coronary flow reserve, microvascular resistance indices, and acetylcholine provocation testing) enables comprehensive characterisation of coronary physiology and vasomotor function. This review proposes a pragmatic framework linking diagnostic findings to targeted therapy through a test-to-endotype-to-therapy paradigm. We summarise the strengths and limitations of each modality, discuss implementation challenges, and highlight the clinical relevance of endotype-driven management. By shifting from a stenosis-centred to a physiology- and mechanism-based approach, this strategy has the potential to close the longstanding gap between diagnosis and treatment in patients with ischaemia beyond obstructive coronary disease. Full article

A significant proportion of patients undergoing invasive coronary angiography for angina have no obstructive coronary artery disease (CAD). In such patients, coronary microvascular dysfunction (CMD) and vasospastic angina (VSA) represent key pathophysiological mechanisms. We report a case of a 58-year-old male with exertional chest pain and exercise ECG changes typical of left main or multivessel CAD. Coronary computed tomography angiography (CCTA) showed borderline stenosis of the distal left main coronary artery. Coronary angiography revealed no critical stenosis. A comprehensive functional assessment demonstrated reduced coronary flow reserve (CFR = 2.0) and an elevated index of microcirculatory resistance (IMR = 25), consistent with CMD. An intracoronary acetylcholine provocation test induced severe focal vasospasm of the mid-left anterior descending artery (LAD) with ST-segment elevation and anginal pain, promptly relieved by nitroglycerin, confirming VSA. This case highlights the diagnostic and clinical importance of invasive functional testing in patients with angina and non-obstructive coronary arteries (ANOCA/INOCA). The coexistence of CMD and VSA (two distinct but overlapping pathophysiological endotypes) is increasingly recognized as a marker of adverse prognosis. Functional coronary assessment should be considered in all patients with angina and non-obstructive coronary arteries, as identifying mixed endotypes enables precise, mechanism-guided therapy. Full article

Coronary artery spasm (CAS) is a common endotype in patients with angina with non-obstructive coronary arteries. Pathophysiologically, the presence of CAS among arteries is not normal, as evidenced by several interacting mechanisms involving CAS development, including the endothelium, vascular smooth muscle cells, adventitia, autonomic nervous system, local inflammation, and systemic inflammation. Clinically, CAS is a dynamic process with a threshold effect on presentation; it can present as silent ischemia, atypical chest pain, resting angina, chronic coronary syndrome, acute coronary syndrome, variant angina, and even sudden cardiac arrest. Incomplete intracoronary provocation testing to exclude CAS as the etiology of chronic or acute coronary syndrome leads to an incorrect diagnosis and, subsequently, inappropriate treatment. Identification of the correct endotypes of chronic and acute coronary syndromes is critical for the selection of appropriate therapy, which thus affects disease outcome. Therefore, it is essential to complete intracoronary provocation testing for both the right and left coronary arteries to reach a correct diagnosis regarding CAS, including epicardial vasospasm and microvascular spasm. If CAS is found not to be the cause of myocardial ischemia, then a microvascular functional assessment is the next step to identify the etiology of the ischemic event. A comprehensive assessment of CAS is essential before appropriate treatments can be started. Full article

Background/Objectives: No-reflow phenomenon (NRP) is a frequent and clinically relevant complication during percutaneous coronary intervention (PCI) of saphenous vein grafts (SVGs). The Naples Prognostic Score (NPS), a composite index reflecting systemic inflammation and nutritional status, may help identify patients at increased risk before the procedure. We investigated whether NPS predicts NRP in patients undergoing PCI/percutaneous transluminal coronary angioplasty (PTCA) for SVG stenosis. Methods: In this retrospective multicenter observational study, consecutive post-coronary artery bypass grafting patients undergoing PCI/PTCA for SVG stenosis were analyzed. NRP was defined as post-procedural thrombolysis in myocardial infarction (TIMI) flow grade <3 in the absence of dissection, residual stenosis, or vasospasm. NPS (0–4) was calculated from serum albumin, total cholesterol, neutrophil-to-lymphocyte ratio, and lymphocyte-to-monocyte ratio. Independent predictors of NRP were assessed using logistic regression, and discrimination was evaluated by receiver operating characteristic (ROC) analysis. Results: Among 252 patients, 55 (21.8%) developed NRP. NPS was significantly higher in the NRP group than in the normal-reflow group (2.61 ± 0.95 vs. 1.73 ± 0.95; p < 0.001). In multivariable analysis, NPS independently predicted NRP (per 1-point increase: odds ratio 2.577, 95% CI 1.428–5.384; p < 0.001 for univariate and 6.077, 95% CI 3.194–11.563; p < 0.001 for multivariate analysis), together with high thrombus burden (TIMI thrombus grades 4–5). NPS showed good discrimination for NRP (AUC 0.742; p < 0.001), with 75% sensitivity and 66% specificity at the optimal cut-off. Conclusions: NPS is a simple, readily available score that independently predicts angiographic no-reflow during SVG PCI and may aid preprocedural risk stratification and tailoring of preventive strategies. Full article

Acute and Chronic Coronary Syndromes represent two major medical challenges and are the leading cause of cardiovascular mortality and morbidity. While Chronic Coronary Syndrome (CCS) can be defined as the whole group of structural and/or functional abnormalities involving coronary arteries before and after an acute event, Acute Coronary Syndrome (ACS) encompasses the condition of acute myocardial ischemia (with or without consequent myocardial injury and troponin release) due to dynamic mechanisms such as athero-thrombosis or vasospasm. Because of this complex interplay between structural and functional mechanisms arising from both the epicardial and microvascular compartments, a comprehensive approach to fully investigate the whole spectrum of coronary disease is therefore essential. To address this issue, the invasive functional assessment has evolved through the years, from a way to guide revascularization to a meticulous protocol for characterizing ischemia-leading mechanisms and stratifying prognosis both in ACS and CCS. However, coronary physiology remains underused in clinical practice, and multiple gaps in knowledge still exist; on top of this, there is increasing heterogeneity regarding how to perform functional assessment, with different protocols proposed by various centers. The aim of this review is to summarize the evidence in the field of coronary physiology, and to discuss how and when to use it at its best. Full article

Background: Thyrotoxicosis is a systemic condition with well-documented cardiovascular effects, but its role as a precipitant of acute coronary syndromes (ACS) is often overlooked. This review summarizes clinical cases and original studies from the last 20 years, describing ACS triggered by thyrotoxicosis. Methods: Following PRISMA 2020 guidelines, we searched PubMed, Scopus, and Embase for reports published between 2004–2025. Only case reports and original articles were included. Data extracted included demographics, ECG findings, angiography results, thyroid function, etiology of hyperthyroidism, and outcomes. Results: A total of 35 cases were identified. The mean age was in the fourth decade of life, with a female predominance (57%, 20 out of 35). More than half of the patients presented with ST-segment elevation myocardial infarction (STEMI) or STEMI equivalents (21 out of 35; 60%). Electrocardiographic abnormalities most often involved anterior or inferior leads. Coronary angiography revealed normal vessels or diffuse vasospasm in 18 cases (51%), while thrombotic occlusion was observed in 4 cases (11%), spontaneous dissection in 2 cases (6%), and myocardial bridging in 3 cases (9%). The leading cause of thyrotoxicosis was Graves’ disease (≈65%), followed by painless thyroiditis, iatrogenic causes, and gestational hyperthyroidism. Thyroid storm was reported in approximately 20% of cases and was associated with malignant ventricular arrhythmias or sudden cardiac death. Conclusions: Thyrotoxicosis should be recognized as a rare but important trigger of ACS, especially in young patients without traditional risk factors. Pathophysiological mechanisms include coronary vasospasm, increased myocardial oxygen demand, and hypercoagulability. Early recognition may prevent unnecessary revascularization and optimize outcomes through integrated endocrine and cardiac management. Full article

Background: Ischemia with no obstructive coronary artery disease (INOCA) is characterized by myocardial ischemia in the absence of significant coronary artery stenosis. Despite the lack of major obstructive lesions, patients often present with chest pain, making diagnosis and management a significant challenge. Materials and Methods: A comprehensive search strategy of electronic databases (2000 to 2024) was used to identify studies assessing pathophysiology, diagnosis, surgical treatments, interventions, and outcomes in INOCA. Clinical trials, observational studies, case-control studies, and cohort studies were included. Results: Emerging surgical treatments may have a role in certain subgroups of INOCA patients, particularly those with severe and persistent symptoms or underlying pathophysiological factors that do not respond adequately to pharmacological therapies. Transmyocardial revascularization (TMR) and sympathetic denervation procedures reduce coronary vasospasm in refractory angina. Trials have shown promise for coronary sinus occlusion. Autologous stem cell therapy is an innovative surgical approach that has shown promise in early trials but remains investigational. Selective surgical cardiac vein retroperfusion remains largely experimental, with limited clinical data. Conclusions: This review highlights the need for ongoing research and clinical trials to assess the effectiveness of surgical and nonsurgical options in INOCA. Although current data on surgical interventions is limited, these treatments may offer hope for patients with refractory symptoms. A personalized and multidisciplinary approach to management is essential for optimal patient outcomes. Full article

Acute myocardial infarction (AMI) in young adults, though less common than in older populations, is an emerging clinical concern with increasing incidence and diverse etiologies. Unlike classic atherosclerotic presentations, a significant proportion of AMI cases in individuals under 45 years are due to nonatherothrombotic mechanisms such as coronary vasospasm, spontaneous coronary artery dissection (SCAD), vasculitis, hypercoagulable states, and drug-induced coronary injury. This manuscript aims to explore the multifactorial nature of AMI in young adults through a focused review of current evidence and a series of illustrative clinical cases. We present and analyze four distinct cases of young patients with AMI, each demonstrating different pathophysiological mechanisms and risk profiles—including premature atherosclerosis, substance use, human immunodeficiency virus (HIV)-related coronary disease, and SCAD. Despite the heterogeneity of underlying causes, early diagnosis, individualized management, and aggressive secondary prevention were key to favorable outcomes. Advanced imaging, lipid profiling, and risk factor modification played a central role in guiding therapy. AMI in young adults requires heightened clinical suspicion and a comprehensive, multidisciplinary approach. Early intervention and recognition of nontraditional risk factors are essential to improving outcomes and preventing recurrent events in this vulnerable population. Full article

Background/Objectives: Donation after circulatory death (DCD) has emerged to expand the heart-donor pool, but many DCD donors have risk factors such as cocaine or methamphetamine use. Stimulant use can cause coronary vasospasm and premature coronary artery disease, leading to routine donor coronary angiography (left heart catheterization, LHC) for coronary screening. However, performing LHC in DCD donors is challenging. We examined whether omitting LHC in stimulant-exposed DCD donors affects outcomes. Methods: A retrospective analysis was performed using the United Network for Organ Sharing (UNOS) database (2019–2024) to identify adult heart transplant recipients from DCD donors with documented cocaine or amphetamine use. Donors were stratified by whether antemortem LHC was performed. The primary outcome was 1-year recipient survival; secondary outcomes included graft failure and acute rejection. Kaplan–Meier survival curves and Cox regression analyses were performed. Results: A total of 485 DCD heart transplant recipients were identified; 135 (28%) donors underwent LHC and 350 (72%) did not. Recipient characteristics were similar between groups. No significant differences in 30-day (6% vs. 3%; p = 0.11), 90-day (6% vs. 3%; p = 0.21), or 1-year survival (7% vs. 6%; p = 0.48) were observed between the LHC and non-LHC cohorts. Graft failure and complication rates were also similar. However, among stimulant-exposed DCD donors with diabetes, an absence of LHC was associated with higher recipient mortality (HR 5.86, 95% CI: 1.57–21.87; p = 0.008). Conclusions: Routine donor coronary angiography may be unnecessary for stimulant-exposed DCD donors without additional risk factors. Omitting LHC did not compromise transplant outcomes. A selective LHC approach for high-risk DCD donors (e.g., diabetic donors) could safely expand the donor pool. Full article

Myocardial infarction with nonobstructive coronary arteries (MINOCA) is an increasingly recognized clinical entity characterized by myocardial injury in the absence of a significant coronary artery obstruction. MINOCA encompasses a diverse range of pathophysiological mechanisms, including coronary plaque disruption, coronary vasospasm, coronary microvascular dysfunction, thromboembolism, and spontaneous coronary artery dissection. A systematic diagnostic approach is essential to identify the underlying etiology and guide appropriate management strategies. Advanced imaging techniques, particularly cardiac magnetic resonance, play a pivotal role in distinguishing ischemic from non-ischemic myocardial injury and refining prognosis. Despite growing awareness, standardized treatment protocols remain limited, with current management largely extrapolated from strategies used in obstructive coronary artery disease. Notably, MINOCA is significantly more prevalent in women, emphasizing the need to understand sex-related differences in its pathophysiology, presentation, and clinical outcomes. This narrative review offers a comprehensive and up-to-date overview of MINOCA, including a dedicated chapter on sex-related considerations. It integrates recent advancements and highlights the importance of personalized management strategies. Full article

Myocardial bridging (MB), a congenital variant where a coronary artery segment is tunneled within the myocardium, is increasingly recognized as a contributor to coronary endothelial and vasomotor dysfunction. Beyond the hallmark systolic compression observed on angiography, MB disrupts endothelial integrity, impairs the release of vasoactive substances, and induces vasomotor abnormalities. These effects exacerbate ischemic symptoms and predispose to atherosclerosis in the proximal segment, particularly in conditions such as ischemia/myocardial infarction with nonobstructive coronary arteries. Recent studies underscore MB’s association with coronary vasospasm, microvascular endothelial dysfunction, and adverse cardiovascular outcomes, including sudden cardiac death. These findings highlight the interplay between MB’s structural anomalies and functional impairments, with factors such as the bridge’s length, depth, and orientation influencing its hemodynamic significance. Advances in imaging and coronary physiology assessment, including acetylcholine testing and stress diastolic fractional flow reserve/iFR/RFR, have enhanced diagnostic precision. This review explores the multifaceted impact of MB on coronary physiology, emphasizing its role in endothelial dysfunction and vasomotor regulation. Recognizing MB’s contribution to cardiovascular disease is essential for accurate diagnosis and tailored management strategies aimed at mitigating ischemic risk and improving patient outcomes. Full article

Kounis syndrome (KS) is a rare condition where hypersensitivity reactions trigger coronary vasospasm, destabilization of atherosclerotic plaques, or stent thrombosis, posing diagnostic and therapeutic challenges due to its overlap with acute coronary syndrome (ACS) and the absence of specific guidelines. This study reviews cases of KS from the Institute of Cardiovascular Disease to highlight clinical presentations, triggers, and treatment strategies. We analyzed four cases of KS treated at our institution between 2019 and 2024. Detailed clinical histories, laboratory findings, imaging studies, and treatment plans were reviewed. Patients were classified by KS subtype based on coronary anatomy and pathophysiological mechanisms. Management strategies were tailored to each subtype, combining myocardial revascularization, antiplatelet therapy, and treatment for allergic reactions. The series included two cases of Type I KS in patients with structurally normal coronary arteries and two cases of Type II KS involving pre-existing atherosclerosis. No Type III KS was observed. Triggers included insect stings, antibiotics, iodinated contrast agents, and anesthetics. Coronary angiography confirmed the diagnosis in all cases. Treatments included percutaneous coronary interventions, dual antiplatelet therapy, and prophylactic antihistamines or corticosteroids. All patients experienced favorable outcomes, although diagnostic delays were noted in cases with atypical presentations. KS remains underdiagnosed, especially in emergency settings where it mimics ACS. Early recognition and multidisciplinary management involving allergology and cardiology are crucial. Future research should focus on safer diagnostic tools, understanding the pathophysiology, and developing evidence-based preventive strategies. Increasing the awareness of KS and its inclusion in ACS differentials are essential to improving patient outcomes and preventing recurrences. Full article

Background: Antineutrophil cytoplasm antibody (ANCA)-associated vasculitis usually affects small blood vessels and is characterized by the presence of circulating autoantibodies (c-ANCA or p-ANCA). The risk of cardiovascular events is threefold higher compared to general population, and cardiac manifestations include myocarditis, pericarditis, valvulitis, aortitis, or coronary arteritis. Coronary involvement is very rare, but it is a potentially life-threatening manifestation. Methods: We present an atypical cardiac scenario of p-ANCA vasculitis. Results: A 68-year-old woman with known p-ANCA vasculitis and stage 5 chronic kidney disease (CKD) on hemodialysis presented with dizziness accompanied by low blood pressure and chest pain. Electrocardiogram on arrival showed slightly ST-T changes, with negative cardiac biomarkers and no abnormalities in cardiac regional wall motion. Five hours after presentation, the patient repeated chest pain, accompanied by a drop in blood pressure and junctional escape rhythm. The highly sensitive cardiac troponin I (hs-cTnI) was raised at 560 ng/L. Coronary angiography showed coronary arteries without significant stenosis. The provocative test with intracoronary ergonovine demonstrated coronary vasospasm of the anterior descending artery accompanied by chest pain, with resolution after intracoronary nitroglycerin. Under amlodipine, nitrate, acetylsalicylic acid, statin and corticosteroids the patient did not experience the recurrence of angina. Conclusions: This case illustrates coronary involvement, manifested as coronary spasm with favorable outcomes, in systemic vasculitis. The underlying mechanism is immune-mediated inflammation in vascular walls. Full article

Coronary aneurysms are typically defined as sections of a coronary artery where the diameter is more than 1.5 times that of an adjacent normal segment. In rare circumstances, these aneurysms can become exceedingly large, leading to the classification of giant coronary artery aneurysms. Despite their occurrence, there is no clear consensus on the precise definition of giant coronary artery aneurysms, and their etiology remains somewhat ambiguous. Numerous potential causes have been suggested, with atherosclerosis being the most prevalent in adults, accounting for up to 50% of cases. In pediatric populations, Kawasaki disease and Takayasu arteritis are the primary causes. Although often discovered incidentally, coronary artery aneurysms can lead to severe complications. These complications include local thrombosis, distal embolization, rupture, and vasospasm, which can result in ischemia, heart failure, and arrhythmias. The optimal approach to medical, interventional, or surgical management of these aneurysms is still under debate and requires further clarification. This literature review aims to consolidate current knowledge regarding coronary artery aneurysms’ pathophysiology, emphasizing their definition, causes, complications, and treatment strategies. Recent research has begun to explore the molecular mechanisms involved in the formation and progression of coronary artery aneurysms. Various molecules, such as matrix metalloproteinases (MMPs), inflammatory cytokines, and growth factors, play crucial roles in the degradation of the extracellular matrix and the remodeling of vascular walls. Elevated levels of MMPs, particularly MMP-9, have been associated with the weakening of the arterial wall, contributing to aneurysm development. Inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukins (IL-1β and IL-6) have been implicated in promoting inflammatory responses that further degrade vascular integrity. Additionally, growth factors such as vascular endothelial growth factor (VEGF) may influence angiogenesis and vascular remodeling processes. Understanding these molecular pathways is essential for developing targeted therapies aimed at preventing the progression of coronary artery aneurysms and improving patient outcomes. Full article