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Background Diagnostic strategies depend on non-standardized workup, and the causes of myocardial infarction with non-obstructive coronary arteries remain unclear for some patients. Intracoronary imaging is recommended for detecting the missed causes by coronary angiography. Myocardial infarction with non-obstructive coronary arteries is a heterogeneous entity; a meta-analysis of myocardial infarction with non-obstructive coronary artery studies demonstrated that all-cause mortality rate at 1 year is 4.7%, and its prognosis is not so favourable. Case summary A 62-year-old man without remarkable medical history complained of acute chest pain at rest, which resolved at his arrival. Although echocardiography and electrocardiogram exhibited normal findings, the concentration of high-sensitive cardiac troponin T increased up to 0.384 from 0.04 ng/mL. Coronary angiography was performed, and mild stenosis of the proximal right coronary artery was detected. He was discharged without catheter intervention and medications as he reported no symptoms. He returned 8 days later because of inferoposterior ST-segment elevation myocardial infarction with ventricular fibrillation. Emergent coronary angiography showed that the mild stenosis of the proximal right coronary artery had progressed to total occlusion. Optical coherence tomography after thrombectomy revealed rupture of the thin-cap fibroatheroma and protruding thrombus. Discussion Patients presenting with myocardial infarction with non-obstructive coronary arteries and plaque disruption and/or thrombus detected by optical coherence tomography do not show normal coronaries on coronary angiography. Aggressive investigation into plaque disruption using intracoronary imaging is recommended even if coronary angiography demonstrates mild stenosis to prevent a fatal attack for suspicious cases of myocardial infarction with non-obstructive coronary arteries. [ABSTRACT FROM AUTHOR]

Vulnerable plaque plays a pivotal role in the pathogenesis of acute coronary syndrome (ACS), being responsible for most ACS. The concept of vulnerable plaque has evolved with advancements in basic and clinical investigations along with developments and rapid expansion of coronary imaging modalities. Intravascular ultrasound (IVUS) is the first widely applied clinical technology with sufficient tissue penetration and enables us to identify vulnerable plaque and comprehensively understand the pathophysiology of ACS. In this review, we summarize current clinical evidence established by IVUS and the recent advancements in our understanding of vulnerable plaque and its role in ACS management. [ABSTRACT FROM AUTHOR]

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• Mechanism for the occurrence of acute myocardial infarction (MI) has not been clarified. • Many silent plaque disruptions are detected in the coronary artery. • Many vulnerable plaques may disrupt and heal without causing acute MI. • Blood thrombogenicity changes dynamically due to many factors. • Blood thrombogenicity increase may directly trigger the onset of acute MI. Although the mechanism for the occurrence of acute myocardial infarction (MI) has been investigated by many pathological and clinical studies, it has not been adequately clarified yet. Although the disruption of vulnerable plaque is a well-known cause of acute MI, there are many silent plaque disruptions detected in the coronary artery by intravascular imaging studies. Therefore, many vulnerable plaques may disrupt and heal without causing acute MI. Some additional mechanisms other than the disruption of vulnerable plaque would be essential for the onset of acute MI. On the other hand, blood thrombogenicity would change dynamically due to circadian rhythms and many other factors. The combination of plaque and blood thrombogenicity would play an important and determinant role for the onset of acute MI. [ABSTRACT FROM AUTHOR]

Background/Aim: Myocardial infarction with non-obstructive coronary arteries (MINOCA) is an increasingly recognized entity. Recent studies have shown that MINOCA is not a benign syndrome, with younger MINOCA patients having outcomes comparable to their myocardial infarction with obstructive coronary artery disease (MI-CAD) counterparts. In this study, we will describe the demographic, clinical and angiographic characteristics of MINOCA patients in our hospital. Methods: In this retrospective cohort study, all patients who underwent coronary angiography with the diagnosis of acute coronary syndrome during September 2016-April 2019 were screened and those with MINOCA were detected. We described the demographic, clinical, and angiographic characteristics of MINOCA patients and compared the etiologic and pathophysiological mechanisms. Results: A total of 3855 patients with acute coronary syndrome were screened and 155 were diagnosed with MINOCA, with a total prevalence of 4.02%. Among them, 48.4% were female and the overall mean age was 55.04 (13.57) years. Plaque disruption was the most common cause of MINOCA (48.4%), which was followed by microvascular dysfunction and slow flow (9.7%). We compared plaque disruption and other causes to find that age (58.31 (13.76) vs 51.89 (12.68) P=0.003), hypertension (37 (48.7%) vs 25 (31.6%) P=0.034), prior coronary artery disease history (16 (21.1%) vs 2 (2.5%) P=0.001) and creatinine clearance (67.35 (IQR: 25.8) vs 74.0 (IQR: 28.58) P=0.009) were higher in patients with plaque disruption than those without. Conclusions: MINOCA is a diagnosis of exclusion with numerous potential causes. The etiological and pathophysiological mechanisms of plaque disruption are different from other causes of MINOCA and the correct treatment approach determines the prognosis. [ABSTRACT FROM AUTHOR]

Purpose of review: Myocardial infarction with non-obstructive coronary arteries (MINOCA) is found in up to 6% of patients presenting with acute coronary syndrome. These patients represent a group with unique pathophysiology and treatment needs. This review summarizes recent advancement in the understanding of the causes and diagnostic work up of patients presenting with MINOCA. Recent findings: Historically the importance of MINOCA has been under-recognized, and the condition was considered a more benign form of acute coronary syndrome. More recently consensus documents from major cardiac societies have highlighted the unique aspects of MINOCA in terms of etiology, diagnosis, and management. Central to this is the understanding that MINOCA should be considered a working diagnosis and prompt detailed investigation into the underlying pathophysiological cause and, where available, the institution of guideline-based medical therapies. Summary: The diagnosis of MINOCA is increasingly being recognized as important both because it identifies a group of patients who differ clinically from those with obstructive coronary artery disease and because it necessitates further diagnostic work up. MINOCA is associated with excess morbidity and mortality, and there is a paucity of data to guide treatment strategies in this heterogeneous group of patients. Further work allows more accurate understanding of risks and optimal management in this population. [ABSTRACT FROM AUTHOR]

Aims: Unstable atherosclerotic plaques have increased activity of myeloperoxidase (MPO). We examined whether molecular magnetic resonance imaging (MRI) of intraplaque MPO activity predicts future atherothrombosis in rabbits and correlates with ruptured human atheroma., Methods and Results: Plaque MPO activity was assessed in vivo in rabbits ( n = 12) using the MPO-gadolinium (Gd) probe at 8 and 12 weeks after induction of atherosclerosis and before pharmacological triggering of atherothrombosis. Excised plaques were used to confirm MPO activity by liquid chromatography-tandem mass spectrometry (LC-MSMS) and to determine MPO distribution by histology. MPO activity was higher in plaques that caused post-trigger atherothrombosis than plaques that did not. Among the in vivo MRI metrics, the plaques' R1 relaxation rate after administration of MPO-Gd was the best predictor of atherothrombosis. MPO activity measured in human carotid endarterectomy specimens ( n = 30) by MPO-Gd-enhanced MRI was correlated with in vivo patient MRI and histological plaque phenotyping, as well as LC-MSMS. MPO-Gd retention measured as the change in R1 relaxation from baseline was significantly greater in histologic and MRI-graded American Heart Association (AHA) type VI than type III-V plaques. This association was confirmed by comparing AHA grade to MPO activity determined by LC-MSMS., Conclusion: We show that elevated intraplaque MPO activity detected by molecular MRI employing MPO-Gd predicts future atherothrombosis in a rabbit model and detects ruptured human atheroma, strengthening the translational potential of this approach to prospectively detect high-risk atherosclerosis., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Introduction: MINOCA is a clinical syndrome that encompasses a subgroup of heterogeneous patients who present with myocardial infarction yet do not have any significant coronary artery obstruction on angiogram. As many as one in ten patients with acute myocardial infarction (AMI) will not have an occluded coronary artery, and the reported prevalence keeps rising, in part due to better recognition of this syndrome. Current guidelines offer several diagnostic algorithms but MINOCA remains largely under-recognised and little is known about whether patients might benefit from a more specific treatment modality. Areas covered: We review pathogenesis, diagnosis, prognosis, and management of MINOCA. Expert commentary: Due to the significant heterogeneity of MINOCA patients, a more efficient management strategy may solely rely on an individualized approach in order to improve outcomes. [ABSTRACT FROM AUTHOR]

Mouse models of atherosclerosis are extensively being used to study the mechanisms of atherosclerotic plaque development and the results are frequently extrapolated to humans. However, major differences have been described between murine and human atherosclerotic lesions and the determination of similarities and differences between these species has been largely addressed recently. This study takes over and extends previous studies performed by our group and related to the biomechanical characterization of both mouse and human atherosclerotic lesions. Its main objective was to determine the distribution and amplitude of mechanical stresses including peak cap stress (PCS) in aortic vessels from atherosclerotic apoE-/- mice, in order to evaluate whether such biomechanical data would be in accordance with the previously suggested lack of plaque rupture in this model. Successful finite element analysis was performed from the zero-stress configuration of aortic arch sections and mainly indicated (1) the modest role of atherosclerotic lesions in the observed increase in residual parietal stresses in apoE-/- mouse vessels and (2) the low amplitude of murine PCS as compared to humans. Overall, the results from the present study support the hypothesis that murine biomechanical properties and artery size confer less propensity to rupture for mouse lesions in comparison with those of humans. [ABSTRACT FROM AUTHOR]

Abstract: Objective: Inflammation and structural factors such as a thin fibrous cap, positive remodeling and large lipid pool have been established as factors associated with coronary plaque instability. This study aimed to investigate the hypothesis that the differential in coronary artery compliance between stenotic and adjacent arterial segments is another factor associated with unstable coronary disease. Methods: Forty-one patients undergoing a percutaneous coronary intervention were classified as unstable coronary syndrome (n =19) or stable angina (n =22). Intravascular ultrasound was used to assess external elastic lamina (EEL) cross-sectional area at diastole and systole. Aortic pressure was determined from the coronary guiding catheter. Coronary cross-sectional compliance (C) was calculated as the quotient of systolic-to-diastolic area differential and pulse pressure. C was measured within the stenosis and the adjacent reference segments. Results: EEL cross-sectional area was greater in systole than in diastole in the reference segments, but did not differ within the lesion site. C was greater in the distal reference than the stenotic segments (7.7±13.1 vs. 0.0±12.3mm2 mmHg−1 ×103, p =0.003). When dichotomized by clinical presentation, the distal-to-stenosis compliance difference was only significant in the unstable coronary syndrome group (stable: distal 4.1±13.3 vs. stenosis –0.3±13.2mm2 mmHg−1 ×103, ANOVA p =0.48; unstable: distal 11.9±11.9 vs. stenosis 0.1±11.6mm2 mmHg−1 ×103, ANOVA p =0.006, distal-to-stenosis difference p =0.001). Conclusions: A difference between stenotic and distal reference segment coronary compliance was evident in unstable, but not stable coronary artery disease patients. Coronary compliance differential would increase cyclical forces in the plaque shoulder region, which may contribute to plaque disruption. [Copyright &y& Elsevier]

Abstract: Background: Autopsy studies have revealed a high incidence of thrombus formation in patients who died of acute myocardial infarction (AMI) or sudden coronary death. However, the incidence of thrombus formation and plaque disruption in patients with non-cardiac death (NCD) remains unclear. Methods: To evaluate the incidence and morphological characteristics of thrombi and plaque disruption in patients with NCD, we examined 102 hearts from NCD autopsy cases and 19 from those who had died of AMI. Results: We found fresh coronary thrombi in 10 cases with NCD and in 14 with AMI (10% vs. 75%, p <0.001). Seven and three thrombi were associated with plaque erosion and rupture, respectively among the NCD cases. The incidence of plaque rupture was significantly higher in AMI than in NCD (54% vs. 3%, p <0.001). The size of coronary thrombi in NCD cases was small and the luminal areas were not significantly affected. Plaques beneath thrombi in NCD had a smaller lipid core and a thicker fibrous cap than those in AMI. Among risk factors for cardiovascular events, hypertension and diabetes mellitus were significantly associated with the incidence of thrombosis in patients with NCD. Conclusion: Coronary thrombosis is a frequent complication in patients with NCD. These small thrombi might not be associated with the onset of clinical events, but with plaque progression in atherosclerosis. [Copyright &y& Elsevier]

Abstract: Background: The balance between degradation and synthesis of extracellular matrix determines its content in atherosclerotic tissue. To examine the role of expression balance of matrix metalloproteinases (MMPs) to their inhibitors, tissue inhibitors of metalloproteinases (TIMPs) and tissue factor pathway inhibitor-2 (TFPI-2) in the development and disruption of atherosclerotic plaque, these gene expressions in human carotid plaque were quantitatively determined by real-time reverse transcription (RT)-polymerase chain reaction (PCR) method. Methods: Total RNA for cDNA synthesis was extracted from tissues in 24 patients with carotid endarterectomy. The amounts of cDNAs for MMP-1, -2, -3 and -9, TFPI-2 and TIMP-1, -2 and -3 were determined by real-time RT-PCR method, and normalized with glutaraldehyde 3-dehydrogenase. Results: In plaques, the expression MMP-1 (1.53±0.25, mean±S.E.M.), MMP-3 (1.99±0.59) and MMP-9 (2.00±0.51) was augmented compared to those in the adjacent control regions (0.60±0.16, 0.46±0.18 and 0.58±0.21, respectively, p <0.05). The expression of TFPI-2 was lower in plaques (0.32±0.08) than in controls (0.94±0.23, p <0.01). Although the expression of TIMP-1 was higher in plaques (1.28±0.23) than in controls (0.81±0.10, p <0.05), the indices of MMP-1/TIMP-1, MMP-3/TIMP-3 and MMP-9/TIMP-1 were still significantly higher in plaques. Interestingly, MMP-9 and the resulting MMP-9/TIMP-1 balance in plaques with disruption were significantly higher (3.36±1.52 and 1.66±0.12, n =11) than those in non-disrupted plaques (1.11±0.52 and 0.76±0.12, n =13, p <0.05). Conclusion: With the decreased expression of TFPI-2, upregulation of MMPs in atherosclerotic plaque was disproportional to that of TIMPs, suggesting that imbalanced degradation and synthesis of extracellular matrix persists in advanced lesions, particularly in plaques with disruption. [Copyright &y& Elsevier]

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Objective: To determine the role of healed plaque disruption in the generation of chronic high grade coronary stenosis.Methods: Coronary arteries obtained at necropsy were perfuse fixed with formal saline for 24 hours at 100 mg Hg. The percentage lumen diameter stenosis was measured in each 3 mm segment containing a plaque, using the lumen size at the nearest histologically normal segment as the reference point. Each segment was prepared for histological examination and stained with Sirius red and immunohistochemistry for smooth muscle actin. Healed disruption was considered to be present when under polarised light there was a break in the yellow-white dense collagen of the cap filled in by more loosely arranged green collagen. Increased smooth muscle density in the green staining areas was required. Each section was read independently by two observers; any segment with discordant views was considered negative.Material: 31 men aged 51-69 dying suddenly of ischaemic heart disease. 39 coronary arteries were studied containing 256 separate plaques, after excluding coronary arteries with old total occlusions, an acute culprit thrombotic lesion, diffuse disease without normal arterial segments, and arteries related to old myocardial scars.Results: 16 of 99 plaques causing < 20% diameter stenosis had prior disruption. In the 21-50% stenosis range 16 of 86 plaques showed healed disruption. Stenosis >/= 51% by diameter was present in 71 plaques, 52 of which showed a healed disruption pattern. The difference between stenosis < 50% and stenosis >/= 51% was significant by the chi(2) test (p < 0.001).Conclusions: Subclinical episodes of plaque disruption followed by healing are a stimulus to plaque growth that occurs suddenly and is a major factor in causing chronic high grade coronary stenosis. This mechanism would explain the phasic rather than linear progression of coronary disease observed in angiograms carried out annually in patients with chronic ischaemic heart disease. [ABSTRACT FROM AUTHOR]

Numerous pathological, clinical, angiographic and angioscopic studies have demon-strated that acute coronary syndromes (unstable angina, acute myocardial infarction and is-chemic sudden death) are most frequently the consequence of plaque disruption (plaque rup-ture or superficial plaque erosion) and consequent coronary thrombosis. Several serial angiographic studies have demonstrated that nearly 60–70% of acute coronary syndromes evolve from mildly to moderately obstructive atherosclerotic plaques. Coronary plaque disruption appears to be a function of both the composition of the plaque (plaque vulnerability ) as well as extrinsic triggers that may precipitate plaque disruption in a vulnerable plaque. Vulner-ability for plaque disruption appears to be largely determined by the size of the lipid-rich atheromatous core, the thickness of the fibrous cap covering the core, and the presence of ongoing inflammation within and underneath the cap. Inflammatory cells may play a critical role in plaque disruption through the elaboration of matrix degrading metalloproteinases or MMPs (collagenases, gelatinases, stromelysins and matrilysin) and by inhibition of function and survival of matrix-synthesizing smooth muscle cells. Inflammatory cells may also play a critical role in triggering thrombosis following plaque disruption through the tissue factor pathway. In addition, stresses resulting from hemodynamic and mechanical forces may precipitate plaque disruption, particularly at points where the fibrous cap is weakest, such as at its shoulders. The degree of thrombosis following plaque disruption is determined by the thrombogenicity of the disrupted plaque, disturbed local rheology and systemic thrombotic-thrombolytic milieu. Surges in sympathetic activity provoked by sudden vigorous exercise, emotional stress – including anger, or cold weather, may also trigger plaque disruption. These observations have led to the concept of plaque stabilization as a new clinical strategy for the prevention of acute coronary syndromes. Plaque stabilization can be achieved through pharmacologic and lifestyle-modifying interventions that reduce vulnerability to plaque disruption by altering plaque composition and/or inflammatory activity within the plaque. [ABSTRACT FROM AUTHOR]

A major factor invoking coronary thrombosis is disruption of an atherosclerotic plaque. Studies comparing intact and disrupted plaques have been used to define the characteristics of vulnerable plaques i.e. those at risk of disruption. The characteristics are a lipid core occupying over 50% of overall plaque volume, a thin plaque cap, a large absolute number and density of macrophages, and a reduction in the smooth muscle content of the plaque. Such vulnerable plaques make up a small proportion of all the plaques present in most individuals. Angiographic stenosis, however, does not predict vulnerability because there is no relation between core size or plaque size with stenosis A large proportion of disruption episodes go unnoticed clinically because the thrombus does not sufficiently encroach on the lumen to cause ischaemia These subclinical episodes, however, will invoke plaque growth. Plaque disruption is followed by a smooth muscle proliferative repair response analogous to that occurring after angioplasty. In both situations exuberant repair leads to post event stenosis Reconstruction of coronary lesions at autopsy shows that 70% of high grade stenosis (angiographic >50% diameter) have had an episode of healed disruption. Such data highlight the role of plaque disruption in the generation of advanced stenotic lesions irrespective of whether an acute clinical event occurred. Any therapeutic intervention which increases plaque stability, i.e. resistance to disruption, would reduce the acute ischaemic event rate but also slow the generation of new high grade stenoses. [ABSTRACT FROM PUBLISHER]