RESUMEN
As the important factors in coronary artery thrombosis, endothelial injury and M1 macrophage polarization are closely related to the expression of miR-34a-5p. Exosomes in plasma are mainly derived from platelets and play an important role in thrombosis. Based on these facts, this study was conducted to investigate the acting mechanism of platelet-derived exosomes (PLT-exo) in the effects of endothelial injury and M1 macrophage polarization on coronary artery thrombosis. Firstly, rats were divided into the sham-operated group and the coronary microembolization (CME) group, and their plasma-derived exosomes were extracted to detect the expression of miR-34a-5p. Next, the PLT-exo were extracted from healthy volunteers and then co-cultured with ox-LDL-induced endothelial cells and LPS-induced macrophages, respectively. Subsequently, the expression of IL-1ß, IL-6, TNF-α, and ICAM-1 in endothelial cells was measured, and the level of markers related to M1 macrophage polarization and Sirt1/NF-κB pathway was detected. Finally, the above indicators were examined again after PLT-exo combined with miR-34a-5p mimic were co-cultured with endothelial cells and macrophages, respectively. The results demonstrated that the expression of miR-34a-5p in the CME group was up-regulated compared with the sham-operated group. In cell experiments, PLT-exo modulated the Sirt1/NF-κB pathway by inhibiting the expression of intracellular miR-34a-5p and down-regulated the expression of IL-1ß, IL-6, TNF-α, and ICAM-1 in endothelial cells and M1 macrophage polarization. After the transfection with miR-34a-5p mimic, endothelial cell inflammatory injury and M1 macrophage polarization increased to varying degrees. In conclusion, PLT-exo can alleviate coronary artery thrombosis by reducing endothelial cell inflammation and M1 macrophage polarization via inhibiting miR-34a-5p expression. In contrast, miR-34a-5p overexpression in PLT-exo may exacerbate these pathological injuries in coronary artery thrombosis.
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Plaquetas , Células Endoteliales , Exosomas , Inflamación , Macrófagos , MicroARNs , MicroARNs/genética , MicroARNs/metabolismo , Exosomas/metabolismo , Animales , Macrófagos/metabolismo , Humanos , Plaquetas/metabolismo , Ratas , Inflamación/metabolismo , Inflamación/genética , Inflamación/patología , Masculino , Células Endoteliales/metabolismo , Trombosis Coronaria/metabolismo , Trombosis Coronaria/genética , Trombosis Coronaria/patología , Técnicas de Cocultivo , Ratas Sprague-DawleyRESUMEN
The precise features of lesions in non-ST-segment elevation myocardial infarction (NSTEMI) patients with total occlusion (TO) of the infarct-related artery (IRA) are still unclear. This study employs optical coherence tomography (OCT) to investigate pathological features in NSTEMI patients with or without IRA TO and explores the relationship between thrombus types and IRA occlusive status. This was a single-center retrospective study. A total of 202 patients diagnosed with NSTEMI were divided into two groups: those with Thrombolysis In Myocardial Infarction (TIMI) flow grade 0 before percutaneous coronary intervention (PCI) (referred to as the TO group, n = 100) and those TIMI flow grade 1-3 (referred to as the Non-TO group, n = 102). Baseline characteristics, coronary angiography findings, and OCT results were collected. Multivariate logistic analysis identified factors influencing TO in NSTEMI. The category of NSTEMI was further subdivided based on the type of electrocardiogram (ECG) into two subgroups: ST segment unoffset myocardial infarction (STUMI) and ST segment depression myocardial infarction (STDMI). This division allows for a more specific classification of NSTEMI cases. The TO group had a younger age, higher male representation, more smokers, lower hypertension and cerebrovascular disease incidence, lower left ventricular ejection fraction (LVEF), and higher creatine kinase myocardial band (CKMB) and creatine kinase (CK) peak levels. In the TO group, LCX served as the main IRA (52.0%), whereas in the Non-TO group, LAD was the predominant IRA (45.1%). Compared to the Non-TO group, OCT findings demonstrated that red thrombus/mixed thrombus was more common in the TO group, along with a lower occurrence of white thrombus (p < 0.001). The TO group exhibited a higher prevalence of STUMI (p = 0.001), whereas STDMI was more commonly observed in the Non-TO group (p = 0.001). NSTEMI presents as STUMI and STDMI distinct entities. Red thrombus/mixed thrombus in IRA often indicates occlusive lesions with STUMI on ECG. White thrombus suggests non-occlusive lesions with STDMI on ECG.
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Angiografía Coronaria , Trombosis Coronaria , Vasos Coronarios , Electrocardiografía , Infarto del Miocardio sin Elevación del ST , Intervención Coronaria Percutánea , Valor Predictivo de las Pruebas , Tomografía de Coherencia Óptica , Humanos , Masculino , Femenino , Estudios Retrospectivos , Persona de Mediana Edad , Infarto del Miocardio sin Elevación del ST/diagnóstico por imagen , Infarto del Miocardio sin Elevación del ST/terapia , Anciano , Trombosis Coronaria/diagnóstico por imagen , Trombosis Coronaria/patología , Factores de Riesgo , Vasos Coronarios/diagnóstico por imagen , Vasos Coronarios/fisiopatología , Análisis Multivariante , Modelos Logísticos , Oclusión Coronaria/diagnóstico por imagen , Oclusión Coronaria/fisiopatología , Circulación Coronaria , Distribución de Chi-Cuadrado , Oportunidad RelativaRESUMEN
Important forensic diagnostic indicators of sudden death in coronary atherosclerotic heart disease, such as acute or chronic myocardial ischemic changes, sometimes make it difficult to locate the ischemic site due to the short death process, the lack of tissue reaction time. In some cases, the deceased died of sudden death on the first-episode, resulting in difficulty for medical examiners to make an accurate diagnosis. However, clinical studies on coronary instability plaque revealed the key role of coronary spasm and thrombosis caused by their lesions in sudden coronary death process. This paper mainly summarizes the pathological characteristics of unstable coronary plaque based on clinical medical research, including plaque rupture, plaque erosion and calcified nodules, as well as the influencing factors leading to plaque instability, and briefly describes the research progress and technique of the atherosclerotic plaques, in order to improve the study on the mechanism of sudden coronary death and improve the accuracy of the forensic diagnosis of sudden coronary death by diagnosing different pathologic states of coronary atherosclerotic plaques.
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Enfermedad de la Arteria Coronaria , Trombosis Coronaria , Placa Aterosclerótica , Humanos , Placa Aterosclerótica/complicaciones , Placa Aterosclerótica/patología , Trombosis Coronaria/complicaciones , Trombosis Coronaria/patología , Factores de Riesgo , Enfermedad de la Arteria Coronaria/complicaciones , Muerte Súbita Cardíaca/etiología , Muerte Súbita Cardíaca/patología , Vasos Coronarios/diagnóstico por imagen , Vasos Coronarios/patologíaRESUMEN
Coronary artery disease (CAD) remains the leading cause of death in the Western world in individuals >20 years of age. CAD is the most common substrate underlying sudden cardiac death (SCD) in the Western world, being responsible for 50-75% of SCDs. In individuals dying suddenly with coronary thrombosis, plaque rupture occurs in 65%, plaque erosion in 30% and calcified nodule in 5%. We evaluated the extent of calcification in radiographs of hearts from patients dying of SCD and showed that calcification is absent in nearly 50% of erosion cases whereas only 10% of plaque rupture show no calcification. Conversely, stable plaques with >75% cross-sectional area luminal narrowing show the severest calcification (moderate to severe) in nearly 50% of cases. Identifying individuals who are susceptible to atherosclerosis may help reduce the incidence of SCD. The identification of coronary calcifications by noninvasive tools, however, only captures a fraction of complicating coronary lesions.
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Enfermedad de la Arteria Coronaria , Trombosis Coronaria , Placa Aterosclerótica , Humanos , Vasos Coronarios/diagnóstico por imagen , Vasos Coronarios/patología , Placa Aterosclerótica/patología , Enfermedad de la Arteria Coronaria/patología , Trombosis Coronaria/complicaciones , Trombosis Coronaria/patología , Muerte Súbita Cardíaca/etiología , Muerte Súbita Cardíaca/prevención & control , Muerte Súbita Cardíaca/epidemiología , Factores de RiesgoRESUMEN
BACKGROUND: Chronic total occlusion (CTO) is a high-risk factor for stent thrombosis, but little is known about the difference in neointimal healing between CTO and non-CTO lesions regarding implanted stents. We investigated factors affecting neointimal healing after stent implantation for CTO and non-CTO lesions using angioscopy. METHODS: We retrospectively evaluated 106 stents in 85 consecutive patients between March 2016 and July 2020. Their average age was 68⯱â¯11â¯years, and participants (73 male and 12 female) underwent follow-up angiography and angioscopy 1â¯year after percutaneous coronary intervention (PCI). The stents (nâ¯=â¯106) were divided into three groups according to the lesion status at the previous PCI: CTO (nâ¯=â¯17), acute coronary syndrome (ACS) (nâ¯=â¯35), and stable coronary artery disease without CTO or non-CTO (nâ¯=â¯54). RESULTS: The neointimal stent coverage grade was significantly lower in the CTO and ACS groups than in the non-CTO group (0.4⯱â¯0.5, 0.9⯱â¯0.8, and 1.4⯱â¯0.8, respectively, pâ¯<â¯0.001). Thrombi were significantly more frequent in CTO and ACS than in non-CTO (71â¯%, 51â¯%, and 15â¯%, respectively, pâ¯<â¯0.001). The yellow grade in CTO was comparable to that in ACS but significantly higher in CTO than in non-CTO (CTO vs. ACS vs. non-CTO 1.5⯱â¯0.7, 1.4⯱â¯0.6, and 0.9⯱â¯0.7, respectively, pâ¯=â¯0.007). CONCLUSIONS: Delayed healing occurs in stents implanted for CTO lesions. Longer dual-antithrombotic therapy may be beneficial.
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Oclusión Coronaria , Trombosis Coronaria , Intervención Coronaria Percutánea , Humanos , Masculino , Femenino , Persona de Mediana Edad , Anciano , Intervención Coronaria Percutánea/efectos adversos , Angioscopía , Trombosis Coronaria/patología , Estudios Retrospectivos , Angiografía Coronaria/efectos adversos , Neointima , Resultado del Tratamiento , Oclusión Coronaria/diagnóstico por imagen , Oclusión Coronaria/terapia , Enfermedad CrónicaRESUMEN
We describe the internal structure, spatial organization and dynamic formation of coronary artery thrombi from ST-segment elevation myocardial infarction patients. Scanning electron microscopy (SEM) revealed significant differences among four groups of patients (<2 hours; 2-6 hours; 6-12 hours, and >12 hours) related to the time of ischemia. Coronary artery thrombi from patients presenting less than 2 hours after the infarction were almost entirely composed of platelets, with small amounts of fibrin and red blood cells. In contrast, thrombi from late presenters (>12 hours) consisted of mainly platelets at the distal end, where clotting was initiated, with almost no platelets at the proximal end, while the red blood cell content went from low at the initiating end to more than 90% at the proximal end. Furthermore, fibrin was present mainly on the outside of the thrombi and older thrombi contained thicker fibers. The red blood cells in late thrombi were compressed to a close-packed, tessellated array of polyhedral structures, called polyhedrocytes. Moreover, there was redistribution from the originally homogeneous composition to fibrin and platelets to the outside, with polyhedrocytes on the interior. The presence of polyhedrocytes and the redistribution of components are signs of in vivo clot contraction (or retraction). These results suggest why later thrombi are resistant to fibrinolytic agents and other treatment modalities, since the close-packed polyhedrocytes form a nearly impermeable seal. Furthermore, it is of particular clinical significance that these findings suggest specific disparate therapies that will be most effective at different stages of thrombus development.
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Plaquetas/patología , Trombosis Coronaria , Eritrocitos/patología , Fibrina/análisis , Fibrinolíticos , Infarto del Miocardio con Elevación del ST , Coagulación Sanguínea/efectos de los fármacos , Coagulación Sanguínea/fisiología , Trombosis Coronaria/diagnóstico por imagen , Trombosis Coronaria/tratamiento farmacológico , Trombosis Coronaria/metabolismo , Trombosis Coronaria/patología , Resistencia a Medicamentos/fisiología , Femenino , Fibrinolíticos/administración & dosificación , Fibrinolíticos/efectos adversos , Humanos , Masculino , Microscopía Electrónica de Rastreo/métodos , Persona de Mediana Edad , Infarto del Miocardio con Elevación del ST/etiología , Infarto del Miocardio con Elevación del ST/terapia , Trombectomía/métodos , Factores de Tiempo , Tiempo de TratamientoRESUMEN
Cardiovascular disease, including myocardial infarction (MI), is the leading cause of death globally. Current antithrombotic medications used during MI treatment are predominantly directed towards platelet inhibition and, to a lesser extent, anticoagulation. Bleeding is a major risk of such treatment and could be circumvented by targeting other causative factors essential for arterial thrombus formation. We sought to re-evaluate the cellular composition of arterial thrombus in order to better understand mechanisms that lead to coronary artery thrombosis in acute MI. We performed detailed histological and immunohistochemical analysis of coronary artery thrombi aspirated from 26 patients undergoing emergency percutaneous coronary intervention for acute ST elevated myocardial infarction (STEMI). Coronary arterial thrombi had an unanticipated cellular heterogeneity. Neutrophil extracellular traps (NETs) were observed in thrombi as identified by anti-citrullinated histone 3 and anti-myeloperoxidase staining. Increased abundance of NETs was seen directly surrounding erythrocytes. Extracellular iron and erythrocyte fragments were also associated with areas of NETs suggesting a possible link. Our results shed light on potential involvement of erythrocytes in coronary arterial thrombosis through activation of platelets and induction of NETs. If supported by further in vitro and in vivo studies, novel therapies to inhibit NET formation or coagulation activation by erythrocyte release products, could bolster current myocardial infarction treatment.
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Trombosis Coronaria , Eritrocitos , Trampas Extracelulares , Infarto del Miocardio/complicaciones , Neutrófilos/patología , Anciano , Coagulación Sanguínea , Plaquetas/patología , Trombosis Coronaria/etiología , Trombosis Coronaria/patología , Vasos Coronarios/patología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Infarto del Miocardio/patologíaRESUMEN
[Figure: see text].
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Apolipoproteína L1/genética , Negro o Afroamericano/genética , Enfermedad de la Arteria Coronaria/genética , Trombosis Coronaria/genética , Variación Genética , Placa Aterosclerótica , Adulto , Autopsia , Causas de Muerte , Enfermedad de la Arteria Coronaria/etnología , Enfermedad de la Arteria Coronaria/mortalidad , Enfermedad de la Arteria Coronaria/patología , Trombosis Coronaria/etnología , Trombosis Coronaria/mortalidad , Trombosis Coronaria/patología , Muerte Súbita Cardíaca/etnología , Muerte Súbita Cardíaca/patología , Femenino , Estudios de Asociación Genética , Predisposición Genética a la Enfermedad , Haplotipos , Humanos , Masculino , Maryland/epidemiología , Persona de Mediana Edad , Necrosis , Fenotipo , Sistema de Registros , Medición de Riesgo , Factores de Riesgo , Rotura EspontáneaRESUMEN
ABSTRACT: Percutaneous coronary intervention has become the main revascularization strategy for coronary artery disease. Compared with early percutaneous coronary angioplasty and the extensive clinical application of bare metal stents, drug-eluting stents can significantly reduce the stenosis caused by the elastic retraction of plaque and neoatherosclerosis (NA), but there is still a high incidence of in-stent restenosis (ISR), which restricts the clinical efficacy of stent implantation. In-stent neoatherosclerosis (ISNA), defined as atherosclerotic lesions in the neointima, is one of the main causes of late stent failure. ISNA plays an important role in stent thrombosis and ISR. The rate of target lesion revascularization and in-stent thrombosis is high when NA arises. Therefore, it is of great clinical significance to explore the occurrence of NA and its development mechanism after stent implantation to prevent ISR and improve stent implantation efficacy and associated clinical prognosis. In this article, we systematically reviewed the existing clinical research on ISNA and the role of optical coherence tomography in its evaluation.
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Enfermedad de la Arteria Coronaria/terapia , Reestenosis Coronaria/etiología , Trombosis Coronaria/etiología , Vasos Coronarios/patología , Neointima , Intervención Coronaria Percutánea/instrumentación , Placa Aterosclerótica , Stents , Animales , Reestenosis Coronaria/diagnóstico por imagen , Reestenosis Coronaria/patología , Trombosis Coronaria/diagnóstico por imagen , Trombosis Coronaria/patología , Vasos Coronarios/diagnóstico por imagen , Stents Liberadores de Fármacos , Humanos , Intervención Coronaria Percutánea/efectos adversos , Valor Predictivo de las Pruebas , Factores de Riesgo , Tomografía de Coherencia Óptica , Resultado del TratamientoRESUMEN
BACKGROUND: Calcified nodule (CN) has a unique plaque morphology, in which an area of nodular calcification causes disruption of the fibrous cap with overlying luminal thrombus. CN is reported to be the least frequent cause of acute coronary thrombosis, and the pathogenesis of CN has not been well studied. OBJECTIVES: The purpose of this study is to provide a comprehensive morphologic assessment of the CN in addition to providing an evolutionary perspective as to how CN causes acute coronary thrombosis in patients with acute coronary syndromes. METHODS: A total of 26 consecutive CN lesions from 25 subjects from our autopsy registry were evaluated. Detailed morphometric analysis was performed to understand the plaque characteristics of CN and nodular calcification. RESULTS: The mean age was 70 years, with a high prevalence of diabetes and chronic kidney disease. CNs were equally distributed between men and women, with 61.5% of CNs found in the right coronary artery (n = 16), mainly within its mid-portion (56%). All CNs demonstrated surface nonocclusive luminal thrombus, consisting of multiple nodular fragments of calcification, protruding and disrupting the overlying fibrous cap, with evidence of endothelial cell loss. The degree of circumferential sheet calcification was significantly less in the culprit section (89° [interquartile range: 54° to 177°]) than in the adjacent proximal (206° [interquartile range: 157° to 269°], p = 0.0034) and distal (240° [interquartile range: 178° to 333°], p = 0.0004) sections. Polarized picrosirius red staining showed the presence of necrotic core calcium at culprit sites of CNs, whereas collagen calcium was more prevalent at the proximal and distal regions of CNs. CONCLUSIONS: Our study suggests that fibrous cap disruption in CN with overlying thrombosis is initiated through the fragmentation of necrotic core calcifications, which is flanked-proximally and distally-by hard, collagen-rich calcification in coronary arteries, which are susceptible to mechanical stress.
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Síndrome Coronario Agudo/complicaciones , Trombosis Coronaria/etiología , Vasos Coronarios/patología , Muerte Súbita Cardíaca/etiología , Calcificación Vascular/complicaciones , Síndrome Coronario Agudo/diagnóstico por imagen , Anciano , Anciano de 80 o más Años , Trombosis Coronaria/patología , Vasos Coronarios/diagnóstico por imagen , Muerte Súbita Cardíaca/patología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Calcificación Vascular/diagnóstico por imagen , Calcificación Vascular/patología , Microtomografía por Rayos XRESUMEN
Coronary ectasia is a rare vessel defect that represents a pathological and incidental finding in routine coronary angiography performed for other coronary syndromes. This defect exposes to the risk of intra-coronary thrombosis by blood stasis due to the turbulent blood flow in those dilated areas that can lead to sudden death. We report an autopsy case of a male subject suddenly deceased. A medico-legal autopsy concluded an ischemic heart failure due to a vascular thrombosis by a blood clot in a coronary ectasia. Our case report aimed to discuss the mechanisms of sudden death attributed to coronary artery ectasia.
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Vasos Coronarios/patología , Muerte Súbita Cardíaca/etiología , Dilatación Patológica/patología , Adulto , Colágeno/metabolismo , Trombosis Coronaria/patología , Humanos , Masculino , Miocardio/patología , Edema Pulmonar/patología , Túnica Media/metabolismo , Túnica Media/patologíaRESUMEN
BACKGROUND: Cardiac injury is common in patients who are hospitalized with coronavirus disease 2019 (COVID-19) and portends poorer prognosis. However, the mechanism and the type of myocardial damage associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain uncertain. METHODS: We conducted a systematic pathological analysis of 40 hearts from hospitalized patients dying of COVID-19 in Bergamo, Italy, to determine the pathological mechanisms of cardiac injury. We divided the hearts according to presence or absence of acute myocyte necrosis and then determined the underlying mechanisms of cardiac injury. RESULTS: Of the 40 hearts examined, 14 (35%) had evidence of myocyte necrosis, predominantly of the left ventricle. Compared with subjects without necrosis, subjects with necrosis tended to be female, have chronic kidney disease, and have shorter symptom onset to admission. The incidence of severe coronary artery disease (ie, >75% cross-sectional narrowing) was not significantly different between those with and without necrosis. Three of 14 (21.4%) subjects with myocyte necrosis showed evidence of acute myocardial infarction, defined as ≥1 cm2 area of necrosis, whereas 11 of 14 (78.6%) showed evidence of focal (>20 necrotic myocytes with an area of ≥0.05 mm2 but <1 cm2) myocyte necrosis. Cardiac thrombi were present in 11 of 14 (78.6%) cases with necrosis, with 2 of 14 (14.2%) having epicardial coronary artery thrombi, whereas 9 of 14 (64.3%) had microthrombi in myocardial capillaries, arterioles, and small muscular arteries. We compared cardiac microthrombi from COVID-19-positive autopsy cases to intramyocardial thromboemboli from COVID-19 cases as well as to aspirated thrombi obtained during primary percutaneous coronary intervention from uninfected and COVID-19-infected patients presenting with ST-segment-elevation myocardial infarction. Microthrombi had significantly greater fibrin and terminal complement C5b-9 immunostaining compared with intramyocardial thromboemboli from COVID-19-negative subjects and with aspirated thrombi. There were no significant differences between the constituents of thrombi aspirated from COVID-19-positive and -negative patients with ST-segment-elevation myocardial infarction. CONCLUSIONS: The most common pathological cause of myocyte necrosis was microthrombi. Microthrombi were different in composition from intramyocardial thromboemboli from COVID-19-negative subjects and from coronary thrombi retrieved from COVID-19-positive and -negative patients with ST-segment-elevation myocardial infarction. Tailored antithrombotic strategies may be useful to counteract the cardiac effects of COVID-19 infection.
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COVID-19/virología , Trombosis Coronaria/etiología , Infarto del Miocardio , Miocardio/patología , Anciano , COVID-19/patología , Trombosis Coronaria/patología , Trombosis Coronaria/virología , Vasos Coronarios/patología , Vasos Coronarios/virología , Femenino , Corazón/virología , Humanos , Italia , Masculino , Persona de Mediana Edad , Infarto del Miocardio/patología , Infarto del Miocardio/virología , SARS-CoV-2 , Infarto del Miocardio con Elevación del ST/epidemiología , Infarto del Miocardio con Elevación del ST/virologíaRESUMEN
ABSTRACT: The 2019 novel coronavirus disease (COVID-19) has spread worldwide, infiltrating, infecting, and devastating communities in all locations of varying demographics. An overwhelming majority of published literature on the pathologic findings associated with COVID-19 is either from living clinical cohorts or from autopsy findings of those who died in a medical care setting, which can confound pure disease pathology. A relatively low initial infection rate paired with a high biosafety level enabled the New Mexico Office of the Medical Investigator to conduct full autopsy examinations on suspected COVID-19-related deaths. Full autopsy examination on the first 20 severe acute respiratory syndrome coronavirus 2-positive decedents revealed that some extent of diffuse alveolar damage in every death due to COVID-19 played some role. The average decedent was middle-aged, male, American Indian, and overweight with comorbidities that included diabetes, ethanolism, and atherosclerotic and/or hypertensive cardiovascular disease. Macroscopic thrombotic events were seen in 35% of cases consisting of pulmonary thromboemboli and coronary artery thrombi. In 2 cases, severe bacterial coinfections were seen in the lungs. Those determined to die with but not of severe acute respiratory syndrome coronavirus 2 infection had unremarkable lung findings.
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COVID-19/mortalidad , Pulmón/patología , Adulto , Distribución por Edad , Anciano , Anciano de 80 o más Años , Autopsia , Índice de Masa Corporal , Edema Encefálico/patología , Cardiomegalia/patología , Comorbilidad , Trombosis Coronaria/patología , Bases de Datos Factuales , Hígado Graso/patología , Femenino , Patologia Forense , Glomeruloesclerosis Focal y Segmentaria/patología , Hepatomegalia/patología , Humanos , Pulmón/diagnóstico por imagen , Masculino , Persona de Mediana Edad , Nefroesclerosis/patología , New Mexico/epidemiología , Sobrepeso/epidemiología , Pandemias , Derrame Pleural/diagnóstico por imagen , Derrame Pleural/patología , Edema Pulmonar/diagnóstico por imagen , Edema Pulmonar/patología , Distribución por Sexo , Streptococcus pneumoniae/aislamiento & purificación , Tomografía Computarizada por Rayos X , Cuerpo Vítreo/química , Imagen de Cuerpo EnteroRESUMEN
BACKGROUND: Microbial translocation from inflamed periodontal pockets into coronary atheroma via systemic circulation is one of the proposed pathways that links periodontitis and myocardial infarction (MI). The purpose of this systematic review is to determine the reported prevalence of periodontal microorganisms in coronary atheroma and/or aspirated clot samples collected from MI patients with periodontal disease. METHODOLOGY: The "Preferred Reporting Items for Systematic Reviews and Meta-Analyses" (PRISMA) guidelines were followed. Six databases were systematically searched using Medical Subject Headings/Index and Entree terms. After a thorough screening, fourteen publications spanning over ten years (2007-2017) were eligible for this systematic review and meta-analysis. RESULTS: Out of 14 included studies, 12 reported presence of periodontal bacterial DNA in coronary atherosclerotic plaque specimens. Overall, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans were the most frequently detected periodontal bacterial species. Meta-analysis revealed that the prevalence of P. gingivalis was significantly higher than A. actinomycetemcomitans in coronary atheromatous plaque samples. Apart from periodontal microbes, DNA from a variety of other microbes e.g. Pseudomonas fluorescens, Streptococcus species, Chlamydia pneumoniae were also recovered from the collected samples. CONCLUSION: Consistent detection of periodontal bacterial DNA in coronary atheroma suggests their systemic dissemination from periodontal sites. It should further be investigated whether they are merely bystanders or induce any structural changes within coronary arterial walls.
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Bacterias/aislamiento & purificación , Enfermedad de la Arteria Coronaria/microbiología , Trombosis Coronaria/microbiología , Infarto del Miocardio/microbiología , Enfermedades Periodontales/microbiología , Periodoncio/microbiología , Placa Aterosclerótica , Bacterias/clasificación , Bacterias/genética , Enfermedad de la Arteria Coronaria/epidemiología , Enfermedad de la Arteria Coronaria/patología , Trombosis Coronaria/epidemiología , Trombosis Coronaria/patología , Humanos , Infarto del Miocardio/epidemiología , Infarto del Miocardio/patología , Enfermedades Periodontales/epidemiología , Factores de RiesgoRESUMEN
While the advent of drug-eluting stents has been clinically effective in substantially reducing the rates of major stent-related adverse events compared with bare metal stents, vascular biological problems such as neointimal hyperplasia, delayed re-endothelialization, late stent thrombosis are not eliminated and, increasingly, neoatherosclerosis is the underlying mechanism for very late stent failure. Further understanding regarding the mechanisms underlying the biological responses to stent deployment is therefore required so that new and improved therapies can be developed. This review will discuss the accumulating evidence that the chemokines, small inflammatory proteins, play a role in each key biological process of stent biocompatibility. It will address the chemokine system in its specialized roles in regulating the multiple facets of vascular biocompatibility including neointimal hyperplasia, endothelial progenitor cell (EPC) mobilization and re-endothelialization after vascular injury, platelet activation and thrombosis, as well as neoatherosclerosis. The evidence in this review suggests that chemokine-targeting strategies may be effective in controlling the pathobiological processes that lead to stent failure. Preclinical studies provide evidence that inhibition of specific chemokines and/or broad-spectrum inhibition of the CC-chemokine class prevents neointimal hyperplasia, reduces thrombosis and suppresses the development of neoatherosclerosis. In contrast, however, to these apparent deleterious effects of chemokines on stent biocompatibility, the CXC chemokine, CXCL12, is essential for the mobilization and recruitment of EPCs that make important contributions to re-endothelialization post-stent deployment. This suggests that future chemokine inhibition strategies would need to be correctly targeted so that all key stent biocompatibility areas could be addressed, without compromising important adaptive biological responses.
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Materiales Biocompatibles , Quimiocinas/metabolismo , Enfermedad de la Arteria Coronaria/terapia , Vasos Coronarios/metabolismo , Intervención Coronaria Percutánea/instrumentación , Stents , Animales , Quimiocinas/inmunología , Enfermedad de la Arteria Coronaria/inmunología , Enfermedad de la Arteria Coronaria/metabolismo , Enfermedad de la Arteria Coronaria/patología , Reestenosis Coronaria/inmunología , Reestenosis Coronaria/metabolismo , Reestenosis Coronaria/patología , Trombosis Coronaria/inmunología , Trombosis Coronaria/metabolismo , Trombosis Coronaria/patología , Vasos Coronarios/inmunología , Vasos Coronarios/patología , Stents Liberadores de Fármacos , Humanos , Hiperplasia , Neointima , Intervención Coronaria Percutánea/efectos adversos , Diseño de Prótesis , Transducción de Señal , Resultado del TratamientoRESUMEN
As the degree of luminal narrowing increases, shear stress increases, and high shear stress is known to activate platelets. However, the relationship between the degree of luminal narrowing and the composition of thrombus in patients with plaque erosion has not been studied. A total of 148 patients with plaque erosion and thrombus detected by optical coherence tomography were divided into tertiles based on the minimum lumen area (MLA) at the culprit lesion. Thrombus was categorized as platelet-rich or fibrin-rich. Among 148 patients, 50 (34%) were in the mild stenosis group, 49 (33%) were in the moderate stenosis group, and 49 (33%) were in the severe stenosis group. The composition of thrombus was significantly different among the 3 groups (prevalence of platelet-rich thrombus was 60% in the mild stenosis group; 78% in the moderate stenosis group; and 84% in the severe stenosis group; P = 0.021). The pattern of fibrin-rich thrombus showed the opposite: 40%, 22%, and 16%, respectively. In the multivariate analysis, current smoking was independently associated with fibrin-rich thrombus (odds ratio [OR] 2.364 [95% CI 1.004-5.567], P = 0.049). This study demonstrated that platelet-rich thrombus was the predominant type of thrombus in plaque erosion. The prevalence of fibrin-rich thrombus was highest in the mild stenosis group.
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Plaquetas/patología , Trombosis Coronaria/patología , Placa Aterosclerótica/patología , Adulto , Anciano , Constricción Patológica/metabolismo , Constricción Patológica/patología , Angiografía Coronaria , Trombosis Coronaria/complicaciones , Trombosis Coronaria/metabolismo , Vasos Coronarios/metabolismo , Vasos Coronarios/patología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Placa Aterosclerótica/complicaciones , Placa Aterosclerótica/metabolismo , Plasma Rico en Plaquetas/metabolismoRESUMEN
Arterial thrombus formation is thought to be initiated by platelet adhesion to the subendothelial matrix, but ruptured atherosclerotic plaques are characterized by substantial reduction of matrix proteins compared with stable plaques. Intraplaque erythrocytes and/or fibrin have been reported in high-risk coronary plaques. The aims of the current study were to identify factors that provide scaffolds for platelets at the sites of ruptured coronary plaques and investigate depositions of iron and bilirubin as hemoglobin catabolites in the ruptured plaques. Histological characteristics of plaque components and the thrombus interface were examined in 73 acute coronary aspirated thrombi. Necrotic debris (95%), macrophages (95%), and cholesterin clefts (81%) were observed frequently at the ruptured plaque and thrombus interface. A fibrous matrix (47%), calcification (32%), and extracellular deoxyribonucleic acid (15%) were identified as small foci. Tissue factor was localized in the necrotic core and macrophages. Fibrin and von Willebrand factor were consistently deposited within the plaques and beneath platelet aggregations. The citrullinated histone H3-immunopositive area accounted for only 0.5% of the plaque area. Bilirubin and iron depositions were detected in approximately 20% of the plaques in addition to biliverdin reductase and ferritin expression in macrophages. Fibrin and von Willebrand factor rather than matrix proteins and neutrophil extracellular traps may be major adhesive molecules at the sites of ruptured plaques. Iron and bilirubin deposits may be markers for rupture-prone plaques.
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Plaquetas/patología , Trombosis Coronaria/patología , Fibrina/análisis , Placa Aterosclerótica/patología , Factor de von Willebrand/análisis , Anciano , Anciano de 80 o más Años , Bilirrubina/análisis , Femenino , Humanos , Hierro/análisis , Masculino , Persona de Mediana Edad , Agregación PlaquetariaRESUMEN
BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and its resultant clinical presentation, coronavirus disease 2019 (COVID-19), is an emergent cause of mortality worldwide. Cardiac complications secondary to this infection are common; however, the underlying mechanisms of such remain unclear. A detailed cardiac evaluation of a series of individuals with COVID-19 undergoing postmortem evaluation is provided, with 4 aims: (1) describe the pathological spectrum of the myocardium; (2) compare with an alternate viral illness; (3) investigate angiotensin-converting enzyme 2 expression; and (4) provide the first description of the cardiac findings in patients with cleared infection. METHODS: Study cases were identified from institutional files and included COVID-19 (n=15: 12 active, 3 cleared), influenza A/B (n=6), and nonvirally mediated deaths (n=6). Salient information was abstracted from the medical record. Light microscopic findings were recorded. An angiotensin-converting enzyme 2 immunohistochemical H-score was compared across cases. Viral detection encompassed SARS-CoV-2 immunohistochemistry, ultrastructural examination, and droplet digital polymerase chain reaction. RESULTS: Male sex was more common in the COVID-19 group (P=0.05). Nonocclusive fibrin microthrombi (without ischemic injury) were identified in 16 cases (12 COVID-19, 2 influenza, and 2 controls) and were more common in the active COVID-19 cohort (P=0.006). Four active COVID-19 cases showed focal myocarditis, whereas 1 case of cleared COVID-19 showed extensive disease. Arteriolar angiotensin-converting enzyme 2 endothelial expression was lower in COVID-19 cases than in controls (P=0.004). Angiotensin-converting enzyme 2 myocardial expression did not differ by disease category, sex, age, or number of patient comorbidities (P=0.69, P=1.00, P=0.46, P=0.65, respectively). SARS-CoV-2 immunohistochemistry showed nonspecific staining, whereas ultrastructural examination and droplet digital polymerase chain reaction were negative for viral presence. Four patients (26.7%) with COVID-19 had underlying cardiac amyloidosis. Cases with cleared infection had variable presentations. CONCLUSIONS: This detailed histopathologic, immunohistochemical, ultrastructural, and molecular cardiac series showed no definitive evidence of direct myocardial infection. COVID-19 cases frequently have cardiac fibrin microthrombi, without universal acute ischemic injury. Moreover, myocarditis is present in 33.3% of patients with active and cleared COVID-19 but is usually limited in extent. Histological features of resolved infection are variable. Cardiac amyloidosis may be an additional risk factor for severe disease.
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COVID-19 , Trombosis Coronaria , Fibrina/metabolismo , Miocardio , SARS-CoV-2/metabolismo , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Enzima Convertidora de Angiotensina 2/biosíntesis , COVID-19/metabolismo , COVID-19/mortalidad , COVID-19/patología , Niño , Preescolar , Trombosis Coronaria/metabolismo , Trombosis Coronaria/mortalidad , Trombosis Coronaria/patología , Femenino , Regulación Enzimológica de la Expresión Génica , Humanos , Inmunohistoquímica , Lactante , Masculino , Persona de Mediana Edad , Miocardio/metabolismo , Miocardio/patologíaAsunto(s)
Infecciones por Coronavirus/patología , Miocarditis/patología , Miocardio/patología , Neumonía Viral/patología , Tropismo Viral/fisiología , Adulto , Anciano , Enzima Convertidora de Angiotensina 2 , Betacoronavirus/genética , COVID-19 , Oclusión Coronaria/patología , Oclusión Coronaria/virología , Trombosis Coronaria/patología , Trombosis Coronaria/virología , Vasos Coronarios/patología , Vasos Coronarios/virología , Síndrome de Liberación de Citoquinas/patología , Citocinas/sangre , Femenino , Corazón/virología , Humanos , Masculino , Miocarditis/virología , Pandemias , Peptidil-Dipeptidasa A/metabolismo , SARS-CoV-2 , Tropismo Viral/genéticaRESUMEN
Sudden cardiac death (SCD) is an important public health problem that accounts for approximately 15% to 20% of global deaths. Our retrospective study aimed to analyze etiological distribution and epidemiological data of 128 cases with SCD as death cause based on autopsies between 2010 and 2019. The mean age of SCD cases was 57.09, with the highest incidence in older than 60 years (43.8%). Male/female ratio was 4.5:1, peaking with 9.2:1 in the 41- to 60-year age group. Deaths occurred mostly at home (41.4%). Coronary atherosclerotic heart disease (CAD) was main SCD cause (65.6%) with cardiac tamponade (10.9%), unexplained SCD (8.6%), and hypertrophic cardiomyopathy (7.8%) after it. A total of 71.2% of CAD cases had coronary artery stenosis of greater than 75% and 92.9% had atherosclerotic degeneration in the left anterior descending artery. Based on the body mass index-based normal heart weights table, 91.7% of CAD cases had cardiomegaly. This study showed CAD, cardiomegaly, and high body mass index concurrence as a very important SCD risk. Because SCD incidence increases in older than 40 years, determining risk groups through regular medical examinations and inspections, older than 30 years would provide implementation of preventive measures. Some cardiac diseases causing sudden death are undetectable despite detailed autopsy and histopathological examinations. Including postmortem cardiogenetic analysis among routine techniques in sudden deaths would lower sudden unexplained death diagnosis rates.