Figure 2 - uploaded by Genevieve M Crane
Content may be subject to copyright.
e Dystrophic calcification. (A and B) Unenhanced axial (A) and contrast-enhanced oblique coronal maximum intensity projection (B) CT images in a one-month-old full- term baby boy with delivery complicated by enterovirus myocarditis. Images show marked circumferential left ventricular calcifications predominantly affecting the subepicardial myocardium ( arrows ). The child expired shortly thereafter. 

e Dystrophic calcification. (A and B) Unenhanced axial (A) and contrast-enhanced oblique coronal maximum intensity projection (B) CT images in a one-month-old full- term baby boy with delivery complicated by enterovirus myocarditis. Images show marked circumferential left ventricular calcifications predominantly affecting the subepicardial myocardium ( arrows ). The child expired shortly thereafter. 

Source publication
Article
Full-text available
Myocardial calcifications are not uncommonly encountered by the cardiac imager and may have a range of imaging appearances, from focal calcific deposits to diffuse myocardial involvement. A number of pathological processes can both cause and result from myocardial calcification; therefore, accurate identification and characterization are important....

Contexts in source publication

Context 1
... calcifications can arise from a number of different etiologies. Calcium within the myocardium indicates underlying pathology associated with morbidity and mortality. It is therefore important to report and characterize myocardial calcifications when they are visible on diagnostic imaging examinations. Radiographs, CT, and echocardiography can detect myocardial calcifications. While imaging features are often nonspecific, the combination of imaging pattern and clinical history may help clinicians determine the etiology and clinical significance of myocardial calcifications when they are discovered. Pathologic calcification in any tissue represents abnormal accumulation of calcium salts. Two basic forms are recog- nized: dystrophic and metastatic. 1 Traditionally, the most broad classification of myocardial calcifications follows this categorization and adds “idiopathic calcification” as a third form 2 ; however, the validity and clinical utility of this classification scheme is unknown. Dystrophic calcification represents the sequelae of local tissue damage and cellular necrosis. It is not associated with abnormalities in serum calcium levels or calcium homeostasis; however, hypercalcemia will accentuate the process. 1 Coagu- lative, caseous, and liquefactive necrosis can all result in dystrophic calcification. 1 According to Perkins, 1 dystrophic calcification is initiated by membrane damage that leads to concentration of calcium ions within membrane-bound vesicles. Phospholipids within the vesicle membrane are hydro- lyzed with the aid of phosphatases and the resulting phosphate group binds to calcium. Mineral deposits eventually accumulate near the cell membrane, where a structural change occurs and calcium phosphate microcrystals form. Progressive crystallization can result in deposits that are intracellular, extracellular, or both. 1 Dystrophic calcification is more prevalent than metastatic calcification. The most common etiology is previous myocardial infarction leading to myocyte necrosis 2 e 4 (Fig. 1). Calcium deposition is accentuated by the ischemia-induced local microenvironment, including relative alkalinity, decreased calcium solubility, and carbon dioxide production, 2 with 1 study demonstrating dystrophic calcifications in 8% of myocardial infarctions older than 6 years. 5 A number of other causes of dystrophic myocardial calcification have been reported, including traumatic, infectious and/or inflammatory, and neoplastic processes (Table 1; Fig. 2). Several cases have been reported in which the primary pathology is located outside the myocardium, for example caseous calcification of the mitral annulus 6 and calcified pericarditis 3 extending into the adjacent ...
Context 2
... decreased calcium solubility, and carbon dioxide production, 2 with 1 study demonstrating dystrophic calcifications in 8% of myocardial infarctions older than 6 years. 5 A number of other causes of dystrophic myocardial calci- fication have been reported, including traumatic, infectious and/or inflammatory, and neoplastic processes (Table 1; Fig. 2). Several cases have been reported in which the primary pathology is located outside the myocardium, for example caseous calcification of the mitral annulus 6 and calcified pericarditis 3 extending into the adjacent myocardium. . The patient had a history of aortic coarctation, patent ductus arteriosus, and mitral valve stenosis status ...
Context 3
... difficult cases. Coronary artery calcifications have a linear, tubular, or tram-track configura- tion and follow an expected anatomic course. Pericardial calcifications are usually chunky but oriented in a linear configuration and usually spare the apex 2,19 (Fig. 11). Calcifi- cations of the mitral annulus are arranged in dense ring-like clumps (Figs. 12 and 13), whereas valvular and great vessel calcifications are thin and curvilinear and located in an ex- pected anatomic location. 2 ...

Similar publications

Article
Full-text available
Neurodegenerative diseases are a heterogeneous group of disorders that are characterized by the progressive dysfunction and loss of neurons. Here, we distil and discuss the current state of modeling in the area of neurodegeneration, and objectively compare the gaps between existing clinical knowledge and the mechanistic understanding of the major p...
Article
Full-text available
Despite the ubiquity of endogenous emotions and their role in both resilience and pathology, the processes supporting their generation are largely unknown. We propose a neural component process model of endogenous generation of emotion (EGE) and test it in two fMRI experiments (N=32/293) where participants generated and regulated positive and negat...
Article
Full-text available
Mineral nanoparticles form in physiological and pathological processes occurring in the human body. The calcium phosphate mineral phase of the particles has affinity for proteins and lipids, but the complete profiling of the organic molecules that bind to the particles has not been described in detail. We report here a comprehensive analysis of org...
Article
Full-text available
Although microRNAs have been elaborated to participate in various physiological and pathological processes, their functions in TRAIL resistance of acute myeloid leukemia (AML) remain obscure. In this study, we detected relatively lower expression levels of miR-424&27a in TRAIL-resistant and semi-resistant AML cell lines as well as newly diagnosed p...

Citations

... Dystrophic calcifications comprise ischemic, traumatic, infectious, inflammatory and neoplastic etiologies. Metastatic calcifications are caused, inter alia, by renal failure or hyperparathyroidism (Nance Jr et al., 2015). ...
Article
The ancient Egyptians considered the heart to be the most important organ. The belief that the heart remained in the body is widespread in the archeological and paleopathological literature. The purpose of this study was to perform an overview of the preserved intrathoracic structures and thoracic and abdominal cavity filling, and to determine the prevalence and computed tomography (CT) characteristics of the myocardium in the preserved hearts of ancient Egyptian mummies. Whole‐body CT examinations of 45 ancient Egyptian mummies (23 mummies from the Ägyptisches Museum und Papyrussammlung, Berlin, Germany, and 22 mummies from the Museo Egizio, Turin, Italy) were systematically assessed for preserved intrathoracic soft tissues including various anatomical components of the heart (pericardium, interventricular septum, four chambers, myocardium, valves). Additionally, evidence of evisceration and cavity filling was documented. In cases with identifiable myocardium, quantitative (measurements of thickness and density) and qualitative (description of the structure) assessment of the myocardial tissue was carried out. Heart structure was identified in 28 mummies (62%). In 33 mummies, CT findings demonstrated evisceration, with subsequent cavity filling in all but one case. Preserved myocardium was identified in nine mummies (five male, four female) as a mostly homogeneous, shrunken structure. The posterior wall of the myocardium had a mean maximum thickness of 3.6 mm (range 1.4–6.6 mm) and a mean minimum thickness of 1.0 mm (range 0.5–1.7 mm). The mean Hounsfield units (HU) of the myocardium at the posterior wall was 61 (range, 185–305). There was a strong correlation between the HU of the posterior wall of the myocardium and the mean HU of the muscles at the dorsal humerus ( R = 0.77; p = 0.02). In two cases, there were postmortem changes in the myocardium, most probably due to insect infestation. To our knowledge, this is the first study to investigate the myocardium systematically on CT scans of ancient Egyptian mummies. Strong correlations between the densities of the myocardium and skeletal muscle indicated similar postmortem changes of the respective musculature during the mummification process within individual mummies. The distinct postmortem shrinking of the myocardium and the collapse of the left ventriclular cavity in several cases did not allow for paleopathological diagnoses such as myocardial scarring.
... Myocardial calcification occurs following myocardial injury or necrosis, including myocardial infarction, cardiac surgery, and myocarditis (1)(2)(3)(4). We herein report a case of fulminant myocarditis with diffuse myocardial calcification and its pathological autopsy results. ...
... Metastatic calcification results from a systemic process (hypercalcemia and/or abnormalities of calcium homeostasis) in patients with chronic renal failure on hemodialysis, primary or secondary hyperparathyroidism, and dietary calcium and vitamin D deficiency (3). However, dystrophic calcification occurs where necrosis or damage to myocardial cells has occurred, such as in myocardial infarction, cardiac surgery, or systemic disorders, such as sepsis, irrespective of serum calcium concentration (1,2). Few reports of myocardial calcification caused by myocarditis exist, and the mechanism is yet to be described (5). ...
... Calcified myocardium may be an arrhythmogenic substrate, such as ventricular tachycardia (9). In addition, massive myocardial calcification often causes restrictive physiology with or without systolic dysfunction (1). Therefore, myocarditis patients with massive myocardial calcification may have a poorer prognosis than those without it. ...
Article
Full-text available
Myocardial calcification in myocarditis is rare and may be linked to poor outcomes. We herein report a case of fulminant myocarditis with massive myocardial calcification and its pathological outcomes at autopsy. A 49-year-old man experienced chest pain and was diagnosed with acute myocarditis. His cardiac function did not recover despite mechanical circulatory support in combination with V-A extracorporeal membrane oxygenation and IMPELLA CP®. He eventually developed sepsis and gastrointestinal bleeding and died on day 27. Diffuse myocardial calcification was observed on computed tomography at autopsy. The pathological autopsy depicted that calcification filled every myocardial cell in the left ventricle.
... Myocardial calcifications are usually categorized as either dystrophic or metastatic. Dystrophic myocardial calcifications are often seen following years after infarction or after infection as a response to tissue necrosis (Nance Jr et al., 2015). However, metastatic myocardial calcifications can present itself after any disturbance in calcium homeostasis including ESKD . ...
... Cardiac involvement is a rare complication, although dysfunction of the heart is a common complication of severe sepsis and shock [1]. Myocardial calcifications are described as dystrophic when they occur in injured myocardium in a patient with normal calcium homeostasis and as metastatic when they occur in intact myocardium in a patient with abnormal calcium homeostasis [2]. We present the case of a middle-aged male who presented with severe leptospirosis with cardiac involvement and developed diffuse myocardial calcifications. ...
... Metastatic calcification occurs as a consequence of systemic process, i.e., hypercalcemia or abnormalities of calcium homeostasis, and can appear in normal or unhealthy tissue. Metastatic calcifications are usually found in patients on hemodialysis (with chronic kidney failure), but they have also appeared in patients with oxaluria, primary, secondary, or tertiary hyperparathyroidism, and a nutritional deficit of calcium and vitamin D [2,9]. Different etiologies of dystrophic myocardial calcification have been described. ...
... The etiology of myocardial calcification can also be multifactorial. Also, a number of inflammatory processes can affect both the heart and the kidney, resulting in dystrophic calcification aggravated by abnormal calcium metabolism [2]. Myocardial calcifications can develop days to weeks after sepsis onset [9]. ...
Article
Full-text available
Severe leptospirosis is defined by multiple organ failure. Cardiac involvement is an uncommon complication in patients with leptospirosis, and the pathophysiology of it is not well understood. Diffuse myocardial calcifications connected with sepsis are infrequent, and their effect on heart function is hard to predict. They can lead to conduction disorders and arrhythmias, thereby causing sudden death. Myocardial calcifications are usually revealed incidentally by radiological investigations such as computed tomography (CT) scan in patients with or after sepsis and are commonly unidentified in practice because most cases progress gradually. This case report involves a 51-year-old male who presented to the emergency department with sepsis. The patient was diagnosed with leptospirosis, causing septic cardiomyopathy and diffuse calcifications of the myocardium of the left ventricle. This case highlights the importance of multimodality imaging and a multidisciplinary approach to diagnoses since early recognition and treatment are essential. Follow-up of such patients is necessary to monitor the systolic function of the left ventricle and cardiac arrhythmia.
... 1 It is associated with poor prognosis. The calcifications correspond to areas of un-excitability and represent a fixed boundary of re-entry circuits acting as substrate for scar related re-entrant VT. 2,3 Although it indicates likely non-viable myocardium, our decision to re-vascularize left main coronary artery was to protect the left circumflex territory. This case emphasizes that dystrophic myocardial calcification, which can sometimes be picked up in routine chest X-ray, can cause scar-related VT. ...
Article
Full-text available
Extensive myocardial dystrophic calcification is rare and indicates a poor prognosis with a risk of arrhythmia and recurrent heart failure. We present a long term survivor of extensive myocardial infarction presenting as myocardial calcification related unstable ventricular tachycardia needing an implantable cardioverter defibrillator.
... Clinically, it is more common in end-stage renal disease, hypercalcaemia, PTH, and poisoning, and the process is slow and usually takes several years. 15 Dystrophic calcification mainly occurs in damaged tissues, suggesting local tissue damage and cell necrosis. Generally, it progresses rapidly, without systemic calcium metabolism disorders, and the serum calcium level is usually average. ...
Article
Full-text available
Background Early myocardial calcifications secondary to fulminant myocarditis (FM) are rare, and their natural evolution and effects on cardiac function are poorly understood. Here, we followed the patient for 4 years to observe the development of cardiac calcification and its impact on heart function. Case summary A 16-year-old man was hospitalized with a fever and cough for 1 day. The patient was previously healthy and had no history of heart disease or specific family conditions. The patient was positive for anti-Epstein–Barr virus IgG and IgM. The computed tomography (CT) scan showed no coronary lesions. Cardiogenic shock and recurrent ventricular fibrillation developed on the third day after admission, and the patient received rescue therapy such as endotracheal intubation, defibrillation, extracorporeal membrane oxygenation, and corticosteroids. On the 13th day of admission, a CT scan revealed significant calcification in the left ventricular wall. The patient was discharged after 30 days in the hospital. After discharge, his left ventricular calcification peaked at 6 months and gradually subsided after that, and his left ventricular function slowly returned to normal at 12 months. Discussion In younger patients, myocardial calcifications secondary to FM may occur as early as 13 days and affect cardiac function. After proper treatment and rehabilitation, the patient’s myocardial calcification can gradually subside and the cardiac function can gradually recover. For FM patients, timely and comprehensive intensive treatment, including heart, lung, and kidney replacement therapy and early administration of hormone preparations, may be beneficial to the early recovery of patients.
... Keywords: Myocardium; Cardiac Imaging Techniques; Child (Source: MeSH) INTRODUCCIÓN El depósito de calcio en las células miocárdicas es el resultado de una reacción distrófica provocada por una lesión tisular. Múltiples procesos patológicos pueden fungir como causa y consecuencia de las calcificaciones miocárdicas (1). Si bien la fisiopatología no está claramente esclarecida, se han descrito dos formas de calcificaciones: distróficas y metastásicas. ...
... Si bien la fisiopatología no está claramente esclarecida, se han descrito dos formas de calcificaciones: distróficas y metastásicas. Las calcificaciones distróficas se han asociado a lesiones cardíacas directas y necrosis celular, mientras las calcificaciones metastásicas se han relacionado con alteraciones en la homeostasis del calcio, como ocurre en la enfermedad renal severa e hiperparatiroidismo (1)(2)(3). Los hallazgos histológicos de ambos tipos de calcificaciones coinciden en la formación de hidroxiapatita que se inicia en las mitocondrias y luego se propaga al resto de las fibras miocárdicas, lo que sugiere que el desarrollo de ambos tipos de calcificaciones es a través de un mecanismo similar (4). ...
Article
Full-text available
Objetivo: Describir los hallazgos clínicos e imagenológicos de niños con calcificaciones miocárdicas distróficas. Métodos: En este estudio retrospectivo revisamos imágenes de tomografía computarizada (TC) de niños con calcificaciones distróficas miocárdicas. Se extrajo la información de las historias clínicas de los pacientes, incluyendo el diagnóstico, las comorbilidades y el tratamiento. Se realizó una búsqueda bibliográfica en PubMed y SciELO de reportes de caso y series de casos que incluyeran pacientes menores de 18 años con calcificaciones miocárdicas. Resultados: Se incluyeron siete pacientes, 5 (71,4%) varones, con una mediana de edad de 1,1 años [RIQ 0.8 - 6.3]. Todas las imágenes de TC mostraron calcificaciones miocárdicas transmurales, que se observaron por primera vez mediante ecocardiografía en tres pacientes. Las calcificaciones miocárdicas afectaban al ventrículo izquierdo en 3 pacientes, a ambos ventrículos en 2 y sólo al ventrículo derecho en otros 2 pacientes. Un paciente también presentaba calcificaciones distróficas vasculares y pulmonares. Mientras que la necesidad de oxigenación por membrana extracorpórea (ECMO) y el antecedente de trasplante cardíaco fueron las comorbilidades asociadas más comunes en nuestro estudio, la insuficiencia renal y la sepsis son las etiologías más descritas en la literatura. La mortalidad fue elevada tanto en nuestra cohorte (43%) como en la literatura (40%). Conclusiones: Los pacientes pediátricos con condiciones críticas, como sepsis, insuficiencia renal, necesidad de ECMO, y aquellos sometidos a trasplante de corazón, pueden desarrollar calcificaciones miocárdicas transmurales. Estas calcificaciones no presentan una distribución característica entre los ventrículos que sea atribuible a una enfermedad de base específica. Sin embargo, de manera conjunta, están asociadas con altas tasas de mortalidad.
... Besides excessive extracellular matrix synthesis, another pathological aspect of cardiac fibrosis is predisposition for myocardial calcification. Myocardial calcification has been reported (4) to occur in sepsis (5,6), renal disease and failure (5)(6)(7)(8), and areas of endomyocardial fibrosis (9,10). Indeed, myocardial calcification is one of the common causes of cardiac conduction blocks, arrhythmias, and contractile dysfunction and is associated with adverse cardiac outcomes (4,11,12). ...
... Myocardial calcification has been reported (4) to occur in sepsis (5,6), renal disease and failure (5)(6)(7)(8), and areas of endomyocardial fibrosis (9,10). Indeed, myocardial calcification is one of the common causes of cardiac conduction blocks, arrhythmias, and contractile dysfunction and is associated with adverse cardiac outcomes (4,11,12). ...
Article
Full-text available
Myocardial fibrosis and calcification associate with adverse outcomes in nonischemic heart failure. Cardiac fibroblasts (CF) transition into myofibroblasts (MF) and osteogenic fibroblasts (OF) to promote myocardial fibrosis and calcification. However, common upstream mechanisms regulating both CF-to-MF transition and CF-to-OF transition remain unknown. microRNAs are promising targets to modulate CF plasticity. Our bioinformatics revealed downregulation of miR-129-5p and upregulation of its targets small leucine-rich proteoglycan Asporin (ASPN) and transcription factor SOX9 as common in mouse and human heart failure (HF). We experimentally confirmed decreased miR-129-5p and enhanced SOX9 and ASPN expression in CF in human hearts with myocardial fibrosis and calcification. miR-129-5p repressed both CF-to-MF and CF-to-OF transition in primary CF, as did knockdown of SOX9 and ASPN. Sox9 and Aspn are direct targets of miR-129-5p that inhibit downstream β-catenin expression. Chronic Angiotensin II infusion downregulated miR-129-5p in CF in WT and TCF21-lineage CF reporter mice, and it was restored by miR-129-5p mimic. Importantly, miR-129-5p mimic not only attenuated progression of myocardial fibrosis, calcification marker expression, and SOX9 and ASPN expression in CF but also restored diastolic and systolic function. Together, we demonstrate miR-129-5p/ASPN and miR-129-5p/SOX9 as potentially novel dysregulated axes in CF-to-MF and CF-to-OF transition in myocardial fibrosis and calcification and the therapeutic relevance of miR-129-5p.
... Calcification of a blood-vessel wall is frequently detected on CT examination for patients on dialysis or with atherosclerosis, whereas it is rarely detected in parenchymal organs, such as the adrenal glands, the myocardium, and/ or the skeletal muscle. The mechanism of organ calcification can be divided into metastatic and dystrophic processes, which are caused by abnormalities in calcium or phosphate metabolism and by cellular damage or necrosis induced by infarction, trauma, inflammation, infection, and drugs, respectively [10,15]. In addition, metastatic calcification occurs gradually over a period spanning months or even years, whereas dystrophic calcification occurs rapidly, sometimes in a matter of days to weeks [11,12]. ...
Article
Full-text available
Purpose: The purpose of this study was to investigate the incidence of multiple organ calcification and the correlation between multiple organ calcification and clinical severity in patients with thrombocytopenia, anasarca, fever, reticulin fibrosis, renal dysfunction, and organomegaly (TAFRO) syndrome. Methods: We retrospectively identified 13 patients with TAFRO syndrome who were treated at our hospital between February 2019 and March 2021. Computed tomography (CT) images of TAFRO patients, which were acquired at admission and one month after admission, were evaluated. Additionally, clinical and laboratory data related to organ calcification and severity classification of TAFRO syndrome were investigated. The correlation between the presence of organ calcification on CT and TAFRO syndrome-severity classification was evaluated. Results: One month after admission, calcification of the myocardium, adrenal glands, gallbladder wall, pancreas, kidney, skeletal muscle, and skin were observed in 38%, 46%, 15%, 15%, 15%, 23%, and 15% of the thirteen patients, respectively. The occurrence rate of calcifications in the myocardium, adrenal glands, and skeletal muscle was significantly higher in patients with a grade 4 or higher clinical severity than in those with a level up to grade 3 (p = 0.001, p = 0.005, and p = 0.035, respectively). Conclusions: Our results suggest that the higher the clinical severity in patients with TAFRO syndrome, the higher is the frequency of calcification in the myocardium, adrenal glands, and skeletal muscle; therefore, the assessment of these organ calcifications on CT images may be useful in predicting the severity of TAFRO syndrome.
... A massive myocardial calcification is a rare sequel of extensive MI, 1) associated with poor prognosis by causing complications such as chronic heart failure and arrhythmia. 2) We report a rare case of a long-term survivor of MI with extensive myocardial calcification. The patient described here had not received revascularization but maintained GDMT for the management of post-MI heart failure. ...