Myocardial Calcification Research Articles

Increased Susceptibility of Cardiac Tissue to PM2.5-Induced Toxicity in Uremic Cardiomyopathic Rats Is Linked to Elevated Levels of Mitochondrial Dysfunction.

Patients with chronic kidney disease (CKD) frequently develop uremic cardiomyopathy, characterized by mitochondrial dysfunction as one of its pathologically significant mediators. Given that PM2.5 specifically targets cardiac mitochondria, exacerbating toxicity, this study addresses the potential alterations in the severity of PM2.5 toxicity in the context of CKD conditions. Female Wistar rats were exposed to PM2.5 at a concentration of 250 μg/m3 daily for 3 h for 21 days after which an adenine-induced CKD model was developed. While both PM2.5 exposure and the induction of CKD in rats lead to cardiomyopathy, the CKD animals exposed to PM2.5 exhibited a notably severe extent of myocardial hypertrophy and fibrosis. ECG recordings in CKD+ PM2.5 animals revealed a depressed ST segment and prolonged QRS interval, with both PM2.5 and CKD animals displaying an elevated ST segment. Subcellular level analysis confirmed a significantly low mitochondrial copy number and a severe decline in mitochondrial bioenergetic function in the CKD+ PM2.5 group. The prominent decline in PGC1-α further affirmed the severe mitochondrial functional deterioration in CKD+ PM2.5 animals compared to other experimental groups. Additionally, myocardial calcification was enhanced in CKD+ PM2.5 animals, heightening the susceptibility of CKD animals to PM2.5 toxicity. In summary, our findings suggest that the increased vulnerability of CKD myocardium to PM2.5-induced toxicity may be attributed to severe mitochondrial damage and increased calcification in the myocardium.

Heart of Stone: Cardiogenic Shock from Myocardial and Mitral Valve Calcification with Systolic Anterior Motion (SAM) Defect after Valve Replacement in a Patient on Chronic Hemodialysis (CHD)

Heart of Stone: Cardiogenic Shock from Myocardial and Mitral Valve Calcification with Systolic Anterior Motion (SAM) Defect after Valve Replacement in a Patient on Chronic Hemodialysis (CHD)

Myocardial calcification: case reports and a systematic review.

Myocardial calcification is an unusual condition in which excess calcium is deposited in the myocardium. Herein, we report two cases of myocardial calcification from our clinical experience. Furthermore, we conduct a systematic review to examine the clinical course and associated pathologies of myocardial calcification. This systematic review was registered in PROSPERO (CRD42023463285). PubMed and Scopus were searched according to the following inclusion criteria: (i) case reports or case series describing patients with myocardial calcification; (ii) diagnosis of myocardial calcification by computed tomography (CT); (iii) adequate description of patients, including their chief complaint, medical history, evaluations, and treatments; and (iv) publication in English. Among the 75 patients, 24 had sepsis, 14 had myocarditis, and 37 had other pathologies. The mortality rate was 33% for patients with sepsis, 14% for patients with myocarditis, and 11% for patients with other pathologies. Follow-up CT findings beyond 2 years were reported in six patients, showing that the CT findings of myocardial calcification persisted but subsided over time. Autopsy was performed in seven patients, and extensive interstitial fibrosis and collection of inflammatory cells were observed in patients with myocarditis, sepsis, and ischaemic heart disease. While various medical conditions can cause myocardial calcification, accompanying conditions commonly reported with myocardial calcification were sepsis and myocarditis. The CT findings of myocardial calcification tend to regress over time if the underlying disease can be treated.

Cardiac arrest and myocardial calcification in a child

Cardiac arrest and myocardial calcification in a child

Massive Myocardial Calcification: A Rare Autopsy Finding

Introduction: Myocardial calcification is rare and occur by two mechanisms- dystrophic and metastatic. It can present with variable clinical manifestations like congestive heart failure, cardiomyopathy, arrhythmia and sudden cardiac death. Case Report: Post mortem viscera of a 50 year old male was received in the department of pathology with alleged history of burns, who died after two weeks of hospital treatment. There was no past history or investigation available in the post mortem papers. Whole heart, pieces of brain, both lungs, liver, spleen and both kidneys were received. On gross examination no abnormality was observed in any of these viscera. Microscopic examination revealed extensive calcification in anterior, lateral & posterior walls of left ventricle of the heart. Sections from kidney showed features of chronic tubulointerstitial nephritis. Conclusion: Myocardial calcification is rare and mostly diagnosed incidentally or on autopsy. Extensive sampling of heart and other viscera might help in finding the etiology in such rare cases of massive calcification in myocardium . Antemortem diagnosis can be made with computed tomography (CT) scan and endomyocardial biopsy.

Electrocardiographic Variants of Ventricular Predominance in Arrhythmogenic Cardiomyopathy

Desmoglein-2 and Desmocollin-2 mutations cause different types of arrhythmogenic cardiomyopathy either dominant right, biventricular or dominant left forms. These two mutations present with myocardial cell necrosis and calcification [1,2]. Signs of electrocardiographic right ventricular hypertrophy can be found in more than 50% [3] besides typical ECG criteria of arrhythmogenic cardiomyopathy like right precordial epsilon waves and T-wave inversions [4], QRS fragmentation [5], localized right precordial QRS prolongation [6], terminal activation delay [7], and large Q-waves, small R-waves and T-wave inversion in lead aVR [8].

Hearts of stone: Rapidly progressive left ventricular myocardial calcifications in severe sepsis: Case series.

Rapidly progressive left ventricular myocardial calcification (RPLVMC) is a rare phenomenon of severe sepsis which is associated with long-term complications like irreversible cardiomyopathy and arrhythmias. To date, only 19 cases have been reported in literature. We present a case series of two patients with RPLVMC which manifested within a period of days in the setting of severe sepsis. Unique to previous case reports, the patients in the current case series had no pre-existing systemic risk factors such as end-stage kidney disease or endocrinological dysfunction. This case series aims to increase awareness of RPLVMC in severe sepsis, improve its opportunistic detection on routine medical imaging (namely chest x-ray and computed tomography), and spur future research to develop potential prevention strategies.

Massive myocardial calcification as an aetiology of heart failure.

Massive myocardial calcification as an aetiology of heart failure.

Extensive myocardial calcifications: a systematic literature review of a rare pathological phenomenon.

Myocardial calcifications (MC) represent a relatively rare pathological process, which may accompany different cardiovascular conditions and can be broadly categorized as dystrophic or metastatic. Myocardial infarction (MI) has been traditionally regarded as the main cause of MC overall; however, no updated comprehensive data on the relative incidence of different forms of MC is available. The purpose of this systematic review of the literature is to analyze the currently available evidence on MC in terms of pathophysiology, diagnosis, and clinical presentation. A total of 241 studies including a total of 368 patients affected by extensive MC were included in the final review. The majority of patients (69.8%) presented with dystrophic MC. Endomyocardial fibrosis (EMF) represents the single most common etiology of MC (24.2%), while sepsis/acute systemic inflammatory syndrome (SIRS) and chronic kidney disease were identified as the second and third most common causes respectively. The relative incidence of etiologies also varies across the years, with MI being more represented before 1990, and sepsis/SIRS becoming the single most common cause of MC after 1990. Multimodality imaging was used in the work-up of MC in 42.7% of cases. The most commonly employed imaging modality overall was echocardiography (51.9%), while after 1990 computed tomography scan became the most widely used tool (70.1%). The present systematic review provides new insights into the pathophysiology of MC. Previously thought to be mainly a consequence of ischemic heart disease, our data indicate that other diseases, namely EMF and sepsis/SIRS, are indeed the main conditions associated with MC. The importance of multimodality imaging in the work-up of MC is also highlighted.

Kiosk 9Q-TA-04 - Acute Myocardial Calcification Demonstrated on Multimodal Imaging

Kiosk 9Q-TA-04 - Acute Myocardial Calcification Demonstrated on Multimodal Imaging

Cor triatriatum sinister with dextrocardia in association with ostium secundum atrial septal defect, subpulmonary ventricular septal defect and bicuspid pulmonary valve in a pig

Necropsy of a 52-day-old Camborough pig revealed numerous cardiac malformations. The positional relationship of the atria, ventricles and great vessels was a mirror image type (I, L and L): inverted arrangement of the atria, with a left-sided right atrium and right-sided left atrium (situs inversus); inverted arrangement of the ventricles, with a left-sided morphological right ventricle and right-sided morphological left ventricle (L-loop); and aortic valve to the front left relative to the pulmonary valve (L-malposed). The major malformations included an ostium secundum atrial septal defect, cor triatriatum sinister (CTS), a subpulmonary ventricular septal defect and a bicuspid pulmonary valve. Histological examination revealed myocyte hypertrophy, focal myocardial necrosis and calcification in the left morphological right ventricle of the heart. To the best of our knowledge, this is the first report of CTS in pigs. Although the individual malformations found in the present case are not unique, an unusual combination of these cardiac malformations has not been described in animals.

Calcium Jacket of Left Ventricle: An Aristocracy of the Monster

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.

Histopathological spectrum of cardiovascular findings in forensic autopsies in Hadoti region: A prospective study of one year

Heart diseases are now the biggest killer in the world. Many cardiovascular pathologies are concealed and found incidentally on post mortem examination. To analyse spectrum of histopathological lesions (related or unrelated to cause of death) in heart autopsies in Hadoti region of Rajasthan. This was a one year prospective hospital-based study. A total of 133 whole heart specimen underwent detailed gross and microscopic examination. Most common histopathological finding was atherosclerosis, seen in 63 cases out of 133 autopsied hearts (47.3%), followed by myocardial hypertrophy in 31 cases and myocardial infarction in 20 cases. Age related changes were seen in 10 cases, severe congestion in 10 cases, myocardial fibrosis in 7 cases. 1 case each of infective endocarditis, myocardial calcification, ventricular rupture, myocarditis, LAD stent, fat embolism was noted. 51 hearts did not reveal any sort of pathology. Correlation of age with atherosclerosis showed a significant p value (0.0009). Males showed a slightly higher prevalence of atherosclerosis but it was not statistically significant. We had 39 (29.3%) cases of sudden cardiac deaths (SCD). SCD cases showed similar histopathological spectrum as all other causes of deaths, but percentage of each heart pathology was much higher in SCD. Most common finding among SCD cases was coronary artery disease (23 cases), followed by myocardial hypertrophy (22 cases) and myocardial infarction (13 cases). Myocardial Fibrosis was seen in 3 cases, age related changes in 2 cases, ventricular rupture in 1 case and severe congestion in 1 case. 61.5% SCD cases showed combination of two or more pathologies. Five SCD cases did not reveal any pathology.In our study heart pathologies make a major contribution towards ill health and death in our society, atherosclerosis being the most common finding.

Pacemaker lead insertion sites contribute to abnormalities of myocardial function and histopathology

Ventricular pacing can cause myocardial dysfunction, but how lead anchoring to the myocardium affects function has not been studied. The purpose of this study was to evaluate patterns of regional and global ventricular function in patients with a ventricular lead using cine cardiac computed tomography (CCT) and histology. This was a single-center retrospective study with 2 groups of patients with a ventricular lead: (1) those who underwent cine CCT from September 2020 to June 2021 and (2) those whose cardiac specimen was analyzed histologically. Regional wall motion abnormalities on CCT were assessed in relation to lead characteristics. For the CCT group, 122 ventricular lead insertion sites were analyzed in 43 patients (47% female; median age 19 years; range 3-57 years). Regional wall motion abnormalities were present at 51 of 122 lead insertion sites (42%) in 23 of 43 patients (53%). The prevalence of a lead insertion-associated regional wall motion abnormality was higher with active pacing (55% vs 18%; P < .001). Patients with lead insertion-associated regional wall motion abnormalities had a lower systemic ventricular ejection fraction (median 38% vs 53%; P < .001) than did those without regional wall motion abnormalities. For the histology group, 3 patients with 10 epicardial lead insertion sites were studied. Myocardial compression, fibrosis, and calcifications were commonly present directly under active leads. Lead insertion site-associated regional wall motion abnormalities are common and associated with systemic ventricular dysfunction. Histopathological alterations including myocardial compression, fibrosis, and calcifications beneath active leads may explain this finding.

The Controversies of Coronary Artery Disease in End-Stage Kidney Disease Patients: A Narrative Review.

Cardiovascular disease (CVD) accounts for more than 50% of deaths among patients with end-stage kidney disease (ESKD). Approximately 40-50% of ESKD patients have clinically significant coronary artery disease (CAD) due to atherosclerosis which accounts for a significant proportion of CVD risk. However, other CVD pathologies including myocardial fibrosis, vascular calcification and arterial stiffening play important contributory roles. The pathophysiology of CAD in ESKD is distinct from the general population. ESKD patients is typically have diffuse multi-vessel involvement with increased calcification that involves both intimal and medial layers of the arterial wall. There is a complex interplay between an increased burden of traditional Framingham risk factors and exposure to non-traditional risk factors including chronic inflammation and dialysis per se. Established treatments for CAD risk factors including cholesterol lowering with statin therapy have attenuated effects and ESKD patients also have worse outcomes after revascularisation. Recent trials such as the Canakinumab Anti-Inflammatory Thrombosis Outcomes Study (CANTOS) have established that direct modulation of inflammation improves CVD outcomes in the general population, which may prove to be a potential attractive therapeutic target in ESKD patients. Multiple retrospective observational studies comparing mortality outcomes between haemodialysis (HD) and peritoneal dialysis (PD) patients have been inconclusive. Randomised trials on this issue of clinical equipoise are clearly warranted but are unlikely to be feasible. Screening for stable CAD in asymptomatic ESKD patients remains a clinical dilemma which is unique to chronic dialysis patients being assessed for kidney transplantation. This has become particularly relevant in light of the recent ISCHEMIA-CKD trial which demonstrated no difference between optimal medical therapy and revascularisation upon CVD outcomes or mortality. The optimal strategy for screening is currently being investigated in the ongoing large international multi-centre CARSK trial. Here we discuss the pathophysiology, risk modification, treatment, screening and future directions of CAD in ESKD.

Myocardial fibrosis and calcification are attenuated by microRNA-129-5p targeting Asporin and Sox9 in cardiac fibroblasts.

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.

Myocardial calcification: a rare consequence of streptococcal toxic shock

A 51-year-old woman presented to our emergency room with a 4-day history of fever, chills, abdominal pain, vomiting, and diarrhoea.

PO-04-170 AUTOMATED CT-BASED PREDICTION OF VENTRICULAR ARRHYTHMIA

Robust risk stratification of post-myocardial infarction (MI) ventricular tachycardia (VT) is desirable to overcome the limitations of left ventricular ejection fraction (LVEF), the currently used criterion for implanting cardiac defibrillator devices. We hypothesized, that a fully automated CT-based technology could predict VT in post-MI patients. A fully automated CT image processing pipeline was implemented including AI-based LV wall segmentation followed by joint analysis and quantification of wall thickness (WT), intramural fat, and myocardial calcification (Fig.1A). A cohort of 132 patients with prior MI (66±11 years, 37±10% LVEF) with implanted cardiac devices underwent CT scan, and were subsequently followed by remote monitoring over an average of 6.6 years (80 ± 31 months). We analyzed the relationship between CT markers (WT, fat, calcification) and VT events at follow-up. Analysis of the wall thickness layers showed the optimal WT-derived marker was the ratio between areas of WT < 3mm and WT< 5mm (no VT 0.57±0.45 vs. VT 0.89±0.55; p<0.01). The amount of myocardial calcification was also found higher in patients with VT (no VT 0.10±0.38ml vs. VT 0.47±1.57ml, p=0.039), while the amount of fat did not differ significantly between groups (no VT 1.14±1.38ml vs. VT 1.21±1.01ml, p=0.771). The optimal cut-off for the WT 3/5mm ratio was 0.3. On Kaplan Meier analysis, this WT ratio was a powerful predictor of VT-free survival (Fig.1B, log rank P<0.01). In contrast, a LVEF<35% was not found to significantly relate to VT-free survival (Fig.1C, P=0.77). Automated analysis of post-MI scar is doable from CT images, allowing for improved risk stratification of future VT. The area of severe wall thinning divided by the total area of thinning appears to be the best marker of risk.

Acute myocardial calcification in a patient with fulminant myocarditis.

Relationship with Industry: None A 38-year-old man was admitted with a 3-week history of rapid clinical deterioration. The patient presented with multisystem inflammatory syndrome associated with multi-organ failure (white blood and polynuclear cells counts at respectively 54.40 and 51.60 *109/L; C-reactive protein, Ferritin and Fibrinogen levels at respectively, 214 mg/L, 1624 μg/L, and 8.31 g/L; and creatinine and bilirubin levels at respectively 397 μmol/L (4,49 mg/dL) and 57 μMol/L (3,33 mg/dL)). Large screening and multiple testing for bacterial and viral infections remained negative in a patient with Covid-19 infection 3-months earlier without vaccination. The patient was transferred to the Intensive Care Unit necessitating mechanical ventilation, hemodialysis, and inotropic support. Rapidly, diffuse ST elevation on electrocardiogram and increased levels of high-sensitivity cardiac I troponin (hs-cTnI = 135000 ng/L) and natriuretic peptide (NT-ProBNP = 72114 ng/L) were found. Coronary angiogram showed no significant coronary disease and transthoracic echocardiography (TTE) showed reduced left ventricular ejection fraction (LVEF = 40%). Cardiac magnetic resonance imaging confirmed diffuse and extensive gadolinium uptake. Despite negative cardiac biopsies, the diagnosis of fulminant myocarditis was made and the patient underwent corticosteroids bolus and intravenous immunoglobulin therapies. Clinical evolution was deemed favourable with a progressive decrease in systemic inflammatory process associated with a decrease in cardiac biomarkers levels. However, 2 weeks later, chest X-ray (Panel A) and TTE (Panel B) showed acute and impressive left ventricular calcified remodelling process with diffuse epicardial calcification and septal patchy fibrosis (whites triangles). The positron emission tomography (PET-CT) confirmed the diffuse FDG uptakes suggesting persistent local inflammatory process (Panel C) associated with large epicardial calcified remodelling (Panel D). The patient was discharged 1 month after the index admission with optimized heart-failure therapy and planned follow-up at the Heart Failure Clinic.

Fulminant myocarditis with massive myocardial calcification in an infant.

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