Cardiac Death In Young Adults Research Articles

Asymptomatic Adult Type ALCAPA Syndrome Coexisting with Bicuspid Aortic Valve- A Case Report

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA), also known as Bland-White-Garland syndrome (BWGS) is a rare variant of the congenital anomalies of the coronary arteries. Two forms, the infantile (most common) and the adult types (rare) of these syndromic manifestations have been reported in the literature. Affected infants present with myocardial infarction and congestive heart failure. Few of them survive the first year of life, without appropriate surgical intervention. Adult type ALCAPA syndrome is one of the important causes of malignant cardiac arrhythmias, acute coronary syndromes, valvular pathologies and sudden cardiac death in young adults and adults. Asymptomatic adult type ALCAPA is uncommon, much more so its coexistence with bicuspid aortic valve (BAV). We present a 65-year-old patient with ALCAPA and BAV, who was largely asymptomatic. She had ligation of the ALCAPA, and aortic valve replacement, with a very good outcome.

Peptide-Based Targeting of the L-Type Calcium Channel Corrects the Loss-of-Function Phenotype of Two Novel Mutations of the CACNA1 Gene Associated With Brugada Syndrome.

Brugada syndrome (BrS) is an inherited arrhythmogenic disease that may lead to sudden cardiac death in young adults with structurally normal hearts. No pharmacological therapy is available for BrS patients. This situation highlights the urgent need to overcome current difficulties by developing novel groundbreaking curative strategies. BrS has been associated with mutations in 18 different genes of which loss-of-function (LoF) CACNA1C mutations constitute the second most common cause. Here we tested the hypothesis that BrS associated with mutations in the CACNA1C gene encoding the L-type calcium channel (LTCC) pore-forming unit (Cavα1.2) is functionally reverted by administration of a mimetic peptide (MP), which through binding to the LTCC chaperone beta subunit (Cavβ2) restores the physiological life cycle of aberrant LTCCs. Two novel Cavα1.2 mutations associated with BrS were identified in young individuals. Transient transfection in heterologous and cardiac cells showed LoF phenotypes with reduced Ca2+ current (ICa). In HEK293 cells overexpressing the two novel Cavα1.2 mutations, Western blot analysis and cell surface biotinylation assays revealed reduced Cavα1.2 protein levels at the plasma membrane for both mutants. Nano-BRET, Nano-Luciferase assays, and confocal microscopy analyses showed (i) reduced affinity of Cavα1.2 for its Cavβ2 chaperone, (ii) shortened Cavα1.2 half-life in the membrane, and (iii) impaired subcellular localization. Treatment of Cavα1.2 mutant-transfected cells with a cell permeant MP restored channel trafficking and physiologic channel half-life, thereby resulting in ICa similar to wild type. These results represent the first step towards the development of a gene-specific treatment for BrS due to defective trafficking of mutant LTCC.

Abstract 13599: A Truncated Mutation in Filamin C Reveals Non-myocyte Contributions to Hypertrophic Cardiomyopathy in Ipsc-derived Cardiac Fibroblasts

Introduction: Hypertrophic cardiomyopathy (HCM) is a cardiac genetic disorder that affects 1:500 individuals and represents one of the main causes of sudden cardiac death in young adults. Several mutations have been associated with HCM, including MYH7 and FLNC . The discovery of induced pluripotent stem cells (IPSC), has provided a unique patient- and disease-specific model to study cardiac disease. Although iPSC derived cardiomyocytes (IPSC-CMs) can provide a genetically diverse human model to study mechanisms of disease, the heart relies in a three-dimensional network of cells that actively participate in the development of hypertrophy. Hypothesis: We hypothesize that mutations causing HCM affect not only CMs, but other non-myocyte cell types such as cardiac fibroblasts contributing to the phenotype of the disease. Methods: IPSCs were reprogrammed from an HCM patient harboring a pathogenic mutation on FLNC (p. Ile616Aspfs*4) using Sendai virus. Cells were differentiated to cardiomyocytes (IPSC-CMs) and cardiac fibroblasts (IPSC-CFs) and cultured for 30 days before analysis. Gene expression, morphology and wound healing (WH) were analyzed in IPSC-CMs and IPSC-CFs. Results: We observed that IPSC-CFs show higher expression of FLNC than IPSC-CMs (CT CM: 1.04±0.19 vs CT CF: 4.05±0.97, **p<0.01). Besides, FLNC mutated (MT) IPSC-CFs showed lower expression of FLNC when compared to controls (CT), with no changes in expression in IPSC-CMs. Expression of the fibrotic markers POSTN , SMA and THY1 was higher in IPSC-CFs from MT. Immunostaining revealed changes in morphology in IPSC-CFs of MT with accumulation of FLNC in the nucleus. Treatment with TGF-b showed upregulation of CCL2 , SMA , POSTN , COL1A1 and FLNC in MT IPSC-CFs. Wound healing assay revealed no changes in cell migration between CT and MT, although TGF-b treatment increased WH % in MT (MT: 22.5±1.5% vs MT TGF: 59.4±6.5% at 8hs, **p<0.01). Conclusions: Based on our results, we conclude that CFs play an important role on the development of HCM; with higher changes in gene expression, cell migration and morphology than those observed in CMs. Further functional studies will provide evidence of the effects of these changes on the phenotype of the disease.

Eosinophilic Myocarditis as a Cause of Death: A Case Diagnosed at Autopsy

Abstract Introduction/Objective Eosinophilic (Loffler) myocarditis is a rare disease defined by the influx of eosinophils into the endocardium and myocardium. Etiologies are numerous and include drug or hypersensitivity reactions, hypereosinophilic syndrome, hematologic malignancies, and parasitic infections. It is a diagnostically challenging entity. Presenting symptoms recorded in the literature are indefinite and nonspecific; heart failure, demonstrable arrhythmia, and elevated cardiac biomarkers. This is especially the case among younger, otherwise healthy patients without classical risk factors for atherosclerotic coronary artery disease. Methods Herein we present several cases of sudden cardiac death in young adults, including a case of unknown eosinophilic myocarditis, which highlights the potential trials in the diagnosis of this disease. Results Autopsies were performed on several adults (age range, 30-40 years) thought to have died of cardiac causes. This included a 30-year-old African American female with no significant known medical history who presented with a chief complaint of palpitations. The initial clinical impression at an outside institution was of cardiac amyloidosis. But the Technetium99 scan was inconclusive. Despite clinical management, she developed ventricular arrhythmias and could not be resuscitated. There was a vague history of taking nutritional supplements from a local grocery store. Gross findings at autopsy included circumferential subepicardial erythema, thymic enlargement (60g), and congested lungs. The heart was thoroughly sampled. Microscopic examination revealed diffuse infiltration of eosinophils, mast cells, lymphocytes and macrophages with mild myocyte necrosis and interstitial edema in all sections. There were no giant cells, no interstitial deposition of amorphous acellular material and no focus of infarcted myocardium. Thymic sections were histologically normal. Acetylcholine receptor antibody panel was negative. Conclusion We conclude that eosinophilic myocarditis though rare (0.5% unsuspected and 0.1% suspected cases), is a distinctive cause of death with a specific microscopic presentation. Our case also included thymic enlargement at autopsy – a finding not previously noted.

Abstract MP114: Cardiotropic Adenovirus Increases Arrhythmia Susceptibility During Acute Infection

Myocarditis is responsible for up to 42% of sudden cardiac death in young adults yet mechanisms underlying virally-induced arrhythmia remain elusive. Adenovirus is a leading etiological agent of myocarditis but due to species-specificity, in vivo models are limited. Altered cardiac gap junction function underlies sudden cardiac death and given that gap junctions also propagate antiviral immune responses, we hypothesized adenovirus would target intercellular coupling, leading to arrhythmogenesis. Employing a recently described strain of mouse adenovirus, MAdV-3, we investigated cardiotropism, arrhythmia susceptibility, and molecular mechanisms of a virally-induced arrhythmogenic substrate. Adult C57BL/6 mice were inoculated with MAdV-3 and infection allowed to progress for one week. Viral genomes were detected by qPCR to measure tissue tropism together with whole animal histopathology. Echo- and electrocardiography were used to measure cardiac function and electrical activity. Viral effects on transcription and junctional protein/ion channel expression and localization were quantified using RT-qPCR, confocal microscopy, and western blotting. Finally, ex vivo optical mapping was employed to test conduction defects and susceptibility to arrhythmia. We find MAdV-3 viral genomes specifically enriched in heart tissue, confirming cardiotropism. Immune cell infiltration was not detected in the heart and no cardiomyopathy was apparent by echocardiography. RR interval widening, however, does occur in MAdV-3 infected mice with reductions in cardiac ion channel and gap junction mRNA transcripts. Optical mapping experiments show that conduction velocity is altered in acutely infected hearts and norepinephrine challenge uncovered electrical impairment presenting as atrioventricular dissociation with increased premature ventricular contraction burden. Our data demonstrate that MAdV-3 is cardiotropic and acute infection result in changes in cardiac electrical activity prior to development of cardiomyopathy or a detectable immune response. MAdV-3 infection is a novel model for adenoviral myocarditis, providing insights into viral subversion of cardiac intercellular coupling and mechanisms of arrhythmogenesis.

Relation of Late Gadolinium Enhancement and Extracellular Volume Fraction to Ventricular Arrhythmias in Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HC) represents a major cause of sudden cardiac death in young adults. Late gadolinium enhancement (LGE) and extracellular volume (ECV) by T1 mapping are cardiac magnetic resonance (CMR) techniques to quantify fibrosis in HC. The relationships of LGE and ECV with ventricular arrhythmia, left ventricular (LV) diastolic function, and risk factors for sudden cardiac death (SCD) in HC are unclear. We studied 103 HC patients (mean age 51 ± 14, 42% women) who underwent CMR from 2012 to 2014. Global LGE and mean ECV were evaluated in relation to history of nonsustained ventricular tachycardia (NSVT), diastolic function by echocardiography, and SCD risk factors. LGE was present in 71 (69%) subjects. Wide variation was demonstrated in LGE (0.5% to 45.9%) and mean ECV (17.6% to 47.4%). Prevalence of NSVT increased continuously with LGE and was greater in subjects with ECV above the study population mean (27%). Increased LGE was associated with LV diastolic dysfunction and LV wall thickness. In conclusion, while ECV appears to have a threshold (27%) above which it is associated with NSVT, LGE demonstrates a more robust relationship with NSVT and measures of diastolic dysfunction.

TMEM43-S358L mutation enhances NF-\u03baB-TGF\u03b2 signal cascade in arrhythmogenic right ventricular dysplasia/cardiomyopathy

Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is a genetic cardiac muscle disease that accounts for approximately 30% sudden cardiac death in young adults. The Ser358Leu mutation of transmembrane protein 43 (TMEM43) was commonly identified in the patients of highly lethal and fully penetrant ARVD subtype, ARVD5. Here, we generated TMEM43 S358L mouse to explore the underlying mechanism. This mouse strain showed the classic pathologies of ARVD patients, including structural abnormalities and cardiac fibrofatty. TMEM43 S358L mutation led to hyper-activated nuclear factor κB (NF-κB) activation in heart tissues and primary cardiomyocyte cells. Importantly, this hyper activation of NF-κB directly drove the expression of pro-fibrotic gene, transforming growth factor beta (TGFβ1), and enhanced downstream signal, indicating that TMEM43 S358L mutation up-regulates NF-κB-TGFβ signal cascade during ARVD cardiac fibrosis. Our study partially reveals the regulatory mechanism of ARVD development.

Familiäre Arrhythmieerkrankungen mit strukturell normalen Herzen

ZusammenfassungAngeborene kardiale Ionenkanalerkrankungen/familiäre Arrhythmieerkrankungen sind häufige Ursachen für arrhythmogene Synkopen und den plötzlichen Herztod bei jungen Erwachsenen. Sie sind mittlerweile bei rechtzeitiger Diagnose und adäquater antiarrhythmischer Therapie gut beherrschbar. Der (verbesserten) Risikostratifizierung kommt in der Behandlung eine entscheidende Rolle zu. Da sich das arrhythmogene Risiko mit der Zeit ändern kann, sind regelmäßige Verlaufskontrollen indiziert. Die genetischen und pathophysiologischen Grundlagen werden zunehmend besser verstanden und so gezieltere (mechanismusbasierte) Therapien möglich.

NF-κB-mediated metabolic remodelling in the inflamed heart in acute viral myocarditis

Acute viral myocarditis (VM), characterised by leukocyte infiltration and dysfunction of the heart, is an important cause of sudden cardiac death in young adults. Unfortunately, to date, the pathological mechanisms underlying cardiac failure in VM remain incompletely understood. In the current study, we investigated if acute VM leads to cardiac metabolic rewiring and if this process is driven by local inflammation. Transcriptomic analysis of cardiac biopsies from myocarditis patients and a mouse model of VM revealed prominent reductions in the expression of a multitude of genes involved in mitochondrial oxidative energy metabolism. In mice, this coincided with reductions in high-energy phosphate and NAD levels, as determined by Imaging Mass Spectrometry, as well as marked decreases in the activity, protein abundance and mRNA levels of various enzymes and key regulators of cardiac oxidative metabolism. Indicative of fulminant cardiac inflammation, NF-κB signalling and inflammatory cytokine expression were potently induced in the heart during human and mouse VM. In cultured cardiomyocytes, cytokine-mediated NF-κB activation impaired cardiomyocyte oxidative gene expression, likely by interfering with the PGC-1 (peroxisome proliferator-activated receptor (PPAR)-γ co-activator) signalling network, the key regulatory pathway controlling cardiomyocyte oxidative metabolism. In conclusion, we provide evidence that acute VM is associated with extensive cardiac metabolic remodelling and our data support a mechanism whereby cytokines secreted primarily from infiltrating leukocytes activate NF-κB signalling in cardiomyocytes thereby inhibiting the transcriptional activity of the PGC-1 network and consequently modulating myocardial energy metabolism.

Survival and weak chaos.

Survival analysis in biology and reliability theory in engineering concern the dynamical functioning of bio/electro/mechanical units. Here we incorporate effects of chaotic dynamics into the classical theory. Dynamical systems theory now distinguishes strong and weak chaos. Strong chaos generates Type II survivorship curves entirely as a result of the internal operation of the system, without any age-independent, external, random forces of mortality. Weak chaos exhibits (a) intermittency and (b) Type III survivorship, defined as a decreasing per capita mortality rate: engineering explicitly defines this pattern of decreasing hazard as ‘infant mortality’. Weak chaos generates two phenomena from the normal functioning of the same system. First, infant mortality—sensu engineering—without any external explanatory factors, such as manufacturing defects, which is followed by increased average longevity of survivors. Second, sudden failure of units during their normal period of operation, before the onset of age-dependent mortality arising from senescence. The relevance of these phenomena encompasses, for example: no-fault-found failure of electronic devices; high rates of human early spontaneous miscarriage/abortion; runaway pacemakers; sudden cardiac death in young adults; bipolar disorder; and epilepsy.

Progranulin ameliorates coxsackievirus-B3-induced viral myocarditis by downregulating Th1 and Th17 cells

Viral myocarditis, which is caused by Coxsackievirus B3 (CVB3) infection, is a leading reason of sudden cardiac death in young adults. Progranulin (PGRN), a pleiotropic growth factor, has been shown to exert anti-inflammatory function in a variety of inflammatory diseases. However, the expression and function of PGRN in the pathogenesis of viral myocarditis remain largely unknown. In this study, we found that PGRN levels in plasma and cardiac tissues were significantly upregulated post CVB3 infection, and negative correlated with disease severity. PGRN deficiency significantly exacerbated, whereas recombinant PGRN treatment attenuated CVB3-induced myocarditis in mice. PGRN downregulated Th1 and Th17 cell responses and cytokine production in vitro and in vivo, whereas its effect on viral myocarditis was Treg cell independent. Furthermore, PGRN regulated Th1 and Th17 cells differentiation through inhibition of the JAK/STAT pathway. Therefore, our findings reveal a critical role for PGRN in reducing CVB3-induced myocarditis and suggest that PGRN maybe a novel therapeutic treatment for viral myocarditis.

Brugada Syndrome: A Primer for Nurse Practitioners

Abstract Brugada syndrome (BrS) is a less known cardiac condition which falls into the category of a channelopathies. BrS has been diagnosed for more than 2 decades. Currently BrS remains a major cause of sudden cardiac death in young adults who have no known abnormal heart structure. Nurse practitioners' awareness of the clinical presentation, diagnosis, treatment, and ongoing care is essential for maximizing patient outcomes.

High-throughput sequencing and better understanding of aetiological spectrum of Hypertrophic cardiomyopathy

Background and objective Hypertrophic cardiomyopathy (HCM) is one of the leading causes of sudden cardiac death in young adults, with a prevalence of 1/500 in the general population. HCM is a genetic disease usually related to a sarcomeric gene mutation. Despite advances in knowledge, elucidation of the genetic cause is reached in only 30–60% of cases with conventional Sanger sequencing and analysis of a limited number of genes (usually the five major sarcomeric genes). We hypothesized that high-throughput sequencing of a large panel of genes will allow a more comprehensive evaluation of the etiologic spectrum of HCM. Methods and results We used high-throughput sequencing technology, with a panel of 107 genes (all the various cardiomyopathies and arrhythmia genes) that we recently developed (Nimblegen capture then Illumina MiSeq sequencing), in a cohort of 97 unrelated patients with HCM. We detected 2740 variants including 99 variants that we classified as pathogenic using restrictive criteria. A pathogenic mutation was identified (i) in 31 patients (32% of cohort of patients) in the group of 5 conventional sarcomeric genes (MYBPC3, MYH7, TNNT2, MYL2, TNNI3) including patients with multiple mutations, (ii) in 8 patients (8%) with a mutation in the group of additional sarcomeric genes (such as MYH6), (iii) in 4 patients (4%) with a mutation in the group of non-sarcomeric genes previously associated to HCM (such as GLA responsible for Fabry disease) and (iv) in additional patients with a mutation in new genes not yet reported in HCM (such as AKAP9). Conclusion High-throughput sequencing of a large panel of genes associated with hereditary heart diseases allowed us to determine the large genetic spectrum of HCM. We confirmed the prominent role of sarcomeric genes, highlighted the role of non-sarcomeric causes (some with specific therapeutics) and identified mutations in potential new genes responsible for the disease.

Abstract 21374: Adenovirus Targets Cardiac Gap Junctions to Facilitate Viral Replication

Myocarditis is a leading cause of sudden cardiac death in young adults, accounting for 20% of cases under 40 years of age in the United States. Adenovirus is a major etiological agent in this disease yet much remains unknown regarding pathogenesis and predisposition to infection. During adenoviral infection, viral proteins uncouple cell cycle checkpoints for viral DNA genome replication to occur. Connexin43 (Cx43) gap junctions play an essential role in propagation of action potentials to precipitate each heartbeat. Cx43 has also been implicated in cell cycle regulation, leading us to hypothesize that adenovirus targets Cx43 to facilitate viral replication, resulting in arrhythmogenic alterations in cardiac intercellular communication. We find reduced Cx43 expression at the mRNA and protein level within 24 hours of infection with adenovirus type 5 (Ad5) in human epithelial cells. Studies in human induced pluripotent stem cell-derived cardiomyocytes reveal alterations in calcium transient propagation and reduced Cx43 protein levels. Growth factor signaling is activated by early Ad5 proteins and is known to negatively regulate gap junction coupling. We performed genetic screens and have identified the viral protein E4-ORF1 as sufficient in suppression of Cx43 expression and modulation of cardiac transcription factors. siRNA-mediated knockdown of Cx43 protein enhances viral genome replication while transient overexpression of Cx43 significantly inhibits late viral protein synthesis and genome replication. Finally, using dominant-negative trafficking-dead and closed-channel Cx43 mutants, we conclude that inhibition of Ad5 replication by Cx43 is gap junction dependent. Together, these data provide novel insight into molecular mechanisms underlying arrhythmogenic viral myocarditis in addition to understanding the role of Cx43 in adenoviral pathogenesis. Revealing viral mechanisms of gap junction dissolution will contribute not just to the development of novel antiviral therapeutics, but will also provide insight into fundamental Cx43 biology relevant to other forms of heart disease.

Sudden unexplained cardiac deaths in young adults: a call for multidisciplinary approach

The investigation of death in young (<35 years), previously fit individuals, calls for a detailed autopsy with emphasis placed upon the examination of the heart. In most instances, the cause of cardiac death can be identified during autopsy. However, a large percentage of sudden deaths remain unexplained even after comprehensive medicolegal investigation, including autopsy, and are labelled as autopsy-negative sudden unexplained cardiac death (SUD). Still, when you look to the law, an autopsy, a much needed truth-finding-instrument, usually is not mandatory and is left up to the discretion of various medical or legal authorities, which when making a decision, balance various, often conflicting interests of the state and society on the one hand and of the deceased and his family on the other. Cardiac molecular autopsy calls for a close cooperation between medical examiner, pathologist, family physician, cardiologist, geneticist, and the relatives. Multidisciplinary approach and the identification of genetic cause of SUD enable proper genetic counselling for surviving relatives as well as for implementing specific preventive/therapeutic strategies, e.g. implantable cardioverter-defibrillator (ICD) implantation.

Identification of a novel hypertrophic cardiomyopathy-associated mutation using targeted next-generation sequencing.

Hypertrophic cardiomyopathy (HCM), one of the most common forms of myocardial diseases, is the major cause of sudden cardiac death in young adults and competitive athletes. Analyses of gene mutations associated with HCM are valuable for its molecular diagnosis, genetic counseling, and management of familial HCM. To dissect the relationship between the clinical presentation and gene mutations of HCM, the genetic characterizations of 19 HCM-related genes in 18 patients (8 cases from 6 pedigrees with familial HCM and 10 cases without familial HCM) were detected using next-generation sequencing (NGS). As a result, 12 disease-related mutations were identified in the 18 subjects, including 6 single mutations and 3 double mutations [MYBPC3 (p.Gln998Glu) plus TNNI3 (p.Arg145Gly), PRKAG2 (p.Gly100Ser) plus MYBPC3 (p.Lys1209Serfs*28) and TNNI3 (p.Glu124Gln) plus GLA (p.Trp47*)]. The 3 heterozygous double mutations were discovered for the first time in the malignant familial HCM patients. Of the 6 single mutations, a novel mutation was found in tafazzin (TAZ, p.Ile208Val), and a mutation in β-myosin heavy chain gene (MYH7, p.Arg54Gln), which was reported as rare in the general population, was firstly found in one HCM patient. Identification of novel and rare mutations in HCM patients have added new data to the spectrum of gene mutations associated with this disease. These findings provide an essential basis for the molecular diagnosis and better management of family members at risk of familial HCM.

Mort subite d’un homme jeune dans le cadre de séquelles tardives d’une pathologie pédiatrique : à propos d’un cas

In France, sudden death is responsible every year for 40,000 deaths. The most frequent etiology is cardiac disease. Atheromatous-related pathology is the most common etiology beyond 35, but cardiomyopathies and channelopathies are responsible for a significant number of deaths in young adults. Some acquired disorders can also cause sudden cardiac death. We report the case of a 17-year-old man who died suddenly after sport. Autopsy and pathological study found multiple giant coronary aneurysms. Thrombosis and fibrous scar of myocardial ischemic events were observed. These lesions were in favor of late sequelae of Kawasaki disease. Kawasaki disease is a rare but not exceptional cause of sudden cardiac death in young adults. In the lack of known clinical history, some aspects, even not specific, should evoke this diagnosis. Even in front of apparent good clinical tolerance, these sequelae require appropriate follow-up because of a significant risk of sudden death.

A rare presentation of spontaneous ventricular tachycardia in young adult

Arrhythmogenic right ventricular dysplasia (ARVD) is a common cause of sudden cardiac death in young adults. It is a disease that has a wide spectrum of presentation. Early identification of the disorder is of paramount importance considering the fatal complications. Here, with this case, a rare sporadic presentation of ARVD, we try to discuss the various presentations, methods of diagnosis and options for treatment for this frequently masquerading and occasionally fatal disorder of cardiac myocytes.

Prevalence of congenital coronary artery anomalies as shown by multi-slice computed tomography coronary angiography: a single-centre study from Turkey.

ObjectiveCoronary artery anomaly (CAA) is a remarkable etiological factor for sudden cardiac death in young adults. The incidence of CAA is unknown, with most reliable data available based on postmortem/angiography investigations. This study aimed to assess the prevalence of different forms of coronary anomalies, and to investigate the relationships between demographic data and occurrence of CAA.MethodsA total of 2401 consecutive patients (1805 men; mean age, 56 ± 11.7 years), who were referred between January 2005 and December 2008 for noninvasive multi-slice computed tomography (MSCT) imaging, were retrospectively analysed.ResultsA total of 225 cases (191 men; mean age, 55.9 ± 12) of CAAs were identified (9.37%). Because 11 patients had multiple muscular bridges of the coronary arteries, 236 coronary artery anomalies were found in these 225 patients. Cases were classified into three groups: group 1, coronary anomalies of origin and distribution (n = 36, 1.5%); group 2, anomalies of intrinsic coronary arterial anatomy (n = 180, 7.49%); and group 3, anomalies of coronary termination (n = 9, 0.4%).ConclusionThe prevalence of CAA was 9.37% in our single-centre study, which is consistent with previous research. A minimally invasive tool, such as MSCT angiography, should be used to identify CAA.

Modern Imaging of Myocarditis: Possibilities and Challenges

Myocarditis is known as the chameleon of cardiac diseases. The symptoms and the course of disease vary greatly so that it is often challenging to establish a diagnosis. Early and accurate diagnosis is of utmost importance, since myocarditis is one of the leading causes of sudden cardiac death in young adults and represents an important precursor to dilated cardiomyopathy. Due to the constraints of the routinely used diagnostic approach, including clinical history and examination, laboratory testing, and electrocardiogram, different imaging modalities have emerged over the last decades as contributors to the noninvasive diagnosis of myocarditis. With this interdisciplinary review we would like to present the current state-of-the-art imaging of myocarditis across all available imaging modalities (i. e., echocardiography, cardiac magnetic resonance, cardiac computed tomography, and nuclear medicine). Furthermore, we present novel imaging techniques that might become useful in the near future for easier and more accurate diagnosis of this highly relevant disease. • Different imaging modalities are increasingly used in the diagnostic workup of myocarditis. • Several emerging imaging techniques are currently on the way to becoming part of the clinical routine. • This review summarizes the diagnostic value of echocardiography, CMR, CT, and nuclear medicine imaging. • There is special focus on the possibilities and challenges of novel imaging tools within the different modalities.