“Echocardiographic response” to sacubitril-valsartan: does it decrease defibrillation implantation, as well as the incidence of malignant arrhythmias? Response

Introduction. Brugada syndrome accounts for about 4% of sudden cardiac deaths (SCD). It is characterized by an ST-segment elevation in the right precordial electrocardiogram (EKG) leads.Case Presentation. We describe a 39-year-old healthy Caucasian man who was admitted to the intensive care unit after being cardioverted from ventricular fibrillation (VF) arrest. His past history was significant for an episode of syncope one month prior to this presentation for which he was admitted to an outlying hospital. EKG during that admission showed ST elevations in V1 and V2 leads, a pattern similar to Type 1 Brugada. A diagnosis of Brugada syndrome was missed and the patient had a cardiac arrest a month later. We discuss a short review of Brugada syndrome and emphasize the need to look for it in patients presenting with SCD and malignant arrhythmias.Conclusion. Physicians should always consider Brugada syndrome in the differential diagnosis of ST-segment elevation in anterior precordial leads of EKG and associated VT/VF. Although more than 17 years have passed since the first case was reported, increased awareness of this syndrome is needed to identify patients with EKG changes and treat them accordingly to prevent incidence of (SCD) and its deleterious complications.

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Disordered Myocardial Ca2+ Homeostasis Results in Substructural Alterations That May Promote Occurrence of Malignant Arrhythmias

Physiological Research ◽

10.33549/physiolres.933388 ◽

2016 ◽

pp. S139-S148 ◽

Cited By ~ 5

Author(s):

N. TRIBULOVA ◽

V. KNEZL ◽

B. SZEIFFOVA BACOVA ◽

T. EGAN BENOVA ◽

C. VICZENCZOVA ◽

...

Keyword(s):

Atrial Fibrillation ◽

Intact Animal ◽

Electron Microscopic Examination ◽

Atrial Pacing ◽

Cardiac Cell ◽

Cell Coupling ◽

Electron Microscopic ◽

Tissue Samples ◽

The Impact ◽

Malignant Arrhythmias

We aimed to determine the impact of Ca2+-related disorders induced in intact animal hearts on ultrastructure of the cardiomyocytes prior to occurrence of severe arrhythmias. Three types of acute experiments were performed that are known to be accompanied by disturbances in Ca2+ handling. Langedorff-perfused rat or guinea pig hearts subjected to K+-deficient perfusion to induce ventricular fibrillation (VF), burst atrial pacing to induce atrial fibrillation (AF) and open chest pig heart exposed to intramyocardial noradrenaline infusion to induce ventricular tachycardia (VT). Tissue samples for electron microscopic examination were taken during basal condition, prior and during occurrence of malignant arrhythmias. Cardiomyocyte alterations preceding occurrence of arrhythmias consisted of non-uniform sarcomere shortening, disruption of myofilaments and injury of mitochondria that most likely reflected cytosolic Ca2+ disturbances and Ca2+ overload. These disorders were linked with non-uniform pattern of neighboring cardiomyocytes and dissociation of adhesive junctions suggesting defects in cardiac cell-to-cell coupling. Our findings identified heterogeneously distributed high [Ca2+]i-induced subcellular injury of the cardiomyocytes and their junctions as a common feature prior occurrence of VT, VF or AF. In conclusion, there is a link between Ca2+-related disorders in contractility and coupling of the cardiomyocytes pointing out a novel paradigm implicated in development of severe arrhythmias.

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Histopathological Analysis of the Pro-Arrhythmogenic Changes in a Suspected Chagas Disease Sudden Death

Heart Research - Open Journal ◽

10.17140/hroj-7-155 ◽

2020 ◽

Vol 7 (1) ◽

pp. 11-16

Author(s):

Héctor O. Rodríguez ◽

Keyword(s):

Sudden Death ◽

Chagas Disease ◽

Vital Signs ◽

Histopathological Analysis ◽

Ischemic Disease ◽

Chronic Myocarditis ◽

Massive Necrosis ◽

Structural Disease ◽

Death Cases ◽

Malignant Arrhythmias

Background Sudden death is the principal cause of fatality in Chagas disease, afflicting to non-symptomatic patients younger than 50-years. For this, sudden death associated with chagasic malignant arrhythmias is underdiagnosed and their pathophysiological basis is poorly understood. Aims In this sense, this work aimed to analyze the histopathological alterations in cardiac structures specialized in the generation/conduction of action potential in an anatomopathological case of non-diagnosed sudden death living in a Chagasic endemic area. Methods The donor was a woman, 62-year-old, which ingressed without vital signs to the emergency room of “Antonio María Pineda” hospital, without any apparent antecedents of cardiac disease. The gross examination was normal, with no external evidence of structural/ischemic disease. Results Microscopic examination revealed nodal like cell depopulation, microvascular disturbances, chronic myocarditis with mononuclear and mast cell infiltrate plus extracellular matrix reaction, and profuse damage of neural structures placed in nodal region. Amastigote nest of Trypanosoma cruzi (T. cruzi) was detected. Conclusion These findings suggest a complex association among parasite persistence, sinus disease, micro-ischemia foci, and neural inflammation in the genesis of malignant arrhythmias of Chagas disease despite the absence of structural disease or massive necrosis. It is important to perform a protocol of examination for no explained sudden death cases in chagasic endemic countries, to avoid misdiagnosed of sudden death associated with Chagas disease.

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Case Report: Hypothyroidism Misdiagnosed as Fulminant Myocarditis in a Child

Frontiers in Cardiovascular Medicine ◽

10.3389/fcvm.2021.698089 ◽

2021 ◽

Vol 8 ◽

Author(s):

Nanjun Zhang ◽

Shuran Shao ◽

Yu Yan ◽

Yimin Hua ◽

Kaiyu Zhou ◽

...

Keyword(s):

Pediatric Patients ◽

Gamma Globulin ◽

Hemodynamic Instability ◽

Fulminant Myocarditis ◽

Common Disease ◽

Delay In Diagnosis ◽

Possible Cause ◽

Cardiac Enlargement ◽

Malignant Arrhythmias ◽

Third Degree Atrioventricular Block

Background: Hypothyroidism can lead to bradycardia, reduced cardiac output, cardiac enlargement, and abnormal electrocardiogram. However, hemodynamic instability and malignant arrhythmias due to hypothyroidism is rarely reported in children.Patient Findings: We report the case of a child with third-degree atrioventricular block, cardiogenic shock, and Adams Stokes Syndrome, who was initially misdiagnosed with fulminant myocarditis and was later found to have hypothyroidism during treatment.Summary: The child's condition did not improve after the administration of gamma globulin, methylprednisolone, and isoproterenol. Even after the placement of temporary pacemakers, the therapeutic effect was still not ideal. Upon reviewing the medical history, the child's condition improved rapidly after levothyroxine supplementation.Conclusions: Hypothyroidism is a common disease, but secondary severe cardiovascular lesions are particularly rare in children. Therefore, the delay in diagnosis can lead to serious cardiovascular manifestations. When pediatric patients develop severe AVB and bradycardia, hypothyroidism should be considered as a possible cause.

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