scholarly journals Drug-induced life-threatening arrhythmias and sudden cardiac death: A clinical perspective of long QT, short QT and Brugada syndromes

2018 ◽  
Vol 37 (5) ◽  
pp. 435-446 ◽  
Author(s):  
Diogo Ramalho ◽  
João Freitas
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Hyun Sok Yoo ◽  
Nancy Medina ◽  
María Alejandra von Wulffen ◽  
Natalia Ciampi ◽  
Analia Paolucci ◽  
...  

Abstract Background The congenital long QT syndrome type 2 is caused by mutations in KCNH2 gene that encodes the alpha subunit of potassium channel Kv11.1. The carriers of the pathogenic variant of KCNH2 gene manifest a phenotype characterized by prolongation of QT interval and increased risk of sudden cardiac death due to life-threatening ventricular tachyarrhythmias. Results A family composed of 17 members with a family history of sudden death and recurrent syncopes was studied. The DNA of proband with clinical manifestations of long QT syndrome was analyzed using a massive DNA sequencer that included the following genes: KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2, ANK2, KCNJ2, CACNA1, CAV3, SCN1B, SCN4B, AKAP9, SNTA1, CALM1, KCNJ5, RYR2 and TRDN. DNA sequencing of proband identified a novel pathogenic variant of KCNH2 gene produced by a heterozygous frameshift mutation c.46delG, pAsp16Thrfs*44 resulting in the synthesis of a truncated alpha subunit of the Kv11.1 ion channel. Eight family members manifested the phenotype of long QT syndrome. The study of family segregation using Sanger sequencing revealed the identical variant in several members of the family with a positive phenotype. Conclusions The clinical and genetic findings of this family demonstrate that the novel frameshift mutation causing haploinsufficiency can result in a congenital long QT syndrome with a severe phenotypic manifestation and an elevated risk of sudden cardiac death.


2019 ◽  
Vol 5 (1 (P)) ◽  
pp. 12
Author(s):  
Dicky Armein Hanafy

Sudden cardiac death is one of the leading causes of death in the western industrial nations. Most people are affected by coronary heart disease (coronary heart disease, CHD) or heart muscle (cardiomyopathy). These can lead to life-threatening cardiac arrhythmias. If the heartbeat is too slow due to impulse or conduction disturbances, cardiac pacemakers will be implanted. High-frequency and life-threatening arrhythmias of the ventricles (ventricular tachycardia, flutter or fibrillation) cannot be treated with a pacemaker. In such cases, an implantable cardioverter-defibrillator (ICD) is used, which additionally also provides all functions of a pacemaker. The implantation of a defibrillator is appropriate if a high risk of malignant arrhythmias has been established (primary prevention). If these life-threatening cardiac arrhythmias have occurred before and are not caused by a treatable (reversible) cause, ICD implantation will be used for secondary prevention. The device can stop these life-threatening cardiac arrhythmias by delivering a shock or rapid impulse delivery (antitachycardic pacing) to prevent sudden cardiac death. Another area of application for ICD therapy is advanced heart failure (heart failure), in which both main chambers and / or different wall sections of the left ventricle no longer work synchronously. This form of cardiac insufficiency can be treated by electrical stimulation (cardiac resynchronization therapy, CRT). Since the affected patients are also at increased risk for sudden cardiac death, combination devices are usually implanted, which combine heart failure treatment by resynchronization therapy and the prevention of sudden cardiac death by life-threatening arrhythmia of the heart chambers (CRT-D device). An ICD is implanted subcutaneously or under the pectoral muscle in the area of the left collarbone. Like pacemaker implantation, ICD implantation is a routine, low-complication procedure today.


Iatrogenicity ◽  
2018 ◽  
pp. 62-76
Author(s):  
Aalap Narichania ◽  
Yasuhiro Yokoyama ◽  
Win K. Shen

ESC CardioMed ◽  
2018 ◽  
pp. 2337-2341
Author(s):  
Jens Cosedis Nielsen ◽  
Jens Kristensen

The most common reason for sudden cardiac death is ischaemic heart disease. Patients who survive cardiac arrest are at particularly high risk of recurrent ventricular arrhythmia and sudden cardiac death, and are candidates for secondary prevention defined as ‘therapies to reduce the risk of sudden cardiac death in patients who have already experienced an aborted cardiac arrest or life-threatening arrhythmias’. The mainstay therapy for secondary prevention of sudden cardiac death is implantation of an implantable cardioverter defibrillator. Furthermore, revascularization and optimal medical therapy for heart failure and concurrent cardiovascular diseases should be ensured.


2020 ◽  
pp. 070674372094842
Author(s):  
Pao-Huan Chen ◽  
Shang-Ying Tsai ◽  
Chun-Hung Pan ◽  
Hu-Ming Chang ◽  
Yi-Lung Chen ◽  
...  

Objective: The pathogenesis of sudden cardiac death may differ between younger and older adults in schizophrenia, but evidence remains scant. This study investigated the age effect on the incidence and risk of the physical and psychiatric comorbidity for sudden cardiac death. Methods: Using 2000 to 2016 data from the Taiwan National Health Insurance Research Database and Department of Health Death Certification System, we identified a national cohort of 170,322 patients with schizophrenia, 1,836 of whom had a sudden cardiac death. Standardized mortality ratios (SMRs) were estimated. Hazard ratios and population attributable fractions of distinctive comorbidities for sudden cardiac death were assessed. Results: The SMRs of sudden cardiac death were all >1.00 across each age group for both sexes, with the highest SMR in male patients aged <35 years (30.88, 95% CI: 26.18–36.18). The fractions of sudden cardiac death attributable to hypertension and congestive heart failure noticeably increased with age. By contrast, the fraction attributable to drug-induced mental disorder decreased with age. Additionally, chronic hepatic disease and sleep disorder increased the risk of sudden cardiac death in patients aged <35 years. Dementia and organic mental disorder elevated the risk in patients aged between 35–54 years. Ischemic heart disease raised the risk in patients aged ≥55 years. Conclusions: The risk is increased across the lifespan in schizophrenia, particularly for younger male patients. Furthermore, physical and psychiatric comorbidities have age-dependent risks. The findings suggest that prevention strategies targeted toward sudden cardiac death in patients with schizophrenia must consider the age effect.


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