Hypertension, left ventricular hypertrophy, and sudden cardiac death

Shenasa, Mohammad; Shenasa, Hossein

doi:10.1016/j.ijcard.2017.03.002

Cited by 173 publications

(126 citation statements)

References 22 publications

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“…SCD was defined as unexpected death without obvious noncardiac causes occurring within 24 h of being in normal health [14,22]. Because cardiac hypertrophy is an established risk factor for SCD [25,30], subjects were placed into three groups according to the cardiac size, namely SCD with cardiac hypertrophy (SCH), compensated cardiac hypertrophy (CCH), and control. Cardiac hypertrophy was defined as hypertrophy with a ratio of heart weight to body height >2.5 g/cm [31].…”

Section: Subjectsmentioning

confidence: 99%

“…However, retrospective studies including autopsies have reported that numerous SCD cases have coronary atherosclerosis and left ventricular hypertrophy [22,23]. Therefore, it is generally accepted that the primary direct cause of SCD is malignant ventricular arrhythmias based on the structural and electrical remodeling secondary to coronary artery disease and pressure overload [24,25]. Studies are required to elucidate myocardial molecular changes that contribute to pathological remodeling.…”

Section: Introductionmentioning

confidence: 99%

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Myocardial cathepsin D is downregulated in sudden cardiac death

et al. 2020

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Cathepsins are the major lysosomal proteases that maintain intracellular homeostasis. Herein, we investigated the alterations in myocardial cathepsin expression during aging, cardiac hypertrophy, and sudden cardiac death (SCD). Cardiac tissue and blood were sampled from autopsy cases. Subjects were classified into three groups: SCD with cardiac hypertrophy (SCH), compensated cardiac hypertrophy (CCH), and control. Immunoblotting was performed for the major cardiac cathepsins and their targets: cathepsin B, D, and L (CTSB/D/L), p62, ATP synthase subunit c (ATPSC), and α-synuclein (ASNC). Immunohistochemical analysis and ELISA using serum samples were performed for CTSD. Cardiac CTSB and CTSD were upregulated with age (r = 0.63 and 0.60, respectively), whereas the levels of CTSL, p62, ATPSC, and ASNC remained unchanged. In age-matched groups, cardiac CTSD was significantly downregulated in SCH (p = 0.006) and CTSL was moderately downregulated in CCH (p = 0.021); however, p62, ATPSC, and ASNC were not upregulated in cardiac hypertrophy. Immunohistochemistry also revealed decreased myocardial CTSD levels in SCH, and serum CTSD levels were relatively lower in SCH cases. Overall, these results suggest that upregulation of cardiac CTSB and CTSD with age may compensate for the elevated proteolytic demand, and that downregulation of CTSD is potentially linked to SCH. OPEN ACCESS Citation: Kakimoto Y, Sasaki A, Niioka M, Kawabe N, Osawa M (2020) Myocardial cathepsin D is downregulated in sudden cardiac death. PLoS ONE 15(3): e0230375. https://doi.org/10.

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Section: Subjectsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Myocardial cathepsin D is downregulated in sudden cardiac death

et al. 2020

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“…These cells mainly compensate for the increase in pressure load by inducing hypertrophy, which will increase energy and oxygen consumption in cardiomyocytes. If the load continues to increase, the reduction of the coronary blood supply can lead to myocardial ischaemia, hypoxia or even apoptosis . Apoptosis arrests the process of oxidative phosphorylation and reduces the production of adenosine triphosphate, which leads to energy barrier .…”

Section: Introductionmentioning

confidence: 99%

“…If the load continues to increase, the reduction of the coronary blood supply can lead to myocardial ischaemia, hypoxia or even apoptosis. [3] Apoptosis arrests the process of oxidative phosphorylation and reduces the production of adenosine triphosphate, which leads to energy barrier. [4] Cardiomyocyte apoptosis is regarded as a key determinant of cardiac structure and function [5,6] and results in a decrease in cardiomyocyte quantity.…”

Section: Introductionmentioning

confidence: 99%

Icariside II prevents hypertensive heart disease by alleviating endoplasmic reticulum stress via the PERK/ATF-4/CHOP signalling pathway in spontaneously hypertensive rats

Yue

et al. 2018

Journal of Pharmacy and Pharmacology

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Objectives Reducing endoplasmic reticulum stress (ERS)‐induced cardiomyocyte apoptosis is a key strategy for preventing hypertensive heart disease. In our previous study, Icariside II can improve left ventricular remodelling in spontaneously hypertensive rats (SHRs). This study aims to determine whether Icariside II can exert its effect by inhibiting ERS‐induced cardiomyocyte apoptosis via the PERK/ATF‐4/CHOP signalling pathway. Methods Spontaneously hypertensive rats were randomly divided into model group and Icariside II groups. The rats in the Icariside II groups were intragastrically administrated with Icariside II 4, 8 and 16 mg/kg from 14 to 26 week‐age, respectively. The left ventricular function was measured at the 18, 22 and 26 week‐age by small animal ultrasound. At the end of the 26th week, cardiomyocyte apoptosis was analysed and the levels of GRP78, PERK, ATF‐4 and CHOP gene and protein were detected. Key findings The function of left ventricular became declined with age in SHRs, but improved in Icariside II groups. Myocardial apoptosis was aggravated in SHRs, but alleviated in Icariside II groups. Icariside II could reduce the levels of GRP78, PERK, ATF‐4, CHOP gene and protein that increased in SHRs. Conclusions Icariside II prevents hypertensive heart disease by alleviating ERS‐induced cardiomyocyte apoptosis, and its mechanism is related to the impediment of the PERK/ATF‐4/CHOP signalling pathway.

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“…또한 유전적인 원인이 나 다른 질병에 의한 이차적인 좌심실 과부하에 의해 병리학적 으로 증가한 상태가 될 수 있다 [6]. 좌심실에 과부하를 주는 대표 적인 원인으로는 고혈압이 잘 알려져 있다 [1]. 이러한 좌심실 비 대에 영향을 미치는 유전자를 발굴하기 위한 전장 유전체 상관 분석도 여러 연구진에서 진행되었다 [7][8][9][10].…”

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Genetic Polymorphisms ofSLC8A1Are Associated with Hypertension and Left Ventricular Hypertrophy in the Korean Population

Park

Kim

Jin

2019

Korean J Clin Lab Sci.

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Hypertension (HTN) is one of the major chronic diseases, and HTN is defined as being in a state of continuous high blood pressure. Left ventricular hypertrophy (LVH) is a condition in which the mass of the left ventricle has increased, and HTN is a leading cause of LVH. HTN and LVH are known to be caused by the interaction of environmental factors and genetic factors. It has been reported that the polymorphisms of SLC8A1, among the genetic factors that affect high blood pressure, are related to salt sensitivity hypertension. In this study, the genetic polymorphisms of SLC8A1 were chosen based on the Korean Genome and Epidemiology data. Logistic regression analysis was then performed for HTN and LVH. Linear regression analysis was also performed for systolic blood pressure (SBP) and diastolic blood pressure (DBP). As a result, 5 SNPs showed statistically significant associations (P＜0.05) with HTN, and 10 SNPs showed statistically significant associations with LVH. rs1002671 and rs9789739 showed significant correlation at the same time with HTN and LVH. These results suggest that the polymorphisms of the SLC8A1 gene are linked to the development of HTN and LVH in Koreans. We expect these results to help us understand the pathogenic mechanisms for HTN and LVH. Candidate gene analysisHypertension Left ventricular hypertrophy SLC8A1 SNP 서 론 고혈압(hypertension, HTN)은 지속적으로 혈압이 높은 상 태를 의미하는 것으로 주요한 만성질환 중 한 가지이다. 이렇게 혈압이 높은 상태를 유지하게 되면 좌심실 비대, 가슴막 손상 기 능 장애, 승모판 역류 등을 포함한 고혈압에 의한 심장질환을 유 발하는 주요한 원인이 된다. 이러한 변화는 심방세동과 심실 부 정맥과 같은 부정맥으로 이어지며 급성심장사(sudden cardiac death, SCD)의 위험인자로도 알려져 있다[1]. 고혈압은 다양한 환경적 및 유전적 위험 인자들의 상호 작용으로 발생하는 질환 으로 잘 알려져 있는데, 환경적인 요인뿐만 아니라 고혈압에 영 향을 미치는 유전적 요인에 대한 연구도 활발하게 진행되고 있 다[2-4]. 특히 일반적인 고혈압에 비하여 염분에 대해 민감하게 증가하는 고혈압(salt sensitive hypertension)은 심혈관 질환 발병의 증가와 생존율 감소와 관련이 있는 것으로 밝혀졌다[5]. 좌심실 비대(left ventricular hypertrophy, LVH)는 심근세 Korean J Clin Lab Sci. 2019;51(3):286-293

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Hypertension, left ventricular hypertrophy, and sudden cardiac death

Cited by 173 publications

References 22 publications

Myocardial cathepsin D is downregulated in sudden cardiac death

Myocardial cathepsin D is downregulated in sudden cardiac death

Icariside II prevents hypertensive heart disease by alleviating endoplasmic reticulum stress via the PERK/ATF-4/CHOP signalling pathway in spontaneously hypertensive rats

Genetic Polymorphisms ofSLC8A1Are Associated with Hypertension and Left Ventricular Hypertrophy in the Korean Population

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