Sudden Cardiac Death in Hypertensive Patients

Verdecchia, Paolo; Angeli, Fabio; Cavallini, Claudio; Aita, Adolfo; Turturiello, Dario; Fano, Michelantonio De; Reboldi, Gianpaolo

doi:10.1161/hypertensionaha.119.12684

Cited by 50 publications

(36 citation statements)

References 70 publications

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“…Anti-arrhythmic effects of sacubitril/valsartan in SHR arrhythmia. 11 Therefore, our results matched a specific pathophysiology of SCD with the available therapies to improve outcomes in patients with hypertensive heart disease. The current SHR model, characterized by ventricular hypertrophy and diastolic dysfunction, is associated with increased fibrosis, collagen deposition, and risk of SCD.…”

Section: Discussionsupporting

confidence: 63%

“…Previous studies have shown that LCZ696 improves systolic function, electrophysiological benefits, and down‐regulation of sodium and potassium channel protein expression, which are important contributors to systolic dysfunction‐related ventricular arrhythmia 9,10 . On the other hand, the rate of sudden cardiac death (SCD) is 0.3 per 100 patient‐years in hypertensive patients without cardiovascular diease 11 . SCD even accounts for around 20% of deaths in hypertensive patients with diastolic dysfunction and HF, which is also associated with malignant ventricular arrhythmia 2,12–15 .…”

Section: Introductionmentioning

confidence: 99%

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Reverse electromechanical modelling of diastolic dysfunction in spontaneous hypertensive rat after sacubitril/valsartan therapy

et al. 2020

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Aims Hypertension is a significant risk for the development of left ventricular hypertrophy, diastolic dysfunction, followed by heart failure and sudden cardiac death. While therapy with sacubitril/valsartan (SV) reduces the risk of sudden cardiac death in patients with heart failure and systolic dysfunction, the effect on those with diastolic dysfunction remains unclear. We hypothesized that, in the animal model of hypertensive heart disease, treatment with SV reduces the susceptibility to ventricular arrhythmia. Methods and results Young adult female spontaneous hypertensive rats (SHRs) were randomly separated into three groups, which were SHRs, SHRs treated with valsartan, and SHRs treated with SV. In addition, the age-matched and weight-matched Wistar Kyoto rats were considered as controls, and there were 12 rats in each group. In vivo ventricular tachyarrhythmia induction and in vitro optical mapping were used to measure the inducibility of ventricular arrhythmias and to characterize the dynamic properties of electrical propagation. The level of small-conductance Ca 2+-activated potassium channel type 2 (KCNN2) was analysed in cardiac tissue. Compared with SHR with left ventricular hypertrophy, treatment with SV significantly improved cardiac geometry (relative wall thickness, 0.68 ± 0.11 vs. 0.76 ± 0.13, P < 0.05) and diastolic dysfunction (isovolumetric relaxation time, 59.4 ± 3.2 vs. 70.5 ± 4.2 ms, P < 0.05; deceleration time of mitral E wave, 46 ± 4.8 vs. 42 ± 3.8, P < 0.05). The incidence of induced ventricular arrhythmia was significantly reduced in SHR treated with SV compared with SHR (ventricular tachycardia, 1.14 ± 0.32 vs. 2.91 ± 0.5 episodes per 10 stimuli, P < 0.001; ventricular fibrillation, 1.72 ± 0.31 vs. 5.81 ± 0.42 episodes per 10 stimuli, P < 0.001). The prolonged action potential duration (APD) and increase of the maximum slope of APD restitution were observed in SHR, while the treatment of SV improved the arrhythmogeneity (APD, 37.12 ± 6.18 vs. 92.41 ± 10.71 ms at 250 ms pacing cycle length, P < 0.001; max slope 0.29 ± 0.01 vs. 1.48 ± 0.04, P < 0.001). These effects were strongly associated with down-regulation of KCNN2 (0.38 ± 0.07 vs. 0.74 ± 0.12 ng/ml, P < 0.001). The treatment of SV also decreased the level of N-terminal pro-B-type natriuretic peptide, cardiac bridging integrator-1, and intramyocardial fibrosis of SHR. Conclusions In conclusion, synergistic blockade of the neprilysin and the renin-angiotensin system by SV in SHRs results in KCNN2-associated electrical remodelling in ventricle, which stabilizes electrical dynamics and attenuates arrhythmogenesis.

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Section: Discussionsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Reverse electromechanical modelling of diastolic dysfunction in spontaneous hypertensive rat after sacubitril/valsartan therapy

et al. 2020

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“…Although being male was an associated risk factor for ECG-LVH, LVH was a greater risk factor for cardiac death among females than among males 27 . Strong evidence was observed that ECG-LVH was a risk predictor of cardiovascular events including coronary heart disease, stroke and sudden cardiac death 2 , 3 , 8 , 28 – 30 . When LVH continued to progress, the prevalence of patients with cardiovascular diseases and their complications were more likely to increase.…”

Section: Discussionmentioning

confidence: 99%

“…Left ventricular hypertrophy (LVH) is considered a cardiac condition secondary to both structural and functional adaptation of the heart leading to many life-threatening complications like myocardial ischemia, left ventricular (LV) dysfunction, heart failure and even sudden cardiac death [1][2][3][4] . Several studies reported that the potential risk…”

Section: Abbreviationsmentioning

confidence: 99%

Prevalence and associated factors of electrocardiographic left ventricular hypertrophy in a rural community, central Thailand

Viwatrangkul

Lawanwisut

Leekhaphan

et al. 2021

Sci Rep

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Left ventricular hypertrophy (LVH) is considered a cardiac condition with life-threatening complications. Detected LVH is a strong predictor of cardiovascular diseases and death. This condition is normally diagnosed at offices. We aimed to determine the prevalence and associated factors of electrocardiographic-LVH (ECG-LVH) among adults in a Thai rural community. A cross-sectional study was conducted in Na-Yao rural community of Thailand in 2020. A total of 638 individuals aged ≥ 20 years were interviewed using standardized structured questionnaires related to demographic information, risk behaviors, comorbidities and anthropometric measurements. LVH was determined by Sokolov-Lyon and Cornell criteria based on the collected electrocardiograms. The prevalence of ECG-LVH among adults was 6.6%. The factors independently associated with ECG-LVH were being male (AORs 2.04, 95% CI 1.05–3.98), history of diabetes mellitus (AORs 1.01, 95% CI 1.01–1.02), and hypertensive crisis ≥ 180/110 mmHg (AORs 7.24, 95% CI 1.31–39.92). However, resting heart rate was negatively associated with ECG-LVH (p < 0.05). Our data emphasized that LVH was one of the significant health problems among adults in a rural community. This condition could lead to severe complications. Thus, effective detection and public health interventions should be provided at the community level.

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“…A study followed for an average of 10.3 years a cohort of 3242 initially untreated patients with hypertension without evidence of coronary or cerebrovascular heart disease at entry. 20 During follow-up, SCD occurred in 33 patients at a rate of 0.10 per 100 patient-years (95% confidence interval [CI], 0.07-0.14). The rate of SCD was 0.07 and 0.30 per 100 patient-years, respectively, in the cohort of patients without and with ECG LVH ( P < .01).…”

Section: Sudden Cardiac Death In Hf With Near-normal/normal Lvefmentioning

confidence: 99%

Sudden Arrhythmic Death at the Higher End of the Heart Failure Spectrum

et al. 2019

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The risk of sudden cardiac death (SCD) is high in heart failure (HF) patients. Sudden arrhythmic death (SAD) is a frequent cause of exit in HF patients at the lower end of the HF spectrum, and implantable cardioverter–defibrillators have been recommended to prevent these life-threatening rhythm disturbances in select patients. However, less is known regarding the cause of SCD in patients at the upper end of the HF spectrum, despite the fact that the majority of out-of-hospital SCD victims have unknown or near-normal/normal left ventricular ejection fraction (LVEF). In this review, we report the epidemiology, summarize the mechanisms, discuss the diagnostic challenges, and propose a stepwise approach for the prevention of SAD in HF with near-normal/normal LVEF.

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Sudden Cardiac Death in Hypertensive Patients

Cited by 50 publications

References 70 publications

Reverse electromechanical modelling of diastolic dysfunction in spontaneous hypertensive rat after sacubitril/valsartan therapy

Reverse electromechanical modelling of diastolic dysfunction in spontaneous hypertensive rat after sacubitril/valsartan therapy

Prevalence and associated factors of electrocardiographic left ventricular hypertrophy in a rural community, central Thailand

Sudden Arrhythmic Death at the Higher End of the Heart Failure Spectrum

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