Prevention of sudden cardiac death in persons living with HIV infection

2021 ◽  
Vol 19 ◽  
Author(s):  
Jean-Jacques Monsuez ◽  
Marilucy Lopez-Sublet

: Persons living with HIV infection (PLWH) have been recognized to have an increased risk of sudden cardiac death (SCD). Prevention of this risk should theoretically be included in their long-term management. However, only a few approaches have been proposed to optimize such interventions. Targeting detection of the commonly associated conditions such as coronary artery disease, left ventricular dysfunction, heart failure, QT interval prolongation and ventricular arrhythmias is the first step of this prevention. However, although detection of the risk of SCD is a suitable challenge in PLWH, it remains uncertain whether optimized treatment of the identified risks would unequivocally translate into a decrease in SCD rates.

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tuomas Kenttä ◽  
Bruce D Nearing ◽  
Kimmo Porthan ◽  
Jani T Tikkanen ◽  
Matti Viitasalo ◽  
...  

Introduction: Noninvasive identification of patients at risk for sudden cardiac death (SCD) remains a major clinical challenge. Abnormal ventricular repolarization is associated with increased risk of lethal ventricular arrhythmias and SCD. Hypothesis: We investigated the hypothesis that spatial repolarization heterogeneity can identify patients at risk for SCD in general population. Methods: Spatial R-, J- and T-wave heterogeneities (RWH, JWH and TWH, respectively) were automatically analyzed with second central moment technique from standard digital 12-lead ECGs in 5618 adults (46% men; age 50.9±12.5 yrs.) who took part in Health 2000 Study, an epidemiological survey representative of the entire Finnish adult population. During average follow-up of 7.7±1.4 years, a total of 72 SCDs occurred. Thresholds of RWH, JWH and TWH were based on optimal cutoff points from ROC curves. Results: Increased RWH, JWH and TWH (Fig.1) in left precordial leads (V4-V6) were univariately associated with SCD (P<0.001, each). When adjusted with clinical risk markers (age, gender, BMI, systolic blood pressure, cholesterol, heart rate, left ventricular hypertrophy, QRS duration, arterial hypertension, diabetes, coronary heart disease and previous myocardial infarction) JWH and TWH remained as independent predictors of SCD. Increased TWH (≥102μV) was associated with a 1.9-fold adjusted relative risk (95% confidence interval [CI]: 1.2 - 3.1; P=0.011) and increased JWH (≥123μV) with a 2.0-fold adjusted relative risk for SCD (95% CI: 1.2 - 3.3; P=0.004). When both TWH and JWH were above threshold, the adjusted relative risk for SCD was 3.2-fold (95% CI: 1.7 - 6.2; P<0.001). When all heterogeneity measures (RWH, JWH and TWH) were above threshold, the risk for SCD was 3.7-fold (95% CI: 1.6 - 8.6; P=0.003). Conclusions: Automated measurement of spatial J- and T-wave heterogeneity enables analysis of high patient volumes and is able to stratify SCD risk in general population.


Circulation ◽  
2020 ◽  
Vol 141 (18) ◽  
pp. 1477-1493 ◽  
Author(s):  
Yihui Wang ◽  
Chunyan Li ◽  
Ling Shi ◽  
Xiuyu Chen ◽  
Chen Cui ◽  
...  

Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a hereditary heart disease characterized by fatty infiltration, life-threatening arrhythmias, and increased risk of sudden cardiac death. The guideline for management of ARVC in patients is to improve quality of life by reducing arrhythmic symptoms and to prevent sudden cardiac death. However, the mechanism underlying ARVC-associated cardiac arrhythmias remains poorly understood. Methods: Using protein mass spectrometry analyses, we identified that integrin β1 is downregulated in ARVC hearts without changes to Ca 2+ -handling proteins. As adult cardiomyocytes express only the β1D isoform, we generated a cardiac specific β1D knockout mouse model and performed functional imaging and biochemical analyses to determine the consequences of integrin β1D loss on function in the heart in vivo and in vitro. Results: Integrin β1D deficiency and RyR2 Ser-2030 hyperphosphorylation were detected by Western blotting in left ventricular tissues from patients with ARVC but not in patients with ischemic or hypertrophic cardiomyopathy. Using lipid bilayer patch clamp single channel recordings, we found that purified integrin β1D protein could stabilize RyR2 function by decreasing RyR2 open probability, mean open time, and increasing mean close time. Also, β1D knockout mice exhibited normal cardiac function and morphology but presented with catecholamine-sensitive polymorphic ventricular tachycardia, consistent with increased RyR2 Ser-2030 phosphorylation and aberrant Ca 2+ handling in β1D knockout cardiomyocytes. Mechanistically, we revealed that loss of DSP (desmoplakin) induces integrin β1D deficiency in ARVC mediated through an ERK1/2 (extracellular signal–regulated kinase 1 and 2)–fibronectin–ubiquitin/lysosome pathway. Conclusions: Our data suggest that integrin β1D deficiency represents a novel mechanism underlying the increased risk of ventricular arrhythmias in patients with ARVC.


2013 ◽  
Vol 304 (12) ◽  
pp. H1697-H1707 ◽  
Author(s):  
Matthew F. Pizzuto ◽  
Gen Suzuki ◽  
Michael D. Banas ◽  
Brendan Heavey ◽  
James A. Fallavollita ◽  
...  

Many survivors of sudden cardiac death (SCD) have normal global ventricular function and severe coronary artery disease but no evidence of symptomatic ischemia or infarction before the development of lethal ventricular arrhythmias, and the trigger for ventricular tachycardia (VT)/ventricular fibrillation (VF) remains unclear. We sought to identify the role of spontaneous ischemia and temporal hemodynamic factors preceding SCD using continuous telemetry of left ventricular (LV) pressure and the ECG for periods up to 5 mo in swine ( n = 37) with hibernating myocardium who experience spontaneous VT/VF in the absence of heart failure or infarction. Hemodynamics and ST deviation at the time of VT/VF were compared with survivors with hibernating myocardium as well as sham controls. All episodes of VT/VF occurred during sympathetic activation and were initiated by single premature ventricular contractions, and the VT degenerated into VF in ∼ 30 s. ECG evidence of ischemia was infrequent and no different from those that survived. Baseline hemodynamics were no different among groups, but LV end-diastolic pressure during sympathetic activation was higher at the time of SCD (37 ± 4 vs. 26 ± 4 mmHg, P < 0.05) and the ECG demonstrated QT shortening (155 ± 4 vs. 173 ± 5 ms, P < 0.05). The week before SCD, both parameters were no different from survivors. These data indicate that there are no differences in the degree of sympathetic activation or hemodynamic stress when VT/VF develops in swine with hibernating myocardium. The transiently elevated LV end-diastolic pressure and QT shortening preceding VT/VF raises the possibility that electrocardiographically silent subendocardial ischemia and/or mechanoelectrical feedback serve as a trigger for the development of SCD in chronic ischemic heart disease.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Kelvin C Chua ◽  
Carmen Teodorescu ◽  
Audrey Uy-Evanado ◽  
Kyndaron Reinier ◽  
Kumar Narayanan ◽  
...  

Introduction: If we are to improve risk stratification for sudden cardiac death (SCD) we should extend beyond the LV ejection fraction (LVEF). The frontal QRS-T angle has been shown to predict risk of SCD but its value independent of LVEF has not been investigated. Hypothesis: We hypothesize that a wide frontal QRS-T angle predicts SCD independent of LVEF. Methods: Cases of adult sudden cardiac arrest with an available electrocardiogram before the event were identified from a large ongoing population based study of SCD in the Northwest US (population approx. one million). Subjects with a computable frontal QRS-T angle were included. A total of 686 SCD cases (mean age 67.4 years; 95% CI, 52.5 to 82.3 years; 68.2% males; 83.5% whites) met criteria, and were compared to 871 controls with and without coronary artery disease (mean age 66.8 years, 55.3 to 78.3 years; 67.7% males; 90.6% whites) from the same geographical region. Results: The mean frontal QRS-T angle was higher in SCD cases (73.9 degrees; 95% CI, 17.5 to 130.3 degrees, p<0.0001) compared to controls (51.1 degrees; 95% CI 5.0 to 97.2 degrees). Using a cut-off of more than 90 degrees, the frontal QRS-T angle was predictive of SCD, and remained predictive, after adjusting for age, sex, left ventricular ejection fraction (LVEF), prolonged QTc, prolonged QRS duration and baseline comorbidities (OR 1.80; 95% CI, 1.27 to 2.55, p=0.001). On the receiver operating characteristic (ROC) curve, the QRS-T angle demonstrated an area-under-curve (AUC) value of 0.614. Compared to the lowest quartile of QRS-T angle, the highest quartile had nearly a triple increase in the risk of SCD (OR 2.71; 95% CI; 2.03 to 3.60; p<0.0001). Conclusion: A wide QRS-T angle greater than 90 degrees is associated with increased risk of sudden cardiac death independent of left ventricular ejection fraction.


Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Muammar M Kabir ◽  
Elyar Ghafoori ◽  
Jonathan W Waks ◽  
Sunil K Agarwal ◽  
Dan E Arking ◽  
...  

Background: Respiration causes heart movement in the chest and proportional change in the heart’s electrical axis. The ECG can be used to measure respiration-related heart motion. The effect of respiration on the ECG is usually considered an artifact. However, it is unknown whether pattern of heart motion due to respiration holds any prognostic value. Method: After excluding those with atrial fibrillation, or atrial or ventricular premature contractions at baseline visit, 14613 ARIC cohort participants (mean age 54.0±5.8 y; 6595 [45.1%] men; 10744 [73.5%] white, 1311 [9.0%] with prevalent cardiovascular disease (CVD)) were included. The digital resting ECG was analyzed using custom Matlab software. The absolute magnitude of the displacement of the heart due to respiration was calculated on X (left-right), Y (up-down), and Z (anterior-posterior) axes. Sudden cardiac death (SCD) and non-coronary heart disease (CHD) death served as competing outcomes in our analysis. Results: In CVD-free participants (as compared to prevalent CVD group) heart moved more on X axis (137±46 vs. 128±47 μV; P<0.0001), and less on Z axis (123±52 vs. 127±60 μV; P=0.05). During a median follow-up of 14 years 278 SCDs (96 in CVD group) and 1619 non-CHD (279 in CVD group) deaths occurred. In competing risk analysis that adjusted for age, gender, race, history of myocardial infarction, CHD, heart failure, systolic blood pressure, anti-hypertensive medications, diabetes, smoking, total cholesterol, high density lipoprotein, level of physical activity, use of beta-blockers, left ventricular hypertrophy on ECG and QRS duration, the absolute magnitude of respiration-related heart movement on X axis (SHR 0.74; 95%CI 0.59-0.93; P=0.009) and Z axis (SHR 1.19; 95%CI 1.01-1.41; P=0.042) associated with SCD (but not with non-CHD death) in CVD group, but not in CVD-free participants. Conclusion: Greater respiration-caused heart motion on Z axis and smaller - on X axis likely reflects cardiomegaly and is associated with increased risk of SCD in patients with CVD.


Author(s):  
David A. Wohl ◽  
Jeffrey T. Kirchner

Upon completion of this chapter, the reader should be able to • To gain a greater understanding of the pathophysiology of CVD and myocardial infarction in persons living with HIV infection. • To understand the link of chronic HIV infection as it relates to increased risk of CVD and myocardial infarction....


2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
F D"ascenzi ◽  
F Valentini ◽  
S Pistoresi ◽  
F Frascaro ◽  
P Pietro ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. The etiology of sudden cardiac death (SCD) in young people is still debated. The aim of this meta-analysis was to identify the most frequent causes of SCD in individuals aged ≤35 years, the differences between athletes and nonathletes and among geographic areas. Methods.  Studies published between 01/01/1990 and 01/31/2020 and evaluating post-mortem the etiology of SCD in young individuals (≤35 years) were included. Individuals were divided in athletes and nonathletes. Studies that did not report separately data between athletes and nonathletes were excluded. Results. Thirty-four studies met the inclusion criteria and a total population of 5,060 victims of SCD were analysed (2,890 athletes, 2,170 nonathletes). Structurally normal heart, hypertrophic cardiomyopathy (HCM), idiopathic left ventricular hypertrophy, and anomalous origin of coronary arteries (AOCA) were the most frequent causes of SCD in athletes while coronary artery disease (CAD), arrhythmogenic cardiomyopathy (ACM), and channelopathies were frequent causes of SCD in nonathletes. The number of SCDs due to ischemic heart disease (19.6% vs. 9.1%, p = 0.009), ACM (11.5% vs. 4.7%, p = 0.03) and channelopathies (8.4% vs. 1.9%, p = 0.02) was higher in nonathletes comparing with athletes. SCD due to non-ischemic left ventricular scar (5.1% vs. 1.1%, p = 0.01) was more frequent in athletes. HCM (p = 0.01) and AOCA (p = 0.004) were more frequently cause of SCD in US while ACM (p = 0.001), structurally normal heart (p = 0.02), and channelopathies (p = 0.02) in Europe. Conclusions. Structurally normal heart, HCM, AOCA were frequent causes of SCD in athletes while CAD, ACM and channelopathies in nonathletes. The causes of SCD differ between US and Europe.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M.A.E Haukilahti ◽  
L Holmstrom ◽  
J Vahatalo ◽  
T.V Kentta ◽  
L Pakanen ◽  
...  

Abstract Background Inferolateral T wave inversion has been associated with increased risk of mortality and sudden cardiac death (SCD) in general population. However, the association between isolated T inversion and SCD is still unclear. Purpose The purpose of this study was to examine whether isolated T inversion associates with SCD, and find out possible gender differences. Methods FinGesture Study has systematically collected clinical data and medico-legal autopsy data from 5,869 consecutive SCD victims (mean age 64.9±12.4 yrs.) in Northern of Finland between years 1998 and 2017. Previously recorded electrocardiograms (ECG) were available and analyzed in 1,101 subjects. The control group consisted of 7,217 subjects representative of Finnish general population (mean age 51.5±12.4 yrs.). T inversion was interpreted isolated if there was at least two T inversions ≥−0.1 mV in at least two contiguous leads, and there were no ECG signs of left ventricular hypertrophy (LVH) defined by Sokolow-Lyon criteria or bunchle brand block (BBB) attached to it. Results In a current study, isolated T inversion was more common finding among SCD victims compared to general population: isolated T inversion in any leads 10.9% vs. 0.9% (SCD vs. general population, p&lt;0.001), laterally 7.7% vs. 0.1% (p&lt;0.001), inferiorly 3.2% vs. 0.5% (p&lt;0.001) and anteriorly 2.9% vs. 0.4% (p&lt;0.001). Particularly, isolated T inversion seemed to assoaciate with ischemic SCD taking into account that 61.5% of the total isolated T inversions were seen in ischemic SCD victims (p=0.018). In addition, 62.1% of the inferior isolated T inversions (p=0.023) and 61.7% of the lateral isolated T inversions (p=0.031) were in ischemic SCD victims versus 37.9% and 38.3% in non-ischemic SCD victims, respectively. The prevalence of isolated T inversion in any lead was also higher among male SCD victims compared to female victims (12.8% vs. 8.2%, p&lt;0.001, respectively). There was no statistically significant difference in the prevalence of LVH and strain changes between the populations. Among bundle branch blocks left BBB was predictably more typical in SCD victims (5.8% vs. 0.5%, p&lt;0.001). Conclusion We noticed an association between isolated T inversion and SCD. The association was most prominent in males and in those with ischemic etiology of SCD. Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): The Finnish Medical Foundation, Finnish Foundation for Cardiovascular Research


2003 ◽  
Vol 12 (3) ◽  
pp. 259-271 ◽  
Author(s):  
Christian C. Evans ◽  
Sandra L. Cassady

Objective:To describe the underlying conditions that predispose athletes to sudden cardiac death (SCD) and review signs and symptoms that indicate an athlete is at risk.Data Sources:MEDLINE, theLos Angeles TimesandTriathlon Timesarchives, and other sources identified in the references of articles initially located therein. A total of 43 references were included.Conclusions:Most cases of SCD in younger athletes (≤35 years) are attributable to multiple hereditary conditions, with familial hyper-trophic cardiomyopathy being the primary cause, whereas the major cause of SCD in older athletes (>35 years) is coronary artery disease. Health-care professionals evaluating athletes should pay particular attention to past medical and family history. Items in an athlete’s screening that suggest increased risk include a history of chest pain, syncope, excessive shortness of breath, irregular heart rate or murmur, or a history of SCD in an immediate family member.


Author(s):  
Omar Elsaka

Background: Sudden cardiac death (SCD) remains a major open clinical and public health problem, with an estimated 300,000 deaths per year in the United States. The possibility of identifying potential SCD victims is limited by the large size of the large number of SCD victims and the apparent time-dependent risk of sudden death. The latter refers to the tendency of SCDs to detect other cardiovascular events during the most dangerous period of 6–18 months following a major cardiovascular event and the risk of subsequent collapse. The combination of time and lake size provides the basis for future research to find more vulnerable people. Pathologically, SCD can be seen as an interaction between some electrophysiological events that causes abnormalities in cardiac structure, temporal dysfunction, and malignant arrhythmias. Structural deformities represent an anatomical matrix of chronic risk and include the effects of electrophysiological anatomical abnormalities such as coronary artery disease, left ventricular hypertrophy, myopathic ventricles, and bypass leaflets in the myocardium. Conclusion: Macroscopic cardiac features are common in about one-third of young SCD victims. However, in 79% of them, histological studies reveal hidden pathological features such as local myocarditis, heart disease and motor system disorders. A total of 16 (6%) victims had no evidence of systemic heart disease and the mechanism of SCD was not described.


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