Sudden cardiac death: epidemiology and prevention

Mapping Intimacies ◽

10.1093/med/9780199687039.003.0005 ◽

2015 ◽

Author(s):

Hans-Richard Arntz

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Sudden Cardiac Death ◽

Cardiac Death ◽

Beta Blockers ◽

Left Ventricular ◽

Industrialized Countries ◽

Pharmacological Prevention ◽

Increased Risk ◽

Genetically Determined

Even if sudden cardiac death is considered to be the most frequent cause of death in adults in industrialized countries, its incidence varies widely, depending on the definition and the source and quality of underlying data. It is estimated that about 70-80% of cases are due to coronary heart disease. The remaining 20% are attributable to a wide variety of inborn, genetically determined or acquired diseases, including a small group with hitherto undefined background. Prevention primarily encompasses the treatment of cardiovascular risk factors to avoid manifestations of coronary heart disease. Furthermore, preventive strategies are targeted to define groups of patients with an increased risk for sudden cardiac death or individuals at risk in specific populations, e.g. competitive athletes. A major target group are patients with impaired left ventricular function, preferentially due to myocardial infarction. These patients, and some less clearly defined patient groups with non-ischaemic cardiomyopathy and heart failure, may benefit from the insertion of an implantable cardioverter-defibrillator. With regard to pharmacological prevention, treatment of the underlying condition is the mainstay, since no antiarrhythmic substance-with the exemption of beta-blockers in some situations-has shown to be of efficacy.

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Evidence for the Cardioprotective Effects of Omega-3 Fatty Acids

Annals of Pharmacotherapy ◽

10.1345/aph.1a314 ◽

2002 ◽

Vol 36 (12) ◽

pp. 1950-1956 ◽

Cited By ~ 35

Author(s):

Douglas N Carroll ◽

Mary T Roth

Keyword(s):

Myocardial Infarction ◽

Fatty Acids ◽

Coronary Heart Disease ◽

Heart Disease ◽

Sudden Cardiac Death ◽

Cardiac Death ◽

Serum Triglyceride ◽

Biomedical Literature ◽

Omega 3 ◽

Increased Risk

OBJECTIVE: To review available literature regarding the cardiovascular effects of marine-derived ω-3 fatty acids and evaluate the benefit of these fatty acids in the prevention of coronary heart disease. DATA SOURCES: Biomedical literature accessed through a MEDLINE search (1966–April 2002). Search terms included fish oil, omega-3 fatty acid, sudden death, hypertriglyceridemia, myocardial infarction, and mortality. DATA SYNTHESIS: Following an early 1970's observational investigation that ω-3 fatty acids may reduce the occurrence of myocardial infarction—related deaths in Greenland Eskimos, additional trials have been conducted that support this finding. Epidemiologic and clinical trial data suggest that ω-3 fatty acids may reduce the risk of cardiovascular-related death by 29–52%. In addition, the risk of sudden cardiac death was found to be reduced by 45–81%. Possible mechanisms for these beneficial effects include antiarrhythmic properties, improved endothelial function, antiinflammatory action, and reductions in serum triglyceride concentrations. ω-3 Fatty acids are fairly well tolerated; potential adverse effects include bloating and gastrointestinal distress, “fishy taste” in the mouth, hyperglycemia, increased risk of bleeding, and a slight increase in low-density-lipoprotein cholesterol. CONCLUSIONS: ω-3 Fatty acids may be beneficial and should be considered in patients with documented coronary heart disease. They may be particularly beneficial for patients with risk factors for sudden cardiac death.

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Abstract P105: Small Magnitude of the Heart Movement Due to Respiration is Associated With Sudden Cardiac Death

Circulation ◽

10.1161/circ.131.suppl_1.p105 ◽

2015 ◽

Vol 131 (suppl_1) ◽

Author(s):

Muammar M Kabir ◽

Elyar Ghafoori ◽

Jonathan W Waks ◽

Sunil K Agarwal ◽

Dan E Arking ◽

...

Keyword(s):

Sudden Cardiac Death ◽

Cardiac Death ◽

Beta Blockers ◽

Density Lipoprotein ◽

Absolute Magnitude ◽

Left Ventricular ◽

Small Magnitude ◽

Increased Risk ◽

Heart Motion ◽

The Absolute

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.

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Dealing with Sudden Cardiac Death: Who Deserves Device Implantation

ACI (Acta Cardiologia Indonesiana) ◽

10.22146/aci.47675 ◽

2019 ◽

Vol 5 (1 (P)) ◽

pp. 12

Author(s):

Dicky Armein Hanafy

Keyword(s):

Heart Failure ◽

Coronary Heart Disease ◽

Heart Disease ◽

Sudden Cardiac Death ◽

Cardiac Arrhythmias ◽

Cardiac Death ◽

Cardiac Insufficiency ◽

Resynchronization Therapy ◽

Icd Implantation ◽

Life Threatening

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.

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Prevention of sudden cardiac death in persons living with HIV infection

Current HIV Research ◽

10.2174/1570162x19666210922154011 ◽

2021 ◽

Vol 19 ◽

Author(s):

Jean-Jacques Monsuez ◽

Marilucy Lopez-Sublet

Keyword(s):

Sudden Cardiac Death ◽

Hiv Infection ◽

Cardiac Death ◽

Left Ventricular ◽

Qt Interval Prolongation ◽

Increased Risk ◽

Persons Living With Hiv ◽

Artery Disease ◽

Optimized Treatment ◽

Living With Hiv

: 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.

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Abstract 15714: Prediction of Sudden Cardiac Death With Automated High-Throughput Analysis of T-Wave Heterogeneity in Standard 12-Lead Electrocardiogram

Circulation ◽

10.1161/circ.130.suppl_2.15714 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Tuomas Kenttä ◽

Bruce D Nearing ◽

Kimmo Porthan ◽

Jani T Tikkanen ◽

Matti Viitasalo ◽

...

Keyword(s):

At Risk ◽

Relative Risk ◽

Sudden Cardiac Death ◽

General Population ◽

Cardiac Death ◽

Left Ventricular ◽

Adjusted Relative Risk ◽

T Wave ◽

Increased Risk ◽

Patients At Risk

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.

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Integrin β1D Deficiency–Mediated RyR2 Dysfunction Contributes to Catecholamine-Sensitive Ventricular Tachycardia in Arrhythmogenic Right Ventricular Cardiomyopathy

Circulation ◽

10.1161/circulationaha.119.043504 ◽

2020 ◽

Vol 141 (18) ◽

pp. 1477-1493 ◽

Cited By ~ 3

Author(s):

Yihui Wang ◽

Chunyan Li ◽

Ling Shi ◽

Xiuyu Chen ◽

Chen Cui ◽

...

Keyword(s):

Ventricular Tachycardia ◽

Sudden Cardiac Death ◽

Right Ventricular ◽

Cardiac Death ◽

Arrhythmogenic Right Ventricular Cardiomyopathy ◽

Left Ventricular ◽

Polymorphic Ventricular Tachycardia ◽

Ventricular Cardiomyopathy ◽

Open Probability ◽

Increased Risk

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.

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Kidney dysfunction predicts sudden cardiac death in women with coronary heart disease

Nature Clinical Practice Nephrology ◽

10.1038/ncpneph0842 ◽

2008 ◽

Vol 4 (7) ◽

pp. 348-348

Keyword(s):

Coronary Heart Disease ◽

Heart Disease ◽

Sudden Cardiac Death ◽

Cardiac Death ◽

Kidney Dysfunction

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Daytime peak incidence of death due to the ischemic heart disease

American Journal of BioMedicine ◽

10.18081/2333-5106/014-04/213-227 ◽

2014 ◽

Vol 2 (4) ◽

pp. 213-227

Author(s):

Janet H. Wilenky ◽

Hsin Chang

Keyword(s):

Myocardial Infarction ◽

Coronary Heart Disease ◽

Heart Disease ◽

Sudden Cardiac Death ◽

Cardiac Death ◽

Early Morning ◽

Morning Peak ◽

Circadian Time ◽

Ventricular Dysrhythmias ◽

Relationship Of

Myocardial infarction, myocardial ischemia, ventricular dysrhythmias, and sudden cardiac death occur most frequently in the morning, especially in the first few hours after awakening. Among individual patients, however, this pattern may vary widely. Up to 80% of individuals who suffer sudden cardiac death have coronary heart disease; the epidemiology of sudden cardiac death to a great extent parallels that of coronary heart disease. This review describes circadian patterns in cardiovascular disease processes and analyses the findings of recent studies by searched, from PubMed, ISI Web of Science, Google Scholar and Scopus databases in a time period between late 1970s through July 2013. The circadian pattern of numerous cardiovascular events (myocardial infarction, sudden cardiac death, stroke) reveals a peak in the early hours of the morning, which occurs in more than 20% of patients with arterial hypertension, and can be regularly detected in combined 24-h-ABPM/EKG examinations. The awareness of an increased incidence of myocardial infarction and sudden cardiac death in the early morning hours, shortly after waking, has stimulated an interest in the relationship of these events and the occurrence of both silent and symptomatic myocardial ischaemia. A number of studies have been reported that examine both the physiological triggers and the underlying causes of these events. Beta-adrenergic blockers have been shown to abolish the early morning peak of myocardial infarction and blunt the morning peak in sudden cardiac death. Newer calcium antagonists, such as amlodipine, have been demonstrated to control angina throughout a 24-hour period. Aspirin is effective in preventing morning infarction. Approaching the pathophysiology of circadian time-dependent sudden cardiac death has implication for future prevention and treatment.

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