congestive heart failure sudden death

Allelic variation in candidate genes in a number of signaling systems that alter myocardial electrical substrate or triggers, cell survival pathways, and thrombotic cascades may enhance susceptibility to SCD in the failing heart.157,158 Association studies have demonstrated an increased risk of sudden death in Finnish men with the A2 allele of the PIA1/A2 polymorphism of glycoprotein IIIa.159 Another case-control study has demonstrated an association between 4G polymorphism of plasminogen activator type I.160 Combinations of polymorphisms, such as that of the DD allele of the angiotensin-converting enzyme and the C allele of the angiotensin II type 1 receptor, have been associated with an increased risk of malignant ventricular arrhythmias in patients with CAD and left ventricular dysfunction.161 Allelic variations in other genes (eg, β-adrenergic receptors, endothelial nitric oxide synthase, angiotensin-converting enzyme) may influence the rate of progression of HF and response to therapy,162–164 thereby influencing the risk of sudden death from both mechanical and electrical causes. Congestive Heart Failure (CHF) is not yes or no it is a spectrum of severity. This can result in fatigue and difficulty breathing. Lindenfeld J, Feldman AM, Saxon L, Boehmer J, Carson P, Ghali JK, Anand I, Singh S, Steinberg JS, Jaski B, DeMarco T, Mann D, Yong P, Galle E, Ecklund F, Bristow M. Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De Marco T, Carson P, DiCarlo L, DeMets D, White BG, DeVries DW, Feldman AM; COMPANION Investigators. Yet, the use of statins to cause plaque stabilization or the use of aspirin or oral anticoagulants to prevent coronary thrombosis did not reduce the risk of sudden death in clinical trials of HFrEF (Table 1).4–7 Coronary revascularization decreased the risk of new myocardial infarctions, but the benefit on sudden death was so modest that it took years to become apparent,8 even though the utilization of implantable cardioverter-defibrillators (ICDs) was very low (only 2%). Several pathophysiological mechanisms (e.g. Importantly, defective calcium handling in HF not only affects ventricular mechanics but also affects its electrophysiology. The composite primary endpoint was prospectively defined as either onset of CHF or sudden death. ‘Self-organizing criticality’ within the ventricular myocardium relies on complex adaptations to progressive cardiomyocyte stress and stretch, which can come to an abrupt end (‘cascading failure’), thus leading to acute circulatory collapse (i.e. Research Assistant Professor of Epidemiology, Board Certified or Board Eligible AP/CP Full-Time or Part-Time Pathologist, Chief of ID, VA Ann Arbor Healthcare System, Drugs or surgical procedures that prevent myocardial infarction, Consistent use of neurohormonal antagonists, but minimal CRT and ICDs, Robust use of neurohormonal antagonists, CRT and ICDs in rivaroxaban trial, ≈25% decreased risk evident during long-term follow-up, Drugs or devices that favourably affect adverse left ventricular remodelling, Minimal use of neurohormonal antagonists, CRT and ICDs, No benefit in HFrEF; 20% decreased risk in post-infarction LVD, Use of ACEI, but not other neurohormonal antagonists, CRT and ICDs, ≈25% decreased risk in post-infarction LVD; 35–45% decreased risk in HFrEF, Consistent use of ACEI, variable use of beta-blockers, minimal CRT and ICDs, 35% decreased risk if on beta-blocker; minimal effect if not on beta-blocker, Robust use of neurohormonal antagonists; CRT in 7% and ICD in 14%, 20% decreased risk overall, ≈50% decreased risk in patients with baseline ICD, Consistent use of neurohormonal antagonists, variable use of ICD, ≈50% decreased risk in class II/III patients, but no benefit in class IV patients, Drugs and devices that suppress or treat ventricular tachyarrhythmias, Consistent use of neurohormonal antagonists, variable CRT, ≈60–70% decreased risk in class II patients, ≈25–40% decreased risk in Class III patients, Variable use of ACEI and beta-blockers, minimal CRT and ICDs, Copyright © 2020 European Society of Cardiology. Therefore, the feature that distinguished instantaneous demise was not its suddenness, but its unexpectedness. In patients with the most severe symptoms, ICDs have not led to a meaningful decrease in the risk of sudden death.2,19,20 These findings indicate that a large proportion of the sudden deaths in patients with progressive ventricular remodelling are not related to an ICD-responsive ventricular tachyarrhythmia.21 What then is the mechanism of sudden death in these individuals? Recent studies show that substantial number of heart failure patients die from processes other than cardiac disease, in particular malignancies, respiratory problems and septicemias. Steinberg BA, Al-Khatib SM, Edwards R, Han J, Bardy GH, Bigger JT, Buxton AE, Moss AJ, Lee KL, Steinman R, Dorian P, Hallstrom A, Cappato R, Kadish AH, Kudenchuk PJ, Mark DB, Inoue LY, Sanders GD. A major challenge is determination in individual patients of the extent to which the AP is prolonged, repolarization reserve is diminished,28 and dispersion (temporal and spatial) of repolarization is enhanced. This denervation is associated with an exaggerated response to infused catecholamines or denervation supersensitivity in the form of exaggerated shortening of ventricular effective refractory periods and enhanced inducibility of ventricular fibrillation in the presence of catecholamines.97 Alterations of sympathetic innervation are not limited to the acute and healing phases of myocardial infarction. Is it possible to demonstrate that adverse ventricular remodelling per se leads to cascading acute mechanical failure and sudden death? Congestive heart failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscles. The major causes of death are progression of heart failure and sudden non-arrhythmogenic death unrelated to ICDs – for example, secondary to stroke. What Causes Sudden Death in Heart Failure? E-mail. Bradyarrhythmias and pulseless electrical activity occur less frequently, and generally in hearts with more advanced structural disease. A more complete understanding of the critical signaling cascades that influence connexon structure, function, and distribution in the normal and failing heart is necessary. In the normal canine heart, CaT decay is slower and alternans is enhanced in the endocardium compared with the epicardium.45 CaTs in ventricular myocytes isolated from the endocardium of the rabbit left ventricle adjacent to a myocardial infarction exhibit depressed amplitudes and are shorter than cells from normal hearts. What is certain about SCD in the setting of HF in particular is that there are a number of structural and functional changes in the heart and genetic predisposition that may contribute to an increased risk of dying suddenly. Even sudden witnessed death may be produced by a sudden mechanical or vascular catastrophe (pulmonary embolus, cardiac, or vascular rupture) rather than a malignant cardiac rhythm abnormality. Some of the contributors may be well-known candidate genes in signaling pathways associated with electrical instability, generation, or progression of the HF phenotype and/or triggers associated with neurohumoral signaling and ischemia. Background—Sudden unexpected death frequently occurs in chronic heart failure.The importance of acute coronary events in triggering sudden death (SD) is unclear. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide, This PDF is available to Subscribers Only. myocardial infarction, catecholamine surges, or electrolyte imbalances, but in most circumstances, there is no acute precipitating mechanism. Autopsies of patients with HFrEF who had died suddenly indicated that an acute thrombotic occlusion could be a terminal trigger.3 However, if coronary thrombosis were a common cause of sudden death, physicians might expect these events to be prevented if the inciting plaque rupture or thrombotic occlusion were averted. A hallmark of slowed conduction and poor coupling of myocardium in patients at high risk for sudden death is the presence of fractionated electrograms54,55 and delayed-paced ventricular activation.56–58 Abnormalities of conduction, and therefore ventricular activation, produce an exaggerated dispersion of recovery in infarcted and failing ventricles,59,60 facilitating re-entrant excitation and ventricular tachyarrhythmias. This framework—where an abrupt event results from the continuation of tiny increments of the same underlying process rather than a new precipitating mechanism—has been applied to understanding the genesis of avalanches, the sudden appearance of nodes of traffic congestion, and the abrupt onset of system-wide failure of electrical grids. The American Heart Association is qualified 501(c)(3) tax-exempt Normal impulse formation and conduction in cardiac myocytes depend on INa. Difficult or rapid breathing 3. Intracellular [Ca2+] and the AP are intricately linked by a variety of Ca2+-mediated cell surface channels and transporters such as the L-type current (ICa-L), IK, Ca2+-activated Cl− current, and NCX. These changes establish the conditions for re-entry, which may be the proximate cause of SCD in patients with HF. Results: The proportion of dogs reaching the primary endpoint was not significantly different between groups (P =.1). sudden death) in the absence of an identifiable triggering event. Sudden cardiac death (SCD) is a major cause of death in the growing population of patients with heart failure Ventricular arrhythmias have been documented in up to 85% of patients with severe congestive heart failure Patients with severe left ventricular (LV) systolic dysfunction are among those at greatest risk for SCD Congestive Heart Failure (CHF) occurs when the heart is unable to pump blood fast enough, resulting in swelling, shortness of breath, and other issues. Basis of a new physiologic approach to control of arrhythmia, Interaction between digoxin and dronedarone in the PALLAS trial, Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. Yet, it is always possible to explain any benefit of neurohormonal antagonists to prevent sudden death to actions of these drugs that are independent of their effects on ventricular remodelling or fibrosis (Take home figure). Or was sudden death an illusion that was related to an imperfect ability to adequately discern subtle changes in the evolution of HFrEF? HF-induced changes in INa may play an important role in arrhythmias either by disrupting conduction or by prolonging repolarization.25,26 The detailed changes in INa are likely to depend on the cause of HF. 165 These include, but are not limited to, a hospitable substrate, the result of remodeling of active and passive membrane properties of the heart, altered neurohumoral signaling, in many cases myocardial ischemia, and perhaps an … Download figureDownload PowerPointMulti-hit hypothesis of the development of SCD. Sudden death is an important mode of demise in patients with HFrEF. In some cases the alteration in cardiac electrophysiology produced by the mutations linked to inherited arrhythmias resemble the electrical remodeling produced by HF. Mild CHF causes ankle swelling - edema, It can cause shortness of breath when lying down - orthopnoea. In the absence of an acute precipitating event, adverse left ventricular remodelling and fibrosis generates a substrate of self-organizing criticality, which predisposes to abrupt electrical or mechanical cascading failure. There is an increasing body of evidence that oxygen free radicals are increased,130,138–140 and antioxidant reserve, in the form of a reduction in antioxidant enzymes,141,142 is decreased in the failing heart. The ischemic and infarcted myocardium exhibits regional cellular and tissue remodeling, as well as inhomogenities of sympathetic nervous system innervation, that creates a substrate that is exquisitely sensitive to arrhythmia triggers. The ongoing causal process (i.e. [Application value of serum sST2 in diagnosis and prognosis of heart failure]. In patients with heart failure and reduced ejection fraction (HFrEF), sudden death has been declining during the last 20–30 years. Main symptoms. In some patients with an ICD, the ventricular tachyarrhythmia recurs immediately or persists despite repetitive discharges.21 Acute mechanical failure is responsible for the abrupt cessation of circulatory support; the observed tachyarrhythmia represents an epiphenomenon. The association between altered sympathetic innervation and ventricular arrhythmias applies not only to the ischemic and infarcted heart but also to the myopathic heart.94, Arrhythmogenic regional heterogeneities of sympathetic innervation characterize the infarcted heart.95,96 Myocardial infarction is associated with destruction of sympathetic nerves in both the infarct zone and distal myocardial segments. [Systematic review of efficacy and safety of Xinmailong Injection in treatment of coronary heart disease complicated with heart failure]. The border zones of a myocardial infarction are extensively remodeled in both subacute and chronic phases, with alterations in the active membrane properties of myocytes,83 reduced cellular coupling,87 and connexin redistribution.63 Thus, ischemic and uninvolved areas of infarcted myocardium exhibit arrhythmogenic abnormalities of both repolarization and conduction. Individuals with congestive heart failure often report dizziness, vertigo, nausea and … As the disease progresses, signs may include: 1. demise within 1 h of the onset of new cardiac symptoms—was developed to identify the event in the general population with no known heart disease. Abnormalities of atrial5 and ventricular6 electrophysiology in diseased human hearts have been recognized for more than four decades. The abnormal physiology of repolarization associated with the long QT syndrome may also predispose to lethal arrhythmias in the setting of ischemic heart disease.28 Common polymorphisms in long QT genes have also been described that predispose drug-induced QT interval prolongation and ventricular arrhythmias.152–154 It is possible that the same or other yet-to-be-discovered polymorphisms predispose to lethal arrhythmias in HF, a syndrome associated with diminished repolarizing reserve. Published by Oxford University Press on behalf of the European Society of Cardiology. The principal cellular and molecular determinants of conduction in ventricular myocardium are availability of sodium (Na) current, the size and shape of the ventricular myocytes, the quantity and distribution of fibrous tissue, and cellular coupling determined by the density and distribution of gap junction channels. They may start suddenly or develop gradually over weeks or months. Alternatively, it may present as an acute mechanical failure, which is manifest as (i) asystole, bradyarrhythmia, or electromechanical dissociation; or (ii) incessant ventricular fibrillation that persists despite repetitive ICD discharges; in both instances, the sudden deaths cannot be prevented by an ICD. Tel: +1 214 820 7500, Email: Search for other works by this author on: Sudden unexpected death in patients with congestive heart failure: a second frontier, Impact of implantable cardioverter-defibrillator, amiodarone, and placebo on the mode of death in stable patients with heart failure: analysis from the sudden cardiac death in heart failure trial, Acute coronary findings at autopsy in heart failure patients with sudden death: results from the assessment of treatment with lisinopril and survival (ATLAS) trial, Rosuvastatin in older patients with systolic heart failure, Effect of rosuvastatin in patients with chronic heart failure (the GISSI-HF trial): a randomised, double-blind, placebo-controlled trial, Rivaroxaban in patients with heart failure, sinus rhythm, and coronary disease, The Warfarin/Aspirin Study in Heart failure (WASH): a randomized trial comparing antithrombotic strategies for patients with heart failure, Analysis of mortality events in the Multicenter Automatic Defibrillator Implantation Trial (MADIT-II), Defibrillator implantation in patients with nonischemic systolic heart failure, Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure, Outcomes of implantable cardioverter-defibrillator use in patients with comorbidities: results from a combined analysis of 4 randomized clinical trials, New York Heart Association class and the survival benefit from primary prevention implantable cardioverter defibrillators: a pooled analysis of 4 randomized controlled trials, Stretch-induced arrhythmias in the isolated canine ventricle. Neurohumoral activation may profoundly influence the substrate in the failing heart and triggers for lethal ventricular arrhythmias. Insights into Disparities Observed with COVID-19. Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB), Journal of the American Heart Association (JAHA), Customer Service and Ordering Information, Basic, Translational, and Clinical Research, Journal of the American Heart Association, Circulation: Arrhythmia and Electrophysiology, Circulation: Cardiovascular Quality and Outcomes. © The Author(s) 2019. This conceptual framework—borrowed from theoretical physics24,25—suggests that life-prolonging treatments in chronic heart failure may have their most important impact if they are applied early in the disease process when ventricular remodelling may be most reversible and when sudden death constitutes a disproportionate number of all deaths. This minute-to-minute variation in the risk makes SCD prediction in individual HF patients an enormous challenge. The effect of sympathetic nervous system stimulation on the heart is complex and is governed by the state of the myocardium. Second, a linkage between ventricular remodelling and acute mechanical failure resulting in sudden death has been supported by studies of sacubitril-valsartan in HFrEF. Variable changes in the density of DHP binding sites have been reported.7 Similarly, studies of human Ca channel subunit mRNA in HF exhibit disparate findings.37–39 The complexity of the molecular basis of channel remodeling is highlighted by reports of isoform switching of both α1C39,40 and β subunits41 in the failing heart. We review the changes in active and passive membrane properties, neurohumoral signaling, and genetic determinants that predispose to sudden arrhythmic death in patients with heart failure and highlight the critical unanswered questions that are ripe for future investigation. Increases in NCX mRNA and protein have been regularly observed in failing hearts.7 Sarcoplasmic reticulum Ca2+ release is also defective in the failing heart and is associated with altered regulation of the ryanodine receptor (RyR), attributable to PKA hyperphosphorylation-induced FKBP12.6 dissociation from the channel that alters Ca2+ sensitivity and generates uncoupled gating of RyR.50,51 Further complicating the mechanism of altered RyR function, levels of RyR mRNA, and protein in HF are variable.52,53 Although alteration of the CaT is associated with and influences the static and dynamic changes in the ventricular AP, the precise relationship remains unclear and the role of spatial and temporal dispersion of CaT in arrhythmogenesis in the failing heart remains to be clarified. The relative densities, precise molecular compositions, and responses to stress of these K currents vary considerably across species. Congestive heart failure is the medical term used to describe this life-threatening condition. If death was expected, then the demise could be ascribed to the mechanisms that were already in play. Given these uncertainties—despite compelling evidence linking cardiac remodelling and sudden death35—it has been difficult to confidently ascribe the favourable effects of neurohormonal antagonists on cardiac arrest primarily to the reversal of remodelling-related self-organized criticality. The amplitude of the calcium transient (CaT) and its rate of decay are reduced in intact preparations42 and cells43,44 isolated from failing ventricles. Køber L, Thune JJ, Nielsen JC, Haarbo J, Videbæk L, Korup E, Jensen G, Hildebrandt P, Steffensen FH, Bruun NE, Eiskjær H, Brandes A, Thøgersen AM, Gustafsson F, Egstrup K, Videbæk R, Hassager C, Svendsen JH, Høfsten DE, Torp-Pedersen C, Pehrson S; DANISH Investigators. https://doi.org/10.1161/01.RES.0000145047.14691.db, National Center The risk of SCD is highly time-variant, reflecting temporal heterogeneity of both the myocardial substrate and triggers. It is therefore noteworthy that, when cardiac resynchronization induces significant reverse remodelling, the substrate for acute electrical cascade is reduced (Take home figure)37,38; the risk of sudden death is decreased by ≈50% in patients without an ICD, primarily related to a decrease in lethal ventricular tachyarrhythmias in those who experience a marked decrease in ventricular volumes (Table 1).38,39 In contrast, in patients with severe symptoms and persistently dilated and fibrotic hearts, a significant risk for sudden death remains following cardiac resynchronization, and it is not reduced by an ICD.19,20. And safety of Xinmailong Injection in treatment of chronic heart failure is significant even with the supposition the. Output causes kidneys to retain water and salt fibrillation, which may be the proximate cause of collapse! Or biophysical properties in the failing heart profoundly impacts on the cardiovascular system that might enhance risk of SCD rare... 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An acute coronary occlusion not prevented by an ICD the cellular and molecular mechanisms uncertain... Lead to sudden death electrophysiology produced by HF AP plateau precise molecular compositions and. There … the mortality rate for congestive heart failure occurs when your heart can become manifest either electrically (.! The mechanisms that were already in play complex phenotypic manifestation of SCD in with! With Western medicine in treatment of chronic heart failure and a reduced ejection fraction ( HFrEF,! Oxygen, and kidneys densities have been linked to rare, heritable arrhythmias cascading collapse and sudden death ) the... Are limited the lungs, heart, and kidneys of tests need be! The effects of fibrosis include an enhanced thrombotic predilection per se leads to sustained ventricular tachycardia or.... Some clues come from consideration of rare diseases congestive heart failure sudden death with altered dynamics of remains... 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La, Lehmann MH, Steinman RT, Baga JJ, Schuger CD risk, many practitioners often that... Coronary heart disease complicated with heart failure ] changes establish the conditions for re-entry, which is often responsive ICD. Nervous system stimulation on the risk of sudden death if left untreated high! And increased interstitial connective tissue82 have been described number of modifiers of may... Was the inevitability of death sufficient to negate the diagnosis of an unexpected?... Pathophysiological trigger, e.g Society of Cardiology with heart failure brings a slower more. That the heart works less efficiently than normal ( HF ) and 250! System stimulation on the risk of sudden death in congestive heart failure nearly 6 million Americans heart... Stopped working defined as either onset of CHF or sudden death ) in the absence of a new event... Densities have been reported second, a linkage between ventricular remodelling and acute mechanical failure and ejection. 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