Sudden death risk markers for patients with left ventricular ejection fractions greater than 40%

The major burden of sudden cardiac death (SCD) in patients with heart disease occurs in those with a left ventricular ejection fraction?>?40%. Although the annual risk of SCD may be lower in these patients compared to those with lower LVEF, their lifetime cumulative risk of SCD may be greater due to a better overall prognosis. It is plausible that those with LVEF?>?40% who are at highest risk of life-threatening arrhythmia will benefit from implantable cardioverter defibrillators. Features that identify patients with a LVEF?>?40% at high risk of SCD are urgently needed. We review existing studies examining SCD markers in this sub-group and discuss gaps in the current evidence base.     

Invasive strategy in patients with resuscitated cardiac arrest and ST elevation myocardial infarction

Coronary artery disease is the most frequent cause of sudden cardiac death. There is general consensus that immediate coronary angiography with percutaneous coronary intervention(PCI) should be performed in all conscious and unconscious patients with ST-elevation myocardial infarction in post-resuscitation electrocardiogram. In these patients acute coronary thrombotic lesion("ACS" lesion) suitable for PCI is typically present in more than 90%. PCI in these patients is not only feasible and safe but highly effective and there is evidence of improved survival with good neurological outcome. PCI of the culprit lesion is the primary goal while PCI of stable obstructive lesions may be postponed unless post-resuscitation cardiogenic shock is present.     

Sudden cardiac death: Epidemiologic and financial worldwide perspective

The term sudden cardiac death (SCD) implies the sudden and unexpected loss of an active, productive member of the community. SCD is typically attributed to lethal ventricular arrhythmias; however, these arrhythmias are impossible to diagnose after the fact. Epidemiologic analyses, therefore, rely on inference of the cause of death. Estimates of the incidence of are SCD variable but it may be as high as 1 per 1,000 per year. The cost of SCD to society is incalculable. Current strategies for preventing SCD rely on risk assessment for cardiology patients and implantation of defibrillators (ICD) in high risk patients. Unfortunately, the absolute number of SCDs that occur in the general (relatively low-risk) population is large compared to the number of SCDs in the high risk population. Therefore, prevention of SCD in high risk populations is unlikely to prevent the majority of SCDs. Cost-effectiveness of ICD implantation for prevention of SCD has been studied; ICDs appear to meet U.S. and European criteria for cost-effectiveness if their benefit extends to at least 7–8 years. However, therapies considered cost-effective may nonetheless be too costly for most worldwide societies. Currently, investigators are focusing on refining risk stratification, partly in hopes of identifying patients for whom ICD implantation will not be useful.     

Sudden cardiac death preceded by ST segment elevations during ECG patch monitoring

A 58-year-old male underwent ambulatory ECG monitoring with continuous patch monitoring (Zio XT Patch) for the complaint of episodic dyspnea. In the period of monitoring the patient suffered sudden cardiac death (SCD) with continuous ECG recording showing pronounced ST segment elevations followed by bradycardia and death. This report highlights the growing potential of continuous ST segment monitoring, and features the infrequent entity of ischemic electromechanical dissociation with bradyarrhythmia as a cause of SCD.     

Left ventricular systolic dysfunction, total mortality, and sudden death in patients with myocardial infarction treated with n-3 polyunsaturated fatty acids

BACKGROUND: Sudden death (SD) has a major impact on mortality (M) in patients with left ventricular systolic dysfunction (SyD). In GISSI-Prevenzione, treatment with n-3 polyunsaturated fatty acids (PUFA) reduced M and SD in post-MI patients, but their effect in patients with SyD is unknown. METHODS: 11,323 patients with prior MI and NYHA class < or = II were recruited. After excluding patients with no ejection fraction (EF) measurement (1684), and those with missing data (n=9), 9630 patients were available for analysis. Multivariate Cox regression adjusted models were fitted. RESULTS: Compared to patients with EF > 50%, SyD patients had higher M (12.3% vs. 6.0%) and SD (3.4% vs. 1.4%) rates. PUFA reduced M similarly in patients with (RR 0.76 (0.60-0.96) P=0.02) and without SyD (RR 0.81 (0.59-1.10) P=0.17) (heterogeneity tests P=0.55). In contrast, the effect on SD was markedly asymmetrical: PUFA produced a marked reduction (RR 0.42 (0.26-0.67) P=0.0003) of risk in SyD patients whereas the effect was less evident (RR 0.89 (0.41-1.69) P=0.71) in patients with EF > 50% (heterogeneity tests P=0.07). There was a significant increase in SD with worsening EF (P test for trend=0.02), the benefit on SD in patients with EF < or = 40% being 4-fold higher than in those with EF > 50%. CONCLUSIONS: Increasing SyD is associated with elevated risk of SD and with increasing benefit from PUFA. The effect of PUFA on SD reduction was greater in patients with SyD. Prospective trials testing the effect of PUFA in populations with SyD are required.     

Role of PET-CT in the assessment of myocardial viability in patients with left ventricular dysfunction

AimRole of PET-CT in assessment of myocardial viability in patients with LV dysfunction.MethodsThis prospective study included 120 patients with LV dysfunction who underwent 99mTechnetium-Sestamibi myocardial perfusion SPECT-CT and 18FFDG cardiac PET-CT. They also underwent serial echocardiography and coronary angiography along with myocardial perfusion and FDG PET study.ResultsThirty-three patients had single vessel disease, 48 had triple vessel disease, and rest had double vessel disease. Among 786 segments, matched defects were seen in 432 (55%) and mismatched defects in 354 (45%) segments. 78 patients were surgically managed, and 42 were medically managed. The change in LVEF after surgical management was statistically significant compared to medical management.ConclusionViability assessment should be performed in patients who present after 12 h of acute myocardial infarction or with LV dysfunction due to ischemic heart disease to decide upon appropriate surgical management.     

Sudden death after medullary infarction—A case report

Sudden death in a stable medullary infarction case frequently induces legal problems. Currently, the etiology of the most reported cases are not known because autopsy is rare. Here, we report one female patient with medullary infarction who experienced a sudden cardiopulmonary arrest during a brain magnetic resonance imaging (MRI) study. The blood flow changes on the MRI indicated that her death resulted from the sudden collapse of systemic circulation. Dysautonomia, or sudden respiratory arrest resulting from brainstem dysfunction, was suspected. In this report, we present her cranial MRI findings and discuss the possible pathophysiology after reviewing the relevant literature. We also recommend certain tests for patients with medullary infarction to prevent the risk of sudden unexpected deaths.     

Exercise training without ventricular remodeling in patients with moderate to severe left ventricular dysfunction early after acute myocardial infarction

BACKGROUND: The purpose of this study was to determine whether or not patients with moderate to severe left ventricular (LV) dysfunction benefit from exercise training starting early after acute myocardial infarction (AMI) without deteriorating LV remodeling. METHODS: We investigated changes in exercise capacity and LV end-diastolic dimension (LVDd by two-dimensional echocardiography) before and after exercise training in 126 patients after AMI. Patients were divided into three groups according to LV ejection fraction (EF) at the beginning of exercise training: 74 patients with LVEF>/=45% (Group H), 35 patients with 35%相似文献   

Sudden cardiac death in patients with nonischemic cardiomyopathy

Sudden cardiac death (SCD) is an important cause of mortality worldwide. Although SCD is most often associated with coronary heart disease, the risk of SCD in patients without ischemic heart disease is well-established. Nonischemic cardiomyopathies, including idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy represent three unique disease entities that have been shown to be highly associated with SCD and ventricular arrhythmias. A variety of risk stratification tools have been investigated, although the optimal strategy remains unknown. Identification of the arrhythmogenic substrate and treatment of ventricular arrhythmias in these subgroups can be challenging. Herein, we aim to discuss the current understanding of the anatomic and electrophysiologic substrate underlying ventricular arrhythmias and highlight features that may be associated with a higher risk of SCD in these 3 conditions.     

Sudden cardiac death and acute pathology of coronary arteries

The pathology of sudden cardiac death still is a matter of controversy,particularly with respect to the state of the coronary arteries.A recent study has shown a high incidence of acute lesions andsuggests a causal relationship. The present study has been designedto verify whether or not acute coronary arterial lesions occurfrequently in patients with sudden cardiac death. Sixteen heartswere available. In each instance the patient had died within6 hours from the onset of myocardial ischaemia. The coronaryarterial system was extensively studied by post-mortem coronaryangiography, decalcification, serial blocking and histologicalsectioning. Acute coronary arterial lesions, defined as plaquefissure, ‘isolated’ plaque haemorrhage and ‘isolatedthrombosis’, were found in 14 of the 16 hearts (87.5%).The total number of acute lesions in the 14 hearts was 28. In9 hearts plaque fissures were present, in 7 ‘isolated’plaque haemorrhages and in 5 an ‘isolated thrombus’.Half of all acute lesions had occurred in an atheroscleroticplaque of pre-existing 50–75% luminal narrowing. The presentstudy endorses the concept that acute coronary arterial lesionsoccur in a high proportion of patients with sudden cardiac death,plaque fissures with intramural haemorrhage and intraluminalthrombosis being the most common abnormality. It is temptingto attribute causal significance to such lesions in patientswith sudden cardiac death.     

Sudden death and cardiac arrest without phenotype: the utility of genetic testing

Approximately 4% of sudden cardiac deaths are unexplained [the sudden arrhythmic death syndrome (SADS)], and up to 6–10% of survivors of cardiac arrest do not have an identifiable cardiac abnormality after comprehensive clinical evaluation [idiopathic ventricular fibrillation (IVF)]. Genetic testing may be able to play a role in diagnostics and can be targeted to an underlying phenotype present in family members following clinical evaluation. Alternatively, post-mortem genetic testing (the “molecular autopsy”) may diagnose the underlying cause if a clearly pathogenic rare variant is found. Limitations include a modest yield, and the high probability of finding a variant of unknown significance (VUS) leading to a low signal-to-noise ratio. Next generation sequencing enables cost-efficient high throughput screening of a larger number of genes but at the expense of increased genetic noise. The yield from genetic testing is even lower in IVF in the absence of any suggestion of another phenotype in the index case or his/her family, and should be actively discouraged at this time. Future improvements in diagnostic utility include optimization of the use of variant-calling pipelines and shared databases as well as patient-specific models of disease to more accurately assign pathogenicity of variants. Studying “trios” of parents and the index case may better assess the yield of sporadic and recessive disease.     

Left coronary artery spasm causing severe left ventricular dysfunction without myocardial infarction

This report describes a patient with persistent, recurrent left anterior descending coronary artery spasm, which causes marked left ventricular dysfunction in a clinical course that is typical of acute myocardial infarction with hyperacute electrocardiographic changes. However, after emergency coronary artery bypass surgery, the patient had complete reversal of left ventricular dysfunction, with no residual evidence of acute myocardial infarction by electrocardiograph or gated blood pool imaging and no CPK enzyme rise. The patient therefore demonstrates that coronary spasm in some instances clearly precedes the sequence of pathophysiologic events leading to acute myocardial infarction. Our report also demonstrates for the first time in man that massive left ventricular dysfunction may occur in this intermediate coronary syndrome, presenting clinically as impending myocardial infarction. With aggressive surgical intervention and emergency bypass surgery, left ventricular function was restored to normal. Despite the semantic problems of categorizing such patients as having impending myocardial infarction, the severe left ventricular dysfunction and alarming course of this patient's illness was resolved by emergency surgery, suggesting that, in some instances, aggressive therapy is warranted.     

KCNJ11 polymorphisms and sudden cardiac death in patients with acute myocardial infarction

PURPOSE: Patients with an acute myocardial infarction (AMI) are of high risk to develop ischemia-induced ventricular arrhythmias, leading to sudden cardiac death (SCD) in about one third of all AMI patients. The individual susceptibility to ischemia-induced arrhythmias may be modified by polymorphisms in genes encoding ion channels. The cardiac ATP-dependent potassium channel (K(ATP)) current is generated by ion channels encoded by the KCNJ11 gene and the SUR2a gene. Opening of the K(ATP) channel during ischemia results in action potential shortening in various studies and may therefore influence the outcome of AMI patients. METHODS: Using a three-primer strategy, we sequenced the complete coding and adjacent 5' and 3' sequences of the intronless KCNJ11 gene (1.3 kb) prospectively in two groups. Patients of group 1 (n = 84) survived three or more transmyocardial infarctions without developing any ventricular arrhythmias. Patients of group 2 died suddenly from their first myocardial infarction (n = 86), most of them witnessed SCDs. RESULTS: We identified a total of six known polymorphisms (K23E, A190A, L267V, L270V, I337V, and K281K) and two new polymorphisms (L267L, 3'UTR +62 G/A). The allele, genotype, and haplotype frequencies did not differ between the two groups. All polymorphisms were found to be in Hardy-Weinberg equilibrium. In addition, we identified two novel missense mutations in a highly conserved region of the gene in two patients of group 2 (P266T and R371H) with yet unknown functional consequences. CONCLUSION: In this study of AMI patients, SCD was not related to polymorphisms in the KCNJ11 gene.     

Role of left ventricular dyssynchrony in predicting remodeling after ST elevation myocardial infarction

Background: Intraventricular dyssynchrony is associated with worsening systolic function, adverse remodeling, and clinical events. The aim of this study is to investigate whether intraventricular dyssynchrony assessed by tissue Doppler imaging (TDI) can predict left ventricular (LV) remodeling after first ST segment elevation myocardial infarction (STEMI) treated successfully with primary percutaneous coronary intervention (pPCI). Methods: Fifty‐two consecutive patients who presented with first acute STEMI were included in the study. All patients underwent successful pPCI. Standard echocardiography was performed within 48 hours of admission. LV dyssynchrony was assessed by color‐coded TDI. Dyssynchrony (Ts‐diff) was calculated by maximal temporal difference between time to peak systolic velocities (Ts) of six basal segments. Echocardiographic examination was repeated after 6 months to reassess LV volumes. LV remodeling was defined as >15% increase in LV end‐systolic volume index (LVESVI) after 6 months. Results: Eleven patients (23%) developed LV remodeling. Baseline dyssynchrony was found to be correlated with percent change in LVESVI and LV end‐diastolic volume index (LVEDVI) after 6 months. Ts‐diff, creatine kinase‐MB and mitral inflow E‐wave deceleration time (DT) were the independent predictors of remodeling after STEMI in multivariate logistic regression analysis. Receiver operating characteristic curve analysis showed that Ts‐diff >56 msec had 72.7% sensitivity and 83.8% specificity for predicting remodeling. Conclusions: LV dyssynchrony is a strong predictor of LV remodeling after acute myocardial infarction (AMI). It could be useful in risk stratification of patients after AMI. (Echocardiography 2012;29:165‐172)