Left cardiac sympathetic denervation in children with Jervell Lange-Nielsen syndrome and drug refractory torsades - A case series.

INTRODUCTION: Long QT syndrome is an inherited malignant channelopathy which leads to life-threatening arrhythmia, with multiple genotypes. Jervell and Lange-Nielsen syndrome (JLNS) is an autosomal recessive subtype of this disease, characterized by congenital sensorineural deafness and a high incidence of sudden cardiac death (SCD). METHODOLOGY: We prospectively followed up six children who underwent left cardiac sympathetic denervation (LCSD) for JLNS in view of high-risk features despite being on maximally tolerated doses of oral propranolol. RESULTS: Mean age at diagnosis was 2.75 ± 0.39 years, with a significant delay between onset of symptoms and diagnosis (mean 7.2 ± 3.5 months). All had sensorineural hearing loss, conforming to the JLNS phenotype. Mean QTc interval was 603 ± 93 ms, with T wave alternans (TWA) seen in all cases. All were started on propranolol and subsequently subjected to LCSD, and 3 underwent AAI permanent pacemaker implantation. Over a mean follow-up of 20 months, there was a significant reduction in QTc (603 ± 93 ms to 501 ± 33 ms, p = .04), which was persistent on follow-up (525 ± 41 ms) and only two out of six had persistent T wave alternans on ECG (p < .01). None of these children had presyncope, syncope, seizures, torsades de pointes, cardiac arrest or death on follow up following LCSD. CONCLUSION: Jervell Lange-Nielsen syndrome is a subtype of LQTS with high-risk features. LCSD, an effective therapeutic option for those having symptoms despite being on propranolol, results in significant reduction of QTc interval and amelioration of symptoms.

Electroconvulsive Therapy in Patients With Cardiac Implantable Electronic Devices: A Case Report and Systematic Review of Published Cases.

OBJECTIVE: The aims of the study were to report the case of a 54-year-old man with recurrent depressive disorder with multiple medical comorbidities having a dual-chamber pacemaker, treated successfully with 11 sessions of electroconvulsive therapy, and to conduct a systematic review of published cases documenting the use of electroconvulsive therapy (ECT) in patients with cardiac implantable electronic devices (CIEDs) for treating major psychiatric disorders. METHODS: We searched electronic databases (MEDLINE, PubMed, Google Scholar, Embase, Cochrane Library, PsycINFO, and Crossref) and included studies reporting on the use of electroconvulsive therapy in patients with CIEDs. RESULTS: Thirty-five publications across 53 years (1967-2021) reported on 76 patients (including current report) who received a pooled total of 979 modified ECT sessions. The most common adverse events were premature ventricular contraction and hypertension. There have been no reports of serious adverse effects that necessitated the cessation of ECT. CONCLUSIONS: Electroconvulsive therapy is a safe and efficacious treatment for major psychiatric disorders, and the presence of CIEDs should not delay or deter the use of ECT in these patients.

What are the atrioventricular delays in right ventricular apical and septal pacing for optimal hemodynamics in patients with normal left ventricular function?

INTRODUCTION: There is a surge of interest in alternate site pacing to prevent pacing-induced left ventricular dysfunction. However, little is known regarding the appropriate atrioventricular (AV) delay between right ventricular (RV) septal and RV apical pacing for optimal hemodynamic benefit. OBJECTIVES: To determine the programmed values of atrial sensed and atrial paced AV delays in basal RV septal and apical RV pacing that results in the maximum delivered stroke volume (SV). METHODS: We calculated the Doppler-derived SV at various sensed and paced AV delays in 50 patients with complete AV block implanted with a dual-chamber pacemaker (group A: 25 RV apical pacing; group B: 25 RV septal pacing). The hemodynamic difference in terms of the SV between sensed and paced AV delay, corresponding to the site of RV pacing was then compared for statistical significance. RESULTS: In group A, maximal SV was derived at a sensed AV delay of 123.2 ± 11 ms and paced AV delay of 129.2 ± 10 ms, and in group B, at a sensed AV delay of 123.6 ± 8 ms and paced AV delay of and 132.8 ± 7 ms. At these intervals, there was no difference in the SV between septal and apical RV pacing (P = .28 and .22, respectively). CONCLUSION: The atrial sensed and atrial paced AV delays for septal and apical RV pacing for optimal hemodynamics are similar. For optimal hemodynamics, the atrial paced AV delay is longer than the atrial sensed AV delay.

Short-term response to phenytoin sodium in Andersen-Tawil syndrome-1 with a cardiac-dominant phenotype.

BACKGROUND: Andersen-Tawil syndrome (ATS) is a rare familial periodic paralysis that typically also affects the heart and skeletal system. Ventricular arrhythmias (VAs) are profound and difficult to control, but minimally symptomatic. In this report, we describe an atypical phenotype of ATS in two related families. We also report our experience with phenytoin sodium for the control of resistant VAs in these patients. METHODS AND RESULTS: Between 2014 and 2018, seven siblings were diagnosed with ATS on the basis of cardiac arrhythmias and genetic evaluation. Heterozygous mutation with c.431G > C (p.G144A) in exon 2 of KCNJ2 gene was observed in all patients. Characteristic cardiac manifestations were noted in all patients but periodic paralysis or objective neurological involvement was distinctly absent. Phenytoin was considered for control of symptomatic VA in three patients. Intake of oral phenytoin (5 mg/kg/day) for 1 month completely suppressed VA (<1% in 24-h Holter monitoring) in two patients, and significantly in the third (8% per 24 h) patient. Phenytoin was well-tolerated in all three patients. CONCLUSIONS: We describe a cardiac-predominant phenotype in ATS. ATS should be suspected in patients with typical cardiac manifestations even in the absence of periodic paralysis. Our initial experience with short-term use of phenytoin for control of resistant VAs is encouraging.

A novel prediction model for risk stratification in patients with a type 1 Brugada ECG pattern.

BACKGROUND: Risk stratification in Brugada syndrome remains a controversial and unresolved clinical problem, especially in asymptomatic patients with a type 1 ECG pattern. The purpose of this study is to derive and validate a prediction model based on clinical and ECG parameters to effectively identify patients with a type 1 ECG pattern who are at high risk of major arrhythmic events (MAE) during follow-up. METHODS: This study analysed data from 103 consecutive patients with Brugada Type 1 ECG pattern and no history of previous cardiac arrest. The prediction model was derived using logistic regression with MAE as the primary outcome, and patient demographic and electrocardiographic parameters as potential predictor variables. The model was externally validated in an independent cohort of 42 patients. RESULTS: The final model (Brugada Risk Stratification [BRS] score) consisted of 4 independent predictors (1 point each) of MAE during follow-up (median 85.3 months): spontaneous type 1 pattern, QRS fragments in inferior leads≥3,S wave upslope duration ratio ≥ 0.8, and T peak - T end ≥ 100 ms. The BRS score (AUC = 0.95,95% CI 0.0.92-0.98) stratifies patients with a type 1 ECG pattern into low (BRS score ≤ 2) and high (BRS score ≥ 3) risk classes, with a class specific risk of MAE of 0-1.1% and 92.3-100% across the derivation and validation cohorts, respectively. CONCLUSIONS: The BRS score is a simple bed-side tool with high predictive accuracy, for risk stratification of patients with a Brugada Type 1 ECG pattern. Prospective validation of the prediction model is necessary before this score can be implemented in clinical practice.

Fosphenytoin for control of electrical storm in acute myocardial infarction and Purkinje fiber-mediated arrhythmias.

BACKGROUND: Purkinje fiber-mediated arrhythmias in the setting of acute myocardial infarction are poorly responsive to conventional antiarrhythmic therapy, increases overall mortality and often requires radiofrequency ablation (RFA) for control. In this study, we report the use of intravenous Fosphenytoin for the control of arrhythmic storm in patients with acute myocardial infarction. METHODS AND RESULTS: Six patients with acute myocardial infarction (5 AW/1 LW) and Purkinje-triggered ventricular arrhythmias refractory to conventional antiarrhythmics were treated with intravenous Fosphenytoin before considering RFA. Arrhythmia control was obtained in all patients after the initial bolus dose. Breakthrough episodes were seen in 5/6 within 24-36 hours of the initial bolus, necessitating a second bolus. Complete arrhythmia control was obtained in all patients within 72 hours and 5/6 patients were successfully discharged from the hospital. One patient succumbed to sepsis in hospital while another patient succumbed to Sub Dural Hematoma after 3 months. CONCLUSIONS: Intravenous Fosphenytoin should be considered before RFA for control of Purkinje fiber-mediated refractory arrhythmias in acute myocardial infarction patients.

Bio-width index: a novel biomarker for prognostication of long term outcomes in patients with anaemia and heart failure.

BACKGROUND: The utility of biomarkers for prognostication of long term outcomes in patients with anaemia and heart failure(HF) is not well defined. The objective of this study was to assess the ability of a novel biomarker, bio-width index (BWI),to improve risk stratification in patients with anaemia and acutely decompensated heart failure(ADHF), in comparison to conventional markers, B-type natriuretic peptide(BNP) and red- cell distribution width(RDW). METHODS: Data from 1569 consecutive patients with ADHF treated at a multidisciplinary HF unit was analysed in this study. The bio-width index (BWI) was calculated by multiplying BNP to RDW and dividing the product by 10 (BWI = BNP x RDW/10). The primary outcome was one year all-cause mortality. RESULTS: During follow up (median 422 days), subjects with anaemia had significantly higher one year mortality (49.6 vs. 30.5%, p < .001). Cox regression analysis revealed that, BWI(HR 2.13, 95%CI 2.02-2.24, p = .018) as well as BNP(HR 1.86, 95%CI 1.78-1.94, p = .024), and RDW (HR 1.98, 95%CI 1.91-2.05, p = .033) were all independent predictors of one year mortality after adjusting for conventional risk factors. BWI had a higher discriminative ability compared to BNP(AUC 0.90 vs. 0.75, p < .001) and RDW(AUC 0.90 vs. 0.81, p = .012). The patients with higher BWI ( >1024.9) had a higher one year mortality(85.1 vs. 29.2%, p < .001). In addition, BWI significantly improved the net reclassification compared to both BNP(p = .002) and RDW(p = .018). CONCLUSIONS: In patients with anaemia and ADHF, bio-width index is superior to the established biomarkers such as BNP and RDW in prognostication of long term mortality.

The Utility of Exercise Testing in Risk Stratification of Asymptomatic Patients With Type 1 Brugada Pattern.

INTRODUCTION: Risk stratification of asymptomatic patients with a Brugada type 1 ECG pattern remains an unresolved clinical conundrum. In contrast to provocative pharmacological testing in Brugada syndrome, there is limited data on the role of exercise stress testing as a risk stratification modality. The objective of this study was to evaluate the utility of exercise testing in asymptomatic patients with type 1 Brugada pattern to prognosticate major arrhythmic events (MAE) during follow-up. METHODS AND RESULTS: Treadmill exercise testing was conducted for 75 asymptomatic patients with type 1 Brugada pattern and for 88 healthy control subjects. The clinical end point of MAE was defined as the occurrence of sudden cardiac death (SCD) or resuscitated ventricular fibrillation (VF). During a follow-up of 77.9 ± 28.9 months, eight MAE occurred (five VF and three SCD). Multivariate Cox regression analysis showed that the following were independent predictors of MAE in asymptomatic patients with a type 1 Brugada pattern: increase in S wave upslope duration ratio >30% at peak exercise (HR 1.35, 95% CI 1.08-10.97, P = 0.023), augmentation of J point elevation in lead aVR >2 mm in late recovery (HR 1.88, 95% 1.21-15.67, P = 0.011), and delayed HR recovery (HR 1.14, 95% CI 1.06-18.22, P = 0.042). A high-risk cohort was identified by the final step-wise regression model with good accuracy (specificity = 98.4%, sensitivity = 62.5%) and discriminative power (AUC = 0.93, 95% CI 0.89-0.96, P = 0.002). Kaplan-Meier analysis revealed increasing MAE in subjects with one, two, or three predictors, respectively (log rank P < 0.001). CONCLUSIONS: Exercise testing in asymptomatic patients with type 1 Brugada pattern aids in identification of high-risk patients and provides a unique window of opportunity for early intervention.

Radiofrequency Ablation of Left Atrial Reentrant Tachycardias in Rheumatic Mitral Valve Disease: A Case Series.

BACKGROUND: Left atrial (LA) reentrant tachycardias are not uncommon in regions where rheumatic heart disease is prevalent. Some of these arrhythmias may be curable by radiofrequency ablation (RFA). However, there are limited data pertaining to this in existing literature. CASE REPORT: Three patients who had rheumatic mitral valve disease with past history of surgical-/catheter-based intervention and having no significant residual disease had symptomatic atrial flutter despite optimal medical management. An electrophysiological study confirmed an LA focal/micro-reentrant mechanism in all. There was patchy scarring of the LA, and successful RFA of these arrhythmias could be achieved. CONCLUSION: The focal nature of the scar in these patients may suggest that the rheumatic involvement of the atrium or the hemodynamic consequence of the vulvar lesion causes nonuniform insult to the atrial tissue and limited scar. At least in some patients with limited scarring, early RFA may help in the maintenance of sinus rhythm.

'Optimized' LV only pacing using a dual chamber pacemaker as a cost effective alternative to CRT.

BACKGROUND: Cardiac Resynchronization therapy (CRT) remains largely under-used in developing countries owing to the high cost of therapy. In this pilot study, we explore 'optimized' Left Ventricle Only Pacing (LVOP) as a cost effective alternative to cardiac resynchronization therapy in selected patients with heart failure. HYPOTHESIS: In economically poorer patients with heart failure, left bundle branch block (LBBB) and intact AV node conduction, synchronization can be obtained using a dual chamber pacemaker (leads in right atrium and Left ventricle) with the help of 2D strain imaging. METHODS AND RESULTS: 4 patients underwent LVOP for symptomatic heart failure. Post procedure 'optimization' was done using 12 lead electrocardiography and 2D- Strain imaging. Difference between Time to Peak longitudinal strain and Aortic valve Closure (Diff TPL-AC) was calculated for each segment at different AV delays and the AV delay with the smallest Diff TPL-AC was programmed. The mean AV delay that resulted in electrical and mechanical synchrony was 150 ms. After a mean follow up of 6 months, all patients had improved by at least 1 NYHA class. The mean reduction in QRS duration post procedure was -54.5 ± 22.82 ms and the mean improvement in EF was 7 ± 2.75%. CONCLUSION: Optimized LVOP using 2D strain and ECG can be a cost-effective alternative to CRT in patients with LBBB, heart failure and normal AV node conduction.

Familial atrioventricular nodal re-entrant tachycardia: A case seriers and a systematic review.

Multiple reports of familial clustering suggest that genetic factors may contribute in the pathogenesis of atrioventricular nodal re-entrant tachycardia (AVNRT). We report three cases of AVNRT in a father and his two sons along with a review of literature of other similar cases. Electrophysiological studies induced typical AVNRT, which was successfully eliminated by radiofrequency ablation in all of them. Of the 22 reported cases, 96% had typical (slow-fast) variant of AVNRT. The predominant pattern of inheritance appears to be autosomal dominant, though other patterns may exist. Further research is needed to understand the genetic influence of AVNRT and its pathophysiology.

Evaluation of baseline ECG in patients undergoing Oral Flecainide Challenge test for suspected Brugada Syndrome: An analysis of lead II.

BACKGROUND AND OBJECTIVES: We analyzed Lead II in patients undergoing an Oral Flecainide Challenge test (FCT), to identify any pointers that could predict a positive FCT and thereby help in recognition of latent BS. METHODS: The following parameters in lead II were retrospectively analyzed from the pre-test ECG in 62 patients undergoing FCT for suspected BS: The presence or absence of S waves, S wave amplitude, duration and upslope duration; J point parameters- Early repolarization, QRS notch, and QRS Slur; ST segment parameters-lack of isoelectric ST segment, ST duration and QT interval. RESULTS: 48 had positive FCT (Group-1) while 14 were negative for FCT(Group-2). Lack of an isoelectric ST segment (50% vs 14.29%, p = 0.018) and slurring of QRS (33.33% vs 0%, p = 0.014) was more common in Group-1 than Group-2. Group-1 had shorter ST segment duration (median 81.5 (IQR 64-103.5) vs 110 (IQR 90-132), p = 0.002) and shorter ST: QT ratio (median 0.28 (IQR 0.22-0.35) vs 0.23 (0.18-0.27), p = 0.007). QRS notch/depressed J point (87.5%), QRS slur (100%), and lack of isoelectric ST segment (92.31%) had high sensitivity for predicting an inducible Type 1 Brugada pattern. Combining two parameters- ST: QT ratio<0.24 and lack of isoelectric ST segment-considerably improved the specificity (73.3%), and the positive predictive value of the test to 76%. The results remained accurate when validated in a small prospective cohort. CONCLUSION: Shortened ST segment in Lead II, lack of isoelectric ST segment, slurred QRS and ST/QT ratio <0.24 are predictive of underlying Brugada pattern in baseline ECG.

Histopathological Study of Left and Right Atria in Isolated Rheumatic Mitral Stenosis With and Without Atrial Fibrillation.

BACKGROUND: Mitral stenosis (MS) has the highest incidence of atrial fibrillation (AF) in chronic rheumatic valvular disease. There are very few studies in isolated MS comparing histopathological changes in patients with sinus rhythm (SR) and AF. OBJECTIVES: To analyze the histological changes associated with isolated MS and compare between changes in AF and SR. METHODS: This was a prospective study in patients undergoing valve replacement surgery for symptomatic isolated MS who were divided into 2 groups, Group I AF (n = 13) and Group II SR (n = 10). Intra-operative biopsies performed from 5 different sites from both atria were analyzed for 10 histopathologic changes commonly associated with AF. RESULTS: On multivariate analysis, myocytolysis (odds ratio [OR]: 1.48, P = 0.05) was found to be associated with AF, whereas myocyte hypertrophy (OR: 0.21, P = 0.003), and glycogen deposition (OR: 0.43, P = 0.002) was associated with SR. Interstitial fibrosis the commonest change was uniformly distributed across both atria irrespective of the rhythm. CONCLUSION: In rheumatic MS, SR is associated with myocyte hypertrophy whereas AF is associated with myocytolysis. Endocardial inflammation is more common in left atrial appendage irrespective of rhythm. Interstitial fibrosis is seen in >90% of patients distributed in both the atria and is independent of the rhythm. Amyloid and Aschoff bodies are uncommon and the rest of the changes are uniformly distributed across both the atria.

Suicidal Zinc Phosphide Poisoning Unmasking Brugada Syndrome and Triggering Near Fatal Ventricular Arrhythmia.

Brugada syndrome (BrS) is an inherited channelopathy associated with increased incidence of ventricular arrhythmias and has many acquired triggers. Zinc phosphide (ZnP) is a rodenticide and is commonly implicated in suicidal poison ingestion. ZnP poisoning can cause myocardial toxicity and death. We report a case of ZnP poisoning that triggered a type I Brugada pattern and ventricular fibrillation in a 67-year-old male. He had no other features of toxicity and recovered later. As metal phosphide is the commonest toxin involved in suicidal poisoning in India and BrS being endemic here, this case highlights an important clinical problem.

Association of Transforming Growth Factor-ß Superfamily Genes with Non-Regression of Pulmonary Artery Hypertension Following Balloon Mitral Valvotomy: A Pilot Study.

BACKGROUND AND AIM OF THE STUDY: Pulmonary arterial hypertension (PAH) is a common accompaniment of rheumatic mitral stenosis (MS), with 70% of patients showing evidence of different grades of PAH. The latter condition is found to be a prognostic factor influencing disease outcome even after interventional or surgical therapy. The cause of the non-regression of PAH following successful balloon mitral valvotomy (BMV) is not clear. Hence, the study aim was to determine if there is an association of mutations in the genes of the TGF-ß superfamily and non-regression of PAH in patients who undergo a successful BMV. METHODS: Forty-six patients who underwent BMV and fulfilled the recruitment criteria were enrolled prospectively in this case-control study. Among the patients, 27 had non-regression of PAH while 19 had regression of PAH and served as controls. The mean age of the population was 32.63 ± 10.65 years. RESULTS: No statistically significant differences were identified in any of the baseline parameters between the two groups. None of the samples had BMPR2 or ACVRL1 mutations. Ten of the patients and four of the controls were positive for Endoglin mutation, but the inter-group difference was not statistically significant (p = 0.25) CONCLUSIONS: The present study - the first of its kind - showed that deletion-duplication mutations in the BMPR2 or ACVRL1 genes may not be associated with non-regression of PAH, even after successful BMV, or in a wider sense serve as a contributor to PAH in rheumatic MS. The association of Endoglin mutation and non-regression of PAH warrants further investigation in a larger population.

Isolated rheumatic severe tricuspid regurgitation.

Severe isolated tricuspid regurgitation (TR) is very rare, with most cases of TR being functional and secondary to pulmonary hypertension from left heart pathologies. We report an unusual case of a young Nigerian male, who presented to us with dyspnea, repeated hospital admissions for heart failure, and a childhood history of rheumatic fever. Echocardiogram showed massively dilated right atrium and ventricle, noncoaptation of thickened tricuspid valve with torrential free tricuspid regurgitation. Other valves were normal. Cardiac MRI showed normal right ventricular function and viability. Patient underwent tricuspid valve replacement with 35-mm St. Jude valve.

Flecainide challenge test: Predictors of unmasking of type 1 Brugada ECG pattern among those with non-type 1 Brugada ECG pattern.

BACKGROUND: Many subjects in community have non-type 1 Brugada pattern ECG with atypical symptoms, relevance of which is not clear. Provocative tests to unmask type 1 Brugada pattern in these patients would help in diagnosing Brugada Syndrome. However sensitivity and specificity of provocating drugs are variable. METHODS: We studied 29 patients referred to our institute with clinical presentation suggestive but not diagnostic of Brugada or with non-Type 1 Brugada pattern ECG. Flecainide Challenge Test (FCT) was done in these patients (IV Flecainide test in 4 patients and Oral Flecainide in 25 patients). Resting 12-lead ECG with standard precordial leads and ECG with precordial leads placed 1 Intercostal space above were performed after flecainide administration every 5 min for first 30 min and every 30 min thereafter until ECG became normal or upto 6 h. The positivity was defined as inducible Type 1 Brugada pattern in atleast 2 right sided leads. RESULT: Median age was 35(range = 5-65) years. In 16 (55%) patients the Type 1 Brugada pattern was unmasked. There were no episodes of major AV block, atrial or ventricular tachyarrhythmia. Three groups were considered for analysis: Group 1(n = 9) - FCT Positive among patients with non-type 1 Brugada ECG pattern, Group 2(n = 4) - FCT Negative among the patients with non-type 1 Brugada ECG pattern, and Group 3(n = 7) - FCT Positive among patients with no spontaneous Brugada ECG pattern. Binary logistic regression analysis found that family h/o SCD was predictive of FCT positivity in Group 1 (Odd's ratio 21, 95% Confidence interval 1.04 to 698.83, p = 0.004). CONCLUSION: Oral flecainide is useful and safe for unmasking of Type I Brugada pattern. In our study, among the many variables studied, family history of sudden cardiac death was the only predictor of flecainide test positivity among those with non-Type 1 Brugada pattern.

Acute outcome of treating patients admitted with electrical storm in a tertiary care centre.

BACKGROUND: Electrical storm (ES) is a life threatening emergency. There is little data available regarding acute outcome of ES. AIMS: The study aimed to analyze the acute outcome of ES, various treatment modalities used, and the factors associated with mortality. METHODS: This is a retrospective observational study involving patients admitted with ES at our centre between 1/1/2007 and 31/12/2013. RESULTS: 41 patients (mean age 54.61 ± 12.41 years; 86.7% males; mean ejection fraction (EF) 44.51 ± 16.48%) underwent treatment for ES. Hypokalemia (14.63%) and acute coronary syndrome (ACS) (14.63%) were the commonest identifiable triggers. Only 9 (21.95%) patients already had an ICD implanted. Apart from antiarrhythmic drugs (100%), deep sedation (87.8%), mechanical ventilation (24.39%) and neuraxial modulation using left sympathetic cardiac denervation (21.95%) were the common treatment modalities used. Thirty-three (80.49%) patients could be discharged after a mean duration of 14.2 ± 2.31 days. Eight (19.5%) patients died in hospital. The mortality was significantly higher in those with EF < 35% compared to those with a higher EF (8 (42.11% vs 0 (0%), p = 0.03)). There was no significant difference in mortality between those with versus without a structural heart disease (8 (21.1% vs 0 (0%), p = 0.32)). Comparison of mortality an ACS with ES versus ES of other aetiologies (3 (50%) vs 5 (14.29) %, p = 0.076)) showed a trend towards significance. CONCLUSION: With comprehensive treatment, there is reasonable acute survival rate of ES. Hypokalemia and ACS are the commonest triggers of ES. Patients with low EF and ACS have higher mortality.