Publications by authors named "Robert J Myerburg"

151 Publications

Association of SGLT2 inhibitors with arrhythmias and sudden cardiac death in patients with type 2 diabetes or heart failure: A meta-analysis of 34 randomized controlled trials.

Heart Rhythm 2021 Mar 20. Epub 2021 Mar 20.

Division of Cardiology, University of Miami Miller School of Medicine, Miami, Florida. Electronic address:

Background: Sodium-glucose cotransporter 2 inhibitors (SGLT2is) reduce hospitalizations and death from heart failure (HF), but their effect on arrhythmia expression has been poorly investigated.

Objective: The purpose of this study was to evaluate the association of SGLT2i with arrhythmias in patients with type 2 diabetes mellitus (T2DM) or HF.

Methods: We searched PubMed and ClinicalTrials.gov. Two independent investigators identified randomized double-blind trials that compared SGLT2i with placebo or active control for adults with T2DM or HF. Primary outcomes were incident atrial arrhythmias, ventricular arrhythmias (VAs), and sudden cardiac death (SCD).

Results: We included 34 randomized (25 placebo-controlled and 9 active-controlled) trials with 63,166 patients (35,883 SGLT2i vs 27,273 control: mean age 53-67 years; 63% male). Medications included canagliflozin, dapagliflozin, empagliflozin, or ertugliflozin. Except for 1 study of HF, all patients had T2DM. Follow-up ranged from 24 weeks to 5.7 years. The cumulative incidence of events was low: 3.6, 1.4, and 2.5 per 1000 patient-years for atrial arrhythmias, VA and SCD, respectively. SGLT2i therapy was associated with a significant reduction in the risk of incident atrial arrhythmias (odds ratio 0.81; 95% confidence interval 0.69-0.95; P = .008) and the "SCD" component of the SCD outcome (odds ratio 0.72; 95% confidence interval 0.54-0.97; P = .03) compared with control. There was no significant difference in incident VA or the "cardiac arrest" SCD component between groups.

Conclusion: SGLT2i are associated with significantly reduced risks of incident atrial arrhythmias and SCD in patients with T2DM. Prospective trials are warranted to confirm the antiarrhythmic effect of SGLT2i and whether this is a class or drug-specific effect.
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http://dx.doi.org/10.1016/j.hrthm.2021.03.028DOI Listing
March 2021

Non-Atherosclerotic causes of Myocardial Ischemia: With emphasis on spontaneous dissection of coronary arteries.

Trends Cardiovasc Med 2021 Feb 17. Epub 2021 Feb 17.

Division of Cardiology, Professor of Medicine and Physiology, American Heart Association Chair in Cardiovascular Research, University of Miami Miller School of Medicine, Miami, Florida. Electronic address:

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http://dx.doi.org/10.1016/j.tcm.2021.02.003DOI Listing
February 2021

Osteopontin and LDLR Are Upregulated in Hearts of Sudden Cardiac Death Victims With Heart Failure With Preserved Ejection Fraction and Diabetes Mellitus.

Front Cardiovasc Med 2020 30;7:610282. Epub 2020 Nov 30.

Division of Cardiology, Department of Medicine, University of Miami Leonard M. Miller School of Medicine, Miami, FL, United States.

Diabetes mellitus (DM) is associated with increased risk of sudden cardiac death (SCD), particularly in patients with heart failure with preserved ejection fraction (HFpEF). However, there are no known biomarkers in the population with DM and HFpEF to predict SCD risk. This study was designed to test the hypothesis that osteopontin (OPN) and some proteins previously correlated with OPN, low-density lipoprotein receptor (LDLR), dynamin 2 (DNM2), fibronectin-1 (FN1), and 2-oxoglutarate dehydrogenase-like (OGDHL), are potential risk markers for SCD, and may reflect modifiable molecular pathways in patients with DM and HFpEF. Heart tissues were obtained at autopsy from 9 SCD victims with DM and HFpEF and 10 age and gender-matched accidental death control subjects from a Finnish SCD registry and analyzed for the expression of OPN and correlated proteins, including LDLR, DNM2, FN1, and OGDHL by immunohistochemistry. We observed a significant upregulation in the expression of OPN, LDLR, and FN1, and a marked downregulation of DNM2 in heart tissues of SCD victims with DM and HFpEF as compared to control subjects ( < 0.01). The dysregulated protein expression of OPN, LDLR, FN1, and DNM2 in patients with DM and HFpEF who experienced SCD provides novel potential modifiable molecular pathways that may be implicated in the pathogenesis of SCD in these patients. Since secreted OPN and soluble LDLR can be measured in plasma, these results support the value of further prospective studies to assess the predictive value of these plasma biomarkers and to determine whether tuning expression levels of OPN and LDLR alters SCD risk in patients with DM and HFpEF.
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http://dx.doi.org/10.3389/fcvm.2020.610282DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7734052PMC
November 2020

Network meta-analysis of His bundle, biventricular, or right ventricular pacing as a primary strategy for advanced atrioventricular conduction disease with normal or mildly reduced ejection fraction.

J Cardiovasc Electrophysiol 2020 06 20;31(6):1482-1492. Epub 2020 Apr 20.

Division of Cardiology, University of Miami Miller School of Medicine, Miami, Florida.

Introduction: Although right ventricular pacing (RVP) may impair ventricular function, it is commonly used for advanced atrioventricular block (AVB) and normal or mildly reduced ejection fraction (EF). We aimed to compare His bundle pacing (HBP), biventricular pacing (BiVP), and RVP for advanced AVB in patients with normal or mildly reduced EF.

Methods And Results: MEDLINE, Embase, Cochrane CENTRAL, ClinicalTrials.gov, Scopus, and Web of Science were searched. Outcomes were all-cause death, heart failure hospitalizations (HFH), EF, left ventricular volumes, 6-minute walk test, and QRS duration. HBP or BiVP was compared with RVP. Subsequently, network meta-analysis compared the three pacing options. Our protocol was registered in PROSPERO (CRD42018094132). Six studies compared BiVP and RVP (704 vs 614 patients) and four compared HBP and RVP (463 vs 568 patients). Follow-up was 6 months to 5 years. There was significantly lower mortality and HFH with HBP or BiVP as compared with RVP (odds ratio [OR], 0.66, [0.51-0.85], P = .002; OR, 0.61 [0.45-0.82], P < .001, respectively]. HBP or BiVP also showed significant increase in EF and decrease in QRS duration (mean difference [MD], 5.27 [3.86-6.69], P < .001; MD -42.2 [-51.2 to -33.3], P < .001, respectively). In network meta-analysis, HBP and BiVP were associated with significantly improved survival compared to RVP, with surface under the cumulative ranking curve (SUCRA) probability of 79.4%, 69.4%, and 1.2% for HBP, BiVP, and RVP, respectively. For HFH, SUCRA probability was 91.5%, 57.2%, and 1.3%, respectively.

Conclusion: HBP or BiVP were the superior strategies to reduce all-cause death and HFH for advanced AVB with normal or mildly reduced EF, with no significant difference between BiVP and HBP.
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http://dx.doi.org/10.1111/jce.14490DOI Listing
June 2020

Electrocardiographic associations with myocardial fibrosis among sudden cardiac death victims.

Heart 2020 Jul 22;106(13):1001-1006. Epub 2020 Mar 22.

Research Unit of Internal Medicine, Medical Research Center, University of Oulu and University Hospital of Oulu, Oulu, Finland.

Objective: A major challenge in reducing the incidence of sudden cardiac death (SCD) is the identification of patients at risk. Myocardial fibrosis has a substantial association with SCD risk but is difficult to identify among general populations. Our aim was to find electrocardiographic (ECG) markers of myocardial fibrosis among SCD victims.

Methods: Study population was acquired from the Fingesture study, which has gathered data from 5869 consecutive autopsied SCD victims in Northern Finland between 1998 and 2017. The degree of fibrosis was determined in histological samples taken from the heart during autopsy and was categorised into four groups: (1) no fibrosis, (2) scattered mild fibrosis, (3) moderate patchy fibrosis and (4) substantial fibrosis. We were able to collect ECGs from 1100 SCD victims.

Results: The mean age of the study subjects was 66±13 years and 75% were male. QRS duration in ECG correlated with the degree of fibrosis (p<0.001, β=0.153). Prevalence of fragmented QRS complex, pathological Q waves and T wave inversions correlated with increased degree of fibrosis (p<0.001 in each). Depolarisation abnormalities were observed both in ischaemic and non-ischaemic heart disease. Repolarisation abnormalities reached statistical significance only among ischaemic SCD victims. An abnormal ECG was observed in 75.3% of the subjects in group 1, 73.7% in group 2, 88.5% in group 3 and 91.7% in group 4 patients (p<0.001).

Conclusions: Myocardial fibrosis was associated with QRS prolongation, deep Q waves, T wave inversions and QRS fragmentation. The results provide potentially useful non-invasive early recognition of patients with fibrotic cardiomyopathy and risk of SCD.
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http://dx.doi.org/10.1136/heartjnl-2019-316105DOI Listing
July 2020

Genetic determinants of responsiveness to mesenchymal stem cell injections in non-ischemic dilated cardiomyopathy.

EBioMedicine 2019 Oct 21;48:377-385. Epub 2019 Oct 21.

Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, FL, United States; Cardiovascular Division, University of Miami Miller School of Medicine, Miami, FL, United States. Electronic address:

Background: Non-ischemic dilated cardiomyopathy (NIDCM) responds variably to intramyocardial injection of mesenchymal stem cells (MSCs). We hypothesized that NIDCM genotype may influence responsiveness to MSC therapy and performed genotyping on all patients in the POSEIDON-DCM trial.

Methods: POSEIDON-DCM patients (n = 34) underwent genetic sequence analysis and deletion/duplication testing. The results were classified as positive for pathological variants (PV+; n = 8), negative for any variants (V-; n = 6), or as variants of uncertain significance (VUS; n = 20). All outcomes of therapy were analysed for each category of genetic results.

Findings: The 3 groups were indistinguishable at baseline with regard to ejection fraction (EF), demographics, medication use, or functional parameters. V- patients had an increase in EF at 12 months: +13.6% (IQR = +7.8%; +20.5%; p = 0.002), compared with VUS (+6.5%; IQR = +0.9%, +11.1%; p = 0.005) and PV+(-5.9%; IQR = -12.7%, +1.0; p = 0.2; p = 0.01 between groups). Six-minute walk distance improved in V- patients, but not in VUS and PV+. V- patients improved MLHFQ, compared to the other 2 groups, which did not improve over time. EPCCFUs increased by 9.7 ± 1.9 in V- (p = 0.009) compared to VUS and PV+ patients. V- patients had one-year survival (100%) compared with VUS (85%) and PV+ (40%; p = 0.015 log-rank). Similarly, MACE rates were lower in V- (0%) than PV+ (61.9%) or VUS (42.2%; p = 0.021 log-rank).

Interpretation: Our findings support the concept that the genetic profile of NIDCM patients plays a role in responsiveness to MSC therapy, with V- patients more likely to benefit and the converse for PV+. This observation emphasizes the need for further genetic studies, because of important implications for the management of NIDCM syndromes.
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http://dx.doi.org/10.1016/j.ebiom.2019.09.043DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6838383PMC
October 2019

A meta-analysis of arrhythmia endpoints in randomized controlled trials of transendocardial stem cell injections for chronic ischemic heart disease.

J Cardiovasc Electrophysiol 2019 11 3;30(11):2492-2500. Epub 2019 Oct 3.

Division of Cardiology, University of Miami Miller School of Medicine, Miami, Florida.

Introduction: The electrophysiologic impact of cell-based therapy on the injured myocardium remains highly controversial. We aimed to perform a meta-analysis of studies comparing arrhythmia burden following transendocardial stem cell therapy vs placebo in patients with chronic ischemic heart disease (CIHD).

Methods And Results: PubMed, Embase, and Cochrane Central Register of Controlled Trials were searched. No restriction of stem cell type was specified. The outcomes included sustained supraventricular or ventricular arrhythmias (VAs), sudden cardiac death (SCD), and resuscitated sudden cardiac arrest (SCA). Effect sizes were reported as odds ratio (OR) and 95% CI. Poisson regression was used to account for zero-events data. Twelve randomized trials that included 736 patients (384 in the cell therapy group and 352 in the placebo group) were analyzed. Six different cell types were used. Follow-up ranged from 6 to 12 months. There was a significant decrease in risk of SCD in the cell therapy group, (FE OR, 0.19 [0.04, 0.93]; P = .04). In subgroup analysis, there was a significantly lower risk of SCD or resuscitated SCA in the cell therapy group limited to studies that did not use skeletal myoblasts, (FE OR, 0.23 [0.06, 0.83]; P = .03). There was no significant difference in the incidence of sustained VA between groups (FE OR, 0.91 [0.47, 1.77]; P = .8), even after stratifying by cell type. There was no difference in supraventricular arrhythmias between groups.

Conclusion: Nonskeletal myoblast transendocardial cell therapy was associated with a significantly lower risk of SCD or resuscitated SCA compared to control, with no proarrhythmic effects.
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http://dx.doi.org/10.1111/jce.14185DOI Listing
November 2019

Refractory ventricular tachycardia storm associated with severe hypokalemia in Fanconi syndrome.

HeartRhythm Case Rep 2019 Jul 24;5(7):374-378. Epub 2019 Apr 24.

Cardiovascular Division, Miller School of Medicine, University of Miami, Miami, Florida.

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http://dx.doi.org/10.1016/j.hrcr.2019.04.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6630180PMC
July 2019

Association of Silent Myocardial Infarction and Sudden Cardiac Death.

JAMA Cardiol 2019 08;4(8):796-802

Research Unit of Internal Medicine, Medical Research Center Oulu, University of Oulu and Oulu University Hospital, Oulu, Finland.

Importance: Myocardial infarction in the absence of major or unrecognized symptoms are characterized as silent (SMI). The prevalence of SMI among individuals who experience sudden cardiac death (SCD), with or without concomitant electrocardiographic (ECG) changes, has not previously been described in detail from large studies to our knowledge.

Objective: To determine the prevalence of SMI in individuals who experience SCD without a prior diagnosis of coronary artery disease (CAD) and to detect ECG abnormalities associated with SMI-associated SCD.

Design, Setting, And Participants: This case-control study compared autopsy findings, clinical characteristics, and ECG markers associated with SMI in a consecutive cohort of individuals in the Finnish Genetic Study of Arrhythmic Events (Fingesture) study population who were verified to have had SCD. The Fingesture study consists of individuals who had autopsy-verified SCD in Northern Finland between 1998 and 2017. Individuals who had SCD with CAD and evidence of SMI were regarded as having had cases; those who had SCD with CAD without SMI were considered control participants. Analyses of ECG tests were carried out by investigators blinded to the SMI data. Data analysis was completed from October 2018 through November 2018.

Main Outcomes And Measures: Silent MI was defined as a scar detected by macroscopic and microscopic evaluation of myocardium without previously diagnosed CAD. Clinical history was obtained from medical records, previously recorded ECGs, and a standardized questionnaire provided to the next of kin. The hypothesis tested was that SMI would be prevalent in the population who had had SCD with CAD, and it might be detected or suspected from findings on ECGs prior to death in many individuals.

Results: A total of 5869 individuals were included (2459 males [78.8%]; mean [SD] age, 64.9 [12.4] years). The cause of SCD was CAD in 4392 individuals (74.8%), among whom 3122 had no history of previously diagnosed CAD. Two individuals were excluded owing to incomplete autopsy information. An ECG recorded prior to SCD was available in 438 individuals. Silent MI was detected in 1322 individuals (42.4%) who experienced SCD without a clinical history of CAD. The participants with SMI were older than participants without MI scarring (mean [SD] age, 66.9 [11.1] years; 65.5 [11.6] years; P < .001) and were more often men (1102 of 1322 [83.4%] vs 1357 of 1798 [75.5%]; P < .001). Heart weight was higher in participants with SMI (mean [SD] weight, 483 [109] g vs 438 [106] g; P < .001). In participants with SMI, SCD occurred more often during physical activity (241 of 1322 [18.2%] vs 223 of 1798 [12.4%]; P < .001). A prior ECG was abnormal in 125 of the 187 individuals (66.8%) who had SCD after SMI compared with 139 of 251 (55.4%) of those who had SCD without SMI (P = .02).

Conclusions And Relevance: Many individuals who experienced SCD associated with CAD had a previously undetected MI at autopsy. Previous SMI was associated with myocardial hypertrophy and SCD during physical activity. Premortem ECGs in a subset with available data were abnormal in 67% of the individuals who had had a SCD after an SMI.
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http://dx.doi.org/10.1001/jamacardio.2019.2210DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6624824PMC
August 2019

HRS 40th anniversary viewpoints: Reflections on a career in cardiac electrophysiology- Parallel pathways and intersections.

Heart Rhythm 2019 07;16(7):1129-1130

Division of Cardiology, University of Miami Miller School of Medicine, Miami, Florida. Electronic address:

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http://dx.doi.org/10.1016/j.hrthm.2019.04.027DOI Listing
July 2019

Prediabetes and Risk for Cardiac Death Among Patients With Coronary Artery Disease: The ARTEMIS Study.

Diabetes Care 2019 07 10;42(7):1319-1325. Epub 2019 May 10.

Research Unit of Internal Medicine, Medical Research Center Oulu, University of Oulu and Oulu University Hospital, Oulu, Finland.

Objective: To compare cardiac mortality in patients with CAD and prediabetes with that in CAD patients with normal glycemic status and type 2 diabetes.

Research Design And Methods: The Innovation to Reduce Cardiovascular Complications of Diabetes at the Intersection (ARTEMIS) study included patients with CAD after revascularization (79%), optimal medical therapy, or both. Patients had type 2 diabetes ( = 834), impaired glucose tolerance (IGT; = 314), impaired fasting glucose (IFG; = 103), or normal glycemic status ( = 697) as defined on the basis of the results of an oral glucose tolerance test. The primary end point was cardiac death. Major adverse cardiac event (MACE: cardiac death, heart failure, or acute coronary syndrome) and all-cause mortality were secondary end points.

Results: During a mean ± SD follow-up of 6.3 ± 1.6 years, 101 cardiac deaths, 385 MACEs, and 208 deaths occurred. Patients with IGT tended to have 49% lower adjusted risk for cardiac death ( = 0.069), 32% lower adjusted risk for all-cause mortality ( = 0.076), and 36% lower adjusted risk for MACE ( = 0.011) than patients with type 2 diabetes. The patients with IFG had 82% lower adjusted risk for all-cause mortality ( = 0.015) than the patients with type 2 diabetes, whereas risks for cardiac death and MACE did not differ significantly between the two groups. The adjusted risks for cardiac death, MACE, and all-cause mortality among patients with IGT and IFG did not significantly differ from those risks among patients with normal glycemic status.

Conclusions: Cardiac mortality or incidence of MACE in patients with CAD with prediabetes (i.e., IGT or IFG after revascularization, optimal medical therapy, or both) does not differ from those values in patients with normal glycemic status.
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http://dx.doi.org/10.2337/dc18-2549DOI Listing
July 2019

Usefulness of Single Nucleotide Polymorphisms as Predictors of Sudden Cardiac Death.

Am J Cardiol 2019 06 20;123(12):1900-1905. Epub 2019 Mar 20.

Division of Cardiology, Department of Medicine, Miller School of Medicine, University of Miami, Miami, Florida.

The pathophysiology of sudden cardiac death (SCD) remains incompletely understood. Genetic mutations can create a favorable substrate for SCD. Our aim is to evaluate the evidence of single nucleotide polymorphisms (SNPs) as predictors of SCD. We searched the Medline database (2000 to 2017) and selected all case-control or cohort studies that reported associations between SNPs and SCD. Our search terms included "polymorphisms" and "sudden death." We collected the study design, population ethnic background, gene testing strategy, the association between the SNP and SCD, and the cardiovascular comorbidities of the population. Our search yielded 723 studies, of which we included 24 based upon our inclusion criteria. The studies had a total population of 78,165 participants, with a median age of 62.5 years (IQR 56 to 66) and 35% (IQR 13 to 32) were female. Almost all studies were conducted in white patients of European descent and the most commonly used genetic strategy was candidate gene panels. Fifteen of the studies had a case-control design that included SCD patients without known heart disease as the comparison group and the other 9 studies included patients with heart failure and coronary artery disease. The studies evaluated 53 SNPs and the most common genetic loci were SCN5A, RyR2, CASQ2, NOSA1P, and AGTR. SNPs with the 3 strongest statistically significant ORs >1 were: rs6684209 of CASQ2 (odds ratio [OR] 19), rs3814843 of CALM1 (OR 5.5), and rs35594137 of GJA5 (OR 3.6). In Conclusion, many SNPs are associated with SCD, with the strongest associations seen in SNPs of genes related to intracellular calcium handling. These findings were generated primarily using a candidate gene strategy in white patients with European descent.
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http://dx.doi.org/10.1016/j.amjcard.2019.02.058DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7175955PMC
June 2019

Sudden Cardiac Death in Women.

Circulation 2019 02;139(8):1012-1021

From Research Unit of Internal Medicine (M.A.E.H., L.H., J.V., T.K., J.T., J.P., H.H., M.J.J.), Medical Research Center Oulu, University of Oulu and University Hospital of Oulu, Finland.

Background: Despite recent progress in profiling of risk for sudden cardiac death (SCD) and prevention and intervention of cardiac diseases, SCD remains a major cause of death. Among women, the incidence of SCD is significant, but lower than in men, particularly in the premenopausal and early postmenopausal years. Possibly, as a consequence of the difference in population burden, the mechanisms and risk markers of SCD are not as well defined for women. The aim of this study was to determine the autopsy findings and causes of death among women in a large SCD population. Additionally, we sought to classify prior ECG characteristics in male and female subjects with SCD.

Methods: The Fingesture study has systematically collected clinical and autopsy data from subjects with SCD in Northern Finland between 1998 and 2017. The cohort consists of 5869 subjects with SCD. Previously recorded ECGs were available and analyzed in 1101 subjects (18.8% of total population; and in 25.3% of women).

Results: Female subjects with SCD were significantly older than men: 70.1±13.1 years versus 63.5±11.8 years (mean ± standard deviation, P<0.001). The most frequently identified cause of death was ischemic heart disease in both sexes: 71.7% among women versus 75.7% among men, P=0.005. In contrast, women were more likely to have nonischemic cause of SCD than men (28.3% versus 24.3%, P=0.005). The prevalence of primary myocardial fibrosis was higher among women (5.2%, n=64) than in men (2.6%, n=120; P<0.001). Female subjects with SCD were more likely to have normal prior ECG tracings (22.2% versus 15.3% in men, P<0.001). A normal ECG was even more common among nonischemic female subjects with SCD (27.8% versus 16.2% in men, P=0.009). However, ECG markers of left ventricular hypertrophy, with or without repolarization abnormalities, were more common among women (8.2%; 17.9%) than in men (4.9%; 10.6%, P=0.036; P<0.001, respectively).

Conclusions: Women were considerably older at the time of SCD and more commonly had nonischemic causes. Women were also more likely to have a prior normal ECG than men, but an increased marker for SCD risk based on ECG criteria for left ventricular hypertrophy with repolarization abnormalities was more commonly observed in women.
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http://dx.doi.org/10.1161/CIRCULATIONAHA.118.037702DOI Listing
February 2019

Type 2 diabetes and coronary artery disease: Preserved ejection fraction and sudden cardiac death.

Heart Rhythm 2018 10;15(10):1450-1456

Research Unit of Internal Medicine, Medical Research Center Oulu, University of Oulu and Oulu University Hospital, Oulu, Finland.

Background: Previous studies have shown that type 2 diabetes (DM2) is associated with sudden cardiac death (SCD) risk in post-myocardial infarction patients. The treatment of coronary artery disease (CAD) as well as DM2 has changed over time.

Objective: The purpose of this study was to compare the incidence of SCD in DM2 and nondiabetic patients with CAD and preserved ejection fraction (EF) in a prospective observational study (ARTEMIS study).

Methods: In 834 DM2 patients and 1112 nondiabetic patients with CAD enrolled, the EF measured ≥3 months after qualifying was 63% ± 10% in DM2 patients and 65% ± 8% in nondiabetic patients (P < .01). The primary end point was SCD or resuscitation from sudden cardiac arrest (SCA). All-cause mortality, cardiac mortality, non-SCD, hospitalization for heart failure, and acute coronary syndrome were secondary end points.

Results: During a mean follow-up of 6.3 ± 1.6 years, SCDs/SCAs occurred in 50 patients. The prevalence of SCD/SCA was higher in DM2 patients (4.1%) than in nondiabetic patients (1.4%) (adjusted hazard ratio 2.6; 95% confidence interval 1.3-5.3; P < .01). However, the non-SCD component of cardiac mortality was not significantly different between DM2 and nondiabetic patients. In addition, heart failure hospitalizations were more common in DM2 patients (8.4%) than in nondiabetic patients (2.9%) (P < .001). The annual cardiac mortality in nondiabetic patients with CAD was 0.50%, which was lower than the 0.59% reported in the general Finnish population.

Conclusion: DM2 is an independent risk factor for SCD/SCA in CAD patients with preserved EF. Cardiac mortality in nondiabetic CAD patients is slightly lower than that in the general population in the present treatment era.
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http://dx.doi.org/10.1016/j.hrthm.2018.06.017DOI Listing
October 2018

Editorial commentary: Ethnic and racial disparities and differences in sudden cardiac death burden and survival: How do we close the gap?

Trends Cardiovasc Med 2019 02 30;29(2):127-128. Epub 2018 Jul 30.

Department of Medicine, Division of Cardiology, Miller School of Medicine, University of Miami, 1400 NW 12th Ave, Suite 4062, Miami, FL 33136, United States.

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http://dx.doi.org/10.1016/j.tcm.2018.07.011DOI Listing
February 2019

Remembering Dr. Agustin Castellanos-1927-2017.

J Interv Card Electrophysiol 2018 Aug 24;52(3):251-254. Epub 2018 Jun 24.

Division of Cardiology (D-39), University of Miami Miller School of Medicine, P. O. Box 016960, Miami, FL, 33101, USA.

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http://dx.doi.org/10.1007/s10840-018-0399-yDOI Listing
August 2018

Primary Myocardial Fibrosis as an Alternative Phenotype Pathway of Inherited Cardiac Structural Disorders.

Circulation 2018 06;137(25):2716-2726

Research Unit of Internal Medicine, University of Oulu and University Hospital of Oulu, Finland (M.J.J., L.H., K.K., H.V.H.).

Background: Myocardial fibrosis is a common postmortem finding among young individuals with sudden cardiac death. Because there is no known single cause, we tested the hypothesis that some cases of myocardial fibrosis in the absence of identifiable causes (primary myocardial fibrosis [PMF]) are associated with genetic variants.

Methods: Tissue was obtained at autopsy from 4031 consecutive individuals with sudden cardiac death in Northern Finland, among whom PMF was the only structural finding in 145 subjects with sudden cardiac death. We performed targeted next-generation sequencing using a panel of 174 genes associated with myocardial structure and ion channel function when autopsies did not identify a secondary basis for myocardial fibrosis. All variants with an effect on protein and with a minor allele frequency <0.01 were classified as pathogenic or variants of uncertain significance on the basis of American College of Medical Genetics consensus guidelines.

Results: Among the 96 specimens with DNA passing quality control (66%), postmortem genetic tests identified 24 variants of known or uncertain significance in 26 subjects (27%). Ten were pathogenic/likely pathogenic variants in 10 subjects (10%), and 14 were variants of uncertain significance in 11 genes among 16 subjects (17%). Five variants were in genes associated with arrhythmogenic right ventricular cardiomyopathy, 6 in hypertrophic cardiomyopathy-associated genes, and 11 in dilated cardiomyopathy-associated genes; 2 were not associated with these disorders. Four unique variants of uncertain significance cosegregated among multiple unrelated subjects with PMF. No pathogenic/likely pathogenic variants were detected in ion channel-encoding genes.

Conclusions: A large proportion of subjects with PMF at autopsy had variants in genes associated with arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, and hypertrophic cardiomyopathy without autopsy findings of those diseases, suggesting that PMF can be an alternative phenotypic expression of structural disease-associated genetic variants or that risk-associated fibrosis was expressing before the primary disease. These findings have clinical implications for postmortem genetic testing and family risk profiling.
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http://dx.doi.org/10.1161/CIRCULATIONAHA.117.032175DOI Listing
June 2018

Cardiac and Noncardiac Causes of Apparent Sudden Arrhythmic Deaths: Shadows in a Spectrum.

Circulation 2018 06;137(25):2701-2704

Division of Cardiology, University of Miami Miller School of Medicine, FL.

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http://dx.doi.org/10.1161/CIRCULATIONAHA.118.034594DOI Listing
June 2018

The Screening ECG and Cardiac Risks.

JAMA 2018 06;319(22):2277-2279

Division of Cardiology, University of Miami Miller School of Medicine, Miami, Florida.

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http://dx.doi.org/10.1001/jama.2018.6766DOI Listing
June 2018

Health Care Costs After Cardiac Arrest in the United States.

Circ Arrhythm Electrophysiol 2018 04;11(4):e005689

Sinai Hospital of Baltimore, LifeBridge Health Cardiovascular Institute, MD (A.A.D., M.M.). Division of Cardiology, Johns Hopkins University, Baltimore, MD (A.A.D.). Department of Internal Medicine, University of Connecticut Health Center, Farmington (M.S.A.). Cardiovascular Division, University of Miami Miller School of Medicine, FL (S.P., T.J.Z., M.G.C., R.D.M., R.J.M.). University of Michigan Health System, Ann Arbor (M.M.).

Background: This study was designed to estimate the costs of index hospitalizations after cardiac arrest in the United States.

Methods And Results: We used the US Nationwide Inpatient Sample (2003-2012) to identify patients with cardiac arrest. Log transformation of inflation-adjusted cost was determined for care to patient outcomes. Overall, an estimated 1 387 396 patients were hospitalized after cardiac arrest. The mean age of the cohort was 66 years, 45% were women, and the majority were white. Inpatient procedures included coronary angiography (15%), percutaneous coronary intervention (7%), intra-aortic balloon pump (4.4%), therapeutic hypothermia (1.1%), and mechanical circulatory support (0.1%). The rates of therapeutic hypothermia increased from zero in 2003 to 2.7% in 2012 (<0.001). Both hospital charges and inflation-adjusted cost increased linearly over time. In a multivariate analysis, predictors of inflation-adjusted cost included large hospital size, urban teaching hospital, and length of stay. Among comorbidities, atrial fibrillation or fluid and electrolytes imbalance was most associated with cost. Among selected interventions, the cost was significantly increased with automatic implantable cardioverter defibrillators (odds ratio, 1.83; <0.001), intra-aortic balloon pump (odds ratio, 1.50; <0.001), hypothermia (odds ratio, 1.28; <0.001), and extracorporeal membrane oxygenation (odds ratio, 2.38; <0.001).

Conclusions: In the period between 2003 and 2012, postcardiac arrest hospitalizations resulted in a steady rise in associated health care cost, likely related to increased length of stay, medical procedures, and systems of care. Although targeted cost containment for postarrest interventions may reduce the finance burden, there is an increasing need for funding research into prediction and prevention of cardiac arrest, which offers greater societal benefit.
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http://dx.doi.org/10.1161/CIRCEP.117.005689DOI Listing
April 2018

Improvements in Outcomes and Disparities of ST-Segment-Elevation Myocardial Infarction Care: The Miami-Dade County ST-Segment-Elevation Myocardial Infarction Network Project.

Circ Cardiovasc Qual Outcomes 2017 12;10(12)

From the Sinai Hospital of Baltimore, LifeBridge Health Cardiovascular Institute, MD (A.A.D., M.M.); Division of Cardiology, Johns Hopkins University, Baltimore, MD (A.A.D.); Cardiovascular Division (R.J.M., V.C., D.G.R., M.G.C.) and Division of Emergency Medicine (K.S.S.), University of Miami Miller School of Medicine, FL; Wertheim College of Medicine, Miami Cardiac and Vascular Institute, Baptist Health and Florida International University (T.F.); Department of Emergency Medicine, Memorial Healthcare System, Hollywood, FL (F.M.K.); Department of Emergency Medicine, Jackson Memorial Hospital, Miami, FL (M.G.); and University of Michigan Health System, Ann Arbor (M.M.).

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http://dx.doi.org/10.1161/CIRCOUTCOMES.117.004038DOI Listing
December 2017

Sudden Cardiac Death: Interface Between Pathophysiology and Epidemiology.

Card Electrophysiol Clin 2017 12;9(4):515-524

Division of Cardiology, University of Miami Miller School of Medicine, D-39, PO Box 016960, Miami, FL 33101, USA.

The population incidence of sudden cardiac arrest (SCA) and sudden cardiac death have not changed appreciably during the decades of improvement in general outcomes from cardiovascular diseases, but the age, clinical circumstances, and pathophysiologic mechanisms have. The epidemiology and pathophysiology of SCA are linked, in that mechanisms of SCA can be modeled based on substrate and expression characteristics. The goal for the future is to expand pathophysiologic and epidemiologic interactions to achieve strong individual risk prediction, to complement the limits of application of population risk data to individuals.
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http://dx.doi.org/10.1016/j.ccep.2017.07.003DOI Listing
December 2017

2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.

Circulation 2018 09;138(13):e210-e271

Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with industry may apply; see Appendix 1 for detailed information. Section numbers pertain to those in the full-text guideline. †ACC/AHA Representative. ‡HRS Representative. §ACC/AHA Task Force on Performance Measures Liaison/HFSA Representative. ‖ACC/AHA Task Force on Clinical Practice Guidelines Liaison.

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http://dx.doi.org/10.1161/CIR.0000000000000548DOI Listing
September 2018

2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.

Circulation 2018 09;138(13):e272-e391

Writing committee members are required to recuse themselves from voting on sections to which their specific relationships with industry may apply; see Appendix 1 for detailed information. †ACC/AHA Representative. ‡HRS Representative. §ACC/AHA Task Force on Performance Measures Liaison/HFSA Representative. ‖ACC/AHA Task Force on Clinical Practice Guidelines Liaison.

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http://dx.doi.org/10.1161/CIR.0000000000000549DOI Listing
September 2018

Signalling the risk of sudden cardiac death: the ECG and beyond.

Eur Heart J 2017 10;38(40):3026-3028

Division of Cardiology, University of Miami Miller School of Medicine, Miami, FL, USA.

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http://dx.doi.org/10.1093/eurheartj/ehx420DOI Listing
October 2017

Sudden Cardiac Arrest Risk Assessment: Population Science and the Individual Risk Mandate.

JAMA Cardiol 2017 06;2(6):689-694

Division of Cardiology, University of Miami Miller School of Medicine, Miami, Florida.

Importance: High-resolution stratification of risk of sudden cardiac arrest (SCA) in individual patients is a tool that is necessary for achieving effective and efficient application of data generated by population-based research. This concept is at the core of initiatives for merging cost effectiveness with maximized clinical efficiency and individual patient treatment.

Observations: For this review, we analyzed data on sudden cardiac death and SCA available from population studies that included large longitudinal and cross-sectional databases, observational cohort studies, and randomized clinical trials. In the context of population science, we treated clinical trials as small, scientifically rigid population studies that generate outcomes focused on defined segments of the population. Application of probabilistic outcomes from these available sources to individual patients generally and patients at risk for SCA and sudden cardiac death in particular is limited by the diversity of the study population based on inclusion criteria and/or the absence of uniformly large effect sizes. Limited information is available on the requirements for defining small high-risk density subgroups that would lead to identification of individuals at a sufficiently high probability of SCA to have a significant effect on clinical decision making.

Conclusions And Relevance: Synthesis of available population and clinical science data demonstrates the limitations for prediction and prevention of SCA and sudden cardiac death and provides justification for a research mandate for improving risk prediction at the level of individual patients. This leads to suggested approaches to new data generation and required research funding to address this large public health burden.
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http://dx.doi.org/10.1001/jamacardio.2017.0266DOI Listing
June 2017