Author
Mark E. Anderson
Other affiliations: Vanderbilt University, University of Colorado Denver, Vanderbilt University Medical Center ...read more
Bio: Mark E. Anderson is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Ca2+/calmodulin-dependent protein kinase & Medicine. The author has an hindex of 72, co-authored 252 publications receiving 17510 citations. Previous affiliations of Mark E. Anderson include Vanderbilt University & University of Colorado Denver.
Papers published on a yearly basis
Papers
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TL;DR: In Fig. 4c of this Article, the y axis values were wrongly given as 0, 20, 40, 60 and 80 in the middle and the lower panels.
Abstract: Nature Communications 6: Article number: 6081 (2015); Published 20 January 2015; Updated 3 June 2015. In Fig. 4c of this Article, the y axis values were wrongly given as 0, 20, 40, 60 and 80 in the middle and the lower panels. The correct values should read 0, 10, 20, 30 and 40 for the middle and 0,1, 2, 3 and 4 for the lower panels.
1,029 citations
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TL;DR: It is shown that oxidation of paired regulatory domain methionine residues sustains CaMKII activity in the absence of Ca2+/CaM and highlights the critical importance of oxidation-dependent CaMK II activation to AngII and ischemic myocardial apoptosis.
989 citations
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TL;DR: CaMKII inhibition substantially prevented maladaptive remodeling from excessive βAR stimulation and myocardial infarction, and induced balanced changes in excitation-contraction coupling that preserved baseline and βAR-stimulated physiological increases in cardiac function.
Abstract: Beta-adrenergic receptor (betaAR) stimulation increases cytosolic Ca(2+) to physiologically augment cardiac contraction, whereas excessive betaAR activation causes adverse cardiac remodeling, including myocardial hypertrophy, dilation and dysfunction, in individuals with myocardial infarction. The Ca(2+)-calmodulin-dependent protein kinase II (CaMKII) is a recently identified downstream element of the betaAR-initiated signaling cascade that is linked to pathological myocardial remodeling and to regulation of key proteins involved in cardiac excitation-contraction coupling. We developed a genetic mouse model of cardiac CaMKII inhibition to test the role of CaMKII in betaAR signaling in vivo. Here we show CaMKII inhibition substantially prevented maladaptive remodeling from excessive betaAR stimulation and myocardial infarction, and induced balanced changes in excitation-contraction coupling that preserved baseline and betaAR-stimulated physiological increases in cardiac function. These findings mark CaMKII as a determinant of clinically important heart disease phenotypes, and suggest CaMKII inhibition can be a highly selective approach for targeting adverse myocardial remodeling linked to betaAR signaling.
563 citations
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New York University1, Cedars-Sinai Medical Center2, University of Virginia3, Harvard University4, University of Iowa5, Northwestern University6, Rhode Island Hospital7, Indiana University8, Tufts University9, National Institutes of Health10, Washington University in St. Louis11, Johns Hopkins University12, University of Wisconsin-Madison13, Vanderbilt University14, Case Western Reserve University15, University of Washington16
TL;DR: In this paper, the authors proposed a method for predicting and preventing sudden cardiac death (SCD) in the general population, which can manifest as ventricular tachycardia, ventricular fibrillation (VF), pulseless electric activity (PEA), or asystole.
Abstract: Despite the significant decline in coronary artery disease (CAD) mortality in the second half of the 20th century,1 sudden cardiac death (SCD) continues to claim 250 000 to 300 000 US lives annually.2 In North America and Europe the annual incidence of SCD ranges between 50 to 100 per 100 000 in the general population.3,–,6 Because of the absence of emergency medical response systems in most world regions, worldwide estimates are currently not available.7 However, even in the presence of advanced first responder systems for resuscitation of out-of-hospital cardiac arrest, the overall survival rate in a recent North American analysis was 4.6%.8 SCD can manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), pulseless electric activity (PEA), or asystole. In a significant proportion of patients, SCD can present without warning or a recognized triggering mechanism. The mean age of those affected is in the mid 60s, and at least 40% of patients will suffer SCD before the age of 65.4 Consequently, enhancement of methodologies for prediction and prevention of SCD acquires a unique and critical importance for management of this significant public health issue.
Prediction and prevention of SCD is an area of active investigation, but considerable challenges persist that limit the efficacy and cost-effectiveness of available methodologies.7,9,10 It was recognized early on that optimization of SCD risk stratification will require integration of multi-disciplinary efforts at the bench and bedside, with studies in the general population.11,–,13 This integration has yet to be effectively accomplished. There is also increasing awareness that more investigation needs to be directed toward identification of early predictors of SCD.14 Significant advancements have occurred for risk prediction in the inherited channelopathies15,–,17 and …
540 citations
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TL;DR: In this paper, the y axis values were wrongly given as 0, 20, 40, 60 and 80 in the middle and the lower panels, respectively, in Fig. 4c of this article.
Abstract: Nature Communications 6: Article number: 6081 (2015); Published 20 January 2015; Updated 3 June 2015. In Fig. 4c of this Article, the y axis values were wrongly given as 0, 20, 40, 60 and 80 in the middle and the lower panels. The correct values should read 0, 10, 20, 30 and 40 for the middle and 0,1, 2, 3 and 4 for the lower panels.
436 citations
Cited by
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TL;DR: The manipulation of fluids in channels with dimensions of tens of micrometres — microfluidics — has emerged as a distinct new field that has the potential to influence subject areas from chemical synthesis and biological analysis to optics and information technology.
Abstract: The manipulation of fluids in channels with dimensions of tens of micrometres--microfluidics--has emerged as a distinct new field. Microfluidics has the potential to influence subject areas from chemical synthesis and biological analysis to optics and information technology. But the field is still at an early stage of development. Even as the basic science and technological demonstrations develop, other problems must be addressed: choosing and focusing on initial applications, and developing strategies to complete the cycle of development, including commercialization. The solutions to these problems will require imagination and ingenuity.
8,260 citations
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TL;DR: 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation are published.
Abstract: 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC)
6,599 citations
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TL;DR: Mozaffarian, Dariush, Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Judd, Suzanne E; Kissela, Brett M; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Matchar, David B
Abstract: Author(s): Mozaffarian, Dariush; Benjamin, Emelia J; Go, Alan S; Arnett, Donna K; Blaha, Michael J; Cushman, Mary; de Ferranti, Sarah; Despres, Jean-Pierre; Fullerton, Heather J; Howard, Virginia J; Huffman, Mark D; Judd, Suzanne E; Kissela, Brett M; Lackland, Daniel T; Lichtman, Judith H; Lisabeth, Lynda D; Liu, Simin; Mackey, Rachel H; Matchar, David B; McGuire, Darren K; Mohler, Emile R; Moy, Claudia S; Muntner, Paul; Mussolino, Michael E; Nasir, Khurram; Neumar, Robert W; Nichol, Graham; Palaniappan, Latha; Pandey, Dilip K; Reeves, Mathew J; Rodriguez, Carlos J; Sorlie, Paul D; Stein, Joel; Towfighi, Amytis; Turan, Tanya N; Virani, Salim S; Willey, Joshua Z; Woo, Daniel; Yeh, Robert W; Turner, Melanie B; American Heart Association Statistics Committee and Stroke Statistics Subcommittee
5,076 citations
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TL;DR: The objective of this study was to establish a baseline level of confidence that the once-in-a-lifetime implantation trial—Reduce Inappropriate Therapy protocol can be trusted to provide safe and effective treatment for cardiac arrhythmia and stroke-like episodes.
Abstract: 2D
: two-dimensional
99mTc-DPD
: 99mTechnetium-3,3-diphosphono- 1,2-propanodi-carboxylic acid
ACE
: angiotensin-converting enzyme
AF
: atrial fibrillation
AL
: amyloid light chain
AR
: aortic regurgitation
ARB
: angiotensin receptor blocker
ATTR
: amyloidosis-transthyretin type
AV
: atrioventricular
BiVAD
: biventricular assist device
BNP
: brain natriuretic peptide
BPM
: Beats per minute
CCS
: Canadian Cardiovascular Society
CFC
: cardiofacialcutaneous
CHA2DS2-VASc
: Congestive Heart failure, hypertension, Age ≥75 (doubled), Diabetes, Stroke (doubled), Vascular disease, Age 65–74, and Sex (female)
CMR
: cardiac magnetic resonance
CRT
: cardiac resynchronization therapy
CRT-D
: cardiac resynchronization therapy-defibrillator
CRT-P
: Cardiac resynchronization therapy with a pacemaker
CT
: computed tomography
DC
: direct current
DNA
: deoxyribonucleic acid
E/A
: ratio of mitral peak velocity of early filling (E) to mitral peak velocity of late filling (A)
E/e’
: ratio of early transmitral flow velocity (E) to early mitral annulus velocity (e’)
EACTS
: European Association for Cardio-Thoracic Surgery
ECG
: electrocardiogram
EF
: ejection fraction
EPS
: electrophysiological study
ESC
: European Society of Cardiology
FDA
: (US) Food and Drug Administration
FHL1
: four and a half LIM domains 1
HAS-BLED
: hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile INR, elderly (>65 years), drugs/alcohol concomitantly
HCM
: hypertrophic cardiomyopathy
hs-cTnT
: high sensitivity cardiac troponin T
HTS
: high throughput sequencing
ICD
: implantable cardioverter defibrillator
ILR
: implantable loop recorder
INR
: international normalized ratio
IUD
: intrauterine device
LA
: left atrium
LAMP-2
: lysosome-associated membrane protein 2
LBBB
: left bundle branch block
LEOPARD
: Lentigines, ECG abnormalities, Ocular hypertelorism, Pulmonary stenosis, Abnormal genitalia, Retardation of growth, and sensory-neural Deafness
LGE
: late gadolinium enhancement
LV
: left ventricular
LVAD
: left ventricular assist device
LVH
: left ventricular hypertrophy
LVOTO
: left ventricular outlow tract obstruction
MADIT-RIT
: Multicenter Automatic Defibrillator Implantation Trial—Reduce Inappropriate Therapy
MAPK
: mitogen activated protein kinase
MELAS
: mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes
MERFF
: myoclonic epilepsy with ragged red fibres
MRA
: mineralocorticoid receptor antagonist
MYBPC3
: myosin-binding protein C, cardiac-type
MYH7
: myosin-7 (s-myosin heavy chain)
MYL3
: myosin light chain 3
NOAC
: new oral anticoagulants
NSVT
: non-sustained ventricular tachycardia
NT-proBNP
: N-terminal pro brain natriuretic peptide
NYHA
: New York Heart Association
OAC
: oral anticoagulants
o.d.
: omni die (every day)
PC-CMR
: phase contrast cardiac magnetic resonance
PDE5
: phosphodiesterase type 5
PET
: positron emission tomography
PRKAG2
: gamma-2 sub-unit of the adenosine monophosphate-activated protein kinase
RAAS
: renin angiotensin aldosterone system
RV
: right ventricular
SAM
: systolic anterior motion
SCD
: sudden cardiac death
SAA
: septal alcohol ablation
S-ICD™
: Subcutaneous lead implantable cardioverter defibrillator
SPECT
: single photon emission computed tomography
SSFP
: steady-state free precession
SVT
: supraventricular tachycardia
TOE
: transoesophageal echocardiography
TNNI3
: troponin I, cardiac muscle
TNNT2
: troponin T, cardiac muscle
TPM1
: tropomyosin alpha-1 chain
TTE
: transthoracic echocardiography
TTR
: transthyretin
VF
: ventricular fibrillation
VKA
: vitamin K antagonist
VT
: ventricular tachycardia
WHO
: World Health Organization
Guidelines summarize and evaluate all available evidence at the time of the writing process, on a particular issue with the aim of assisting health professionals in selecting the best management strategies for an individual patient, with a given condition, taking into account the impact on outcome, as well as the risk-benefit-ratio of particular diagnostic or therapeutic means. Guidelines and recommendations should help the health professionals to make decisions in their daily practice. However, the final decisions concerning an individual patient must be made by the responsible health professional(s) in consultation with the patient and caregiver as appropriate.
A great number of Guidelines have been issued in recent years by the European Society of Cardiology (ESC) as well as by other societies and organisations. Because of the impact on clinical practice, quality criteria for the development of guidelines have been established in order to make all decisions transparent to the user. The recommendations for formulating and issuing ESC Guidelines can be found on the ESC website (http://www.escardio.org/guidelines-surveys/esc-guidelines/about/Pages/rules-writing.aspx). ESC Guidelines represent the official position of the ESC on a given topic and are regularly updated.
Members of this Task Force were selected by the ESC to represent professionals involved with the medical care of patients with this pathology. Selected experts in the field undertook a comprehensive review of the published evidence for management (including diagnosis, treatment, prevention and rehabilitation) of a given condition according to ESC Committee for Practice Guidelines (CPG) policy. A critical evaluation of diagnostic and therapeutic procedures was performed including assessment of the risk-benefit-ratio. Estimates of expected health outcomes for larger populations were included, where data exist. The level of evidence and the strength of recommendation of particular management options were weighed and graded according to predefined scales, as outlined in Tables 1 and 2 .
The experts of …
3,276 citations
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TL;DR: The pathways that regulate ROS homeostasis are crucial for mitigating the toxicity of ROS and provide strong evidence about specificity in ROS signalling.
Abstract: Reactive oxygen species (ROS) have been shown to be toxic but also function as signalling molecules. This biological paradox underlies mechanisms that are important for the integrity and fitness of living organisms and their ageing. The pathways that regulate ROS homeostasis are crucial for mitigating the toxicity of ROS and provide strong evidence about specificity in ROS signalling. By taking advantage of the chemistry of ROS, highly specific mechanisms have evolved that form the basis of oxidant scavenging and ROS signalling systems.
2,941 citations