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AN: CV Complications Leading to SCD - Coggle Diagram
AN: CV Complications Leading to SCD
Mitral Valve Prolapse
Bc ? Increased vagal tone
Oka 1987
Mitral valve motion abnormal Simone 1994
Yahalom 2013
Increased vagal tone
ishizawa 2008
Vagal tone becomes lower the longer the illness. Associated with higher mortality. Nakai 2015
Galetta 2003
prevalences
MVP Oka 1987
Di cola 2014, deaths due to cardiac, SD, CV comp
Marin 2019
Mainly attributable to C events Nakai 2015
Longer duration = higher mortality
SCD general Michaud 2009
AN morbidity - thinks estimates are inflated - provides own morality estimates Keshaviah 2014
Brady and QT prolong are most common cardio abnormalities Giovinazzo 2018
pericardial effusions more common more weightless Docx 2010
cardiac complication in AN Abuzeid 2010
Mitral valve motion abnormality Simone 1994
CV and mortality Yahalom 2013
Orthostatic hypotension Shamim 2003
worldwide cases Sadar 2015
mortality rates underestimated
bradycardia Sadar 2015
Standardised mortality ratios Arcelus 2011
Other
Ipecac Ho 1998
Low plasma zinc causing cardiomyopathy Rosenblum 2020
Multiple bilateral pulmonary thromboembolism Derman 2006
Cardiac tamponade Kircher 2012
AMI
Is rare. Abuzeid 2010
Recommendations
Any AN death to be reported and autopsy performed Dermat 2006
Further study need to find out cause of sudden death in AN Krantz 2020
SCD
Causes ofSCD
Mechanism of AN deaths is unclear
Derman 2006
Mechanism controversial Krantz 2012
Whether long QTc is a feature, whether repo varies with AN severity
Krantz 2020
Sudden deaths supposedly attributed to V tachyarrythmias Farasat 2020
bradyarythmias more common than tacky and possibly a mechanism farasat 2020
Brady and QT prolong degenerate into vent fib or Torsades de pointes which is likely what causes the SCD Giovinazzo 2018
SCD associated with structural remodelling in hypertrophy and HF Tomaselli 2000
Also associated with potassium and Ca++ handling abnormalities Tomaselli 2000
HF
Channelopathies (sodium potassium, calcium) leading to arythmias Ji 2004
Abnormalities in these channels are from mutations in genes encoding channel proteins Ji 2004
Genetic mutations have been identified to be involved in hypertrophy + SCD, but notably cTNT is highly associate with SCD but only mildly with hypertrophy, Marian 1998
SCD channel-patties which disturb depolarisation gradients among other things Martin 2013
Cause in general population linked to inherited arrhythmia, for which there is a candidate gene. Lu 2012
In general population is associated with LQTS and specific gene mutations Vincent 1998
SCD cause in general pop linked to congenital arrhythmic disorders such as LQTS and Brugada syndrome Michaud 2009
SCD gen pop caused by channel-patties sodium and potassium Kocic 2002
Cahnnelopathies in 15-18% of SCD deaths Cann 2017
Risk of death linked to QT prolongation, which could be hypokalaemia or remodelling, Ravaldi 2003
Occurred with refeeding
Abed 2014 alongside other salt deficiencies
J-Lobera 2012
Other risk factors include duration of illness, low plasma albumin
SCD in AN is due to arrhythmia Abuzeid 2010
Low PNS activity increases risk in general pop Algra 1993
CV complication usually the cause of SCD in AN J-Lobera 2012
Causes of deaths and rate varies widely, suffers from misreporting due to poor definitions Neumarker 1997
Significant risk of death associated with AN and CV complications Mont 2003
All Eds have elevated mortality Smink 2012
Endocrine causes
T3 and T4
Metabolic state
Bannai 1988
FT# IGF1 GH, correlation between GH/IGF1 imbalance FT3 and cardiac hypotrophy Carlomagno 2011
link between weightless and low FT3 Marin 2019
QT interval
Elongated
Dawano 2016
Acquired LQTS Tran 2020
Janzen 2019 BUT QTc is normal
Abed 2014
Normal
Largest study. prolongation only with extrinsic factors Krantz 2020
Padfield 2016
Facchini 2006
doesn't correlate to disease severity Krantz 2011
Takotsubo
Elongated QT Dawano 2016
complication of AN and hypoglycaemia Elikowski 2018
Volman 2011
QT dispersion
Greater
Franzoni 2002
Potassium supplementation normalises it
Risk may be linked to low RMR Krantz 2005
marker of arrhythmic risk Krantz 2005
increased QT interval dispersion as a marker of SCD ventricular arrhythmia J-Lobera 2012
Hypokalemia
Autonomic nervous system dysfunction causes Cardio dysfunction
reduced SNS, increased PNS, ishizawa 2008
vasospasm?
Repolarisation dysfunction
Krantz 2011
Padfield 2016
NO conduction abnormalities
Chu 2019
Janzen 2019
Reversibility of CV complications
HR normalisation with weight restoration
Farasat 2020
BP, HR, QT, QTc intervals and QT and QTc dispersion all reversible Ulger 2006
Low R wave amplitude in V6 not reversible
Pericardial effusions Docx 2010
LV mass, LV vol reversible, but wall stress and EF did not change. Sutton 1985
EF improved from 10-15 to 40 Abed 2014
QT int normalised
hypophosphatemia, hypokalemia, hypocalcemia, and hypomagnesemia with refeeding
orthostasis/hypotension = 3wks reseeding. Shamim 2003
Olivares 2005, LVmass, LV ED dimension, CO and QT interval and dispersion allimproved
HR, HRV, CO, LVM, exercise cap, QT int, QT dis p all reversible Mont 2003
hypotrophy
GH resistance, low FT3 best predictors after haemodynamic load and BMI Carlomagno 2011
LVM smaller in AN when controlling for BSA
Chu 2019
Low volumes. no myocardial fibrosis
Low haemodynamic load leads to hypotrophy Romano 2003 LVM
Simone 1994, associated with less filling and systolic dysfunction
LVM less controlled for BSA and BP, NO change in LV shape
Sutton 1985 mass and vol lower but architecture normal
Hypotensive effect of fasting -> decrease in after load -> reduction in mass, Sutton 1985
Shape was changed in such a way that wall stress remained in normal range
Galetta 2003
Olivares 2005
93% decreased LVM 70% decreased wall thickness Mont 2003
EF
Right and Left vent. <60%, smaller than controls. Chu 2019
Romano 2003
Abed 2014
Bradycardia / HR
Janzen 2019 HR lower
Romano 2003 Lower HR SV CO EF but Resistance higher
HRV
Greater in AN
Galetta 2003
Mont 2003
Abed 2014
Tachycardia
Possibly life threatening condition at play. Mori 2004
Associated with unfavourable outcome Tokumara 2012
Yahalom 2013
HF and hypotension too
orthostatic hypotension
Shamim 2003
Sadar 2015
Mont 2003
particularly norctural bradycardia
Pericardial effusions
Docx 2010
Risk of ED genetics, environment, personality Culbert 2015
