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__NOTOC__
[[Congestive heart failure digoxin|Digoxin]]
{{COVID-19 associated Heart Failure}}
'''For patient information, click [[Xyz (patient information)|here]]'''


{{CMG}}; {{AE}} {{Mitra}}
;Shown below is an image that summarizes the steps in the chronic management of patients with heart failure.


{{SK}}  
{| class="wikitable
!ACE-I !! Starting dose!! Target dose
|-
| Captopril||align="center"|6.25 mg t.i.d.||align="center"|50 mg t.i.d.
|-
| Enalapril||align="center"|2.5 mg b.i.d.||align="center"|10-20 mg b.i.d.
|-
| Lisinopril||align="center"|> 2.5-5 mg daily||align="center"| 20-35 mg daily
|-
| Ramipril||align="center"|> 2.5 mg b.i.d.||align="center"| 5 mg b.i.d.
|-
| Trandolapril||align="center"|> 0.5 mg daily||align="center"| 4 mg daily
|}


==[[Heart Failure overview|Overview]]==


*Patients with chronic heart failure (HF) may be at higher risk of developing severe COVID-19 infection due to the advanced age and the presence of multiple comorbidities.
*Both de novo acute heart failure and acute decompensation of chronic heart failure can occur in patients with COVID-19.


==[[Heart Failure historical perspective|Historical Perspective]]==


==[[Heart Failure classification|Classification]]==


==[[Heart Failure pathophysiology|Pathophysiology]]==
: '''[[Congestive heart failure acute pharmacotherapy|Acute Pharmacotherapy]]'''
: '''[[Congestive heart failure with preserved EF pharmacotherapy|Chronic Pharmacotherapy in HFpEF]]


*Presumed pathophysiologic mechanisms for the development of new or worsening heart failure in patients with COVID-19 include:<ref name="pmid32219357">{{Cite pmid|32219357}}</ref> <ref name="pmid32360242">{{Cite pmid|32360242}}</ref> <ref name="pmid32186331">{{Cite pmid|32186331}}</ref> <ref name="pmid30625066">{{Cite pmid|30625066}}</ref> <ref name="pmid32140732">{{Cite pmid|32140732}}</ref>   
**Acute exacerbation of chronic heart failure
**Acute myocardial injury (which in turn can be caused by several mechanisms)
**Stress cardiomyopathy (i.e., Takotsubo cardiomyopathy)
**Impaired myocardial relaxation resulting in diastolic dysfunction [i.e., Heart failure with preserved ejection fraction (HFpEF)]
**Right-sided heart failure, secondary to pulmonary hypertension caused by hypoxia and acute respiratory distress syndrome (ARDS)


==[[Heart Failure causes|Causes]]==
:'''[[Congestive heart failure treatment of underlying causes|Treatment of underlying causes]] | [[Congestive heart failure treatment of associated conditions|Associated conditions]]'''


==[[Heart Failure differential diagnosis|Differentiating Heart Failure from other Diseases]]==


==[[Heart Failure epidemiology and demographics|Epidemiology and Demographics]]==


==[[Heart Failure risk factors|Risk Factors]]==


==[[Heart Failure screening|Screening]]==
: [[Congestive heart failure biventricular pacing or cardiac resynchronization therapy|Biventricular Pacing or Cardiac Resynchronization Therapy (CRT)]] | [[Congestive heart failure implantation of intracardiac defibrillator|Implantation of Intracardiac Defibrillator]] | [[Congestive heart failure ultrafiltration|Ultrafiltration]] | [[Congestive heart failure left ventricular assist devices|Left Ventricular Assist Devices (LVADs)]] | [[Congestive heart failure cardiac transplantation|Cardiac Transplantation]] | [[Congestive heart failure cardiac surgery|Cardiac Surgery]]


==[[Heart Failure natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
: '''[[Chronic Pharmacotherapy|Chronic Pharmacotherapy in HFrEF]]:'''
:'''[[Congestive heart failure drugs to avoid|Drugs to Avoid]] | [[Congestive heart failure drug interactions|Drug Interactions]]'''


  | |  |  | [[Congestive heart failure calcium channel blockers|Ca Channel Blockers]] | [[Congestive heart failure vasodilators|Nitrates]] | [[Congestive heart failure vasodilators|Hydralazine]] | [[Congestive heart failure positive inotropics|Positive Inotropics]] | [[Congestive heart failure anticoagulants|Anticoagulants]] |  | [[Congestive heart failure antiarrhythmic Drugs|Antiarrhythmic Drugs]] | [[Congestive heart failure other pharmacotherapies#Nutritional Supplements|Nutritional Supplements]] | [[Congestive heart failure other pharmacotherapies#Hormonal Therapies|Hormonal Therapies]] | [[Congestive heart failure lifestyle modification|Lifestyle modification]]
: '''[[Device therapy for heart failure with reduced ejection fraction]]''': [[Implantable cardioverter-defibrillator]] | [[Cardiac resynchronization therapy]] | [[ Devices under evaluation]]


==Diagnosis==
[[Xyz diagnostic study of choice|Diagnostic study of choice]] | [[Xyz history and symptoms|History and Symptoms]] | [[Xyz physical examination|Physical Examination]] | [[Xyz laboratory findings|Laboratory Findings]] | [[Xyz electrocardiogram|Electrocardiogram]] | [[Xyz x ray|X-Ray Findings]] | [[Xyz echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Xyz CT scan|CT-Scan Findings]] | [[Xyz MRI|MRI Findings]] | [[Xyz other imaging findings|Other Imaging Findings]] | [[Xyz other diagnostic studies|Other Diagnostic Studies]]


====Symptoms and signs====
*Dyspnea: may overlap with dyspnea due to concomitant respiratory involvement and ARDS due to COVID-19 infection
*Lower limb edema
*Orthopnea
*Paroxysmal nocturnal dyspnea
*Confusion and altered mentation
*Cool extremities
*Cyanosis
*Syncope
*Fatigue
*Hemoptysis
*Palpitations
*Weakness
*Wheezing or cardiac asthma
*Distended jugular veins
*Crackles on auscultation


| [[Xyz physical examination|Physical Examination]] | [[Heart Failure laboratory findings|Laboratory Findings]] | [[Heart Failure electrocardiogram|Electrocardiogram]]
*Efficacy: Low
====Electrocardiography (ECG)====
**Sinus rhythm is maintained in <20% of patients
*There is no specific electrocardiographic sign for acute heart failure in COVID-19 patients.
**Symtoms are reduced in >=20%.
*The ECG may help in identifying preexisting cardiac abnormalities and precipitating factors such as ischemia, myocarditis, and arrhythmias.
*These ECG findings may include:
**Low QRS Voltage
**Left ventricular hypertrophy
**Left atrial enlargement
**Left bundle branch block
**Poor R progression
**ST-T changes
| [[Xyz x ray|X-Ray Findings]]
====Chest x-ray (CXR)====
*The Chest x-ray may show evidence of:
**Cardiomegaly
**Pulmonary congestion
**Increased pulmonary vascular markings.
*Signs of pulmonary edema may be obscured by underlying respiratory involvement and ARDS due to COVID-19.  
| [[Heart Failure echocardiography and ultrasound|Echocardiography and Ultrasound]]


====Echocardiography====
=====Adverse effects=====
*A complete standard transthoracic (TTE) has not been recommended in COVID-19 patients considering the limited personal protective equipment (PPE) and the risk of exposure of additional health care personnel.<ref name="pmid32391912">{{Cite pmid|32391912}}</ref>
*Bradycardia
*To deal with limited resources (both personal protective equipment and personnel) and reducing the exposure time of personnel, a focused TTE to find gross abnormalities in cardiac structure/function seems satisfactory.
*Hypotension
*In addition, bedside options, which may be performed by the trained personnel who might already be in the room with these patients, might also be considered. These include:
*Edema
**Cardiac point-of-care ultrasound (POCUS)
**Focused cardiac ultrasound study (FoCUS)
**Critical care echocardiography
*Cardiac ultrasound can help in assessing the following parameters:
**Left ventricular systolic function (ejection fraction) to distinguish systolic dysfunction with a reduced ejection fraction (<40%) from diastolic dysfunction with a preserved ejection fraction.
**Left ventricular diastolic function
**Left ventricular structural abnormalities, including LV size and LV wall thickness
**Left atrial size
**Right ventricular size and function
**Detection and quantification of valvular abnormalities
**Measurement of systolic pulmonary artery pressure
**Detection and quantification of pericardial effusion
**Detection of regional wall motion abnormalities/reduced strain that would suggest an underlying ischemia
| [[Heart Failure CT scan|CT-Scan Findings]] | [[Heart Failure MRI|MRI Findings]] | [[Heart Failure other imaging findings|Other Imaging Findings]] | [[Heart Failure other diagnostic studies|Other Diagnostic Studies]]
====Cardiac biomarkers====
*Cardiac Troponins:
**Elevated cardiac troponin levels suggest the presence of myocardial cell injury or death.
**Cardiac troponin levels may increase in patients with chronic or acute decompensated HF.<ref name="pmid20863950">{{Cite pmid|20863950}}</ref>
*Natriuretic Peptides:
**Natriuretic peptides (BNP/NT-proBNP) are released from the heart in response to increased myocardial stress and are quantitative markers of increased intracardiac filling pressure.<ref name="pmid28062628">{{Cite pmid|28062628}}</ref>
**Elevated BNP and NT-proBNP are of both diagnostic and prognostic significance in patients with heart failure.
**Increased BNP or NT-proBNP levels have been demonstrated in COVID-19 patients.
**Increased NT-proBNP level was associated with worse clinical outcomes in patients with severe COVID-19.<ref name="pmid32293449">{{Cite pmid|32293449}}</ref> <ref name="pmid32232979">{{Cite pmid|32232979}}</ref>
**However, increased natriuretic peptide levels are frequently seen among patients with severe inflammatory or respiratory diseases.<ref name="pmid18298480">{{Cite pmid|18298480}}</ref> <ref name="pmid16442916">{{Cite pmid|16442916}}</ref> <ref name="pmid28322314">{{Cite pmid|28322314}}</ref> <ref name="pmid23837838">{{Cite pmid|23837838}}</ref> <ref name="pmid21478812">{{Cite pmid|21478812}}</ref>
**Therefore, routine measurement of BNP/NT-proBNP has not been recommended in COVID-19 patients, unless there is a high suspicion of HF based on clinical grounds.


==Treatment==
=====Contraindications=====
[[Heart Failure medical therapy|Medical Therapy]]
*Bradycardia
*Hypotension
*Heart failure with depressed ejection fraction


*Patients with chronic heart failure are recommended to continue their previous guideline-directed medical therapy, including beta-blockers, ACEI or ARB, and mineralocorticoid receptor antagonists. <ref name="pmid31129923">{{Cite pmid|31129923}}</ref>
*Acute heart failure in the setting of COVID-19 is generally treated similarly to acute heart failure in other settings. These may include:
**Fluid restriction
**Diuretic therapy
**Vasopressors and/or inotropes
**Ventricular assisted devices and extracorporeal membrane oxygenation (ECMO)
*Beta-blockers should not be initiated during the acute stage due to their negative inotropic effects.<ref name="pmid24251454">{{Cite pmid|24251454}}</ref>
*Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) should be used with caution in patients with acute heart failure due to their effect on fluid and sodium retention.<ref name="pmid12656651">{{Cite pmid|12656651}}</ref>


| [[Heart Failure interventions|Interventions]] | [[Heart Failure surgery|Surgery]] | [[Heart Failure primary prevention|Primary Prevention]] | [[Heart Failure secondary prevention|Secondary Prevention]] | [[Heart Failure cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Xyz future or investigational therapies|Future or Investigational Therapies]]
=====Contraindications=====
*[[Bradycardia]]
*[[Hypotension]]


==Case Studies==
=====Precautions during treatment=====
[[Xyz case study one|Case #1]]
*Monitor for [[bradycardia]]


[[Category: (name of the system)]]
 
<ref>{{cite book | last = LastName | first = FirstName | title = Diagnostic and statistical manual of mental disorders : DSM-5 | publisher = American Psychiatric Association,American Psychiatric Association | location = Arlington, VA Washington, D.C | year = 2013 | isbn = 978-0-89042-554-1 }}</ref>
 
<ref> ....</ref>
 
==Books by Psychologists and Psychiatrists==
* Beck, A. T., Rush, A. J., Shaw, B. F., Emery, G. (1987). ''Cognitive therapy of depression''. New York: Guilford.
* Burns, David D. (1999). ''Feeling Good : The New Mood Therapy''. Avon.
* Griffin, J., Tyrrell, I. (2004) ''How to lift Depression – Fast''.  HG Publishing. ISBN 1-899398-41-4
* [[Edith Jacobson|Jacobson, Edith]]: "Depression; Comparative Studies of Normal, Neurotic, and Psychotic Conditions", International Universities Press, 1976, ISBN 0-8236-1195-7
* Klein, D. F., & Wender, P. H. (1993). ''Understanding depression: A complete guide to its diagnosis and treatment''. New York: Oxford University Press.
* Kramer, Peter D. (2005). ''Against Depression''. New York: Viking Adult.
* Plesman, J. (1986). [http://books.google.com/books?lr=&ie=ISO-8859-1&q=foreword+Jurriaan+Plesman&btnG=Search Getting off the Hook], Sydney Australia. A self-help book available on the internet.
* Rowe, Dorothy (2003). ''Depression: The way out of your prison''. London: Brunner-Routledge.
* Sarbadhikari, S. N. (ed.) (2005) ''Depression and Dementia: Progress in Brain Research, Clinical Applications and Future Trends''. Hauppauge, [[Nova Science Publishers]]. ISBN 1-59454-114-0.
* Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). ''Comprehensive guide to interpersonal psychotherapy''. New York: Basic Books.
* Bieling, Peter J. & Anthony, Martin M. (2003) ''Ending The Depression Cycle.'' New Harbinger Publications. ISBN 1572243333
* For books on male depression, see [[Terrence Real]]
 
===Historical Account===
*[[David Healy (psychiatrist)|Healy, David]]. (1999). ''The Antidepressant Era'', Paperback Edition, Harvard University Press. ISBN 0-674-03958-0
[[af:Kliniese depressie]]
[[ar:الاكتئاب عند الإنسان]]
[[bs:Klinička depresija]]
[[ca:Depressió]]
[[cs:Deprese (psychologie)]]
[[da:Depression]]
[[de:Depression]]
[[et:Depressioon]]
[[el:Κλινική κατάθλιψη]]
[[es:Depresión]]
[[eo:Deprimo]]
[[fr:Dépression (médecine)]]
[[ko:우울증]]
[[hr:Klinička depresija]]
[[id:Depresi]]
[[it:Depressione (malattia)]]
[[he:דיכאון]]
[[ku:Klînîk depresyon]]
[[la:Depressio (psychiatria)]]
[[lt:Depresija]]
[[hu:Depresszió]]
[[ms:Kemurungan]]
[[nl:Klinische depressie]]
[[nds-nl:Depressie (psychologie)]]
[[ja:うつ病]]
[[no:Depresjon (sykdom)]]
[[nn:Depresjon]]
[[oc:Depression]]
[[uz:Klinik depressiya]]
[[pl:Depresja (choroba)]]
[[pt:Depressão nervosa]]
[[ro:Depresie (boală)]]
[[ru:Большая депрессия (психиатрия)]]
[[simple:Depression (illness)]]
[[sk:Depresia (psychológia)]]
[[sr:Klinička depresija]]
[[fi:Masennus]]
[[sv:Depression]]
[[vi:Trầm cảm]]
[[tr:Klinik depresyon]]
[[uk:Депресія (медицина)]]
[[yi:קלינישע דעפרעסיע]]
[[zh:憂鬱症]]
 
{{WH}}
{{WS}}
 
[[Category:Disease]]
[[Category:Psychiatry]]
[[Category:Medical emergencies]]
 
==Medical Therapy==
[[Antidepressant]] drugs include [[selective serotonin reuptake inhibitor]]s, such as [[escitalopram oxalate]] (Lexapro), [[citalopram]] (Celexa), [[fluoxetine]] (Prozac), [[paroxetine]] (Paxil), and [[sertraline]] (Zoloft), are the primary medications considered for patients, having fewer side effects than the older [[monoamine oxidase inhibitor]]s (MAOIs). 
 
The effect size is very small for moderate depression but increased with severity reaching the [[NICE]] criteria for 'clinical significance' for very severe depression.<ref>{{cite web |url=http://medicine.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pmed.0050045 |title=Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration |accessdate=2008-02-26 |author=Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT |authorlink= |coauthors= |date=February 2008 |format=htm |work= |publisher=PLoS Medicine |pages= |language= |archiveurl= |archivedate= |quote=}}</ref> This result is consistent with the earlier clinical studies where only patients with severe depression benefited from the treatment with a tricyclic antidepressant [[imipramine]] or from psychotherapy more than from the placebo treatment.<ref name="pmid2684085">{{cite journal |author=Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR, Docherty JP |title=National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments |journal=Arch. Gen. Psychiatry |volume=46 |issue=11 |pages=971–82; discussion 983 |year=1989 |pmid=2684085 |doi=}}</ref><ref name="pmid7593878">{{cite journal |author=Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D |title=Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program |journal=J Consult Clin Psychol |volume=63 |issue=5 |pages=841–7 |year=1995 |pmid=7593878 |doi=}}</ref><ref name="pmid1853989">{{cite journal |author=Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, Watkins JT, Imber SD, Leber WR, Moyer J |title=Patient predictors of response to psychotherapy and pharmacotherapy: findings in the NIMH Treatment of Depression Collaborative Research Program |journal=Am J Psychiatry |volume=148 |issue=8 |pages=997–1008 |year=1991 |pmid=1853989 |doi=}}</ref>  According to the STAR*D [[randomized controlled tria]]l, about 50% of patients with major depression have a response and about 30% of have remission of symptoms with usage of [[citalopram]].<ref name="pmid16390886">{{cite journal| author=Trivedi MH, Rush AJ, Wisniewski SR, Nierenberg AA, Warden D, Ritz L et al.| title=Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. | journal=Am J Psychiatry | year= 2006 | volume= 163 | issue= 1 | pages= 28-40 | pmid=16390886 | doi=10.1176/appi.ajp.163.1.28 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16390886  }} </ref>
 
[[Bupropion]] (Wellbutrin, Zyban), an atypical [[antidepressant]] that acts as a [[norepinephrine reuptake inhibitor|norepinephrine]] and [[dopamine reuptake inhibitor]], is also considered to be effective in the treatment of depression,<ref>{{cite journal | author = Fava M, Rush AJ, Thase ME, Clayton A, Stahl SM, Pradko JF, Johnston JA. | title = 15 years of clinical experience with bupropion HCl: from bupropion to bupropion SR to bupropion XL | journal = Prim Care Companion J Clin Psychiatry| volume = 7|issue = 3|pages = 106–113| year = 2005 |pmid=16027765 }}</ref> without sexual dysfunction or sexual side effects<ref> For the review, see: {{cite journal | author = Clayton AH| title = Antidepressant-Associated Sexual Dysfunction: A Potentially Avoidable Therapeutic Challenge | journal =  Primary Psychiatry| volume = 10| issue=1 |pages = 55–61 | year = 2003}}</ref> and without weight gain. Bupropion has also been shown to be more effective than [[SSRI]]s at improving symptoms such as [[hypersomnia]] and [[fatigue (medical)|fatigue]] in depressed patients.<ref>{{cite journal | author = Baldwin DS, Papakostas GI| title = Symptoms of Fatigue and Sleepiness in Major Depressive Disorder | journal =  J Clin Psychiatry| volume = 67 (suppl 6)| pages = 9–15 | year = 2006 |pmid=16848671}}</ref>
 
Measurement-based care, which guides mediation based on serial measurement of psychometric testing, improves outcomes according to randomized controlled trials<ref name="pmid16390886">{{cite journal| author=Trivedi MH, Rush AJ, Wisniewski SR, Nierenberg AA, Warden D, Ritz L et al.| title=Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. | journal=Am J Psychiatry | year= 2006 | volume= 163 | issue= 1 | pages= 28-40 | pmid=16390886 | doi=10.1176/appi.ajp.163.1.28 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16390886  }} </ref><ref name="pmid22807244">{{cite journal| author=Yeung AS, Jing Y, Brenneman SK, Chang TE, Baer L, Hebden T et al.| title=Clinical Outcomes in Measurement-based Treatment (Comet): a trial of depression monitoring and feedback to primary care physicians. | journal=Depress Anxiety | year= 2012 | volume= 29 | issue= 10 | pages= 865-73 | pmid=22807244 | doi=10.1002/da.21983 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22807244  }} </ref>.
 
====Predictors of a response to treatment====
=====Severity of depression=====
The effectiveness is antidepressants may<ref name="pmid20051569">{{cite journal| author=Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD,  Shelton RC et al.| title=Antidepressant drug effects and depression  severity: a patient-level meta-analysis. | journal=JAMA | year= 2010 |  volume= 303 | issue= 1 | pages= 47-53 | pmid=20051569 |  doi=10.1001/jama.2009.1943 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20051569  }} </ref> or may not<ref name="pmid31303567">{{cite journal| author=Hieronymus F, Lisinski A, Nilsson S, Eriksson E| title=Influence of baseline severity on the effects of SSRIs in depression: an item-based, patient-level post-hoc analysis. | journal=Lancet Psychiatry | year= 2019 | volume=  | issue=  | pages=  | pmid=31303567 | doi=10.1016/S2215-0366(19)30216-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31303567  }} </ref><ref name="pmid22393205">{{cite journal|  author=Gibbons RD, Hur K, Brown CH, Davis JM, Mann JJ| title=Benefits  From Antidepressants: Synthesis of 6-Week Patient-Level Outcomes From  Double-blind Placebo-Controlled Randomized Trials of Fluoxetine and  Venlafaxine. | journal=Arch Gen Psychiatry | year= 2012 | volume=  |  issue=  | pages=  | pmid=22393205 |  doi=10.1001/archgenpsychiatry.2011.2044 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22393205  }} </ref>  depend on the severity of a patient's depression. This relationship may  be due to the declining effect of placebo among more severely depressed  patients.
 
{| class="wikitable
|+ The effectiveness of antidepressants depending on severity of depression<ref name="pmid20051569">{{cite journal|  author=Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD,  Shelton RC et al.| title=Antidepressant drug effects and depression  severity: a patient-level meta-analysis. | journal=JAMA | year= 2010 |  volume= 303 | issue= 1 | pages= 47-53 | pmid=20051569 |  doi=10.1001/jama.2009.1943 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20051569  }} </ref>
!American Psychiatric Association<br/>classification of severity<ref name="isbn1-58562-218-4">{{cite book |author=First, Michael B. |title=Handbook of Psychiatric Measures, Second Edition |publisher=American Psychiatric Publishing, Inc |location= |year=2007 |pages= |isbn=1-58562-218-4 |oclc= |doi= |accessdate=}}</ref>!! [http://healthnet.umassmed.edu/mhealth/HAMD.pdf Hamilton Depression Rating Scale]<br/>(HDRS)!![[Number needed to treat]]<ref name="pmid20051569"/>!!Clinical significance<br/>(NICE)<ref>National Institute for Clinical Excellence. [http://guidance.nice.org.uk/CG90 Depression: Management of Depression in Primary and Secondary Care]. London, England: National Institute for Clinical Excellence; 2009.</ref>
|-
| Mild to moderate||align="center"|< 19||align="center"|16||align="center"|No
|-
| Severe||align="center"|19 - 22||align="center"|11||align="center"|No
|-
| Very severe||align="center"|> 22||align="center"| &nbsp;4||align="center"|Yes
|}
 
=====Genetic variations=====
Variations in the GRIK4 ([[glutamate]] receptor, ionotropic, kainate 4 protein) and HTR2A ([[serotonin|5-hydroxytryptamine]] receptor) genes predict response to citalopram.<ref name="pmid17671280">{{cite journal| author=Paddock S, Laje G, Charney D, Rush AJ, Wilson AF, Sorant AJ et al.| title=Association of GRIK4 with outcome of antidepressant treatment in the STAR*D cohort. | journal=Am J Psychiatry | year= 2007 | volume= 164 | issue= 8 | pages= 1181-8 | pmid=17671280 | doi=10.1176/appi.ajp.2007.06111790 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17671280  }} </ref>
 
====Treatment failure====
{| class="wikitable" align="right"
|+ Treatment after monotherapy failure<br/>(VAST-D Study)<ref name="pmid28697253">{{cite journal| author=Mohamed S, Johnson GR, Chen P, Hicks PB, Davis LL, Yoon J et al.| title=Effect of Antidepressant Switching vs Augmentation on Remission Among Patients With Major Depressive Disorder Unresponsive to Antidepressant Treatment: The VAST-D Randomized Clinical Trial. | journal=JAMA | year= 2017 | volume= 318 | issue= 2 | pages= 132-145 | pmid=28697253 | doi=10.1001/jama.2017.8036 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28697253  }} </ref>
! colspan="2"|Intervention!!colspan="2"|Outcome
|-
! Medication!! Mode final dose!!Remission %!! Quit 2˚ [[Drug toxicity|ADR]]s (%)
|-
| colspan="4"| Switch medications
|-
| [[Bupropion]] SR||align="right"|200 mg twice daily||align="center"|22.3%||style="background-color:coral;text-align:center"|10%
|-
| colspan="4"| Augment medications
|-
| [[Aripiprazole]]||align="right"|10 mg|| style="background-color:lightgreen;text-align:center"|29% || style="text-align:center"|5%
|-
| [[Bupropion]] SR||align="right"|300 mg daily ||style="text-align:center"|27%||align="center"|7%
|}
 
After starting medications, treatment should be switched if there is no response within one month.<ref name="ngc24158 >American Psychiatric Association (APA). [http://www.guideline.gov/content.aspx?id=24158 Practice guideline for the treatment of patients with major depressive disorder]. 3rd ed. Arlington (VA): American Psychiatric Association (APA); 2010 Oct. 152 p. [1170 references]</ref>
 
When treated with monotherapy for depression, approximately 30% of patients have remission of symptoms while 50% have a response to medications.<ref name="pmid16390886">{{cite journal |author=Trivedi MH, Rush AJ, Wisniewski SR, ''et al'' |title=Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice |journal=The American journal of psychiatry |volume=163 |issue=1 |pages=28–40 |year=2006 |pmid=16390886 |doi=10.1176/appi.ajp.163.1.28}}</ref>
 
For patients with inadequate response, [[randomized controlled trial]]s provide guidance.<ref name="pmid28697253">{{cite journal| author=Mohamed S, Johnson GR, Chen P, Hicks PB, Davis LL, Yoon J et al.| title=Effect of Antidepressant Switching vs Augmentation on Remission Among Patients With Major Depressive Disorder Unresponsive to Antidepressant Treatment: The VAST-D Randomized Clinical Trial. | journal=JAMA | year= 2017 | volume= 318 | issue= 2 | pages= 132-145 | pmid=28697253 | doi=10.1001/jama.2017.8036 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28697253  }} </ref><ref name="pmid16554526">{{cite journal |author=Trivedi MH, Fava M, Wisniewski SR, ''et al'' |title=Medication augmentation after the failure of SSRIs for depression |journal=N. Engl. J. Med. |volume=354 |issue=12 |pages=1243–52 |year=2006 |pmid=16554526 |doi=10.1056/NEJMoa052964}}</ref>
 
* The original VAST-D trial, that did not include [[aripiprazole]], confirms that augmenting with bupropion is the most effective of options other than augmentation with [[aripiprazole]]. In this trial, either adding sustained-release [[bupropion]] ("bupropion was 200 mg per day during weeks 1 and 2, increasing to 300 mg per day by week 4 and to 400 mg per day (the final dose) during week 6") or [[buspirone]] (up to 60 mg per day) for augmentation as a second drug can cause remission in approximately 30% of patients ([[bupropion]] may be more effective than [[buspirone]])<ref name="pmid16554526"/>, while switching medications can achieve remission in about 25% of patients<ref name="pmid16554525">{{cite journal |author=Rush AJ, Trivedi MH, Wisniewski SR, ''et al'' |title=Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression |journal=N. Engl. J. Med. |volume=354 |issue=12 |pages=1231–42 |year=2006 |pmid=16554525 |doi=10.1056/NEJMoa052963}}</ref>. Alternatively, "extended-release venlafaxine, the starting daily dose of 37.5 mg for 7 days was increased to 75 mg from day 8 to 14, to 150 mg from day 15 to 27, to 225 mg from day 28 to 41, to 300 mg from day 42 to 62, and to 375 mg from day 63 onward."<ref name="pmid16554525"/>
* The PReDICT trial found that among patients who initially were treated with either an SSRI or CBT, remission was increased when the opposite treatment (CBT or SSRI) was added to non-remitters<ref name="pmid30764648">{{cite journal| author=Dunlop BW, LoParo D, Kinkead B, Mletzko-Crowe T, Cole SP, Nemeroff CB et al.| title=Benefits of Sequentially Adding Cognitive-Behavioral Therapy or Antidepressant Medication for Adults With Nonremitting Depression. | journal=Am J Psychiatry | year= 2019 | volume=  | issue=  | pages= appiajp201818091075 | pmid=30764648 | doi=10.1176/appi.ajp.2018.18091075 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30764648  }} </ref>.
* The newer VAST-D trial found that augmentation with [[aripiprazole]] is effective.<ref name="pmid28697253"/> The dose of aripiprazole  was 2 mg of with titration to 5, 10, or 15 mg daily as guided by measurement-based care using the PHQ-9.<ref name="pmid28697253"/> ''However'', aripiprazole led to more [[adverse drug reaction]]s including somnolence, akathisia, and weight gain. The second most effective was augmentation with [[buproprion]] starting at 150 mg sustained release to 300 mg or 400 mg daily as guided by measurement-based care using the PHQ-9.
 
* More recently, [[mirtazapine]], was found not to add to SSRIs<ref name="pmid30381374">{{cite journal| author=Kessler DS, MacNeill SJ, Tallon D, Lewis G, Peters TJ, Hollingworth W et al.| title=Mirtazapine added to SSRIs or SNRIs for treatment resistant depression in primary care: phase III randomised placebo controlled trial (MIR). | journal=BMJ | year= 2018 | volume= 363 | issue=  | pages= k4218 | pmid=30381374 | doi=10.1136/bmj.k4218 | pmc=6207929 | url=https://www.ncbi.nlm.n

Latest revision as of 13:58, 19 September 2021

Digoxin

Shown below is an image that summarizes the steps in the chronic management of patients with heart failure.
ACE-I Starting dose Target dose
Captopril 6.25 mg t.i.d. 50 mg t.i.d.
Enalapril 2.5 mg b.i.d. 10-20 mg b.i.d.
Lisinopril > 2.5-5 mg daily 20-35 mg daily
Ramipril > 2.5 mg b.i.d. 5 mg b.i.d.
Trandolapril > 0.5 mg daily 4 mg daily



Acute Pharmacotherapy
Chronic Pharmacotherapy in HFpEF


Treatment of underlying causes | Associated conditions



Biventricular Pacing or Cardiac Resynchronization Therapy (CRT) | Implantation of Intracardiac Defibrillator | Ultrafiltration | Left Ventricular Assist Devices (LVADs) | Cardiac Transplantation | Cardiac Surgery
Chronic Pharmacotherapy in HFrEF:
Drugs to Avoid | Drug Interactions
 | |  |  | Ca Channel Blockers | Nitrates | Hydralazine | Positive Inotropics | Anticoagulants |  | Antiarrhythmic Drugs | Nutritional Supplements | Hormonal Therapies | Lifestyle modification
Device therapy for heart failure with reduced ejection fraction: Implantable cardioverter-defibrillator | Cardiac resynchronization therapy | Devices under evaluation


  • Efficacy: Low
    • Sinus rhythm is maintained in <20% of patients
    • Symtoms are reduced in >=20%.
Adverse effects
  • Bradycardia
  • Hypotension
  • Edema
Contraindications
  • Bradycardia
  • Hypotension
  • Heart failure with depressed ejection fraction


Contraindications
Precautions during treatment


[1]

[2]

Books by Psychologists and Psychiatrists

  • Beck, A. T., Rush, A. J., Shaw, B. F., Emery, G. (1987). Cognitive therapy of depression. New York: Guilford.
  • Burns, David D. (1999). Feeling Good : The New Mood Therapy. Avon.
  • Griffin, J., Tyrrell, I. (2004) How to lift Depression – Fast. HG Publishing. ISBN 1-899398-41-4
  • Jacobson, Edith: "Depression; Comparative Studies of Normal, Neurotic, and Psychotic Conditions", International Universities Press, 1976, ISBN 0-8236-1195-7
  • Klein, D. F., & Wender, P. H. (1993). Understanding depression: A complete guide to its diagnosis and treatment. New York: Oxford University Press.
  • Kramer, Peter D. (2005). Against Depression. New York: Viking Adult.
  • Plesman, J. (1986). Getting off the Hook, Sydney Australia. A self-help book available on the internet.
  • Rowe, Dorothy (2003). Depression: The way out of your prison. London: Brunner-Routledge.
  • Sarbadhikari, S. N. (ed.) (2005) Depression and Dementia: Progress in Brain Research, Clinical Applications and Future Trends. Hauppauge, Nova Science Publishers. ISBN 1-59454-114-0.
  • Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). Comprehensive guide to interpersonal psychotherapy. New York: Basic Books.
  • Bieling, Peter J. & Anthony, Martin M. (2003) Ending The Depression Cycle. New Harbinger Publications. ISBN 1572243333
  • For books on male depression, see Terrence Real

Historical Account

  • Healy, David. (1999). The Antidepressant Era, Paperback Edition, Harvard University Press. ISBN 0-674-03958-0

af:Kliniese depressie ar:الاكتئاب عند الإنسان bs:Klinička depresija ca:Depressió cs:Deprese (psychologie) da:Depression de:Depression et:Depressioon el:Κλινική κατάθλιψη eo:Deprimo ko:우울증 hr:Klinička depresija id:Depresi it:Depressione (malattia) he:דיכאון ku:Klînîk depresyon la:Depressio (psychiatria) lt:Depresija hu:Depresszió ms:Kemurungan nl:Klinische depressie nds-nl:Depressie (psychologie) no:Depresjon (sykdom) nn:Depresjon oc:Depression uz:Klinik depressiya simple:Depression (illness) sk:Depresia (psychológia) sr:Klinička depresija fi:Masennus sv:Depression uk:Депресія (медицина) yi:קלינישע דעפרעסיע

Template:WH Template:WS

Medical Therapy

Antidepressant drugs include selective serotonin reuptake inhibitors, such as escitalopram oxalate (Lexapro), citalopram (Celexa), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft), are the primary medications considered for patients, having fewer side effects than the older monoamine oxidase inhibitors (MAOIs).

The effect size is very small for moderate depression but increased with severity reaching the NICE criteria for 'clinical significance' for very severe depression.[3] This result is consistent with the earlier clinical studies where only patients with severe depression benefited from the treatment with a tricyclic antidepressant imipramine or from psychotherapy more than from the placebo treatment.[4][5][6] According to the STAR*D randomized controlled trial, about 50% of patients with major depression have a response and about 30% of have remission of symptoms with usage of citalopram.[7]

Bupropion (Wellbutrin, Zyban), an atypical antidepressant that acts as a norepinephrine and dopamine reuptake inhibitor, is also considered to be effective in the treatment of depression,[8] without sexual dysfunction or sexual side effects[9] and without weight gain. Bupropion has also been shown to be more effective than SSRIs at improving symptoms such as hypersomnia and fatigue in depressed patients.[10]

Measurement-based care, which guides mediation based on serial measurement of psychometric testing, improves outcomes according to randomized controlled trials[7][11].

Predictors of a response to treatment

Severity of depression

The effectiveness is antidepressants may[12] or may not[13][14] depend on the severity of a patient's depression. This relationship may be due to the declining effect of placebo among more severely depressed patients.

The effectiveness of antidepressants depending on severity of depression[12]
American Psychiatric Association
classification of severity[15]		 Hamilton Depression Rating Scale
(HDRS)		 Number needed to treat[12] Clinical significance
(NICE)[16]
Mild to moderate < 19 16 No
Severe 19 - 22 11 No
Very severe > 22  4 Yes
Genetic variations

Variations in the GRIK4 (glutamate receptor, ionotropic, kainate 4 protein) and HTR2A (5-hydroxytryptamine receptor) genes predict response to citalopram.[17]

Treatment failure

Treatment after monotherapy failure
(VAST-D Study)[18]
Intervention Outcome
Medication Mode final dose Remission % Quit 2˚ ADRs (%)
Switch medications
Bupropion SR 200 mg twice daily 22.3% 10%
Augment medications
Aripiprazole 10 mg 29% 5%
Bupropion SR 300 mg daily 27% 7%

After starting medications, treatment should be switched if there is no response within one month.[19]

When treated with monotherapy for depression, approximately 30% of patients have remission of symptoms while 50% have a response to medications.[7]

For patients with inadequate response, randomized controlled trials provide guidance.[18][20]

  • The original VAST-D trial, that did not include aripiprazole, confirms that augmenting with bupropion is the most effective of options other than augmentation with aripiprazole. In this trial, either adding sustained-release bupropion ("bupropion was 200 mg per day during weeks 1 and 2, increasing to 300 mg per day by week 4 and to 400 mg per day (the final dose) during week 6") or buspirone (up to 60 mg per day) for augmentation as a second drug can cause remission in approximately 30% of patients (bupropion may be more effective than buspirone)[20], while switching medications can achieve remission in about 25% of patients[21]. Alternatively, "extended-release venlafaxine, the starting daily dose of 37.5 mg for 7 days was increased to 75 mg from day 8 to 14, to 150 mg from day 15 to 27, to 225 mg from day 28 to 41, to 300 mg from day 42 to 62, and to 375 mg from day 63 onward."[21]
  • The PReDICT trial found that among patients who initially were treated with either an SSRI or CBT, remission was increased when the opposite treatment (CBT or SSRI) was added to non-remitters[22].
  • The newer VAST-D trial found that augmentation with aripiprazole is effective.[18] The dose of aripiprazole was 2 mg of with titration to 5, 10, or 15 mg daily as guided by measurement-based care using the PHQ-9.[18] However, aripiprazole led to more adverse drug reactions including somnolence, akathisia, and weight gain. The second most effective was augmentation with buproprion starting at 150 mg sustained release to 300 mg or 400 mg daily as guided by measurement-based care using the PHQ-9.
  • More recently, mirtazapine, was found not to add to SSRIs<ref name="pmid30381374">{{cite journal| author=Kessler DS, MacNeill SJ, Tallon D, Lewis G, Peters TJ, Hollingworth W et al.| title=Mirtazapine added to SSRIs or SNRIs for treatment resistant depression in primary care: phase III randomised placebo controlled trial (MIR). | journal=BMJ | year= 2018 | volume= 363 | issue= | pages= k4218 | pmid=30381374 | doi=10.1136/bmj.k4218 | pmc=6207929 | url=https://www.ncbi.nlm.n
  1. ↑ LastName, FirstName (2013). Diagnostic and statistical manual of mental disorders : DSM-5. Arlington, VA Washington, D.C: American Psychiatric Association,American Psychiatric Association. ISBN 978-0-89042-554-1.
  2. ↑ ....
  3. ↑ Kirsch I, Deacon BJ, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT (February 2008). "Initial Severity and Antidepressant Benefits: A Meta-Analysis of Data Submitted to the Food and Drug Administration" (htm). PLoS Medicine. Retrieved 2008-02-26.
  4. ↑ Elkin I, Shea MT, Watkins JT, Imber SD, Sotsky SM, Collins JF, Glass DR, Pilkonis PA, Leber WR, Docherty JP (1989). "National Institute of Mental Health Treatment of Depression Collaborative Research Program. General effectiveness of treatments". Arch. Gen. Psychiatry. 46 (11): 971–82, discussion 983. PMID 2684085.
  5. ↑ Elkin I, Gibbons RD, Shea MT, Sotsky SM, Watkins JT, Pilkonis PA, Hedeker D (1995). "Initial severity and differential treatment outcome in the National Institute of Mental Health Treatment of Depression Collaborative Research Program". J Consult Clin Psychol. 63 (5): 841–7. PMID 7593878.
  6. ↑ Sotsky SM, Glass DR, Shea MT, Pilkonis PA, Collins JF, Elkin I, Watkins JT, Imber SD, Leber WR, Moyer J (1991). "Patient predictors of response to psychotherapy and pharmacotherapy: findings in the NIMH Treatment of Depression Collaborative Research Program". Am J Psychiatry. 148 (8): 997–1008. PMID 1853989.
  7. ↑ 7.0 7.1 7.2 Trivedi MH, Rush AJ, Wisniewski SR, Nierenberg AA, Warden D, Ritz L; et al. (2006). "Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice". Am J Psychiatry. 163 (1): 28–40. doi:10.1176/appi.ajp.163.1.28. PMID 16390886.
  8. ↑ Fava M, Rush AJ, Thase ME, Clayton A, Stahl SM, Pradko JF, Johnston JA. (2005). "15 years of clinical experience with bupropion HCl: from bupropion to bupropion SR to bupropion XL". Prim Care Companion J Clin Psychiatry. 7 (3): 106–113. PMID 16027765.
  9. ↑ For the review, see: Clayton AH (2003). "Antidepressant-Associated Sexual Dysfunction: A Potentially Avoidable Therapeutic Challenge". Primary Psychiatry. 10 (1): 55–61.
  10. ↑ Baldwin DS, Papakostas GI (2006). "Symptoms of Fatigue and Sleepiness in Major Depressive Disorder". J Clin Psychiatry. 67 (suppl 6): 9–15. PMID 16848671.
  11. ↑ Yeung AS, Jing Y, Brenneman SK, Chang TE, Baer L, Hebden T; et al. (2012). "Clinical Outcomes in Measurement-based Treatment (Comet): a trial of depression monitoring and feedback to primary care physicians". Depress Anxiety. 29 (10): 865–73. doi:10.1002/da.21983. PMID 22807244.
  12. ↑ 12.0 12.1 12.2 Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC; et al. (2010). "Antidepressant drug effects and depression severity: a patient-level meta-analysis". JAMA. 303 (1): 47–53. doi:10.1001/jama.2009.1943. PMID 20051569.
  13. ↑ Hieronymus F, Lisinski A, Nilsson S, Eriksson E (2019). "Influence of baseline severity on the effects of SSRIs in depression: an item-based, patient-level post-hoc analysis". Lancet Psychiatry. doi:10.1016/S2215-0366(19)30216-0. PMID 31303567.
  14. ↑ Gibbons RD, Hur K, Brown CH, Davis JM, Mann JJ (2012). "Benefits From Antidepressants: Synthesis of 6-Week Patient-Level Outcomes From Double-blind Placebo-Controlled Randomized Trials of Fluoxetine and Venlafaxine". Arch Gen Psychiatry. doi:10.1001/archgenpsychiatry.2011.2044. PMID 22393205.
  15. ↑ First, Michael B. (2007). Handbook of Psychiatric Measures, Second Edition. American Psychiatric Publishing, Inc. ISBN 1-58562-218-4.
  16. ↑ National Institute for Clinical Excellence. Depression: Management of Depression in Primary and Secondary Care. London, England: National Institute for Clinical Excellence; 2009.
  17. ↑ Paddock S, Laje G, Charney D, Rush AJ, Wilson AF, Sorant AJ; et al. (2007). "Association of GRIK4 with outcome of antidepressant treatment in the STAR*D cohort". Am J Psychiatry. 164 (8): 1181–8. doi:10.1176/appi.ajp.2007.06111790. PMID 17671280.
  18. ↑ 18.0 18.1 18.2 18.3 Mohamed S, Johnson GR, Chen P, Hicks PB, Davis LL, Yoon J; et al. (2017). "Effect of Antidepressant Switching vs Augmentation on Remission Among Patients With Major Depressive Disorder Unresponsive to Antidepressant Treatment: The VAST-D Randomized Clinical Trial". JAMA. 318 (2): 132–145. doi:10.1001/jama.2017.8036. PMID 28697253.
  19. ↑ American Psychiatric Association (APA). Practice guideline for the treatment of patients with major depressive disorder. 3rd ed. Arlington (VA): American Psychiatric Association (APA); 2010 Oct. 152 p. [1170 references]
  20. ↑ 20.0 20.1 Trivedi MH, Fava M, Wisniewski SR; et al. (2006). "Medication augmentation after the failure of SSRIs for depression". N. Engl. J. Med. 354 (12): 1243–52. doi:10.1056/NEJMoa052964. PMID 16554526.
  21. ↑ 21.0 21.1 Rush AJ, Trivedi MH, Wisniewski SR; et al. (2006). "Bupropion-SR, sertraline, or venlafaxine-XR after failure of SSRIs for depression". N. Engl. J. Med. 354 (12): 1231–42. doi:10.1056/NEJMoa052963. PMID 16554525.
  22. ↑ Dunlop BW, LoParo D, Kinkead B, Mletzko-Crowe T, Cole SP, Nemeroff CB; et al. (2019). "Benefits of Sequentially Adding Cognitive-Behavioral Therapy or Antidepressant Medication for Adults With Nonremitting Depression". Am J Psychiatry: appiajp201818091075. doi:10.1176/appi.ajp.2018.18091075. PMID 30764648.
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