wikidoc - Recent changes [en]

Congestive heart failure Management of Acute heart failure

2026-04-18T10:39:34Z

Transitional care plan: components (Class 1 recommendation):[2]

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	\|MedCond =Congestive heart failure\|Mannitol}}		\|MedCond =Congestive heart failure\|Mannitol}}

			=== '''Transitional care plan:''' ===

			* '''Structure of early post-discharge follow-up''':
			* It has two distinct events:<ref name=":3" />
			*# '''Follow-up phone call within 2-3 days of discharge'''
			*# '''Clinic visit within 7-14 days of hospital discharge'''
			* The first post-discharge appointment provides the opportunity to reassess clinical status, provide additional patient education, review medications and adjust doses, and address issues that might lead to readmission or worsening HF.

			==== '''Transitional care plan components''' (Class 1 recommendation):<ref name=":0" /> ====

			* Addressing any precipitating causes of worsening HF identified in the hospital

			* Adjusting diuretics based on volume status (including weight) and electrolytes
			* Coordination of safety laboratory checks (e.g., electrolytes after initiation or intensification of GDMT)
			* '''Plans for GDMT optimization''', including:
			** Plans for resuming medications held in the hospital
			** Plans for initiating new medications
			** '''Plans for titration of GDMT to goal doses as tolerated'''
			* Reinforcing HF education and assessing compliance with medical therapy and lifestyle modifications
			* Addressing high-risk characteristics (comorbid conditions, limitations in psychosocial support, impaired health literacy)
			* Referral to cardiac rehabilitation where appropriate
			* Referral to palliative care specialists in selected patients

	==References==		==References==

User:Nehal Eid

2026-04-18T10:30:11Z

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	'''Wikidoc contributions:'''		'''Wikidoc contributions:'''

			[[Intravenous drug use (recreational)]]

	[[Juvenile idiopathic arthritis]]		[[Juvenile idiopathic arthritis]]

	[[~~Sudden cardiac death~~]]		[[Hypertension and Blood Pressure Control in Diabetics]]

	[[~~Cosibelimab-ipdl~~]]		[[Lipid Management in Diabetics]]

	[[~~Olezarsen~~]]		[[Coronary heart disease in Diabetics]]

	[[~~Intravenous drug use (recreational)~~]]		[[Congestive heart failure Management of Acute heart failure]]

	[[~~Hypertension and Blood Pressure Control in Diabetics~~]]		[[Sudden cardiac death]]

	[[~~Lipid Management in Diabetics~~]]		[[Cosibelimab-ipdl]]

	[[~~Coronary heart disease in Diabetics~~]]		[[Olezarsen]]

Congestive heart failure Management of Acute heart failure

2026-04-18T10:28:06Z

Show changes

Advances in catheter based physical treatments

2026-04-16T16:09:32Z

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 __NOTOC__
-{{CMG}}
+{{CMG}} {{AE}} {{ACM}}
 ==Overview==
@@ Line 11: / Line 11: @@
 * developing ways of adequately binding the drugs to the stainless surface of the [[stent]] struts (the coating must stay bound despite marked handling and stent deformation stresses) and
 * developing coating controlled release mechanisms that release the drug slowly over about 30 days.
 ==References==

Rheumatoid arthritis overview

2026-04-16T12:40:15Z

Medical Therapy

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 ==Medical Therapy==
 The mainstay of treatment of [[rheumatoid arthritis]] is pharmacotherapy. Early diagnosis of [[rheumatoid arthritis]] is helpful in treatment. Choice of treatment depends on various factors such as stage of [[disease]], comorbid conditions, stage of therapy and presence of severe prognostic signs. There are two types of therapies- non-pharmacological therapy and pharmacological therapy. There are different drug regimen depending upon the stage of the disease. In active stage, combined therapy include disease-modifying antirheumatic drugs ([[DMARDs]]) are used along with the [[anti-inflammatory drugs]]. Therapy for resistant disease and flares is the addition of oral [[glucocorticoids]]. In case of the flare, add another [[DMARDs]] with [[methotrexate]] or replace with another [[DMARDs]].
 ==Surgical Therapy==

Acute lymphoblastic leukemia medical therapy

2026-04-16T12:02:57Z

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	{{Acute lymphoblastic leukemia}}		{{Acute lymphoblastic leukemia}}

	{{CMG}} {{shyam}} {{AE}} {{RT}} {{CLG}} {{ACM}}		{{CMG}} {{shyam}} {{AE}} {{RT}} {{CLG}} {{ACM}} {{MSD}}

	==Overview==		==Overview==

Coronary heart disease overview

2026-04-16T12:01:21Z

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	__NOTOC__		__NOTOC__
	{{Coronary heart disease}} {{CMG}}		{{Coronary heart disease}} {{CMG}} {{AE}} {{MSD}}

	==Overview==		==Overview==
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	==Treatment==		==Treatment==
	===Medical Therapy===		===Medical Therapy===
	Goals for treating coronary artery disease include lowering [[blood pressure]], ~~maintaining [[~~HbA1c~~]] levels to less than~~ 7%, and lowering [[LDL]] cholesterol. Long-term treatment will generally depend on the symptoms and severity of disease, and include [[aspirin]], [[ACE inhibitors]], and other ani-coagulant and anti-platelet regimens. The mainstay of treatment for [[chronic stable angina\|stable angina]] which occurs with exertion, includes [[nitroglycerin]]. When unstable angina causes symptoms at rest, or in the setting of an acute [[myocardial infarction]], the immediate therapy is [[morphine]], [[oxygen]], [[nitrate]] and [[aspirin]]. [[Angioplasty]] may also be required in cases of [[acute coronary syndrome]].		Goals for treating coronary artery disease include lowering [[blood pressure]], managing diabetes with cardiovascular-risk-reducing agents such as SGLT2 inhibitors and GLP-1 receptor agonists, independent of HbA1c target<ref name="pmid39289001">{{cite journal \|vauthors=Galli M, Gragnano F, Vrints C, Andreotti F \|title=2024 ESC guidelines on chronic coronary syndromes: what is new in pharmacotherapy? \|journal=Eur Heart J Cardiovasc Pharmacother \|volume=10 \|issue=7 \|pages=572–574 \|date=November 2024 \|pmid=39289001 \|doi=10.1093/ehjcvp/pvae069 \|url=}}</ref>, and lowering [[LDL]] cholesterol. Long-term treatment will generally depend on the symptoms and severity of disease, and include [[aspirin]], [[ACE inhibitors]], and other ani-coagulant and anti-platelet regimens.Low-dose colchicine (0.5 mg daily) should also be considered as an adjunctive anti-inflammatory therapy for long-term management. <ref name="pmid37558377">{{cite journal \|vauthors=Nelson K, Fuster V, Ridker PM \|title=Low-Dose Colchicine for Secondary Prevention of Coronary Artery Disease: JACC Review Topic of the Week \|journal=J Am Coll Cardiol \|volume=82 \|issue=7 \|pages=648–660 \|date=August 2023 \|pmid=37558377 \|doi=10.1016/j.jacc.2023.05.055 \|url=}}</ref> The mainstay of treatment for [[chronic stable angina\|stable angina]] which occurs with exertion, includes [[nitroglycerin]]. When unstable angina causes symptoms at rest, or in the setting of an acute [[myocardial infarction]], the immediate therapy is [[morphine]], supplemental oxygen (only if SpO₂ <90%), nitrate, and aspirin. [[Angioplasty]] may also be required in cases of [[acute coronary syndrome]].Beta-blockers should be used selectively: they are indicated when LVEF is <50%, or in the presence of angina, arrhythmias, or hypertension, but are no longer routinely recommended for all patients with chronic coronary disease.<ref name="pmid38766996">{{cite journal \|vauthors=Khorsandi M, Blumenthal RS, Blaha MJ, Kohli P \|title=The ABCs of the 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA guideline for the management of patients with chronic coronary disease \|journal=Clin Cardiol \|volume=47 \|issue=5 \|pages=e24284 \|date=May 2024 \|pmid=38766996 \|pmc=11103637 \|doi=10.1002/clc.24284 \|url=}}</ref>

	===Primary Prevention===		===Primary Prevention===
	The [[LDL]] target in primary prevention depends upon the patient's [[risk factors]]. If the ~~patient has CHD or its equivalent~~, ~~then the LDL goal is under 100 mg~~/dl. ~~If the patient has 2~~ risk ~~factors~~, the LDL ~~goal is 130 mg~~/dl. ~~If the patient has~~ < ~~2 risk factors~~, ~~the LDL goal~~ is < ~~160 mg~~/dl. Attempts should be made to reduce [[triglyceride]] levels and to increase [[HDL]] levels. The underlying causes for existing [[dyslipidemia]]s should be identified and appropriately managed. Drugs that cause dyslipidemias should be avoided. Patients should be evaluated reguarly for the presence of risk factors for coronary heart disease, and those with increased risk should be counseled on the beneficial effects of daily [[aspirin]] therapy. Patients should also regularly be counseled about modifying risk factors such as [[obesity]], [[hypertension]], [[smoking]], and the benefits of an [[exercise]] plan.		The [[LDL]] target in primary prevention depends upon the patient's [[risk factors]]. LDL targets in primary prevention should be guided by estimated 10-year ASCVD risk using the PREVENT™ equations<ref name="urlACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology">{{cite web \|url=https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia \|title=ACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology \|format= \|work= \|accessdate=}}</ref>. Statin therapy is recommended for those with intermediate risk (5–<10%) and reasonable for those with borderline risk (3–<5%) after shared decision-making, with the goal of achieving at least a 50% LDL-C reduction from baseline<ref name="urlACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology">{{cite web \|url=https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia \|title=ACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology \|format= \|work= \|accessdate=}}</ref>.Non-statin therapies — including ezetimibe, bempedoic acid, and PCSK9 inhibitors should be considered when statin therapy alone is insufficient.<ref name="urlACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology">{{cite web \|url=https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia \|title=ACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology \|format= \|work= \|accessdate=}}</ref> Attempts should be made to reduce [[triglyceride]] levels and to increase [[HDL]] levels.Coronary artery calcium (CAC) scoring and Lp(a) measurement should be considered to further refine cardiovascular risk and guide treatment intensity.<ref name="urlACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology">{{cite web \|url=https://www.acc.org/latest-in-cardiology/journal-scans/2026/03/13/15/20/acc-aha-release-new-clinical-guideline-for-managing-dyslipidemia \|title=ACC, AHA Release New Clinical Guideline For Managing Dyslipidemia - American College of Cardiology \|format= \|work= \|accessdate=}}</ref> The underlying causes for existing [[dyslipidemia]]s should be identified and appropriately managed. Drugs that cause dyslipidemias should be avoided. Patients should be evaluated reguarly for the presence of risk factors for coronary heart disease, and those with increased risk should be counseled on the beneficial effects of daily [[aspirin]] therapy. Patients should also regularly be counseled about modifying risk factors such as [[obesity]], [[hypertension]], [[smoking]], and the benefits of an [[exercise]] plan.

	===Secondary Prevention===		===Secondary Prevention===
	Patients who should be treated with secondary prevention are those with established atherosclerosis including peripheral artery		Patients who should be treated with secondary prevention are those with established atherosclerosis including peripheral artery disease; carotid artery disease; atherosclerotic aortic disease; diabetes and those with a 10-year ASCVD risk >20% by contemporary risk calculators (e.g., PREVENT™ equations or SCORE2).<ref name="url2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines \| Circulation">{{cite web \|url=https://www.ahajournals.org/doi/10.1161/CIR.0000000000001423 \|title=2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines \| Circulation \|format= \|work= \|accessdate=}}</ref> There are 13 aspects of secondary prevention: Smoking cessation; blood pressure control; lipid-lowering; increasing physical activity; weight loss; diabetes control; antiplatelet agents/anticoagulants; RAS blockers; beta-blockers; depression management; cardiac rehabilitation, influenza vaccine and low-dose colchicine (0.5 mg/day) for anti-inflammatory residual risk reduction.<ref>SEC Working Group for the 2024 ESC guidelines for the management of chronic coronary syndromes and SEC Guidelines Committee. (2025). Comments on the ESC 2024 guidelines for the management of chronic coronary syndromes. ''Revista Espanola de Cardiologia (English Ed.)'', ''78''(3), 170–175. <nowiki>https://doi.org/10.1016/j.rec.2024.10.007</nowiki></ref> Please note that secondary prevention guidelines, especially, those involving medication, may differ between [[Unstable Angina\|UA/NSTEMI]]; [[STEMI]]; and [[Chronic Stable Angina]].
	disease; carotid artery disease; atherosclerotic aortic disease; diabetes and those with a ~~Framingham Risk Score of~~ > 20%.
	There are 12 aspects of secondary prevention: Smoking cessation; blood pressure control; lipid-lowering; increasing physical activity; weight loss; diabetes control; antiplatelet agents/anticoagulants; RAS blockers; beta-blockers; depression management; cardiac rehabilitation ~~and~~ influenza vaccine. Please note that secondary prevention guidelines, especially, those involving medication, may differ between [[Unstable Angina\|UA/NSTEMI]]; [[STEMI]]; and [[Chronic Stable Angina]].

	==References==		==References==

Sandbox

2026-04-16T00:52:30Z

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			== ACS Treatment ==
			Primary Prevention:

	~~{{familytree/start}}~~		'''Equivalent intensity for CHD-risk equivalents (LoE: A):''' Patients with established CHD should be targeted for secondary prevention. Crucially, patients with a '''CHD risk equivalent''' — defined as atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or a Framingham-calculated 10-year risk exceeding 20% — should receive '''the same intensity of risk factor intervention''' as those with overt, clinically apparent CHD.
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| A01 \| \| \| \| \| \|A01=Adult ALL }}~~
	~~{{familytree \| \|,\|-\|-\|-\|v\|-\|-\|-\|-\|-\|-\|+\|-\|-\|-\|-\|-\|-\|-\|-\|-\|.\| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| D01 \| \| D02 \| \| \| \| \| D03 \| \| \| \| \| \| \| \| D05 \| \| \| \|D01=Burkitt Leukemia\|D02=PH-Positive B-ALL\|D03=PH-negative B-ALL\|D05=T-ALL}}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|,\|-\|-\|^\|-\|-\|.\| \| \| \|,\|-\|-\|^\|-\|-\|.\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	{{familytree \| E01 \| \| E02 \| \| E03 \| \| \| \| E04 \| \| E05 \| \| \| \| E06 \| \| \|E01=R-hyper CVAD<br> DA-R-EPOCH\|E02=Chemotherapt+TKI <br> Blinatumomab+TKI\|E03=Younger adults\|E04=Older Adults\|E05=ETP\|E06=Non ETP}}
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \|}}~~
	{{familytree \| \|!\| \| \| \|!\| \| \| F01 \| \| \| \| F02 \| \| F03 \| \| \| \| F04 \| \|F01=Chemotherapy+<br>blinatumomab\|F02=Chemotherapy+<br>blinatumumab+InO <br>Chemotherapy-free blinatumomab + InO\|F03=Chemotherapy+pegAsp+<br>nelarabine+venetoclax\|F04=Chemotherapy+pegAsp+<br>nelarabine}}
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|`\|-\|-\|-\|^\|-\|-\|-\|^\|-\|-\|v\|-\|-\|^\|-\|-\|-\|^\|-\|-\|-\|-\|-\|~~'~~\| \| \| }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| G01 \| \| \| \| \| \| \| \| \| \| \| \| \| \|G01=<div style="float: left; text~~-~~align~~: ~~left; height~~: ~~3em; width: 20em;">~~ '''~~Measurable residual disease monitoring~~'''~~<br> </div>}} }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \| \| \| \| \| }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| H01 \| \| \| \| \| \| \| \| \| \| \| \| \| \| \|H01=<div style="float: left; text~~-~~align: left;">~~'''~~Alloegenic hematopoietic stem cell transplant~~''' ~~<br>•Ph-like ALL~~ with ~~CRLF2 and JAK vairants<br>•High-risk cytogenetics in B-ALL<br>•High-risk Ph-positive B-ALL: IZKF1 genotype<br>•T-ALL: ETP-ALL<br>•Persistent measurable residual disease by NGS<br> </div>}}~~
	~~{{familytree/end}}~~

User:Hasnain Ali

2026-04-14T19:59:22Z

Recently Edited Topics

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	I create original content on my areas of interest and refresh older chapters to keep the medical information current.		I create original content on my areas of interest and refresh older chapters to keep the medical information current.

	* Medical Officer with Dept. of Neurology, Liaquat University hospital Hyderabad/Jamshoro, Pakistan.		* Resident Medical Officer with Dept. of Neurology, Liaquat University hospital Hyderabad/Jamshoro, Pakistan.

	I provide inpatient and outpatient neurological care, managing up to 5 inpatients daily and around 30 clinic and emergency patients per week. Alongside clinical duties, I participated in multidisciplinary academic activities and contributed to research through systematic data collection and documentation.		I provide inpatient and outpatient neurological care, managing up to 5 inpatients daily and around 30 clinic and emergency patients per week. Alongside clinical duties, I participated in multidisciplinary academic activities and contributed to research through systematic data collection and documentation.
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	*'''Dr. Ruth. K. M. Pfau Civil hospital Karachi, Pakistan (July/2021 - Jan/2022)'''<br>'''Position:''' Intern/House officer<br>'''Supervisor Attending:''' Multiple		*'''Dr. Ruth. K. M. Pfau Civil hospital Karachi, Pakistan (July/2021 - Jan/2022)'''<br>'''Position:''' Intern/House officer<br>'''Supervisor Attending:''' Multiple

			==Recently Edited Topics==
			* [[Transient global amnesia\|Transient Global Amnesia]]

Low back pain conservative management

2026-04-14T16:24:46Z

Physical Therapy

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	According to a [[systematic review]] of [[randomized controlled trial]]s by the [[Cochrane Collaboration]], massage therapy, compared to inactive controls, over the short-term significantly reduced pain (SMD=0.75; large) and improved function (SMD=0.72; large).<ref name="pmid26329399">{{cite journal\| author=Furlan AD, Giraldo M, Baskwill A, Irvin E, Imamura M\| title=Massage for low-back pain. \| journal=Cochrane Database Syst Rev \| year= 2015 \| volume= 9 \| issue= \| pages= CD001929 \| pmid=26329399 \| doi=10.1002/14651858.CD001929.pub3 \| pmc= \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26329399 }} </ref> However, the Cochrane concluded "very little confidence that massage is an effective treatment".		According to a [[systematic review]] of [[randomized controlled trial]]s by the [[Cochrane Collaboration]], massage therapy, compared to inactive controls, over the short-term significantly reduced pain (SMD=0.75; large) and improved function (SMD=0.72; large).<ref name="pmid26329399">{{cite journal\| author=Furlan AD, Giraldo M, Baskwill A, Irvin E, Imamura M\| title=Massage for low-back pain. \| journal=Cochrane Database Syst Rev \| year= 2015 \| volume= 9 \| issue= \| pages= CD001929 \| pmid=26329399 \| doi=10.1002/14651858.CD001929.pub3 \| pmc= \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26329399 }} </ref> However, the Cochrane concluded "very little confidence that massage is an effective treatment".

	===~~Mckenzie Method~~===		=== Physical Therapy===
	The Mckenzie Method has been shown to be a modestly effective therapy for adults with chronic low back pain. A 2011 summary of 4 studies showed consistent significant improvement in pain and function although only one study had a large enough population to demonstrate effect sizes on pain and functional outcomes, 0.50 and 0.39 respectively.<ref name="pmid22135496">{{cite journal\| author=Dunsford A, Kumar S, Clarke S\| title=Integrating evidence into practice: use of McKenzie-based treatment for mechanical low back pain. \| journal=J Multidiscip Healthc \| year= 2011 \| volume= 4 \| issue= \| pages= 393-402 \| pmid=22135496 \| doi=10.2147/JMDH.S24733 \| pmc=PMC3215349 \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22135496 }} </ref>		The Mckenzie Method has been shown to be a modestly effective therapy for adults with chronic low back pain. A 2011 summary of 4 studies showed consistent significant improvement in pain and function although only one study had a large enough population to demonstrate effect sizes on pain and functional outcomes, 0.50 and 0.39 respectively.<ref name="pmid22135496">{{cite journal\| author=Dunsford A, Kumar S, Clarke S\| title=Integrating evidence into practice: use of McKenzie-based treatment for mechanical low back pain. \| journal=J Multidiscip Healthc \| year= 2011 \| volume= 4 \| issue= \| pages= 393-402 \| pmid=22135496 \| doi=10.2147/JMDH.S24733 \| pmc=PMC3215349 \| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22135496 }} </ref>

			A [[randomized controlled trial]] in 2015 found minimal benefit.<ref name="v851">{{cite journal \| last1=Fritz \| first1=Julie M. \| last2=Magel \| first2=John S. \| last3=McFadden \| first3=Molly \| last4=Asche \| first4=Carl \| last5=Thackeray \| first5=Anne \| last6=Meier \| first6=Whitney \| last7=Brennan \| first7=Gerard \| title=Early Physical Therapy vs Usual Care in Patients With Recent-Onset Low Back Pain: A Randomized Clinical Trial \| journal=JAMA \| volume=314 \| issue=14 \| date=2015-10-13 \| issn=0098-7484 \| doi=10.1001/jama.2015.11648 \| pmid = 26461996 \| page=1459 \| url=http://jama.jamanetwork.com/article.aspx?doi=10.1001/jama.2015.11648 \| access-date=2026-04-12}}</ref> Outcomes were measured with the Oswestry Disability Index (ODI: range 0 to 100) which has a recommended minimum clinically important difference (MCID) of 6<ref name="pmid11175676">{{cite journal \| last1=Fritz \| first1=J. M. \| last2=Irrgang \| first2=J. J. \| title=A comparison of a modified Oswestry Low Back Pain Disability Questionnaire and the Quebec Back Pain Disability Scale \| journal=Physical Therapy \| volume=81 \| issue=2 \| date=2001 \| issn=0031-9023 \| pmid=11175676 \| doi=10.1093/ptj/81.2.776 \| pages=776–788 \| url=https://pubmed.gov/11175676 \| access-date=2026-04-14}}</ref>. While both the intervention and usual care group had improvement well above the MCID, the "Mean Difference Between Groups in Change from Baseline" were less than 4 at all time points.

	===Pilates===		===Pilates===

Back pain

2026-04-12T19:14:31Z

Treatment

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	==Treatment==		==Treatment==

	[[Back pain medical therapy\|Medical Therapy]] \| [[Back pain surgery\|Surgery]] \| [[Back pain primary prevention\|Primary Prevention]] \| [[Back pain secondary prevention\|Secondary Prevention]] \| [[Back pain cost-effectiveness of therapy\|Cost-Effectiveness of Therapy]] \| [[Back pain future or investigational therapies\|Future or Investigational Therapies]] \| [[Back pain monitoring response to therapy\| Monitoring Response to Therapy]]		[[Back pain medical therapy\|Medical Therapy]] \| [[Low back pain conservative management]] \| [[Back pain surgery\|Surgery]] \| [[Back pain primary prevention\|Primary Prevention]] \| [[Back pain secondary prevention\|Secondary Prevention]] \| [[Back pain cost-effectiveness of therapy\|Cost-Effectiveness of Therapy]] \| [[Back pain future or investigational therapies\|Future or Investigational Therapies]] \| [[Back pain monitoring response to therapy\| Monitoring Response to Therapy]]

	==Lecture==		==Lecture==

File:Zoliflodacin.jpg

2026-04-11T14:35:03Z

Basir Gill uploaded File:Zoliflodacin.jpg

New page

Template:SS

2026-04-09T17:52:01Z

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	[[User:~~ShiSheng~~\|~~Sheng Shi~~, ~~M.D.~~]] [mailto:~~shengshi~~@~~wikidoc~~.~~org~~]		[[User:Sophia Saad\|Sophia Saad, Associate Editor - WikiDoc]] [mailto:scsaad23@yahoo.com]

Olezarsen

2026-04-08T08:33:21Z

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	\|aOrAn=an		\|aOrAn=an
	\|drugClass=Oligonucleotide		\|drugClass=Oligonucleotide

Cosibelimab-ipdl

2026-04-08T08:32:42Z

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	\|aOrAn=a		\|aOrAn=a
	\|drugClass=programmed death ligand-1 (PD-L1) blocking antibody		\|drugClass=programmed death ligand-1 (PD-L1) blocking antibody

User:Nehal Eid

2026-04-08T08:28:46Z

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	[[User:Nehal Eid\|Nehal Eid, M.D.]][mailto:nehalelsaeed98@gmail.com]		[[User:Nehal Eid\|Nehal Eid, M.D.]][mailto:nehalelsaeed98@gmail.com]

			'''Wikidoc contributions:'''

			[[Juvenile idiopathic arthritis]]

			[[Sudden cardiac death]]

			[[Cosibelimab-ipdl]]

			[[Olezarsen]]

			[[Intravenous drug use (recreational)]]

			[[Hypertension and Blood Pressure Control in Diabetics]]

			[[Lipid Management in Diabetics]]

			[[Coronary heart disease in Diabetics]]

Sudden cardiac death prognosis

2026-04-07T15:45:12Z

Prognosis of cardiac arrest in young athletes:

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	==== Prognosis of cardiac arrest in young athletes: ====		==== Prognosis of cardiac arrest in young athletes: ====

			* 58% survival rate was reported by the US Commotio Cordis Registry in 216 persons with sudden cardiac arrest due to commotio cordis (cardiac arrest due to VF triggered by blunt chest trauma) (age range, 0.2-51 years;mean,15years, 95% male) from 2006 through 2012.<ref name=":9">Maron BJ, Haas TS, Ahluwalia A, Garberich RF, Estes NA III, Link MS. Increasing survival rate from commotio cordis.HeartRhythm.2013;10(2):219-223. doi:10.1016/j.hrthm.2012.10.034</ref>
			* Prompt resuscitation and participation in organized competitive sports was associated with higher survival rates. Multivariate analysis identified participation in recreational sports with lower survival (odds ratio [OR] compared with organized competitive sports, 0.33; 95%CI,0.16-0.67) and onsite automated external defibrillator with higher survival (OR, 4.61; 95% CI, 1.43-14.88).<ref name=":9" />
			* Individuals aged 18 to 35 years with sports-related sudden cardiac arrest in Germany and France showed improved survival to hospital discharge with public automated external defibrillator use prior to EMS arrival (OR, 6.25; 95% CI, 1.48 43.20); individuals with sudden cardiac arrest who received both immediate bystander CPR and automated external defibrillator had 91%survival.<ref>Bohm P, Meyer T, Narayanan K, et al. Sports-related sudden cardiac arrest in young adults. Europace. 2023;25(2):627-633. doi:10.1093/ europace/euac172</ref>
			* A recent meta-analysis demonstrated that in sports related sudden cardiac arrest, bystander presence (OR, 2.55; 95%CI, 1.48-4.37), bystander CPR (OR, 3.84; 95% CI, 2.36-6.25), and bystander automated external defibrillator use (OR, 5.25; 95%CI,3.58-7.70) were associated with improved survival.<ref>Michelland L, Murad MH, Bougouin W, et al. Association between basic life support and survival in sports-related sudden cardiac arrest: a meta-analysis. Eur Heart J. 2023;44(3):180-192. doi:10.1093/eurheartj/ehac586</ref>

	==References==		==References==

Sudden cardiac death epidemiology and demographics

2026-04-07T15:38:11Z

Cardiac arrest in young athletes:

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	* Commotio cordis is cardiac arrest precipitated by chest blunt force sufficient to trigger VF.<ref>Maron BJ, Estes NA III. Commotio cordis. N Engl J Med. 2010;362(10):917-927.doi:10.1056/ NEJMra0910111</ref>,<ref>Peng T, Derry LT, Yogeswaran V, Goldschlager NF. Commotio cordis in 2023. SportsMed.2023;53 (8):1527-1536. doi:10.1007/s40279-023-01873-6</ref> Although commotio cordis incidence is unknown, more than 90% of cases in the US occur among individuals younger than 25 years.<ref name=":8">Maron BJ, Ahluwalia A, Haas TS, Semsarian C, Link MS, Estes NA III. Global epidemiology and JAMA March18,2025 Volume 333,Number11 (Reprinted) demographics of commotio cordis. HeartRhythm. 2011;8(12):1969-1971. doi:10.1016/j.hrthm.2011.07. 014</ref> Commotio cordis is common in baseball, softball, and football in the US, whereas soccer, cricket, and hockey were the sports most commonly associated with it in non-US populations.<ref name=":8" />		* Commotio cordis is cardiac arrest precipitated by chest blunt force sufficient to trigger VF.<ref>Maron BJ, Estes NA III. Commotio cordis. N Engl J Med. 2010;362(10):917-927.doi:10.1056/ NEJMra0910111</ref>,<ref>Peng T, Derry LT, Yogeswaran V, Goldschlager NF. Commotio cordis in 2023. SportsMed.2023;53 (8):1527-1536. doi:10.1007/s40279-023-01873-6</ref> Although commotio cordis incidence is unknown, more than 90% of cases in the US occur among individuals younger than 25 years.<ref name=":8">Maron BJ, Ahluwalia A, Haas TS, Semsarian C, Link MS, Estes NA III. Global epidemiology and JAMA March18,2025 Volume 333,Number11 (Reprinted) demographics of commotio cordis. HeartRhythm. 2011;8(12):1969-1971. doi:10.1016/j.hrthm.2011.07. 014</ref> Commotio cordis is common in baseball, softball, and football in the US, whereas soccer, cricket, and hockey were the sports most commonly associated with it in non-US populations.<ref name=":8" />
	* 58% survival rate was reported by the US Commotio Cordis Registry in 216 persons with sudden cardiac arrest due to commotio cordis (age range, 0.2-51 years;mean,15years,95%male) from 2006 through 2012.<ref name=":9">Maron BJ, Haas TS, Ahluwalia A, Garberich RF, Estes NA III, Link MS. Increasing survival rate from commotio cordis.HeartRhythm.2013;10(2):219-223. doi:10.1016/j.hrthm.2012.10.034</ref>
	* Prompt resuscitation and participation in organized competitive sports was associated with higher survival rates. Multivariate analysis identified participation in recreational sports with lower survival (odds ratio [OR] compared with organized competitive sports, 0.33; 95%CI,0.16-0.67) and onsite automated external defibrillator with higher survival (OR, 4.61; 95% CI, 1.43-14.88).<ref name=":9" />
	*

	==References==		==References==

Sudden cardiac death prognosis

2026-04-07T15:37:06Z

Prognosis of Sudden Cardiac Arrest Survivors

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	:* Women between 15-45 years old<ref name="pmid20228684">{{cite journal \|vauthors=Topjian AA, Localio AR, Berg RA, Alessandrini EA, Meaney PA, Pepe PE, Larkin GL, Peberdy MA, Becker LB, Nadkarni VM \|title=Women of child-bearing age have better inhospital cardiac arrest survival outcomes than do equal-aged men \|journal=Crit Care Med \|volume=38 \|issue=5 \|pages=1254–60 \|date=May 2010 \|pmid=20228684 \|pmc=3934212 \|doi=10.1097/CCM.0b013e3181d8ca43 \|url=}}</ref>		:* Women between 15-45 years old<ref name="pmid20228684">{{cite journal \|vauthors=Topjian AA, Localio AR, Berg RA, Alessandrini EA, Meaney PA, Pepe PE, Larkin GL, Peberdy MA, Becker LB, Nadkarni VM \|title=Women of child-bearing age have better inhospital cardiac arrest survival outcomes than do equal-aged men \|journal=Crit Care Med \|volume=38 \|issue=5 \|pages=1254–60 \|date=May 2010 \|pmid=20228684 \|pmc=3934212 \|doi=10.1097/CCM.0b013e3181d8ca43 \|url=}}</ref>
	:*Rapid intervention with a [[defibrillator]] increases [[survival rates]].<ref>{{cite journal \|author=Eisenberg MS, Mengert TJ \|title=Cardiac resuscitation \|journal=N. Engl. J. Med. \|volume=344 \|issue=17 \|pages=1304–13 \|year=2001 \|month=April \|pmid=11320390 \|doi= \|url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=11320390&promo=ONFLNS19}}</ref><ref name="pmid12826637">{{cite journal \|author=Bunch TJ, White RD, Gersh BJ, ''et al'' \|title=Long-term outcomes of out-of-hospital cardiac arrest after successful early defibrillation \|journal=N. Engl. J. Med. \|volume=348 \|issue=26 \|pages=2626–33 \|year=2003 \|month=June \|pmid=12826637 \|doi=10.1056/NEJMoa023053 \|url=}}</ref>		:*Rapid intervention with a [[defibrillator]] increases [[survival rates]].<ref>{{cite journal \|author=Eisenberg MS, Mengert TJ \|title=Cardiac resuscitation \|journal=N. Engl. J. Med. \|volume=344 \|issue=17 \|pages=1304–13 \|year=2001 \|month=April \|pmid=11320390 \|doi= \|url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=11320390&promo=ONFLNS19}}</ref><ref name="pmid12826637">{{cite journal \|author=Bunch TJ, White RD, Gersh BJ, ''et al'' \|title=Long-term outcomes of out-of-hospital cardiac arrest after successful early defibrillation \|journal=N. Engl. J. Med. \|volume=348 \|issue=26 \|pages=2626–33 \|year=2003 \|month=June \|pmid=12826637 \|doi=10.1056/NEJMoa023053 \|url=}}</ref>

			==== Prognosis of cardiac arrest in young athletes: ====

	==References==		==References==

Sudden cardiac death epidemiology and demographics

2026-04-07T15:35:25Z

Race

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	*In a US study from 1999 through 2015 (n = 31492), Black individuals younger than 34 years had a higher incidence of presumed sudden cardiac deaths (1.88 per 100000 person-years in 2015) than Hispanic individuals (0.66 per 100000 person-years),and White individuals (1.17 per 100000 person-years),<ref>El-AssaadI, Al-Kindi SG, Aziz PF. Trends of out-of-hospital sudden cardiac death among children and youngadults. Pediatrics. 2017;140(6): e20171438. doi:10.1542/peds.2017-1438</ref> which may be due to inequitable access to care <ref>Noonan AS, Velasco-Mondragon HE, Wagner FA. Improving the health of African Americans in the USA: an overdue opportunity for social justice. Public Health Rev. 2016;37:12. doi:10. 1186/s40985-016-0025-4</ref> and racial disparities among out-of hospital resuscitation attempts.		*In a US study from 1999 through 2015 (n = 31492), Black individuals younger than 34 years had a higher incidence of presumed sudden cardiac deaths (1.88 per 100000 person-years in 2015) than Hispanic individuals (0.66 per 100000 person-years),and White individuals (1.17 per 100000 person-years),<ref>El-AssaadI, Al-Kindi SG, Aziz PF. Trends of out-of-hospital sudden cardiac death among children and youngadults. Pediatrics. 2017;140(6): e20171438. doi:10.1542/peds.2017-1438</ref> which may be due to inequitable access to care <ref>Noonan AS, Velasco-Mondragon HE, Wagner FA. Improving the health of African Americans in the USA: an overdue opportunity for social justice. Public Health Rev. 2016;37:12. doi:10. 1186/s40985-016-0025-4</ref> and racial disparities among out-of hospital resuscitation attempts.
	*White individuals were more likely to receive bystander CPR after a witnessed cardiac arrest and postresuscitation care than were Black and Hispanic persons in several US based studies.<ref>Toy J, Bosson N, Schlesinger S,Gausche-Hill M. Racial and ethnic disparities in the provision of bystander CPR after witnessed out-of-hospital cardiac arrest in the United States. Resuscitation. 2023;190:109901. doi:10.1016/j.resuscitation.2023. 109901</ref><ref>Casey SD, Mumma BE.Sex,race,and insurance status differences in hospital treatment and outcomes following out-of-hospital cardiac arrest. Resuscitation. 2018;126:125-129. doi:10.1016/j. resuscitation.2018.02.027</ref>		*White individuals were more likely to receive bystander CPR after a witnessed cardiac arrest and postresuscitation care than were Black and Hispanic persons in several US based studies.<ref>Toy J, Bosson N, Schlesinger S,Gausche-Hill M. Racial and ethnic disparities in the provision of bystander CPR after witnessed out-of-hospital cardiac arrest in the United States. Resuscitation. 2023;190:109901. doi:10.1016/j.resuscitation.2023. 109901</ref><ref>Casey SD, Mumma BE.Sex,race,and insurance status differences in hospital treatment and outcomes following out-of-hospital cardiac arrest. Resuscitation. 2018;126:125-129. doi:10.1016/j. resuscitation.2018.02.027</ref>

			=== Cardiac arrest in young athletes: ===

			* Commotio cordis is cardiac arrest precipitated by chest blunt force sufficient to trigger VF.<ref>Maron BJ, Estes NA III. Commotio cordis. N Engl J Med. 2010;362(10):917-927.doi:10.1056/ NEJMra0910111</ref>,<ref>Peng T, Derry LT, Yogeswaran V, Goldschlager NF. Commotio cordis in 2023. SportsMed.2023;53 (8):1527-1536. doi:10.1007/s40279-023-01873-6</ref> Although commotio cordis incidence is unknown, more than 90% of cases in the US occur among individuals younger than 25 years.<ref name=":8">Maron BJ, Ahluwalia A, Haas TS, Semsarian C, Link MS, Estes NA III. Global epidemiology and JAMA March18,2025 Volume 333,Number11 (Reprinted) demographics of commotio cordis. HeartRhythm. 2011;8(12):1969-1971. doi:10.1016/j.hrthm.2011.07. 014</ref> Commotio cordis is common in baseball, softball, and football in the US, whereas soccer, cricket, and hockey were the sports most commonly associated with it in non-US populations.<ref name=":8" />
			* 58% survival rate was reported by the US Commotio Cordis Registry in 216 persons with sudden cardiac arrest due to commotio cordis (age range, 0.2-51 years;mean,15years,95%male) from 2006 through 2012.<ref name=":9">Maron BJ, Haas TS, Ahluwalia A, Garberich RF, Estes NA III, Link MS. Increasing survival rate from commotio cordis.HeartRhythm.2013;10(2):219-223. doi:10.1016/j.hrthm.2012.10.034</ref>
			* Prompt resuscitation and participation in organized competitive sports was associated with higher survival rates. Multivariate analysis identified participation in recreational sports with lower survival (odds ratio [OR] compared with organized competitive sports, 0.33; 95%CI,0.16-0.67) and onsite automated external defibrillator with higher survival (OR, 4.61; 95% CI, 1.43-14.88).<ref name=":9" />
			*

	==References==		==References==

Sudden cardiac death screening

2026-04-07T15:15:15Z

Screening in young athletes:

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	**LQTS Risk Calculator		**LQTS Risk Calculator
	**VA calculator		**VA calculator

			=== Screening in young athletes: ===
			The American Heart Association–American College of Cardiology consensus statement<ref name=":1">Maron BJ, Levine BD, Washington RL, Baggish AL, Kovacs RJ, Maron MS; American Heart Association Electrocardiography and Arrhythmias Committee of Council on Clinical Cardiology, Council on Cardiovascular Disease in Young, Council on Cardiovascular and Stroke Nursing, Council on Functional Genomics and Translational Biology, and American College of Cardiology. Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities: Task Force 2: preparticipation screening for cardiovascular disease in competitive athletes: a scientific statement from the American Heart Association and AmericanCollege of Cardiology. Circulation. 2015;132(22):e267-e272.</ref> on preparticipation screening recommends the American Heart Association 14-point screening guide, including a comprehensive history taking and a physical examination for young athletes (class I recommendation), but does not recommend routine ECG screening of young adults (athletes and non-athletes) in the general population (class III), due to concerns about diagnostic accuracy, cost-effectiveness, and availability of physicians and equipment needed for screening. ECG or transthoracic echocardiography should only be performed in select individuals in whom genetic,congenital,or other cardiovascular abnormalities are suspected or identified (class IIb).<ref name=":1" />

			However, recent ESC guideline recommends a 12-lead ECG as part of preparticipation for all competitive athletes younger than 35 years (class IIa).<ref name="pmid36017572" /> This recommendation was supported by outcome data from the Veneto region, which showed declining incidence of sudden death in young competitive athletes after introduction of a nationwide prescreening program using ECG.<ref>Corrado D, Basso C, Pavei A, Michieli P, Schiavon M,ThieneG. Trends in sudden cardiovascular death in young competitive athletes after implementation of a preparticipation screening program. JAMA.2006;296(13):1593-1601. doi:10.1001/jama.296.13.1593</ref> Some data suggest that compared with history and physical examination, ECG may provide superior accuracy to identify potential risk of sudden death, primarily due to detection of preexcitation syndromes (sensitivity 88% vs 19%, specificity 98% vs 75%).<ref>Williams EA, Pelto HF, Toresdahl BG, et al. Performance of the American Heart Association (AHA)14-point evaluation versus electrocardiography for the cardiovascular screening of high school athletes: a prospective 996 study. J AmHeartAssoc.2019;8(14):e012235. doi:10.1161/JAHA.119.012235</ref>,<ref>Goff NK, Hutchinson A, Koek W, Kamat D. Meta-analysis on the effectiveness of ECG screening for conditions related to sudden cardiac death in young athletes. Clin Pediatr (Phila). 2023;62(10):1158-1168. doi:10.1177/ 00099228231152857</ref>

			In the last 2 decades, preparticipation screening for early identification of young competitive athletes at risk of sudden cardiac arrest in high school, college, and professional settings has been investigated. A comparable incidence of cardiovascular deaths was found between 1993 and 2015 in these studies screening competitive athletes. In the Veneto region of Italy, where ECG is routinely employed as part of preparticipation screening, and those in the US (Minnesota), where preparticipation prescreening is limited to history and physical examination.<ref>Maron BJ, Haas TS, Doerer JJ, Thompson PD, Hodges JS. Comparison of U.S.and Italian experiences with sudden cardiac deaths in young competitive athletes and implications for preparticipation screening strategies. Am J Cardiol. 2009;104(2):276-280. doi:10.1016/j.amjcard.2009. 03.037</ref>

Sudden cardiac death risk factors

2026-04-06T16:54:56Z

Risk Factors

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	__NOTOC__		__NOTOC__
	{{Sudden cardiac death}}		{{Sudden cardiac death}}
	{{CMG}} {{AE}} {{Sara.Zand}} {{EdzelCo}}		{{CMG}} {{AE}} {{Sara.Zand}} {{EdzelCo}} {{Nehal}}

	==Overview==		==Overview==
	Common [[risk factors]] related to underlying [[coronary artery disease]] ([[CAD]]) and [[inherited]] causes in the development of [[ sudden cardiac arrest]] ([[SCA]]) are [[hypertension]], [[male]] [[gender]]		Common [[risk factors]] related to underlying [[coronary artery disease]] ([[CAD]]) and [[inherited]] causes in the development of [[ sudden cardiac arrest]] ([[SCA]]) are [[hypertension]], [[male]] [[gender]]
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	:*[[Early repolarization]] patten in early phase of [[MI]]<ref name="NaruseTada2012">{{cite journal\|last1=Naruse\|first1=Yoshihisa\|last2=Tada\|first2=Hiroshi\|last3=Harimura\|first3=Yoshie\|last4=Hayashi\|first4=Mayu\|last5=Noguchi\|first5=Yuichi\|last6=Sato\|first6=Akira\|last7=Yoshida\|first7=Kentaro\|last8=Sekiguchi\|first8=Yukio\|last9=Aonuma\|first9=Kazutaka\|title=Early Repolarization Is an Independent Predictor of Occurrences of Ventricular Fibrillation in the Very Early Phase of Acute Myocardial Infarction\|journal=Circulation: Arrhythmia and Electrophysiology\|volume=5\|issue=3\|year=2012\|pages=506–513\|issn=1941-3149\|doi=10.1161/CIRCEP.111.966952}}</ref>		:*[[Early repolarization]] patten in early phase of [[MI]]<ref name="NaruseTada2012">{{cite journal\|last1=Naruse\|first1=Yoshihisa\|last2=Tada\|first2=Hiroshi\|last3=Harimura\|first3=Yoshie\|last4=Hayashi\|first4=Mayu\|last5=Noguchi\|first5=Yuichi\|last6=Sato\|first6=Akira\|last7=Yoshida\|first7=Kentaro\|last8=Sekiguchi\|first8=Yukio\|last9=Aonuma\|first9=Kazutaka\|title=Early Repolarization Is an Independent Predictor of Occurrences of Ventricular Fibrillation in the Very Early Phase of Acute Myocardial Infarction\|journal=Circulation: Arrhythmia and Electrophysiology\|volume=5\|issue=3\|year=2012\|pages=506–513\|issn=1941-3149\|doi=10.1161/CIRCEP.111.966952}}</ref>
	:*Family history of premature death (sudden and unexpected) before age 50 attributed to [[heart]] disease in > 1 relative, presence of [[heart]] disease in close relative less than age 50, presence of ion [[channelopathies]] in family members		:*Family history of premature death (sudden and unexpected) before age 50 attributed to [[heart]] disease in > 1 relative, presence of [[heart]] disease in close relative less than age 50, presence of ion [[channelopathies]] in family members

			=== Sudden Cardiac Arrest in Young Athletes: ===
			Generally, athletes are considered healthier than young adults in the general population. In studies of children and young adults, incidence of sudden death in athletes was reported to be low at approximately 1 per 100000 person-years.<ref name=":0">Maron BJ, Haas TS, Murphy CJ, Ahluwalia A, Rutten-RamosS. Incidence and causes of sudden death in U.S. college athletes. J Am Coll Cardiol. 2014;63(16):1636-1643. doi:10.1016/j.jacc.2014.01. 041</ref>,<ref>Risgaard B, Winkel BG, Jabbari R, et al. Sports-related sudden cardiac death in a competitive and a non competitive athlete population aged 12 to 49 years: data from an unselected nationwide study in Denmark.Heart Rhythm.2014;11(10):1673-1681. doi:10.1016/j.hrthm. 2014.05.026</ref> However in a prospective study of 11168 adolescent soccer players (mean age, 16.4 years, 95% male) in the English Football Association cardiac screening program from 1996 through 2016, the incidence of sudden death was 6.8 per 100000 person-years.<ref>Malhotra A, Dhutia H, Finocchiaro G, et al. Outcomes of cardiac screening in adolescent soccer players. N Engl J Med.2018;379(6):524-534. doi: 10.1056/NEJMoa1714719</ref> Most common cause of cardiac arrests in young athletes are:

			# Sudden arrhythmic death syndrome
			# Coronary anomalies
			# Myocarditis
			# Valvular disease.<ref name=":0" />,<ref>Finocchiaro G, Papadakis M, Robertus JL, et al. Etiology of sudden death in sports: insights from a United Kingdom regional registry. J AmColl Cardiol. 2016;67(18):2108-2115. doi:10.1016/j.jacc.2016.02. 062</ref>

			A meta-analysis evaluating sudden cardiac death etiology in individuals younger than 35 years from 2010 through 2020 demonstrated that the following cardiac conditions were more common among athletes than nonathletes: hypertrophic cardiomyopathy(11.9%vs3.9%;P = .002),dilated cardiomyopathy (3.6% vs 0.8%; P = .047), and anomalous coronary arteries (7.2% vs 1.9%; P = .009).<ref>D’Ascenzi F, Valentini F, Pistoresi S, et al. Causes of sudden cardiac death in young athletes and non-athletes: systematic review and meta-analysis: sudden cardiac death in the young. Trends Cardiovasc Med. 2022;32(5):299-308. doi:10.1016/j.tcm.2021.06.001</ref>

	==References==		==References==

User:Fernanda Servin

2026-04-06T16:31:01Z

User account Fernanda Servin was created by Alberto Castro Molina

User:Adrian Gutierrez

2026-04-06T16:05:58Z

User account Adrian Gutierrez was created by Alberto Castro Molina

Sudden cardiac death screening

2026-04-06T14:53:42Z

← Older revision		Revision as of 14:53, 6 April 2026
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	__NOTOC__		__NOTOC__
	{{Sudden cardiac death}}		{{Sudden cardiac death}}
	{{CMG}} {{AE}} {{Sara.Zand}} {{EdzelCo}}		{{CMG}} {{AE}} {{Sara.Zand}} {{EdzelCo}} {{Nehal}}

	==Overview==		==Overview==
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	==Screening==		==Screening==
	*~~[[Screening]]~~ in the ~~first relative~~ of [[patients]] with [[sudden cardiac arrest~~]] should be done if there is concern about inherited causes~~ of [[cardiac arrest]].		*If the phenotype in a patient resuscitated after sudden cardiac arrest is established, a recent expert consensus statement<ref name=":0">Stiles MK, Wilde AAM, Abrams DJ, et al. 2020 APHRS/HRS expert consensus statement on the investigation of decedents with sudden unexplained death and patients with sudden cardiac arrest, and of their families. Heart Rhythm. 2021;18(1):e1-e50. doi:10.1016/j.hrthm.2020.10.010</ref> recommends genetic testing focused on potential candidate genes and clinical evaluation of family members to identify relatives who have or are at risk of developing a clinical condition.
			*If the cause of sudden cardiac arrest is not determined, first-degree relatives may undergo clinical evaluation, including ECG, cardiac imaging, ambulatory monitoring, and provocative testing.
			*Psychological evaluation and treatment of grief and post traumatic stress in survivors and their immediate family members by trained mental health professionals is recommended.<ref name=":0" />
	*Several [[SCD]] [[risk calculators]] are available for all age groups <ref name="pmid31155932">{{cite journal\| author=Wahbi K, Ben Yaou R, Gandjbakhch E, Anselme F, Gossios T, Lakdawala NK \| display-authors=etal\| title=Development and Validation of a New Risk Prediction Score for Life-Threatening Ventricular Tachyarrhythmias in Laminopathies. \| journal=Circulation \| year= 2019 \| volume= 140 \| issue= 4 \| pages= 293-302 \| pmid=31155932 \| doi=10.1161/CIRCULATIONAHA.118.039410 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31155932 }} </ref> <ref name="pmid30915475">{{cite journal\| author=Cadrin-Tourigny J, Bosman LP, Nozza A, Wang W, Tadros R, Bhonsale A \| display-authors=etal\| title=A new prediction model for ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy. \| journal=Eur Heart J \| year= 2019 \| volume= 40 \| issue= 23 \| pages= 1850-1858 \| pmid=30915475 \| doi=10.1093/eurheartj/ehz103 \| pmc=6568197 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30915475 }} </ref> <ref name="pmid32418493">{{cite journal\| author=Miron A, Lafreniere-Roula M, Steve Fan CP, Armstrong KR, Dragulescu A, Papaz T \| display-authors=etal\| title=A Validated Model for Sudden Cardiac Death Risk Prediction in Pediatric Hypertrophic Cardiomyopathy. \| journal=Circulation \| year= 2020 \| volume= 142 \| issue= 3 \| pages= 217-229 \| pmid=32418493 \| doi=10.1161/CIRCULATIONAHA.120.047235 \| pmc=7365676 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32418493 }} </ref> <ref name="pmid31411652">{{cite journal\| author=Norrish G, Ding T, Field E, Ziólkowska L, Olivotto I, Limongelli G \| display-authors=etal\| title=Development of a Novel Risk Prediction Model for Sudden Cardiac Death in Childhood Hypertrophic Cardiomyopathy (HCM Risk-Kids). \| journal=JAMA Cardiol \| year= 2019 \| volume= 4 \| issue= 9 \| pages= 918-927 \| pmid=31411652 \| doi=10.1001/jamacardio.2019.2861 \| pmc=6694401 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31411652 }} </ref> <ref name="pmid24126876">{{cite journal\| author=O'Mahony C, Jichi F, Pavlou M, Monserrat L, Anastasakis A, Rapezzi C \| display-authors=etal\| title=A novel clinical risk prediction model for sudden cardiac death in hypertrophic cardiomyopathy (HCM risk-SCD). \| journal=Eur Heart J \| year= 2014 \| volume= 35 \| issue= 30 \| pages= 2010-20 \| pmid=24126876 \| doi=10.1093/eurheartj/eht439 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24126876 }} </ref>		*Several [[SCD]] [[risk calculators]] are available for all age groups <ref name="pmid31155932">{{cite journal\| author=Wahbi K, Ben Yaou R, Gandjbakhch E, Anselme F, Gossios T, Lakdawala NK \| display-authors=etal\| title=Development and Validation of a New Risk Prediction Score for Life-Threatening Ventricular Tachyarrhythmias in Laminopathies. \| journal=Circulation \| year= 2019 \| volume= 140 \| issue= 4 \| pages= 293-302 \| pmid=31155932 \| doi=10.1161/CIRCULATIONAHA.118.039410 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31155932 }} </ref> <ref name="pmid30915475">{{cite journal\| author=Cadrin-Tourigny J, Bosman LP, Nozza A, Wang W, Tadros R, Bhonsale A \| display-authors=etal\| title=A new prediction model for ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy. \| journal=Eur Heart J \| year= 2019 \| volume= 40 \| issue= 23 \| pages= 1850-1858 \| pmid=30915475 \| doi=10.1093/eurheartj/ehz103 \| pmc=6568197 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30915475 }} </ref> <ref name="pmid32418493">{{cite journal\| author=Miron A, Lafreniere-Roula M, Steve Fan CP, Armstrong KR, Dragulescu A, Papaz T \| display-authors=etal\| title=A Validated Model for Sudden Cardiac Death Risk Prediction in Pediatric Hypertrophic Cardiomyopathy. \| journal=Circulation \| year= 2020 \| volume= 142 \| issue= 3 \| pages= 217-229 \| pmid=32418493 \| doi=10.1161/CIRCULATIONAHA.120.047235 \| pmc=7365676 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32418493 }} </ref> <ref name="pmid31411652">{{cite journal\| author=Norrish G, Ding T, Field E, Ziólkowska L, Olivotto I, Limongelli G \| display-authors=etal\| title=Development of a Novel Risk Prediction Model for Sudden Cardiac Death in Childhood Hypertrophic Cardiomyopathy (HCM Risk-Kids). \| journal=JAMA Cardiol \| year= 2019 \| volume= 4 \| issue= 9 \| pages= 918-927 \| pmid=31411652 \| doi=10.1001/jamacardio.2019.2861 \| pmc=6694401 \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31411652 }} </ref> <ref name="pmid24126876">{{cite journal\| author=O'Mahony C, Jichi F, Pavlou M, Monserrat L, Anastasakis A, Rapezzi C \| display-authors=etal\| title=A novel clinical risk prediction model for sudden cardiac death in hypertrophic cardiomyopathy (HCM risk-SCD). \| journal=Eur Heart J \| year= 2014 \| volume= 35 \| issue= 30 \| pages= 2010-20 \| pmid=24126876 \| doi=10.1093/eurheartj/eht439 \| pmc= \| url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24126876 }} </ref>
	**[[HCM Risk-Kids Score]] is a validated [[risk calculator]] used for [[patients]] with [[hypertrophic cardiomyopathy]] ([[HCM]]) who are up to 16 years of [[age]].		**[[HCM Risk-Kids Score]] is a validated [[risk calculator]] used for [[patients]] with [[hypertrophic cardiomyopathy]] ([[HCM]]) who are up to 16 years of [[age]].

Sudden cardiac death other diagnostic studies

2026-04-06T14:33:31Z

Postmortem Genetic Investigation:

← Older revision		Revision as of 14:33, 6 April 2026
(2 intermediate revisions by the same user not shown)
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	===Genetic testing===		===Genetic testing===
	* ~~Genetic testing of young adults may be useful~~ for ~~diagnosis~~ and ~~treatment of cardiomyopathies~~ and ~~primary arrhythmia syndromes~~.Genetic ~~testing of first-degree family members may help identify asymptomatically affected relatives. The reported diagnostic yield~~ of ~~genetic testing among individuals with~~ sudden ~~arrhythmic death syndrome(normal heart at autopsy with no cause of death identified) is 13% to 34%, whereas~~ the yield ~~of genetic testing of survivors of~~ sudden cardiac ~~arrest resuscitated~~ from ~~idiopathic ventricular arrhythmias is 2~~% to 22%.It is used to identify [[genetic]] composition of an individual and determine whether genetic variation modifications are present leading to [[Brugada syndrome]], [[long QT syndrome]] ([[LQTS]]), [[hypertrophic cardiomyopathy]] ([[HCM]]), and [[dilated cardiomyopathy]] ([[DCM]]) <ref name="~~pmid33831308~~">~~{{cite journal\| author=James CA~~, ~~Jongbloed JDH~~, ~~Hershberger RE~~, ~~Morales~~ A~~, Judge DP, Syrris P \| display~~-~~authors=etal\| title=International Evidence Based Reappraisal of Genes Associated With Arrhythmogenic Right Ventricular Cardiomyopathy Using the Clinical Genome Resource Framework~~. ~~\| journal=Circ Genom Precis Med \| year= 2021 \| volume= 14 \| issue= 3 \| pages= e003273 \| pmid=33831308 \|~~ doi=10.~~1161~~/~~CIRCGEN~~.~~120~~.~~003273 \| pmc=8205996 \| url=https~~:~~//www~~.~~ncbi~~.~~nlm.nih.gov/entrez/eutils~~/~~elink~~.~~fcgi?dbfrom=pubmed&tool=sumsearch~~.~~org/cite&retmode=ref&cmd=prlinks&id=33831308 }}~~ </ref> <ref name="~~pmid32429735~~">~~{{cite journal\| author=~~Lahrouchi N, ~~Tadros R, Crotti L~~, ~~Mizusawa Y~~, ~~Postema PG, Beekman L \| display~~-~~authors=etal\| title=Transethnic Genome-Wide Association Study Provides Insights~~ in ~~the Genetic Architecture and Heritability~~ of ~~Long QT Syndrome~~. ~~\| journal=Circulation \| year= 2020 \| volume= 142 \| issue= 4 \| pages= 324~~-~~338 \| pmid=32429735 \|~~ doi=10.~~1161~~/~~CIRCULATIONAHA~~.~~120~~.~~045956 \| pmc=7382531 \| url=https:~~/~~/www~~.~~ncbi~~.~~nlm~~.~~nih~~.~~gov~~/~~entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org~~/~~cite&retmode=ref&cmd=prlinks&id=32429735 }}~~ </ref> <ref name="~~pmid33164571~~">~~{{cite journal\| author=Wijeyeratne YD~~, ~~Tanck MW~~, ~~Mizusawa Y~~, ~~Batchvarov V, Barc J, Crotti L \| display-authors=etal\| title=SCN5A Mutation Type and a Genetic Risk Score Associate Variably With Brugada Syndrome Phenotype~~ in ~~SCN5A Families~~. ~~\| journal=Circ Genom Precis Med \| year= 2020 \| volume= 13 \| issue=~~ 6 ~~\| pages= e002911 \| pmid=33164571 \|~~ doi=10.~~1161~~/~~CIRCGEN~~.~~120~~.~~002911 \| pmc=7748043 \| url=https:~~/~~/www~~.~~ncbi~~.~~nlm~~.~~nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=~~ref~~&cmd~~=~~prlinks&id=33164571 }} <~~/~~ref~~> <ref name="~~pmid33495597~~">~~{{cite journal\| author=Harper AR~~, ~~Goel~~ A, ~~Grace C~~, ~~Thomson KL~~, ~~Petersen SE~~, ~~Xu X \| display~~-~~authors~~=~~etal\| title~~=~~Common genetic variants and modifiable risk factors underpin hypertrophic cardiomyopathy susceptibility and expressivity. \| journal~~=~~Nat Genet \| year~~= ~~2021 \| volume~~= ~~53 \| issue~~= ~~2 \| pages~~= ~~135-142 \| pmid~~=~~33495597 \| doi~~=~~10.1038/s41588-020-00764-0 \| pmc~~=~~8240954 \| url~~=~~https~~:~~//www~~.~~ncbi~~.~~nlm~~.~~nih~~.~~gov~~/~~entrez/eutils/elink~~.~~fcgi?dbfrom=pubmed&tool=sumsearch~~.~~org~~/~~cite&retmode=~~ref~~&cmd~~=~~prlinks&id=33495597 }} <~~/~~ref~~> <ref name="~~pmid33495596~~">~~{{cite journal\| author=Tadros R~~, ~~Francis C~~, ~~Xu X~~, ~~Vermeer AMC~~, ~~Harper AR~~, ~~Huurman R \| display-authors=etal\| title=Shared genetic pathways contribute to risk~~ of ~~hypertrophic~~ and ~~dilated cardiomyopathies with opposite directions~~ of ~~effect~~. ~~\| journal=Nat Genet \| year=~~ 2021 ~~\| volume= 53 \| issue= 2 \| pages= 128~~-~~134 \| pmid=33495596 \|~~ doi=10.~~1038~~/~~s41588-020-00762-~~2 ~~\| pmc=7611259 \| url=https~~:~~//www~~.~~ncbi~~.~~nlm~~.~~nih~~.~~gov/entrez~~/~~eutils/elink~~.~~fcgi?dbfrom=pubmed&tool=sumsearch~~.~~org/cite&retmode=ref&cmd=prlinks&id=33495596 }}~~ </ref> <ref ~~name="pmid31504448"~~>~~{{cite journal\| author=Tadros R~~, ~~Tan HL~~, ~~ESCAPE-NET Investigators~~. ~~El Mathari S, Kors JA, Postema PG \| display~~-~~authors=etal\| title=Predicting cardiac electrical response to sodium-channel blockade and Brugada syndrome using polygenic risk scores~~. ~~\| journal=Eur~~ Heart ~~J \| year= 2019 \| volume= 40 \| issue= 37 \| pages= 3097~~-~~3107 \| pmid=31504448 \|~~ doi=10.~~1093~~/~~eurheartj~~/~~ehz435 \| pmc=6769824 \| url=https~~://~~www~~.~~ncbi~~.~~nlm~~.~~nih~~.~~gov~~/~~entrez/eutils/elink~~.~~fcgi?dbfrom=pubmed&tool=sumsearch~~.~~org/cite&retmode=ref&cmd=prlinks&id=31504448 }}~~ </ref>.
			====== Postmortem Genetic Investigation: ======

			* Its use increased recently for research purposes and to inform family members about potentially inherited disease. It investigates the association between genotypes and etiology by autopsy.
			* Genetic studies of sudden deaths in young adults demonstrate that the genetic yield for pathogenic or likely pathogenic variants in autopsy-confirmed sudden cardiac deaths ranged from 13% to 34%.<ref name=":1">Bagnall RD, Weintraub RG, Ingles J, et al. A prospective study of sudden cardiac death among children and young adults. NEnglJMed.2016;374 (25):2441-2452. doi:10.1056/NEJMoa1510687</ref>,<ref>Christiansen SL, Hertz CL, Ferrero-Miliani L, et al. Genetic investigation of 100 heart genes in sudden unexplained death victims in a forensic setting. Eur J HumGenet.2016;24(12):1797-1802. doi:10.1038/ejhg.2016.118</ref>,<ref name=":3">Lahrouchi N, Raju H, Lodder EM, et al.Utility of post-mortem genetic testing in cases of sudden arrhythmic death syndrome.JAmCollCardiol. 2017;69(17):2134-2145. doi:10.1016/j.jacc.2017.02. 046</ref>,<ref>Hansen BL, Jacobsen EM, Kjerrumgaard A, et al. Diagnostic yield in victims of sudden cardiac death and their relatives. Europace. 2020;22(6): 964-971. doi:10.1093/europace/euaa056</ref>-,<ref name=":2">Webster G,Puckelwartz MJ,Pesce LL, et al. Genomic autopsy of sudden deaths in young individuals. JAMA Cardiol. 2021;6(11):1247-1256. doi:10.1001/jamacardio.2021.2789</ref>. These yields are obtained after careful etiologic assessment by comprehensive postmortem investigation (including toxicology) for accurate genotype-phenotype correlation.
			* Sudden arrhythmic death without an apparent cause identified by autopsy is often attributed to arrhythmia syndromes. Of 490 prospectively ascertained sudden cardiac deaths by autopsy in persons aged 1 to 35 years in Australia,<ref name=":1" /> 113 were adjudicated as sudden arrhythmic death syndrome (ie,normal structural heart) and underwent genetic testing. Clinically relevant pathogenic or likely pathogenic variants in cardiac genes were found in 27%; major associated disorders included LQTS, Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy, and CPVT.
			* Another study, 103 sudden cardiac deaths defined by autopsy in persons aged 1 to 44years without known CVD referred from 24 US medical examiners’ offices identified pathogenic or likely pathogenic variants associated with dilated cardiomyopathy, hypertrophic cardiomyopathy, LQTS, and arrhythmogenic right ventricular cardiomyopathy in13%.<ref name=":2" />
			* However, the total number of eligible sudden deaths was not reported, so it is unclear how this applies to all young adults with sudden cardiac death. A single center prospective study in the UK revealed that among 303 referred family members of individuals who had sudden arrhythmic death syndrome, 128 (42%) were diagnosed with inherited cardiac diseases including Brugada syn drome,LQTS,and dilated cardiomyopathy.<ref>Papadakis M, Papatheodorou E,Mellor G, et al. The diagnostic yield of Brugada syndrome after sudden death with normal autopsy.JAmColl Cardiol. 2018;71(11):1204-1214. doi:10.1016/j.jacc. 2018.01.031</ref>

			====== Genetic Testing of Cardiac Arrest Survivors: ======
			Genetic testing of sudden cardiac arrest survivors and additional cardiac screening of family members may detect previously unknown cardiomyopathy, such as dilated cardiomyopathy, hypertrophic cardiomyopathy, or primary arrhythmia syndrome.<ref>Krahn AD, Healey JS, Chauhan V, et al. Systematic assessment of patients with unexplained cardiac arrest: Cardiac Arrest Survivors With Preserved Ejection Fraction Registry (CASPER). Circulation. 2009;120(4):278-285. doi:10.1161/CIRCULATIONAHA.109.853143</ref>,<ref name=":3" />,<ref name=":2" /> Genetic testing of survivors is recommended if the results are likely to aid diagnosis,management, or family screening (classI,level B).<ref>Stiles MK, Wilde AAM, Abrams DJ, et al.2020 APHRS/HRS exper tconsensus statement on the investigation of decedents with sudden unexplained death andpatients with sudden cardiac arrest, and of their families. Heart Rhythm. 2021;18(1):e1-e50. doi:10.1016/j.hrthm.2020.10.010</ref> However, the yield of genetic testing from studies of survivors with clinically unexplained VT/VF targeting arrhythmia and cardiomyopathy genes ranged from 2% to 22%, which is lower than the percentage of pathogenic or likely pathogenic variants in cardiac genes among those who had sudden cardiac death (ie, nonsurvivors).<ref>Mellor G, Laksman ZWM, Tadros R, et al. Genetic testing in the evaluation of unexplained cardiac arrest: from the CASPER(Cardiac Arrest Survivors With Preserved Ejection Fraction Registry). Circ Cardiovasc Genet. 2017;10(3):e001686. doi:10.1161/CIRCGENETICS.116.001686</ref><ref>Visser M, Dooijes D, van der Smagt JJ, et al. Next-generation sequencing of a large gene panel in patients initially diagnosed with idiopathic ventricular fibrillation. Heart Rhythm. 2017;14(7): 1035-1040. doi:10.1016/j.hrthm.2017.01.010</ref><ref>Leinonen JT, Crotti L, Djupsjöbacka A, et al. The genetics underlying idiopathic ventricular fibrillation: a special role for catecholaminergic polymorphic ventricular tachycardia? Int J Cardiol. 2018;250:139-145. doi:10.1016/j.ijcard.2017.10.016</ref><ref>Asatryan B, Schaller A, Seiler J, et al. Usefulness of genetic testing in sudden cardiac arrest survivors with or without previous clinical evidence of heart disease. AmJCardiol. 2019;123 (12):2031-2038. doi:10.1016/j.amjcard.2019.02.061</ref>

Sudden cardiac death prognosis

2026-04-05T12:42:38Z

Prognosis of Sudden Cardiac Death

← Older revision		Revision as of 12:42, 5 April 2026
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	==Prognosis of Sudden Cardiac ~~Death~~==		==Prognosis of Sudden Cardiac Arrest Survivors==
	*Prognosis of in-hospital cardiac arrest is generally better than out-of-hospital [[cardiac arrest]] and the 1-year survival rate of patients who survived to hospital discharge was approximately 25% in the GWTG-R registry.<ref name="ViraniAlonso2020">{{cite journal\|last1=Virani\|first1=Salim S.\|last2=Alonso\|first2=Alvaro\|last3=Benjamin\|first3=Emelia J.\|last4=Bittencourt\|first4=Marcio S.\|last5=Callaway\|first5=Clifton W.\|last6=Carson\|first6=April P.\|last7=Chamberlain\|first7=Alanna M.\|last8=Chang\|first8=Alexander R.\|last9=Cheng\|first9=Susan\|last10=Delling\|first10=Francesca N.\|last11=Djousse\|first11=Luc\|last12=Elkind\|first12=Mitchell S.V.\|last13=Ferguson\|first13=Jane F.\|last14=Fornage\|first14=Myriam\|last15=Khan\|first15=Sadiya S.\|last16=Kissela\|first16=Brett M.\|last17=Knutson\|first17=Kristen L.\|last18=Kwan\|first18=Tak W.\|last19=Lackland\|first19=Daniel T.\|last20=Lewis\|first20=Tené T.\|last21=Lichtman\|first21=Judith H.\|last22=Longenecker\|first22=Chris T.\|last23=Loop\|first23=Matthew Shane\|last24=Lutsey\|first24=Pamela L.\|last25=Martin\|first25=Seth S.\|last26=Matsushita\|first26=Kunihiro\|last27=Moran\|first27=Andrew E.\|last28=Mussolino\|first28=Michael E.\|last29=Perak\|first29=Amanda Marma\|last30=Rosamond\|first30=Wayne D.\|last31=Roth\|first31=Gregory A.\|last32=Sampson\|first32=Uchechukwu K.A.\|last33=Satou\|first33=Gary M.\|last34=Schroeder\|first34=Emily B.\|last35=Shah\|first35=Svati H.\|last36=Shay\|first36=Christina M.\|last37=Spartano\|first37=Nicole L.\|last38=Stokes\|first38=Andrew\|last39=Tirschwell\|first39=David L.\|last40=VanWagner\|first40=Lisa B.\|last41=Tsao\|first41=Connie W.\|title=Heart Disease and Stroke Statistics—2020 Update: A Report From the American Heart Association\|journal=Circulation\|volume=141\|issue=9\|year=2020\|issn=0009-7322\|doi=10.1161/CIR.0000000000000757}}</ref>.Survival after out of hospital cardiac arrest and in hospital cardiac arrest has continued to improve over time according to the guideline.		*Prognosis of in-hospital cardiac arrest is generally better than out-of-hospital [[cardiac arrest]] and the 1-year survival rate of patients who survived to hospital discharge was approximately 25% in the GWTG-R registry.<ref name="ViraniAlonso2020">{{cite journal\|last1=Virani\|first1=Salim S.\|last2=Alonso\|first2=Alvaro\|last3=Benjamin\|first3=Emelia J.\|last4=Bittencourt\|first4=Marcio S.\|last5=Callaway\|first5=Clifton W.\|last6=Carson\|first6=April P.\|last7=Chamberlain\|first7=Alanna M.\|last8=Chang\|first8=Alexander R.\|last9=Cheng\|first9=Susan\|last10=Delling\|first10=Francesca N.\|last11=Djousse\|first11=Luc\|last12=Elkind\|first12=Mitchell S.V.\|last13=Ferguson\|first13=Jane F.\|last14=Fornage\|first14=Myriam\|last15=Khan\|first15=Sadiya S.\|last16=Kissela\|first16=Brett M.\|last17=Knutson\|first17=Kristen L.\|last18=Kwan\|first18=Tak W.\|last19=Lackland\|first19=Daniel T.\|last20=Lewis\|first20=Tené T.\|last21=Lichtman\|first21=Judith H.\|last22=Longenecker\|first22=Chris T.\|last23=Loop\|first23=Matthew Shane\|last24=Lutsey\|first24=Pamela L.\|last25=Martin\|first25=Seth S.\|last26=Matsushita\|first26=Kunihiro\|last27=Moran\|first27=Andrew E.\|last28=Mussolino\|first28=Michael E.\|last29=Perak\|first29=Amanda Marma\|last30=Rosamond\|first30=Wayne D.\|last31=Roth\|first31=Gregory A.\|last32=Sampson\|first32=Uchechukwu K.A.\|last33=Satou\|first33=Gary M.\|last34=Schroeder\|first34=Emily B.\|last35=Shah\|first35=Svati H.\|last36=Shay\|first36=Christina M.\|last37=Spartano\|first37=Nicole L.\|last38=Stokes\|first38=Andrew\|last39=Tirschwell\|first39=David L.\|last40=VanWagner\|first40=Lisa B.\|last41=Tsao\|first41=Connie W.\|title=Heart Disease and Stroke Statistics—2020 Update: A Report From the American Heart Association\|journal=Circulation\|volume=141\|issue=9\|year=2020\|issn=0009-7322\|doi=10.1161/CIR.0000000000000757}}</ref>.Survival after out of hospital cardiac arrest and in hospital cardiac arrest has continued to improve over time according to the guideline.
	*60% to 78% of young adults hospitalized after resuscitation from sudden cardiac arrest do not survive to hospital discharge.<ref>Deasy C, Bray JE, Smith K, Harriss LR, Bernard SA, Cameron P. Out-of-hospital cardiac arrests in young adults in Melbourne,Australia. Resuscitation. 2011;82(7):830-834. doi:10.1016/j.resuscitation.2011. 03.008</ref>,<ref name=":2" />,<ref>Fovaeus H, Holmen J, Mandalenakis Z, Herlitz J, Rawshani A, Castellheim AG.Out-of-hospital cardiac arrest: survival in children and young adults over 30 years,a nationwide registry-based cohort study. Resuscitation. 2024;195:110103. doi:10.1016/ j.resuscitation.2023.110103</ref> This in-hospital mortality rate is similar to that of older adults who were resuscitated to hospitalization (≈65%).<ref>Ricceri S, Salazar JW, Vu AA, Vittinghoff E, Moffatt E, Tseng ZH. Factors predisposing to survival after resuscitation for sudden cardiac arrest. J AmColl Cardiol. 2021;77(19):2353-2362. doi:10.1016/j.jacc.2021.03.299</ref>		*60% to 78% of young adults hospitalized after resuscitation from sudden cardiac arrest do not survive to hospital discharge.<ref>Deasy C, Bray JE, Smith K, Harriss LR, Bernard SA, Cameron P. Out-of-hospital cardiac arrests in young adults in Melbourne,Australia. Resuscitation. 2011;82(7):830-834. doi:10.1016/j.resuscitation.2011. 03.008</ref>,<ref name=":2" />,<ref>Fovaeus H, Holmen J, Mandalenakis Z, Herlitz J, Rawshani A, Castellheim AG.Out-of-hospital cardiac arrest: survival in children and young adults over 30 years,a nationwide registry-based cohort study. Resuscitation. 2024;195:110103. doi:10.1016/ j.resuscitation.2023.110103</ref> This in-hospital mortality rate is similar to that of older adults who were resuscitated to hospitalization (≈65%).<ref>Ricceri S, Salazar JW, Vu AA, Vittinghoff E, Moffatt E, Tseng ZH. Factors predisposing to survival after resuscitation for sudden cardiac arrest. J AmColl Cardiol. 2021;77(19):2353-2362. doi:10.1016/j.jacc.2021.03.299</ref>
			*The 10-year survival rate of sudden cardiac arrest survivors aged 40 years or younger was 90% in an Australian registry.<ref>Andrew E, Nehme Z, Wolfe R, Bernard S, Smith K. Long-term survival following out-of-hospital cardiac arrest. Heart. 2017;103(14):1104-1110. doi: 10.1136/heartjnl-2016-310485</ref>The rate of recurrent arrest (both out of and in the hospital) or death in survivors aged 18 to 39 years in a Swedish registry was approximately 15% a year after the out-of-hospital cardiac arrest.<ref>Hellsén G, Rawshani A, Skoglund K, et al. Predicting recurrent cardiac arrest in individuals surviving out-of-hospital cardiac arrest. Resuscitation. 2023;184:109678. doi:10.1016/j.resuscitation.2022. 109678</ref>

			One-year overall mortality of subcutaneous ICD recipients aged 15 to 34 years was 4.3% in one cohort,90 whereas the VT or VF recurrence rate estimated by subcutaneous ICD recording in secondary prevention recipients (age not reported) in a separate study was 9.9% at 1year and15.8% at 3years.<ref>Boersma LV, Barr CS, Burke MC ,et al; EFFORTLESS and IDE Study Investigators. Performance of the subcutaneous implantable cardioverter-defibrillator in patients with a primary prevention indication with and without a reduced ejection fraction versus patients with a secondary prevention indication. Heart Rhythm. 2017;14(3): 367-375. doi:10.1016/j.hrthm.2016.11.025</ref>
	*<i><u>Factors associated poor [[prognosis]] after in-hospital [[cardiac arrest]] include</u></i>:<ref name="Chan2012">{{cite journal\|last1=Chan\|first1=Paul S.\|title=A Validated Prediction Tool for Initial Survivors of In-Hospital Cardiac Arrest\|journal=Archives of Internal Medicine\|volume=172\|issue=12\|year=2012\|pages=947\|issn=0003-9926\|doi=10.1001/archinternmed.2012.2050}}</ref><ref name="pmid21596693">{{cite journal \|vauthors=Ebell MH, Afonso AM \|title=Pre-arrest predictors of failure to survive after in-hospital cardiopulmonary resuscitation: a meta-analysis \|journal=Fam Pract \|volume=28 \|issue=5 \|pages=505–15 \|date=October 2011 \|pmid=21596693 \|doi=10.1093/fampra/cmr023 \|url=}}</ref>		*<i><u>Factors associated poor [[prognosis]] after in-hospital [[cardiac arrest]] include</u></i>:<ref name="Chan2012">{{cite journal\|last1=Chan\|first1=Paul S.\|title=A Validated Prediction Tool for Initial Survivors of In-Hospital Cardiac Arrest\|journal=Archives of Internal Medicine\|volume=172\|issue=12\|year=2012\|pages=947\|issn=0003-9926\|doi=10.1001/archinternmed.2012.2050}}</ref><ref name="pmid21596693">{{cite journal \|vauthors=Ebell MH, Afonso AM \|title=Pre-arrest predictors of failure to survive after in-hospital cardiopulmonary resuscitation: a meta-analysis \|journal=Fam Pract \|volume=28 \|issue=5 \|pages=505–15 \|date=October 2011 \|pmid=21596693 \|doi=10.1093/fampra/cmr023 \|url=}}</ref>
	:*Age > 70 years old		:*Age > 70 years old

Sudden cardiac death post arrest care and prevention

2026-04-05T12:33:04Z

2022 ESC Guidelines for the management of patients with ventricular arrythymias and the prevention of sudden cardiac death [2]

Show changes

← Older revision		Revision as of 00:52, 16 April 2026
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			== ACS Treatment ==
			Primary Prevention:

	~~{{familytree/start}}~~		'''Equivalent intensity for CHD-risk equivalents (LoE: A):''' Patients with established CHD should be targeted for secondary prevention. Crucially, patients with a '''CHD risk equivalent''' — defined as atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or a Framingham-calculated 10-year risk exceeding 20% — should receive '''the same intensity of risk factor intervention''' as those with overt, clinically apparent CHD.
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| A01 \| \| \| \| \| \|A01=Adult ALL }}~~
	~~{{familytree \| \|,\|-\|-\|-\|v\|-\|-\|-\|-\|-\|-\|+\|-\|-\|-\|-\|-\|-\|-\|-\|-\|.\| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| D01 \| \| D02 \| \| \| \| \| D03 \| \| \| \| \| \| \| \| D05 \| \| \| \|D01=Burkitt Leukemia\|D02=PH-Positive B-ALL\|D03=PH-negative B-ALL\|D05=T-ALL}}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|,\|-\|-\|^\|-\|-\|.\| \| \| \|,\|-\|-\|^\|-\|-\|.\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	{{familytree \| E01 \| \| E02 \| \| E03 \| \| \| \| E04 \| \| E05 \| \| \| \| E06 \| \| \|E01=R-hyper CVAD<br> DA-R-EPOCH\|E02=Chemotherapt+TKI <br> Blinatumomab+TKI\|E03=Younger adults\|E04=Older Adults\|E05=ETP\|E06=Non ETP}}
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \|}}~~
	{{familytree \| \|!\| \| \| \|!\| \| \| F01 \| \| \| \| F02 \| \| F03 \| \| \| \| F04 \| \|F01=Chemotherapy+<br>blinatumomab\|F02=Chemotherapy+<br>blinatumumab+InO <br>Chemotherapy-free blinatumomab + InO\|F03=Chemotherapy+pegAsp+<br>nelarabine+venetoclax\|F04=Chemotherapy+pegAsp+<br>nelarabine}}
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|!\| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| \|!\| \| \| \| \| \|!\| \| \| }}~~
	~~{{familytree \| \|`\|-\|-\|-\|^\|-\|-\|-\|^\|-\|-\|v\|-\|-\|^\|-\|-\|-\|^\|-\|-\|-\|-\|-\|~~'~~\| \| \| }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| G01 \| \| \| \| \| \| \| \| \| \| \| \| \| \|G01=<div style="float: left; text~~-~~align~~: ~~left; height~~: ~~3em; width: 20em;">~~ '''~~Measurable residual disease monitoring~~'''~~<br> </div>}} }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \| \| \| \| \| }}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| H01 \| \| \| \| \| \| \| \| \| \| \| \| \| \| \|H01=<div style="float: left; text~~-~~align: left;">~~'''~~Alloegenic hematopoietic stem cell transplant~~''' ~~<br>•Ph-like ALL~~ with ~~CRLF2 and JAK vairants<br>•High-risk cytogenetics in B-ALL<br>•High-risk Ph-positive B-ALL: IZKF1 genotype<br>•T-ALL: ETP-ALL<br>•Persistent measurable residual disease by NGS<br> </div>}}~~
	~~{{familytree/end}}~~