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Tuberculosis electrocardiogram

SophiaSaad — Tue, 04 Aug 2026 22:03:02 GMT

User:Nehal Eid

Nehal Eid — Tue, 04 Aug 2026 20:54:44 GMT

← Older revision		Revision as of 20:54, 4 August 2026
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			[[File:WhatsApp Image 2025-01-21 at 3.49.56 PM (2).jpg\|thumb\|Nehal Eid, M.D.]]
	[[User:Nehal Eid\|Nehal Eid, M.D.]][mailto:nehalelsaeed98@gmail.com]		[[User:Nehal Eid\|Nehal Eid, M.D.]][mailto:nehalelsaeed98@gmail.com]

File:WhatsApp Image 2025-01-21 at 3.49.56 PM (2).jpg

Nehal Eid — Tue, 04 Aug 2026 20:47:56 GMT

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Nehal Eid, M.D.

User:Nehal Eid

Nehal Eid — Tue, 04 Aug 2026 20:43:24 GMT

← Older revision		Revision as of 20:43, 4 August 2026
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	[[User:Nehal Eid\|Nehal Eid, M.D.]][mailto:~~nehaleid.md~~@gmail.com]		[[User:Nehal Eid\|Nehal Eid, M.D.]][mailto:nehalelsaeed98@gmail.com]

	== Education ==		== Education ==

Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Follow-Up and Surveillance

Nehal Eid — Tue, 04 Aug 2026 20:35:19 GMT

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Tuberculosis electrocardiogram

Nehal Eid — Tue, 04 Aug 2026 20:09:13 GMT

Overview

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User:Nehal Eid

Nehal Eid — Tue, 04 Aug 2026 19:46:39 GMT

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(3 intermediate revisions by the same user not shown)
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	[[User:Nehal Eid\|Nehal Eid, M.D.]][mailto:~~nehalelsaeed98~~@gmail.com]		[[User:Nehal Eid\|Nehal Eid, M.D.]][mailto:nehaleid.md@gmail.com]

	== Education ==		== Education ==
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	# Alhaque Roomi, M. H., '''Eid, N'''., & Visaria, A. (2025). Association Between Sleep Duration and Angina Characteristics in United Sta<span id="ctl00_rpPublication_ctl02_lblPublicationAuthors"></span><span id="ctl00_rpPublication_ctl03_lblPublicationAuthors"></span>tes Adults. ''American Journal of Medicine Open'', ''14'', 100109. <nowiki>https://doi.org/10.1016/j.ajmo.2025.100109</nowiki>		# Alhaque Roomi, M. H., '''Eid, N'''., & Visaria, A. (2025). Association Between Sleep Duration and Angina Characteristics in United Sta<span id="ctl00_rpPublication_ctl02_lblPublicationAuthors"></span><span id="ctl00_rpPublication_ctl03_lblPublicationAuthors"></span>tes Adults. ''American Journal of Medicine Open'', ''14'', 100109. <nowiki>https://doi.org/10.1016/j.ajmo.2025.100109</nowiki>
			# Mohammed O, Kim SH, Karthikeyan A, '''Eid N''', Reimann RS, Kanniyan AS, Joy B, Dascălu AC, Nanna GJ, Romero-Acero LM, Nanna M. Effica<span id="ctl00_rpPublication_ctl02_lblPublicationAuthors"></span><span id="ctl00_rpPublication_ctl03_lblPublicationAuthors"></span>cy and Safety of SGLT-2 Inhibitors in Patients with Uncontrolled or Resistant Hypertension: A Pilot Meta-Analysis of Randomized Clinical Trials. High Blood Press Cardiovasc Prev. 2026 Jul 31. doi: 10.1007/s40292-026-00817-1. Epub ahead of print. PMID: 42538499.

			== Wikidoc contributions ==
	~~'''~~Wikidoc contributions~~:'''~~

	[[Intravenous drug use (recreational)]]		[[Intravenous drug use (recreational)]]
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	[[Cardiac resynchronization therapy device management]]		[[Cardiac resynchronization therapy device management]]

			[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER)]]

	[[Cosibelimab-ipdl]]		[[Cosibelimab-ipdl]]

	[[Olezarsen]]		[[Olezarsen]]

Tuberculosis electrocardiogram

SophiaSaad — Tue, 04 Aug 2026 18:54:59 GMT

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Percutaneous Intervention for Coarctation of the Aorta

Anum Ijaz — Tue, 04 Aug 2026 17:27:30 GMT

Associated coronary risk

← Older revision		Revision as of 17:27, 4 August 2026
(One intermediate revision by the same user not shown)
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	{{CMG}}; {{AE}} {{AIJ}}		{{CMG}}; {{AE}} {{AIJ}}

	==Overview==		==Overview==
	Percutaneous treatment of [[coarctation of the aorta]] (CoA) comprises [[balloon angioplasty]] (BA) and endovascular [[stent]] implantation (SI). Both are established alternatives to open surgical repair for discrete native and recurrent CoA in older children, adolescents, and adults. Stent implantation is the preferred percutaneous modality over BA alone, offering superior hemodynamic results, lower aneurysm rates, and fewer acute complications. Current ACC/AHA and EACTS/STS guidelines endorse endovascular stenting alongside surgery as a Class I option for adults with significant CoA and [[hypertension]]. Surgical repair remains the reference standard for neonates, infants, and complex arch anatomy, whereas percutaneous intervention is the treatment of choice for most recurrent CoA and an increasingly accepted first-line option for discrete native CoA in appropriately sized patients.		Percutaneous treatment of [[coarctation of the aorta]] (CoA) comprises [[balloon angioplasty]] (BA) and endovascular [[stent]] implantation (SI). Both are established alternatives to open surgical repair for discrete native and recurrent CoA in older children, adolescents, and adults. Stent implantation is the preferred percutaneous modality over BA alone, offering superior hemodynamic results, lower aneurysm rates, and fewer acute complications. Current ACC/AHA and EACTS/STS guidelines endorse endovascular stenting alongside surgery as a Class I option for adults with significant CoA and [[hypertension]]. Surgical repair remains the reference standard for neonates, infants, and complex arch anatomy, whereas percutaneous intervention is the treatment of choice for most recurrent CoA and an increasingly accepted first-line option for discrete native CoA in appropriately sized patients.
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	Percutaneous Intervention is indicated for '''significant CoA''', defined by upper-extremity [[hypertension]] (resting, ambulatory, or exercise-induced) or [[left ventricular hypertrophy]] combined with one of the gradient/anatomic criteria below.<ref name="2022Aortic">{{cite journal \|author=Isselbacher EM, Preventza O, Hamilton Black J III, et al \|title=2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines \|journal=Journal of the American College of Cardiology \|year=2022 \|volume=80 \|issue=24 \|pages=e223-e393 \|doi=10.1016/j.jacc.2022.08.004}}</ref><ref name="2025ACHD" />		Percutaneous Intervention is indicated for '''significant CoA''', defined by upper-extremity [[hypertension]] (resting, ambulatory, or exercise-induced) or [[left ventricular hypertrophy]] combined with one of the gradient/anatomic criteria below.<ref name="2022Aortic">{{cite journal \|author=Isselbacher EM, Preventza O, Hamilton Black J III, et al \|title=2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines \|journal=Journal of the American College of Cardiology \|year=2022 \|volume=80 \|issue=24 \|pages=e223-e393 \|doi=10.1016/j.jacc.2022.08.004}}</ref><ref name="2025ACHD" />

	{\| class="wikitable"		{\| class="wikitable"
	\|~~+ Criteria defining hemodynamically significant coarctation~~		\|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
	! Diagnostic test !! Index !! Threshold		\| Diagnostic test
			\|Index
			\|Threshold
	\|-		\|-
	\| Upper- vs. lower-extremity BP \|\| Systolic BP difference \|\| >20 mmHg		\| Upper- vs. lower-extremity BP \|\| Systolic BP difference \|\| >20 mmHg
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	===Indications for Stent Implantation (AHA Scientific Statement)===		===Indications for Stent Implantation (AHA Scientific Statement)===

	{\| class="wikitable"		{\| class="wikitable"
	\|+		\|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
	! No. !! Indication		\| No.
			\|Indication
	\|-		\|-
	\| 1 \|\| Recurrent CoA in patients of sufficient size, with a stent expandable to adult size, and transcatheter gradient >20 mmHg		\| 1 \|\| Recurrent CoA in patients of sufficient size, with a stent expandable to adult size, and transcatheter gradient >20 mmHg
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	AHA Scientific Statement 2011, reproduced in Goldstein & Kreutzer, JACC 2021<ref name="Goldstein2021" />		AHA Scientific Statement 2011, reproduced in Goldstein & Kreutzer, JACC 2021<ref name="Goldstein2021" />
	===Indications for Balloon Angioplasty (AHA Scientific Statement)===		===Indications for Balloon Angioplasty (AHA Scientific Statement)===
	{\| class="wikitable"		{\| class="wikitable"
	\|+		\|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
	! No. !! Indication		\| No.
			\| Indication
	\|-		\|-
	\| 1 \|\| Recoarctation with gradient >20 mmHg and suitable anatomy, irrespective of age		\| 1 \|\| Recoarctation with gradient >20 mmHg and suitable anatomy, irrespective of age
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	* '''Success criteria''' vary by source: the EACTS/STS 2024 guideline defines success by an acceptably low residual stenosis and residual gradient <!-- exact EACTS residual-stenosis/gradient thresholds TRUNCATED in audits; verify against Czerny et al., EJCTS 2024 -->; a meta-analysis reported that stenting achieves a residual gradient ≤20 mmHg in ~99.5% of cases vs. ~89.5% with BA alone.<ref name="EACTS2024" />		* '''Success criteria''' vary by source: the EACTS/STS 2024 guideline defines success by an acceptably low residual stenosis and residual gradient <!-- exact EACTS residual-stenosis/gradient thresholds TRUNCATED in audits; verify against Czerny et al., EJCTS 2024 -->; a meta-analysis reported that stenting achieves a residual gradient ≤20 mmHg in ~99.5% of cases vs. ~89.5% with BA alone.<ref name="EACTS2024" />
	* Further dilation may be performed per hemodynamic/angiographic findings; additional overlapping covered stents may be placed for endoleak or wall injury proximal/distal to the initial stent.<ref name="Taggart2016" />		* Further dilation may be performed per hemodynamic/angiographic findings; additional overlapping covered stents may be placed for endoleak or wall injury proximal/distal to the initial stent.<ref name="Taggart2016" />
			[[File:Percutaneous Intervention of coractation .png\|400px\|thumb\|right\|The image shows severe discrete native coarctation, the immediate angiographic result after stent implantation, and follow-up MRI/CT confirming stent position without recoarctation. <ref>Thanopoulos, B. V., Eleftherakis, N., Tzanos, K., Skoularigis, I., & Triposkiadis, F. (2008). Stent implantation for adult aortic coarctation. ''Journal of the American College of Cardiology'', ''52''(22), 1815–1816. <nowiki>https://doi.org/10.1016/j.jacc.2008.03.068</nowiki></ref>]]
	===Post-procedural antiplatelet/anticoagulation protocol===		===Post-procedural antiplatelet/anticoagulation protocol===
	* [[Aspirin]] daily for a minimum of '''6 months'''.<ref name="Hamdan2001" /><ref name="Taggart2016" />		* [[Aspirin]] daily for a minimum of '''6 months'''.<ref name="Hamdan2001" /><ref name="Taggart2016" />
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	* Given the high prevalence of ASCVD risk factors in this population, the 2025 ACC/AHA guideline recommends a target systolic BP <!-- specific SBP target TRUNCATED in both audits (both end at "target systolic BP"); verify against Gurvitz et al., JACC 2025 --> for these patients.<ref name="2025ACHD" />		* Given the high prevalence of ASCVD risk factors in this population, the 2025 ACC/AHA guideline recommends a target systolic BP <!-- specific SBP target TRUNCATED in both audits (both end at "target systolic BP"); verify against Gurvitz et al., JACC 2025 --> for these patients.<ref name="2025ACHD" />

	===Associated coronary risk===		===Associated coronary artery risk===
	The 2025 ACC/AHA guideline emphasizes that premature coronary artery disease in CoA patients is multifactorial, driven by hypertension, hyperlipidemia, type 2 diabetes, and inherent vascular dysfunction; aggressive cardiovascular risk-factor modification is warranted.<ref name="2025ACHD" />		The 2025 ACC/AHA guideline emphasizes that premature coronary artery disease in CoA patients is multifactorial, driven by hypertension, hyperlipidemia, type 2 diabetes, and inherent vascular dysfunction; aggressive cardiovascular risk-factor modification is warranted.<ref name="2025ACHD" />

	===Surveillance after percutaneous intervention===		===Surveillance after percutaneous intervention===
	{\| class="wikitable"		{\| class="wikitable"
	\|~~+ Recommended follow~~-~~up intervals (months) by physiological stage~~		\|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
	! Test !! Stage A !! Stage B !! Stage C !! Stage D		\| Test
			\| Stage A
			\| Stage B
			\| Stage C
			\| Stage D
	\|-		\|-
	\| Acute [[CAD]]\|\| 24 \|\| 24 \|\| 6–12 \|\| 3–6		\| Acute [[CAD]]\|\| 24 \|\| 24 \|\| 6–12 \|\| 3–6
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	<ref name="2018ACHD" />		<ref name="2018ACHD" />

	'''Note:''' The 2025 ACC/AHA ACHD guideline updates some intervals: Stage C ACHD cardiologist visits are now every 12 months (previously 6–12), and Stage D ECG and ACHD visit are now every 6 months (previously 12 and 3–6, respectively). The 2025 table includes only three rows (ACHD visit, ECG, TTE) and does not specify CMR/CCT or exercise-test intervals; the 2018 recommendations for those modalities should be followed until updated. The 2025 guideline additionally notes that exercise testing every 5 years is reasonable in CoA patients with hypertension already on antihypertensive therapy, to assess adequacy of BP control.<ref name="2025ACHD" />

	'''ACC/AHA Appropriate Use Criteria for post-stent imaging:'''		'''ACC/AHA Appropriate Use Criteria for post-stent imaging:'''

EVAR

Anum Ijaz — Tue, 04 Aug 2026 17:03:56 GMT

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Thoracic Endovascular Aortic Repair (TEVAR)

Anum Ijaz — Tue, 04 Aug 2026 16:23:40 GMT

← Older revision		Revision as of 16:23, 4 August 2026
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	* '''Frozen elephant trunk (FET)''': A single-stage hybrid operation combining total aortic arch replacement (under circulatory arrest) with antegrade delivery of a stent-graft into the descending aorta. The stent-graft component provides a landing zone for potential future distal TEVAR extension. Early series report 30-day mortality of 5%, stroke of 5%, and transient SCI of 5%.<ref name="chu2019">{{cite journal\|author=Chu MWA, Losenno KL, Dubois LA, et al.\|title=Early Clinical Outcomes of Hybrid Arch Frozen Elephant Trunk Repair With the Thoraflex Hybrid Graft\|journal=The Annals of Thoracic Surgery\|year=2019\|volume=107\|issue=1\|pages=47-53\|doi=10.1016/j.athoracsur.2018.07.091}}</ref>		* '''Frozen elephant trunk (FET)''': A single-stage hybrid operation combining total aortic arch replacement (under circulatory arrest) with antegrade delivery of a stent-graft into the descending aorta. The stent-graft component provides a landing zone for potential future distal TEVAR extension. Early series report 30-day mortality of 5%, stroke of 5%, and transient SCI of 5%.<ref name="chu2019">{{cite journal\|author=Chu MWA, Losenno KL, Dubois LA, et al.\|title=Early Clinical Outcomes of Hybrid Arch Frozen Elephant Trunk Repair With the Thoraflex Hybrid Graft\|journal=The Annals of Thoracic Surgery\|year=2019\|volume=107\|issue=1\|pages=47-53\|doi=10.1016/j.athoracsur.2018.07.091}}</ref>
	* '''Two-stage hybrid arch repair''': First-stage total arch replacement with conventional elephant trunk, followed by second-stage TEVAR using the elephant trunk as a proximal landing zone. A series of 55 patients reported 0% in-hospital mortality for both stages and 5-year survival of 67%.<ref name="yoshitake2019">{{cite journal\|author=Yoshitake A, Iida Y, Yamazaki M, et al.\|title=Midterm Results of 2-Stage Hybrid Arch Repair for Extensive Aortic Arch Aneurysms\|journal=Annals of Vascular Surgery\|year=2019\|volume=56\|pages=97-102\|doi=10.1016/j.avsg.2018.07.063}}</ref>		* '''Two-stage hybrid arch repair''': First-stage total arch replacement with conventional elephant trunk, followed by second-stage TEVAR using the elephant trunk as a proximal landing zone. A series of 55 patients reported 0% in-hospital mortality for both stages and 5-year survival of 67%.<ref name="yoshitake2019">{{cite journal\|author=Yoshitake A, Iida Y, Yamazaki M, et al.\|title=Midterm Results of 2-Stage Hybrid Arch Repair for Extensive Aortic Arch Aneurysms\|journal=Annals of Vascular Surgery\|year=2019\|volume=56\|pages=97-102\|doi=10.1016/j.avsg.2018.07.063}}</ref>
			[[File:Hybrid technique TEVAR.png\|400px\|thumb\|right\|The following figure from a JACC State-of-the-Art Review shows sequential CT imaging (preoperative, postoperative, and 1-year follow-up) of a type A dissection treated with the frozen elephant trunk technique, demonstrating progressive aortic remodeling and false lumen thrombosis <ref>Vilacosta, I., San Román, J. A., di Bartolomeo, R., Eagle, K., Estrera, A. L., Ferrera, C., Kaji, S., Nienaber, C. A., Riambau, V., Schäfers, H.-J., Serrano, F. J., Song, J.-K., & Maroto, L. (2021). Acute aortic syndrome revisited: JACC state-of-the-art review. ''Journal of the American College of Cardiology'', ''78''(21), 2106–2125. <nowiki>https://doi.org/10.1016/j.jacc.2021.09.022</nowiki></ref>]]
	* '''Debranching with TEVAR''': Surgical revascularization of arch vessels (carotid-carotid bypass, carotid-subclavian bypass) followed by TEVAR extending into the arch, reserved for patients who are not candidates for open arch replacement.		* '''Debranching with TEVAR''': Surgical revascularization of arch vessels (carotid-carotid bypass, carotid-subclavian bypass) followed by TEVAR extending into the arch, reserved for patients who are not candidates for open arch replacement.

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	== Devices ==		== Devices ==
	Several FDA-approved thoracic stent-graft platforms are available:		Several FDA-approved thoracic stent-graft platforms are available:
	{\| class="wikitable"		{\| class="wikitable"
	\|-		\|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
	! Device !! Graft Material !! Stent Frame !! Notes		\|Device
			\|Graft Material
			\|Stent Frame
			\|Notes
	\|-		\|-
	\| Gore TAG / Conformable TAG (CTAG) \|\| ePTFE \|\| Nitinol exoskeleton \|\| Most widely used device (~60% of BTAI repairs); the CTAG with ACTIVE CONTROL system allows staged deployment and angulation control<ref name="mariani2019">{{cite journal \|author=Mariani C, van der Weijde E, Smith T, et al. \|title=The GORE TAG Conformable Thoracic Stent Graft With the New ACTIVE CONTROL Deployment System \|journal=Journal of Vascular Surgery \|year=2019 \|volume=70 \|issue=2 \|pages=432-437 \|doi=10.1016/j.jvs.2018.11.015}}</ref>		\| Gore TAG / Conformable TAG (CTAG) \|\| ePTFE \|\| Nitinol exoskeleton \|\| Most widely used device (~60% of BTAI repairs); the CTAG with ACTIVE CONTROL system allows staged deployment and angulation control<ref name="mariani2019">{{cite journal \|author=Mariani C, van der Weijde E, Smith T, et al. \|title=The GORE TAG Conformable Thoracic Stent Graft With the New ACTIVE CONTROL Deployment System \|journal=Journal of Vascular Surgery \|year=2019 \|volume=70 \|issue=2 \|pages=432-437 \|doi=10.1016/j.jvs.2018.11.015}}</ref>
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	Endoleaks occur in up to 20–30% of patients after TEVAR and represent the most important risk factor for aortic rupture.<ref name="ripley2025" /><ref name="zierler2018">{{cite journal \|author=Zierler RE, Jordan WD, Lal BK, et al. \|title=The Society for Vascular Surgery Practice Guidelines on Follow-Up After Vascular Surgery Arterial Procedures \|journal=Journal of Vascular Surgery \|year=2018 \|volume=68 \|issue=1 \|pages=256-284 \|doi=10.1016/j.jvs.2018.04.018}}</ref> The 2022 ACC/AHA guidelines classify endoleaks into five types:<ref name="isselbacher2022" />		Endoleaks occur in up to 20–30% of patients after TEVAR and represent the most important risk factor for aortic rupture.<ref name="ripley2025" /><ref name="zierler2018">{{cite journal \|author=Zierler RE, Jordan WD, Lal BK, et al. \|title=The Society for Vascular Surgery Practice Guidelines on Follow-Up After Vascular Surgery Arterial Procedures \|journal=Journal of Vascular Surgery \|year=2018 \|volume=68 \|issue=1 \|pages=256-284 \|doi=10.1016/j.jvs.2018.04.018}}</ref> The 2022 ACC/AHA guidelines classify endoleaks into five types:<ref name="isselbacher2022" />

	{\| class="wikitable"		{\| class="wikitable"
	\|-		\|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
	! Type !! Mechanism !! Management		\| Type
			\|Mechanism
			\|Management
	\|-		\|-
	\| I (IA proximal / IB distal) \|\| Leak at attachment site; persistent sac pressurization \|\| Represents treatment failure; requires immediate intervention		\| I (IA proximal / IB distal) \|\| Leak at attachment site; persistent sac pressurization \|\| Represents treatment failure; requires immediate intervention
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	\| V (endotension) \|\| Sac expansion without an identifiable endoleak \|\| Continued surveillance; intervention if progressive		\| V (endotension) \|\| Sac expansion without an identifiable endoleak \|\| Continued surveillance; intervention if progressive
	\|}		\|}

			[[File:Endoleaks EVAR.png\|400px\|right\|This figure demonstrates triple-phase CTA imaging of Type IA, Type II, and Type III endoleaks after endovascular aortic repair, showing noncontrast, arterial, and delayed venous phases for each type <ref>(N.d.). Jamanetwork.Com. Retrieved 4 August 2026, from <nowiki>https://jamanetwork.com/journals/jamasurgery/article-abstract/2807722?utm_source=openevidence&utm_medium=referral</nowiki></ref>]]

	Type I and III endoleaks are treatment failures requiring urgent reintervention.<ref name="zierler2018" /> In a series of 82 TAA patients treated with TEVAR, 11% required reintervention at 60 months, primarily for type I endoleaks (7%).<ref name="upchurch2021" />		Type I and III endoleaks are treatment failures requiring urgent reintervention.<ref name="zierler2018" /> In a series of 82 TAA patients treated with TEVAR, 11% required reintervention at 60 months, primarily for type I endoleaks (7%).<ref name="upchurch2021" />

File:Percutaneous Intervention of coractation .png

Anum Ijaz — Tue, 04 Aug 2026 15:57:39 GMT

Anum Ijaz uploaded File:Percutaneous Intervention of coractation .png

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Percutaneous Intervention for Coarctation of the Aorta

Anum Ijaz — Tue, 04 Aug 2026 15:50:09 GMT

← Older revision		Revision as of 15:50, 4 August 2026
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	~~{{Interventions infobox~~
	~~\| Name = Percutaneous Intervention of coarctation of aorta~~
	~~\| Image = \|~~
	~~Caption = \|~~
	~~ICD10 = \|~~
	~~ICD9 = {{ICD9proc\|39.51}}, {{ICD9proc\|39.52}}, {{ICD9proc\|39.7}} \|~~
	~~MeshID = \|~~
	~~OPS301 = \|~~
	~~OtherCodes = \|~~
	~~HCPCSlevel2 =~~
	}}

			{{CMG}}; {{AE}} {{AIJ}}
	{{CMG}} {{AE}} {{AIJ}}

	==Overview==		==Overview==
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	! Test !! Stage A !! Stage B !! Stage C !! Stage D		! Test !! Stage A !! Stage B !! Stage C !! Stage D
	\|-		\|-
	\| ~~ACHD cardiologist visit~~ \|\| 24 \|\| 24 \|\| 6–12 \|\| 3–6		\| Acute [[CAD]]\|\| 24 \|\| 24 \|\| 6–12 \|\| 3–6
	\|-		\|-
	\| ECG \|\| 24 \|\| 24 \|\| 12 \|\| 12		\| [[ECG]]\|\| 24 \|\| 24 \|\| 12 \|\| 12
	\|-		\|-
	\| TTE \|\| 24 \|\| 24 \|\| 12 \|\| 12		\| [[TTE]]\|\| 24 \|\| 24 \|\| 12 \|\| 12
	\|-		\|-
	\| CMR/CCT \|\| 36–60 \|\| 36–60 \|\| 12–24 \|\| 12–24		\| [[CMR]]/CCT \|\| 36–60 \|\| 36–60 \|\| 12–24 \|\| 12–24
	\|-		\|-
	\| Exercise test \|\| 36 \|\| 24 \|\| 24 \|\| 12		\| Exercise test \|\| 36 \|\| 24 \|\| 24 \|\| 12
	\|}		\|}
	Abbreviations: CMR = Cardiovascular magnetic resonance; CCT= Cardiovascular computed topography.		Abbreviations: CMR = [[Cardiovascular magnetic resonance imaging (CMR)\|Cardiovascular magnetic resonance]]; CCT= Cardiovascular computed topography.

	<ref name="2018ACHD" />		<ref name="2018ACHD" />

Diabetes mellitus type 1 Diagnostic study of choice

Anum Ijaz — Tue, 04 Aug 2026 14:30:08 GMT

@@ Line 98: / Line 98: @@
 '''Abbreviations:''' DKA = [[diabetic ketoacidosis]]; FPG = [[Fasting plasma glucose|fasting plasma glucose]]; GAD65 = glutamic acid decarboxylase 65; HbA1c = [[glycosylated hemoglobin]]; IA-2 = insulinoma-associated antigen 2; IAA = insulin autoantibodies; LADA = latent autoimmune diabetes in adults; MODY = maturity-onset diabetes of the young; T1DM = type 1 diabetes mellitus; T2DM = type 2 diabetes mellitus; ZnT8 = zinc transporter 8.
-===Clinical Pearls===
 ==References==

Diabetes mellitus type 1 medical therapy

Anum Ijaz — Tue, 04 Aug 2026 14:22:23 GMT

← Older revision		Revision as of 14:22, 4 August 2026
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	Individuals with T1DM should never have insulin completely discontinued in the hospital setting due to the risk of DKA; basal insulin must be continued even when NPO. CGM use in the hospital is increasingly supported.<ref name="pmid_ada2026_s16"/>		Individuals with T1DM should never have insulin completely discontinued in the hospital setting due to the risk of DKA; basal insulin must be continued even when NPO. CGM use in the hospital is increasingly supported.<ref name="pmid_ada2026_s16"/>

	~~===Clinical Pearls===~~

	* Never discontinue basal insulin in a patient with T1DM, even when NPO or during illness — this is the most common precipitant of DKA.
	* Euglycemic DKA (~10% of DKA presentations) can occur with near-normal glucose, particularly with SGLT2 inhibitor use, pregnancy, or reduced carbohydrate intake.<ref name="pmid_ada2026_s16"/>
	* The "500 rule" (ICR = 500 ÷ TDD) and "1800 rule" (ISF = 1800 ÷ TDD) are starting estimates only; titrate based on individual response and CGM data.
	* CV ≤36% on CGM is a key safety metric; higher variability is associated with increased severe hypoglycemia risk.<ref name="pmid_jama2026"/><ref name="pmid34593612"/>
	* Overbasalization — suspect when there is a large bedtime-to-morning glucose differential, frequent nocturnal hypoglycemia, or high glycemic variability; redistribute insulin toward prandial dosing.<ref name="pmid_ada2026_s9"/>
	* Statin therapy should be considered for all adults with T1DM aged ≥40 years and for younger adults with additional risk factors or long disease duration (≥20 years).<ref name="pmid34593612"/><ref name="pmid_manrique2024"/>

	~~===Common Pitfalls===~~

	* '''Misdiagnosis as type 2 diabetes in adults:''' Adult-onset T1DM is frequently misclassified; check islet autoantibodies and C-peptide when clinical features are atypical (normal BMI, rapid progression to insulin requirement, DKA at presentation).
	* '''Failure to prescribe glucagon:''' All patients on insulin should have glucagon prescribed; caregivers must be trained in its use.
	* '''Inadequate DKA transition:''' Stopping IV insulin without adequate subcutaneous insulin overlap (30–60 minutes) leads to DKA recurrence.
	* '''Ignoring psychosocial burden:''' Diabetes distress, burnout, and disordered eating are highly prevalent and directly impair glycemic outcomes; routine screening is essential.
	* '''Delaying technology adoption:''' CGM and AID systems have robust evidence for benefit across all age groups; cost and access barriers should be actively addressed rather than accepted.
	* '''Using SGLT2 inhibitors without DKA risk mitigation:''' If used off-label, requires structured education on ketone monitoring, insulin dose maintenance, and sick-day rules.
	* '''Applying type 2 diabetes cardiovascular risk calculators to T1DM:''' Standard ASCVD risk calculators may underestimate risk in T1DM; T1DM-specific risk tools should be considered when available.

	==References==		==References==

Downstream TFIIB recognition element gene transcriptions

Marshallsumter — Tue, 04 Aug 2026 06:43:58 GMT

dBRE samplings

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	48. GTTTTTT IDC 1 (~~3396~~)		48. GTTTTTT IDC 1 (3386)

	(c) (C/T) A (A/C/T) (A/C) (A/C) (A/C) (A/C)		(c) (C/T) A (A/C/T) (A/C) (A/C) (A/C) (A/C)
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	4. (1) np +30 TGGGGTG +36 ± 50 1		4. (1) np +30 TGGGGTG +36 ± 50 1
	5. TGGGTTA 0		5. TGGGTTA 0
	6. TGGGTTG 0		6. TGGGTTG IDC 1 (10068)
	7. TGGTATA 0		7. TGGTATA 0
	8. TGGTATG 0		8. TGGTATG 0
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	48. TTTTTTG IDC 2 (3386) (115350)		48. TTTTTTG IDC 1 (3386)
			49. TTTTTTG IDC 1 (115350)

	(ci) (A/C) (A/C) (A/C) (A/C) (A/C/T) A (C/T)		(ci) (A/C) (A/C) (A/C) (A/C) (A/C/T) A (C/T)

User:Paris Tran

Basir Gill — Mon, 03 Aug 2026 23:14:09 GMT

User account Paris Tran was created by Basir Gill and password was sent by email DrKumo's intern

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Basir Gill — Mon, 03 Aug 2026 19:30:17 GMT

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Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Follow-Up and Surveillance

Nehal Eid — Mon, 03 Aug 2026 19:19:28 GMT

Created page with "{{CMG}}; {{AE}} {{Nehal}}"

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{{CMG}}; {{AE}} {{Nehal}}

Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) natural history, complications and prognosis

Nehal Eid — Mon, 03 Aug 2026 19:17:01 GMT

Prognosis after M-TEER

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			{{CMG}}; {{AE}} {{Nehal}}
	__NOTOC__		__NOTOC__

	==Natural history, complications, and prognosis==		==Natural history, complications, and prognosis==

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	===Prognosis after M-TEER===		===Prognosis after M-TEER===
	Mitral transcatheter edge-to-edge repair (M-TEER) reduces, but does not eliminate, the event burden associated with HFrEF and significant SMR.		Mitral transcatheter edge-to-edge repair (M-TEER) reduces, but does not eliminate, the event burden associated with HFrEF and significant SMR.<ref name="Stone2023" />

	{\| class="wikitable"		{\| class="wikitable"
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	\| 91.5%		\| 91.5%
	\| HR 0.53; 95% CI 0.44–0.64		\| HR 0.53; 95% CI 0.44–0.64
	\|}		\|}Most of the hospitalization benefit occurred during the first 3 years and most of the mortality benefit during the first 2 years. Interpretation of later curve convergence is limited by progression of the underlying cardiomyopathy and protocol-permitted crossover from the control group after 2 years.<ref name="Stone2023" />
	~~<ref name="Stone2023" />~~

	Most of the hospitalization benefit occurred during the first 3 years and most of the mortality benefit during the first 2 years. Interpretation of later curve convergence is limited by progression of the underlying cardiomyopathy and protocol-permitted crossover from the control group after 2 years.<ref name="Stone2023" />

	MITRA-FR did not demonstrate a reduction in death or unplanned heart-failure hospitalization at 1 or 2 years. This neutral result, compared with COAPT, indicates that the COAPT mortality and hospitalization effects should not be generalized to every SMR phenotype.<ref name="Obadia2018">{{cite journal \|author=Obadia JF, Messika-Zeitoun D, Leurent G, et al. \|title=Percutaneous Repair or Medical Treatment for Secondary Mitral Regurgitation \|journal=The New England Journal of Medicine \|year=2018 \|volume=379 \|issue=24 \|pages=2297-2306 \|doi=10.1056/NEJMoa1805374}}</ref>		MITRA-FR did not demonstrate a reduction in death or unplanned heart-failure hospitalization at 1 or 2 years. This neutral result, compared with COAPT, indicates that the COAPT mortality and hospitalization effects should not be generalized to every SMR phenotype.<ref name="Obadia2018">{{cite journal \|author=Obadia JF, Messika-Zeitoun D, Leurent G, et al. \|title=Percutaneous Repair or Medical Treatment for Secondary Mitral Regurgitation \|journal=The New England Journal of Medicine \|year=2018 \|volume=379 \|issue=24 \|pages=2297-2306 \|doi=10.1056/NEJMoa1805374}}</ref>

Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) natural history, complications and prognosis

Nehal Eid — Mon, 03 Aug 2026 19:10:10 GMT

Created page with "__NOTOC__ ==Natural history, complications, and prognosis== ===Natural history during guideline-directed medical therapy=== Ventricular secondary mitral regurgitation (SMR) in heart failure with reduced ejection fraction (HFrEF) is a dynamic lesion whose severity may change substantially after optimization of guideline-directed medical therapy (GDMT) and cardiac resynchronization therapy (CRT). In a prospective cohort of 2,254 ambulatory patients with..."

New page

__NOTOC__

==Natural history, complications, and prognosis==

===Natural history during guideline-directed medical therapy===
Ventricular secondary [[mitral regurgitation]] (SMR) in [[heart failure with reduced ejection fraction]] (HFrEF) is a dynamic lesion whose severity may change substantially after optimization of [[guideline-directed medical therapy]] (GDMT) and [[cardiac resynchronization therapy]] (CRT).

In a prospective cohort of 2,254 ambulatory patients with HFrEF who underwent baseline and 12-month echocardiography, the proportion with nonsignificant SMR increased from 67.6% to 79.5%. Among patients with moderate or severe SMR at baseline, 57.5% improved to nonsignificant SMR. Patients whose SMR improved had long-term outcomes comparable to those who never had significant SMR.<ref name="Ferrero2026">{{cite journal |author=Ferrero C, Codina P, Lupón J, et al. |title=Secondary Mitral Regurgitation Trajectories and Prognosis With Intensification of Guideline-Directed Medical Therapy in Heart Failure |journal=JACC: Heart Failure |year=2026 |volume=14 |issue=7 |pages=103001 |doi=10.1016/j.jchf.2026.103001}}</ref>

Conversely, persistent moderate or severe SMR after treatment optimization was associated with increased:

* All-cause mortality: hazard ratio (HR) 1.60; 95% confidence interval (CI) 1.36–1.89.
* All-cause mortality or heart-failure hospitalization: HR 1.59; 95% CI 1.36–1.85.

These associations persisted over a median follow-up of 4.5 years and indicate that the post-GDMT SMR trajectory is more prognostically informative than a single baseline severity measurement.<ref name="Ferrero2026" />

===Prognosis with medical therapy alone===
Persistent significant SMR promotes progressive volume overload and adverse left-ventricular remodeling. Its clinical course may be complicated by recurrent heart-failure decompensation, pulmonary hypertension, right-ventricular dysfunction or failure, functional tricuspid regurgitation, atrial fibrillation, and cardiorenal syndrome.<ref name="OGara2020">{{cite journal |author=O'Gara PT, Mack MJ |title=Secondary Mitral Regurgitation |journal=The New England Journal of Medicine |year=2020 |volume=383 |issue=15 |pages=1458-1467 |doi=10.1056/NEJMcp1903331}}</ref>

The medically treated control population in COAPT provides a contemporary estimate for selected patients with symptomatic severe SMR despite maximally tolerated GDMT:

* Death or heart-failure hospitalization occurred in approximately 67% by 2 years, 87% by 3 years, and 91.5% by 5 years.<ref name="Mack2021">{{cite journal |author=Mack MJ, Lindenfeld J, Abraham WT, et al. |title=3-Year Outcomes of Transcatheter Mitral Valve Repair in Patients With Heart Failure |journal=Journal of the American College of Cardiology |year=2021 |volume=77 |issue=8 |pages=1029-1040 |doi=10.1016/j.jacc.2020.12.047}}</ref><ref name="Stone2023">{{cite journal |author=Stone GW, Abraham WT, Lindenfeld J, et al. |title=Five-Year Follow-up after Transcatheter Repair of Secondary Mitral Regurgitation |journal=The New England Journal of Medicine |year=2023 |volume=388 |issue=22 |pages=2037-2048 |doi=10.1056/NEJMoa2300213}}</ref>
* Five-year all-cause mortality was 67.2%.
* The annualized heart-failure hospitalization rate was 57.2% per year.<ref name="Stone2023" />

These estimates apply to the COAPT enrollment profile: patients with persistent symptoms despite maximally tolerated GDMT, moderate-to-severe or severe SMR, left-ventricular ejection fraction of 20%–50%, and no marked chamber dilation or severe right-heart involvement. They should not be extrapolated without qualification to patients with substantially different ventricular or right-heart disease.<ref name="Hahn2024">{{cite journal |author=Hahn RT, Lindenfeld J, Lim SD, Mack MJ, Burkhoff D |title=Structural Cardiac Interventions in Patients With Heart Failure: JACC Scientific Statement |journal=Journal of the American College of Cardiology |year=2024 |volume=84 |issue=9 |pages=832-847 |doi=10.1016/j.jacc.2024.05.061}}</ref>

Maximally tolerated GDMT should not be equated with achievement of target doses. In a post hoc COAPT analysis, only 2.2% of patients tolerated target doses of all three evaluated GDMT classes, most frequently because of hypotension or renal dysfunction.<ref name="Hahn2024" />

===Prognosis after M-TEER===
Mitral transcatheter edge-to-edge repair (M-TEER) reduces, but does not eliminate, the event burden associated with HFrEF and significant SMR.

{| class="wikitable"
|+ Five-year outcome trajectory in COAPT
|-
! Outcome
! M-TEER plus GDMT
! GDMT alone
! Effect estimate
|-
| Annualized heart-failure hospitalization
| 33.1% per year
| 57.2% per year
| HR 0.53; 95% CI 0.41–0.68
|-
| All-cause mortality
| 57.3%
| 67.2%
| HR 0.72; 95% CI 0.58–0.89
|-
| Death or heart-failure hospitalization
| 73.6%
| 91.5%
| HR 0.53; 95% CI 0.44–0.64
|}
<ref name="Stone2023" />

Most of the hospitalization benefit occurred during the first 3 years and most of the mortality benefit during the first 2 years. Interpretation of later curve convergence is limited by progression of the underlying cardiomyopathy and protocol-permitted crossover from the control group after 2 years.<ref name="Stone2023" />

MITRA-FR did not demonstrate a reduction in death or unplanned heart-failure hospitalization at 1 or 2 years. This neutral result, compared with COAPT, indicates that the COAPT mortality and hospitalization effects should not be generalized to every SMR phenotype.<ref name="Obadia2018">{{cite journal |author=Obadia JF, Messika-Zeitoun D, Leurent G, et al. |title=Percutaneous Repair or Medical Treatment for Secondary Mitral Regurgitation |journal=The New England Journal of Medicine |year=2018 |volume=379 |issue=24 |pages=2297-2306 |doi=10.1056/NEJMoa1805374}}</ref>

Mean effective regurgitant orifice area was 0.40–0.41 cm² in COAPT, 0.31 cm² in MITRA-FR, and 0.23–0.25 cm² in RESHAPE-HF2, while mean left-ventricular end-diastolic volumes were largest in MITRA-FR. Benefit appears greatest when MR severity is disproportionate to the degree of left-ventricular remodeling. This framework is not fully explanatory: RESHAPE-HF2 reported no apparent heterogeneity of treatment effect across subgroups defined by baseline echocardiographic measurements, despite 23% of enrolled patients having an effective regurgitant orifice area below 0.20 cm².<ref name="Stolz2025">{{cite journal |author=Stolz L, Stocker TJ, Lurz P, Hausleiter J |title=Growing Evidence for Edge-to-Edge Repair in Secondary Mitral Regurgitation: What to Learn From COAPT, MITRA-FR, and RESHAPE-HF2 |journal=JACC: Cardiovascular Interventions |year=2025 |volume=18 |issue=7 |pages=927-932 |doi=10.1016/j.jcin.2025.01.429}}</ref><ref name="Anker2024">{{cite journal |author=Anker SD, Friede T, von Bardeleben RS, et al. |title=Transcatheter Valve Repair in Heart Failure with Moderate to Severe Mitral Regurgitation |journal=The New England Journal of Medicine |year=2024 |volume=391 |issue=19 |pages=1799-1809 |doi=10.1056/NEJMoa2314328}}</ref><ref name="Gupta2024">{{cite journal |author=Gupta A, Packer M, Makkar R, Grayburn P |title=A Volume-Based Framework Reconciling COAPT, MITRA-FR, and RESHAPE-HF2 |journal=Journal of the American College of Cardiology |year=2024 |volume=84 |issue=24 |pages=2376-2379 |doi=10.1016/j.jacc.2024.08.029}}</ref>

COAPT did not demonstrate significant left-ventricular reverse remodeling attributable to device therapy. Persistence of the underlying ventricular cardiomyopathy helps explain why absolute mortality and hospitalization rates remain high despite durable MR reduction.<ref name="Hahn2024" />

RESHAPE-HF2 met its primary composite endpoint of recurrent heart-failure hospitalization or cardiovascular death in patients with moderate-to-severe SMR (rate ratio 0.64; 95% CI 0.48–0.85). The trial was not powered to demonstrate an isolated all-cause mortality benefit; this should not be interpreted as a negative mortality signal.<ref name="Anker2024" /> Improvement in health status occurred across baseline Kansas City Cardiomyopathy Questionnaire strata, indicating that poor baseline health status alone should not be used as a futility marker.<ref name="Butler2026">{{cite journal |author=Butler J, Khan MS, Friede T, et al. |title=Mitral Transcatheter Edge-to-Edge Repair and Outcomes According to Baseline Health Status: The RESHAPE-HF2 Trial |journal=European Heart Journal |year=2026 |volume=47 |issue=19 |pages=2290-2304 |doi=10.1093/eurheartj/ehaf1035}}</ref>

===Durability, recurrence, and reintervention===
Reduction of SMR after M-TEER is generally durable through 3 years. Pooled data suggest that combined M-TEER failure, defined as recurrent MR or mitral reintervention, remains below approximately 10%–13% through 3 years but increases to approximately 22% by 5 years in SMR.<ref name="Mariani2026">{{cite journal |author=Mariani A, Stolz L, von Bardeleben RS, et al. |title=Durability of Mitral Valve Transcatheter Edge-to-Edge Repair: An Expert Overview |journal=JACC: Cardiovascular Interventions |year=2026 |volume=19 |issue=9 |pages=1057-1070 |doi=10.1016/j.jcin.2026.02.019}}</ref>

Late failure in ventricular SMR is predominantly functional and is usually related to progressive left-ventricular remodeling rather than structural failure of the implanted device. Reported recurrence and reintervention rates vary according to MR definition, underlying ventricular phenotype, device generation, procedural result, and duration of follow-up; therefore, a single recurrence estimate should not be applied to all treated populations.<ref name="Mariani2026" />

===Prognosis relative to surgery===
MATTERHORN randomized 210 patients with heart failure and secondary MR to M-TEER or mitral valve surgery. At 1 year, the composite of death, heart-failure hospitalization, mitral reintervention, ventricular assist-device implantation, or stroke occurred in 16.7% after M-TEER and 22.5% after surgery. The estimated mean difference was −6 percentage points (95% CI −17 to 6), meeting the prespecified noninferiority criterion.<ref name="Baldus2024">{{cite journal |author=Baldus S, Doenst T, Pfister R, et al. |title=Transcatheter Repair versus Mitral-Valve Surgery for Secondary Mitral Regurgitation |journal=The New England Journal of Medicine |year=2024 |volume=391 |issue=19 |pages=1787-1798 |pmid=39216093 |doi=10.1056/NEJMoa2408739}}</ref>

Major adverse events within 30 days occurred in 14.9% after M-TEER compared with 54.8% after surgery.<ref name="Baldus2024" /> Applicability to a strictly HFrEF population is limited because mean left-ventricular ejection fraction was 43.0±11.7%, representing a broader ventricular-function range than the pivotal HFrEF-focused trials.

===Late device-related and hemodynamic complications===
Acute periprocedural and device complications are addressed in the procedural-therapy microchapter. This section is limited to late abnormalities that materially influence prognosis.

In a prospective registry of 128 patients undergoing systematic transesophageal echocardiography 6 months after M-TEER:

* New partial or complete single-leaflet device attachment was detected in 7.8%.
* The proportion with an elevated mean transmitral gradient increased from 13.3% immediately after the procedure to 18% at 6 months.
* Severe recurrent or residual MR was present in 13.3%.
* Mean transmitral gradient ≥5 mm Hg predicted death or heart-failure rehospitalization at 2 years: HR 2.30; 95% CI 1.10–4.81.
* Severe MR at 6 months predicted death or heart-failure rehospitalization: HR 3.26; 95% CI 1.18–8.99.

Several clinically important abnormalities were identified by transesophageal echocardiography but not by transthoracic imaging alone.<ref name="Bartkowiak2024">{{cite journal |author=Bartkowiak J, Kassar M, Brülisauer SJ, et al. |title=Findings From Transoesophageal Echocardiographic Follow-Up After Mitral Transcatheter Edge-to-Edge Repair |journal=EuroIntervention |year=2024 |volume=20 |issue=20 |pages=e1298-e1308 |doi=10.4244/EIJ-D-24-00297 |pmid=39432254}}</ref>

===Long-term prognostic markers===
The major determinants of prognosis after M-TEER are the severity of the underlying cardiomyopathy, the quality and durability of MR reduction, right-heart involvement, and avoidance of clinically significant transmitral obstruction.

{| class="wikitable"
|-
! Prognostic factor
! Evidence and clinical significance
|-
| '''Persistent SMR after GDMT or CRT'''
| Persistent moderate or severe SMR is associated with increased mortality and heart-failure hospitalization, whereas regression to nonsignificant SMR identifies a substantially more favorable trajectory.<ref name="Ferrero2026" />
|-
| '''Residual MR ≥2+'''
| Residual MR is consistently associated with death, recurrent heart-failure hospitalization, and later progression to severe MR. Observational analyses reported HRs of 2.1 for all-cause mortality and 2.3 for heart-failure rehospitalization after acute procedural failure with residual MR >2+.<ref name="BenShoshan2020">{{cite journal |author=Ben-Shoshan J, Overtchook P, Buithieu J, et al. |title=Predictors of Outcomes Following Transcatheter Edge-to-Edge Mitral Valve Repair |journal=JACC: Cardiovascular Interventions |year=2020 |volume=13 |issue=15 |pages=1733-1748 |doi=10.1016/j.jcin.2020.03.025}}</ref>
|-
| '''Quality of MR reduction'''
| In EXPAND, 1-year death or first heart-failure hospitalization occurred in 29.7% of patients with MR ≤1+ compared with 69.6% of those with MR ≥2+.<ref name="Orban2023">{{cite journal |author=Orban M, Rottbauer W, Williams M, et al. |title=Transcatheter Edge-to-Edge Repair for Secondary Mitral Regurgitation With Third-Generation Devices in Heart Failure Patients—Results From the Global EXPAND Post-Market Study |journal=European Journal of Heart Failure |year=2023 |volume=25 |issue=3 |pages=411-421 |doi=10.1002/ejhf.2770}}</ref>
|-
| '''Iatrogenic mitral stenosis'''
| A small post-procedural mitral valve area or elevated mean transmitral gradient is associated with mortality, heart failure, and reintervention. Reported adverse thresholds include valve area ≤1.94 cm² and mean gradient >4.4–5 mm Hg, but no universally accepted prognostic cutoff exists.<ref name="BenShoshan2020" /><ref name="Bartkowiak2024" />
|-
| '''Right-ventricular dysfunction and secondary tricuspid regurgitation'''
| Right-ventricular dysfunction and significant tricuspid regurgitation are associated with worse prognosis and should be assessed separately from left-sided disease. Right-heart involvement is partly dynamic: reverse right-ventricular remodeling and reduction in tricuspid regurgitation severity may occur in up to 50% after successful M-TEER; atrial fibrillation and right-ventricular dilation predict failure of tricuspid regurgitation to improve.<ref name="Groger2024">{{cite journal |author=Gröger M, Felbel D, Paukovitsch M, et al. |title=Insulin-Like Growth Factor Binding Protein 2 Predicts Right Ventricular Reverse Remodeling and Improvement of Concomitant Tricuspid Regurgitation After Transcatheter Edge-to-Edge Mitral Valve Repair |journal=Clinical Cardiology |year=2024 |volume=47 |issue=12 |pages=e70041 |doi=10.1002/clc.70041}}</ref>
|-
| '''Advanced ventricular or systemic disease'''
| Marked left-ventricular remodeling, pulmonary vascular disease, advanced renal dysfunction, and frailty identify patients with greater residual risk and potential procedural futility.<ref name="Lander2023">{{cite journal |author=Lander MM, Brener MI, Goel K, et al. |title=Mitral Interventions in Heart Failure |journal=JACC: Heart Failure |year=2023 |volume=11 |issue=8 Pt 2 |pages=1055-1069 |doi=10.1016/j.jchf.2023.07.016}}</ref>
|}

===Prognostic risk stratification===

====Clinical MitraScore (Raposeiras-Roubin)====
The clinical MitraScore is an unweighted eight-item preprocedural model derived in the MIVNUT registry and externally validated in the GIOTTO registry. One point is assigned for each of the following predictors, producing a score from 0 to 8:<ref name="Raposeiras2022">{{cite journal |author=Raposeiras-Roubin S, Adamo M, Freixa X, et al. |title=A Score to Assess Mortality After Percutaneous Mitral Valve Repair |journal=Journal of the American College of Cardiology |year=2022 |volume=79 |issue=6 |pages=562-573 |doi=10.1016/j.jacc.2021.11.041}}</ref>

* Age ≥75 years
* [[Anemia]]
* [[Estimated glomerular filtration rate]] <60 mL/min/1.73 m²
* [[Left ventricular ejection fraction]] <40%
* [[Peripheral arterial disease]]
* [[Chronic obstructive pulmonary disease]]
* High-dose loop-diuretic therapy
* No renin–angiotensin system inhibitor therapy

Each additional point was associated with a 55% relative increase in mortality risk (HR 1.55; 95% CI 1.44–1.67). Discrimination was modest:

* Derivation cohort c-statistic: 0.70; 95% CI 0.66–0.73.
* GIOTTO validation cohort c-statistic: 0.66.
* EuroSCORE II c-statistic: 0.61.
* [[Society of Thoracic Surgeons]] score c-statistic: 0.57.<ref name="Raposeiras2022" />

In the OCEAN-Mitral registry, which included 3,745 patients across different MR subtypes, the clinical MitraScore demonstrated a c-statistic of 0.63 with good calibration. Compared with the low-risk group:

* Moderate risk, score 3–4: mortality HR 1.92; 95% CI 1.59–2.33.
* High risk, score 5–8: mortality HR 4.16; 95% CI 3.25–5.33.

Adding a Clinical Frailty Scale score ≥4 improved prognostic performance beyond the conventional MitraScore, STS score, and EuroSCORE II, although further validation is required.<ref name="Nonaka2025">{{cite journal |author=Nonaka H, Asami M, Horiuchi Y, et al. |title=Validation of MitraScore in Diverse Mitral Regurgitation Subtypes: Insights From the OCEAN-Mitral Registry |journal=International Journal of Cardiology |year=2025 |volume=436 |pages=133427 |doi=10.1016/j.ijcard.2025.133427 |pmid=40441608}}</ref>

Important limitations include modest discrimination, development in a mixed-etiology M-TEER population rather than an exclusively HFrEF-SMR cohort, and dependence on medical-therapy variables. Omission of these treatment variables reduces discrimination. Absence of renin–angiotensin system inhibitor therapy is partly a marker of GDMT intolerance or undertreatment rather than an immutable risk factor and may be modifiable before referral.<ref name="Raposeiras2022" />

{{Caution|The name '''MitraScore''' refers to two unrelated instruments. The clinical MitraScore described above is a preprocedural 0–8-point mortality model. The MITRA-PRO intraprocedural MitraScore is a separate 0–14-point multimodal assessment of residual MR that combines left-atrial v-wave pressure, left-ventricular angiography, two-dimensional echocardiographic MR assessment, and bubble testing during volume challenge. A final score ≤3 defines an optimal procedural result, whereas ≥4 indicates a suboptimal result with relevant residual MR. The instruments must not be conflated.<ref name="Boekstegers2023">{{cite journal |author=Boekstegers P, Hausleiter J, Schmitz T, et al. |title=Intraprocedural Residual Mitral Regurgitation and Survival After Transcatheter Edge-to-Edge Repair: Prospective German Multicenter Registry (MITRA-PRO) |journal=JACC: Cardiovascular Interventions |year=2023 |volume=16 |issue=5 |doi=10.1016/j.jcin.2022.12.015}}</ref>}}

====Other prognostic tools====
{| class="wikitable"
|-
! Tool
! Outcome and performance
! Limitations
|-
| '''EuroSMR risk score'''
| An artificial-intelligence-derived 18-variable model developed in 4,172 and validated in 428 patients with SMR. It predicted 1-year mortality with an area under the curve (AUC) of 0.789; among the highest-risk 5%, 1-year mortality was 72.7% and mortality or absence of clinical improvement was 83.2%.<ref name="Hausleiter2024">{{cite journal |author=Hausleiter J, Lachmann M, Stolz L, et al. |title=Artificial Intelligence-Derived Risk Score for Mortality in Secondary Mitral Regurgitation Treated by Transcatheter Edge-to-Edge Repair: The EuroSMR Risk Score |journal=European Heart Journal |year=2024 |volume=45 |issue=11 |pages=922-936 |doi=10.1093/eurheartj/ehad871}}</ref>
| Requires multiple clinical, laboratory, treatment, and echocardiographic variables; the extreme-risk subgroup constituted only 2.6% of the cohort.
|-
| '''COAPT risk score'''
| Predicts death or heart-failure hospitalization at 2 years.
| External validation in 344 patients showed poor discrimination in COAPT-eligible and COAPT-noneligible groups, with AUC ≤0.61.<ref name="Gasecka2025">{{cite journal |author=Gąsecka A, Jasińska-Gniadzik K, D'Ascenzo F, et al. |title=External Validation of COAPT Risk Score in Patients Who Underwent Transcatheter Edge-to-Edge Repair of Severe, Functional Mitral Regurgitation |journal=The American Journal of Cardiology |year=2025 |volume=238 |pages=8-15 |doi=10.1016/j.amjcard.2024.11.028}}</ref>
|-
| '''MITRALITY and comparative models'''
| In a single-center comparison, MITRALITY had the best discrimination for 1-year mortality and the composite of mortality or heart-failure hospitalization: AUC 0.74 overall and 0.72 in SMR.
| Performance remained moderate; surgical risk scores, MitraScore, and baseline NT-proBNP alone performed poorly in this comparison.<ref name="DeSaMarchi2024">{{cite journal |author=de Sá Marchi MF, van den Dorpel M, Calomeni P, et al. |title=Comparative Analysis of Different Risk Prediction Tools After Mitral Transcatheter Edge-to-Edge Repair |journal=International Journal of Cardiology |year=2024 |volume=401 |pages=131826 |doi=10.1016/j.ijcard.2024.131826}}</ref>
|}

No prognostic score should be used as the sole determinant of M-TEER candidacy. Current tools have, at best, moderate discrimination and should support multidisciplinary assessment, shared decision-making, and identification of patients at extreme risk.

===Phenotype-based prognosis===
Unsupervised hierarchical clustering of 22 baseline clinical, echocardiographic, and laboratory variables in COAPT (n=614) identified three distinct SMR phenotypes, characterized by clinical risk, comorbidity burden, and cardiac-damage stage. The primary outcome was heart-failure hospitalization or cardiovascular death at 2 years. The phenotypes were subsequently assessed in MITRA-FR.<ref name="Bonnet2026">{{cite journal |author=Bonnet G, Rommel KP, Redfors B, et al. |title=Phenotypic Diversity and Outcomes of Transcatheter Mitral Repair for Secondary Mitral Regurgitation: Insights From the COAPT and MITRA-FR Trials |journal=JACC: Cardiovascular Interventions |year=2026 |volume=19 |issue=9 |pages=1087-1104 |pmid=42120116 |doi=10.1016/j.jcin.2026.02.030}}</ref>

{| class="wikitable"
|+ SMR phenotypes identified in COAPT
|-
! Cluster
! Proportion of COAPT
! Principal characteristics
! Relative reduction in heart-failure hospitalization or cardiovascular death with M-TEER
|-
| '''1'''
| 21%
| Low clinical risk with substantial left-ventricular cardiac damage; highest 2-year survival
| 46%
|-
| '''2'''
| 43%
| Intermediate clinical risk with biventricular cardiac damage
| 49%
|-
| '''3'''
| 36%
| High clinical risk and comorbidity burden, comparatively low cardiac damage, and less severe SMR
| 34%; no observed survival benefit
|}

Cluster 3 accounted for 48% of the MITRA-FR population. Multidimensional phenotyping that integrates cardiac damage, comorbidity burden, and clinical risk may explain some of the heterogeneity between M-TEER trials more effectively than any single variable. These exploratory phenotypes have not been established as formal candidacy, deferral, or futility criteria.<ref name="Bonnet2026" />

===Guideline context===
Both American and European guidelines emphasize optimization of GDMT, including CRT when indicated, before mitral intervention and recommend multidisciplinary heart-team assessment. Secondary summaries agree that restoration of mitral competence is not curative but differ in their characterization of the formal M-TEER recommendation class.<ref name="Coisne2023">{{cite journal |author=Coisne A, Lancellotti P, Habib G, et al. |title=ACC/AHA and ESC/EACTS Guidelines for the Management of Valvular Heart Diseases: JACC Guideline Comparison |journal=Journal of the American College of Cardiology |year=2023 |volume=82 |issue=8 |pages=721-734 |doi=10.1016/j.jacc.2023.05.061}}</ref><ref name="Ostrominski2024">{{cite journal |author=Ostrominski JW, DeFilippis EM, Bansal K, et al. |title=Contemporary American and European Guidelines for Heart Failure Management: JACC: Heart Failure Guideline Comparison |journal=JACC: Heart Failure |year=2024 |volume=12 |issue=5 |pages=810-825 |doi=10.1016/j.jchf.2024.02.020}}</ref>

* Optimization of GDMT and indicated CRT before intervention is described as Class I-C in the American guideline and Class I-B in the European guideline.<ref name="Coisne2023" />
* A 2023 guideline-comparison analysis describes different Class IIa/IIb positions across the American and European documents, whereas a 2024 JACC scientific statement characterizes both as Class IIa for chronic severe SMR with persistent NYHA class II–IV symptoms despite optimal GDMT and COAPT-like criteria.<ref name="Coisne2023" /><ref name="Hahn2024" />
* The American guideline defines severe chronic secondary MR (stages C and D) as effective regurgitant orifice area ≥0.40 cm², regurgitant volume ≥60 mL, and regurgitant fraction ≥50%. It notes that not every criterion will be present in each patient, that severity grading requires integration of quantitative and clinical findings, that two-dimensional proximal isovelocity surface area measurement may underestimate true effective regurgitant orifice area because of crescentic proximal convergence, and that regurgitant volume may be lower in low-flow states.<ref name="Otto2021">{{cite journal |author=Otto CM, Nishimura RA, Bonow RO, et al. |title=2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease |journal=Journal of the American College of Cardiology |year=2021 |volume=77 |issue=4 |pages=e25-e197 |doi=10.1016/j.jacc.2020.11.018}}</ref>
* Interpretive commentary describes the combined American and European position as effective regurgitant orifice area ≥0.40 cm² with regurgitant volume ≥60 mL, or effective regurgitant orifice area ≥0.30 cm² with regurgitant volume ≥40 mL in the presence of an ellipsoid proximal isovelocity surface area zone. The lower numeric combination is not stated as a discrete alternative threshold in the American stage table.<ref name="Stolz2025" />
* Quantitative MR thresholds must be interpreted relative to left-ventricular volume. Identical effective regurgitant orifice area and regurgitant-volume values may produce markedly different regurgitant fractions in ventricles of different end-diastolic volumes.<ref name="Bonow2020">{{cite journal |author=Bonow RO, O'Gara PT, Adams DH, et al. |title=2020 Focused Update of the 2017 ACC Expert Consensus Decision Pathway on the Management of Mitral Regurgitation |journal=Journal of the American College of Cardiology |year=2020 |volume=75 |issue=17 |pages=2236-2270 |doi=10.1016/j.jacc.2020.02.005}}</ref>

Both guideline documents evaluated in these comparisons predate RESHAPE-HF2 and MATTERHORN. The existing COAPT-like Class IIa position does not comprehensively reflect the subsequent evidence: RESHAPE-HF2 demonstrated reduction in heart-failure hospitalization among patients with less severe SMR, while MATTERHORN provided randomized evidence in a population with a broader, predominantly mid-range ejection-fraction profile. Whether intervention benefits patients with truly moderate SMR remains unresolved and requires further randomized evaluation.<ref name="Stolz2025" />

Because the secondary sources do not characterize the recommendation class identically, the discrepancy should not be harmonized without review of the current primary ACC/AHA and ESC/EACTS guideline documents.



===Prognostic interpretation===
* SMR severity should be interpreted after optimization of GDMT and CRT because regression identifies a substantially better prognosis.
* Persistent moderate SMR should not automatically be considered benign; contemporary trajectory data associate it with increased mortality and heart-failure hospitalization.<ref name="Ferrero2026" />
* A technically successful M-TEER procedure does not cure the underlying cardiomyopathy. In COAPT, 57.3% of treated patients died and 73.6% died or were hospitalized for heart failure within 5 years.<ref name="Stone2023" />
* Residual MR at discharge and during follow-up is among the most clinically useful modifiable post-procedural prognostic markers.<ref name="BenShoshan2020" /><ref name="Orban2023" /><ref name="Bartkowiak2024" />
* Continued clinical and echocardiographic surveillance remains necessary because functional recurrence and transmitral obstruction may become apparent after discharge.<ref name="Mariani2026" /><ref name="Bartkowiak2024" />
* Absence of renin–angiotensin system inhibitor therapy within the clinical MitraScore may identify treatment intolerance or undertreatment and should not automatically be interpreted as fixed biological risk.<ref name="Raposeiras2022" />
* A mortality benefit comparable to COAPT has not been established across all SMR phenotypes. Cluster analysis indicates that absent survival benefit may be concentrated in a phenotype characterized by high clinical risk and comorbidity burden, comparatively low cardiac damage, and less severe SMR. This phenotype comprised 36% of COAPT and 48% of MITRA-FR, but the finding remains hypothesis-generating and should not independently determine candidacy.<ref name="Bonnet2026" />

==References==
{{Reflist|2}}

[[Category:Cardiology]]
[[Category:Surgery]]
[[Category:Up-To-Date]]

Influenza other diagnostic studies

Mohammed Braizat — Mon, 03 Aug 2026 17:38:28 GMT

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Gerald Chi — Mon, 03 Aug 2026 16:15:38 GMT

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Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Treatment

Nehal Eid — Mon, 03 Aug 2026 13:44:47 GMT

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Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER)

Nehal Eid — Mon, 03 Aug 2026 13:41:08 GMT

Treatment

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	==[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) imaging and assessment\|Imaging and assessment]]==		==[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) imaging and assessment\|Imaging and assessment]]==

	~~[[Preprocedural imaging and anatomic suitability assessment]] \| [[echocardiography and ultrasound\|Echocardiography and Ultrasound]] \| [[Other Imaging Findings / Other Diagnostic Studies]]~~


	==[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Treatment\|Treatment]]==		==[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Treatment\|Treatment]]==

	[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Medical therapy (GDMT optimization before and after M-TEER)]] \| [[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Periprocedural and Post-Procedural Antithrombotic Therapy]] \| [[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Comparison with surgery]]

	== [[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) natural history, complications and prognosis\|Natural History, Complications and Prognosis]] ==		== [[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) natural history, complications and prognosis\|Natural History, Complications and Prognosis]] ==

Dyspepsia medical therapy

Fahad Hasan — Mon, 03 Aug 2026 02:50:21 GMT

Step 1: Helicobacter pylori Eradication

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Diabetes mellitus type 1 Diagnostic study of choice

Hiba Tullah — Sun, 02 Aug 2026 18:15:41 GMT

Inflammatory bowel disease

Omar Soliman — Sun, 02 Aug 2026 15:24:49 GMT

Classification

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	__NOTOC__		__NOTOC__
	{{Inflammatory bowel disease}}		{{Inflammatory bowel disease}}
	{{CMG}} ; {{AE}} {{ADG}}~~<br>~~		{{CMG}} ; {{AE}} {{ADG}} ; {{OS}}
	{{SK}} IBD ;		{{SK}} IBD ;
	{{Infobox medical condition		{{Infobox medical condition
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	Classification may change over time with longitudinal follow-up.		Classification may change over time with longitudinal follow-up.

	~~== Etiologic framework ==~~

	~~IBD results from inappropriate immune activation against intestinal microbial communities in genetically susceptible individuals.~~

	~~Disease development reflects interaction between:~~

	* Host genetics.
	* Intestinal microbiome alterations.
	* Intestinal epithelial barrier dysfunction.
	* Innate and adaptive immune responses.
	* Environmental exposures.

	~~=== Genetic pathways ===~~

	~~Important genetic associations include:~~

	* '''NOD2 variants''' — strongly associated with Crohn disease.
	* '''ATG16L1''' and autophagy pathways.
	* '''IL-23/Th17 immune axis.'''

	~~=== Environmental contributors ===~~

	~~Potential contributors include:~~

	* Westernized dietary patterns.
	* Smoking.
	* Altered microbial diversity.
	* Antibiotic exposure.
	* Urbanization and industrialization.

	== Epidemiology and disease burden ==		== Epidemiology and disease burden ==
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	==== Genetic factors ====		==== Genetic factors ====
	* ~~[[Mutation\|Mutations]] in the [[~~NOD2~~\|CARD15]] gene (also known as the NOD2 [[gene]]) are~~ associated with Crohn's disease.
	* ~~Mutations of the transporter proteins such as OCTN1~~ and ~~OCTN2~~ and ~~scaffolding proteins such as the MAGUK family are believed to cause ulcerative colitis~~.		Important genetic associations include:

			* '''NOD2 variants''' — strongly associated with Crohn disease.
			* '''ATG16L1''' and autophagy pathways.
			* '''IL-23/Th17 immune axis.'''
			== Etiologic framework ==

			IBD results from inappropriate immune activation against intestinal microbial communities in genetically susceptible individuals.

			=== Environmental contributors ===

			Potential contributors include:

			* Westernized dietary patterns.
			* Smoking.
			* Altered microbial diversity.
			* Antibiotic exposure.
			* Urbanization and industrialization.

	==== Environmental factors ====		==== Environmental factors ====
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	==Classification==		==Classification==
	Inflammatory bowel disease ~~can be classified into~~ Crohn's disease and ulcerative colitis.		Inflammatory bowel disease consists of Crohn's disease and ulcerative colitis. Microscopic colitis is a related inflammatory colitis characterized by chronic inflammation of the colon.
	~~{{familytree/start}}~~
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| A01 \| \| \| \| \| \|A01=~~Inflammatory ~~Bowel Disease}}~~		* Inflammatory bowel disease and related inflammatory colitides
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| }}~~		** Crohn's disease
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| \|,\|-\|-\|-\|-\|-\|-\|-\|-\|^\|-\|-\|-\|-\|-\|-\|.\| \| }}~~		*** Based on region involved
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| B01 \| \| \| \| \| \| \| \| \| \| \| \| \| \| B02 \|B01=~~Crohn's ~~Disease\|B02=Ulcerative colitis}}~~		**** Ileocolic Crohn's disease
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| \|!\| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \|!\| }}~~		**** Crohn's ileitis
	~~{{familytree \| \| \| \| \| \| \| \|,\|-\|-\|-\|-\|-\|^\|-\|-\|-\|-\|-\|.\| \| \| \| \| \| \| \| \| \|!\|}}~~		**** Crohn's colitis
	~~{{familytree \| \| \| \| \| \| \| Z01 \| \| \| \| \| \| \| \| \| \| Z02 \| \| \| \| \| \| \| \| \|!\| \|Z01=~~Based on ~~Region~~ involved~~\|Z02=Based on Severity}}~~		*** Based on disease behavior
	~~{{familytree \| \| \| \|,\|-\|-\|-\|+\|-\|-\|-\|.\| \| \| \|,\|-\|-\|-\|+\|-\|-\|-\|.\| \| \| \| \| \|!\| \| }}~~		**** Stricturing disease
	~~{{familytree \| \| \| C01 \| \| C02 \| \| C03 \| \| C04 \| \| C05 \| \| C06 \| \| \| \| \|!\| \|C01=~~Ileocolic Crohn's disease~~\|C02=~~Crohn's ileitis~~\|C03=~~Crohn's colitis~~\|C04=~~Stricturing disease~~\|C05=~~Penetrating disease~~\|C06=~~Inflammatory disease}}		**** Penetrating disease
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \|,\|-\|-\|-\|-\|-\|^\|-\|-\|-\|.\| \| }}~~		**** Inflammatory disease
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| Z01 \| \| \| \| \| \| \| \| Z02 \| \|Z01=~~Based on ~~Region involved\|Z02=~~Based on ~~Severity}}~~		** Ulcerative colitis
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \|,\|-\|-\|-\|^\|-\|.\| \| \| \|,\|-\|-\|-\|+\|-\|-\|-\|v\|-\|-\|-\|.\| }}~~		*** Based on extent
	~~{{familytree \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| \| C01 \| \| \| \| C02 \| \| C03 \| \| C04 \| \| C05 \| \| C06 \| C01=Distal UC\|C02=Proximal UC\|C03=Mild\|C04=~~Moderate~~\|C05=~~Severe~~\|C06=Flumiant\|}}~~		**** Distal ulcerative colitis
	{{~~familytree~~/end}}		**** Proximal ulcerative colitis
			**** Pancolitis
			*** Based on severity
			**** Mild
			**** Moderate
			**** Severe
			** Microscopic colitis
			*** Collagenous colitis
			*** Lymphocytic colitis
			{{tree list/end}}

	==Differential diagnosis==		==Differential diagnosis==

Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) imaging and assessment

Nehal Eid — Sun, 02 Aug 2026 14:56:40 GMT

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	==[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) imaging and assessment\|Imaging and assessment]]==		==[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) imaging and assessment\|Imaging and assessment]]==

	~~[[Preprocedural imaging and anatomic suitability assessment]] \| [[echocardiography and ultrasound\|Echocardiography and Ultrasound]] \| [[Other Imaging Findings / Other Diagnostic Studies]]~~


	==[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Treatment\|Treatment]]==		==[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Treatment\|Treatment]]==

	[[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Medical therapy (GDMT optimization before and after M-TEER)]] \| [[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Periprocedural and Post-Procedural Antithrombotic Therapy]] \| [[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) Comparison with surgery]]

	== [[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) natural history, complications and prognosis\|Natural History, Complications and Prognosis]] ==		== [[Percutaneous mitral repair as treatment in HFrEF (MitraClip/TEER) natural history, complications and prognosis\|Natural History, Complications and Prognosis]] ==

← Older revision		Revision as of 18:15, 2 August 2026
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	===Diagnostic Criteria for Diabetes Mellitus===		===Diagnostic Criteria for Diabetes Mellitus===

	The diagnosis of diabetes mellitus is established by any one of the following criteria.<ref name="ada2026s2">{{cite journal \|author=American Diabetes Association Professional Practice Committee \|title=2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes-2026 \|journal=Diabetes Care \|volume=49 \|issue=Suppl 1 \|pages=S27–S49 \|year=2026 \|doi=10.2337/dc26-S002}}</ref>		The diagnosis of diabetes mellitus is established by any one of the following criteria.<ref name="ada2026s2">{{cite journal \|author=American Diabetes Association Professional Practice Committee \|title=2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes-2026 \|journal=Diabetes Care \|volume=49 \|issue=Suppl 1 \|pages=S27–S49 \|year=2026 \|pmid=41358893 \|doi=10.2337/dc26-S002}}</ref>

	{\| class="wikitable"		{\| class="wikitable"
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	'''Confirmatory testing:''' In the absence of unequivocal hyperglycemia (classic symptoms plus random glucose ≥200 mg/dL), the diagnosis requires two abnormal test results- either from the same sample or from two separate time points. If two different tests are discordant, the test above the diagnostic threshold should be repeated.<ref name="ada2026s2"/>		'''Confirmatory testing:''' In the absence of unequivocal hyperglycemia (classic symptoms plus random glucose ≥200 mg/dL), the diagnosis requires two abnormal test results- either from the same sample or from two separate time points. If two different tests are discordant, the test above the diagnostic threshold should be repeated.<ref name="ada2026s2"/>

	'''Plasma glucose versus HbA1c in acute-onset T1DM:''' Because dysglycemia progression can be rapid in T1DM, '''HbA1c is less sensitive than plasma glucose''' for diagnosing acute-onset disease and may underestimate the degree of hyperglycemia.<ref name="jama2026">{{cite journal \|author=Jacobsen LM, Schatz DA \|title=Type 1 Diabetes: A Review \|journal=JAMA \|year=2026 \|doi=10.1001/jama.2026.0048}}</ref><ref name="~~pmid29894873~~">{{cite journal \|author=DiMeglio LA, Evans-Molina C, Oram RA \|title=Type 1 diabetes \|journal=Lancet \|volume=391 \|issue=10138 \|pages=2449–2462 \|year=2018 \|pmid=~~29894873~~ \|doi=10.1016/S0140-6736(18)31320-5}}</ref> Plasma glucose (fasting, random with symptoms, or OGTT) should be used preferentially when acute-onset T1DM is suspected; HbA1c remains useful for assessing the chronicity of hyperglycemia.<ref name="ada2026s2"/>		'''Plasma glucose versus HbA1c in acute-onset T1DM:''' Because dysglycemia progression can be rapid in T1DM, '''HbA1c is less sensitive than plasma glucose''' for diagnosing acute-onset disease and may underestimate the degree of hyperglycemia.<ref name="jama2026">{{cite journal \|author=Jacobsen LM, Schatz DA \|title=Type 1 Diabetes: A Review \|journal=JAMA \|year=2026 \|pmid=41697686 \|doi=10.1001/jama.2026.0048}}</ref><ref name="pmid29916386">{{cite journal \|author=DiMeglio LA, Evans-Molina C, Oram RA \|title=Type 1 diabetes \|journal=Lancet \|volume=391 \|issue=10138 \|pages=2449–2462 \|year=2018 \|pmid=29916386 \|doi=10.1016/S0140-6736(18)31320-5}}</ref> Plasma glucose (fasting, random with symptoms, or OGTT) should be used preferentially when acute-onset T1DM is suspected; HbA1c remains useful for assessing the chronicity of hyperglycemia.<ref name="ada2026s2"/>

	===Confirming the Diagnosis as Type 1 Diabetes===		===Confirming the Diagnosis as Type 1 Diabetes===
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	* '''Insulin autoantibodies (IAA):''' more common in children; can be positive with exogenous insulin exposure; sensitivity ~52-54%, specificity ~99-100%<ref name="pmid36401613"/>		* '''Insulin autoantibodies (IAA):''' more common in children; can be positive with exogenous insulin exposure; sensitivity ~52-54%, specificity ~99-100%<ref name="pmid36401613"/>

	Standardized islet autoantibody testing is recommended for classification of diabetes in adults with phenotypic features overlapping T1DM (e.g., younger age at diagnosis, unintentional weight loss, ketoacidosis, or short time to insulin treatment) (ADA 2026, Recommendation 2.10, Level E).<ref name="ada2026s2"/> The commonly cited "<35 years of age" threshold derives from the ADA/EASD consensus (as restated in the AACE 2026 statement) rather than from Recommendation 2.10, which uses non-numeric descriptors.<ref name="aace2026">{{cite journal \|author=Samson SL, Vellanki P, Blonde L, ''et al.'' \|title=American Association of Clinical Endocrinology Consensus Statement: Algorithm for Management of Adults With Type 2 Diabetes - 2026 Update \|journal=Endocr Pract \|volume=32 \|issue=4 \|pages=473–518 \|year=2026 \|doi=10.1016/j.eprac.2026.01.006}}</ref> Autoantibody results may be falsely negative (masked) if tested while on corticosteroids or immunosuppressants.<ref name="aace2026"/>		Standardized islet autoantibody testing is recommended for classification of diabetes in adults with phenotypic features overlapping T1DM (e.g., younger age at diagnosis, unintentional weight loss, ketoacidosis, or short time to insulin treatment) (ADA 2026, Recommendation 2.10, Level E).<ref name="ada2026s2"/> The commonly cited "<35 years of age" threshold derives from the ADA/EASD consensus (as restated in the AACE 2026 statement) rather than from Recommendation 2.10, which uses non-numeric descriptors.<ref name="aace2026">{{cite journal \|author=Samson SL, Vellanki P, Blonde L, ''et al.'' \|title=American Association of Clinical Endocrinology Consensus Statement: Algorithm for Management of Adults With Type 2 Diabetes - 2026 Update \|journal=Endocr Pract \|volume=32 \|issue=4 \|pages=473–518 \|year=2026 \|pmid=41842862 \|doi=10.1016/j.eprac.2026.01.006}}</ref> Autoantibody results may be falsely negative (masked) if tested while on corticosteroids or immunosuppressants.<ref name="aace2026"/>

	The ADA 2026 Standards offer the '''AABBCC''' mnemonic to flag adults in whom T1DM should be suspected over T2DM: '''A'''ge (<35 years), '''A'''utoimmunity (personal or family history), '''B'''ody habitus (BMI <25 kg/m²), '''B'''ackground (family history of T1DM), '''C'''ontrol (inability to reach glycemic goals on noninsulin therapies), and '''C'''omorbidities (e.g., checkpoint inhibitor–associated diabetes).<ref name="ada2026s2"/>		The ADA 2026 Standards offer the '''AABBCC''' mnemonic to flag adults in whom T1DM should be suspected over T2DM: '''A'''ge (<35 years), '''A'''utoimmunity (personal or family history), '''B'''ody habitus (BMI <25 kg/m²), '''B'''ackground (family history of T1DM), '''C'''ontrol (inability to reach glycemic goals on noninsulin therapies), and '''C'''omorbidities (e.g., checkpoint inhibitor–associated diabetes).<ref name="ada2026s2"/>
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	\|}		\|}

	This staging framework became clinically actionable with the FDA approval of teplizumab (TZIELD). The current FDA label indicates teplizumab for adult and pediatric patients aged ≥1 year with stage 2 T1DM to delay onset of stage 3 disease, and separately for pediatric patients aged 8-17 years with recently diagnosed stage 3 T1DM to delay the decline in endogenous insulin production. (Note: ADA 2026 Recommendation 3.17 [Level B] still references age ≥8 years for stage 2 treatment, so the guideline and the current label diverge; the FDA label is the authoritative regulatory source.)<ref name="tzieldpi">{{cite web \|title=TZIELD (teplizumab-mzwv) Prescribing Information \|publisher=U.S. Food and Drug Administration \|url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/761183s000lbl.pdf}}</ref><ref name="ada2026s3">{{cite journal \|author=American Diabetes Association Professional Practice Committee \|title=3. Prevention or Delay of Diabetes and Associated Comorbidities: Standards of Care in Diabetes-2026 \|journal=Diabetes Care \|volume=49 \|issue=Suppl 1 \|pages=S59–S85 \|year=2026 \|doi=10.2337/dc26-S003}}</ref> Detailed screening protocols and monitoring of autoantibody-positive individuals are covered in the [[Diabetes mellitus type 1 screening\|Screening]] microchapter.		This staging framework became clinically actionable with the FDA approval of teplizumab (TZIELD). The current FDA label indicates teplizumab for adult and pediatric patients aged ≥1 year with stage 2 T1DM to delay onset of stage 3 disease, and separately for pediatric patients aged 8-17 years with recently diagnosed stage 3 T1DM to delay the decline in endogenous insulin production. (Note: ADA 2026 Recommendation 3.17 [Level B] still references age ≥8 years for stage 2 treatment, so the guideline and the current label diverge; the FDA label is the authoritative regulatory source.)<ref name="tzieldpi">{{cite web \|title=TZIELD (teplizumab-mzwv) Prescribing Information \|publisher=U.S. Food and Drug Administration \|url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2023/761183s000lbl.pdf}}</ref><ref name="ada2026s3">{{cite journal \|author=American Diabetes Association Professional Practice Committee \|title=3. Prevention or Delay of Diabetes and Associated Comorbidities: Standards of Care in Diabetes-2026 \|journal=Diabetes Care \|volume=49 \|issue=Suppl 1 \|pages=S59–S85 \|year=2026 \|pmid=41358891 \|doi=10.2337/dc26-S003}}</ref> Detailed screening protocols and monitoring of autoantibody-positive individuals are covered in the [[Diabetes mellitus type 1 screening\|Screening]] microchapter.

	===Diagnostic Approach===		===Diagnostic Approach===
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	* Plasma glucose, not HbA1c, is the preferred diagnostic test for acute-onset T1DM - HbA1c may be falsely normal with rapid onset.		* Plasma glucose, not HbA1c, is the preferred diagnostic test for acute-onset T1DM - HbA1c may be falsely normal with rapid onset.
	* GAD65 is the single most sensitive autoantibody in adults; a standardized multiplex panel of GAD65 + IA-2 + ZnT8 achieves ~94–96% sensitivity at 98–100% specificity (IASP 2024 workshop).<ref name="dc2026iasp">{{cite journal \|author=Marzinotto I, Pittman DL, Achenbach P, ''et al.'' \|title=Interlaboratory evaluation of multiplex autoantibody assay performance in the Islet Autoantibody Standardization Program 2024 Workshop \|journal=Diabetes Care \|volume=49 \|issue=4 \|pages=607–615 \|year=2026 \|doi=10.2337/dc25-1326}}</ref>		* GAD65 is the single most sensitive autoantibody in adults; a standardized multiplex panel of GAD65 + IA-2 + ZnT8 achieves ~94–96% sensitivity at 98–100% specificity (IASP 2024 workshop).<ref name="dc2026iasp">{{cite journal \|author=Marzinotto I, Pittman DL, Achenbach P, ''et al.'' \|title=Interlaboratory evaluation of multiplex autoantibody assay performance in the Islet Autoantibody Standardization Program 2024 Workshop \|journal=Diabetes Care \|volume=49 \|issue=4 \|pages=607–615 \|year=2026 \|pmid=41575380 \|doi=10.2337/dc25-1326}}</ref>
	* Misdiagnosis as T2DM occurs in up to ~40% of adults with new-onset T1DM (ADA 2026; the earlier Lancet estimate was as high as 50%)- maintain a low threshold for autoantibody testing when clinical features are atypical.<ref name="ada2026s2"/><ref name="~~pmid29894873~~"/>		* Misdiagnosis as T2DM occurs in up to ~40% of adults with new-onset T1DM (ADA 2026; the earlier Lancet estimate was as high as 50%)- maintain a low threshold for autoantibody testing when clinical features are atypical.<ref name="ada2026s2"/><ref name="pmid29916386"/>
	* Two or more autoantibodies with normoglycemia (stage 1) confer ~100% lifetime risk of progression to clinical T1DM.<ref name="jama2026"/>		* Two or more autoantibodies with normoglycemia (stage 1) confer ~100% lifetime risk of progression to clinical T1DM.<ref name="jama2026"/>
	* Wait ≥2 weeks after DKA resolution before measuring C-peptide to avoid glucotoxicity-related suppression.<ref name="pmid35676794"/>		* Wait ≥2 weeks after DKA resolution before measuring C-peptide to avoid glucotoxicity-related suppression.<ref name="pmid35676794"/>