Cardiology
Photo
🔵 𝙈𝙚𝙘𝙝𝙖𝙣𝙞𝙨𝙢𝙨 𝙤𝙛 𝘼𝙣𝙜𝙞𝙤𝙥𝙡𝙖𝙨𝙩𝙮 𝙖𝙣𝙙 𝙎𝙩𝙚𝙣𝙩𝙞𝙣𝙜
#CCU_CORONARY
1️⃣. 𝘿𝙞𝙨𝙧𝙪𝙥𝙩𝙞𝙤𝙣 𝙤𝙛 𝙋𝙡𝙖𝙦𝙪𝙚 𝙖𝙣𝙙 𝙩𝙝𝙚 𝘼𝙧𝙩𝙚𝙧𝙞𝙖𝙡 𝙒𝙖𝙡𝙡
==============================
The inflated balloon exerts pressure against the plaque
and the arterial wall, causing fracturing and splitting.
• Concentric (round or circumferential) lesions
fracture and split at the thinnest and weakest points.
• Eccentric lesions split at the junction of plaque
and the normal arterial wall.
• Dissection or separation of the plaque from
vessel wall releases the restraining effect
caused by the lesion and results in a larger lumen.
👉This is the major mechanism of balloon angioplasty.
2️⃣. 𝙇𝙤𝙨𝙨 𝙤𝙛 𝙀𝙡𝙖𝙨𝙩𝙞𝙘 𝙍𝙚𝙘𝙤𝙞𝙡
===============
• Balloon dilatation causes stretching and thinning
of the medial musculature of the vessel wall.
• Stretching causes the vessel wall to temporarily
lose its elastic (recoil) properties.
• The degree of elastic recoil is affected by
the balloon-to-artery size ratio.
• Almost all vessels have some elastic recoil and,
over time, will recoil, which is a contributing
mechanism to restenosis.
• The major initial benefit of stenting is elimination
of elastic recoil, which maintains a large lumen over time.
3️⃣. 𝙍𝙚𝙙𝙞𝙨𝙩𝙧𝙞𝙗𝙪𝙩𝙞𝙤𝙣 & 𝘾𝙤𝙢𝙥𝙧𝙚𝙨𝙨𝙞𝙤𝙣 𝙤𝙛 𝙋𝙡𝙖𝙦𝙪𝙚
=============================
• During angioplasty, balloon pressure causes
denudation of vessel wall lining (endothelial)
cells and extrusion or pushing out of plaque components.
• There may be some extrusion longitudinally of
the softer lipid material, but this effect accounts
for a very small part of the overall effect.
💢 𝙋𝘾𝙄 𝙨𝙪𝙘𝙘𝙚𝙨𝙨 𝙙𝙚𝙛𝙞𝙣𝙚𝙙 𝙗𝙮
=================
Angiographic, Procedural, and Clinical criteria.
💜 𝘼𝙣𝙜𝙞𝙤𝙜𝙧𝙖𝙥𝙝𝙞𝙘 𝙎𝙪𝙘𝙘𝙚𝙨𝙨
================
• Final minimum stenosis diameter reduction to <10%.
❤️ 𝙋𝙧𝙤𝙘𝙚𝙙𝙪𝙧𝙖𝙡 𝙎𝙪𝙘𝙘𝙚𝙨𝙨
==============
• Angiographic success without in-hospital
major clinical complications
(e.g., death, m [MI], emergency CABG).
• MI is often defined as the development of
Q-waves in addition to elevation of troponins
three times the upper limits of normal value.
• Cardiac troponin T and I as measurements of
myocardial necrosis are more sensitive and
specific than CK-MB.
• Enzyme elevations in the absence of new
Q-waves is counted as MI, peri-procedural.
• There is no consensus on what level of troponin
alone is clinically important enough to change
major management following the interventional procedure.
💚 𝘾𝙡𝙞𝙣𝙞𝙘𝙖𝙡 𝙎𝙪𝙘𝙘𝙚𝙨𝙨
============
• A clinically successful PCI is an anatomic and
procedural success with relief of signs and/or
symptoms of myocardial ischemia after recovery
from the procedure.
• The long-term clinical success requires that
patient has continued relief of signs ,symptoms
of myocardial ischemia for more than 6 months.
• Restenosis is the principal cause of lack of
long-term clinical success when short-term
clinical success has been achieved.
❇️ 𝙃𝙤𝙬 𝘼𝙣𝙜𝙞𝙤𝙥𝙡𝙖𝙨𝙩𝙮 𝙖𝙣𝙙 𝙎𝙩𝙚𝙣𝙩𝙞𝙣𝙜 𝙒𝙤𝙧𝙠𝙨 ❓
=============================
(𝐀) The artery is filled with atherosclerotic material,
compromising the lumen.
A cross-section of artery is shown on RT side.
(𝘽) Guidewire is positioned past the stenoses
through the lumen.
(𝘾) Balloon catheter is advanced over guidewire.
(𝘿) The balloon is inflated.
(𝙀) The balloon is deflated and withdrawn.
(𝙁) The balloon catheter is exchanged for a stent
(on a balloon).
(𝙂) The stent is expanded.
(𝙃) The expanded stent remains in place after
the deflated balloon is withdrawn.
https://www.tg-me.com/cardiology
#CCU_CORONARY
1️⃣. 𝘿𝙞𝙨𝙧𝙪𝙥𝙩𝙞𝙤𝙣 𝙤𝙛 𝙋𝙡𝙖𝙦𝙪𝙚 𝙖𝙣𝙙 𝙩𝙝𝙚 𝘼𝙧𝙩𝙚𝙧𝙞𝙖𝙡 𝙒𝙖𝙡𝙡
==============================
The inflated balloon exerts pressure against the plaque
and the arterial wall, causing fracturing and splitting.
• Concentric (round or circumferential) lesions
fracture and split at the thinnest and weakest points.
• Eccentric lesions split at the junction of plaque
and the normal arterial wall.
• Dissection or separation of the plaque from
vessel wall releases the restraining effect
caused by the lesion and results in a larger lumen.
👉This is the major mechanism of balloon angioplasty.
2️⃣. 𝙇𝙤𝙨𝙨 𝙤𝙛 𝙀𝙡𝙖𝙨𝙩𝙞𝙘 𝙍𝙚𝙘𝙤𝙞𝙡
===============
• Balloon dilatation causes stretching and thinning
of the medial musculature of the vessel wall.
• Stretching causes the vessel wall to temporarily
lose its elastic (recoil) properties.
• The degree of elastic recoil is affected by
the balloon-to-artery size ratio.
• Almost all vessels have some elastic recoil and,
over time, will recoil, which is a contributing
mechanism to restenosis.
• The major initial benefit of stenting is elimination
of elastic recoil, which maintains a large lumen over time.
3️⃣. 𝙍𝙚𝙙𝙞𝙨𝙩𝙧𝙞𝙗𝙪𝙩𝙞𝙤𝙣 & 𝘾𝙤𝙢𝙥𝙧𝙚𝙨𝙨𝙞𝙤𝙣 𝙤𝙛 𝙋𝙡𝙖𝙦𝙪𝙚
=============================
• During angioplasty, balloon pressure causes
denudation of vessel wall lining (endothelial)
cells and extrusion or pushing out of plaque components.
• There may be some extrusion longitudinally of
the softer lipid material, but this effect accounts
for a very small part of the overall effect.
💢 𝙋𝘾𝙄 𝙨𝙪𝙘𝙘𝙚𝙨𝙨 𝙙𝙚𝙛𝙞𝙣𝙚𝙙 𝙗𝙮
=================
Angiographic, Procedural, and Clinical criteria.
💜 𝘼𝙣𝙜𝙞𝙤𝙜𝙧𝙖𝙥𝙝𝙞𝙘 𝙎𝙪𝙘𝙘𝙚𝙨𝙨
================
• Final minimum stenosis diameter reduction to <10%.
❤️ 𝙋𝙧𝙤𝙘𝙚𝙙𝙪𝙧𝙖𝙡 𝙎𝙪𝙘𝙘𝙚𝙨𝙨
==============
• Angiographic success without in-hospital
major clinical complications
(e.g., death, m [MI], emergency CABG).
• MI is often defined as the development of
Q-waves in addition to elevation of troponins
three times the upper limits of normal value.
• Cardiac troponin T and I as measurements of
myocardial necrosis are more sensitive and
specific than CK-MB.
• Enzyme elevations in the absence of new
Q-waves is counted as MI, peri-procedural.
• There is no consensus on what level of troponin
alone is clinically important enough to change
major management following the interventional procedure.
💚 𝘾𝙡𝙞𝙣𝙞𝙘𝙖𝙡 𝙎𝙪𝙘𝙘𝙚𝙨𝙨
============
• A clinically successful PCI is an anatomic and
procedural success with relief of signs and/or
symptoms of myocardial ischemia after recovery
from the procedure.
• The long-term clinical success requires that
patient has continued relief of signs ,symptoms
of myocardial ischemia for more than 6 months.
• Restenosis is the principal cause of lack of
long-term clinical success when short-term
clinical success has been achieved.
❇️ 𝙃𝙤𝙬 𝘼𝙣𝙜𝙞𝙤𝙥𝙡𝙖𝙨𝙩𝙮 𝙖𝙣𝙙 𝙎𝙩𝙚𝙣𝙩𝙞𝙣𝙜 𝙒𝙤𝙧𝙠𝙨 ❓
=============================
(𝐀) The artery is filled with atherosclerotic material,
compromising the lumen.
A cross-section of artery is shown on RT side.
(𝘽) Guidewire is positioned past the stenoses
through the lumen.
(𝘾) Balloon catheter is advanced over guidewire.
(𝘿) The balloon is inflated.
(𝙀) The balloon is deflated and withdrawn.
(𝙁) The balloon catheter is exchanged for a stent
(on a balloon).
(𝙂) The stent is expanded.
(𝙃) The expanded stent remains in place after
the deflated balloon is withdrawn.
https://www.tg-me.com/cardiology
Telegram
Cardiology
👨💻 @dr_navruz
𝐒𝐭𝐞𝐧𝐭 𝐓𝐡𝐫𝐨𝐦𝐛𝐨𝐬𝐢𝐬
#CCU_CORONARY
Stent Thrombosis, although rare (occur in <1%
patients within the first year), is one of the most
serious complications following stent placement.
More than 80% of patients who experience
stent thrombosis present with acute MI, and
30-day mortality rates in patients with stent
thrombosis range from 10% to 25%.
As a result, prevention and treatment of
this complication are of utmost importance.
————————————————————————-
𝙏𝙝𝙚 𝙢𝙤𝙨𝙩 𝙬𝙞𝙙𝙚𝙡𝙮 𝙪𝙨𝙚𝙙 𝙙𝙚𝙛𝙞𝙣𝙞𝙩𝙞𝙤𝙣 𝙞𝙣𝙫𝙤𝙡𝙫𝙞𝙣𝙜 𝙩𝙝𝙚 𝙘𝙡𝙖𝙨𝙨𝙞𝙛𝙞𝙘𝙖𝙩𝙞𝙤𝙣 𝙖𝙣𝙙 𝙩𝙞𝙢𝙞𝙣𝙜 𝙤𝙛 𝙨𝙩𝙚𝙣𝙩 𝙩𝙝𝙧𝙤𝙢𝙗𝙤𝙨𝙞𝙨 𝙬𝙖𝙨 𝙙𝙚𝙫𝙚𝙡𝙤𝙥𝙚𝙙 𝙗𝙮 𝙩𝙝𝙚 𝘼𝙘𝙖𝙙𝙚𝙢𝙞𝙘 𝙍𝙚𝙨𝙚𝙖𝙧𝙘𝙝 𝘾𝙤𝙣𝙨𝙤𝙧𝙩𝙞𝙪𝙢
𝐃𝐞𝐟𝐢𝐧𝐢𝐭𝐞 stent thrombosis is confirmed by
angiographic or autopsy evidence of thrombus in the setting of an acute coronary syndrome, and
𝐏𝐫𝐨𝐛𝐚𝐛𝐥𝐞 stent thrombosis is defined as
unexplained death within 30 days after stent implantation or acute MI involving the target vessel territory without angiographic confirmation.
𝘼𝙘𝙪𝙩𝙚 𝙩𝙝𝙧𝙤𝙢𝙗𝙤𝙨𝙞𝙨 𝙤𝙘𝙘𝙪𝙧𝙨 𝙬𝙞𝙩𝙝𝙞𝙣 24 𝙝𝙤𝙪𝙧𝙨
(excluding intraprocedural events within
the catheterization laboratory),
𝙎𝙪𝙗𝙖𝙘𝙪𝙩𝙚 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 1 𝙙𝙖𝙮 𝙖𝙣𝙙 30 𝙙𝙖𝙮𝙨,
𝙀𝙖𝙧𝙡𝙮 𝙬𝙞𝙩𝙝𝙞𝙣 30 𝙙𝙖𝙮𝙨
(counting both acute and subacute events),
𝙇𝙖𝙩𝙚 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 30 𝙙𝙖𝙮𝙨 𝙖𝙣𝙙 1 𝙮𝙚𝙖𝙧, and
𝙑𝙚𝙧𝙮 𝙇𝙖𝙩𝙚 𝙖𝙛𝙩𝙚𝙧 1 𝙮𝙚𝙖𝙧.
————————————————————————
𝙏𝙝𝙧𝙤𝙢𝙗𝙤𝙩𝙞𝙘 𝙤𝙘𝙘𝙡𝙪𝙨𝙞𝙤𝙣 is classified as :-
▫️ 𝙋𝙧𝙞𝙢𝙖𝙧𝙮 if it is directly related to the stent implantation
▫️ 𝙎𝙚𝙘𝙤𝙣𝙙𝙖𝙧𝙮 if it occurs at the stent site after
a subsequent intervention to the target lesion.
Risk Factors Stent thrombosis can occur as
a result of many reasons, including •••
𝙋𝙖𝙩𝙞𝙚𝙣𝙩-𝙧𝙚𝙡𝙖𝙩𝙚𝙙 𝙛𝙖𝙘𝙩𝙤𝙧𝙨
———————————-
Patients who 𝙥𝙧𝙚𝙨𝙚𝙣𝙩 𝙬𝙞𝙩𝙝 thrombotic ACS, Smokers, and Diabetes and/or chronic kidney as well as severely depressed left ventricular function
are all more prone to stent thrombosis.
High residual 𝙥𝙡𝙖𝙩𝙚𝙡𝙚𝙩 𝙧𝙚𝙖𝙘𝙩𝙞𝙫𝙞𝙩𝙮 after treatment,
which can be seen in patients with genetic mutations in the enzyme responsible for
converting clopidogrel to its active metabolite,
has been associated with stent thrombosis.
𝙇𝙚𝙨𝙞𝙤𝙣 𝙛𝙖𝙘𝙩𝙤𝙧𝙨 that increase risk of thrombosis include diffuse disease with long stented segments, small vessels, bifurcation disease, and significant inflow or outflow lesions proximal or distal to the stent.
𝙋𝙧𝙤𝙘𝙚𝙙𝙪𝙧𝙖𝙡 𝙛𝙖𝙘𝙩𝙤𝙧𝙨 :
—————————
▫️inadequate stent expansion and/or apposition,
▫️Stent type used (i.e., BMS or DES),
▫️Excessive stent overlap, and
▫️Edge dissections limiting inflow or outflow.
▫️Strut fracture linked to +Risk of thrombosis.
The thicker struts of earlier generation BMS and DES systems have been associated with increased risk of stent thrombosis, and this may have implications in the thrombosis risk of first-generation bioabsorbable scaffolds.
In addition, the polymers used in certain first-generation DES systems may be inherently throm-bogenic and/or prone to mechanical deformation after implantation, serving as a nidus for thombus formation.
𝙋𝙤𝙨𝙩𝙥𝙧𝙤𝙘𝙚𝙙𝙪𝙧𝙖𝙡 𝙧𝙞𝙨𝙠 𝙛𝙖𝙘𝙩𝙤𝙧𝙨:-
—————————————-
▫️ 𝐃iscontinuation Early of dual-antiplatelet
(although the ideal length of treatment
varies by the specific stent system),
▫️ 𝐃elayed re-endothelialization of stent struts
in DES systems due to antiproliferative agent
▫️ 𝐃evelopment of neoatherosclerosis within
the stent leading to plaque rupture.
Specific strategies aimed at reducing the occurrence of stent thrombosis are shown image👇
————————————————————————-
𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐨𝐟 𝐬𝐭𝐞𝐧𝐭 𝐭𝐡𝐫𝐨𝐦𝐛𝐨𝐬𝐢𝐬,
especially when presenting as acute MI,
is almost always 𝙀𝙢𝙚𝙧𝙜𝙚𝙣𝙩 𝙋𝘾𝙄.
▪️Options for restoring perfusion include :
▫️ 𝙏𝙝𝙧𝙤𝙢𝙗𝙚𝙘𝙩𝙤𝙢𝙮 either aspiration or mechanical
#CCU_CORONARY
Stent Thrombosis, although rare (occur in <1%
patients within the first year), is one of the most
serious complications following stent placement.
More than 80% of patients who experience
stent thrombosis present with acute MI, and
30-day mortality rates in patients with stent
thrombosis range from 10% to 25%.
As a result, prevention and treatment of
this complication are of utmost importance.
————————————————————————-
𝙏𝙝𝙚 𝙢𝙤𝙨𝙩 𝙬𝙞𝙙𝙚𝙡𝙮 𝙪𝙨𝙚𝙙 𝙙𝙚𝙛𝙞𝙣𝙞𝙩𝙞𝙤𝙣 𝙞𝙣𝙫𝙤𝙡𝙫𝙞𝙣𝙜 𝙩𝙝𝙚 𝙘𝙡𝙖𝙨𝙨𝙞𝙛𝙞𝙘𝙖𝙩𝙞𝙤𝙣 𝙖𝙣𝙙 𝙩𝙞𝙢𝙞𝙣𝙜 𝙤𝙛 𝙨𝙩𝙚𝙣𝙩 𝙩𝙝𝙧𝙤𝙢𝙗𝙤𝙨𝙞𝙨 𝙬𝙖𝙨 𝙙𝙚𝙫𝙚𝙡𝙤𝙥𝙚𝙙 𝙗𝙮 𝙩𝙝𝙚 𝘼𝙘𝙖𝙙𝙚𝙢𝙞𝙘 𝙍𝙚𝙨𝙚𝙖𝙧𝙘𝙝 𝘾𝙤𝙣𝙨𝙤𝙧𝙩𝙞𝙪𝙢
𝐃𝐞𝐟𝐢𝐧𝐢𝐭𝐞 stent thrombosis is confirmed by
angiographic or autopsy evidence of thrombus in the setting of an acute coronary syndrome, and
𝐏𝐫𝐨𝐛𝐚𝐛𝐥𝐞 stent thrombosis is defined as
unexplained death within 30 days after stent implantation or acute MI involving the target vessel territory without angiographic confirmation.
𝘼𝙘𝙪𝙩𝙚 𝙩𝙝𝙧𝙤𝙢𝙗𝙤𝙨𝙞𝙨 𝙤𝙘𝙘𝙪𝙧𝙨 𝙬𝙞𝙩𝙝𝙞𝙣 24 𝙝𝙤𝙪𝙧𝙨
(excluding intraprocedural events within
the catheterization laboratory),
𝙎𝙪𝙗𝙖𝙘𝙪𝙩𝙚 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 1 𝙙𝙖𝙮 𝙖𝙣𝙙 30 𝙙𝙖𝙮𝙨,
𝙀𝙖𝙧𝙡𝙮 𝙬𝙞𝙩𝙝𝙞𝙣 30 𝙙𝙖𝙮𝙨
(counting both acute and subacute events),
𝙇𝙖𝙩𝙚 𝙗𝙚𝙩𝙬𝙚𝙚𝙣 30 𝙙𝙖𝙮𝙨 𝙖𝙣𝙙 1 𝙮𝙚𝙖𝙧, and
𝙑𝙚𝙧𝙮 𝙇𝙖𝙩𝙚 𝙖𝙛𝙩𝙚𝙧 1 𝙮𝙚𝙖𝙧.
————————————————————————
𝙏𝙝𝙧𝙤𝙢𝙗𝙤𝙩𝙞𝙘 𝙤𝙘𝙘𝙡𝙪𝙨𝙞𝙤𝙣 is classified as :-
▫️ 𝙋𝙧𝙞𝙢𝙖𝙧𝙮 if it is directly related to the stent implantation
▫️ 𝙎𝙚𝙘𝙤𝙣𝙙𝙖𝙧𝙮 if it occurs at the stent site after
a subsequent intervention to the target lesion.
Risk Factors Stent thrombosis can occur as
a result of many reasons, including •••
𝙋𝙖𝙩𝙞𝙚𝙣𝙩-𝙧𝙚𝙡𝙖𝙩𝙚𝙙 𝙛𝙖𝙘𝙩𝙤𝙧𝙨
———————————-
Patients who 𝙥𝙧𝙚𝙨𝙚𝙣𝙩 𝙬𝙞𝙩𝙝 thrombotic ACS, Smokers, and Diabetes and/or chronic kidney as well as severely depressed left ventricular function
are all more prone to stent thrombosis.
High residual 𝙥𝙡𝙖𝙩𝙚𝙡𝙚𝙩 𝙧𝙚𝙖𝙘𝙩𝙞𝙫𝙞𝙩𝙮 after treatment,
which can be seen in patients with genetic mutations in the enzyme responsible for
converting clopidogrel to its active metabolite,
has been associated with stent thrombosis.
𝙇𝙚𝙨𝙞𝙤𝙣 𝙛𝙖𝙘𝙩𝙤𝙧𝙨 that increase risk of thrombosis include diffuse disease with long stented segments, small vessels, bifurcation disease, and significant inflow or outflow lesions proximal or distal to the stent.
𝙋𝙧𝙤𝙘𝙚𝙙𝙪𝙧𝙖𝙡 𝙛𝙖𝙘𝙩𝙤𝙧𝙨 :
—————————
▫️inadequate stent expansion and/or apposition,
▫️Stent type used (i.e., BMS or DES),
▫️Excessive stent overlap, and
▫️Edge dissections limiting inflow or outflow.
▫️Strut fracture linked to +Risk of thrombosis.
The thicker struts of earlier generation BMS and DES systems have been associated with increased risk of stent thrombosis, and this may have implications in the thrombosis risk of first-generation bioabsorbable scaffolds.
In addition, the polymers used in certain first-generation DES systems may be inherently throm-bogenic and/or prone to mechanical deformation after implantation, serving as a nidus for thombus formation.
𝙋𝙤𝙨𝙩𝙥𝙧𝙤𝙘𝙚𝙙𝙪𝙧𝙖𝙡 𝙧𝙞𝙨𝙠 𝙛𝙖𝙘𝙩𝙤𝙧𝙨:-
—————————————-
▫️ 𝐃iscontinuation Early of dual-antiplatelet
(although the ideal length of treatment
varies by the specific stent system),
▫️ 𝐃elayed re-endothelialization of stent struts
in DES systems due to antiproliferative agent
▫️ 𝐃evelopment of neoatherosclerosis within
the stent leading to plaque rupture.
Specific strategies aimed at reducing the occurrence of stent thrombosis are shown image👇
————————————————————————-
𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐨𝐟 𝐬𝐭𝐞𝐧𝐭 𝐭𝐡𝐫𝐨𝐦𝐛𝐨𝐬𝐢𝐬,
especially when presenting as acute MI,
is almost always 𝙀𝙢𝙚𝙧𝙜𝙚𝙣𝙩 𝙋𝘾𝙄.
▪️Options for restoring perfusion include :
▫️ 𝙏𝙝𝙧𝙤𝙢𝙗𝙚𝙘𝙩𝙤𝙢𝙮 either aspiration or mechanical
▫️ and/or 𝙗𝙖𝙡𝙡𝙤𝙤𝙣 𝙖𝙣𝙜𝙞𝙤𝙥𝙡𝙖𝙨𝙩𝙮 with
▫️ Administration of more potent pharmacologic
agents such as 𝙜𝙡𝙮𝙘𝙤𝙥𝙧𝙤𝙩𝙚𝙞𝙣 𝙄𝙄𝙗/𝙄𝙄𝙄𝙖 𝙞𝙣𝙝𝙞𝙗𝙞𝙩𝙤𝙧𝙨
at the discretion of the operator.
▪️𝘼𝙙𝙟𝙪𝙣𝙘𝙩𝙞𝙫𝙚 𝙞𝙢𝙖𝙜𝙞𝙣𝙜 𝙬ith modalities such as
𝙄𝙑𝙐𝙎 𝙤𝙧 𝙊𝘾𝙏 can be very helpful in discerning
the underlying etiology of the thrombosis
(e.g., stent underexpansion/malapposition or
residual dissection) and is recommended prior to
further balloon manipulation of the stented site.
▪️ 𝘼𝙙𝙙𝙞𝙩𝙞𝙤𝙣𝙖𝙡 𝙨𝙩𝙚𝙣𝙩𝙨 𝙖𝙧𝙚 𝙩𝙮𝙥𝙞𝙘𝙖𝙡𝙡𝙮 𝙖𝙫𝙤𝙞𝙙𝙚𝙙 unless
a mechanical reason for the thrombosis
(such as edge dissection) is seen.
▪️ 𝙀𝙫𝙖𝙡𝙪𝙖𝙩𝙞𝙤𝙣 𝙣𝙤𝙣𝙢𝙚𝙘𝙝𝙖𝙣𝙞𝙘𝙖𝙡 𝙘𝙖𝙪𝙨𝙚𝙨 𝙤𝙛 𝙩𝙝𝙧𝙤𝙢𝙗𝙤𝙨𝙞𝙨
such as hypercoagulable state, thrombocytosis,
or aspirin/clopidogrel resistance should considered.
▪️ 𝙀𝙨𝙘𝙖𝙡𝙖𝙩𝙞𝙤𝙣 𝙤𝙛 𝙢𝙖𝙞𝙣𝙩𝙚𝙣𝙖𝙣𝙘𝙚 𝙖𝙣𝙩𝙞𝙥𝙡𝙖𝙩𝙚𝙡𝙚𝙩 𝙩𝙝𝙚𝙧𝙖𝙥𝙮
(e.g., from clopidogrel to more potent oral
antiplatelet therapies such as prasugrel or
ticagrelor) is standard.
https://www.tg-me.com/cardiology
▫️ Administration of more potent pharmacologic
agents such as 𝙜𝙡𝙮𝙘𝙤𝙥𝙧𝙤𝙩𝙚𝙞𝙣 𝙄𝙄𝙗/𝙄𝙄𝙄𝙖 𝙞𝙣𝙝𝙞𝙗𝙞𝙩𝙤𝙧𝙨
at the discretion of the operator.
▪️𝘼𝙙𝙟𝙪𝙣𝙘𝙩𝙞𝙫𝙚 𝙞𝙢𝙖𝙜𝙞𝙣𝙜 𝙬ith modalities such as
𝙄𝙑𝙐𝙎 𝙤𝙧 𝙊𝘾𝙏 can be very helpful in discerning
the underlying etiology of the thrombosis
(e.g., stent underexpansion/malapposition or
residual dissection) and is recommended prior to
further balloon manipulation of the stented site.
▪️ 𝘼𝙙𝙙𝙞𝙩𝙞𝙤𝙣𝙖𝙡 𝙨𝙩𝙚𝙣𝙩𝙨 𝙖𝙧𝙚 𝙩𝙮𝙥𝙞𝙘𝙖𝙡𝙡𝙮 𝙖𝙫𝙤𝙞𝙙𝙚𝙙 unless
a mechanical reason for the thrombosis
(such as edge dissection) is seen.
▪️ 𝙀𝙫𝙖𝙡𝙪𝙖𝙩𝙞𝙤𝙣 𝙣𝙤𝙣𝙢𝙚𝙘𝙝𝙖𝙣𝙞𝙘𝙖𝙡 𝙘𝙖𝙪𝙨𝙚𝙨 𝙤𝙛 𝙩𝙝𝙧𝙤𝙢𝙗𝙤𝙨𝙞𝙨
such as hypercoagulable state, thrombocytosis,
or aspirin/clopidogrel resistance should considered.
▪️ 𝙀𝙨𝙘𝙖𝙡𝙖𝙩𝙞𝙤𝙣 𝙤𝙛 𝙢𝙖𝙞𝙣𝙩𝙚𝙣𝙖𝙣𝙘𝙚 𝙖𝙣𝙩𝙞𝙥𝙡𝙖𝙩𝙚𝙡𝙚𝙩 𝙩𝙝𝙚𝙧𝙖𝙥𝙮
(e.g., from clopidogrel to more potent oral
antiplatelet therapies such as prasugrel or
ticagrelor) is standard.
https://www.tg-me.com/cardiology
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👨💻 @dr_navruz