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History of Heart Failure Definition

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Cardiology
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๐Ÿ”ต ๐™ˆ๐™š๐™˜๐™๐™–๐™ฃ๐™ž๐™จ๐™ข๐™จ ๐™ค๐™› ๐˜ผ๐™ฃ๐™œ๐™ž๐™ค๐™ฅ๐™ก๐™–๐™จ๐™ฉ๐™ฎ ๐™–๐™ฃ๐™™ ๐™Ž๐™ฉ๐™š๐™ฃ๐™ฉ๐™ž๐™ฃ๐™œ
#CCU_CORONARY

1๏ธโƒฃ. ๐˜ฟ๐™ž๐™จ๐™ง๐™ช๐™ฅ๐™ฉ๐™ž๐™ค๐™ฃ ๐™ค๐™› ๐™‹๐™ก๐™–๐™ฆ๐™ช๐™š ๐™–๐™ฃ๐™™ ๐™ฉ๐™๐™š ๐˜ผ๐™ง๐™ฉ๐™š๐™ง๐™ž๐™–๐™ก ๐™’๐™–๐™ก๐™ก
==============================
The inflated balloon exerts pressure against the plaque
and the arterial wall, causing fracturing and splitting.

โ€ข Concentric (round or circumferential) lesions
fracture and split at the thinnest and weakest points.

โ€ข Eccentric lesions split at the junction of plaque
and the normal arterial wall.

โ€ข Dissection or separation of the plaque from
vessel wall releases the restraining effect
caused by the lesion and results in a larger lumen.

๐Ÿ‘‰This is the major mechanism of balloon angioplasty.

2๏ธโƒฃ. ๐™‡๐™ค๐™จ๐™จ ๐™ค๐™› ๐™€๐™ก๐™–๐™จ๐™ฉ๐™ž๐™˜ ๐™๐™š๐™˜๐™ค๐™ž๐™ก
===============
โ€ข Balloon dilatation causes stretching and thinning
of the medial musculature of the vessel wall.

โ€ข Stretching causes the vessel wall to temporarily
lose its elastic (recoil) properties.

โ€ข The degree of elastic recoil is affected by
the balloon-to-artery size ratio.

โ€ข Almost all vessels have some elastic recoil and,
over time, will recoil, which is a contributing
mechanism to restenosis.

โ€ข The major initial benefit of stenting is elimination
of elastic recoil, which maintains a large lumen over time.

3๏ธโƒฃ. ๐™๐™š๐™™๐™ž๐™จ๐™ฉ๐™ง๐™ž๐™—๐™ช๐™ฉ๐™ž๐™ค๐™ฃ & ๐˜พ๐™ค๐™ข๐™ฅ๐™ง๐™š๐™จ๐™จ๐™ž๐™ค๐™ฃ ๐™ค๐™› ๐™‹๐™ก๐™–๐™ฆ๐™ช๐™š
=============================
โ€ข During angioplasty, balloon pressure causes
denudation of vessel wall lining (endothelial)
cells and extrusion or pushing out of plaque components.

โ€ข There may be some extrusion longitudinally of
the softer lipid material, but this effect accounts
for a very small part of the overall effect.

๐Ÿ’ข ๐™‹๐˜พ๐™„ ๐™จ๐™ช๐™˜๐™˜๐™š๐™จ๐™จ ๐™™๐™š๐™›๐™ž๐™ฃ๐™š๐™™ ๐™—๐™ฎ
=================
Angiographic, Procedural, and Clinical criteria.

๐Ÿ’œ ๐˜ผ๐™ฃ๐™œ๐™ž๐™ค๐™œ๐™ง๐™–๐™ฅ๐™๐™ž๐™˜ ๐™Ž๐™ช๐™˜๐™˜๐™š๐™จ๐™จ
================
โ€ข Final minimum stenosis diameter reduction to <10%.

โค๏ธ ๐™‹๐™ง๐™ค๐™˜๐™š๐™™๐™ช๐™ง๐™–๐™ก ๐™Ž๐™ช๐™˜๐™˜๐™š๐™จ๐™จ
==============
โ€ข Angiographic success without in-hospital
major clinical complications
(e.g., death, m [MI], emergency CABG).

โ€ข MI is often defined as the development of
Q-waves in addition to elevation of troponins
three times the upper limits of normal value.

โ€ข Cardiac troponin T and I as measurements of
myocardial necrosis are more sensitive and
specific than CK-MB.

โ€ข Enzyme elevations in the absence of new
Q-waves is counted as MI, peri-procedural.

โ€ข There is no consensus on what level of troponin
alone is clinically important enough to change
major management following the interventional procedure.

๐Ÿ’š ๐˜พ๐™ก๐™ž๐™ฃ๐™ž๐™˜๐™–๐™ก ๐™Ž๐™ช๐™˜๐™˜๐™š๐™จ๐™จ
============
โ€ข 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.

โ€ข The long-term clinical success requires that
patient has continued relief of signs ,symptoms
of myocardial ischemia for more than 6 months.

โ€ข Restenosis is the principal cause of lack of
long-term clinical success when short-term
clinical success has been achieved.

โ‡๏ธ ๐™ƒ๐™ค๐™ฌ ๐˜ผ๐™ฃ๐™œ๐™ž๐™ค๐™ฅ๐™ก๐™–๐™จ๐™ฉ๐™ฎ ๐™–๐™ฃ๐™™ ๐™Ž๐™ฉ๐™š๐™ฃ๐™ฉ๐™ž๐™ฃ๐™œ ๐™’๐™ค๐™ง๐™ ๐™จ โ“
=============================
(๐€) The artery is filled with atherosclerotic material,
compromising the lumen.
A cross-section of artery is shown on RT side.

(๐˜ฝ) Guidewire is positioned past the stenoses
through the lumen.

(๐˜พ) Balloon catheter is advanced over guidewire.

(๐˜ฟ) The balloon is inflated.

(๐™€) The balloon is deflated and withdrawn.

(๐™) The balloon catheter is exchanged for a stent
(on a balloon).

(๐™‚) The stent is expanded.

(๐™ƒ) The expanded stent remains in place after
the deflated balloon is withdrawn.

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๐’๐ญ๐ž๐ง๐ญ ๐“๐ก๐ซ๐จ๐ฆ๐›๐จ๐ฌ๐ข๐ฌ
#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.
โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”-
๐™๐™๐™š ๐™ข๐™ค๐™จ๐™ฉ ๐™ฌ๐™ž๐™™๐™š๐™ก๐™ฎ ๐™ช๐™จ๐™š๐™™ ๐™™๐™š๐™›๐™ž๐™ฃ๐™ž๐™ฉ๐™ž๐™ค๐™ฃ ๐™ž๐™ฃ๐™ซ๐™ค๐™ก๐™ซ๐™ž๐™ฃ๐™œ ๐™ฉ๐™๐™š ๐™˜๐™ก๐™–๐™จ๐™จ๐™ž๐™›๐™ž๐™˜๐™–๐™ฉ๐™ž๐™ค๐™ฃ ๐™–๐™ฃ๐™™ ๐™ฉ๐™ž๐™ข๐™ž๐™ฃ๐™œ ๐™ค๐™› ๐™จ๐™ฉ๐™š๐™ฃ๐™ฉ ๐™ฉ๐™๐™ง๐™ค๐™ข๐™—๐™ค๐™จ๐™ž๐™จ ๐™ฌ๐™–๐™จ ๐™™๐™š๐™ซ๐™š๐™ก๐™ค๐™ฅ๐™š๐™™ ๐™—๐™ฎ ๐™ฉ๐™๐™š ๐˜ผ๐™˜๐™–๐™™๐™š๐™ข๐™ž๐™˜ ๐™๐™š๐™จ๐™š๐™–๐™ง๐™˜๐™ ๐˜พ๐™ค๐™ฃ๐™จ๐™ค๐™ง๐™ฉ๐™ž๐™ช๐™ข

๐ƒ๐ž๐Ÿ๐ข๐ง๐ข๐ญ๐ž stent thrombosis is confirmed by
angiographic or autopsy evidence of thrombus in the setting of an acute coronary syndrome, and

๐๐ซ๐จ๐›๐š๐›๐ฅ๐ž stent thrombosis is defined as
unexplained death within 30 days after stent implantation or acute MI involving the target vessel territory without angiographic confirmation.

๐˜ผ๐™˜๐™ช๐™ฉ๐™š ๐™ฉ๐™๐™ง๐™ค๐™ข๐™—๐™ค๐™จ๐™ž๐™จ ๐™ค๐™˜๐™˜๐™ช๐™ง๐™จ ๐™ฌ๐™ž๐™ฉ๐™๐™ž๐™ฃ 24 ๐™๐™ค๐™ช๐™ง๐™จ
(excluding intraprocedural events within
the catheterization laboratory),

๐™Ž๐™ช๐™—๐™–๐™˜๐™ช๐™ฉ๐™š ๐™—๐™š๐™ฉ๐™ฌ๐™š๐™š๐™ฃ 1 ๐™™๐™–๐™ฎ ๐™–๐™ฃ๐™™ 30 ๐™™๐™–๐™ฎ๐™จ,

๐™€๐™–๐™ง๐™ก๐™ฎ ๐™ฌ๐™ž๐™ฉ๐™๐™ž๐™ฃ 30 ๐™™๐™–๐™ฎ๐™จ
(counting both acute and subacute events),

๐™‡๐™–๐™ฉ๐™š ๐™—๐™š๐™ฉ๐™ฌ๐™š๐™š๐™ฃ 30 ๐™™๐™–๐™ฎ๐™จ ๐™–๐™ฃ๐™™ 1 ๐™ฎ๐™š๐™–๐™ง, and

๐™‘๐™š๐™ง๐™ฎ ๐™‡๐™–๐™ฉ๐™š ๐™–๐™›๐™ฉ๐™š๐™ง 1 ๐™ฎ๐™š๐™–๐™ง.
โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”
๐™๐™๐™ง๐™ค๐™ข๐™—๐™ค๐™ฉ๐™ž๐™˜ ๐™ค๐™˜๐™˜๐™ก๐™ช๐™จ๐™ž๐™ค๐™ฃ is classified as :-

โ–ซ๏ธ ๐™‹๐™ง๐™ž๐™ข๐™–๐™ง๐™ฎ if it is directly related to the stent implantation

โ–ซ๏ธ ๐™Ž๐™š๐™˜๐™ค๐™ฃ๐™™๐™–๐™ง๐™ฎ 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 โ€ขโ€ขโ€ข

๐™‹๐™–๐™ฉ๐™ž๐™š๐™ฃ๐™ฉ-๐™ง๐™š๐™ก๐™–๐™ฉ๐™š๐™™ ๐™›๐™–๐™˜๐™ฉ๐™ค๐™ง๐™จ
โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”-
Patients who ๐™ฅ๐™ง๐™š๐™จ๐™š๐™ฃ๐™ฉ ๐™ฌ๐™ž๐™ฉ๐™ 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 ๐™ฅ๐™ก๐™–๐™ฉ๐™š๐™ก๐™š๐™ฉ ๐™ง๐™š๐™–๐™˜๐™ฉ๐™ž๐™ซ๐™ž๐™ฉ๐™ฎ 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.

๐™‡๐™š๐™จ๐™ž๐™ค๐™ฃ ๐™›๐™–๐™˜๐™ฉ๐™ค๐™ง๐™จ 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.

๐™‹๐™ง๐™ค๐™˜๐™š๐™™๐™ช๐™ง๐™–๐™ก ๐™›๐™–๐™˜๐™ฉ๐™ค๐™ง๐™จ :
โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”
โ–ซ๏ธinadequate stent expansion and/or apposition,
โ–ซ๏ธStent type used (i.e., BMS or DES),
โ–ซ๏ธExcessive stent overlap, and
โ–ซ๏ธEdge dissections limiting inflow or outflow.
โ–ซ๏ธ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.

๐™‹๐™ค๐™จ๐™ฉ๐™ฅ๐™ง๐™ค๐™˜๐™š๐™™๐™ช๐™ง๐™–๐™ก ๐™ง๐™ž๐™จ๐™  ๐™›๐™–๐™˜๐™ฉ๐™ค๐™ง๐™จ:-
โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”-
โ–ซ๏ธ ๐ƒiscontinuation Early of dual-antiplatelet
(although the ideal length of treatment
varies by the specific stent system),

โ–ซ๏ธ ๐ƒelayed re-endothelialization of stent struts
in DES systems due to antiproliferative agent

โ–ซ๏ธ ๐ƒevelopment of neoatherosclerosis within
the stent leading to plaque rupture.

Specific strategies aimed at reducing the occurrence of stent thrombosis are shown image๐Ÿ‘‡
โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”โ€”-
๐“๐ซ๐ž๐š๐ญ๐ฆ๐ž๐ง๐ญ ๐จ๐Ÿ ๐ฌ๐ญ๐ž๐ง๐ญ ๐ญ๐ก๐ซ๐จ๐ฆ๐›๐จ๐ฌ๐ข๐ฌ,
especially when presenting as acute MI,
is almost always ๐™€๐™ข๐™š๐™ง๐™œ๐™š๐™ฃ๐™ฉ ๐™‹๐˜พ๐™„.

โ–ช๏ธOptions for restoring perfusion include :
โ–ซ๏ธ ๐™๐™๐™ง๐™ค๐™ข๐™—๐™š๐™˜๐™ฉ๐™ค๐™ข๐™ฎ either aspiration or mechanical
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โ–ซ๏ธ and/or ๐™—๐™–๐™ก๐™ก๐™ค๐™ค๐™ฃ ๐™–๐™ฃ๐™œ๐™ž๐™ค๐™ฅ๐™ก๐™–๐™จ๐™ฉ๐™ฎ with
โ–ซ๏ธ Administration of more potent pharmacologic
agents such as ๐™œ๐™ก๐™ฎ๐™˜๐™ค๐™ฅ๐™ง๐™ค๐™ฉ๐™š๐™ž๐™ฃ ๐™„๐™„๐™—/๐™„๐™„๐™„๐™– ๐™ž๐™ฃ๐™๐™ž๐™—๐™ž๐™ฉ๐™ค๐™ง๐™จ
at the discretion of the operator.

โ–ช๏ธ๐˜ผ๐™™๐™Ÿ๐™ช๐™ฃ๐™˜๐™ฉ๐™ž๐™ซ๐™š ๐™ž๐™ข๐™–๐™œ๐™ž๐™ฃ๐™œ ๐™ฌith modalities such as
๐™„๐™‘๐™๐™Ž ๐™ค๐™ง ๐™Š๐˜พ๐™ 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.

โ–ช๏ธ ๐˜ผ๐™™๐™™๐™ž๐™ฉ๐™ž๐™ค๐™ฃ๐™–๐™ก ๐™จ๐™ฉ๐™š๐™ฃ๐™ฉ๐™จ ๐™–๐™ง๐™š ๐™ฉ๐™ฎ๐™ฅ๐™ž๐™˜๐™–๐™ก๐™ก๐™ฎ ๐™–๐™ซ๐™ค๐™ž๐™™๐™š๐™™ unless
a mechanical reason for the thrombosis
(such as edge dissection) is seen.

โ–ช๏ธ ๐™€๐™ซ๐™–๐™ก๐™ช๐™–๐™ฉ๐™ž๐™ค๐™ฃ ๐™ฃ๐™ค๐™ฃ๐™ข๐™š๐™˜๐™๐™–๐™ฃ๐™ž๐™˜๐™–๐™ก ๐™˜๐™–๐™ช๐™จ๐™š๐™จ ๐™ค๐™› ๐™ฉ๐™๐™ง๐™ค๐™ข๐™—๐™ค๐™จ๐™ž๐™จ
such as hypercoagulable state, thrombocytosis,
or aspirin/clopidogrel resistance should considered.

โ–ช๏ธ ๐™€๐™จ๐™˜๐™–๐™ก๐™–๐™ฉ๐™ž๐™ค๐™ฃ ๐™ค๐™› ๐™ข๐™–๐™ž๐™ฃ๐™ฉ๐™š๐™ฃ๐™–๐™ฃ๐™˜๐™š ๐™–๐™ฃ๐™ฉ๐™ž๐™ฅ๐™ก๐™–๐™ฉ๐™š๐™ก๐™š๐™ฉ ๐™ฉ๐™๐™š๐™ง๐™–๐™ฅ๐™ฎ
(e.g., from clopidogrel to more potent oral
antiplatelet therapies such as prasugrel or
ticagrelor) is standard.

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