brief prabowo nsteacs.pptx

Morning Report
Physician in Charge
IV : dr. Anastasia / dr. Savitri
IIIA (Ward/IW) : dr. Erick, dr. Ira dan dr. Cik Kahadi
IIIB : dr. Kaputrin dan dr. Teguh
Chief : dr. Yordan dan dr. Astrid
Supervisor : dr. Budi Satrijo, Sp. JP(K)
Supervisor Incovit : dr. Indra Prasetya, Sp.JP(K)
MR Consultant : dr. Budi Satrijo, SpJP (K)

SUBJECTIVE
Mr. P/60 yo/ID 11536070
CHIEF COMPLAINT : Chest Pain
Patient complained about chest pain at 06.00 AM (2 hours before RSSA admission) with VAS
score 8/10, when he was lying on bed. It was heavy-like sensation, without radiated to the back, with
duration more than 30 minutes, and accompanied with cold sweating. Nausea (-), vomiting (-), SOB (-
). There was no stabbing like sensation and chest pain was not affected with inspiration, positional
changes, or food intake. Because the chest pain still persisted, patient directly went to RSSA.
In ER RSSA at 00.30 AM, patient said that chest pain still already felt with VAS 8/10 mmHg. GCS
was 456, BP 160/112 mmHg, HR 81 bpm, RR 26x/min and Sat 99% on NC 3 lpm NC. He was given drip
NTG 40 mcg/min, loading aspilet 4 tab, and CPG 4 tab, and his BP was improved 130 / 90 mmHg, and
chest pain improved with VAS 4/10.
Previously, he suffered from similar chest pain, with VAS score 6/10 while at rest. It was
occured At 05.00 AM (19 hours before RSSA admission). He was taking isosorbide dinitrate 5 mg, with
6 times of repetition, but the chest pain did not Improved.

SUBJECTIVE
Mr. P/60 yo/ID 11536070
PAST MEDICAL HISTORY :
• He had suffered from similar chest pain 1 year ago and checked at private hospital in Malang. He was
diagnosed with NSTEMI, and was referred to other hospital for further management. Coronary
angiography was perform and the result was CAD 3VD + LM disease. Then he planned to be referred to
cardiologist outpatient clinic for consideration for elective PCI or CABG. But patient never came to
control at RSSA because he refused for operation. After that Patient never controlled to any cardiologist
and also didn’t take any medication
• History of DOE (+) while doing moderate-heavy activities since 1 month. OE, PND, Leg swelling,
palpitation, and syncope was denied

SUBJECTIVE
Mr. P/60 yo/ID 11536070
RISK FACTOR :
• He had hypertension since 20 years ago, didn’t routinely consume medication
• He is an a passive smoker for the last 1 year
• History of diabetes mellitus, CKD, CAD and other disease was denied.
FAMILY HISTORY :
History of hypertension on her family was denied
There was no sudden cardiac death and cardiac disease in her family.
He was the 2nd son out of 5 siblings.
Screening for covid-19
There was no cough, fever, sore throat, anosmia, dysgeusia in the last 14 days ago.
History of traveling to red zone area was denied
History of contact with patient confirmed COVID-19 was denied
He lives in orange zone area
He hasn’t yet vaccinated covid-19

OBJECTIVES
Physical Examination :
General appearance moderate ill
BW 65 kg Height 160 cm BMI 25.4 kg/m2
(overweight)
GCS 456, VAS 8/10  drip GTN 40 mcg/min, VAS
4/10
BP 160/112 mmHg drip GTN 40 mcg/min 
130/70 mmHg
PR 100 bpm regular, strong pulse
RR 20 tpm
SpO 99% NC 3 lpm
Tax: 36,50C
Head and Neck :
Anemic conjuctiva +|+; icteric sclera -|-
nostril breathing (-), sternocleidomastoid muscle
retraction (-)
JVP R+1 cmH O
OBJECTIVES
Thorax :
Cor: ictus cordis, palpable at 1 cm lateral MCL V
sinistra
S1-S2 regular normal, murmur (-), gallop (-)
Pulmo:
symmetrical movement, intercostal muscle retraction
(-)
ves/ves Rh -/- wh - / -
ves/ves -/- - / -
Ves/ves +/+ - / -
Abdomen : flat, soefl, bowel sound was normal, liver
and spleen unpalpable, shifting dullness (-)
Extremities : leg swelling -|- , warm acrals, CRT < 2
seconds
Urine output : 350 cc (initial)  inj furosemide 40 mg
 1750 cc/2 hours

ECG at RSSA (April 18th 2022) at 00.30
Sinus rhythm, HR 100 bpm, FA LAD, HA N. normal P wave, PR Int 160 ms. narrow QRS 80 ms. Pathological Q waves in lead III.
ST segmen depression V2 (3 mm), V3(4 mm), V4(4.5 mm). T wave normal. QTc 337 msec. LVH(-), RVH (-), LAE (-), RAE(-).
Conclusion : Sinus tachycardia with ischemia

ECG at CVCU (March 4th 2022)
Sinus rhythm, HR 100 bpm, FA LAD, HA N. normal P wave, PR Int 160 ms. narrow QRS 80 ms. Pathological Q waves in lead III. ST
segmen depression V2 (1 mm), V3(1.5 mm), V4(0.5 mm). Biphasic T wave at V2,V3,V4. QTc 397 msec. LVH(-), RVH (-), LAE (-),
RAE(-).
Conclusion : Sinus tachycardia, with ST-T changes (+)
ECG at RSSA (April 18th 2022) at 2.30

ECG at CVCU (March 4th 2022)
Sinus rhythm, HR 98 bpm, FA LAD, HA N. normal P wave, PR Int 160 ms. narrow QRS 80 ms. Pathological Q waves in lead III. ST
segmen depression V2 (2 mm), V3(1 mm), V4(1 mm). T wave normal. QTc 486 msec. LVH(-), RVH (-), LAE (-), RAE(-).
Conclusion : Sinus tachycardia, ischemia, and prolonged QTc.
ECG at Persada Hospital (May 30th 2021)

CXR at Persada Hospital (May 30th 2021)
AP position, symmetrical, enough inspiration,
enough KV
Soft tissue: Normal
Bone: Costae D/S normal
ICS D/S normal
Trachea: In the middle
Cor: Site: N
Size: CTR 56%
Cardiac waist (+)
Aorta dilatation (+)
Hemidiaphragm:
D: dome shape
S: hard to evaluate
Vascular apex D increased
Costophrenic angles: D: sharp, S: hard to evaluate
Pulmo : Infiltrate (-)
Conclusion :
Cardiomegaly with HHD configuration
Aorta dilatation

CXR at RSSA (April 18th 2022)
AP position, symmetrical, less inspiration, enough
KV
Soft tissue: Normal
Bone: Costae D/S normal
ICS D/S normal
Trachea: In the middle
Cor: Site: N
Size: CTR 67%
Cardiac waist (-)
Hemidiaphragm:
D: dome shape
S: hard to evaluate
Bronchovesicular pattern dextra and sinistra
increased
Costophrenic angles: D: sharp, S: hard to evaluate
Pulmo : Infiltrate (-)
Conclusion :
Cardiomegaly with HHD configuration
Susp. Pleural effusion sinistra

Parameter Result Normal Value
Hb 10 g/dL 11.5 – 18.0 g/dL
Leukocytes 10,500 /µL 4000 - 11000/µL
Hematocrit 31,5 % 35 - 45 %
Thrombocytes 302,000 /µL 150000-450000/µL
Differential count 1/0.3/61.7/25/12 1-2/0-1/3-5/54-62/25-33/3-7
%
NLR 2.48
PPT 10.6 detik 9.4 – 11.3
aPTT 25.2 detik 24.6 – 30.6
INR 1.02 <1.5
Random Blood
Sugar
108 mg/dL <200 mg /dl
SGOT 83 U/L 0-40 U/L
SGPT 24 U/L 0-41 U/L
Albumin 4.08 mg/dl 3.5 – 5.5
Na 140 mmol/L 136 – 145
K 3.47 mmol/L 3.5 – 5.0
Cl 102 mmol/L 98 - 106
Ureum 23.9 mg/dL 16.6-48.5
Creatinin 1.13 mg/dL <1.2
eGFR 70.256 mL/mnt/1.
73 m2
Procalcitonin 0.06 ng/mL <0.1
Troponin I 2.4 ng/mL <0.1
CKMB 105 mg/dL 7-25
CRP 1.41 mg/dL <0.3
Date: April 18th 2022
Laboratory Finding at RSSA

pH 7,45 7.35 – 7.45
pCO2 29,7 mmHg 35 - 45
pO2 120,1 mmHg 80 - 100
HCO3 20,6 mmol/L 21 - 28
BE -3,7 mmol/L -3 - +3
SaO2 99,9 % >95
Respiratory Alkalosis Fully Compensated
Date: April 18th 2022
Blood Gas Analysis at RSSA with NC 4 lpm

Echocardiography at Prima Medika Hospital (May 8th 2021)
Dimensi ruang jantung normal
LV concentric hypertrophy (LVMI 118 g/m2, RWT 0.43)
Fungsi sistolik LV : EF teach 56%, biplane 66%
Fungsi diastolic LV : impaired relaxation (E/A 0.59)
Fungsi sistolik RV : normal (TAPSE 1.63 cm)
Analisa segmental : hipokinetik anteroseptal
setinggi mid, hipokinetik
anterior setinggi apex
Kesimpulan :
Hypertensive heart disease
Diastolic dysfunction LV gr I
Mild MR
Coronary Artery Disease

Coronary angiography at Persada Hospital
LM : stenosis 10% mid-distal
LAD : stenosis 95-99% at osteal-proximal.
CTO at proximal, got collateral from
contralateral
Intermediate : stenosis 90% at osteal-
proximal
LCx : co-dominsasnt. Stenosis 90% at
osteal-proximal. Stenosis 60-70% at distal
RCA : stenosis 60% at osteal-mid. stenosis
40% at RPL. Stenosis 80% at PDA
Conclusion : CAD 3VD
Suggest to : CABG/high cost PCI

Assessment
1. NSTEMI killip II (Very high risk criteria) TIMI 5/7, GRACE 140 CRUSADE 27
2. HF st C fc II dt CAD, HHD
3. Hypertension st II
4. History of smoker

Planning Diagnosis & Therapy
Planning diagnosis
Echocardiography ECG/24 hours, FBG/2hPPBG, HbA1c,
UA, profil lipid
Planning therapy
Pro Early Immediate invasive strategy with IABP backup
Bedrest
O2 NC 2 lpm
Total Fluid 2000 ml/24 h
IVFD NS 0.9% 1000 ml/24 h
Oral Intake 1000 cc/24 hr
Equal fluid balance
Heart Diet 1800 kkal/day
Drip GTN 40 mcg/min
Inj. Enoxaparin 2x60mg sc
Inj. Lansoprazol 1x30mg
Inj. Furosemide 40 mg  3x20mg
Peroral
ASA 320 mg  0-0-80mg
Clopidogrel 300 mg  75mg-0-0
Atorvastatin 0-0-40mg
Captopril 3x25mg
Bisoprolol postponed
Diazepam 0-0-2mg
Laxadyn 0-0-CI
Planning Monitoring
Subjective, Vital Sign, UOP, Bleeding Sign, ECG/24h
Admitted to ICVCU

Condition at the end of the duty
• S: chest pain (-)
• O:
• BP 126/70 mmHg
• HR 90x/min
• RR 20x/min
• Tax 36.5 degrees C
• SpO2 99 % NC 4 lpm
• Rh --+/--+ Wh -/-
• Edema -/-
• Urine output 3000 ml/7hours

www.escardio.org/guidelines
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa575)
©ESC
Table 2 Conditions other than acute type 1 myocardial infarction
associated with cardiomyocyte injury (= cardiac troponin
elevation) (1)
Tachyarrhythmias
Heart failure
Hypertensive emergencies
Critical illness (e.g. shock/ sepsis/ burns)
Myocarditisa
Takotsubo syndrome
Valvular heart disease (e.g. aortic stenosis)
Aortic dissection
Pulmonary embolism, pulmonary hypertension
Renal dysfunction and associated cardiac disease
Bold = most frequent conditions. aIncludes myocardial extension of endocarditis or pericarditis.

©ESC
Table 2 Conditions other than acute type 1 myocardial infarction
associated with cardiomyocyte injury (= cardiac troponin
elevation) (2)
Acute neurological event (e.g. stroke or subarachnoid haemorrhage)
Cardiac contusion or cardiac procedures (CABG, PCI, ablation, pacing, cardioversion, or
endomyocardial biopsy)
Hypo- and hyperthyroidism
Infiltrative diseases (e.g. amyloidosis, haemochromatosis, sarcoidosis, scleroderma)
Myocardial drug toxicity or poisoning (e.g. doxorubicin, 5-fluorouracil, herceptin, snake
venoms)
Extreme endurance efforts
Rhabdomyolysis
Bold = most frequent conditions. aIncludes myocardial extension of endocarditis or pericarditis.

©ESC
Figure 3 (1)
0 h/1 h rule-out and
rule-in algorithm using
high-sensitivity cardiac
troponin assays in
haemodynamically stable
patients presenting with
suspected non-ST-
segment elevation acute
coronary syndrome to the
emergency department.
aOnly applicable if CPO >3 h.

©ESC
Table 4 Differential diagnoses of acute coronary syndromes in the
setting of acute chest pain
Bold = common and/or important differential diagnoses.
aDilated, hypertrophic and restrictive cardiomyopathies may cause angina or chest discomfort.

©ESC
Figure 6
Antithrombotic
treatments in non-ST-
segment elevation acute
coronary syndrome
patients: pharmacological
targets. Drugs with oral
administration are shown
in black letters and drugs
with preferred parenteral
administration in red.
Abciximab (in brackets) is
not supplied anymore.

©ESC
Figure 9 Selection of
non-ST-segment
elevation acute
coronary syndrome
treatment strategy and
timing according to
initial
risk stratification

©ESC
Recommendations for coronary revascularization (1)
Recommendations Class Level
Timing of invasive strategy
An immediate invasive strategy (<2 h) is recommended in patients with at
least one of the following very-high-risk criteria:
• Haemodynamic instability or CS
• Recurrent or refractory chest pain despite medical treatment
• Life-threatening arrhythmias
• Mechanical complications of MI
• Heart failure clearly related to NSTE-ACS
• Presence of ST-segment depression >1 mm in ≥6 leads additional to
ST-segment elevation in aVR and/or V1.
I C

©ESC
Timing of invasive strategy (continued)
An early invasive strategy within 24 h is recommended in patients with any of
the following high-risk criteria:
• Diagnosis of NSTEMI suggested by the diagnostic algorithm
recommended in Section 3
• Dynamic or presumably new contiguous ST/T-segment changes
suggesting ongoing ischaemia
• Transient ST-segment elevation
• GRACE risk score >140.
I A

©ESC
Timing of invasive strategy (continued)
A selective invasive strategy after appropriate ischaemia testing or detection
of obstructive CAD by CCTA is recommended in patients considered at low
risk.
I A
Delayed as opposed to immediate angiography should be considered among
haemodynamically stable patients without ST-segment elevation successfully
resuscitated after out-of-hospital cardiac arrest.
IIa B

©ESC
Figure 13 (1) Central illustration. Management strategy
for non-ST-segment elevation acute coronary syndrome
patients.

©ESC
patients.

©ESC
Supplementary Table 8 Lifestyle recommendations
Smoking
cessation
Use pharmacological and behavioural strategies to help patients quit
smoking. Avoid passive smoking.
Healthy diet Diet high in vegetables, fruit, whole grains; limit saturated fat to <10% of
total. Limit alcohol to <100 g/week or 15 g/day.
Physical
activity
30–60 min moderate physical activity most days, but even irregular activity
is beneficial.
Healthy
weight
Obtain and maintain a healthy weight (BMI 18.5–25 kg/m2) or reduce weight
through recommended energy intake and increased physical activity.
Other Take medication as prescribed.
Sexual activity is low risk for stable patients who are not symptomatic at
low-to-moderate activity levels.
Lifestyle recommendations are based on ESC CCS Guidelines

©ESC
Supplementary Table 9 Healthy diet
Increase consumption of fruit and vegetables (≥200 g each per day)
35–45 g of fibre per day, preferably from whole grains
Moderate nut consumption (30 g unsalted)
1–2 servings of fish per week (one to be oily fish)
Limited lean meat, low-fat dairy products, and liquid vegetable oils
Saturated fats to account for <10% of total energy intake, replace with polyunsaturated fats
Trans unsaturated fats as low as possible, preferably no intake from processed food, and <1%
of total energy intake
≤5–6 g of salt per day
If alcohol is consumed, limiting intake to ≤100 g/week or <15 g/day is recommended
Avoid energy-dense foods such as sugar-sweetened soft drinks
Results are based on the results of a systematic review by de Vries et al.

Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation 42

47
Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation

48

49

50

51

53

54

Intraprocedural stent thrombosis (IPST)
INTRODUCTION
a rare complication leading to poor outcome including STEMI
and sudden cardiac death
47 (0.7%) of 6,591
patients with incident
IPST
 Death within 30 days was higher (12.9% vs 1.4%)
 Mortality within one year was also higher (19.9% vs. 2.7%)
 0.5-2% in the case of elective PCI
 6% in the case of PCI with acute coronary syndromes
Safety concerns regarding an increased risk of stent thrombosis with drug eluting stent (DES) persist while the
incidence, timing, and predictors of stent thrombosis with DES have not been determined
Oktaviono YH. Folia Medica Indonesiana Vol. 52. 2016 : 66-73
Iqbal J, et al. EuroIntervention. 2013,9:62-69

Definition of Intraprocedural Stent Thrombosis
(IPST)
Intra-procedural stent thrombosis (IPST) is defined as an angiographically confirmed
intraluminal filling defect within the stent that results in occlusive or non-occlusive
thrombolysis in myocardial infarction (TIMI) grade-0 or 1 anterograde flow, secondary to the
development of new or increasing thrombus within or adjacent to a recently implanted stent,
occurring during the index procedure or before the percutaneous coronary intervention
(PCI) is completed.
Brener et al. JACC: Cardiovascular Interventions. Vol. 6. 2013: 36-43
IPST has an incidence of 0.7% after drug eluting stent (DES), and <0.01% after bare metal stent (BMS)
implantation in patients without acute myocardial infarction (AMI), thrombus-containing lesions and dissections. It
occurs in <1% of patients with ST-segment elevation myocardial infarction (STEMI).

The Academic Research Consortium (ARC) has
standardized the definitions of ST by categorizing
the specificity of the adjudicated event (definite,
probable, or possible) and its timing relative to
PCI (acute, subacute, late, and very late).
Intra-procedural stent thrombosis (IPST) (i.e., the development of occlusive or non-occlusive new thrombus in or
adjacent to a recently implanted stent before the PCI procedure is completed) is excluded from the ARC ST
definitions.
Claessen et al. JACC: Cardiovascular Interventions. Vol. 7. 2014:1081-1092

End Point Definition of Stent
Thrombosis by
The Academic Research Consortium
(ARC)-2
Garcia et al. Circulation. 2018:137:2635–2650

The most important aspect for the diagnosis and treatment of IPST is
clinical suspicion of early stent thrombosis.
Diagnosis of Intraprocedural Stent thrombosis
(IPST)
The typical clinical presentation of stent thrombosis consists of chest pain and ischemic
electrocardiographic changes in the target vessel territory. However, ST can also present as
sudden death, or it can be asymptomatic in the setting of collateral vessels.
Hyo-Sun Shin, et al. J Lipid Atheroscler. 2014;3(1):43-
48

Coronary intervention-related MI is arbitrarily defined by an elevation of cTn values more than five times
the 99th percentile URL in patients with normal baseline values. In addition, one of the following
elements is required:
1. New ischaemic ECG changes
2. Development of new pathological Q waves
3. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a
pattern consistent with an ischaemic aetiology;
4. Angiographic findings consistent with a procedural flow-limiting complication such as coronary
dissection, occlusion of a major epicardial artery or a side branch occlusion/thrombus, disruption of
collateral flow, or distal embolization.
Criteria for PCI-related MI 48 h after the index procedure (type 4a MI)
Thygesen K, et al. 2018. European Heart Journal 2019, 40: 237–269

When a filling defect is detected angiographically:
 Intravascular ultrasound (IVUS) may be used to detect the underlying
mechanism of ST (underexpansion, malapposition, edge dissection).
 Optical coherence tomography (OCT) is very suitable for visualization
of the stent surface for its higher resolution (10 mm), and its ability to
detect the presence of (sub) clinical thrombus has been experimentally
confirmed.
In this patient, as soon as the action predilatation with balloon and stent, we found ischaemic ECG changes and thrombus
intracatheter in the end of procedure. The ECG monitor back to the baseline soon after we gave loading Ticagrelor 180 mg,
Atorvastatin 40 mg and intracoronary heparin 1000 mg.
Diagnosis of Intraprocedural Stent thrombosis
(IPST)
Genereux P, et al. 2014. Journal of the American College of Cardiology Vol. 63, No. 7, 2014: 619-629

Pathophysiology of Stent
Thrombosis
Many factors are involved including procedural factors/stent, patient factors and lesion
characteristics. Patients with acute coronary syndrome, inflammation and tissue necrosis
were exposed to the circulation so as to strengthen the activity of platelets and easily
formed thrombus.
The material in the form of a polymer stent Cypher (sirolimus) and Taxus
(paclitaxel) DES can cause infiltration of eosinophils suspected
hypersensitivity reaction that can trigger platelet adhesion and activation
cascade coagulant.

There are two kinds of thrombus:
 White thrombus : a platelet-rich thrombus, usually only lead to partial occlusion
 Red thrombus : a rich thrombus fibrin and erythrocytes.
White thrombi composed approximately one-third of specimens retrieved during PCI in a
contemporary sample of patients from a high-volume referral center. Patients with white thrombi
had less ischemic time and had smaller vessels when compared with those with red thrombi.
THROMBUS
Quadros AS, et al. 2012. American Heart Journal Volume 164, Number 4: 554-560

Torrado, J. et al. J Am Coll Cardiol. 2018;71(15):1676–95
Pathogenic Mechanisms
of Stent Thrombosis

Multiple Risk Factors Involved
In The Development Of Stent
Thrombosis

Device-related factors (or stent thrombogenicity), including stent material, surface coating, and the interaction with
adjunctive therapy such as intracoronary brachytherapy.
Platelet activation was greater during the 30 days after implantation of an open-cell versus a closed-cell stent,
which was potentially related to the different scaffolding properties of the stents.
The content of the drugs currently on the DES can be prothrombogenic. Rapamycin and Paclitaxel works by
blocking the migration and proliferation of smooth muscle cells that plays a role in neointimal formation
and restenosis. However, both drugs induce endothelial expression of tissue factor that will bind to the clotting
factor so that the formation of fibrin.
STENT FACTORS

Patient- or lesion-specific factors, including vessel size, acute coronary syndrome/unstable
angina, plaque characteristics, local platelet/coagulation activity, coronary blood flow, and left
ventricular ejection fraction.
A polymorphism of platelet glycoprotein IIIa gene (PlA2) may also be associated with an
increased risk of stent thrombosis.
Other patient characteristics that favor the development of stent thrombosis include diabetes
mellitus, chronic kidney disease, smoker, cancer, DAPT non-responsive, premature cessation of
DAPT, advanced age and hypersensitivity to polymer or drug.
PATIENT- OR LESION-SPECIFIC FACTORS

PREDICTORS OF IPST
Over the past several years, many researchers have investigated potential predictors
of stent thrombosis especially acute and sub-acute categories and identified a number
of angiographic, clinical, procedural and post-procedural risk factors of stent thrombosis
A risk score has been proposed to personalize risk assessment for the occurrence of ST and may be used to identify patients
who might beneﬁt the most from more aggressive antiplatelet therapy after stent implantation.
Iqbal J, et al.. Euro Intervention 2013; 9: 62-69

Predictors of Early and (Very) Late Stent Thrombosis

Predictors of IPST
Clinical risk score for prediction of
stent thrombosis and risk
stratification as developed by Baran
et al
8 significant predictors, with a stratification of
patients in low, medium, and high risk
groups, and has been validated using 1-year
data from 4,820 patients.
PATIENT’S SCORE: 12
Iqbal J, et al.. Euro Intervention 2013; 9: 62-69

Predictors of IPST
Stent Thrombosis Risk Score
(STRS) in predicting early stent
thrombosis (ST) after primary
Percutaneous Coronary Intervention
(PCI).
A total of 569 patients were included, the median
age was 56 years. Early ST was observed in 33
(5.8%) patients.
Early ST rate was 3.3% at STRS of 0-2, which
raised to 5.0% at STR of 3-4, and 17.2% at
STRS of ≥5
Kumar R, et al. Journal Of The Saudi Heart Association 2020;32:256-262

Predictors of IPST
Association of the CHA2DS2VASc Score
with Acute Stent Thrombosis
3,460 consecutive patients with STEMI who
underwent a PPCI.
CHA2DS2VASc scores ≥ 4 were independently
associated with acute stent thrombosis.
Patients with a CHA2DS2VASc score of 4 had a
4.3 times higher risk of acute stent thrombosis
compared to those with a CHA2DS2VASc score of
1.
Tanik OZ, et al. 2019. Med Princ Pract 2019;28:115–123

Predictors of IPST
Integer-Based Risk Score for 1-Year
Deﬁnite/Probable Stent Thrombosis in
Patients With Acute Coronary
Syndromes
6,139 patients undergoing PCI with stent
implantation for ACS.
Risk scores 1 to 6 were considered low risk
(1.36%), 7 to 9 intermediate risk (3.06%), and ≥10
high risk for ST (9.18%).
Brener SJ, et al. 2013. JACC: Cardiovascular Interventions Vol.6, No.1,2013: 36-43

Stent Thrombosis Management
If ST is the case then action targets PTCA for revascularization of blood
vessels should be done immediately. Guidewire selected must be soft and
floppy to ensure free through the lumen of the stent and not crossing through the strut
stent
Aspiration trombhectomy intra coronary thrombus is effective for the treatment of ST especially on stents with a diameter of more than
2.5 mm, large blood vessels and large thrombus. Intracoronary thrombus aspiration can prevent distal embolization.
The existence of intra coronary thrombus is also an indication of the provision of Glycoprotein IIb-IIIa inhibitors.
The success of overcoming the acute thrombosis, characterized by normal blood flow (TIMI 3 flow) with
stenosis <50%.
Nikesh Jain et al. Cardiology and Cardiovascular Research 2019; 3(2): 31-36

Dual anti-platelet (DAPT) should be given as early as possible, especially in all patients
with acute coronary syndrome patients.
Acetylsalicylic acid (ASA) and the P2Y12 receptor antagonists such as clopidogrel, prasugrel and ticagrelor served to increase the
effectiveness of treatment and prevention of stent thrombosis.
PLATO Trial  The effectiveness of Ticagrelor vs Clopidogrel in preventing stent thrombosis
The incidence of stent thrombosis could still occur at 0.5-2% in the case of elective PCI and more than 6% in the case of PCI
with acute coronary syndromes despite using dual antiplatelet
ANTI-PLATELET

Selection of anticoagulation during PCI procedures is also important
 Unfractionated heparin (UFH) is the main option while undergoing
PCI.
From the research HORIZON-AMI, comparing UFH-Glycoprotein IIa/IIIb with direct thrombin
inhibitors bivalirubin as monotherapy, showed a 0.3 vs 1.4%, P <0.001 in the incidence of
Acute ST.
It is important choose the right size stents and perform high-pressure post-dilation effectively (> 14 atm)
To further optimize the prevention ST, lesions calsified, can be handled with the use of rotational atherectomy
so that expansion and better positioning stent.
The use of intracoronary imaging modalities such as Intra Vascular Ultra Sound (IVUS) and Optical
Coherence Tomography (OCT) is very helpful as guiding the expansion and apposition of the stent to be
more adequate
ANTICOAGULANT
PROCEDURE OPTIMIZATION

INTEGRATED STRATEGY OF IPST IN THIS PATIENT
Patient Characteristic Lession Characteristic Stent Characteristic
 Male, 49 y.o
 Insulin treated DM Type
II
 Smoker
 History of ACS 1 month
prior admission
 CAD 3VD with Left
Main Disease
 Lession length > 20
mm with calcification
 Multiple stenting
 Length 38mm
Moderate Risk of Early
Stent Thrombosis
Evidence IPST:
Ischemic ECG Changes
Thrombus Intracatheter
DAPT with Asetyl Salycilic +
Ticagrelor
High Intensity Statin
TIMI Flow 3, residual stenosis 0%
ECG returned to baseline
No chest discomfort during and post
procedure
2nd Generation DES
(Everolimus-eluting
platinum chromium stent)

Conclusions
Intraprocedural Stent Thrombosis was a strong predictor of mortality in patients
undergoing PCI.
This case showed that the present widespread use of DES instead of BMS for coronary
implantation although decreased the future risk of repeat revascularization, increased the
risk of thrombosis.
Prior risk stratification, selection of 2nd generation DES, early potent antiplatelet treatment
and anticoagulant of choice with UFH might be used to reduce the risk of IPST in patients
undergoing stent implantation.

brief prabowo nsteacs.pptx

Recomendados

Recomendados

Más contenido relacionado

Similar a brief prabowo nsteacs.pptx

Similar a brief prabowo nsteacs.pptx (20)

Último

Último (20)

brief prabowo nsteacs.pptx