Coronary artery perforation during percutaneous coronaryRamachandra Barik
Percutaneous coronary intervention (PCI) has considerable
efficacy in the treatment of coronary artery disease, but it is
associated with some complications.[1‑4] One of the uncommon
complications of PCI is a coronary artery perforation, with an
incidence rate of 0.2%–0.6%, which may lead to pericardial
effusion and may consequently progress to cardiac tamponade,
myocardial infarction, and death.[1‑8] We herein present a case
of a right coronary artery (RCA) perforation during PCI.
Perforation management of collaterals
Kambis Mashayekhi, Bad Krotzingen, Germany
11th Experts Live CTO
The annual Euro CTO meeting
September 13th –14th, 2019 - Berlin, Germany
Coronary artery perforation during percutaneous coronaryRamachandra Barik
Percutaneous coronary intervention (PCI) has considerable
efficacy in the treatment of coronary artery disease, but it is
associated with some complications.[1‑4] One of the uncommon
complications of PCI is a coronary artery perforation, with an
incidence rate of 0.2%–0.6%, which may lead to pericardial
effusion and may consequently progress to cardiac tamponade,
myocardial infarction, and death.[1‑8] We herein present a case
of a right coronary artery (RCA) perforation during PCI.
Perforation management of collaterals
Kambis Mashayekhi, Bad Krotzingen, Germany
11th Experts Live CTO
The annual Euro CTO meeting
September 13th –14th, 2019 - Berlin, Germany
Coronary CTO is characterized by heavy atherosclerotic plaque burden within the artery, resulting in complete (or nearly complete) occlusion of the vessel. Although the duration of the occlusion is difficult to determine on clinical grounds, a total occlusion must be present for at least 3 months to be considered a true CTO. Patients with CTO typically have collateralization of the distal vessel on coronary angiography, but these collaterals may not provide sufficient blood flow to the myocardial bed, resulting in ischemia and anginal symptoms. CTO is clinically distinct from acute coronary occlusion, which occurs in the setting of ST-segment–elevation myocardial infarction, or subacute coronary occlusion, discovered with delayed presentation after ST-segment–elevation myocardial infarction. Clinical features and treatment considerations of these entities differ considerably from CTO.
Among patients who have a clinical indication for coronary angiography, the incidence of CTO has been reported to be as high as 15% to 30%. Patients with CTO are referred for angiography because of anginal symptoms or significant ischemia on noninvasive ischemia testing. Patients who are symptomatic will have stable exertional angina resulting from a limitation of collateral vessel flow to meet myocardial oxygen demand with stress. Of patients referred for PCI in clinical trials of CTO PCI, only 10% to 15% of patients are asymptomatic. It is likewise uncommon for patients with CTO to present with an acute coronary syndrome caused by the CTO itself.
A review of the approach and necessary equipment for the endovascular treatment pf Coronary Chronic Total Occlusions including guide catheters, guide wires, micro catheters, snares, balloons, stents and new devices
Coronary CTO is characterized by heavy atherosclerotic plaque burden within the artery, resulting in complete (or nearly complete) occlusion of the vessel. Although the duration of the occlusion is difficult to determine on clinical grounds, a total occlusion must be present for at least 3 months to be considered a true CTO. Patients with CTO typically have collateralization of the distal vessel on coronary angiography, but these collaterals may not provide sufficient blood flow to the myocardial bed, resulting in ischemia and anginal symptoms. CTO is clinically distinct from acute coronary occlusion, which occurs in the setting of ST-segment–elevation myocardial infarction, or subacute coronary occlusion, discovered with delayed presentation after ST-segment–elevation myocardial infarction. Clinical features and treatment considerations of these entities differ considerably from CTO.
Among patients who have a clinical indication for coronary angiography, the incidence of CTO has been reported to be as high as 15% to 30%. Patients with CTO are referred for angiography because of anginal symptoms or significant ischemia on noninvasive ischemia testing. Patients who are symptomatic will have stable exertional angina resulting from a limitation of collateral vessel flow to meet myocardial oxygen demand with stress. Of patients referred for PCI in clinical trials of CTO PCI, only 10% to 15% of patients are asymptomatic. It is likewise uncommon for patients with CTO to present with an acute coronary syndrome caused by the CTO itself.
A review of the approach and necessary equipment for the endovascular treatment pf Coronary Chronic Total Occlusions including guide catheters, guide wires, micro catheters, snares, balloons, stents and new devices
Spontaneous coronary artery dissection (SCAD) is an infrequent and often missed diagnosis among patients presenting with acute coronary syndrome (ACS). Unfortunately, SCAD can result in significant morbidities such as myocardial ischemia and infarction, ventricular arrhythmias and sudden cardiac death. Lack of angiographic recognition from clinicians is a major factor of under-diagnosis. With the advent of new imaging modalities, particularly with intracoronary imaging, there has been improved diagnosis of SCAD. The aim of this paper is to review the epidemiology, etiology, presentation, diagnosis and management of SCAD.
Chronic Total Occlusions: The Road Less TraveledAllina Health
By M. Nicholas Burke, MD. The use of pioneering percutaneous treatments for chronic total occlusions: indications, limitations, outcomes and current research.
Significant, defined as a greater than 50 percent narrowing, left main coronary artery disease is found in 4 to 6 percent of all patients who undergo coronary arteriography. When present, it is associated with multivessel coronary artery disease about 70 percent of the time
High Risk Left main PCI using Impella in post-TAVR patient Abdelkader Almanfi
This presentation describes a novel approach to high risk Left main PCI using Impella device for hemodynamic support in patient who already had TAVR .. this case was presented at at CRT 2016 meeting in Washington DC.
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Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
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The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
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• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
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Lmca dissection
1. Catheter Induced
Leftmain Dissection
Leftmain Dissection
Dr. Dinh Huynh Linh
National Heart Centre Singapore
Vietnam National Heart Institute
Dr. Jack Tan Wei Chieh
National Heart Centre Singapore
2. Case presentation
•
•
59 year old gentleman
•
Thorax CT: bronchus stricture + mediastinal
lymphadenophathy. Will need lung biopsy
•
•
•
•
•
NSTEMI in November 2012
Persistent AF, with history of lower limb artery thrombus. On
warfarin
MPI: inferior-lateral ischaemia.
Angiogram: DVD (RCA + LCx)
PCI in RCA CTO. EF improved, from 24 to 39%
Elective admission for staged PCI in the LCx
3. RCA CTO intervention on Nov 2, 2012
Genous 3.5 x 33 + MultiLink 3.0 x 38
QuickTime™ and a
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Pre-procedure
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Post-procedure
4. Scheduled PCI to mid-LCx
Supposed to be a
straightforward 15-minute
PCI case
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•Type B1 lesion
•Radial approach
•6 French sheath
•EBU 3.75 6F guide
6. First injection
• Dissection?
• Air embolism?
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Suspected acute
LMCA spiral
dissection, extending
into LAD and LCx
8. Clinical course
• Acute LMCA dissection. TIMI 1
flow in both LAD and LCx
• Retrograde dissection to the
coronary sinus
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H.264 decompressor
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• Pt had chest pain, hypotension,
VT, then VF. Multiple
defibrillation performed
• Heparin had already been given
(5500 IU) after catheter
engagement
9. Q1: What to do next?
1. CABG
2. PCI
3. Medical therapy
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10. Q2: What to do next?
1.No mechanical circulatory
support
2.Mechanical circulatory
support: IABP
3.Mechanical circulatory
support : ECMO
4.Other opinion
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11. PCI: open question?
1.To stent backward or
forward?
2.6F or 7F guiding catheter?
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12. Q4: PCI: which guidewire?
1.Hydrophillic guidewire
2.Hydrophobic guidewire
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13. Management
•
The surgical team and ECMO
team were activated
•
Senior consultant was called
for help
•
Strategy: Stent the LMCA,
LAD, LCx
•
•
•
RFA puncture
JL 3.5 6F guide
Fielder 0.014” to distal LAD
QuickTime™ and a
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14. QuickTime™ and a
H.264 decompressor
are needed to see this picture.
Genous 3.5 x 33 stent in LMCA
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The LMCA’s ostium was covered
15. QuickTime™ and a
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QuickTime™ and a
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Restoration of LAD and LCx flow
after LMCA stenting and post-dilatation
16. Stents implantation in LAD and LCx
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QuickTime™ and a
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QuickTime™ and a
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Proximal LAD stent implantation (Coroflex Blue 3.5 x 19 mm)
Coroflex Blue 3.0 x 16 mm in mid LCx
Coroflex Blue 3.0 x 28 mm in ostial LCx (TAP technique)
17. QuickTime™ and a
H.264 decompressor
are needed to see this picture.
QuickTime™ and a
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Final kissing balloon inflation
18. QuickTime™ and a
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are needed to see this picture.
QuickTime™ and a
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Final results
19. QuickTime™ and a
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QuickTime™ and a
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•
Dissection into the left coronary cusp. The right cusp was not involved
•
BP 151/64/86, HR 55 bpm, SpO2 97%
•
Protamin given to neutralize heparin
•
IABP was not inserted due to aortic dissection and stable condition
21. Post-procedural course
•
•
•
•
•
Patient was clinically stable. No chest pain
ECHO: no pericardial effusion, no LV thrombus
No EKG changes
No postprocedural cardiac enzyme elevation
Patient was discharged well 4 days later, on aspirin
100 mg and clopidogrel 75 mg
22. CTA 1 month later
Complete healing of the ascending aorta
12.2012
1.2013
23. Clinical follow-up
•
Follow-up CT: The intramural hematoma in the
posterior wall of the proximal ascending aorta shows
complete resolution
•
Lung cancer was excluded
•
Restart warfarin
•
Life long aspirin. 2 months of clopidogrel
•
Pt recovered uneventfully. No recurrence of angina
24. Literature review
•
•
•
•
•
Catheter induced LMCA dissection:
•
•
Urgent revascularization is mandated
0.008 to 0.02% of diagnostic catheterizations
0.06 to 0.07% of PCI
Ostial LMCA dissection is rarer than RCA dissection
Risk factors: LMCA disease, Amplatz usage, acute MI, catheter
manipulation, hard contrast injection
Retrograde dissection involving the coronary cusp or extending
up the aortic wall < 40 mm: conservative treatment
Boyle AJ et al. management. J Invasive Cardiol. 2006 Oct;18(10):500-3
prevention and Catheter-induced coronary artery dissection: risk factors,
25. What I have learnt
• Guiding catheter can be dangerous, especially if not coaxially engaged
• Vigorous contrast injection can be dangerous
• PCI is a life-saving approach for acute LMCA dissection
• Complete seal-off of the entry site, as well as the
LMCA’s origin, is important to prevent the further
extension of the dissection
• Limited dissection to the aorta can be treated
conservatively, without any surgical intervention
• Always call for help
27. Catheter Induced
Leftmain Dissection
Leftmain Dissection
Dr. Dinh Huynh Linh
National Heart Centre Singapore
Vietnam National Heart Institute
Dr. Jack Tan Wei Chieh
National Heart Centre Singapore
28. Case presentation
•
•
59 year old male
•
•
•
•
•
•
Mediastinal and hilar lymphadenophathy
Persistent AF, on warfarin. History of lower limb artery
thrombus, treated with thrombolysis
NSTEMI in November 2012
MPI: inferior-lateral ischaemia. EF=24%.
Angiogram: double vessel disease
PCI in RCA CTO
Elective admission for checking prior stents in RCA
and PCI in the LCx
29. QuickTime™ and a
H.264 decompressor
are needed to see this picture.
QuickTime™ and a
H.264 decompressor
are needed to see this picture.
The LMCA was stented (Genous 3.5 x 33 mm at 16 atm)
Post-dilate the LMCA with Hiryu 3.5 x 15 mm NC balloon
30. QuickTime™ and a
H.264 decompressor
are needed to see this picture.
QuickTime™ and a
H.264 decompressor
are needed to see this picture.
Proximal LAD stent implantation (Coroflex Blue 3.5 x 19 mm)
31. RCA CTO intervention on Nov 2, 2012
Genous 3.5 x 33 + MultiLink 3.0 x 38
QuickTime™ and a
H.264 decompressor
are needed to see this picture.
Pre-procedure
QuickTime™ and a
H.264 decompressor
are needed to see this picture.
Post-procedure
32. Angiogram on Dec 11, 2012
QuickTime™ and a
H.264 decompressor
are needed to see this picture.
November 2
December 11
33. •
•
•
•
•
•
•
59 year old gentleman.
Persistent AF, on warfarin
Thorax CT: suspected lung maglinancy. Will need lung biopsy
NSTEMI in November 2012 with inferior-lateral ischemia on MPI
Angiogram: DVD (RCA + LCx)
PCI in RCA. EF improved from 24% to 39%
Elective admission for staged PCI in the LCx
Senior consultant punctured the groin while main operator tried to wire via radial approach, but unsuccessful
ascending aorta shows complete resolution
The LMCA ositum: greater elastic + fibrious tissue content
he longest follow-up available in the literature is from the ASAN-MAIN (ASAN Medical Center-Left MAIN Revascularisation) Registry (n=250:BMS n=100, CABG n=250) [41]. In the 10-year follow-up, the adjusted risks of death (HR 0.81; 95%, CI: 0.44 to 1.50; p=0.50) and the composite outcome of death/QWMI/CVA (HR: 0.92; 95% CI: 0.55 to 1.53; p=0.74) were similar between the 2 treatment groups (BMS and CABG). Notably, the rate of TVR was significantly higher in the BMS group (HR: 10.34; 95% CI: 4.61 to 23.18;
p<0.001). For comparison, 5-year follow-up of another population who underwent ULM PCI with DES from the same registry (n=395: DES n=176, CABG n=219) [41] demonstrated no significant differences in death (HR: 0.83; 95% CI: 0.34 to 2.07; p=0.70) or the same composite outcome of death/QWMI/CVA (HR: 0.91; 95% CI: 0.45 to 1.83; p=0.79). The rate of TVR was, however, higher in the DES group compared to the CABG group (HR: 6.22; 95% CI: 2.26 to 17.14; p<0.001); with the effect being less pronounced compared to BMS.
The LMCA ositum: greater elastic + fibrious tissue content
