Coronary flow for the critically ill by Dr Pranesh Jogia
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The intent of this presentation is to provide an update of coronary assessment and management for the adult intensivist. Discussion points will include: 1. An assessment of coronary severity, using established methods, in particular fractional flow reserve (FFR), 2. Which stent- highlight the evolution of the stent to the current generation and what is evolving, 3. How to keep the stent open with current concepts of antiplatelet therapy and how this impacts the critically ill patient 4. What to consider if the ECG is abnormal, but the coronaries are not flow limiting obstruction- an occasional dilemma in the critically ill patient and finally 5. Discussion around a contemporary study regarding cardiogenic shock and coronary ischemia.
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Coronary flow for the critically ill by Dr Pranesh Jogia
- 1. CORONARY FLOW IN THE ICU DR PRANESH JOGIA INTENSIVE CARE SPECIALIST AND CARDIOLOGIST CLINICAL UNIT LEADER ICU, CARDIOLOGY, CARDIOTHORACIC SURGERY WAIKATO HOSPITAL , NZ CRITICALHEART@ICLOUD.COM
- 2. DISCLOSURES • Nothing to disclose
- 3. THE REQUEST CORONARY FLOW FOR THE CRITICALLY ILL- 15 MINUTES • Update for mostly adult intensivists • Overview of coronary angiogram and interventions- how to identify a significant lesion, evidence for various interventions (plasty vs bare metal stent vs DES), • recent advances, etc. • relevant for an ICU audience.
- 4. AIMED AT THE INTENSIVIST 1. Identification of the lesion- what to do about it in the ICU 2. Which stent 3. How to keep the stent open 4. Culprit Shock 5. When you suspect ischemia and the coronaries don’t have flow limiting in the sick patient (ruptured plaque, spasm, takosubo) 6. Not discuss inotropy in ischemic heart disease (levosimendan) 7. Coronaries after cardiac arrest (Will be discussed later in the meeting) 8. Not about IABP
- 5. IDENTIFICATION OF THE LESION • CORONARY ANGIOGRAM • Why do a Coronary Angiogram? • Symptoms in the conscious patient- then risk stratification • Changing in the era of CT coronary Angiography
- 6. CRITICALLY ILL PATIENT • Conscious • Chest pain/ECG changes/troponin elevation • Unconscious • Haemodynamic instability/ telemetry findings • ECG changes/ troponin elevation/ regional wall abnormality
- 8. IDENTIFY LESIONS • No obstructive disease (MI with non obstructive coronary arteries MINOCA) • Mild • Moderate • Severe
- 9. MODERATE LESION… …IS IT SIGNIFICANT? • Causes anguish • Use your thumb to guestimate
- 11. PROBABLY SIGNIFICANT, STENT! • Occulo stent reflex
- 12. FRACTIONAL FLOW RESERVE • Measuring coronary blood flow and pressure provides unique information that complements the angiographic evaluation and facilitates decision-making regarding therapy.
- 14. CT FFR
- 16. Started the evolution of opening occluded vessels with a balloon Problems of acute stent closure (arterial recoil) Dissection Repeat revascularization high
- 17. Resolved issues of arterial recoil Dissection still present but less frequent BUT Restenosis due to neointimal proliferation Repeat revascularization risk remained high due to restenosis
- 18. Developed to deal with the high restenosis rate of BMS Highly successful but identified the problems of Instent thrombosis Lack of vessel endothelialisation promoted thrombus formation Emphasized the importance of Dual antiplatelet therapy
- 19. SECOND GENERATION DES • Promoted Evolution of second generation DES • Better stent profile • Different drug on the scaffold • Resulted in significantly less stent thrombosis • Outcome Profiles are better than BMS • However DAPT has simultaneously evolved likely contributing to better outcomes
- 20. SHOULD A DES OR BMS BE USED? • NORSTENT 2016 Everolimus- or Zotarolimus-eluting stents (second generation) • definite stent thrombosis DES 0.8% and BMS 1.2%
- 22. OTHER OPTIONS • Drug Eluting Balloon • esp when duration of DAPT should be limited • Bioresorbable Vascular scaffold • Considered to be the holy grail • Scaffold essentially dissolves with time leaving only native vessel • Outcomes have not been as good as second generation DES, so work has yet to be done, if at all
- 23. HOW TO KEEP THE STENT OPEN • Once a stent is deployed- risk of instent thrombosis exists. • This risk is reduced with dual antiplatelet agents (DAPT) • Each agent works by a different pathway resulting in greater effect compared to using either agent alone.
- 24. DUAL ANTIPLATELET THERAPY • Aspirin- still cornerstone of antiplatelet therapy • Once upon a time- IV glycoprotein 2b3a inhibitors • Still used when thrombus burden is high • Evolution ADP Inhibitors
- 25. DIFFERENT ADP INHIBITORS Tan, Lam, Yan Cardiovascular Therapeutics 30 (2012) e167–e173
- 26. From: 2017 ESC focused update on dual antiplatelet therapy in coronary artery disease developed in collaboration with EACTSThe Task Force for dual antiplatelet therapy in coronary artery disease of the European Society of Cardiology (ESC) and of the European Association for Cardio-Thoracic Surgery (EACTS) Eur Heart J. 2017;39(3):213-260. doi:10.1093/eurheartj/ehx419 Eur Heart J | The article has been co-published with permission in the European Heart Journal [DOI: 10.1093/eurheartj/ehx419] on behalf of the European Society of Cardiology and European Journal of Cardio-Thoracic Surgery [DOI 10.1093/ejcts/ezx334]
- 27. DUAL ANTIPLATELET THERAPY CAN I STOP IT??!! Bleeding vs Clotting • Life threatening bleeding- no real discussion All other situations: • Currently there is no prescriptive risk calculator or algorithm that guides the clinician • I am never comfortable stopping DAPT less than 6 months for DES • But often it needs to be done
- 28. Egholm et al JACC Vol 68, 24, 2622-2632 2016
- 29. RISK FACTORS FOR INSTENT THROMBOSIS Surgery After DES Implantation JACC VOL 68 24, 2016 Spaulding, Mennuni Factors which make me extra nervous when planning to stop DAPT Extra risks to stent thrombosis Think about keeping a single agent Greatest risk is stopping DAPT
- 30. CULPRIT-SHOCK • Largest contemporary study of Cardiogenic shock • 706 patients in cardiogenic shock- ischemic • Culprit vessel PCI had better outcome then multivessel PCI in shock (opposite to non shock patients) • Fascinating study just to look at Cardiogenic shock in contemporary modern day practice (age up to 90) with current optimal medical therapy • Depressing reading
- 31. CULPRIT-SHOCK • Approximately 80% of the patients were ventilated and approx 90% were on catecholamines • EF 30% (similar to SHOCK) • 28% used mechanical circulatory support… … • Of this • 26% IABP (compared to 86% in SHOCK 1999) • 23% ECMO • 43% used Impella 2.5 or CP (12% of the study popn) • 47% mortality at 30 days despite all efforts (compared to 51% in SHOCK)
- 32. CULPRIT-SHOCK • Mortality remains high - Despite the evolution of stents, timing of intervention and CVS supports
- 33. SUMMARY • CVS intervention continues to evolve • Complexities of PCI and DAPT therapy in the ICU remains complex and relatively evidence free • Cardiogenic Shock associated with myocardial ischemia remains high despite progress
- 34. WAIKATO HOSPITAL CRITICAL CARE NEW ZEALAND Large tertiary centre- Trauma/Neurosurg/Cardio thoracic serving a large geographic territory Exciting Opportunities for INTENSIVISTS and FELLOWS No one will accuse you of being a hobbit Pranesh.Jogia@waikatodhb.health.nz Geoff.mccracken@waikatodhb.health.nz Criticalheart @icloud.com DO GOOD WORK WITH GOOD PEOPLE
- 35. .org
Editor's Notes
- Measuring coronary blood flow and pressure provides unique information that com- plements the angiographic evaluation and facilitates decision-making regarding therapy. Coronary pressure and flow relationships can identify the ischemic potential of a stenosis For translesional pressure (FFR) measurements, the wire pressure is first matched to the guide catheter pressure in the central aortic location, and then the wire is advanced into the artery beyond the stenosis. Baseline pressure is recorded, followed by induction of coronary hyperemia with IC or IV adenosine, continuously recording both guide catheter and sensor-wire pressures. FFR is computed Pressuredistal/ Pressureaorta at maximal hyperemia. Pressuredistal is recorded from the pressure wire, Pressureaorta is recorded from the guide catheter that delivers the pressure wire. Pressure signal artifacts may be reduced by careful attention to technique.
- Theoretical framework by which second-generation drug-eluting stents (DESs) might decrease the risk for myocardial infarction (MI) and cardiovascular death in comparison to bare-metal stents, even though rst-generation DESs did not. (From Bhatt DL. Examination of new drug-eluting stents—top of the class! Lancet 2012;380:1453.)
- Figure 3 Algorithm for DAPT in patients with coronary artery disease. ACS = acute coronary syndrome, BMS = bare-metal stent; BRS = bioresorbable vascular scaffold; CABG = Coronary artery bypass graft; DCB = drug-coated balloon; DES: drug-eluting stent; PCI = percutaneous coronary intervention; Stable CAD = stable coronary artery disease. High bleeding risk is considered as an increased risk of spontaneous bleeding during DAPT (e.g. PRECISE-DAPT score ≥25). Colour-coding refers to the ESC Classes of Recommendations (green = Class I; yellow = Class IIa; orange = Class IIb). Treatments presented within the same line are sorted in alphabetic order, no preferential recommendation unless clearly stated otherwise. <sup>1</sup>: After PCI with DCB 6 months. DAPT should be considered (Class IIa B). <sup>2</sup>: If patient presents with Stable CAD or, in case of ACS, is not eligible for a treatment with prasugrel or ticagrelor. <sup>3</sup>: If patient is not eligible for a treatment with prasugrel or ticagrelor. <sup>4</sup>: If patient is not eligible for a treatment with ticagrelor.
- Important bleeding, and DES was implanted more than a month earlier, stop DAPT. If important risk factors for thrombosis, I would like to keep aspirin on if possible and return to DAPT as soon as safe
- Figure 1 Diagnostic algorithm of myocardial infarction with no obstructive coronary atherosclerosis. First step is represented by clinical history, electrocardiography, cardiac enzymes, echocardiography, coronary angiography, and left ventricular (LV) angiography. Regional wall motion abnormalities with an ‘epicardial pattern’ indicate an epicardial cause of myocardial infarction with no obstructive coronary atherosclerosis: if clinical data suggest coronary artery spasm, intra-coronary acetylcholine (Ach), or ergonovine test should be performed and if there is a clinical doubt of thrombus, intra-vascular ultrasound (IVUS), or optical coherence tomography (OCT) are required. Regional wall motion abnormalities with a ‘microvascular pattern’ indicate a microvascular cause of MINOCA. If clinical data and left ventriculography suggest Takotsubo syndrome (TS) or PVB19 myocarditis, cardiac magnetic resonance (CMR) with contrast medium (CM) is needed. If the latter shows evidence of myocarditis, endomyocardial biopsy (EMB) can be performed to ascertain the aetiology. If clinical data suggest coronary microembolism, TEE, and/or CEE are required to detect a cardiac source of embolism. Finally, if microvascular spasm is suspected, IC Ach test is needed. TEE, transesophageal echocardiography; CEE, contrast-enhanced echocardiography.
- Figure 1 Recommended diagnostic and therapeutic algorithm for myocardial infarction with non-obstructive coronary arteries. * Takotsubo cardiomyopathy cannot be diagnosed with certainty in the acute phase as the definition requires follow-up imaging to document recovery of left ventricular function. In the authors' experience, some patients with apparent takotsubo have unrecognized ischaemic injury or myocarditis. We therefore recommend CMR when takotsubo cardiomyopathy is suspected. ** Plaque disruption (rupture, or erosion) should be suspected and intracoronary imaging considered whenever an alternate aetiology of the clinical presentation such as myocarditis or vasospasm has not been clearly identified, particularly among those patients with evidence of atherosclerosis on the coronary angiogram. Intravascular ultrasound and intracoronary optical coherence tomography frequently show more atherosclerotic plaque than may be appreciated on angiography. They also increase sensitivity for dissection. If intracoronary imaging is to be performed, it is appropriate to carry out this imaging at the time of the acute cardiac catheterization, after diagnostic angiography. Patients should be made aware of the additional information the test can provide and the small increase in risk associated with intracoronary imaging. *** Provocative testing for coronary artery spasm has been safely performed by experienced clinical researchers in selected patients with a recent acute myocardial infarction.<sup>34</sup> However, death cases have been reported (Per Tornvall Tornberg, personal communication) and this should not be a standard procedure among the patients, particularly in the acute phase. **** Clinically suspected myocarditis (no angiographic stenosis ≥ 50% plus non-ischaemic pattern on cardiac magnetic resonance imaging) by ESC Task Force criteria.<sup>36</sup> Diagnosis of certainty and aetiological diagnosis of myocarditis requires EMB (histology, immunohistology, infectious agents by PCR). AMI, acute myocardial infarction; BNP, B-type natriuretic peptide; CRP, C-reactive protein; Hb, hemoglobin; IVUS, intravascular ultrasound; LGE, late gadolinium enhancement; LV, left ventricle; MRI, magnetic resonance imaging; OCT, optical coherence tomography; SO2, Oxygen saturation; WBC, white blood cell count.
- I believe people want to make a difference by doing good work with good people