Ken Rosenfield's guest appearances

Ken Rosenfield

PERTcast

Oren Friedman

John Moriarty

Vic Tapson

Richard Channick

Jim Horowitz

Scott Cameron

Rachel Rosovsky

Robert Lookstein

Jennifer Quail

James Horowitz

Jon Haft

OwlTail

Episode 4: Dr. Rosenfield interviews Dr. Richard Channick on Post PE care! Dr Channick is the current PERT Consortium president and is the Director of the Acute and Chronic Thromboembolic Disease Program within the David Geffen School of Medicine at UCLA.  Dr. Rosenfield is Section Head of Vascular Medicine and Intervention at Mass General Hospital and past PERT president and founder.  What happens after a PE?  Following acute pulmonary embolism some patients do not return to their baseline and may suffer from what is called post PE syndrome. Some of these unfortunate patients develop chronic thromboembolic disease or chronic thromboembolic pulmonary hypertension  Follow Up Clinic  In clinic it's important to assess if patients have returned to their baseline of physical acitivity. If the answer is no, then go for objective testing First step may be getting a follow-up echocardiogram or repeat imaging CTA is extremely helpful for acute pulmonary embolism. CTA is less revealing for chronic pulmonary embolism. VQ scan is the most sensitive test for the chronic pulmonary embolism.  If VQ scan is normal 8 to 10 weeks following acute PE rhythm you do not have any chronic pulmonary embolism Following an abnormal VQ scan next steps should be --&gt; evaluated for CTED or CTEPH.  Define chronic thromboembolic pulmonary hypertension and its characteristics?  CTED or CTEPH is a scar tissue forming in pulmonary vessels is not an acute clot. à higher degree of such vascular obstruction will lead to increase in PVR and eventually PHTN and RV dysfunction. CTED or CTEPH has distinct appearance on imaging: Chronic clot may have appearance of fibrous bands, webs or bands. Appearance is quite different than acute clot. Extremely high pulmonary artery pressure of about 80 or 90 millimeters of Hg suggest chronic right ventricular pressure overload. Bronchial collaterals on CTA may suggest a chronic process.   Acute Vs Chronic Clot on Imaging:  Acute clot will have a central occlusive appearance. Sometimes it is hard to differentiate. If patient has not been anticoagulated in the past you anticoagulate and do a follow-up in 8 to 10 weeks. Signs of RV hypertrophy on the echocardiogram also suggests a chronic process    Treatment of chronic thromboembolic pulmonary hypertension  First-line of treatment is surgical. [It is complicated cardiac surgery that involves expert surgical team. It involves cardiopulmonary bypass, deep hypothermic arrest and needs and expertise.] Balloon pulmonary angioplasty growing evidence. RIOCIGUAT is the only approved drug for CTEPH. Macitentan has been studied but not approved. PDE inhibitors   also have been tried Upfront medical therapy should not delay the referral for the patients who potentially are surgical candidates.   Types of chronic thromboembolic pulmonary disease  and surgical classification  Four levels depend on whether the disease starts If the disease starts proximally it is easier for the surgeon to dissect. It depends where the chronic clots are involving the pulmonary vasculature.  Level 1 disease: Proximal disease Level 2 disease: Lobar disease Level 3 disease segmental disease Level 4 disease sub-segmental disease Basics Concepts of Balloon Pulmonary Angioplasty (BPA)  It involves dilating the narrowed pulmonary segments and improve with the primary pulmonary perfusion and reducing the pulmonary hypertension. First step is to do the pulmonary angiogram. Then match the perfusion defects with the VQ scan.  Work as a team. Goal is not to over distend the pulmonary vasculature. Goal is just to break up the scar or the fibrous tissue and increase distal perfusion. Vascular stenting is not performed usually. BPA is a staged procedure. The session can last anywhere between 2-3 to 12-13 sessions. Each session is 2 to 3 hours involves fair amount of radiation and the contrast. Pulmonary hemorrhage is a very serious complication; BPA has a learning curve. 

Episode 4: Dr. Rosenfield interviews Dr. Richard Channick on Post PE care! Dr Channick is the current PERT Consortium president and is the Director of the Acute and Chronic Thromboembolic Disease Program within the David Geffen School of Medicine at UCLA.  Dr. Rosenfield is Section Head of Vascular Medicine and Intervention at Mass General Hospital and past PERT president and founder. What happens after a PE? <ul> <li>Following acute pulmonary embolism some patients do not return to their baseline and may suffer from what is called post PE syndrome.</li> <li>Some of these unfortunate patients develop chronic thromboembolic disease or chronic thromboembolic pulmonary hypertension</li> </ul> Follow Up Clinic <ul> <li>In clinic it's important to assess if patients have returned to their baseline of physical acitivity. If the answer is no, then go for objective testing</li> <li>First step may be getting a follow-up echocardiogram or repeat imaging</li> <li>CTA is extremely helpful for acute pulmonary embolism. CTA is less revealing for chronic pulmonary embolism. VQ scan is the most sensitive test for the chronic pulmonary embolism.  If VQ scan is normal 8 to 10 weeks following acute PE rhythm you do not have any chronic pulmonary embolism</li> <li>Following an abnormal VQ scan next steps should be --&gt; evaluated for CTED or CTEPH.</li> </ul> Define chronic thromboembolic pulmonary hypertension and its characteristics? <ul> <li>CTED or CTEPH is a scar tissue forming in pulmonary vessels is not an acute clot. à higher degree of such vascular obstruction will lead to increase in PVR and eventually PHTN and RV dysfunction.</li> <li>CTED or CTEPH has distinct appearance on imaging: Chronic clot may have appearance of fibrous bands, webs or bands. Appearance is quite different than acute clot.</li> <li>Extremely high pulmonary artery pressure of about 80 or 90 millimeters of Hg suggest chronic right ventricular pressure overload.</li> <li>Bronchial collaterals on CTA may suggest a chronic process. </li> </ul> Acute Vs Chronic Clot on Imaging: <ul> <li>Acute clot will have a central occlusive appearance.</li> <li>Sometimes it is hard to differentiate. If patient has not been anticoagulated in the past you anticoagulate and do a follow-up in 8 to 10 weeks.</li> <li>Signs of RV hypertrophy on the echocardiogram also suggests a chronic process</li> </ul> Treatment of chronic thromboembolic pulmonary hypertension <ul> <li>First-line of treatment is surgical. [It is complicated cardiac surgery that involves expert surgical team. It involves cardiopulmonary bypass, deep hypothermic arrest and needs and expertise.]</li> <li>Balloon pulmonary angioplasty growing evidence.</li> <li>RIOCIGUAT is the only approved drug for CTEPH. Macitentan has been studied but not approved. PDE inhibitors   also have been tried</li> <li>Upfront medical therapy should not delay the referral for the patients who potentially are surgical candidates. </li> </ul> Types of chronic thromboembolic pulmonary disease  and surgical classification <ul> <li>Four levels depend on whether the disease starts</li> <li>If the disease starts proximally it is easier for the surgeon to dissect. It depends where the chronic clots are involving the pulmonary vasculature.</li> </ul> Level 1 disease: Proximal disease Level 2 disease: Lobar disease Level 3 disease segmental disease Level 4 disease sub-segmental disease Basics Concepts of Balloon Pulmonary Angioplasty (BPA) <ul> <li>It involves dilating the narrowed pulmonary segments and improve with the primary pulmonary perfusion and reducing the pulmonary hypertension.</li> <li>First step is to do the pulmonary angiogram. Then match the perfusion defects with the VQ scan.  Work as a team.</li> <li>Goal is not to over distend the pulmonary vasculature. Goal is just to break up the scar or the fibrous tissue and increase distal perfusion. Vascular stenting is not performed usually.</li> <li>BPA is a staged procedure. The session can last anywhere between 2-3 to 12-13 sessions.</li> <li>Each session is 2 to 3 hours involves fair amount of radiation and the contrast.</li> <li>Pulmonary hemorrhage is a very serious complication; BPA has a learning curve.</li> </ul>

What Happens after a PE? Ken Rosenfield interviews Richard Channick

Episode 2: Oren Friedman interviews Ken Rosenfield on catheter directed lytics. Oren Friedman MDAssociate Director, Cardiac Surgery ICU Pulmonary Critical Care Cedars-Sinai Medical Center Ken Rosenfield, MD, MHCDSSection Head, Vascular Medicine and Intervention Division of Cardiology Mass General Hospital   What is catheter directed thrombolysis (CDT)?  Placing a catheter via femoral or IJs into pulmonary arteries and infusing low dose thrombolytic over extended period. Percutaneous mechanical thrombectomy differs as it involves extracting thrombus from pulmonary artery. (mostly from proximal pulmonary arteries, and no thrombolytic regimen used in this method)  MOA of CDT compared to peripheral systemic thrombolysis  More clot bound thrombolytic directly into the clot compared to around the clot with systemic tPA. Increased local thrombolytic concentration. Reduced tPA and longer duration of infusion—reason for increased safety profile for ICH and major bleeding compared to full dose systemic tPA. (dose is 100 mg, ICH rates 3-5%) CDT also allows improve tPA infusion to into distal pulmonary circulation bed. (Vs percutaneous mechanical embolectomy)  Technical aspects of CDT:  Pulmonary angiogram is not always needed at time of CDT or post CDT. Decision to place unilateral or bilateral catheters (right, left or both branches of pulmonary artery) depends on location of clot based on CTA. Patient are usually monitored in ICU while drugs are infusing, close monitoring and experienced clinical nursing staff should be involved. Heparin during CDT: fix dose 300-500 unit/per catheter sheaths. Hard to achieve targeted aPTT (40-60) given very short duration of infusion. Fibrinogen to guide tPA duration- limited to no data Catheter directed thrombolysis with (EKOS) ultrasound or without ultrasound: We just don’t know. The available data stems from prospective clinical trials with ultrasound catheters. Sedation: be careful with sedation. Use minimum. Avoid intubation for procedure itself.  What is successful CDT?  Goal is to improve hemodynamics, not to remove all thrombus. Drop in pulmonary artery pressures (if monitoring available) or improved RV/LV ratio in pre-vs Post intervention imaging. [Echo or CTA]  Data on CDT  Impact on RV/LV ratio, as primary goal of improvement in many trials (see Table below)     ULTIMA trial: Heparin Vs CDT, with EKOS catheters. Rapid normalization of RV/LV ratio compared to heparin alone in immediate period. No difference at 90 days. Small numbers to show impact on mortality. SEATTLE II trial -- also included massive PE patients. PERFECT registry: prospective registry showing safety and efficacy of CDT. OPTALYSE trial: compared different CDT dosing regimens.     Impact on long term disability like CTED or CTEPH remains to be seen.  Dosing regimens for of CDT: (See Table below)  Higher risk bleeding patients: use as low as dose possible. OPTALYSE trial: Lower dose (as low as 4-8 mg) and shorter duration are effective for hemodynamic improvement. Higher doses were associated with better Miller clot burden improvement with increased risk of bleeding. (2 ICH incidents)   Rali P, Criner J. Am J Respir Crit Care Med. 2018 Sep 1;198(5):588-598

Episode 2: Oren Friedman interviews Ken Rosenfield on catheter directed lytics. Oren Friedman MDAssociate Director, Cardiac Surgery ICU Pulmonary Critical Care Cedars-Sinai Medical Center Ken Rosenfield, MD, MHCDSSection Head, Vascular Medicine and Intervention Division of Cardiology Mass General Hospital What is catheter directed thrombolysis (CDT)? <ul> <li>Placing a catheter via femoral or IJs into pulmonary arteries and infusing low dose thrombolytic over extended period.</li> <li>Percutaneous mechanical thrombectomy differs as it involves extracting thrombus from pulmonary artery. (mostly from proximal pulmonary arteries, and no thrombolytic regimen used in this method)</li> </ul> MOA of CDT compared to peripheral systemic thrombolysis <ul> <li>More clot bound thrombolytic directly into the clot compared to around the clot with systemic tPA.</li> <li>Increased local thrombolytic concentration.</li> <li>Reduced tPA and longer duration of infusion—reason for increased safety profile for ICH and major bleeding compared to full dose systemic tPA. (dose is 100 mg, ICH rates 3-5%)</li> <li>CDT also allows improve tPA infusion to into distal pulmonary circulation bed. (Vs percutaneous mechanical embolectomy)</li> </ul> Technical aspects of CDT: <ul> <li>Pulmonary angiogram is not always needed at time of CDT or post CDT.</li> <li>Decision to place unilateral or bilateral catheters (right, left or both branches of pulmonary artery) depends on location of clot based on CTA.</li> <li>Patient are usually monitored in ICU while drugs are infusing, close monitoring and experienced clinical nursing staff should be involved.</li> <li>Heparin during CDT: fix dose 300-500 unit/per catheter sheaths. Hard to achieve targeted aPTT (40-60) given very short duration of infusion. Fibrinogen to guide tPA duration- limited to no data</li> <li>Catheter directed thrombolysis with (EKOS) ultrasound or without ultrasound: We just don’t know. The available data stems from prospective clinical trials with ultrasound catheters.</li> <li>Sedation: be careful with sedation. Use minimum. Avoid intubation for procedure itself.</li> </ul> What is successful CDT? <ul> <li>Goal is to improve hemodynamics, not to remove all thrombus. Drop in pulmonary artery pressures (if monitoring available) or improved RV/LV ratio in pre-vs Post intervention imaging. [Echo or CTA]</li> </ul> Data on CDT <ul> <li>Impact on RV/LV ratio, as primary goal of improvement in many trials (see Table below)</li> </ul> <ol> <li> <ol> <li>ULTIMA trial: Heparin Vs CDT, with EKOS catheters. Rapid normalization of RV/LV ratio compared to heparin alone in immediate period. No difference at 90 days. Small numbers to show impact on mortality.</li> <li>SEATTLE II trial -- also included massive PE patients.</li> <li>PERFECT registry: prospective registry showing safety and efficacy of CDT.</li> <li>OPTALYSE trial: compared different CDT dosing regimens.</li> </ol> </li> </ol> <ul> <li>Impact on long term disability like CTED or CTEPH remains to be seen.</li> </ul> Dosing regimens for of CDT: (See Table below) <ul> <li>Higher risk bleeding patients: use as low as dose possible.</li> <li>OPTALYSE trial: Lower dose (as low as 4-8 mg) and shorter duration are effective for hemodynamic improvement. Higher doses were associated with better Miller clot burden improvement with increased risk of bleeding. (2 ICH incidents)</li> </ul> Rali P, Criner J. <a href="https://www.ncbi.nlm.nih.gov/pubmed/29672125" rel="nofollow" target="_blank">Am J Respir Crit Care Med.</a> 2018 Sep 1;198(5):588-598

Catheter-Directed Lysis: Oren Friedman interviews Ken Rosenfield