Meeting Update

VeithSymposium: Hot Topics in the Peripheral Vasculature

Compiled by Cath Lab Digest

Compiled by Cath Lab Digest

*Note: the interview with Dr. Engelhardt has been corrected in this online version to reflect the following:

"There is a trial going on at multiple sites in Germany called the ULTrasound Accelerated ThrombolysIs of PulMonAry Embolism (ULTIMA) trial, which is about halfway through enrollment." The original printed text noted only the Frankfurt trial site.


Abbott: Medical Therapy, Not Carotid Surgery or Stenting, for Asymptomatic Carotid Artery Disease

Bell: A Critical Look at Intervention for Asymptomatic Carotid Stenosis

Engelhardt: Catheter-Directed Ultrasound Thrombolysis and the Reduction of Right Ventricular Dysfunction in Acute Pulmonary Embolism

Kwolek: Early Use of the Vortex Angiovac Suction Cannula in the Treatment of Iliac and IVC Thrombosis, and Massive Pulmonary Emboli

The VeithSymposium was held in New York City from November 16-20, 2011.


Medical Therapy, Not Carotid Surgery or Stenting, for Asymptomatic Carotid Artery Disease

Cath Lab Digest talks with Anne L. Abbott, MD, PhD, FRACP, Neurologist and Senior Research Fellow at the Baker IDI Heart and Diabetes Institute in Melbourne, Australia.

Dr. Abbott concludes, based on a detailed analysis, that current medical intervention is superior to the utilization of carotid surgery or angioplasty/stenting for the vast majority of patients with asymptomatic carotid artery disease.

Are we wrong to pursue stenting or surgery for asymptomatic carotid artery disease patients?

Currently, in routine practice, patients with asymptomatic carotid stenosis receive the best chance of a stroke prevention benefit by using optimal medical intervention alone. In this context, medical intervention refers to non-invasive strategies to reduce risk of vascular disease complications, including stroke. It consists primarily of diagnosis of vascular disease risk factors and reduction in risk using education, support of healthy lifestyle habits and appropriate drugs. There are several reasons why patients with asymptomatic carotid stenosis now have the best chance of stroke risk reduction using current, good quality medical intervention alone. Most importantly, there has been a 60-80% fall in the relative risk of ipsilateral stroke in patients with a 50-99% carotid stenosis receiving medical intervention alone over the last 20 to 30 years.1-4 The results are robust. This reflects many advances in the efficacy of medical treatment and improved implementation. We are now seeing an average annual rate of ipsilateral stroke with medical treatment alone of about 0.5%.3 This is approximately:

  • Three times lower than for operated patients in the Asymptomatic Carotid Atherosclerosis Study (ACAS)5;
  • Five times lower than for non-operated patients in ACAS5;
  • Three times lower than for stented patients in the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST)6;
  • Two times lower than for operated patients in CREST6.

The second reason you cite is that we don’t know how to identify asymptomatic carotid disease patients at high risk for stroke.

Yes, that’s the second reason why patients will do better with current medical intervention alone. We cannot reliably identify those at high risk of ipsilateral stroke despite current, good quality medical treatment. There are a number of reasons, including the fact that current optimal medical intervention has been poorly defined; no one has actually defined it properly and measured its impact on the risk of stroke in this population. No one has done risk stratification studies in the context of current best practice medical intervention alone.

So there is not an optimal medical therapy agreed upon by the current medical community?

It comes down to detail. People have been treated for asymptomatic stenosis largely on the basis of their other vascular disease risk factors: coronary heart disease, angina, atrial fibrillation, stroke in other territories, peripheral vascular disease, hypertension, diabetes, smoking and so on. Physicians have largely treated these patients according to these ‘non-asymptomatic carotid stenosis’ risk factors. Over the last few decades, we have accumulated better knowledge about how to define and manage these risk factors from a wide variety of disciplines: hypertension specialists, lipid specialists, diabetes specialists, and so on, and the craft of all these groups has evolved significantly over the last 20 to 30 years. Now it is time to consolidate and agree on the best medical intervention for prevention of vascular disease in a more integrated fashion, and therefore, better define how to best prevent stroke and other complications in patients with asymptomatic carotid stenosis.7

You list a third reason as the barriers in clinical practice to implementing the strict protocols of clinical trials.

Yes. It has been about 15 years since the ACAS study5 was published, and yet it is still quite uncommon to find accurate measures of routine practice surgical outcomes in local hospitals. So it is very hard to know what your local service provider is achieving in terms of peri-procedural stroke and death rates. We do not fully replicate randomized trial methods in routine practice, so it is very hard, of course, to be sure that you are duplicating randomized trial outcomes as well. A number of registries are setting up in different areas, including vascular disease, and that is very good. Measuring fundamental outcomes for the services we provide in hospitals should be routine. We need these measures to make sure we are achieving what we are hoping for and improve services. If you are going to offer any service, whether non-invasive or invasive, we should set up cost-effective ways to measure the outcomes of what we do, routinely. And that’s possible. It’s another story, but it would involve organization of the medical information we collect in daily practice so that it is used for patient reports and, at the same time, integrated into a database. It would require collaboration and some dedicated resources. However, such resources would save hospitals money by helping to demonstrate which services are helpful to patients and which are not.

Do you think that it is because so many disciplines are involved in the treatment of asymptomatic carotid artery disease patients that we lack clear guidelines for treatment?

Tackling vascular disease from multiple ‘organ’-focused directions has allowed for a great deal of expansion in knowledge. However, at this point, yes. There is too much knowledge for one person or one group to ever fully comprehend, let alone keep track of. We need to become more organized and strongly encourage multidisciplinary team approaches to vascular disease, which is a huge societal problem.

What do you view as the future of invasive procedures for asymptomatic carotid artery disease?

First, the routine clinical practice role for invasive carotid procedures, as defined in current guidelines, needs reappraisal. Generally, for instance, surgery is still recommended for ‘generally fit’ patients with asymptomatic carotid stenosis as long as the 30-day peri-operative risk of stroke or death is <3%.8 Recently, some have suggested carotid angioplasty/stenting as an alternative based on the same 30-day procedural risk.9 However, these recommendations are now obsolete. They are based on the results of two or three historical randomized surgical trials in which patients were randomized from 1983-2003, and received inferior medical intervention by today’s standards. As mentioned, we are now measuring, in asymptomatic patients, an average annual ipsilateral stroke rate of about 0.5%.3 This is without defining, and testing the impact, of current ‘best-practice’ medical intervention alone. Therefore, we can conservatively estimate, based on already published studies,  that  <5% of ‘generally fit’, medically managed patients with moderate or severe asymptomatic carotid stenosis will now receive an ipsilateral stroke prevention benefit from carotid endarterectomy (CEA) (or carotid artery stenting, CAS) during their lifetime if they survive an average of 10 years from identification. This is even if the procedural risk of stroke/death is zero.

Further, as mentioned, we cannot yet reliably identify this <5% of patients now likely to benefit from CEA or CAS. In order to identify them, first of all, we would have to define best-practice medical treatment by consensus and then measure the risk of stroke when patients are receiving it. We can expect a very low overall stroke rate, emphasizing the need for large patient numbers, serious collaborative efforts and careful rate calculations. Measuring the risk of ipsilateral stroke and other significant vascular complications in these patients would be immensely useful. This would help define what can now be achieved with medical intervention and set new standards of care. However, one needs to question the effort that will be required to identify those at high risk of stroke, despite current medical intervention, who benefit from additional surgery or stenting. The academic practicality of this would need to be carefully considered, as well as the practicality of translating this later to routine practice. Perhaps we need to consider that the time for an invasive approach to asymptomatic carotid stenosis has now passed and move on to the next problem. For instance, we may get more ‘bang for our buck’ by making sure current best practice medical intervention is received by those who need it, or  improving the outcomes for patients with symptomatic carotid stenosis.

What percentage of carotid artery disease patients are symptomatic versus asymptomatic?

By far, most patients with carotid stenosis are asymptomatic. It is quite a common lesion. About 10% of people, by the time they get to their eighth decade, have asymptomatic carotid stenosis of about 50-99%. It is quite easy to detect with ultrasound, which is relatively cheap and noninvasive. If people do become symptomatic, it can be with their first ipsilateral transient ischemic attack (TIA), which is more common, or first ipsilateral  stroke, without prior TIA. From my 2009 meta-analysis, in the most recently reported studies, first ipsilateral TIA was about twice as common as first ipsilateral stroke.1 The average annual risk of ipsilateral stroke was about 1% and for ipsilateral TIA, about 2%. However, as mentioned above, these absolute average annual rates are continuing to fall as medical intervention and its implementation continue to improve.3

Is medical therapy is less expensive than carotid surgery or stenting?

Yes. That is another argument that comes into it. Medical intervention alone is at least 4-8 times cheaper than surgery or angioplasty/stenting for preventing stroke associated with asymptomatic carotid stenosis.1 However, the first concern is efficacy. Yet, here again, medical treatment alone now offers the best chance of stroke prevention in patients with asymptomatic carotid stenosis.

What is your take-home message?

I would highlight the very good news. The efforts of so many, from so many disciplines, over recent decades have been highly successful in reducing our risk of stroke. These efforts ARE paying off and patients need to understand how much they have to gain by embracing relatively cheap and simple methods to prevent stroke. We should very happy that stroke prevention has become more effective, less traumatic and cheaper.

Dr. Abbott can be contacted at


  1. Abbott AL. Medical (nonsurgical) intervention alone is now best for prevention of stroke associated with asymptomatic severe carotid stenosis: Results of a systematic review and analysis. Stroke. Oct 2009;40(10):e573-583.
  2. Naylor AR, Gaines P, Rothwell P. Who benefits most from interventions for asymptomatic carotid stenosis: Patients or professionals? Eur J Vasc Endovasc Surg. 2009;37:625-632.
  3. Abbott AL. Why All The Landmark Trials Supporting Surgery To Prevent Strokes From Carotid Stenosis Are Now Obsolete: When Is Carotid Intervention Now Indicated. New York Hilton, New York City: Presented at the 37th Annual Vascular and Endovascular Issues, Techniques and Horizons(VEITHsymposium)2010. Ten page conference paper. Available online.
  4. Naylor AR. Time to rethink management strategies in asymptomatic carotid artery disease. Nature reviews. Cardiology. Oct 11 2011, online ahead of print.
  5. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA. 1995;273:1421-1428.
  6. Brott TG, Hobson RW, 2nd, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. Jul 1 2010;363(1):11-23.
  7. Abbott A. Best medical intervention for arterial disease or wishful thinking. Eur J Vasc Endovasc Surg. Apr 2011;41(4):509-510.
  8. Goldstein LB, Adams R, Alberts MJ, et al. Primary prevention of ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council: cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. Jun 20 2006;113(24):e873-923.
  9. Brott TG, Halperin JL, Abbara S, et al. 2011 ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS Guideline on the Management of Patients With Extracranial Carotid and Vertebral Artery Disease: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American Stroke Association, American Association of Neuroscience Nurses, American Association of Neurological Surgeons, American College of Radiology, American Society of Neuroradiology, Congress of Neurological Surgeons, Society of Atherosclerosis Imaging and Prevention, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of NeuroInterventional Surgery, Society for Vascular Medicine, and Society for Vascular Surgery. Stroke. Jan 31 2011.

Catheter-Directed Ultrasound Thrombolysis and the Reduction of Right Ventricular Dysfunction in Acute Pulmonary Embolism

Cath Lab Digest talks with Tod C. Engelhardt, MD, FACS, Chairman of the Cardiovascular and Thoracic Surgery Division of East Jefferson General Hospital, Metairie, Louisiana

Can you tell us about the pulmonary embolism patient population?

There are three categories of pulmonary embolism (PE) patients:

  • Massive PE patients account for 5%. These patients present in cardiogenic shock, so they are the most serious group, and they have a high mortality rate.
  • The submassive group accounts for 40%. Submassive patients are hemodynamically stable, with normal blood pressure, but present with evidence of right ventricular dysfunction or right heart enlargement, so with imminent right heart failure. 
  • The remaining patients, about 55%, will present as minor PE patients, and we normally don’t treat them with anything other than the traditional anticoagulation. The subset of patients in which we are most interested is the submassive group, which accounts for 40% of PE patients. In my opinion, treatment with anticoagulation alone for submassive patients is often inadequate, and that is why we are investigating new ways to treat this subgroup with catheter-directed ultrasound thrombolysis. 

How does it work?

We use a specially designed catheter, the EkoSonic Endovascular System (Ekos Corporation), with two components. The first component is a catheter that fits through a 6 French sheath, usually placed through the femoral vein. It can be passed up over an .035” guide wire, from the femoral vein, up the inferior vena cava into the right atrium. It crosses over the tricuspid valve into the right ventricle and goes up through the right ventricular outflow tract into the pulmonary arteries. The first portion of the catheter has multiple side holes that allow for the delivery of a thrombolytic agent, such as tPA. The second portion of the catheter is a central ultrasonic core, essentially a wire with ultrasonic transducers. Each transducer is very small and is placed about 1 cm apart, and this portion sits inside the first catheter with the side holes. The ultrasonic core vibrates at 2 million cycles per second, or 2 megahertz. The resulting ultrasonic energy breaks up clot by exposing plasminogen receptor sites, making the clot more ‘porous’, so to speak, and allowing delivery of tPA drug into the clot. The ultrasonic waves drive the drug deeper inside the clot. It also allows us to use less tPA, meaning a lower risk of bleeding complications. A systemic dose of tPA, usually 100mg delivered over 1-2 hours, has a 0-3% incidence of intracranial hemorrhage, and an up to 21% incidence of major bleeding, usually in the abdominal cavity.

In our protocol for catheter-directed ultrasound therapy, we have been using a total of 20 mg over 12-20 hours. It is a very slow administration of a much lower dose, and we are getting just as good results as with the systemic dose. The protocol we have been using is 1 mg per hour, and we usually give ½ mg on each side. Patients require ICU stay and a continuous infusion over 20 hours.

The bleeding rate, compared to traditional administration of tPA, has been significantly reduced. When I first started using the catheter, in the first 13 patients, I used an average dose of 45 mg. I would give a bolus dose and then use as much tPA as I thought necessary, because we actually didn’t know how much to give. I had bleeding complications confined to the groin only (groin hematomas). I had 3 out of 28 patients develop groin hematomas that required at least 1 unit of blood transfusion, so I decreased the amount of tPA given and shortened the time of administration. Since we have gone to no more than 20 mg, we have had no bleeding complications, including no groin hematomas.

We published our first 24 cases treating massive and submassive PE patients in Thrombosis Research.1 Three patients were in the massive category, presenting in cardiogenic shock, and the remaining patients were submassive. Our study is ongoing, and probably by the beginning of 2012, we will begin the Seattle Study, a prospective evaluation using the same protocol and the same submassive subset of patients.

What did you find in your analysis regarding right ventricular dysfunction following the catheter treatment?

Practically all patients demonstrated significant reduction in what we call the right ventricular/left ventricular (RV/LV) ratio. If you take the end diastolic volume and measure the diameter of the right ventricle compared to the left ventricle, the result is the RV/LV ratio. Anything greater than 0.9 is an independent predictor of poor outcome in these patients. We found a significant decrease in right ventricular dysfunction with the catheter-directed treatment. With right ventricular enlargement, patients are prone to developing recurrent pulmonary embolism and primary pulmonary hypertension. When you treat a patient with anticoagulation alone, in the submassive PE patients, there will be a subset of patients who, within 7 days, will not have regression of their right ventricular diameter. A significant number, up to 44%, will develop pulmonary hypertension. The main goal of any treatment should be to reverse diameter enlargement and get the RV/LV ratio back to 0.9 or less. We saw this in nearly all of our patients directly after the treatment with catheter-directed thrombolysis using ultrasonic enhancement within 48 hours of presentation to the hospital. They reverted back to the normal ratio.

When patients present, if a PE is entertained as a diagnosis, a CT angiogram (CTA) is done. We measure the right ventricular diameter off of the CT imaging study, which also shows the clot burden in the pulmonary arteries. We do get an echocardiogram as well, and have been able to get a 4-chamber view echocardiogram that corresponds very favorably to the CTA results (we do plan to publish this data). Patients also get a duplex scan of both lower extremities looking for deep venous thrombosis. Once I have the diagnosis and the patient fits the submassive group, we will place the catheter and treat them for the necessary length of time, giving up to 20 mg of tPA. In the next 24 hours, the CTA is repeated, and we judge the results. Nearly all of our submassive patients have had a significant regression in the size of the right ventricle, meaning they are at a much less risk of developing pulmonary hypertension or a repeat pulmonary embolism.

Are there any other studies ongoing?

There is a trial going on at multiple sites in Germany called the ULTrasound Accelerated ThrombolysIs of PulMonAry Embolism (ULTIMA) trial, which is about halfway through enrollment. It is comparing anticoagulation alone to ultrasound-assisted thrombolysis in submassive PE patients. ULTIMA should answer the questions of those physicians wondering which is better, the traditional therapy, heparin and coumadin, or anticoagulation alone, or catheter-directed ultrasound thrombolysis.

Dr. Engelhardt can be contacted at


  1. Engelhardt TC, Taylor AJ, Simprini LA, Kucher N. Catheter-directed ultrasound-accelerated thrombolysis for the treatment of acute pulmonary embolism. Thromb Res 2011 Aug;128(2):149-154.

A Critical Look at Intervention for Asymptomatic Carotid Stenosis

Cath Lab Digest talks with Peter R.F. Bell MD, FRCS, DSC, KBE, Emeritus Professor of Surgery at the University of Leicester, and Honorary Consultant Surgeon at the Leicester Royal Infirmary, London, United Kingdom.

What do you think about intervention for asymptomatic carotid stenosis?

The vast majority of asymptomatic patients do not need an operation or a stent; they need best medical treatment. Only about 5% of asymptomatic patients with a severe stenosis need invasive treatment. The trouble is, we do not know who they are. We need to find out the small number of people who do need invasive treatment, and treat those. Treating the entire asymptomatic population invasively is more trouble than it is worth, and a stent is more dangerous than an operation.

What have the data told us so far?

A paper was published in 2008 which indicated that in the United States in 2005 122,000+ patients with asymptomatic carotid disease with severe stenosis were treated invasively.1 Recent data tells us that using best medical treatment alone for these cases, meaning statins and some kind of antiplatelet treatment like aspirin, blood pressure control and stopping smoking, reduces the risk of a stroke and mortality every year to 0.5%. If we look at the recent CREST trial2, the risk of a stroke per annum, after an operation, is 0.9%, adding 0.4% more risk than using medical treatment alone. If a stent is placed instead, the risk of stroke per annum increases to 1.6%. This means that invasive treatment is causing strokes and stenting is causing almost twice as many as surgery.

The CREST trial data showed that the risk of getting a stroke, death or myocardial infarction (MI) (the trial endpoint) was the same whether a stent was put in or whether an operation was performed. What the CREST endpoint didn’t show was that the risk of stroke, which is what we are trying to stop, was much higher with stenting than with surgery. CREST also did not have a comparative medical treatment arm, and asymptomatic and symptomatic patients were mixed together. Because we know that symptomatic patients are much more at a risk of a stroke than asymptomatic patients, mixing them in this way is unacceptable, and like mixing apples and oranges. In spite of this, and based on this trial, the FDA decided that anybody who has a carotid stenosis, symptomatic or asymptomatic, could have a stent put in, which is complete nonsense and potentially dangerous.

Did they measure severity of the strokes that occurred in CREST?

That’s a very interesting question. Most of these strokes were categorized as ‘minor’, but the trial didn’t actually define what minor and major meant. Minor could mean anything from being able to still walk around, but with a left arm paralyzed, or perhaps being unable able to think straight or speak clearly, but still able to walk around. A major stroke means paralysis down one side. Anything less than paralysis down one side is so-called minor. But minor can be pretty serious.

If anything, asymptomatic patients are worse in terms of overall risk factors, but their actual risk of stroke is lower. There is, therefore, no good reason to stent most asymptomatic patients. In fact, it is a waste of healthcare resources, and it is actually causing strokes.

There is a small number, 5%, of asymptomatic patients, who are at risk of stroke, but right now we cannot confidently state who these patients are. There are techniques available to try and figure out which patients are at risk, but rather than doing that, money is being put into stenting. In the United Kingdom, we tend not to stent or operate on asymptomatic patients. We may treat about 5%, based mainly on intuition, rather than fact, and these are usually operated on. For example, if a patient has a blocked carotid artery on one side and no symptoms, but the other side is narrowed, perhaps to 80%, you may be inclined to treat that side with surgery. This is based on no data, but but seems sensible if one side is blocked. Papers have been published which show that certain categories of asymptomatic patients may be at higher risk. One category is the one I just mentioned. There are also methods of determining whether the plaque is brittle and liable to break off by looking at its composition. One way is with duplex scanning and another is by using transcranial Doppler (TCD), where a special Doppler device is placed over the middle cerebral artery on the patient’s head and can show if tiny bits of clot (emboli) come and go into the brain.

Ultimately, what we should do with asymptomatic patients is test them to see who is the most likely to be at risk of stroke and then only intervene on those people. Right now, Congress has not yet agreed to fund carotid stenting through Medicare. That’s key. What Congress should do is only fund stenting or surgery for asymptomatic cases that fit certain criteria for treatment, and to determine those criteria, we need research to find out who those asymptomatic patients are.

Dr. Bell can be contacted at


  1. McPhee JT, Schanzer A, Messina LM, Eslami MH. Carotid artery stenting has increased rates of postprocedure stroke, death, and resource utilization than does carotid endarterectomy in the United States, 2005. J Vasc Surg 2008 Dec;48(6):1442-1450, 1450.e1.
  2. Brott TG, Hobson RW 2nd, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med 2010 Jul 1;363(1):11-23.

Early Use of the Vortex Angiovac Suction Cannula in the Treatment of Iliac and IVC Thrombosis, and Massive Pulmonary Emboli

Cath Lab Digest talks with Christopher J. Kwolek, MD, of the Harvard Medical School Division of Vascular and Endovascular Surgery and the Massachusetts General Hospital Heart and Vascular Center in Boston, Massachusetts.

Can you tell us about the Angiovac device?

The Angiovac is a large-bore cannula system designed to remove what is called “undesirable intravascular material,” or UIM. This is its official indication from the FDA. While the Angiovac works well for thrombus or clot, it has also been used to remove other material, such as a tumor and/or foreign material inside the vascular system. The concept was developed several years ago by a cardiac surgeon, Dr. Lishan Aklog. While working with Dr. Samuel Goldhaber, one of the world’s experts in pulmonary emboli and treatment of pulmonary venous hypertension, at the Brigham and Women’s Hospital, Dr. Aklog became one of Dr. Goldhaber’s surgical collaborators for the treatment of patients with both acute and chronic emboli. For these patients, there was no device large enough to remove large volumes of thrombus or intravascular material. Of course, there have been new developments with lytics as well as smaller catheters available to try and remove clot. However, Dr. Aklog persisted in thinking that there had to be a better way, and came up with the Angiovac after performing several open procedures. As a cardiac surgeon, he already had experience with partial heart bypass and bypass pumps. Essentially, the Angiovac is a modified cannula that goes into the vein and is is connected to a centrifugal pump with a small trap or reservoir. The device uses the same type of mechanism as a partial left heart bypass, where the pump creates a negative flow or vortex. It is not suction; the idea is not to grab clot like a vacuum cleaner, but rather to create a vortex or negative flow so that there is flow coming back out of the vein. Thrombus or foreign material is drawn back in and goes through a pump. The thrombus or foreign matter becomes trapped in the filter, and then the blood is immediately returned to the patient through another venous cannula. This allows the procedure to be performed with  good hemodynamic stability. Heparin is required, but the Angiovac does not require going on complete bypass, which is what is done for an open pulmonary embolectomy, where the pulmonary artery is opened through a median sternotomy. The Angiovac can be placed through a small incision, either in the neck or the groin. It can also be placed percutaneously through a sheath in the neck or the groin.

I first heard about the device a year ago at a cardiothoracic surgical conference. At that point, physicians had predominantly removed pulmonary emboli, clots in the right atrium, and tumor mass material. They had also performed a few cases for inferior vena cava (IVC) thrombus. It became immediately apparent to me that the Angiovac would be very helpful for the vascular surgery and interventional community to use as a method for the removal of thrombus or other material anywhere in the venous system, not necessarily just in the heart or pulmonary arteries, but also in the iliac, femoral veins  and the IVC.

The Angiovac device is 22 French. It tracks over a 0.035” guide wire, and has a funnel-shaped tip, allowing it to open up and conform to the vessel wall. When the negative flow is started, this design helps keeps it open, allowing the flow and the vortex to bring in any foreign material, and preventing the vessel from collapsing.

We recently began using the Angiovac to treat patients with IVC thrombosis and iliac venous thrombosis. Within the last year, we had seven patients with phlegmasia and massive iliocaval thrombosis. These patients have so much clot in the venous system that it impedes flow out of the leg. That, in turn, impedes blood flow into the leg, and patients become profoundly ischemic and develop compartment syndrome. Historically, mortality rates range from 30-50%, and amputation rates are at about 40%. In these acute patients, time is of the essence, meaning we often do not have the time to try a more traditional approach such as tPA. A few patients also had contraindications to using tPA or catheter-directed thrombolysis; either it didn’t work or they had other, recent major bleeding problems where it couldn’t be safely used. In these seven patients, we were able to both remove the thrombus from the lower part of the leg through a small incision and use the Angiovac to remove thrombus more proximally in the iliocaval system We reestablished bloodflow, and then evaluated the vessels with  intravascular ultrasound and fluoroscopy. If we discovered any narrowing or anatomic problem, we then corrected it with balloons and stents. Preliminarily, at 30 days and 60 days, all of these patients have remained widely patent. CT scans show no remaining thrombus. We are very pleased, since traditionally we have not had any great options for these patients.

At present, Angiovac is two years after first-in-man, with over 106 cases performed. There was one mortality very early on in a patient with a pulmonary embolism. Operators had problems with the cannula and there was a tear in the atrium. There is certainly some risk working in this area, but these are very sick patients. About 20% of cases to date have been for treatment of pulmonary emboli, which was the initial thought behind the development of the Angiovac. Another 25% were used for removal of clots and other masses in the atrium. Over 50% of cases have been for treatment of massive thrombus in the IVC and in the iliac veins.

Traditionally, many patients with pulmonary emboli have been treated with heparin, and more recently with one of the new catheter-directed clot-busting medications. But these approaches take a while to work. In some of these patients who are hemodynamically unstable, there is not a lot of time to get the thrombus out of the pulmonary artery. While I have not personally performed any pulmonary embolism cases, they have been performed by my colleagues at the Massachusetts General Hospital (MGH), including Dr. Ken Rosenfeld, an interventional cardiologist, along with Dr. Gus Vlahakes,  one of our cardiac surgeons. MGH has a multidisciplinary team, including CT surgery, cardiology, and vascular surgery, involved with using the Angiovac and in taking care of these patients. Pulmonary emboli patients often present acutely and need to have something done fairly urgently. The options are to try to perform catheter-directed thrombolysis or perform an open emergency surgical procedure, which can be challenging in these critically ill patients.

Many of the patients with IVC and lower-extremity thrombosis have such a huge burden of thrombus that it would be extremely difficult to try and remove  such a large  clot burden in a short time frame. We also know that as we use the other smaller mechanical thrombectomy devices, then there can be limitations in terms of the amount of use. The smaller catheters tend to hemolyze or chew up the red cells to some extent, and that can cause problems with renal insufficiency.

The Angiovac is large enough to remove large volumes of thrombus very quickly, and at the same time, while the blood goes through a pump, it doesn’t lyse, or macerate the red blood cells significantly, meaning we can simply re-infuse the blood directly back into the patient after it has been filtered.

Dr. Kwolek can be contacted at

Disclosure: Dr. Kwolek reports he is on the Vortex Medical advisory board as a consultant. He does not have any proprietary or patent interest in the company.