3 – Cardiovascular diseases

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Cardiovascular diseases and prevention

Metabolic syndrome-managing the patient at cardiometabolic risk
Moderators: E Diamantopoulos (Greece), S Novo (Italy)
Participants: E Diamantopoulos (Greece), A Nicolaides (Cyprus), A Trichopoulou (Greece), S Novo (Italy), U Pagotto (Italy)

E Diamantopoulos presented an introduction to various definitions of metabolic syndrome. Despite sometimes confusing criteria, every definition has the same core components: abdominal obesity, impaired fasting glucose tolerance, dyslipidemia and arterial hypertension. The prevalence of metabolic syndrome is almost the same in all countries: around 20-25%. From the pathophysiological point of view, visceral fat accumulation and consequent insulin resistance seems to have pivotal roles. It was also highlighted that, according to the studies, abdominal obesity and insulin resistance increase the risk of CV morbidity and mortality. The metabolic syndrome is also a predictor of coronary heart disease, of type 2 diabetes mellitus, and increases CV and overall mortality. Finally, the speaker pointed out that metabolic syndrome is a cluster of cardio-metabolic risk factors with a central role for abdominal obesity, needing appropriate non-pharmacological and pharmacological management strategies. Metabolic syndrome should be used for the identification of individuals at increased risk for future CV disease and can complement Framingham scoring.

A Nicolaides presenting the Cyprus Study demonstrated that plaque morphology assessed by high-resolution ultrasound is a better predictor of CV risk than intimamedia thickness. In the Cyprus Study it was found that in the presence of metabolic syndrome there was a higher prevalence of CV disease. Also in the presence of the metabolic syndrome, intima-media thickness (IMT), total (two common carotid and two common femoral arteries assessed) plaque thickness (TPT), the black (echo lucent) plaque burden (according to the Widder 1-5 classification) and the rate of plaque growth were higher. A Nicolaides concluded that unstable plaque develops earlier in the presence of the metabolic syndrome. Finally, he stressed that future interventional studies in individuals with metabolic syndrome should measure TPT and black plaque burden in addition to IMT.

A Trichopoulou from Athens talked about the challenge of lifestyle and dietary intervention in cardiometabolic care. According to several well-designed studies, adhesion to the Mediterranean diet with its 9 components significantly reduced not only cardiovascular mortality, but also cancer mortality and overall mortality. The result was the same in USA as in Mediterranean and European countries. This dietary approach reduced the incidence of type 2 diabetes mellitus, was not associated with obesity and lowered the systolic and diastolic blood pressure. Mediterranean diet reduces inflammation, has antiatherogenic properties, and is inversely correlated with metabolic syndrome and the associated cardiovascular risk.

S Novo from Italy presented multifactorial drug treatment modalities in patients with metabolic syndrome. In his introduction he highlighted the role of early diagnosis. Individuals with metabolic syndrome commonly manifest insulin resistance, prothrombotic and pro-inflammatory state, and endothelial dysfunction. All guidelines recommend that first-line therapy should be based on lifestyle modification, consisting of the Mediterranean diet and moderate physical activity. When this approach is inadequate, it is recommended that drug treatment is used to reduce the overall impact on cardiovascular disease and type 2 diabetes mellitus risk. Metformin, thiazolidinediones, and acarbose are antihyperglycemic drugs, but they also reduce the incidence of type 2 diabetes mellitus and insulin resistance, and decrease or stabilize visceral adipose tissue mass. Also, angiotensin II receptor blockers and angiotensin-converting enzyme inhibitors reduce the incidence of type 2 diabetes mellitus and insulin resistance. Telmisartan has been considered particularly useful in the treatment of hypertension associated with cardiometabolic risk factors due to its PPR-gamma receptor agonism and improvement of insulin sensitivity. Beta-blockers and thiazide diuretics should be avoided because they can reduce insulin sensitivity, impair lipid profile, and increase type 2 diabetes mellitus incidence. This is not the case of carvedilol, indapamide, or spironolactone. Orlistat and sibutramine are used with a reduced calorie diet plus exercise program to help people who want to lose weight, but the former causes gastrointestinal malabsorbtion syndrome, and the latter may cause hypertension. Statins, fibrates and omega-3 fatty acids normalize dyslipidemia. Statins have additional therapeutic benefits in reducing inflammatory activity. Fibrates effectively reduce triglycerides and increase HDL, and have also shown some anti-inflammatory activity. Lowdose aspirin is also recommended for patients with a prothrombotic state. Rimonabant, the first cannabinoid receptor (CBI) antagonist studied in obesity, modulates cardiometabolic risk factors, through its impact on visceral fat and through direct pathways not related to weight loss. In this issue the lecture of U Pagotto was particularly useful in reminding everyone about the physiologic and pathophysiologic role of cannabinoid receptors, named CB1 and CB2. The ability of the endocannabinoid system to control appetite, food intake, and energy balance has recently received great attention. This system modulates rewarding properties of food by acting at specific mesolimbic areas in the brain. Interestingly, the endocannabinoid system was recently shown to control several metabolic functions by acting on peripheral tissues, such as adipocytes, hepatocytes, the gastrointestinal tract, skeletal muscle, and the pancreas. Visceral obesity seems to involve overactivation of the endocannabinoid system, so drugs that interfere with this overactivation by blocking CB1 receptors are considered valuable candidates for the treatment of obesity and related cardiometabolic risk factors. Recent pharmacological studies with rimonabant in obese patients with and without comorbidities are promising. Rimonabant should not be used, however, in the presence of serious uncontrolled psychiatric problems, because it can cause depression, irritability, and anxiety .

Primary prevention of cardiovascular diseases
Moderators: D Mikhailidis (UK), A Jawien (Poland)
Participants: DB Panagiotakos (Greece), E Liberopoulos (Greece), V Athyros (Greece), G Kolovou (Greece)

The first lecture of this session by DB Panagiotakos dealt with the role of smoking, alcohol intake, and Mediterranean diet in cardiovascular disease risk. As is well known, active smoking is one of the most important risk factors for cardiovascular and peripheral arterial disease. Moreover, exposure of nonsmokers to environmental tobacco smoke has been associated with a substantial increase in the risk of coronary heart disease and perhaps of peripheral atherosclerosis also. According to the lecturer the effect of passive smoking (occasional and regular) is still controversial because of difficulties in objective measurement and quantification of tobacco-smoke exposure. Some studies use self-reported questionnaires, others biochemical indices (C-reactive protein, white blood count, homocysteine level, LDL cholesterol, etc.) in order to establish exposure and quantify the degree of passive smoking. Nevertheless, a meta-analysis of 18 cohort and case-control studies conducted by Jiang provides clear evidence of an increase in the overall relative risk (24-26%) of cardiovascular mortality and morbidity associated with passive smoking. The same results were also found in the ATTICA and GREECS studies. The latter shows that passive smokers have 61% higher risk of recurrent CV event or death after acute myocardial infarction compared with the non-exposed population. In the “Seven Country Study” conducted in 1970s, 10-year follow-up assessing the relationship between dietary habits and cardiovascular events of seven countries showed zero mortality in the Corfu group. The main explanation for this is the Mediterranean diet (diet rich in fruits, vegetables, whole grains, olive oil, fish, nuts, small-moderate amount of alcohol) and the supposed effect of the Mediterranean “way of life”. Since this first study, a large number of trials have shown that the Mediterranean diet significantly reduces (8-32%) CV morbidity and mortality. Dietary factors exert their influence largely through their effects on body weight, blood pressure, plasma lipids, blood coagulation, and inflammatory markers. The author concluded that smoking and passive smoking account for a large proportion of cardiovascular risk and that the Mediterranean diet seems to be an effective means of primary and secondary prevention of cardiovascular disease which can be easily applied in other cultures also.

In the second lecture of this round table E Liberopoulos talked about a twoway strategy of preventing type 2 diabetes mellitus, today’s dangerous with an attendant huge increase in CV complications. The first modality of prevention is lifestyle intervention. Studies conducted in this field, especially the Diabetes Prevention Program (DPP) and the Finnish Diabetes Prevention Study (FDPS), showed that lifestyle changes (including weight loss of about 4 kg, Mediterranean diet, physical activity) significantly reduced the incidence of type 2 diabetes mellitus in prediabetic patients. This effect seems to be evident on a long-term basis also. The major problem is that radical lifestyle modifications are difficult to implement in everyday clinical practice, especially in the long term. Therefore preventive pharmacological interventional modalities were also discussed. The results of trials using metformin, orlistat, acarbose, glitazones, statins, or fibrates are either encouraging or require more extensive evaluation. In addition, studies with antihypertensive drugs (mainly ACE inhibitors and angiotensin II receptor antagonists) showed that these drugs could also reduce progression to type 2 diabetes mellitus in high-risk individuals. Attention is needed in the selection of antihypertensive drugs since beta-blockers and thiazide diuretics increase the risk of new-onset type 2 diabetes mellitus, which during hypertension treatment is very dangerous with an increased risk of stroke. Finally, the speaker stressed the importance of intensive lifestyle interventions for type 2 diabetes mellitus prevention in individuals at high risk. These are, unfortunately, difficult to achieve and sustain in daily practice. Among drugs metformin may be of value especially in younger obese patients with prediabetes, and the glitazones are the most promising pharmacologic agents.

V Athyros used compelling scientific evidence to show that the presence of metabolic syndrome as a clinical entity with cumulative risk of CV events and CV death is a fact and not a fiction. The controversy of this issue is mainly due to the several confusing definitions. Despite the fact that abdominal obesity, glucose metabolism disturbances, hypertension, and dyslipidemia are the main components of this syndrome, there are significant differences in quantifying these variables in different definitions. The WHO definition of 1999 was abandoned because of lack in daily practice applicability. The ATP III\NCEP definition of 2001 has been widely used (3 or more components are present, including abdominal obesity >102 cm men and, >88 cm women, triglycerides>150 mg/dL, HDL<40 mg/dL men, <50 women, blood pressure <130/85 mm Hg and fasting glucose >110 mg/dL), but in 2005 the IDF-EASD-EAS reduced the limit of abdominal obesity to >94 cm in men and >80 cm in women and also the limit of fasting glucose level>100 mg/dL (abdominal obesity plus 2 or more components). In the same year the AHA/NLHBI definition returned to ATP III abdominal obesity values, but the fasting glucose level remained above 100 mg/dL. The prevalence of metabolic syndrome is almost the same in USA and in Europe: about 1 in 4 people in the general population. Of course, the prevalence in different studies depends on the definition used, as stressed by the speaker. As the metabolic syndrome increases by 3.55 the risk of CV mortality, it needs a multifactorial approach, including lifestyle modification and drug treatment as well.

In her exciting lecture, G Kolovou told us about the well known and scientifically proved CV risk of elevated Lp(a), plasma fasting triglycerides and low HDL levels. However, there is less evidence regarding whether or not the proatherogenic role of high postprandial level of plasma triglycerides is an independent risk factor for premature CV disease or not. As postprandial hypertriglyceridemia is associated with fasting lipoproteins, gender, age, body mass index, glucose metabolism, blood pressure, genetic and lifestyle factors, it is not yet entirely clear whether postprandial hyperlipemia is an independent risk factor. The magnitude of the postprandial response appears to play a role in the etiology and progression of CHD. The mechanisms involved in postprandial elevated triglyceride levels are not fully understood, but could involve the malfunction of LP-lipase due to increased cholesterol synthesis in the liver after a reduction of cholesterol absorption from the intestine. The postprandial peak is after 3-4 hours and values above 220 mg/dL seem to be pathological. Many studies show that in the hypertriglyceridemic state the secreted VLDL particles are large and result in formation of small dense LDL particles, which are particularly atherogenic. The main limitation in assessing postprandial lipemia is the lack of an established standard method. Such a method should be easily and widely applicable and reproducible as well.

Statins: a role in protection against cardiac and cerebrovascular events

Moderators: F Fedele (Italy), S Novo (Italy)

Target of LDL-Cholesterol in High-Risk Patients and in Secondary Prevention according to Guidelines
S Novo (Italy)

It is crucial to define a high6risk patient. Individuals with established cardiovascular (CV) disease who have both diabetes mellitus and metabolic syndrome have the highest risk.

There are several disease entities that confer a CV risk similar to that of coronary artery disease (CAD). These CAD “equivalents” are periphery artery disease (PAD), abdominal aortic aneurysm, symptomatic carotid disease, asymptomatic carotid disease, diabetes mellitus, metabolic syndrome, and chronic renal insufficiency. Patients with a very high risk are either those with established CV disease and multiple risk factors or those with established CV disease and only several but poorly controlled risk factors.

Trials concerning primary as well as secondary prevention of CV events have proved the importance of lowering total and especially LDL-cholesterol. The greater the reduction in LDL-cholesterol, the greater the observed reduction in CV events. Statins have shown their efficacy in the reduction of all events and this effect was independent not only of age, gender, hypertension, and diabetes mellitus, but also of the baseline levels of total cholesterol, LDL-cholesterol, HDLcholesterol, and triglycerides. Persistent therapy leads to progressive risk reduction so adherence to the treatment is the key issue. According to the risk profile of an individual patient, the target LDL-cholesterol for the high-risk population should be 100mg/dL or better 70mg/dL. The concept “the lower the better” is valid.

Prevention of Coronary Events
G Novo (Italy)

Many trials have proved that statins effectively prevent major coronary events. The benefit of statin therapy is seen irrespective of baseline LDL-levels (Heart Protection Study). Standard statin doses are able to reduce LDL-cholesterol levels by about 30%. Higher than standard doses decrease LDL-cholesterol levels more, and this is also associated with more significant reduction of CV events (PROVEIT study). Higher doses of statins are well tolerated and the changes in liver and muscle enzymes are not significant. Based on the study results, statin therapy can also be recommended in patients with acute coronary syndrome.

The reduction in coronary events seen with statins is not explained only by lowering of total and LDL-cholesterol, but also by reduction in atherosclerosis progression (decrease in atheroma volume and of percentage of obstruction proved in REVERSAL study) and by stabilization of coronary plaque (anti-inflammatory effect – decreasing C-reactive protein proved in REVERSAL study).

Statins are the cornerstone treatment in coronary prevention. There is no LDLcholesterol level beyond which there are no additional benefits from statin therapy.

Prevention of Cerebrovascular Events
E Diamantopoulos (Greece)

For many years cholesterol was not considered a risk factor for stroke. However, the association was later clearly proved for ischemic stroke. The effect of LDLcholesterol reduction on reduction in stroke incidence has been proved as well (a meta-analysis of statin trials, published in 2005, showed a 21% reduction in stroke without any increase in hemorrhagic stroke). The effect of statins is pleiotropic and comprises not only LDL-cholesterol reduction but also atheromatous plaque stabilization, anti-inflammatory properties, improving endothelial functions, decreasing oxidative stress, enhancing angiogenesis, and reducing ischemic/reperfusion injury. Aggressive statin treatment (atorvastatin 80 mg daily in SPARCLE study) demonstrated a higher efficacy in reducing the incidence of fatal and nonfatal strokes as well as major coronary events and the benefit was significant despite a very slight increase in the incidence of hemorrhagic stroke, compared with the placebo group. The recent AHA guidelines have been updated with a recommendation for statin treatment for all patients with ischemic stroke or transient ischemic attack, even without known coronary artery disease.

Prevention of Events in Patients with Peripheral Arterial Disease
A Balbarini (Italy)

Atherosclerosis is a generalized disease. The presence of peripheral arterial disease (PAD) is a powerful predictor of coronary artery disease (CAD), and both increase with age and have similar risk factors. A 15% prevalence of PAD was found in asymptomatic individuals over 70 years of age. However, asymptomatic persons with lower limb arterial disease have the same risk as patients with intermittent claudication.

The prognosis of patients with PAD is poor; 55% of them die from CAD.

Ankle brachial index is an important predictor of CV events and death. There is a strong correlation between the severity of PAD and survival.

Prevention of CV events in patients with PAD should comprise smoking cessation, lifestyle changes, physical activity, weight loss, lipid lowering, glycemic control, and long-term antiplatelet therapy. Like patients with all clinical forms of atherosclerosis, PAD patients also benefit from statin therapy. The target LDLcholesterol level should be at least 100 mg/dL (2.59 mmol/L).

In PAD patients, it is strongly recommended to assess the global CV risk (ie, to examine the carotid and coronary arteries as well) and to reduce aggressively all modifiable risk factors.

Past, present, and future of antiplatelet therapy for angiologic disorders

Moderators: G Rao (USA), A Halaris (USA)
Participants: D Clement (Belgium), J Fareed (USA), G Rao (USA), A Halaris (USA)

A survey of newer antiplatelet agents
J. Fareed (USA)

Aspirin, clopidogrel, and GP IIb/IIIa inhibitors are the most commonly used antiplatelet drugs. Aspirin activity causes irreversible inhibition of COX-I and is proven to prevent vascular death and to reduce the incidence of nonfatal vascular events. However, the optimal dose and aspirin resistance are still unclear. Clopidogrel, is an active metabolite of thienopyridines and causes irreversible alteration of the platelet P2Y12 receptor and selective inhibition of ADP-induced platelet aggregation. Clopidogrel is commonly used in patients who undergoing percutaneous coronary intervention. Clopidogrel activity has an inter-individual variability and the optimal timing and size of the dose to achieve an acute antiplatelet effect are not yet well established.

Among novel thienopyridines, prasugrel seems to have more rapid onset of action and more platelet inhibition than clopidogrel. Cangrelor and AZ06140 do not require metabolic activation and their action has a rapid onset and offset.

GPIIb/IIIa inhibitors include monoclonal antibodies against the receptor and RGD mimetics and are commonly used to prevent ischemic complications with percutaneous coronary intervention. Their risk-benefit ratio in patients with acute coronary syndrome not undergoing early revascularization is less certain. Efforts to develop oral GPIIb/IIIa antagonists have been unsuccessful.

Proteases as SCH-530348 and E 5555, which block thrombin-mediated activation of platelets, are in various phases of clinical trials. An active thromboxane receptor inhibitor (S 18886) is undergoing phase II evaluation for secondary prevention of stroke.

Despite these developments it should be emphasized that most of the newer antiplatelet drugs are administered with aspirin with which they show variable degrees of interaction.

Aspirin resistance: need for a point-of-care assay.
G. Rao (USA)

The author highlighted the efficacy of aspirin in preventing heart attacks and stroke, but emphasized the fact that several studies have shown that a significant percentage of patients (from 4% to 50%) are nonresponders to the action of this drug. Furthermore, monitoring of aspirin sensitivity, using arachidonic acidinduced platelet aggregation, have not identified a specific diagnostic method.

The author proposed a new reliable instrument to measure coagulation (platelet reactivity POC instrument -PRT) to test aspirin sensitivity alone without agonist. This instrument has a microcapillary with a coil of stainless steel inside and this coil is the site of clot formation. In his personal experience using 325 mg of aspirin in normal subjects and measuring clotting time, aspirin inhibited platelet activation in 30% of subjects. This percentage was not very high and depended on clotting time increase. In conclusion, there is a need to develop a point-of-care assay to monitoring global hemostasis.

Serotonin reuptake inhibitors as antiplatelet drugs: what is the evidence?
A Halaris (USA)

Selective serotonin reuptake inhibitor (SSRI) antidepressants exert their effect by inhibiting the reuptake of serotonin by the presynaptic nerve terminals. They have the same effect on platelets. As demonstrated in several studies, SSRIs reduce the incidence of recurrent MI in post-MI patients who develop depression.

The possible mechanisms of the antithrombotic action of SSRIs are: inhibition of 5-HT reuptake by platelets, formation of weaker platelet aggregates, decreased release of antiplasmins, promotion of fibrinolysis. Platelet inhibition by SSRIs may represent an independent avenue of pharmacological effects responsible for the ultimate success of these drugs in patients, not only with depression, but with coronary artery disease and ischemic stroke. Future strategies in patients after vascular events must consider safe approaches to protect platelets from extensive activation.

Cardiovascular diseases and aneurysms

Selection criteria of endovascular aortic aneurysm repair
Lecture by R Greenhalgh

The endovascular aortic aneurysm repair (EVAR) trial 1 showed that although there was an early operative mortality benefit with endovascular repair, by 4 years there was no difference in survival between patients receiving open or endovascular abdominal aortic aneurysm repair. The EVAR 2 trial remains regrettably unique and randomized patients considered unfit for open repair to either endovascular repair or no intervention. In this trial of unfit patients, the 30-day mortality in the group randomized to endovascular repair was 9% and by 4 years there was no difference in overall survival between those randomized to endovascular repair or no intervention. Moreover, by the 4-year time point about two-thirds of the patients had died. The results of the EVAR trial were the subject of a commentary suggesting that the younger, fitter patient, with a large abdominal aortic aneurysm, would still benefit from having open repair of the aneurysm. This hypothesis was tested using data from EVAR trial 1. There is some evidence to suggest that the fittest patients may benefit the most under a policy of EVAR rather than open repair and this is contrary to the above hypothesis. The publications have highlighted the importance of fitness in patient selection for aneurysm intervention and optimization of patients in terms of fitness and medical therapy should be prioritized as well as consideration of their aneurysm size.

From the start, the EVAR trial participants realized that the fitness of the patient was a key issue with respect to endovascular aneurysm repair. However, it was recognized that endovascular aneurysm repair could be performed in two separate populations of patients and the EVAR scientists recommended keeping these populations separate. The first indication was in patients who were fit for open repair and these patients were recruited to EVAR trial 2. The EVAR trialists tried very hard to get the anesthetists to agree to a precise protocol for entry into EVAR 1 or EVAR 2, but the anesthetists, along with the 41 trial centers, had their own criteria in selecting for endovascular or open repair. Consequently, we made suggestions in terms of renal function, respiratory function, and cardiac function which were pointers to encourage the anesthetists in the way in which they categorized the patients. This was adopted very well and in no small part, contributed to the very low operative mortality achieved across the board in 41 centers in EVAR 1, patients who were otherwise fit for open repair, a remarkable EVAR mortality of 1.7% at 30 days.

Unanswered issues regarding endovascular aortic aneurysm repair (EVAR)

Moderators: R Greenhalgh (UK), D Papadimitriou (Greece)
Participants: P Glovicszki (USA), P Cao (Italy), R Greenhalgh (UK), D Kiskinis (Greece), JB Ricco (France), G Deriu (Italy)

Repair of Abdominal Aortic and Iliac Artery Aneurysms: The Changing Concept of Management at the Mayo Clinic
P Gloviczki (USA)

Since the introduction of endovascular aortic aneurysm repair (EVAR) in the early 1990s, robust data have accumulated from thousands of patients who underwent EVAR with a low early morbidity and mortality. However, the durability and indications for EVAR are questioned by the need for continuous surveillance using expensive imaging studies and the nephrotoxicity of contrast agents, the high cost of the device, complications, late ruptures, and the lack of evidence of improved late mortality and a better quality of life vs. open repair. The risk of late endoleaks at 5 years in a recent report by Greenberg et al was 12% to 15% , representing the primary indication for secondary interventions which occur in 20% of standard patients and 25% of high-risk patients through 5 years.

The proportion of EVAR vs open repair (OR) in the last 5 years has been constant at 47% (512/572).

Results of open repair of abdominal aortic aneurysm (AAA) have continuously improved during the past 5 decades. This can be attributed to progress in evaluation and imaging modalities as well as improved selection of patient at high risk for EVAR. Early mortality in a series of 2452 AAA repairs reported in 1993 at the Mayo Clinic was 2.9%. West and Duncan recently reported a 2.5% 30-day mortality of 247 pararenal aneurysms in patients operated between 1993 and 2003. Knott and Kalra analyzed results of open repair of juxtarenal AAAs and found a 30-day mortality of 0.8% (1/126), with 5 cases of temporary dialysis, but no permanent dialysis, and the same low mortality and complication rate as EVAR. Both elective and emergency open repairs have been durable. At 5 years after open surgery Hallett found graft-related complications in 7% of the patients operated on at the Mayo Clinic.

EVAR has emerged during the last decade as an excellent alternative, but less risky treatment for AAAs. Recently published 5-year results of the FDA approved endografts in the United States showed a decreased early mortality and morbidity compared with open surgical repair with a low rate of late complications. The EVAR 1 trial failed to confirm long-term survival advantage of patients who underwent EVAR. In addition, EVAR was more expensive, and associated with a greater number of complications and reinterventions. The issue, however, remains unanswered since in the EVAR 1 study there was a 3% better aneurysm-related survival. The EVAR 2 study failed to show any benefit of EVAR in those high-risk patients who were unfit for surgery. The US Veterans Administration Hospital data support offering EVAR to high-risk patients and this has been our observation as well: high-risk patients benefit from the low early complications of EVAR. In 555 consecutive patients who underwent elective EVAR for aortic or iliac aneurysm at the Mayo Clinic during the last decade, early mortality was 1.26% (7/555). In open surgery mortality was 7.4% for symptomatic, non-ruptured aneurysms (2/27) and was 11.8% for ruptured aneurysms (2/17). In a comparison of the results in 355 consecutive Mayo Clinic patients with infrarenal AAA (261 had OR, and 94 had EVAR), there was no difference in 30-day mortality (1.1%, 3/261 for OR and 0% for EVAR). There were more high-risk patients in the EVAR group, but cardiac and pulmonary complications were less frequent after EVAR than OR (11% vs. 22%, P=0.02, and 3% vs. 16% , P=0.0001, respectively). Graft-related complications were less frequent after OR (4% vs. 13%, P=0.002). Indications for AAA repair.

Based on data of prospective, randomized, multicenter studies, surgical treatment is recommended for males who harbor an abdominal aortic aneurysm of >5.0 cm. The United States Preventive Services Task Force also found evidence that surgical repair of AAAs 5.5 cm or larger in men aged 65 to 75 years who have ever smoked leads to decreased AAA-specific mortality. At the Mayo Clinic, open repair remains an excellent treatment of AAAs and open surgery (transabdominal, retroperitoneal, or mini-laparotomy) is offered as the first option to many highrisk patients less than 70 years of age. At the Mayo Clinic, EVAR are offered to most high-risk patients with suitable anatomy for endograft repair and to selected patients with symptomatic and ruptured AAAs. With introduction of fenestrated and branched graft technology and with the judicious use of abdominal aortic debranching and retrograde visceral artery revascularization, an increasing number of patients with juxtarenal and paravisceral abdominal aortic aneurysms will undergo endovascular repair in the future.

Gloviczki et al in a recent review of 715 common iliac artery aneurysm (CIAA) repairs, performed in 438 patients between 1986 and 2005, found 396 patients (9%) had elective repair and 42 (10%) had emergency repair. OR was performed in 394 patients (90%). Thirty -day mortality was not different among the groups. Complications were more frequent and hospitalization was longer after OR than EVAR (P<0.05). Freedom from reintervention was similar after OR and EVAR (83% vs. 69%, P=NS), as were survival rates (76% vs. 77%, P=NS).
Gloviczki et al currently recommend elective repair for asymptomatic patients with CIAA >3.5 cm. Although buttock claudication after EVAR remains a concern, results at 3 years support EVAR as first-line treatment in most anatomically suitable patients who require repair of a CIAA. Patients with compressive symptoms or those with iliocaval fistula should be preferentially treated with OR.

Is endovascular aortic aneurysm repair going to become the gold standard for ruptured abdominal aortic aneurysms?
D. Kiskinis (Greece)

The following topics were discussed regarding endovascular aortic aneurysm repair (EVAR) and ruptured abdominal aortic aneurysms (AAAs):

  • Preoperative imaging: CT is necessary for diagnosis of rupture, and other organ pathology, eg, aortocaval fistula, morphology of aneurysm and iliac arteries. Other options for graft sizing are: intravascular ultrasound (not available in every department) and intra-operative angiography and use of a marker catheter.
  • Anesthetic management Hypotensive hemostasis: blood pressure <100 mm Hg is sufficient for vital organ perfusion and decreases the tearing force on the aortic wall. With local anesthesia, which is feasible, hemodynamic instability during induction of general anesthesia is avoided.
  • ype of endograft (aorto, uni-iliac or bifurcated)
  • Postoperative management (compartment syndrome)

The compartment syndrome increases mortality 5-fold. It is monitored through urinary bladder pressure, which is mandatory in every patient after EVAR for ruptured AAA. Decompression laparotomy is performed when bladder pressure is greater than 25 mm Hg

  • Evidence from the literature There are no completed randomized controlled trials comparing EVAR with conventional open surgical repair for the treatment of rAAA. There are only case reports.


There is no high-quality evidence to support the use of EVAR in the treatment of RAAA. EVAR is feasible in selected cases. Repair in selected patients may be associated with a trend to reductions in blood loss, in duration of intensive care treatment, and in mortality.
Follow-up strategies after endovascular aortic aneurysm repair

JB Ricco (France)

Although endovascular aortic aneurysm repair (EVAR) offers immediate advantages over open aneurysm repair, it carries the need for lifelong surveillance to monitor aneurysm size and/or potential complications including endoleak, change in aneurysm size, graft migration, structural failure, and limb outflow impairment. Current modalities for EVAR surveillance include computed tomography (CT) scan and color-flow duplex ultrasound scanning (US). The most important downside of repetitive CT imaging includes renal dysfunction due to intravenous contrast and problems related to radiation exposure. Recent reports have suggested that US is as effective as and even better than CT. Dr Ricco compared both CT and US as modalities of surveillance for endoleak detection and change in aneurysm size after EVAR. He found a small size difference (<5 mm) in abdominal aortic aneurysm (AAA) measurement by CT and US. However, in his practice and in many other studies, US has a low sensitivity and a low predictive value limiting its use. Technical factors can be very important in the diagnostic value of US and they could not duplicate the excellent results of other centers. Recently, noninvasive sac pressure monitoring using implantable sensors has been shown to have the potential to provide a reliable alternative for post-EVAR surveillance.

Finally, recent studies have shown that follow-up surveillance after EVAR is less intense in practice environments outside clinical trials and that these patients with incomplete follow-up have higher fatal complication rates than patients with regular follow-up.

These data expose a potential under-appreciated limitation of EVAR which is dependent on compliance with a monitoring program. Duplex ultrasound “only” surveillance post-EVAR is safe in patients with stable or shrinking AAA after one year of CT follow-up. It seems possible that half of the patients treated with EVAR will be eligible at 3 years for this follow-up modality. This policy should result in cost savings and should avoid the complications associated with CT.
Unfavorable abdominal aortic aneurysm anatomy. Should we challenge endovascular aortic aneurysm repair or proceed with open repair?

G. Deriu (Italy)

The following recommendations were put forward:

  • abdominal aortic aneurysm (AAA) with unfavorable anatomy in low-risk patents: conventional surgery
  • AAA with unfavorable anatomy in high-risk patients:

a) Iliac problems: EVAR
b) Neck problems: pararenal and suprarenal aneurysms: fenestrated or branched grafts

Neck problems: juxtarenal aneurysms with short (<2 cm) or very short (0.7-1 cm) neck, neck calcifications, thrombotic appositions, pyramidal shape, angulations >60%. EVAR is justified considering secondary results since the neck problem, and iliac artery problems are predictive factors for more frequent complications, either periprocedural or during the follow-up.
Duplex guided balloon angioplasty and stenting for infrainguinal occlusive and aneurysmal disease.

Lecture by E Ascher (USA)

The conventional balloon angioplasty of infrainguinal arteries requires the use of fluoroscopy and injection of contrast material. The author reported his personal experience of 303 balloon angioplasties of the superficial femoral and/or popliteal arteries under duplex guidance in 352 patients to avoid the nephrotoxic effect of contrast and to minimize radiation exposure. Critical ischemia was the indication in 37% of cases and severe claudication in 63%. Infrapopliteal angioplasties in 15% of all cases were performed in order to improve the run-off (as well as) after completion of femoral-popliteal angioplasties. For femoral-popliteal segments, overall technical success was 95% (stenosis 99.6%, occlusions 85%). For infrapopliteal arteries, technical success was achieved in 62 of 65 cases, with an overall success rate of 95% (stenosis 96%, occlusions 91%). The overall 30-day survival rate was 100%. Overall limb salvage rates were 94% and 90% at 6 and 12 months, respectively. Twelve-month patency rates for TASC class A, B, C, and D lesions were 90%, 59%, 52%, and 46%, respectively. Duplex-guided balloon angioplasty and stent placement appears to be a safe and effective technique for the treatment of femoral-popliteal and infrapopliteal arterial occlusive disease.