**4. Coronary dissection and acute closure**

#### **4.1 Angiographic definition**

Dissection is defined as disruption of an arterial wall resulting in splitting and separation of the intimal (or subintimal) layers.


Table 3. Standardized criteria for postprocedural lesion morphology63,64

#### **4.2 Pathogenesis and incidence of coronary dissection**

Intima-media cracks and medial dissection can be developed by balloon injury and if dissection involves the adventitia layer, narrowing of the lumen can occur.65 In NHLBI classification, coronary dissection occurs in 32-41% of total balloon procedures. If the lumen narrows >50% or the length of dissection is >10mm, the risk of abrupt vessel closure increases.

In the modern PCI era, where coronary dissection can be promptly resolved by stent implantation, clinically significant dissection is reported only 1.7%. Residual dissection increases the risk of post procedure MI, emergency CABG, and stent thrombosis and mortality also increases threefold.66

Complications of Coronary Intervention 59

When acute chest pain is recognized, nitroglycerin 100-200mcg should be injected into the coronary artery. If activated clotting time is less than 250 sec, additional heparin should be injected. Before the stent era, a size-matched balloon was inflated for at least 5 min and sometimes perfusion balloon was used. Currently, bailout stenting is considered as the most effective tool for abrupt or threatened coronary closure. Additional balloon inflation can recover blood flow to normal. Because the effect of rescue abciximab has been reported in many clinical trials and since it reduces subacute thrombus formation, administration of

In cases of acute closure due to left main coronary artery injury or coronary artery perforation, installation of intra-aortic balloon counterpulsation is necessary and emergency coronary artery bypass grafting (CABG) should be considered. A long dissection which does

Definitions of stent thrombosis (ST) range from "angiographically proven to "clinically suspected" ST with the inclusion of myocardial infarction involving the target vessel to unexplained death (within 30 days). Although the first definition has a well-defined mechanism limited to selected patients undergoing angiography at the time of ST, there is concern for underestimation of the true incidence of ST. On the other hand, the other

**4.5 Managements** 

Fig. 4. Management algorithm of abrupt closure

glycoprotein IIb/IIIa inhibitors is recommended.

not resolve with stenting also needs CABG.

**2. Coronary artery bypass graft** 

**5. Stent thrombosis** 

**5.1 Definition** 

**1. Initial management** 

#### **4.3 Pathogenesis and incidence of abrupt vessel closure**

Coronary balloon dilatation leads to endothelial denudation, intimal fissuring, and medial penetration and extensive damage causes obstructive dissection or intramural hematoma. When subintimal structures are exposed to the blood, then activation of platelets and thrombin formation occur. Obstructive thrombus can be formed with or without medial dissection.

An autopsy finding of patients who experienced abrupt closure within 30 days after balloon angioplasty revealed that over 50% have intimal/medial dissection flaps with or without thrombi. Cases presenting with pure thrombi without dissection was very rare.

It has been reported that the incidence of abrupt closure due to balloon angioplasty or atherectomy is 2-13.5%. About two thirds of cases of abrupt closure arise inside the catheterization laboratory and the majority occurs within the first 6 h after angioplasty. After routine stent implantation had replaced balloon angioplasty, the incidence of abrupt closure was dramatically decreased. Proper deployment technique and supportive drugs such as dual antiplatelet therapy and heparin also contribute toward the lower incidence.

#### **4.4 Clinical manifestations of abrupt closure**

Before the stent era, the incidence of abrupt closure-related mortality, myocardial infarction, and emergency CABG were 5%, 45%, and 55% respectively. However, since bailout stenting had been introduced, the incidence of emergency CABG owing to abrupt closure was reported to be 0.8%. Long term prognosis of abrupt closure in related to the increase of restenosis, 2-year mortality, myocardial infarction, and CABG. Well known predictors of abrupt closure are in Table 4.

 Unstable angina Diabetes mellitus Female gender Advanced age Intraluminal thrombus ACC/AHA score Lesion length ≥2 luminal diameters or >10 mm Extensive proximal tortuosity Bend point ≥45 degrees Branch point Other stenoses ≥50% in same vessel Multivessel disease Ostial right coronary artery Degenerated saphenous vein grafts "Inoperable" surgical status Collaterals originating from target vessel Preangioplasty stenosis 90-99%

Table 4. Predictor of abrupt closure

#### **4.5 Managements**

58 Coronary Interventions

Coronary balloon dilatation leads to endothelial denudation, intimal fissuring, and medial penetration and extensive damage causes obstructive dissection or intramural hematoma. When subintimal structures are exposed to the blood, then activation of platelets and thrombin formation occur. Obstructive thrombus can be formed with or without medial dissection.

An autopsy finding of patients who experienced abrupt closure within 30 days after balloon angioplasty revealed that over 50% have intimal/medial dissection flaps with or without

It has been reported that the incidence of abrupt closure due to balloon angioplasty or atherectomy is 2-13.5%. About two thirds of cases of abrupt closure arise inside the catheterization laboratory and the majority occurs within the first 6 h after angioplasty. After routine stent implantation had replaced balloon angioplasty, the incidence of abrupt closure was dramatically decreased. Proper deployment technique and supportive drugs such as dual antiplatelet therapy and heparin also contribute toward the lower incidence.

Before the stent era, the incidence of abrupt closure-related mortality, myocardial infarction, and emergency CABG were 5%, 45%, and 55% respectively. However, since bailout stenting had been introduced, the incidence of emergency CABG owing to abrupt closure was reported to be 0.8%. Long term prognosis of abrupt closure in related to the increase of restenosis, 2-year mortality, myocardial infarction, and CABG. Well known predictors of

thrombi. Cases presenting with pure thrombi without dissection was very rare.

**4.3 Pathogenesis and incidence of abrupt vessel closure** 

**4.4 Clinical manifestations of abrupt closure** 

Lesion length ≥2 luminal diameters or >10 mm

abrupt closure are in Table 4.

 Intraluminal thrombus ACC/AHA score

 Extensive proximal tortuosity Bend point ≥45 degrees

Ostial right coronary artery

"Inoperable" surgical status

 Preangioplasty stenosis 90-99% Table 4. Predictor of abrupt closure

Other stenoses ≥50% in same vessel

Degenerated saphenous vein grafts

Collaterals originating from target vessel

 Unstable angina Diabetes mellitus Female gender Advanced age

Branch point

Multivessel disease

Fig. 4. Management algorithm of abrupt closure

#### **1. Initial management**

When acute chest pain is recognized, nitroglycerin 100-200mcg should be injected into the coronary artery. If activated clotting time is less than 250 sec, additional heparin should be injected. Before the stent era, a size-matched balloon was inflated for at least 5 min and sometimes perfusion balloon was used. Currently, bailout stenting is considered as the most effective tool for abrupt or threatened coronary closure. Additional balloon inflation can recover blood flow to normal. Because the effect of rescue abciximab has been reported in many clinical trials and since it reduces subacute thrombus formation, administration of glycoprotein IIb/IIIa inhibitors is recommended.

#### **2. Coronary artery bypass graft**

In cases of acute closure due to left main coronary artery injury or coronary artery perforation, installation of intra-aortic balloon counterpulsation is necessary and emergency coronary artery bypass grafting (CABG) should be considered. A long dissection which does not resolve with stenting also needs CABG.

### **5. Stent thrombosis**

#### **5.1 Definition**

Definitions of stent thrombosis (ST) range from "angiographically proven to "clinically suspected" ST with the inclusion of myocardial infarction involving the target vessel to unexplained death (within 30 days). Although the first definition has a well-defined mechanism limited to selected patients undergoing angiography at the time of ST, there is concern for underestimation of the true incidence of ST. On the other hand, the other

Complications of Coronary Intervention 61

In the bare metal stent (BMS) era, most of ST was early ST and very late ST was extremely rare, although several cases of late ST were reported.73,74 Early ST is encountered with a similar or even somewhat lower frequency after drug-eluting stent (DES) compared with BMS. A metaanalysis of 6 studies comparing BMS with sirolimus-eluting stent (SES) reported that early rates of ST were 0.5% with SES and 0.6% with BMS, respectively (*P*=0.55).68 A pooled analysis of 5 trials comparing BMS with paclitaxel-eluting stent (PES) revealed early ST was 0.5% in PES and 0.6% in BMS, respectively (*P*=0.51).69 Although there had been some reported cases of late ST during the BMS era, this was not a clinical concern for most. According to recent a meta-analysis, no differences existed in the incidence of late ST between DES and BMS (0.2% versus 0.3%, 95% CI: 0.35-2.84; *P*=1.00).70 In another meta-analysis of 9 trials comparing SES and PES, no significant differences were detected for up to 1 year of follow-up (Figure 6).93

Fig. 6. Risk of ST in 9 trials directly comparing SES and PES with follow-up to 1 year.93

Fig. 5. Classification based on the time frame of adverse events

**5.2 Incidence** 

broader definitions include events potentially related to disease progression, life threatening arrhythmias, myocardial infarction of non-culprit lesions, and non-cardiac sudden death and therefore overestimate the true incidence. Accounting for these limitations, an academic research consortium (ARC) proposed a new standardised definition of ST (Table 5).67 It is based on 2 principles: level of certainty that ST is underlying mechanism of the adverse event and the time of the adverse event relative to the index procedure.

ST can be classified based on the time of adverse event (Figure 5). Early ST refers to the first 30 days after stent implantation and is further stratified into acute (<24 hours) and subacute (24 hours to 30 days). Late ST is time between 1 month and 1 year. Very late ST means beyond 1 year. The rationale of this classification is to account for different pathophysiological mechanisms that may be at work at various times.

Definite ST

Definite stent thrombosis is diagnosed when either angiographic or pathological confirmation is present

Angiographic confirmation of ST\*

The presence of a thrombus originating in the stent or in the segment 5 mm proximal to the stented region and at least one of the following criteria within a 48-h time window:

Acute onset of ischemic symptoms at rest (typical chest pain >20 min)

New ischemic ECG changes suggestive of acute ischemia

Typical rise and fall in cardiac biomarkers

Pathological confirmation of stent thrombosis

Evidence of recent thrombus within the stent determined at autopsy

#### Probable ST

Clinical definition of probable ST is diagnosed after intracoronary stenting in the following cases

Any unexplained death within the first 30 d

Regardless of the time after the index procedure, any MI that is related to documented acute ischemia in the territory of the implanted stent without angiographic confirmation of ST and in the absence of any other obvious cause

#### Possible ST

Clinical definition of possible ST is diagnosed with any unexplained death from 30 d after intracoronary stenting until the end of trial follow-up

\*The incidental angiographic documentation of stent occlusion in the absence of clinical signs or symptoms (silent occlusion) is (for this purpose) not considered a confirmed stent thrombosis.

Table 5. Definition of ST as Proposed by the Academic Research Consortium67

broader definitions include events potentially related to disease progression, life threatening arrhythmias, myocardial infarction of non-culprit lesions, and non-cardiac sudden death and therefore overestimate the true incidence. Accounting for these limitations, an academic research consortium (ARC) proposed a new standardised definition of ST (Table 5).67 It is based on 2 principles: level of certainty that ST is underlying mechanism of the adverse

ST can be classified based on the time of adverse event (Figure 5). Early ST refers to the first 30 days after stent implantation and is further stratified into acute (<24 hours) and subacute (24 hours to 30 days). Late ST is time between 1 month and 1 year. Very late ST means beyond 1 year. The rationale of this classification is to account for different

Definite stent thrombosis is diagnosed when either angiographic or pathological

The presence of a thrombus originating in the stent or in the segment 5 mm proximal to the stented region and at least one of the following criteria within a 48-h time

Clinical definition of probable ST is diagnosed after intracoronary stenting in the

Regardless of the time after the index procedure, any MI that is related to documented acute ischemia in the territory of the implanted stent without angiographic

Clinical definition of possible ST is diagnosed with any unexplained death from 30 d after

\*The incidental angiographic documentation of stent occlusion in the absence of clinical signs or symptoms (silent occlusion) is (for this purpose) not considered a confirmed stent thrombosis.

Table 5. Definition of ST as Proposed by the Academic Research Consortium67

Acute onset of ischemic symptoms at rest (typical chest pain >20 min)

Evidence of recent thrombus within the stent determined at autopsy

confirmation of ST and in the absence of any other obvious cause

New ischemic ECG changes suggestive of acute ischemia

 Typical rise and fall in cardiac biomarkers Pathological confirmation of stent thrombosis

Any unexplained death within the first 30 d

intracoronary stenting until the end of trial follow-up

event and the time of the adverse event relative to the index procedure.

pathophysiological mechanisms that may be at work at various times.

Definite ST

window:

Probable ST

Possible ST

following cases

confirmation is present

Angiographic confirmation of ST\*

Fig. 5. Classification based on the time frame of adverse events

#### **5.2 Incidence**

In the bare metal stent (BMS) era, most of ST was early ST and very late ST was extremely rare, although several cases of late ST were reported.73,74 Early ST is encountered with a similar or even somewhat lower frequency after drug-eluting stent (DES) compared with BMS. A metaanalysis of 6 studies comparing BMS with sirolimus-eluting stent (SES) reported that early rates of ST were 0.5% with SES and 0.6% with BMS, respectively (*P*=0.55).68 A pooled analysis of 5 trials comparing BMS with paclitaxel-eluting stent (PES) revealed early ST was 0.5% in PES and 0.6% in BMS, respectively (*P*=0.51).69 Although there had been some reported cases of late ST during the BMS era, this was not a clinical concern for most. According to recent a meta-analysis, no differences existed in the incidence of late ST between DES and BMS (0.2% versus 0.3%, 95% CI: 0.35-2.84; *P*=1.00).70 In another meta-analysis of 9 trials comparing SES and PES, no significant differences were detected for up to 1 year of follow-up (Figure 6).93

Fig. 6. Risk of ST in 9 trials directly comparing SES and PES with follow-up to 1 year.93

Complications of Coronary Intervention 63

segment proximal and distal to DES showed paradoxical vasoconstriction, whereas BMS

Incomplete stent apposition resulting from positive arterial remodeling or stent

PCI is not essential in all angina patients. The COURAGE trial, a randomization study comparing PCI and medical therapy in carefully selected patients with stable angina, revealed that there were no significant differences in mortality, acute myocardial infarction, and rehospitalization for acute coronary syndrome.83 It is therefore appropriate to consider medical therapy to the initial treatment option in stable angina patients with relatively low risk. In determining of use of BMS or DES, the risk of restenosis, the probability of bleeding

underexpansion, and penetration of the stent into a necrotic core leads to ST.

Thickness and robustness of neointimal stent coverage

demonstrated normal vasodilatation.

Drug response/interactions

Antithrombotic and anticoagulation therapy

Inhibition of platelet aggregation

Incomplete stent apposition

 Gene polymorphism Left ventricular function Acute coronary syndrome

Coagulation activity

 Renal failure Diabetes mellitus

Procedural factors Dissection

Lesion factors Vessel size Lesion length Thrombus

Stent expansion

Plaque characteristics

 Bifurcation Device factors

 Stent surface Drugs Polymer Table 6. Multifactorial Origin of ST

**3. Incomplete stent apposition** 

**1. Patient and lesion selection** 

**5.6 Prevention** 

Patient factors

Case reports, observational studies, extended follow-up of trials comparing DES with BMS, and meta-analyses of randomized trials have corroborated that very late ST is more common with DES than BMS. Pooled analysis of 4 randomized trials comparing SES with BMS and 5 randomized trials comparing PES with BMS revealed similar rates of late ST but significantly more very late ST (0.6% versus 0% for SES versus BMS, *P*=0.03; 0.7% versus 0.2% for PES versus BMS, *P*=0.03).72

#### **5.3 Clinical sequelae**

The reason why ST attracts attention is that it is associated with much higher mortality compared to other complications. Moreover, ST may be responsible for late complications of MI, including heart failure, arrhythmias, or mechanical complications. The impact of ST depends upon the myocardial area at risk, its viability, the degree of instantly recruitable collaterals, and the availability of rapid reperfusion therapy. The mortality rate varies depending on the definition of ST and follow-up duration (7-45%).73-77 Most ST patients experience myocardial infarction (>66%) with no differences between DES and BMS.71

#### **5.4 Risk factors**

ST is a multifactorial problem related to the stent itself, procedural factors, response to antiplatelet drugs, and lesion factors (Table 6). Many cases of early ST are caused by the procedure itself such as the presence of residual dissections or stent underexpansion. Poor response to antiplatelet drugs is also a documented cause of ST.78 Individual or ethnic differences have been reported and it has been suggested that several genetic polymorphisms are related to this drug resistance. Discontinuation of antiplatelet drugs is one of the most important predictors of ST. Patients noncompliance is the main problem and discontinuation due to dental procedures, surgical procedures or bleeding is also an important predisposing factor for late and very late ST.76

#### **5.5 Pathogenesis**

#### **1. Hypersensitivity reaction with extensive vasculitis**

Virmani and colleagues79 first described a case of local hypersensitivity reaction with extensive vasculitis of the intima, media, and adventitia consisting predominantly of lymphocytes and eosinophils in a patient suffering very late DES thrombosis. Histopathological analysis of an autopsy case revealed aneurysmal dilatation of the vessel wall within the stented segment with incomplete stent apposition and thick fibrin thrombus between the stent and the arterial wall. Most hypersensitivity cases reported to the Food and Drug administration after DES implantation were attributed to the DES itself, especially the polymer coating.

#### **2. Delayed healing and dysfunctional endothelialization**

Another possible explanation is delayed healing and endothelial dysfunction. Delayed healing manifested by persistent fibrin deposition and incomplete reendothelialization emerged as an important discriminator between BMS and DES.80 Physiological evidence of dysfunctional endothelium comes from studies assessing vasomotion 6 months after DES implantation.81,82 Through the use of bicycle exercise during coronary angiography, the

Case reports, observational studies, extended follow-up of trials comparing DES with BMS, and meta-analyses of randomized trials have corroborated that very late ST is more common with DES than BMS. Pooled analysis of 4 randomized trials comparing SES with BMS and 5 randomized trials comparing PES with BMS revealed similar rates of late ST but significantly more very late ST (0.6% versus 0% for SES versus BMS, *P*=0.03; 0.7% versus

The reason why ST attracts attention is that it is associated with much higher mortality compared to other complications. Moreover, ST may be responsible for late complications of MI, including heart failure, arrhythmias, or mechanical complications. The impact of ST depends upon the myocardial area at risk, its viability, the degree of instantly recruitable collaterals, and the availability of rapid reperfusion therapy. The mortality rate varies depending on the definition of ST and follow-up duration (7-45%).73-77 Most ST patients experience myocardial infarction (>66%) with no differences between DES and BMS.71

ST is a multifactorial problem related to the stent itself, procedural factors, response to antiplatelet drugs, and lesion factors (Table 6). Many cases of early ST are caused by the procedure itself such as the presence of residual dissections or stent underexpansion. Poor response to antiplatelet drugs is also a documented cause of ST.78 Individual or ethnic differences have been reported and it has been suggested that several genetic polymorphisms are related to this drug resistance. Discontinuation of antiplatelet drugs is one of the most important predictors of ST. Patients noncompliance is the main problem and discontinuation due to dental procedures, surgical procedures or bleeding is also an

Virmani and colleagues79 first described a case of local hypersensitivity reaction with extensive vasculitis of the intima, media, and adventitia consisting predominantly of lymphocytes and eosinophils in a patient suffering very late DES thrombosis. Histopathological analysis of an autopsy case revealed aneurysmal dilatation of the vessel wall within the stented segment with incomplete stent apposition and thick fibrin thrombus between the stent and the arterial wall. Most hypersensitivity cases reported to the Food and Drug administration after DES implantation were attributed to the DES itself, especially the

Another possible explanation is delayed healing and endothelial dysfunction. Delayed healing manifested by persistent fibrin deposition and incomplete reendothelialization emerged as an important discriminator between BMS and DES.80 Physiological evidence of dysfunctional endothelium comes from studies assessing vasomotion 6 months after DES implantation.81,82 Through the use of bicycle exercise during coronary angiography, the

0.2% for PES versus BMS, *P*=0.03).72

important predisposing factor for late and very late ST.76

**1. Hypersensitivity reaction with extensive vasculitis** 

**2. Delayed healing and dysfunctional endothelialization** 

**5.3 Clinical sequelae** 

**5.4 Risk factors** 

**5.5 Pathogenesis** 

polymer coating.

segment proximal and distal to DES showed paradoxical vasoconstriction, whereas BMS demonstrated normal vasodilatation.

Patient factors Thickness and robustness of neointimal stent coverage Drug response/interactions Gene polymorphism Left ventricular function Acute coronary syndrome Renal failure Diabetes mellitus Antithrombotic and anticoagulation therapy Coagulation activity Inhibition of platelet aggregation Procedural factors Dissection Incomplete stent apposition Stent expansion Lesion factors Vessel size Lesion length Thrombus Plaque characteristics Bifurcation Device factors Stent surface Drugs Polymer

Table 6. Multifactorial Origin of ST

#### **3. Incomplete stent apposition**

Incomplete stent apposition resulting from positive arterial remodeling or stent underexpansion, and penetration of the stent into a necrotic core leads to ST.

#### **5.6 Prevention**

#### **1. Patient and lesion selection**

PCI is not essential in all angina patients. The COURAGE trial, a randomization study comparing PCI and medical therapy in carefully selected patients with stable angina, revealed that there were no significant differences in mortality, acute myocardial infarction, and rehospitalization for acute coronary syndrome.83 It is therefore appropriate to consider medical therapy to the initial treatment option in stable angina patients with relatively low risk. In determining of use of BMS or DES, the risk of restenosis, the probability of bleeding

Complications of Coronary Intervention 65

recently developed.91 The Titan-TINOX stent (Hexacath, Rueil-Malmaison, France) is made of stainless steel coated with a Titanium nitride oxide (TNO) compound. The coating minimizes the leakage of metal residues, mostly nickel, from the metal stent into the arterial wall and, to some extent, attenuates electrical conductivity. Thus, the device was designed to enhance endothelialization and decrease the rate of stent-related thrombosis and restenosis. Stent coating with TNO reduced angiographic and ultrasonic measures of restenosis compared with stainless steel control stents of otherwise identical design in the

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[3] Shaikh F, Maddikunta R, Djelmami-Hani M, Solis J, Allaqaband S, Bajwa T. Stent fracture

[4] Sianos G, Hofma S, Ligthart JM, Saia F, Hoye A, Lemos PA, et al. Stent fracture and restenosis in the drug-eluting era, Catheter Cardiovasc Interv 2004;61:111-116. [5] Lee MS, Jurewitz D, Aragon J, Forrester J, Makkar RR, Kar S. Stent fracture associated

[6]Makaryus AN, Lefkowitz I, Lee AD. Coronary artery stent fracture. Int J Cardiovasc

[7]Yang TH, Kim DI, Park SG, Seo JS, Cho HJ, Seol SH, Kim SM, Kim DK, Kim DS. Clinical

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[10] Rits J, Van Herwaarden JA, Jahrome AK, Krievins D, Moll FL. The incidence of arterial

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[12] Popma JJ, Tiroch K, Almonacid A, Cohen S, Kandzari DE, Leon MB. A qualitative and

[13] Lemos PA, Saia F, Ligthart JM, et al. Coronary restenosis after sirolimus-eluting stent

after femoropopliteal stenting. L Am Coll Cardiol 2005;45:312/315.

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M, Murohara T. Frequency, predictors and outcome of stent fracture after

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implantation: morphological description and mechanistic analysis from a

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**6. References** 

or non-cardiac surgery, and the risk of late ST should be considered. The situations that BMS can be used are as follows.


The need for non-cardiac surgical procedures may arise after recent DES implantation. ST can arise after antiplatelet therapy withdrawal, especially within 12 months after PCI. In a study of 103 stent patients undergoing noncardiac surgery, an alarming 5% mortality rate and 45% complication rate were noted.84 It should be determined whether the surgical procedure can be postponed beyond 12 months after stenting or whether dual antiplatelet therapy can be maintained throughout the perioperative period. However if it is not possible to delay surgery beyond 12 months, balloon angioplasty or BMS implantation can be considered instead of DES implantation.

#### **2. Antiplatelet therapy**

The important of dual antiplatelet maintenance after PCI cannot be emphasized strongly enough. In a registry, 14% discontinued thienopyridine therapy within 30 days after discharge.85 Predictors of premature thienopyridine discontinuation were older age, lower socioeconomic status, preexisting cardiovascular disease, and lack of discharge instructions or cardiac rehabilitation referral. Mortality was about 10 times higher and rehospitalization was almost twice as high in patients without thienopyridine therapy.

The optimal duration of dual antiplatelet therapy after DES implantation is not well established.

The AHA/ACC guidelines are not based upon multicenter trials. Dual antiplatelet therapy is recommended at least 1 month for BMS implantation whereas for DES implantation, adherence to a 12 month regimen is recommended.86 It is also important that surgeons and dentists are advised not to automatically discontinue antiplatelet therapy but rather to consult first with the patient's cardiologist.

#### **3. Technique**

Attention to technical details also may improve results when PCI is performed with DES. Optimal deployment of stents by full expansion throughout their entire length should be ensured and residual dissections should be avoided. Intravascular ultrasound or optical coherence tomography is helpful to avoid stent malapposition. Multiple stenting in bifurcation lesions should be limited to only cases where really needed.

#### **4. Development of new DES**

Because the polymer coatings of DES were suspected to be responsible for some of ST, biodegradable polymers87 and polymer-free DES88 were developed. Another approach banks on drugs with improved healing properties such as antibodies capturing CD34+ endothelial progenitor cells89 or antithrombotic substances90 applied to the stent surface. Biodegradable stents, fully disintegrated in the body over a long period of time, have been recently developed.91 The Titan-TINOX stent (Hexacath, Rueil-Malmaison, France) is made of stainless steel coated with a Titanium nitride oxide (TNO) compound. The coating minimizes the leakage of metal residues, mostly nickel, from the metal stent into the arterial wall and, to some extent, attenuates electrical conductivity. Thus, the device was designed to enhance endothelialization and decrease the rate of stent-related thrombosis and restenosis. Stent coating with TNO reduced angiographic and ultrasonic measures of restenosis compared with stainless steel control stents of otherwise identical design in the prospective, randomized, multicenter trial.92

#### **6. References**

64 Coronary Interventions

or non-cardiac surgery, and the risk of late ST should be considered. The situations that BMS

The need for non-cardiac surgical procedures may arise after recent DES implantation. ST can arise after antiplatelet therapy withdrawal, especially within 12 months after PCI. In a study of 103 stent patients undergoing noncardiac surgery, an alarming 5% mortality rate and 45% complication rate were noted.84 It should be determined whether the surgical procedure can be postponed beyond 12 months after stenting or whether dual antiplatelet therapy can be maintained throughout the perioperative period. However if it is not possible to delay surgery beyond 12 months, balloon angioplasty or BMS implantation can

The important of dual antiplatelet maintenance after PCI cannot be emphasized strongly enough. In a registry, 14% discontinued thienopyridine therapy within 30 days after discharge.85 Predictors of premature thienopyridine discontinuation were older age, lower socioeconomic status, preexisting cardiovascular disease, and lack of discharge instructions or cardiac rehabilitation referral. Mortality was about 10 times higher and rehospitalization

The optimal duration of dual antiplatelet therapy after DES implantation is not well

The AHA/ACC guidelines are not based upon multicenter trials. Dual antiplatelet therapy is recommended at least 1 month for BMS implantation whereas for DES implantation, adherence to a 12 month regimen is recommended.86 It is also important that surgeons and dentists are advised not to automatically discontinue antiplatelet therapy but rather to

Attention to technical details also may improve results when PCI is performed with DES. Optimal deployment of stents by full expansion throughout their entire length should be ensured and residual dissections should be avoided. Intravascular ultrasound or optical coherence tomography is helpful to avoid stent malapposition. Multiple stenting in

Because the polymer coatings of DES were suspected to be responsible for some of ST, biodegradable polymers87 and polymer-free DES88 were developed. Another approach banks on drugs with improved healing properties such as antibodies capturing CD34+ endothelial progenitor cells89 or antithrombotic substances90 applied to the stent surface. Biodegradable stents, fully disintegrated in the body over a long period of time, have been

was almost twice as high in patients without thienopyridine therapy.

bifurcation lesions should be limited to only cases where really needed.

can be used are as follows.

3. Short,focal lesions

5. Non-ostial lesions

**2. Antiplatelet therapy** 

established.

**3. Technique** 

1. De novo lesions of native vessel 2. Reference diameter >3.5mm

4. Patients with no diabetes mellitus

be considered instead of DES implantation.

consult first with the patient's cardiologist.

**4. Development of new DES** 


Complications of Coronary Intervention 67

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**4** 

Roman Škulec

*Czech Republic* 

**Therapeutic Hypothermia** 

**in Cardiac Arrest Survivors** 

*Emergency Medical Service of the Central Bohemian Region,* 

*Department of Anesthesiology and Intensive Care, Charles University in Prague, Faculty of Medicine in Hradec Kralove, University Hospital Hradec Kralove* 

In Europe, cardiac arrest is the leading cause of death. Summary data indicate that the annual incidence of out-of-hospital cardiac arrest (OHCA) treated by Emergency medical systems is 38 per 100,000 population (Atwood et al., 2005). Survival is an estimated 10 % for all initial rhythms. Return of spontaneous circulation (ROSC) is followed by the development of post-cardiac arrest syndrome (PCAS), including post-cardiac arrest brain injury. This has been identified as the main cause of death and the condition limiting a long term quality of life (Edgren et al., 1994). Therapeutic hypothermia (TH) has became a cornerstone of early post-resuscitation care in cardiac arrest survivors (Nolan et al., 2008). So far, it has been the only known post-cardiac arrest intervention which can reduce the risk of unfavourable neurological outcome and decrease mortality. After an advisory statement of the International Liaison Committee on Resuscitation endorsed the use of TH in 2003, it was recommended as a standard therapeutic procedure in cardiac arres patients in the 2005 and 2010 guidelines for resuscitation and emergency cardiac care of the European Resuscitation Council and the American Heart Association (Nolan et al., 2005; Deakin et al., 2011). Accurate and safe management during the procedure of TH is a prerequisite for achieving the optimal neuroprotective effect. Moreover, the combination of TH along with other procedures (urgent myocardial revascularization, goal-directed haemodynamic support, control of blood glucose, ventilation and seizures) improves the goal of reaching a good neurological outcome (Sunde et al., 2007). This chapter summarizes patophysiological

aspects of PCAS, the evidence supporting TH and significant aspects of its practice.

The return of spontaneous circulation after severe complete whole-body ischemia is an unnatural pathophysiological state created by successful cardiopulmonary resuscitation. It is followed by a number of undesirable processes leading to the development of PCAS. The following four key clinical components of PCAS have been identified: a) post-cardiac arrest brain injury, b) post-cardiac arrest myocardial dysfunction, c) systemic ischemia/reperfusion response, and d) persistent precipitating pathology (Nolan et al., 2008). While some of the processes develop very early during cardiac arrest, others follow

**2. Pathophysiology of post-cardiac arrest syndrome** 

**1. Introduction** 

