**6. Signs and symptoms**

Onset of the atherosclerotic plaque and speed of the growth and complications, there are several signs and symptoms. Atherosclerosis can be seen in every artery, but for the coronary atherosclerosis, the result of the disease is coronary artery disease, and the symptoms and the signs are due to this. Because of the impaired blood flow, there is a sort of symptoms. Some of them are in the side of the chest, and some of them are systemic because of the impaired circulation.

• Chest pain

**5. Risk factors**

**a.** Increased age.

LDL.

**5.1. Non-modifiable risk factors**

8 Atherosclerosis - Yesterday, Today and Tomorrow

vascular risk factors:

**d.** Increased lipoprotein(a) level.

myocardial infarction [10].

**5.2. Modifiable risk factors**

cans by smooth muscle cells.

**f.** Stressful lifestyle: better known as Type A personality.

**b.** High-density lipoprotein (HDL) and its major apolipoprotein (ApoA1)

dysfunction.

resistance.

**a.** Exercise

**5.3. Atheroprotective factors**

**b.** Male gender: lack of atheroprotective properties of estrogen which raises HDL and lowers

**c.** Hereditary factors: history of coronary artery disease (CAD) among first-degree relatives at a young age (before 55 for males and before 65 for females). New markers of the cardio-

**e.** Increased homocysteine level: high levels may promote oxidative stress, vascular inflammation, and platelet adhesiveness. And, this process leads to atherosclerosis. A meta-analysis that collected a large number of prospective studies showed a significant association between the serum level of homocysteine and the incidence of cardiovascular disease [9]. Not just with it, increased blood homocysteine levels are shown in patients with acute

**f.** C-reactive protein (CRP), high-sensitivity CRP (hs-CRP), and other markers of inflammation: activate complement and contribute to a sustained inflammatory state. CRP is a biomarker of tissue damage and inflammation. It is an acute-phase reactant and increases in the inflammatory process. But nowadays, it has been used in the diagnosis of the cardiovascular diseases such as CAD. Sara et al. have showed that hs-CRP is associated with coronary endothelial dysfunction in the asymptomatic coronary artery disease [11].

**b.** Tobacco smoking: enhances oxidative modification of LDL, contributes to endothelial dysfunction via oxidant stress, and increases expression of leukocyte adhesion molecules. **c.** Hypertension: increases permeability of the vessel wall to lipoproteins and promotes retention of LDL in the vessel intima by accentuating production of LDL-binding proteogly-

**d.** Diabetes mellitus: enhances glycation of LDL and is associated with endothelial

**e.** Obesity and lack of physical activity: can cause dyslipidemia, hypertension, and insulin

**a.** Dyslipidemia: increased LDL and decreased high-density lipoprotein (HDL).


Coronary atherosclerosis causes coronary artery disease. Complicated atherosclerotic plaque disrupts the blood flow in the coronary circulation. Impaired blood flow causes a corrupted supply and demand of the oxygen and the metabolites in the heart. This results in a decrease in coronary arterial blood flow and a decrease in oxygen supply. There are several symptoms such as chest pain (angina pectoris), dyspnea, syncope, and sometimes pulmonary edema. Increased demand of blood supply and oxygen starts the angina pectoris. Because of the decreased blood flow in coronary artery, sufficient blood cannot be supplied in the increased effort capacity. The spectrum of presentation includes symptoms and signs consistent with the following conditions:

*Exercise echocardiography*: images are taken before and after the treadmill or stationary bike effort test. If exercise echocardiography cannot be performed due to peripheral artery disease, musculoskeletal disorders, etc., drug-stimulated (dobutamine, adenosine, dipyridamole) stress echocardiography can be performed. These drugs increase the cardiac contractility and rhythm. Doses of the drugs increases step by step, and images are taken gradually.

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The purpose is to assess the exercise tolerance of the heart. If there is a myocardial perfusion defect due to coronary artery disease, stress echocardiography can give information about this. The severity of the coronary artery disease can be assessed with this test. Before and after revascularization either PCI or CABG cardiac risk can be evaluated. It can be performed for cardiac risk analyses for noncardiac surgeries. Exercise echocardiography can be used for risk stratification in asymptomatic patients with severe aortic stenosis too [14]. Yao et al. have showed in their clinical study; as the result of the exercise tests, monophasic/normal wall motion was associated with a benign prognosis, but abnormal wall motion responses were

*Myocardial perfusion scintigraphy*: can show us the ischemic parts of the heart due to the occlu-

*Computed tomography (CT)*: conventional thoracoabdominal CT scan can show atherosclerotic calcification and plaques in the aortic or arterial wall. But coronary CT scan can show us the presence of coronary atherosclerosis, the degree of the coronary artery disease, and the occlu-

*Intravenous ultrasound (IVUS)*: can be useful for the controversial lesions. This is an invasive technique that localizes plaques and quantifies plaque seriousness. Virtual histology-intravascular ultrasound (VH-IVUS) can identify plaque components. Optical coherence tomography (OCT), also known as optical frequency domain imaging (OFDI), identifies intimal

*Coronary angiography*: is the gold standard for diagnosis of coronary atherosclerosis and coronary artery disease. Moving image of each coronary artery and the atherosclerotic lesions can be seen. It is the most specific and sensitive test for the diagnosis of coronary artery disease. Coronary angiography can come out to such results. This can be a follow-up with medical therapy, a percutaneous coronary intervention can be necessary, or a coronary artery bypass grafting (CABG) is essential to be performed to the patient. All of the interventions are selected due to the percentage of the affected coronary artery lesion, the lesion type, lesion location, the number of the affected coronary artery, and of course the general condition of the patient. **Treatment:** There are several treatment modalities. These include lifestyle changes, risk factor modification, and medical therapies. But we want to mention about the clinically important

*Percutaneous coronary intervention (PCI)*: it is also known as coronary angioplasty, and this is a nonsurgical technique to treat obstructive coronary artery disease. It can be a choice in stable angina pectoris, in acute myocardial infarction, or in multivessel coronary artery disease. The procedure is performed in angiography catheter laboratory. An x-ray fluoroscopy and opaque fluid are necessary for the procedure. Entry ways for the procedure are femoral

hyperplasia and also detects and quantifies the key features of vulnerable plaque [16].

sive effect of coronary atherosclerosis leading to coronary artery disease.

occlusive coronary artery diseases' invasive treatment.

arteries and radial arteries for the individual cases.

associated with a worse prognosis [15].

sive lesions.


## **7. Diagnosis and treatment**

Atherosclerosis can be seen in all the arterial sites in the whole body as mentioned before. So, the physical examination can give us very important findings. A well-taken medical history and physical examination can be helpful for the diagnosis. Suspicious findings can lead us to make a decision for the advanced examination.

Medical history is the cornerstone of diagnosis. A positive history of typical chest pain, shortness of breath, impaired physical capacity, and the other signs and symptoms are very useful to diagnosis.

Atherosclerosis can cause both coronary artery and peripheral artery diseases. Concomitant coronary and peripheral artery disease prevalence is varied 28–94% in published reports [13]. So, on the calcified peripheral artery, palpation or lack of pulse in the peripheral arteries or signs of the peripheral artery disease are important parts of the physical examination.

What are the parts of the advanced examination?

*Electrocardiography (ECG)*: impaired blood flow in acute events such as acute myocardial infarction and acute coronary syndromes are the changes we can see in the ECG.

*Echocardiography (ECO)*: atherosclerotic calcification or plaque and thickness of aortic wall can be seen in ECO. Ventricular low ejection fraction and impaired contraction of ventricular segments can suspect us for coronary atherosclerosis.

*Stress echocardiography*: this echocardiography can be performed either by exercise method or pharmacological drugs that increase cardiac contractility and rate.

*Exercise echocardiography*: images are taken before and after the treadmill or stationary bike effort test. If exercise echocardiography cannot be performed due to peripheral artery disease, musculoskeletal disorders, etc., drug-stimulated (dobutamine, adenosine, dipyridamole) stress echocardiography can be performed. These drugs increase the cardiac contractility and rhythm. Doses of the drugs increases step by step, and images are taken gradually.

Coronary atherosclerosis causes coronary artery disease. Complicated atherosclerotic plaque disrupts the blood flow in the coronary circulation. Impaired blood flow causes a corrupted supply and demand of the oxygen and the metabolites in the heart. This results in a decrease in coronary arterial blood flow and a decrease in oxygen supply. There are several symptoms such as chest pain (angina pectoris), dyspnea, syncope, and sometimes pulmonary edema. Increased demand of blood supply and oxygen starts the angina pectoris. Because of the decreased blood flow in coronary artery, sufficient blood cannot be supplied in the increased effort capacity. The spectrum of presentation includes symptoms and signs consistent with the following

Atherosclerosis can be seen in all the arterial sites in the whole body as mentioned before. So, the physical examination can give us very important findings. A well-taken medical history and physical examination can be helpful for the diagnosis. Suspicious findings can lead us to

Medical history is the cornerstone of diagnosis. A positive history of typical chest pain, shortness of breath, impaired physical capacity, and the other signs and symptoms are very useful

Atherosclerosis can cause both coronary artery and peripheral artery diseases. Concomitant coronary and peripheral artery disease prevalence is varied 28–94% in published reports [13]. So, on the calcified peripheral artery, palpation or lack of pulse in the peripheral arteries or signs of the peripheral artery disease are important parts of the physical examination.

*Electrocardiography (ECG)*: impaired blood flow in acute events such as acute myocardial

*Echocardiography (ECO)*: atherosclerotic calcification or plaque and thickness of aortic wall can be seen in ECO. Ventricular low ejection fraction and impaired contraction of ventricular seg-

*Stress echocardiography*: this echocardiography can be performed either by exercise method or

infarction and acute coronary syndromes are the changes we can see in the ECG.

conditions:

• Stable angina pectoris

• Congestive heart failure

**7. Diagnosis and treatment**

make a decision for the advanced examination.

What are the parts of the advanced examination?

ments can suspect us for coronary atherosclerosis.

pharmacological drugs that increase cardiac contractility and rate.

• Sudden cardiac arrest

to diagnosis.

• Asymptomatic state (subclinical phase)

10 Atherosclerosis - Yesterday, Today and Tomorrow

• Acute myocardial infarction (AMI) • Chronic ischemic cardiomyopathy

• Unstable angina (i.e., acute coronary syndrome)

The purpose is to assess the exercise tolerance of the heart. If there is a myocardial perfusion defect due to coronary artery disease, stress echocardiography can give information about this. The severity of the coronary artery disease can be assessed with this test. Before and after revascularization either PCI or CABG cardiac risk can be evaluated. It can be performed for cardiac risk analyses for noncardiac surgeries. Exercise echocardiography can be used for risk stratification in asymptomatic patients with severe aortic stenosis too [14]. Yao et al. have showed in their clinical study; as the result of the exercise tests, monophasic/normal wall motion was associated with a benign prognosis, but abnormal wall motion responses were associated with a worse prognosis [15].

*Myocardial perfusion scintigraphy*: can show us the ischemic parts of the heart due to the occlusive effect of coronary atherosclerosis leading to coronary artery disease.

*Computed tomography (CT)*: conventional thoracoabdominal CT scan can show atherosclerotic calcification and plaques in the aortic or arterial wall. But coronary CT scan can show us the presence of coronary atherosclerosis, the degree of the coronary artery disease, and the occlusive lesions.

*Intravenous ultrasound (IVUS)*: can be useful for the controversial lesions. This is an invasive technique that localizes plaques and quantifies plaque seriousness. Virtual histology-intravascular ultrasound (VH-IVUS) can identify plaque components. Optical coherence tomography (OCT), also known as optical frequency domain imaging (OFDI), identifies intimal hyperplasia and also detects and quantifies the key features of vulnerable plaque [16].

*Coronary angiography*: is the gold standard for diagnosis of coronary atherosclerosis and coronary artery disease. Moving image of each coronary artery and the atherosclerotic lesions can be seen. It is the most specific and sensitive test for the diagnosis of coronary artery disease.

Coronary angiography can come out to such results. This can be a follow-up with medical therapy, a percutaneous coronary intervention can be necessary, or a coronary artery bypass grafting (CABG) is essential to be performed to the patient. All of the interventions are selected due to the percentage of the affected coronary artery lesion, the lesion type, lesion location, the number of the affected coronary artery, and of course the general condition of the patient.

**Treatment:** There are several treatment modalities. These include lifestyle changes, risk factor modification, and medical therapies. But we want to mention about the clinically important occlusive coronary artery diseases' invasive treatment.

*Percutaneous coronary intervention (PCI)*: it is also known as coronary angioplasty, and this is a nonsurgical technique to treat obstructive coronary artery disease. It can be a choice in stable angina pectoris, in acute myocardial infarction, or in multivessel coronary artery disease. The procedure is performed in angiography catheter laboratory. An x-ray fluoroscopy and opaque fluid are necessary for the procedure. Entry ways for the procedure are femoral arteries and radial arteries for the individual cases.

Some urgent cases such as acute myocardial infarction PCI can be performed emergent. Primary PCI is called in this situation. But also PCI is used for elective coronary artery disease usually. The procedure starts with a local anesthesia from the arterial puncture side; this can be even femoral or radial artery. Hydrophilic and micro-catheters and guidewires are used to reach coronary arteries. These radiopaque wires are seen easily on fluoroscopy. A balloon angioplasty can be performed to the occlusive lesion. Coronary stents can be implanted to the occluded lesion. Coronary stents vary from bare metal stents to drug eluding stent. These drug eluding stents vary to the first, second, and third generation. Nowadays, fourth-generation bioresorbable stents are mentioned in some clinical trials [17]. Whatever the kind of the stents, the main purpose is to improve blood flow of the myocardium tissue.

*Coronary artery bypass grafting (CABG)*: so, is this the only technique that we can improve blood supply of the myocardium? Is there any other way of myocardial revascularization? The answer is yes. It is coronary artery bypass grafting (CABG). This is an open cardiac surgical procedure. This means that it is more invasive than PCI. But in some cases, PCI cannot be the concluding treatment for the coronary artery disease. Lesion type, region of the lesion, collateral and main side branches extending from the lesion, severity of the lesion, and the number of the lesions is important for the physician to make the choice.

Before explaining CABG, we have to mention the indications and guidelines (**Table 1** and **2**).

*7.1.1.2. Class IIa*

anatomy for both procedures [19].

*7.1.1.3. Class IIb*

*7.1.2. Stable angina*

*7.1.2.1. Class I*

1. LMC stenosis. 2. LMCE disease.

*7.1.2.2. Class IIa*

3. Three-vessel disease.

(1) Proximal LAD (one- or two-vessel disease)

and high-risk criteria on noninvasive testing.

6. Disabling angina refractory to medical therapy.

1. Proximal LAD stenosis with one-vessel disease.

at risk and demonstrable ischemia.

(1) One- or two-vessel disease not involving proximal LAD (if a large territory at risk on non-

Recommendation for the type of revascularization (CABG or PCI) in patients with stable CAD with suitable coronary

4. Two-vessel disease with proximal LAD stenosis and LVEF <50% or demonstrable ischemia. 5. One- or two-vessel disease without proximal LAD stenosis but with a large territory at risk

2. One- or two-vessel disease without proximal LAD stenosis, but with a moderate territory

invasive studies or LVEF <50%, class IIa and IIb become class I indications)

**Table 2.** 2014 ESC/EACTS Guidelines on myocardial revascularization guidelines.

**Recommendation CABG PCI**

One or two-vessel disease without LAD IIb C I C One-vessel disease with proximal LAD I A I A Two-vessel disease with proximal LAD I B I C LMC with SYNTAX score < 22 I B I B LMC with SYNTAX score 23–32 I B IIb B LMC with SYNTAX score > 32 I B III B Three-vessel disease SYNTAX score > 22 I A I B Three-vessel disease SYNTAX score 23–32 I A III B Three-vessel disease SYNTAX score > 32 I A III B

**Class Level Class Level**

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#### **7.1. Guidelines for coronary artery bypass graft surgery**



CABG, coronary artery bypass grafting; DES, drug-eluting stent; DM, diabetes mellitus; LAD, left anterior descending artery; LMC, left main coronary artery disease; LVD, left ventricular dysfunction. \*Y, yes; N, no; C, controversial.

**Table 1.** The reality of myocardial revascularization strategies in patients with isolated coronary artery disease [18].


Recommendation for the type of revascularization (CABG or PCI) in patients with stable CAD with suitable coronary anatomy for both procedures [19].

**Table 2.** 2014 ESC/EACTS Guidelines on myocardial revascularization guidelines.

#### *7.1.1.2. Class IIa*

Some urgent cases such as acute myocardial infarction PCI can be performed emergent. Primary PCI is called in this situation. But also PCI is used for elective coronary artery disease usually. The procedure starts with a local anesthesia from the arterial puncture side; this can be even femoral or radial artery. Hydrophilic and micro-catheters and guidewires are used to reach coronary arteries. These radiopaque wires are seen easily on fluoroscopy. A balloon angioplasty can be performed to the occlusive lesion. Coronary stents can be implanted to the occluded lesion. Coronary stents vary from bare metal stents to drug eluding stent. These drug eluding stents vary to the first, second, and third generation. Nowadays, fourth-generation bioresorbable stents are mentioned in some clinical trials [17]. Whatever the kind of the stents,

*Coronary artery bypass grafting (CABG)*: so, is this the only technique that we can improve blood supply of the myocardium? Is there any other way of myocardial revascularization? The answer is yes. It is coronary artery bypass grafting (CABG). This is an open cardiac surgical procedure. This means that it is more invasive than PCI. But in some cases, PCI cannot be the concluding treatment for the coronary artery disease. Lesion type, region of the lesion, collateral and main side branches extending from the lesion, severity of the lesion, and the

Before explaining CABG, we have to mention the indications and guidelines (**Table 1** and **2**).

CABG, coronary artery bypass grafting; DES, drug-eluting stent; DM, diabetes mellitus; LAD, left anterior descending artery; LMC, left main coronary artery disease; LVD, left ventricular dysfunction. \*Y, yes; N, no; C, controversial.

**Table 1.** The reality of myocardial revascularization strategies in patients with isolated coronary artery disease [18].

**No risk DM LVD No risk DM LVD**

N N N Y Y Y Y Y Y N N N

N N N Y Y Y Y Y Y Y Y Y

Y Y Y N N N Y Y Y C C C

Y Y Y N N N Y Y Y N N N

the main purpose is to improve blood flow of the myocardium tissue.

number of the lesions is important for the physician to make the choice.

**Revascularization CABG DES**

**7.1. Guidelines for coronary artery bypass graft surgery**

*7.1.1. Asymptomatic CAD*

12 Atherosclerosis - Yesterday, Today and Tomorrow

1. LMC stenosis.[18, 20]

3 Three-vessel disease.

Two-vessel disease without LAD Two-vessel disease with LAD

Two-vessel disease + proximal LAD

Three-vessel + proximal LAD

*7.1.1.1. Class I*

2. LMCE disease.

One-vessel disease Proximal LAD

Three-vessel disease

LMC ± other lesions

(1) Proximal LAD (one- or two-vessel disease)

#### *7.1.1.3. Class IIb*

(1) One- or two-vessel disease not involving proximal LAD (if a large territory at risk on noninvasive studies or LVEF <50%, class IIa and IIb become class I indications)

#### *7.1.2. Stable angina*

*7.1.2.1. Class I*


4. Two-vessel disease with proximal LAD stenosis and LVEF <50% or demonstrable ischemia.

5. One- or two-vessel disease without proximal LAD stenosis but with a large territory at risk and high-risk criteria on noninvasive testing.

6. Disabling angina refractory to medical therapy.

#### *7.1.2.2. Class IIa*

1. Proximal LAD stenosis with one-vessel disease.

2. One- or two-vessel disease without proximal LAD stenosis, but with a moderate territory at risk and demonstrable ischemia.

*7.1.3. Unstable angina/non-ST-segment elevation MI (non-STEMI)*

*7.1.3.1. Class I*

1. LMC stenosis.

2. LMCE disease.

3. Ongoing ischemia not responsive to maximal nonsurgical therapy.

*7.1.3.2. Class IIa*

Proximal LAD stenosis with one- or two-vessel disease.

*7.1.3.3. Class IIb*

One- or two-vessel disease without proximal LAD stenosis when PCI not possible (becomes class I if high-risk criteria on noninvasive testing).

*7.1.5.2. Class IIa*

*7.1.6.1. Class I*

*7.1.6.2. Class IIa*

*7.1.7. Failed PCI*

*7.1.7.1. Class I*

*7.1.7.2. Class IIa*

*7.1.7.3. Class IIb*

*7.1.8.1. Class I*

*7.1.8.2. Class IIa*

1. Large territory at risk.

*7.1.8. Previous CABG*

1. Foreign body in critical position.

2. Shock.

2. Three-vessel disease.

1. LMC.

Significant viable territory and noncontractile myocardium.

2. Proximal LAD disease and one- or two-vessel disease. These become class I indications if

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arrhythmia is resuscitated cardiac death or sustained ventricular tachycardia.

2. Nonpatent previous bypass grafts, but with class I indications for native CAD.

2. Vein grafts supplying LAD or large territory are "/> 50% stenosed.

*7.1.6. Life-threatening ventricular arrhythmias*

1. Bypassable one- or two-vessel disease.

1. Ongoing ischemia with significant territory at risk.

2. Shock with coagulopathy and no previous sternotomy.

Shock with coagulopathy and previous sternotomy.

1. Disabling angina refractory to medical therapy.

*7.1.4. ST-segment elevation (Q wave) MI*

*7.1.4.1. Class I*

1. Failed PCI with persistent pain or shock and anatomically feasible.

2. Persistent or recurrent ischemia refractory to medical treatment with acceptable anatomy, which has a significant territory at risk and not a candidate for PCI.

3. Requires surgical repair of post-infarct VSD or MR.

4. Cardiogenic shock in patients <75 years of age who have ST elevation, LBBB, or a posterior MI within 18 hours onset.

5. Life-threatening ventricular arrhythmias in the presence of ≥50% LMC stenosis or threevessel disease.

*7.1.4.2. Class IIa*

1. Primary reperfusion in patients who have failed fibrinolytics or PCI and are in the early stages (6–12 h) of an evolving STEMI.

2. Mortality with CABG is elevated in the first 3–7 days after STEMI/NSTEMI. After 7 days, criteria for CABG in previous section are applied.

*7.1.5. Poor LV function*

*7.1.5.1. Class I*

1. LMC.

2. LMCE.

3. Proximal LAD stenosis and two- to three-vessel disease.

*7.1.5.2. Class IIa*

*7.1.3. Unstable angina/non-ST-segment elevation MI (non-STEMI)*

3. Ongoing ischemia not responsive to maximal nonsurgical therapy.

1. Failed PCI with persistent pain or shock and anatomically feasible.

which has a significant territory at risk and not a candidate for PCI.

One- or two-vessel disease without proximal LAD stenosis when PCI not possible (becomes

2. Persistent or recurrent ischemia refractory to medical treatment with acceptable anatomy,

4. Cardiogenic shock in patients <75 years of age who have ST elevation, LBBB, or a posterior

5. Life-threatening ventricular arrhythmias in the presence of ≥50% LMC stenosis or three-

1. Primary reperfusion in patients who have failed fibrinolytics or PCI and are in the early

2. Mortality with CABG is elevated in the first 3–7 days after STEMI/NSTEMI. After 7 days,

Proximal LAD stenosis with one- or two-vessel disease.

class I if high-risk criteria on noninvasive testing).

3. Requires surgical repair of post-infarct VSD or MR.

*7.1.4. ST-segment elevation (Q wave) MI*

*7.1.3.1. Class I*

1. LMC stenosis. 2. LMCE disease.

14 Atherosclerosis - Yesterday, Today and Tomorrow

*7.1.3.2. Class IIa*

*7.1.3.3. Class IIb*

*7.1.4.1. Class I*

vessel disease.

*7.1.4.2. Class IIa*

*7.1.5. Poor LV function*

*7.1.5.1. Class I*

1. LMC. 2. LMCE.

MI within 18 hours onset.

stages (6–12 h) of an evolving STEMI.

criteria for CABG in previous section are applied.

3. Proximal LAD stenosis and two- to three-vessel disease.

Significant viable territory and noncontractile myocardium.

*7.1.6. Life-threatening ventricular arrhythmias*

*7.1.6.1. Class I*

1. LMC.

2. Three-vessel disease.

*7.1.6.2. Class IIa*

1. Bypassable one- or two-vessel disease.

2. Proximal LAD disease and one- or two-vessel disease. These become class I indications if arrhythmia is resuscitated cardiac death or sustained ventricular tachycardia.

*7.1.7. Failed PCI*

*7.1.7.1. Class I*

1. Ongoing ischemia with significant territory at risk.

2. Shock.

*7.1.7.2. Class IIa*


*7.1.7.3. Class IIb*

Shock with coagulopathy and previous sternotomy.

*7.1.8. Previous CABG*

*7.1.8.1. Class I*

1. Disabling angina refractory to medical therapy.

2. Nonpatent previous bypass grafts, but with class I indications for native CAD.

*7.1.8.2. Class IIa*


Class I: Conditions for which there is evidence and/or general agreement that a given procedure or treatment is useful and effective.

**8. Prevention**

individuals.

and smoking status.

Prevention of the coronary atherosclerosis has to be lifelong. Individuals need to be careful for

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Healthy eating habit for the heart: eating habits are very important in the process of developing atherosclerosis. Healthy diet consists of low amounts of white bread, unsaturated fat products, fast foods, salt, and sugar. It also includes eating dairy products, fruits, vegetables,

After the start of healthy diet for the heart, weight control can be achieved, because over-

Physical activity: stressful and sedentary lifestyles are the risk factors for coronary atherosclerosis. So, a programmed physical activity can improve the fitness level and the health of the

**Figure 2.** Ten year risk of fatal CVD in high risk regions of Europe by gender, age, systolic blood pressure, total cholesterol

risk factors. Adopting a healthy lifestyle. What is inside of this healthy lifestyle?

whole grain, seafood, poultry without skin, lean meats, low-fat milk, or fat-free milk.

weight and obese people have high risk for coronary atherosclerosis.

Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness or efficacy of a procedure.

Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy.

Class IIb: Usefulness/efficacy is less well established by evidence/opinion.

Class III: Conditions for which there is evidence and/or general agreement that the procedure/ treatment is not useful/effective and in some cases may be harmful.

ACC, American College of Cardiology; AHA, American Heart Association; CABG, coronary artery bypass grafting; CAD, coronary artery disease; LAD, left anterior descending artery; LBBB, left bundle branch block, LMC, left main coronary artery; LMCE, left main coronary equivalent; LVEF, left ventricular ejection fraction; MI, myocardial infarction; MR, mitral regurgitation; NSTEMI, non-ST elevation myocardial infarction; PCI, percutaneous transluminal coronary angioplasty; STEMI, ST elevation myocardial infarction; VSD, ventricular septal defect [20].

There are several grafts that are used in CABG. Arterial grafts such as left internal and right internal mammary artery (LIMA and RIMA), especially LIMA has got the longest patency rate (10-year patency is 95%). Radial artery can be used, but it is a muscular artery and has got a predisposition to vasospasm. Vena saphena magna is the most used venous graft.

This procedure can be performed with cardiopulmonary bypass (CPB) machine (on-pump), without CPB (off-pump CABG-OPCAB), or beating heart procedures. In the last decade, minimally invasive techniques are rising to individual cases. MIDCAB (minimally invasive direct coronary artery bypass) can be performed without full median sternotomy. This can serve minimal surgical trauma and avoid wound complication.

TECAB: this is a robotically assisted total endoscopic coronary artery bypass procedure. This is a complex procedure; surgeon has to steep a learning curve. This procedure can perform both on-pump and off-pump CABG.

Awake coronary artery bypass (ACAB) procedure: This avoids side effects of general anesthesia. This includes a minimal invasive procedure without intubation and mechanical ventilatory support. A somatosensory and motor block is made via the T1–T8 level of vertebra. This preserves diaphragmatic ventilation.

Early outcomes after CABG continue to improve, and the early cumulative mortality rate is below 2% and lower than 1% in lower-risk patients. The most common reasons for death are heart failure (65%), neurologic events (7.5%), hemorrhage (7%), respiratory failure (5.5%), and dysrhythmia (5.5%).

The survival rate after isolated CABG is higher than 98% for the first month and 97% for first year, 92% for 5 years, 80% for 10 years, 65% for 15 years, and 51% for 20 years. Usage of LIMA is a predictive parameter for late survival.
