Coronary Stents

Article Author:
Lovely Chhabra
Article Author (Archived):
Muhammad Zain
Article Editor:
Waqas Siddiqui
4/21/2019 4:10:22 PM
PubMed Link:
Coronary Stents


Coronary stents (CS) are tube-like expandable metallic devices which are introduced into coronary arteries that are clogged due to an underlying atherosclerosis disease. This revascularization procedure is termed as a percutaneous coronary intervention (PCI) or coronary angioplasty with stent placement. The coronary stent was first developed in the 1980s and has continued to evolve in terms of shape, structure, and the material used within them. In a pre-stent era, balloon angioplasty was the mainstay of coronary revascularization in which an inflatable balloon-tipped catheter was inserted percutaneously through arterial entry site in extremity and advanced into coronary arteries. On reaching the coronaries, the balloon was inflated to compress atherosclerotic plaque against the vascular wall and restore blood flow to the myocardium. The balloon was withdrawn after deflating. This procedure had major drawbacks such as acute vessel closure due to arterial recoil, coronary arteries dissection, acute arterial thrombosis, and restenosis due to neointimal hyperplasia. With the introduction of coronary stents, coronary dissection and vascular recoil were eliminated due to the expandable, metallic meshwork of the stent which prevents negative remodeling.[1][2][3][1]

Types of Coronary Stents

  1. Bare metal stents (BMS)
  2. Drug-eluting stents (DES)
  3. Bioresorbable scaffold system (BRS)
  4. Drug-eluting balloons (DEB)

DES consists of three components: metallic stent platform, active pharmacological drug agent, and a carrier vehicle. Stainless steel or cobalt chromium is the most common metal and gives long-term mechanical stability to counteract vascular recoil. Commonly used drugs act to block signal transduction and cell cycle progression in different phases thereby blocking SMC proliferation in the stented arterial site. Rapamycin agents bind to the intracellular protein, FKBP-12, that inhibit the protein kinase mammalian target of Rapamycin (mTOR). This intracellular complex increases the expression of p27 and blocks progression of the cell cycle from the G1 phase to the S phase (DNA synthesis). Another drug category is taxanes which interfere with microtubule function which is necessary for M phase (mitosis). So cells get arrested in the G2 phase of the cell cycle. To increase surface area, a carrier vehicle matrix or a polymer coating is used to enable sufficient drug loading and release for a long time. Polymer coating consists of repeating units of biodegradable poly-L-lactide, poly –D, and L-lactic-co-glycolic acid in a regular pattern, which are degraded into lactic acid and glycolic acid that ultimately get converted into water and carbon dioxide. 1 generation DES has sirolimus or paclitaxel coating on a stainless steel base while 2 generation DES has zotarolimus or everolimus coating on top of biocompatible cobalt-chromium or platinum-chromium platform. The drug release is carried out by diffusion through pores in the polymeric coating.

While DEB has only antiproliferative drug coating without underlying metallic structure of the stent, BRS is also devoid of metallic structure and is resorbed completely in few months after serving their purpose. Other stents like bifurcation stents and covered stents are designed for special circumstances such as lesion over vascular bifurcation or coronary artery perforation respectively.[4][5]


Atherosclerosis, which is characterized by the formation of luminal plaques, is the underlying cause of coronary artery disease. Risk factors for the development and progression of atherosclerosis have been studied and classified as modifiable or nonmodifiable.

Modifiable Risk Factors

  • Hyperlipidemia and dyslipidemia
  • Hypertension
  • Diabetes mellitus
  • Cigarette smoking
  • Physical inactivity
  • Obesity 

Non-modifying Risk Factors

  • Age
  • Sex
  • Family history of premature CAD


CAD is the leading cause of morbidity and mortality worldwide and is responsible for approximately 20% of all deaths in the United States. CAD is due to underlying atherosclerosis which leads to plaque formation in the coronary artery's lumen. The actual frequency of atherosclerosis cannot be determined as it is asymptomatic predominantly. It starts early in childhood and develops fatty streaks over time. More advanced and complicated lesions are present in individuals in the fifth or sixth decade of life. In the United States, approximately 14 million individuals experience CAD and its complications with post-myocardial infarction congestive heart failure (CHF) being most common one. Approximately 1.5 million Americans have an acute myocardial infarction (AMI) annually, one-third result in death. In 2009, around 785,000 Americans suffered a first AMI, while 470,000 Americans had a recurrent MI. An estimated 195,000 "silent" heart attacks occur each year. About every 34 seconds, an American will have an AMI. In developed countries, the incidence of AMI is similar to that observed in the United States. The frequency of symptomatic CAD in ethnic immigrant populations in the United States approaches that of the white population which supports the role of environmental factors. In France, the Mediterranean diet with the use of alcohol and its possible HDL-raising benefit, and the predominant use of monosaturated fatty acids (canola oil or olive oil) and omega-3 fatty acids there is a low chance of atherogenesis with all said factors. The reduced incidence of CAD and AMI is a phenomenon is called “French paradox.” The Spanish cohort of the European Prospective Investigation into Cancer and Nutrition suggests that the Mediterranean diet may help lower the risk of the CAD. The frequency of symptomatic CAD is also very high in Great Britain, Scotland, Scandinavia, Finland, and Russia. Symptomatic CAD due to atherosclerosis is rare on the African continent, although recent evidence points to a rapid rise in these statistics due to rapid urbanization and westernization of the rural African populations. The statistics of CAD vary significantly with race. As compared to whites, blacks have higher morbidity and mortality rates of CAD due to higher risk factors such as hypertension, obesity, metabolic syndromes and physical inactivity. Men have a higher prevalence of CAD than women before menopause, but after menopause the rates of CAD for both sexes are similar. 


The early pivotal event in atherogenesis is endothelial cell dysfunction (ED) due to the long-term presence of various cardiovascular risk factors, such as dyslipidemia, chronic uncontrolled hypertension causing shear stress, and uncontrolled diabetes mellitus, which cause non-enzymatic glycosylation of surface lipoproteins on endothelial cells. It is believed that ED causes endothelial nitric oxide synthase (ENOS) dysregulation which leads to decreased production of vasodilator nitric oxide (NO) and increased amount of superoxide which is oxidant. This imbalance between vasodilators (nitric oxide and histamine) and vasoconstrictive factors impairs vascular hemostasis which leads to increased turbulence, shear stress, and ED.

ED causes endothelial cell activation which leads to increased expression of adhesion molecules, activation of platelets and inflammatory cells, and increased permeability of endothelial cells; thus it promotes diffusion of lipids and transmigration of the adherent leukocytes in the presence of chemo-attractant cytokines secreted by inflammatory cells. Both innate and adaptive immunity are involved in atheroma formation. Innate immune cells, such as monocytes, and dendritic cells and adaptive immune cells, such as T lymphocytes, present antigen on their surface to dendritic cells in the interstitium and regional lymph nodes. Monocyte turns into macrophage when it reaches the intima. It engulfs the lipid and turns into lipid-laden foam cells. Activated macrophages, platelets, and dysfunctional endothelial cells produce growth factors which modulate early atherogenesis. These factors include transforming growth factors alpha and beta, thrombin, platelet-derived growth factor, insulin-like growth factor, and angiotensin II. The relative deficiency of endothelium-derived NO further potentiates proliferative stage of plaque maturation

The earliest morphological manifestation of atherosclerosis is fatty streaks which consist of lipid-laden macrophages, T lymphocytes, and smooth muscle cells (SMC). Fatty streaks go on to transform into fibrous plaque due to SMC activation. SMC secretes extracellular collagen matrix which forms the fibrous cap and stabilizes plaque. Due to ongoing inflammation, some macrophages die and releases lipids into extracellular space in the intima, resulting in a necrotic core. Matrix metalloproteinases (MMP) are protease enzymes which are secreted by SMC, and they are very crucial for plaque progression due to their role in extracellular matrix destruction. MMP is counteracted by tissue inhibitor of matrix metalloproteinase (TIMP) and statin drugs. The imbalance between MMP and TIMP can lead to the rupture of the fibrous cap due to excessive extracellular matrix destruction and subsequent activation of platelets and acute thrombosis which leads to a critical level of coronary occlusion. This compromises blood flow to the myocardium. It is manifested as angina to acute myocardial infarction, depending upon the level of arterial occlusion. The luminal obstruction must be between 50% to 70 % to cause flow limitation.

Plaque Remodeling

As the plaque progresses, two types of remodeling can occur: positive and negative.

Positive Remodeling

It is the outward growth of plaque due to underlying compensatory arterial dilation. It does not compromise blood flow, but due to the overburden of unstable plaque, it is at risk for plaque rupture and thrombosis which results in acute myocardial infarction. It does not present as stable angina symptoms because luminal diameters remain the same until plaque ruptures suddenly and presents with acute coronary syndromes.

Negative Remodeling

In this case, the plaque grows inwardly towards the vessel lumen thereby decreasing luminal diameter over time because there is no compensatory vascular dilation. As soon as the luminal obstruction is between 50% and 70%, blood flow to the myocardium is limited, and angina symptoms are more likely to develop. Plaque, in this case, is still at risk of rupture, so acute myocardial infarction can still occur.


According to Stary et al., atherosclerosis is classified in Roman numeral numbers in the sequence of lesion progression.

Type I: (initial) contains scattered isolated lipid-laden macrophage; also called foam cells.

Type II: consists of foam cells mainly in the form of layers; ialso called fatty streaks. 

Type III: is the intermediate stage lesion which contains foam cells in layers and scattered extracellular lipid droplets due to apoptosis of foam cells.

Type IV: consists of an extensive dense accumulation of extracellular lipid which is also termed as lipid core; also called atheroma.

Type Va: These lesions are also termed as fibro-atheroma, and it consists of the fibrous cap on top of atheroma. There is also smooth muscle cells present in an intimal layer which help in the deposition of the extracellular matrix of the fibrous cap. 

  • If fibro-atheroma has calcification, then it is termed as type Vb.
  • One particular type-V lesion in which a lipid core is absent and lipid, in general, is minimal may be referred to as type Vc.

Type VI : The disruption of the lesion surface leading to thrombosis or hemorrhage into lesion is a hallmark of this complicated lesion. These lesions are associated with high mortality and morbidity. Type VI may be subclassified by the superimposed features.

  • Disruption of the surface may be labeled as type VIa.
  • Hematoma or hemorrhage indicates type VIb.
  • Thrombosis indicates type VIc.
  • Type VIabc indicates the presence of all three features.


A major drawback of BMS is in-stent restenosis due to intimal layer injury. Neo-intimal hyperplasia (NIH) is the underlying phenomenon in which intimal injury leads to increase SMC migration and proliferation in the intimal layer thereby leading to restenosis. DES is designed to locally deliver antirestenotic drugs which act to block SMC migration and proliferation at stent site with no systemic adverse drug outcomes. The efficacy of the drug depends upon the diffusion rate, tissue accumulation, distribution, and local vascular toxicity. Thus, a balance should be achieved between adequate drug amount, delivery, and minimal local vascular toxicity. The rate of diffusion depends upon several factors, such as coating thickness, amount of drug loaded, a drug to polymer ratio, and partition coefficient (PC) of the drug. PC is directly proportional to the rate of diffusion.

Drug release has an initial fast phase due to the immediate dissolution of the drug from the outer most layer of the polymer coating. The fast-phase release has first-order kinetic, with the majority of the total available dose-released within the first few days. Later on, a sustained slower-release phase occurs, for the most part, due to slower diffusion-mediated release. The higher loading dose tends to have a greater release during the initial fast-release phase.

The hydrophobic, hydrophilic, or lipophilic nature of a drug also regulates the transport or distribution of the drug in arterial tissue. Hydrophilic drugs mix readily with blood and can distribute into and around local arterial tissue; therefore, there is lower local drug concentration. By contrast, hydrophobic drugs tend to distribute more towards the arterial tissue homogenously, leading to high drug accumulation in arterial tissue and slower clearance. Lipophilic drugs have a slower drug release rate.

Studies have shown that rapamycin and paclitaxel enhance the expression of prothrombotic factors such as tissue factor and plasminogen activator inhibitor-1. In the presence of local drug toxicity in the stent site leading to delayed re-endothelialization, the acidic byproducts (lactic acid and glycolic acid) of polymeric degradation and these prothrombotic factors can cause stent thrombosis due to platelet activation. It is more pronounced when antithrombotic drugs are withdrawn postoperatively. Hypersensitivity towards polymer coating has also been reported which also augments the stent site for chronic inflammation.[6][7][2]

History and Physical

Coronary atherosclerosis is an underlying pathology in ischemic heart disease. Coronary atherosclerosis is predominantly an asymptomatic condition. It starts at an early age, such as in the 20s, as fatty streaks, but it is clinically silent. It only becomes symptomatic once 50% to 70% of the luminal diameter is obstructed due to growing fibrous plaque, leading to end-organ ischemia or infarction. It can be due to the chronic stenotic lesion which grows towards luminal side without thrombus formation (angina) or plaque rupture with superimposed acute thrombosis (acute myocardial infarction).

Patients with symptomatic coronary artery disease present with signs and symptoms which are consistent with following conditions.

  • Stable angina
  • Unstable (prinzemetal) angina
  • Acute myocardial infarction (AMI) which consists of  ST elevation (STEMI) and Non- ST-elevation myocardial infarction (NSTEMI)
  • Sudden cardiac death
  • Chronic ischemic cardiomyopathy
  • Congestive heart failure (CHF)

The most common symptom associated with coronary artery disease is dull, squeezing, or pressure-like chest pain located in the sub-sternal or left side of the chest and radiating to the left arm, neck, or jaw. It may be associated with dyspnea and increased sweating. In stable angina, it is exertional in nature and relieved on resting for a while or ingestion of nitrates, while pain associated with unstable or AMI (STEMI and NSTEMI) occurs at rest. The pain of AMI is partially relieved with nitrates.

Physical Exam

The following signs can be noted in a patient with AMI.

  • Diaphoresis
  • Tachypnea
  • Dyspnea with crackles on lungs auscultation, orthopnea, and paroxysmal nocturnal dyspnea due to left ventricular infarct which leads to reduced LVEF and pooling of blood in lungs.
  • Hypotension or cardiogenic shock due to the following: (1) Left ventricular infarct with reduced LVEF. S3 can be heard on heart auscultation. (2) Right ventricular infarct leading to a decreased venous return to the left heart. The patient can have jugular venous distension (JVD) and pedal edema with normal lungs auscultation.
  • Mitral regurgitation murmur can be heard which is either functional or ischemic
  • Xanthoma/xanthelasma may or may not be present secondary to underlying dyslipidemia
  • Arrhythmias

On physical exam, tachycardia is common in a patient with AMI. While bradycardia can occur due to blockage of the right coronary artery branch which supplies sino-atrial node. Arrhythmias of different types also can be seen secondary to ischemia of myocardium. Acute ischemia or infarction causes hypoxia and depletion of intracellular adenosine triphosphate which shifts the cell to anaerobic glycolysis and lactic acid is accumulated inside the cell. This intracellular acidic environment lowers the PH and activates Na+/H+ and Na+/Ca++ ion exchange channels to dump H+ ion out of the cell and raise intracellular PH. This is accompanied by intracellular calcium overload and increased late sodium current. A lower resting membrane potential is generated in this manner which turns infarcted tissues more excitable and leads to arrhythmias. There are many types of ventricular tachyarrhythmias (VA) present after AMI such as non-sustained ventricular tachycardia (NSVT), sustained ventricular tachycardia (VT), or ventricular fibrillation (VFIB). VA is the most common cause of sudden cardiac death, occurring within 1 hour of AMI. Thrombolysis and percutaneous coronary intervention have reduced the incidence of VA and reduced the burden of SCD in over the past decades. The incidence of VA is directly proportional to the size of an infarct and inversely related to the left ventricular ejection fraction after AMI. 


  • Complete Blood Count (CBC): Anemia can present with chest pain and dyspnea due to the decreased oxygen content of blood.
  • Thyroid Function Test (TSH and fT4): Hyperthyroidism can cause palpitation, arrhythmias or chest pain.
  • Fasting Lipid Profile: Triglyceride, total cholesterol, and low-density lipoproteins (LDL).
  • Electrocardiogram (EKG): Stable angina can give nonspecific T wave abnormalities to T wave flattening or inversion. In STEMI, ST segment can be elevated. Thus it helps to diagnose the condition. NSTEMI is not diagnosed on EKG.
  • Cardiac Enzymes: Creatine kinase such as MB isozymes (CKMB), troponins and lactate dehydrogenase (LDH) is diagnostic for AMI. Troponins are more specific than others, but CKMB is diagnostic for re-infarction cases because its level starts to rise in blood within 4 to 6 hours after AMI, like troponins, peak level is achieved in 12 to 24 hours after AMI, but CKMB level drops to baseline after 36 hours. This is why CKMB is more specific to diagnose re-infarction.
  • Echocardiography: It uses sound waves and creates an image of the heart chambers. It can comment on heart chamber size, wall thickness, wall motion abnormalities, left ventricular ejection fraction (LVEF), and valve structure and function accurately.
  • Exercise tolerance test (ETT): ETT can diagnose the patients with symptomatic coronary artery disease with baseline EKG abnormalities or situations in which coronary artery disease cannot be diagnosed on history alone.
  • Coronary angiography: An iodine-containing contrast agent is injected by a catheter placed at the ostium of coronary arteries and pictures are taken under fluoroscopy to detect flow limitation. Actual plaque burden cannot be documented by angiography because it only shows blood flow. To solve this riddle, intravascular ultrasonography (IVUS) is used.
  • Intravascular ultrasonography (IVUS): IVUS can accurately comment on a plaque with positive remodeling which grows outwardly, but vessel lumen is not stenosed much. IVUS demonstrates presence or absence of a fibrous cap, calcification and ulceration, or cracks on plaque surface. 
  • Doppler Velocity Probes: Atherosclerotic plaque can also be classified as mild, moderate or severe on the basis of coronary flow reserve by using Doppler velocity probes.

Treatment / Management

Coronary artery atherosclerosis remains undiagnosed mostly due to the chronic progression of plaque until it is a significant lesion that limits blood flow. Patients are diagnosed with coronary atherosclerosis after they have a cardiac event. The management goals for these patients are to alleviate symptoms of CAD and to prevent future cardiac events such as angina pectoris, AMI, or death due to a cardiac cause. These goals are achieved by controlling the modifiable risk factors with diet and lifestyle modification and medical management. Risk factors include hypertension, diabetes mellitus, and dyslipidemia. Medical therapy includes nitrates, beta blockers, statins, aspirin, calcium channel blockers and last, but not least, ranolazine. AMI is treated definitely with revascularization by medical or surgical interventions such as thrombolytics or angioplasty with stenting or coronary artery bypass grafting.[8][9][10][11]

Differential Diagnosis

Chest pain is the most common symptom of symptomatic coronary artery disease. Others causes of chest pain should also be ruled out while making the correct diagnosis.

  • Unstable angina
  • Acute myocardial infarction (ST elevation and Non-ST elevation)
  • Aortic dissection
  • Takotasubo cardiomyopathy
  • Vasculitis (Kawasaki Disease in children)
  • Acute pericarditis
  • Myocarditis
  • Gastro-esophageal reflux disease (GERD)
  • Pleuritis
  • Costochondritis
  • Pulmonary embolism


CAD remains the number one cause of death for men and women worldwide. In the United States, around 1.5 million Americans suffer from AMI annually, and one-third of these die. Survivors of AMI have a poor prognosis with a 1.5 to 15 times greater risk of mortality and morbidity than the rest of the population. Historical figures among survivors of AMI show that 25% of the men and 38% of women die within 1 year after having an AMI, 18% of men and 34% of women have a second MI within 6 years of AMI, and 22% of men and 46% of women are diagnosed with CHF due to ischemic cardiomyopathy.

The prognosis depends on the following factors:

  • Presence of angina symptoms
  • Left ventricular ejection fraction
  • Number, location, and extent of coronary artery involvement
  • Coronary revascularization status
  • Cardiac arrhythmias
  • Compliance with medical therapy
  • Aggressive risk control 


Coronary artery disease has following complications.

  • Angina pectoris
  • Sudden cardiac death
  • Congestive heart failure due to ischemic cardiomyopathy
  • Ventricular arrhythmias
  • Pulmonary edema due to reduced LVEF
  • Mechanical complication of AMI such as ventricular free wall rupture leading to cardiac tamponade, interventricular septal rupture.


Consultation with the following personnel is mandatory to manage CAD effectively.

  • Cardiologist
  • Cardiothoracic surgeon
  • Interventional radiologist
  • Cardiac rehabilitation specialist team
  • Nutritionist

Deterrence and Patient Education

Ischemic heart disease (IHD) is the most common cause of death globally. The most cost-effective and clinically significant way of reducing the burden of IHD is primary prevention. Education of the general population regarding a healthy lifestyle, dietary habits, and regular exercise has been shown to reduce the prevalence of IHD. A recent study suggests that education based interventions may improve health-related quality of life. Patients with IHD should be counseled on compliance with medications and lifestyle modifications to alter their risk factors' impact on cardiac health. The patient also should be encouraged to avoid cigarette smoking, eat a low-fat diet that is rich in fruits and vegetables, and exercise regularly. The patient should be counseled to avoid over-exertion. They can resume sexual activity 4 weeks after an AMI event but should not have angina symptoms during sexual activity. Patients should be counseled to join support groups. According to a recent study, women are more likely to benefit from women-only groups while men may prefer to have a mixed-gender group.

Enhancing Healthcare Team Outcomes

Even though there are several treatments for people with ischemic heart disease, the primary care provider and nurse practitioner should emphasize prevention. The most cost-effective and clinically significant way of reducing the burden of IHD is primary prevention. Education of the general population regarding a healthy lifestyle, dietary habits, and regular exercise has been shown to reduce the prevalence of IHD. A recent study suggests that education based interventions may improve health-related quality of life. Patients with IHD should be counseled on compliance with medications and lifestyle modifications to alter their risk factors' impact on cardiac health. The patient also should be encouraged to avoid cigarette smoking, eat a low-fat diet that is rich in fruits and vegetables, and exercise regularly. The patient should be counseled to avoid over-exertion. They can resume sexual activity 4 weeks after an AMI event but should not have angina symptoms during sexual activity. Patients should be counseled to join support groups. According to a recent study, women are more likely to benefit from women-only groups while men may prefer to have a mixed-gender group.


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