Author Archives: laprimaadmin

Coronary heart disease is a major cause of death and disability in developed countries including Malaysia. Stent implantation has become an efficacious treatment for a culprit lesion vessel of the coronary artery. However, 10%–20% restenosis is still an important complication that restricts the clinical safety and efficacy of drug-eluting stents. In-stent restenosis may lead to the recurrence of major cardiovascular adverse events, including angina pectoris, acute myocardial infarction, and even sudden cardiac death. These events are currently serious problems that occur after coronary stent implantation. Malaysia Clinical physicians face a difficult choice for in-stent restenosis treatment. Recent studies indicate that a drug-coated balloon has promising clinical efficacy similar to the drug-eluting stents for treating coronary in-stent restenosis.

Coronary heart disease (CHD) has become the “first killer” that endangers human health. CHD weakens the heart muscle and leads to heart failure and arrhythmias. Percutaneous coronary intervention (PCI) helps in recovering the coronary flow and has become an efficacious treatment for revascularization of the blocked coronary artery.

PCI includes percutaneous transluminal coronary angioplasty (PTCA), stent implantation, and drug-coated balloons (DCBs). The rapid development of stent bioengineering technology and drug carriers has improved the safety and efficacy of stent treatment. Compared with PTCA in which restenosis occurs at the rate of up to 50%, the rate of in-stent restenosis (ISR) in patients with drug-eluting stents (DESs) decreased significantly; however, 10%–20% restenosis is still a major complication, restricting the clinical safety and efficacy of DESs. ISR may lead to a recurrence of major adverse cardiovascular events (MACEs), including angina pectoris, acute myocardial infarction, and even sudden cardiac death.

No stents were available in the early 1970s. Although balloon dilation could reduce coronary artery stenosis, owing to the property of elastic recoil and intimal tear of the vessel wall, vascular restenosis may reoccur again. The vascular retraction rate after simple balloon dilatation angioplasty was as high as 30% to 60% 3 to 6 months postoperatively. In the 1980s, the emergence of bare-metal stents (BMSs) led to a 30% incidence of restenosis. Recent DESs combined with antiproliferative drugs, such as paclitaxel and sirolimus, reduced the incidence of ISR to less than 10%. Although the incidence of ISR is gradually declining, still it cannot be completely prevented.

Although ISR is much less common with the use of DESs than BMSs, the number of stents implanted in interventional practice means that the treatment of ISR remains an important clinical challenge. Malaysia Clinical physicians face a difficult choice for ISR treatment. Accumulative evidence indicates that drug-coated balloon (DCB) angioplasty, as a similar new DES treatment for coronary ISR, have been considered as an alternative option for treating coronary ISR, avoiding repeated stenting after ISR that leads to expose the patient to cost and risk of a prolonged DAPT. Therefore, in this study, we highlight the progress of coronary intervention and the use of DCBs in the treatment of ISR.

In-Stent Restenosis

ISR is defined as new proliferative lesions of more than or equal to 50% of the lumen diameter, involving either the stent segment or adjacent 5 mm segments on both sides of the stent by coronary angiography (CAG). After a successful PCI procedure, coronary stents can fail to maintain vessel patency as a result of either restenosis or thrombosis; restenosis is a gradual re-narrowing of the stent segment that mostly occurs between 3 and 12 months after stent implantation. Restenosis usually presents as recurrent angina but can present as an acute myocardial infarction in approximately 10% of patients. Restenosis can usually be managed by repeat percutaneous revascularization.

The patterns of ISR lesions can be divided into two broad categories: focal—lesions localized within the stent that are <10 mm in length are said to be Type I lesions and can be focal single or focal multiple—and diffuse—diffuse lesions are >10 mm in length and may or may not be confined to the edges of the stent. Type II diffuse lesions are confined to the stent edges, Type III diffuse lesions overhang the stent edges, and Type IV diffuse lesions completely occlude the stent.

Pathology of In-Stent Restenosis

Restenosis was understood to be the result of exuberant smooth muscle cell proliferation and macrophage infiltration inside the stent. Arterial vessels are abundant in elastic fibers that provide vessels with recoiling properties after they are distended by any means. Recoiling occurs within seconds to minutes after the procedure. ISR is mainly caused by neointimal hyperplasia, which occurs in response to local arterial injury sustained during PCI, leading to complex inflammatory and reparative processes. Neointimal hyperplasia first develops as damage to the arterial wall, followed by platelet aggregation at the site of the injury, recruitment of inflammatory cells, proliferation and migration of vascular smooth muscle cells, and collagen deposition.

Deployment of a stent at the lesion site requires inflation of a balloon apposing it in approximation with the vessel wall, thereby stretching the plaque and vessel wall layers. Intima and media tears give rise to a complex inflammatory response; this phenomenon, via multiple mechanisms, can lead to excessive neointimal proliferation, thereby decreasing the minimal luminal diameter (MLD). Neointimal proliferation is a process by which smooth muscle cells and myofibroblasts are mobilized from the media and adventitia of vessel walls, respectively. Redistribution and overgrowth of smooth muscle cells on stent struts cause luminal loss. This process takes months and is almost complete at 6 months; after 6 months, there is a shift in the cellular distribution that causes the collagen and proteoglycan matrix to become the major component of the growing lesion. Interestingly, this shift in cellularity leads to a relative decrease in late luminal loss as a result of the shrinkage in the lesion width. This process occurs from 6 months to 3 years.

Evidence-Based Practice of Treating ISR Using DCBs

The treatment options for ISR include PCI with DESs, DCBs, or PTCA. DCBs and second-generation DESs were equally effective in treating coronary ISR, according to a new systematic review and meta-analysis. Paclitaxel and rapamycin analogues have been proven successful in preventing neointimal hyperplasia and ISR. Different characteristics of these agents may affect their clinical efficacy. Paclitaxel is a diterpenoid compound isolated from the Pacific yew tree. Due to its high lipophilic characteristics, paclitaxel promotes rapid cellular uptake. Paclitaxel inhibits mitotic progression and cell proliferation in the G0-G1 and G2-M phases of the cell cycle. Sirolimus, a rapamycin analogue, forms a complex with the cytosolic immunophilin, FK506 binding protein-12, which in turn blocks the activation of the cell-cycle-specific kinase, mammalian target of rapamycin (mTOR). mTORC1 regulates translation, transcription, cell cycle progression, and survival through the phosphorylation of p70 56 kinase and 4E-BP1.

Drug-coated balloon angioplasty is similar to plain old balloon angioplasty, with the addition of an antiproliferative medication coating on the balloon, which helps reduce and prevent restenosis. The drug coating comprises an active drug and a carrier. The active drugs are paclitaxel and rapamycin. The current DCB prevents the premature release of drugs before the balloon catheter is positioned at a target site and promotes the drugs that are quickly released from the surface of the balloon and absorbed by the target tissue. DCBs were used to treat coronary ISR. Recent clinical trials on DCBs are summarized in Table 1. Scheller et al. reported that a paclitaxel-eluting balloon (PEB) significantly reduced the incidence of ISR compared with POBA in porcine coronary arteries. In a study by Scheller et al., the LLL of PEBs was significantly lower than that of POBA by CAG after 6 months of follow-up; the incidences of ISR and MACEs were also significantly lower than that of POBA. Furthermore, long-term follow-up results also showed a good therapeutic effect with PEBs.

Should you need any further information, please do not hesitate to contact [email protected].

Table 1

Source: Zhang DM, Chen S. In-Stent Restenosis and a Drug-Coated Balloon: Insights from a Clinical Therapeutic Strategy on Coronary Artery Diseases. Cardiol Res Pract. 2020 Oct 25;2020:8104939. doi: 10.1155/2020/8104939. PMID: 33163230; PMCID: PMC7605950.

What is Restenosis?

Restenosis means that a section of blocked artery that was opened up with angioplasty or a stent has become narrowed again.

There are many treatment options in Malaysia for patients who have restenosis after receiving a stent. The first step in treatment is meeting with an experienced cardiac interventionist (a doctor who performs procedures to open up clogged arteries). The doctor can determine the best type of treatment based on the location of the blocked stent, how badly it is blocked, and information about the patient (such as age, type of cardiovascular disease, and other medical conditions). The doctor will perform a catheterization and can use tests during the procedure to get more information about the blockage by looking inside the artery. These tests include intravascular ultrasound (IVUS) and optical coherence tomography (OCT).

MANAGEMENT AND TREATMENT

What are the treatment options for in-stent restenosis?

Re-stenting

If an interventional procedure is needed, the approach will vary depending on if the original stent(s) were fully expanded, how many stents are overlapped, and the length of the re-blockage.

Non-Surgical Options It is possible that the stent was not put in place correctly or that it did not expand the way it should have. An IVUS or OCT can help check to see if either of those problems exist. If so, sometimes the solution is simply re-expanding the stent. This can be done with a high pressure balloon (sometimes assisted by laser to loosen up the firm tissue around the stent). If the stent was well-expanded and the problem is tissue regrowth inside the stent, the best treatment option is often placement of another drug-eluting stent (DES). However, the risk of reblockage increases with the number of overlapping stents. If 2-3 stents are already in place, we usually recommend brachytherapy or occasionally drug-eluting balloon use. Shorter blockages tends to respond better to all of these approaches.

 Please contact [email protected] if there are any questions

Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup, a condition known as atherosclerosis.

Why is it done?

PCI improves blood flow, thus decreasing heart-related chest pain (angina), making you feel better and increasing your ability to be active. PCI is usually scheduled ahead of time.

What is done?

1. A catheter is inserted into the blood vessels either in the groin or in the arm.

2. Using a special type of X-ray called fluoroscopy, the catheter is threaded through the blood vessels into the heart where the coronary artery is narrowed.

3. When the tip is in place, a balloon tip covered with a stent is inflated.

4. The balloon tip compresses the plaque and expands the stent.

5. Once the plaque is compressed and the stent is in place, the balloon is deflated and withdrawn.

6. The stent stays in the artery, holding it open.

Before the procedure:

1. Shortly before your procedure, you may receive a sedative to help you relax. 2. Hair in the groin area around where the catheter will be inserted may be clipped.

3. An intravenous (IV) line is inserted so, if necessary, you can be given medications quickly.

4. Electrodes will be placed on your body to monitor your heart, and a small device called a pulse oximeter may be clipped on a finger or ear to track the oxygen level in your blood.

During the procedure:

1. Most PCIs are conducted with the patient sedated but not asleep.

2. You will lie on your back on a procedure table.

3. A local anaesthetic will be injected into the skin at the site where the catheter will be inserted.

4. Once it has taken effect, the catheter will be inserted into the blood vessels.

5. You may feel a brief sting or pinch as the needle goes through the skin and some pressure within the artery as the catheter is moved. If you are uncomfortable, tell your doctor and if necessary additional pain medication may be given.

6. When the catheter reaches the heart, the contrast dye will be released so the area where the blood vessel is narrowed can be identified.

7. When the dye is released, you may feel a brief flushing sensation or feeling of warmth. Some people experience a salty or metallic taste in the mouth, or a brief headache. A few people may feel nauseated or even vomit, but this is rare. These effects are harmless usually last for only a few minutes.

9. When the narrowing is located, the catheter will be advanced so the special tip can be activated.

10. It is possible to experience some chest pain or discomfort at this point, but your doctor will monitor you carefully and the discomfort should go away quickly.

11. When finished, the catheter will be withdrawn and pressure put on the insertion site to stop the bleeding.

12. Once the bleeding has stopped, a tight bandage will be applied.

13. You will need to remain lying flat during this time.

14. If the catheter was inserted in the groin, you will have to keep your leg straight for several hours.

15. If it was inserted in the arm, your arm will be kept elevated on pillows and kept straight with an arm board.

After the procedure:

1. You will probably go to a recovery room for several hours of observation.

2. You will be asked to remain in bed for 2 to 6 hours, depending upon your specific condition.

3. Pain medication may be given if you experience any discomfort.

4. You will be encouraged to drink water and other fluids to help flush the contrast dye from your body.

5. Most people spend the night in hospital after a PCI.

Should you need any further information, please do not hesitate to contact [email protected].

The ideal treatment for ischemic coronary artery disease (CAD) remains a subject of debate. The two primary revascularization modalities are coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI). Throughout this article, we discuss the history, indications, applications and outcomes of these revascularization procedures. Both PCI and surgical revascularization are advancing rapidly, and it is likely that such advances will continue in the years to come.

Several studies have shown that mechanical revascularization by either CABG or PCI is more effective in relieving angina and improving quality of life.

The ORBITA (Objective Randomised Blinded Investigation with optimal medical Therapy of Angioplasty in stable angina) trial randomized PCI with placebo in patients with stable coronary artery disease due to single-vessel CAD in the presence of moderate angina. This study outlined that symptomatic relief in that cohort might be at least partly due to placebo effect and, importantly, it emphasized the role of optimal medical therapy (OMT).

While bioabsorbable stents have not lived up to the promise and have been pulled out of the market, bioabsorbable stents continue to hold promise. Bioabsorbable magnesium stents are being evaluated. The advantages of biodegradable polymers include high drug-loading capacity, controlled long-term drug release, and full degradation of the polymer over a defined period, resulting in full release of the drug during a well-controlled time interval.

Thromboresistant polymer coatings based on biologic substances such as fibrin, collagen, hyaluronic acid, and biologic oils are being tested. These polymers serve as drug delivery reservoirs for drugs that inhibit neointimal hyperplasia through suppression of platelet activation and the inflammatory response and through inhibition of smooth muscle cell migration and proliferation.

The effect of variable dose and release kinetics of drugs on neointimal hyperplasia is also being studied. Multiple drugs may be delivered at timed intervals through newly designed stents.

Gene-eluting stents are undergoing experimental and clinical trials; these will be usable either alone or in conjunction with other drug-eluting stents (DESs) and may further reduce in-stent restenosis (ISR). The ABSORB trial studied the safety of the bioabsorbable everolimus-eluting stent. At 2 years, the stent was bioabsorbed, with vasomotion restored and restenosis prevented, and was clinically safe, suggesting freedom from late thrombosis.

The TRITON-TIMI 38 trial showed that in patients with acute coronary syndromes with scheduled PCI, prasugrel therapy was associated with significantly reduced rates of ischemic events, including stent thrombosis, but with an increased risk of major bleeding, including fatal bleeding. Overall mortality did not differ significantly between treatment groups. Prasugrel has been approved by the US Food and Drug Administration (FDA). Other antithrombotics are in the pipeline.

Most acute coronary syndromes are caused by rupture of unstable plaques of mild-to-moderate stenosis (< 50%). Stenting of such vulnerable lesions might result in stabilization and prevention of plaque rupture. Likewise, rapid advances have been made in surgical techniques. In the future, PCI and CABG may come to be seen as complementary techniques for myocardial revascularization.
Please let me know if you have any questions [email protected].

Source: Arun Kalyanasundaram, MD, MPH Interventional Cardiology Fellow, Department of Cardiology, Cleveland Clinic

Coronary artery disease is the build-up of plaque in the arteries that supply oxygen-rich blood to your heart. Plaque causes a narrowing or blockage that could result in a heart attack. Symptoms include chest pain or discomfort and shortness of breath. Treatments include lifestyle changes and medications that target your risk factors and/or possibly surgery.

Coronary arteries are the blood vessels that supply oxygen-rich blood to your heart muscle to keep it pumping. The coronary arteries are directly on top of your heart muscle. You have four main coronary arteries:

• The right coronary artery.
• The left coronary artery.
• The left anterior descending artery.
• The left circumflex artery.

Coronary artery disease is caused by atherosclerosis. Atherosclerosis is the build-up of plaque inside your arteries. Plaque consists of cholesterol, fatty substances, waste products, calcium and the clot-making substance fibrin. As plaque continues to collect on your artery walls, your arteries narrow and stiffen. Plaque can clog or damage your arteries, which limits or stops blood flow to your heart muscle. If your heart does not get enough blood, it can’t get the oxygen and nutrients it needs to work properly. This condition is called ischemia. Not getting enough blood supply to your heart muscle can lead to chest discomfort or chest pain (called angina). It also puts you at risk for a heart attack.

Coronary artery disease happens in everyone. The speed at which it develops differs from person to person. The process usually starts when you are very young. Before your teen years, the blood vessel walls start to show streaks of fat. As plaque deposits in your artery’s inner walls, your body fights back against this ongoing process by sending white blood cells to attack the cholesterol, but the attack causes more inflammation. This triggers yet other cells in the artery wall to form a soft cap over the plaque.

This thin cap over the plaque can break open (due to blood pressure or other causes). Blood cell fragments called platelets stick to the site of “the injury,” causing a clot to form. The clot further narrows arteries. Sometimes a blood clot breaks apart on its own. Other times the clot blocks blood flow through the artery, depriving the heart of oxygen and causing a heart attack.

Symptoms of Coronary Artery Disease

You may not know you have coronary artery disease since you may not have symptoms at first. The buildup of plaque in your arteries takes years to decades. But as your arteries narrow, you may notice mild symptoms that indicate your heart is pumping harder to deliver oxygen-rich blood to your body. The most common symptoms are chest pain or shortness of breath, especially after light physical activity like walking upstairs, but even at rest.

Sometimes you won’t know you have coronary artery disease until you have a heart attack. Symptoms of a heart attack include:

• Chest discomfort (angina) described as heaviness, tightness, pressure, aching, burning, numbness, fullness, squeezing or a dull ache. The discomfort can also spread to or only be felt in your left shoulder, arms, neck, back or jaw.
• Feeling tired.
• Dizziness, lightheadedness.
• Nausea.
• Weakness.
• Symptoms of a heart attack in women can be slightly different and include:
• Discomfort or pain in the shoulders, neck, abdomen (belly) and/or back.
• Feeling of indigestion or heartburn.
• Unexplained anxiety.
• Cold sweat.

Procedures and surgery

Interventional procedures are nonsurgical treatments to get rid of plaque buildup in the arteries and prevent blockages. Common procedures are balloon angioplasty and stenting. These procedures are done with a long, thin tube called a catheter. It is inserted into an artery in the wrist or the top of the leg through a small incision and guided to the blocked or narrowed area of the artery. The balloon widens the diameter of the artery to restore blood flow to the heart. A stent (a small metal spring-like scaffold) is left in place to keep your artery open.

Coronary artery bypass graft (CABG) surgery involves creating a new path for blood to flow when there is a blockage in the coronary arteries. In most cases, the surgeon removes blood vessels from your chest, arm or leg, and creates a new pathway to deliver oxygen-rich blood to the heart.

If traditional treatment options are not successful, your cardiologist may recommend other treatment options, such as enhanced external counterpulsation (EECP). In this procedure, inflatable cuffs (like blood pressure cuffs) are used to squeeze the blood vessels in your lower body. This helps improve blood flow to the heart and helps create natural bypasses (collateral circulation) around blocked coronary arteries. Enhanced external counterpulsation is a possible treatment for those with chronic stable angina who can’t have an invasive procedure or bypass surgery and don’t get relief from medication.

If you require any further information, feel free to contact us at [email protected].