LUB-dup, lub-dup ... your heart beats 60 to 90 beats per minute for every minute of your life, even though you are unaware of it most of the time.

In terms of survival, it is the most important organ of ourmr body. It cannot stop, even for a minute, without major consequences to our wellbeing.

While we know that the heart is the primary supplier of oxygenated blood to the body, we tend to forget that the heart itself also needs to be supplied with blood to function.

Blood goes to the heart via three major blood vessels, known as the coronary arteries. They are: the right coronary artery, the left anterior descending coronary artery, and the left circumflex artery, which goes around the heart to its back.

National Heart Institute (also known by its Malay acronym IJN) chief executive officer Tan Sri Dr Robaayah Zambahari likes to think of blood vessels as pipes. "If they are clear, they will flow smoothly. Once there are deposits, there will be narrowings or blockages - medically, it is called stenosis.

"If there are blockages, the blood cannot flow through, and the heart muscles that it supplies will be deprived of oxygen and nutrients," she explains.

Amazingly, our heart muscle can still function with only 10% of blood getting through the blood vessel that supplies it (i.e. a 90% blocked artery).

In this situation, Dr Robaayah says that "you will be okay on rest, but when you exert yourself, you will get symptoms like your heart thumping, which is known as palpitations, shortness of breath, chest pain, etc."

According to Dr Robaayah, who is also a senior consultant cardiologist, autopsies done on soldiers who died in battle have shown that the "deposits" in our blood vessels are already present in our 20s. They start off as fatty streaks, which consist of immune cells, platelets, smooth muscle cells and cholesterol droplets, and are a result of internal injury to the blood vessel wall.

Some of these fatty streaks progress on to form fibrous plaques, which, in addition, to the contents of the fatty streak, also contain connective tissues like collagen and elastin. These fibrous plaques usually protrude into the lumen (or central tube) of the artery, and obstruct blood flow.

According to Dr Robaayah, this can cause up to 60% narrowing of the lumen.

The fibrous plaques also contribute to the hardening, or loss of elasticity, of the blood vessel. The plaques themselves are prone to rupturing, particularly in those arteries that are subject to high blood flow.

Once a plaque ruptures, a blood clot or thrombus will form on the ruptured area to close off the injury and enable it to repair itself. However, the thrombus itself takes up more space and contributes to the blockage of the blood vessel.

With the addition of the thrombus, the fibrous plaque has now progressed to a complicated plaque.

Complicated plaques can also be caused by the accumulation of calcium, particularly in older people, or an emboli, which can be any free-floating object within the blood that eventually gets stuck within a blood vessel.

The formation of a complicated plaque is likely to mean that the artery is now occluded up to at least 80%, says Dr Robaayah.

And while most fibrous plaques tend to form after the age of 40, she says that the process is accelerated in those with risk factors like being overweight, having an unhealthy diet, inadequate exercise, and having conditions like diabetes, high blood pressure (hypertension) and high cholesterol levels.

"We cannot cure this disease, but we can slow the progress by decreasing the risk factors," she says. This includes living a healthy lifestyle by exercising and eating right, as well as treating medical conditions that increase the risk of coronary artery disease (CAD).

Treatment with stents

However, for those who are already experiencing the symptoms of CAD, or who have had a heart attack, more needs to be done.

The usual procedure to see how much, and how many, coronary arteries are blocked is coronary angiography. In this imaging method, a catheter is inserted through the femoral artery at the patient's upper thigh, and is passed through the artery all the way up to the coronary arteries. Once there, the doctor will inject a dye into the arteries, so that any blockages will show up on the x-rays he will take.

Usually, arteries that are over 60% blocked will have to be reopened.

While coronary artery bypass graft surgery is an option and may be the only choice in certain cases, the less invasive method in current use is percutaneous coronary intervention (PCI). (Refer to The PCI procedure.) PCI takes advantage of the fact that the plaques are elastic, and can be compressed to restore the original space of the lumen.

The procedure is similar to angiography, but this time, the catheter carries a deflated balloon and collapsed stent with it. Once the catheter reaches the narrowed spot, the balloon is inflated to compress the plaque.

The stent, which is a metal structure, is also expanded along with the balloon, and is left behind after the procedure to hold the artery open.

Dr Robaayah explains: "The balloon opens up the vessel, but it is elastic, so after awhile, it will collapse. So you need to put in a scaffolding, that is, a wire mesh, to keep it open."

The evolution of stents

The first generation of stents were just metal devices made out of stainless steel, and were known as bare metal stents (BMS). While they did their intended job of compressing the plaques just fine, a problem arose because the body identified the stent as a foreign object and worked against it.

This meant that cardiologists had to prescribe medication to patients to halt the rejection process.

Dr Robaayah says: "We call it the dual anti-platelet therapy (DAPT), to prevent clotting inside the stent." She adds that patients are usually given aspirin, and either clopidogrel or ticlopidine, for a month.

However, another problem was discovered over time.

"But there was also cell growth on the stent," says Dr Robaayah. "In 20-30% of cases, there was excessive cell growth on the stent, leading to restenosis of the artery."

She likened the cell overgrowth, which consists of smooth muscle cells, to the formation of keloids, or an overgrown scar, on the skin.

"So research found a way of preventing the excessive cell growth by putting a drug on the stent."

This resulted in the second generation of stents known as drug-eluting stents (DES). The drugs on these stents - usually a version of sirolimus or paclitaxel - are released into the blood stream, either directly or through timed release.

However, Dr Robaayah says: "Then we have another problem; we have prevented excessive cell growth, but in some cases, the drug is so effective, it completely stops the cell growth, meaning that blood will come into contact with the stent, causing blood clots."

She adds: "So now, we have a new 'enemy'. With DES, we have incidences of drug thrombosis - up to 40% if they stop taking the medication (DAPT). Even if they take the medication, there is still a chance of blood clots.

"So with DES, there is decreased restenosis, but increased blood clotting, especially if the patient stops the medication, or needs to stop it because they need other surgical procedures, for example, tooth extraction."

Because the DAPT works to prevent blood from clotting, this means that patients on it take a longer time to stop bleeding compared to the norm.

Compliance to the one-year regime of DAPT for patients with DES is very important.

"The problem of stent thrombosis occurs if the patient does not take their medication, or forgets to take it, for example, because they feel well," says Dr Robaayah.

Because of this, various drug companies have put time and effort into developing new types of stents that can help overcome this problem.

Latest developments

One of the third generation of stents in the market is the Genous stent. Instead of being coated with a drug, the stent is covered with antibodies that are specific to endothelial progenitor cells.

As Dr Robaayah explains it, "Endothelial progenitor cells (EPCs) produced by the bone marrow, circulate in the body. The new stents have antibodies that 'trap' the EPCs onto the stent. There, the EPCs differentiate into endothelial cells - the same as those lining the inside of the blood vessel - to form a few layers on the stent. This occurs rapidly - just over 72 hours."

She adds that theoretically, this means that not only will the stent not be so exposed to the blood in the artery (and thus, decrease the incidence of blood clots), but also, the endothelial cells will prevent the excessive overgrowth of smooth muscle cells faced by BMS.

Equally important, patients with the Genous stent need only take the DAPT for one month, thus, minimising the risk of non-compliance, as well as allowing them to undergo other surgical procedures quickly, if necessary.

IJN is also involved in the international multi-centre clinical trials of at least two fourth generation stents. (See table)

Local trends

In Malaysia, Dr Robaayah says that all types of stents are still being used. "Cost is an issue," she says, when explaining why local cardiologists still implant BMS.

A bare metal stent costs around RM2,000 (S$840), whereas a drug-eluting stent and the Genous stent can cost between RM6,000-8,000.

She adds however, that a BMS is usually only considered for large vessels, which have lots of space to accommodate narrowing without compromising blood flow too much.

DES are currently the preferred stent for PCI, she says, while the Genous stent is recommended for patients who are likely to need surgical procedures, and those who are likely to forget to take their medication.

She also strictly emphasised that despite undergoing PCI, all patients need to change their unhealthy lifestyle habits and adhere strictly to any medication regime they might have, or else their arteries will only start narrowing again.