Coronary Artery Disease (CAD) is the leading cause of death in most developed and developing countries. Many patients that once developed heart artery blockages would eventually go on to have a heart attack. And if they survived the first one, they would eventually succumb to the ones that came after that. Medicines like statins that could decrease the buildup of fat inside the arteries were not discovered until a few decades ago and the general use of aspirin to prevent heart attacks had not been established.

The big question is of course why heart attacks kill. There are three major ways that a heart attack can kill a person. It all starts with a particular heart artery getting completely blocked up leading to a part of the heart muscle dying from lack of blood. In younger people, it can happen suddenly. In older people, a complete blockage is often preceded by the warning signs like angina or chest pain on exertion or even at rest.

The first way a heart attack kills is by creating a fast and irregular heart rhythm. Normally the heart beats at a regular rate of between sixty and ninety beats a minute. The damaged heart tissue produces a short circuit in the electrical system of the heart due to which the pumping chamber of the heart starts beating three or four hundred times in a minute (ventricular fibrillation-VF). When that happens, the heart can no longer supply blood to the body. The person will become unconscious and ‘brain death’ will occur within a few minutes. The heart itself will also eventually stop working because it cannot even supply itself either.

Most people that die suddenly die because of this. If a person becomes suddenly unconscious and no pulse that can be felt, the reason is often VF and cardio-pulmonary resuscitation (CPR) done by paramedics or others can keep the person alive especially if an electrical ‘defibrillator’ is available to provide a high energy shock to the chest that can often disrupt the short circuit and return a normal heart beat. This might allow the person to survive the heart attack. It is for this reason that defibrillators are now placed in many public places like airports, railway stations and other public places.

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The next reason why people die after a heart attack is because so much of the heart muscle has been damaged that the heart cannot effectively pump enough blood. Many people survive after major heart attacks but eventually they will continue to get worse and die from inadequate heart function. A rough measure of heart function is ejection fraction (EF). Normally a heart pushes out close to two thirds (66 per cent) of the blood in it during every heartbeat. This translates to a 66 per cent EF. Once enough heart muscle has been damaged that the EF goes down to around twenty per cent or lower, the heart will start to fail. The only treatment then is a mechanical heart assist device and eventually a heart transplant.

The third reason why heart attacks kill is because of a rupture of the damaged heart muscle leading to the blood pooling around the heart and preventing it from filling and emptying properly. Ruptures can also involve the wall separating the two pumping chambers or the muscles that hold the heart valves in place. Some such patients might survive long enough to get to a hospital and undergo surgery to repair these problems.

Modern treatment of CAD really started in 1960 when Mason Sones, a cardiologist at the Cleveland Clinic accidentally injected a radiopaque dye into a coronary artery while planning to inject that dye only into the aorta -- the big artery above the heart from where the coronary arteries arise. The patient survived and Sones was able to get a picture of the inside of the coronary artery.

That started ‘selective’ coronary angiography which could provide a clear picture of the inside of the arteries and the site and nature of the blockages present. Important to remember here that the largest coronary artery is no bigger than a lead pencil and the average coronary artery is the size of the lead inside the pencil.

Read also: Heart disease-II

Within a few years cardiac surgeons started performing operations that could bring blood to the arteries beyond the blockage. Initially one end of a vein from the leg was sewn in to the aorta and the other end was sewn in to the coronary artery beyond the blockage (Coronary Artery Bypass Graft-CABG-cabbage). An early innovation was to separate an artery running inside the breast bone (Internal Mammary Artery-Internal Thoracic Artery- IMA/ITA) and sew the lower end into the artery beyond the blockage.

Many coronary arteries and their branches can thus be bypassed during the same operation. By the nineties, millions of these operations had been performed all over the world. And yes, over my professional career I have performed quite a few of them myself and I have done as many as six or seven bypasses on the same patient during one operation.

In 1977, Andreas Gruentzig, a Swiss cardiologist took a catheter with a collapsed balloon on one end and passed it into a blocked coronary artery, placed the balloon at the site of the blockage and pushed the balloon and the blockage opened. And the artery stayed open! Thus started an entirely new treatment of CAD called Percutaneous Transluminal Coronary Angioplasty (PTCA-but known mostly as angioplasty). However, angioplasty did not succeed too well as a standalone procedure and had a high failure rate often requiring urgent open heart surgery.

But then came a new innovation that when combined with angioplasty improved the results remarkably. This innovation was the use of intra coronary stents. Stents are small metal mesh tubes that are placed over a balloon and are dilated in the blockage over the balloon. The open stent then keeps the artery open after the balloon has been withdrawn.

The first stents were made of plain metal and were called bare metal stents (BMS). Soon however newer stents were developed that are coated with special medicines that prevent closure of the blockages even in the presence of a ‘foreign’ body inside the small artery. These stents are called drug eluting stents (DES). Today a vast majority of so called angioplasties are really angioplasties combined with stent placement. And newer blood thinning medicines can prevent closure of these stents over time.

Finally, about stopping an evolving heart attack. The earliest ‘modern’ treatment was the injections of clot busting medicines like Streptokinase that break up the blood clot that is blocking the artery. But this is not that effective in a majority of patients. Today the best treatment of an evolving heart attack is urgent catheterisation and dilatation and stenting of the blocked artery combined with special medicines to break up the present clot.

If this can be done within a few hours of the time when the heart attack starts, a heart attack can be stopped and much of the heart muscle at danger can be saved. All catheter based treatments are called Percutaneous Catheter Interventions (PCI) and are performed by medical doctors and not by heart surgeons.