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Refer to the basic blood supply description in the anatomy blog. In brief, there are three main blood vessels or arteries which supply the heart. Left anterior descending artery, notoriously called the ‘widow-maker’ is the largest and supplies the front of the heart. The other two arteries – left circumflex and the right coronary arteries, surround the heart in the middle and supply the left, right and back sides of the heart (figure 1).
All three arteries divide into various branches, getting smaller as they go further in their course. These three arteries are assigned the responsibility of supplying the entire real estate of the heart.
Cholesterol plaques may develop within the walls of these arteries. Plaques are formed by certain cells in the blood called macrophages ingesting (or eating) fat globules. This is one of the way body gets rid of excess fat through scavenging. Some arteries are especially prone to have these cells ‘settle’ in the walls of the arteries, heart arteries being one of them. Over time these cells may die and release the fat to the vicinity creating a cholesterol filled plaque.
This could be an ongoing process which may slowly obstruct the flow downstream. On occasions the plaque may rupture and expose its innards to the blood. The exposed plaque acts as a magnet for platelets and other clotting agents and starts forming a clot. This can result in a sudden and sometimes complete obstruction of the artery. The heart muscles dependent on the artery for nutrition and oxygen supply are suddenly starved (figure 2). This is one of the most common causes of a heart attack or ‘acute myocardial infarction’.
Plaque formation is accelerated by certain risk factors such as poorly controlled hypertension, diabetes, high cholesterol levels, old age, male gender, obesity, smoking, family history to name a few. Arterial plaques anywhere in the body is a risk factor for plaques in the heart arteries. Exercise primes the heart to function in extreme conditions, makes favorable changes to the heart, open up new channels. Just like long-distance marathon runners learn to optimize their movements and conserve energy for the long run. Lack of exercise does the opposite and the heart does not need to optimize anymore.
Consequence of a heart attack:
If the obstruction is further up in the artery, the amount of heart muscles affected may be massive. Starved muscles behave stunned. They stop contracting, sometimes balloon out, may even rupture; depending on the extent of damage. They are also prone to sudden and persistent electrical activation which could overwhelm the entire electrical system of the heart, short-circuiting it. Heart valves with attachments to the affected walls may malfunction and start leaking. In short, the manifestations may be variable depending on the extent of damage.
Early blood clot is like jelly in consistency but as time progresses and more clotting factors are attracted to it, the clot becomes hard as concrete. Also, the changes described above can be reversible to a large extent if treatment is initiated early. Consequently, detection and treatment as early as possible could give the best outcomes. Once concrete, it becomes difficult to intervene. Also, the stunned muscles die if they remained starved. So ‘time is muscle’!
Chest pain, shortness of breath, funny-feeling fast heart rate and/or dizziness. Chest pain is classically described as dull aching pressure like discomfort, going down the left arm. This textbook description of chest pain however happens in a minority. The pain could be sharp, shooting, stabbing or may have some other unusual characteristics. Some other types of pain, such as abdominal pain, could also signal a heart attack but so could multiple other things. This is where the difficult dilemma comes in, since all the characteristics of pain described above could be caused by number of other things, some completely unrelated to the heart.
During a heart attack, certain proteins contained within the heart muscles leak into the blood, called the troponins. These protein compounds are undetectable under normal circumstances and start rising few minutes to hours after a heart attack. Depending on the extent of the damage, the troponins may continue to rise within the blood. The rising trend in these troponins is used to diagnose a heart attack. An ultrasound of the heart, called the echocardiogram, can show weakening of the damaged heart muscles. Electrocardiogram (ECG) could show changes which are diagnostic of a heart attack, but this does not happen always.
The usual treatment is to attempt opening the obstructed artery/ries if possible, but as mentioned above this may not always be possible. Some hospitals which do not have these capabilities and are further out from a facility with these capabilities, may administer a clot-buster to attempt opening the artery.
The opening of the blockage involves opening a balloon across the obstruction. The un-inflated balloon is first pushed across the obstruction and inflated under pressure (figure 3).
A stent, which is usually a metallic scaffolding, is then placed across the obstruction to keep the artery open (figure 4).
This is a foreign body left in the artery. It is in contact with the blood 24×7, but over time the stent gets covered with a layer of cells, isolating it from the blood. Until then, it is necessary to take certain blood thinners which prevent the platelets (clotting cells) from aggregating. If these medications are not taken as recommended, then the stent is at risk of attracting platelets on itself and clotting off. On the other hand, the stent keeps the artery open, prevents an elastic recoil of the arteries after ballooning and can prevent the plaque from reoccurring through medications contained within the scaffolding.
Prevention of the above involves working on the controllable risk factors mentioned above. Graded exercise under supervised conditions and a heart-healthy diet are recommended.