Whilst many people will make a full recovery from their attack others will unfortunately be less lucky.
Probably the most dangerous time during the course of a heart attack is in the minutes immediately after the coronary artery becomes blocked. This is because the lack of blood flow to the muscle past the blockage and the consequent lack of oxygen causes the muscle to become very prone to becoming electrically unstable. This means that instead of responding to the normal regular electrical discharge of the sinus node (the inbuilt pacemaker area of the heart) and subsequent passage of electricity through the heart, the ventricles become prone to spontaneous and erratic electrical discharges that can cause heart rhythm disturbances called Ventricular Tachycardia or Ventricular Fibrillation (see The Normal Heart Rhythm and Ventricular Arrhythmias). This is very likely to lead to sudden collapse with loss of conciousness and if the patient is not rapidly resuscitated by electrical shock treatment they are likely to die. Electrical shock treatment is very effective in these circumstances. It needs to be delivered quickly after the event both to increase the chance of restoring the normal heart rhythm, but also to minimise the effects of any potential permanent brain damage. This is because the loss of circulation to the brain during the collapse causes irreversible damage to the brain tissue due the loss of oxygen delivery.
Continued anginal pains after a heart attack suggest that there is muscle in the heart wall that is still alive but not receiving a sufficient blood supply to meet all of its requirements even at rest. This may mean that there is another critically narrowed artery in addition to the one that blocked to cause the heart attack. In these circumstances drugs that lower the metabolic requirements of the heart muscle (Beta-blockers) and improve the blood supply to the compromised area (nitrates) will often be used, and the latter may be given by an intravenous infusion (that is continously and directly into a vein).
Angina following a heart attack is likely to be an indication to carry out early coronary angiography. This will show whether angioplasty or by-pass grafting is needed to reduce the risk of further early heart attack. (See Cardiac Catheterisation)
Unlike angina, pericarditis causes pain, not because of lack of oxygen to the heart muscle (ischaemia), but because the sack that contains the heart (the pericardium) becomes inflammed. This means as the two surfaces of the sack rub against each other with movement (caused by the heart beat, breathing or just moving around) the patient experiences pain. This pain tends to be sharp and short lived, although there may be a more persistent dull element to it, and it tends to be relieved as the patient sits up and leans forward.
Although painful, pericarditis is usually not dangerous and often is short-lived. Anti-inflammatory painkillers such as Ibuprofen are often the best treatment.
Very occassionally the inflammation persists and may cause a build-up of fliud within the sack called a pericardial effusion. Again this is usually self-limiting, but in a few cases it may become big enough to cause pressure on the heart, which in turn may compress the pumping chambers reducing the circulation and blood pressure - a condition called cardiac tamponade and in these circumstances the fluid may need to drained from the pericardium. This can normally be done under a local anaesthetic. The diagnosis is confirmed by doing an Echocardiogram which is a simple and painless test using a sophisticated ultrasound machine.
Some patients may experience atrial fibrillation as a consequence of their heart attack. This is usually short-lived and self correcting and rarely requires any treatment over or above that that they are receiving for the heart attack although occasionally medications to slow the heart rate may be needed. (See Atrial fibrillation).
Another consequence of a heart attack can be the onset of new heart failure or the worsening of pre-existing heart failure.
Essentially heart failure occurs when the pumping function of the heart is insufficient to supply all the various tissues of the body with an adequate blood supply. Following a heart attack some muscle of the heart will have died. How strong the pumping function was before the event and how much muscle was lost because of the heart attack will determine the degree, if any, of heart failure.
Often symptoms of heart failure will improve as time goes by after the heart attack. This is because sometimes there are areas of the heart where the muscle had a compromised blood supply from the thrombosis but did not die and as the blood supply improves they recover pumping function. Also transient heart rhythm disturbances may cause reversible heart failure.
For a fuller description of heart failure (not just related to heart attacks) see Heart Failure.
These complications are, thankfully, rare.
If the muscle that has been damaged becomes so weakened that it breaks down this can lead to a hole in the wall of the left ventricle allowing blood to flow out of the heart into the pericardium - cardiac rupture. This may prove fatal.
Similarly, the muscle in the wall between the left and right ventricles may break down causing abnormal flow from one side of the heart to the other - acquired ventricular septal defect. This is also a serious and potentially fatal complication although sometimes cardiac surgery may be helpful.
The mitral valve is opened by contraction of the parts of muscle of the left ventricle (papillary muscles) which have fibrous strings (chords) running to the tips of the valve leaflets. If this part of the muscle is seriously damaged this may lead to the valve becoming very leaky with a lot of back pressure into the lungs causing heart failure. Again this is a very serious condition which may be helped by emergency cardiac surgery.
As mentioned above, ventricular arrhythmias can arise early in the course of a heart attack due to the sudden loss of blood supply to the muscle of the heart and the consequent ischaemia. If the patient is resuscitated from an early cardiac arrest caused by VF or VT this does not mean that they are any more likely to have a subsequent cardiac arrest than anyone else who has had a similar heart attack.
Patients who have significant ventricular arrhythmias later in the course of their heart attack - perhaps days after the initial event are, however, at greater risk of subsequent rhythm disturbances and possibly sudden death from cardiac collapse.
For this reason late onset ventricular arrhythmias are taken seriously and may need specialised investigations to determine the best form of treatment. Some of these will relect an ongoing irritabilty of the muscle due to reduced blood supply and coronary angiography may show that an operation to improve the blood supply to the muscle of the heart is necessary (either angioplasty or CABG's) and this may prevent further rhythm disturbances. Angioplasty and Stents and Coronary Artery By-pass Grafts (CABG's)
In other patients the damaged muscle itself is the cause of the unstable heart rhythm. In these circumstances continued medications to stabilise the heart rhythm may need to be taken. Further depending on the ongoing risk despite best medications it may be necessary to insert what is called an Automated Implantable Cardio-defibrillator (AICD) which is like a larger and more sophisticated pacemaker that can not only pace the heart if it goes too slowly but can also deliver an electrical shock to the inside of the heart if it detects a chaotic heart rhythm.
Further information on this rather complicated subject can be found in the NICE (National Institute of Clinical Excellence) guidance by following the link: NICE Guidance on AICD's