Hospital list

Cardiology/ Cardiothoracic Surgery

Definition by UZ Brussel Medical team

Heart Diseases

• Coronary heart diseases

- Angina pectoris
- Heart Attack

• Structural disorders

- Heart Failure
- Valvular disease
- Congenital defects

• Arrythmia and conductivity disorders

- Bradycardia
- Tachycardia
- Sudden cardiac death

Diseases of the vascular system

• Arterial diseases

- Stenosis
- Aneurysm

• Venous diseases

- Varicose veins
- Deep vein thrombosis
- Venous malformations

• Other diseases

- Diabetic foot ulcers
- Renal ischemia
- Lymphoedema
- Neurovascular and vasospastic diseases


Coronary heart diseases (CHD)

  • Angina pectoris

Angina or angina pectoris is a pressing or squeezing feeling (even sharp pain sometimes) behind the breastbone. It occurs when the heart isn't receiving enough oxygen-rich blood to be able to function properly. Angina is nearly always due to a narrowing of the coronary arteries. The pain is felt mainly during physical effort or strong emotion; because that's when the heart needs more oxygen and will, quite logically, begin to beat faster. Angina usually subsides by itself when the oxygen requirement drops.

  • Heart attack

When a heart attack (or myocardial infarction) occurs, part of the heart muscle may die off because the blood supply to the heart through the coronary arteries has been interrupted. This can lead to (lethal) arrythmia or heart failure. A heart attack always occurs at the place where a blood-vessel has narrowed (stenosis). If a blood clot passing through the blood-vessel remains stuck at the stenosis, this can block the already much reduced blood flow entirely. And the patient suffers a heart attack because the blood can no longer reach parts of the heart muscle lying beyond.

Methods of treatment (medication, PTCA or CABG)

If the tests reveal that your heart isn't getting enough oxygen, there are different methods for treating a heart attack. In some cases it is sufficient to change one's lifestyle or to avoid heavy physical effort. Treatment with medication consisting of blood-thinners (aspirin), blood-vessel dilators (nitrates) and substances that slow the heart rate (beta-blockers) is another possible solution. If still the situation doesn't improve, the cardiologist or heart surgeon will have to proceed to a balloon dilatation, stenting or CABG.
Treating coronary blood-vessels with reduced diameter other than with medication is possible in one of two ways: either through a minimally invasive interventional procedure or through surgery. The ratio of interventional procedures to surgical procedures is about 9 to 1. In these last years the number of operations has dropped considerably thanks to the advance of interventional techniques. Furthermore, a minimally invasive intervention entails fewer risks for the patient, a shorter recovery period and much lower costs.

  • PTCA

PTCA stands for Percutaneous Transluminal Coronary Angioplasty. This procedure is carried out in a "cathlab" (see picture).The patient lies on the operating table, fully conscious. The X-ray machine can move horizontally and vertically to obtain images of the coronary arteries from different angles. A number of patches will be stuck on your chest to monitor your heart rate. Doctors will be able to watch pictures of your coronary arteries on the screens and follow the patient's heart rate and blood pressure closely. When everything is in place, the procedure can begin.
The procedure usually happens through the groin, which is made numb with an injection by the doctor. A sheath (short tube, photo 2) is introduced and then the guiding catheter (long flexible tube, photo 3) is slipped into the aorta all the way up to the coronary artery.
Once the guide wire is in the right place, the balloon catheter will be slipped over it till the balloon reaches the blockage. The doctor now inflates the balloon with a special pump. If an ordinary balloon is used, the plaque will be compressed against the artery wall thus widening the vessel opening sufficiently to provide your heart with oxygen-rich blood. The balloon is then deflated and, once it is empty, is withdrawn over the guide wire and removed from your body. In many instances the doctor will opt to place a stent immediately. The principle is the same, except that outside the balloon there is a stent that will be pressed into the artery wall when the balloon inflates. The stent will make sure that the blood-vessel doesn't shrink again after some time:

-the balloon catheter sitting near the stenosis (1)
-the balloon inflating and pressing the stent into the vessel wall (2) and
-the stent left behind as the catheter is removed (3)

  • CABG

CABG is short for Coronary Artery Bypass Grafting. Many people call this a bypass operation. A CABG is usually performed on people with very serious coronary heart disease who can't be treated effectively in any other way. Patients undergoing bypass surgery don't usually have just one or two blockages, but a number of them. In order to restore the blood flow in your coronary arteries to a good level, the surgeon will remove a healthy blood –vessel from your leg, arm or chest and use it to replace the narrowed coronary artery. The surgeon will attach one end of the vessel to the aorta, and the other end to the sick artery at some point past the blockage. Through this detour oxygenated blood can be delivered to the entire heart once again. A bypass operation considerably reduces the risk of a heart attack.

A surgeon can perform a CABG in two ways: on a heart that has been stopped (the traditional way) or on a beating heart. During a traditional CABG the heart is stopped completely and no blood flows through it anymore. The patient's circulation is taken care of by the so-called heart-lung machine, which takes over all functions of heart and lungs. During an operation on a beating heart no heart-lung machine is used and heart and lungs carry on working. But the heart is steadied with a sort of suction cap so it moves less vigorously. Clearly it is simpler to operate on a still heart than on a beating heart, but this method does have a couple of drawbacks. Research has shown that certain complications occur more frequently with a traditional CABG than with an operation on a beating heart. Thus the risk of stroke is higher and there are more complications with the kidneys, the myocardium and the lungs. On top of that more blood transfusions are needed and the patient has to stay longer in hospital than with a CABG on a beating heart.

Structural disorders

  • Heart Failure

The term heart failure refers to a situation where the heart lacks sufficient pumping power to meet the oxygen needs of the body. Normally at every contraction the heart pumps blood from the left ventricle into the aorta. In patients with heart failure this doesn't happen correctly. A first cause can be a reduced functioning of the heart muscle itself, but heart failure can also be caused by prolonged excess pressure or volume or by a valve defect. But in the Western world heart attacks are the main cause of heart failure (in 60 to 70 % of cases). Other regularly occurring causes are for instance:

- deterioration of the heart muscle by an infection or toxic substances (alcohol)
- chronic lung disease
- diabetes


Once a diagnosis has been reached, doctors will endeavour first and foremost to treat the causes to stop the heart failure getting worse. Thus in the case of patients with coronary disease the pumping problem may be caused in part by ischaemia. Here revascularisation by means of PTCA (more) or CABG (more) may be a solution. Heart failure can also be due to valvular disease or arrythmia which can be cured by means of surgery or an electrophysiological procedure.

But if there is no correctable underlying disorder, doctors will opt for treatment by means of medication and therapy intended to help the patient change his/her lifestyle. Two types of medication are available. Firstly, we have diuretic and vasodilating medication (diuretics and nitrates) and secondly, medication that improves the heart's pumping function (ACE-inhibitors, digoxines and beta-blockers). Lifestyle therapy helps patients with ways to stop smoking, reduce alcohol intake, avoid heavy physical effort, monitor diet etc. They see the doctor regularly, but check their weight themselves (rapid weight increase is probably due to insufficient fluid removal) and take their medication themselves. In case of questions or problems outpatient heart failure patients can see the doctor or a specialised nurse. If complications arise, the patient can be temporarily admitted for intravenous medication till the situation has stabilised.

  • Valvular Disease

Valvular heart disease is the name given to disorders of the heart valves. They can be subdivided into 2 categories:

- Valves don't close properly: as a result blood isn't pumped out  adequately and some of it leaks back. This is called valvular insufficiency. 

- Valve leaflets may be fused or calcified: as a result the valve doesn't open correctly and insufficient blood is pumped. Doctors call this valvular stenosis.

What can cause valvular heart disease?
Valve abnormalities have different possible causes. They may be caused by hereditary predisposition, ageing or illness.

Valvular diseases usually occur in the mitral and aortic valves in the left heart. If the disorder is making it difficult for your heart to pump, an operation may be necessary, even if you have few or no complaints. Otherwise the valve problem could, in time, lead to heart failure.

Treatment of valvular disease

If the valve abnormality isn't too serious, treating with medication may suffice. This medication will help reduce the workload of the heart. Often the doctor will also prescribe anticoagulants to help prevent clotting of the blood.

Balloon dilatation
In some patients the narrowing valve can be opened up without surgery. Usually this concerns stenoses of the mitral or aortic valve, sometimes the pulmonary valve. This procedure is very similar to coronary artery dilatation, except that the balloon used for valve dilatation is many times bigger. The balloon is slipped into the heart through the veins and inflated at the valve thus stretching it open. It has to be said that this procedure is used only very rarely nowadays.

Surgical intervention
Surgery may be necessary in the case of serious valvular disorders or degenerating valves. Your general condition among other things will determine whether or not an operation is carried out as open heart surgery is a major intervention. The operation will involve either replacing or repairing the sick valve.

If a replacement is decided, the sick valve is removed and replaced with a mechanical or a biological valve. The choice of valve will depend on a number of factors, such as age, the patient's case history, medication etc. Mechanical valves are made of very durable material, mainly carbon, synthetic material and metal. They barely wear out and will in principle last a lifetime. People who receive a mechanical valve need to take anticoagulants for the rest of their lives. Biological valves either are made of treated animal tissue (pig or bovine) or are human valves from a donor. The advantage of biological valves is that anticoagulants only need to be taken during the first days after surgery. On the other hand they do wear out and will need to be replaced after a certain period of time.

A third possibility in surgery is for the patient to be his/her own donor. The damaged aortic valve is then replaced by the patient's own pulmonary valve and the latter is replaced by an artificial val

  • Congenital defects

The other 60% of children will need treatment. Often medication is not sufficient and surgery is needed to provide a more structural solution. Most children with a corrected congenital heart defect will need to be monitored by a cardiologist indefinitely. During childhood the pediatric cardiologist provides the follow up. At UZ Brussels we organise joint consultations of the pedriatric cardiologist and the adults' cardiologist for patients coming out of adolescence.

Just under 1% of babies are born with a heart malformation. In Belgium, every year, about 120,000 children are born on average, and so over 1,000 of them will have a congenital heart disease. In the table below you will find the prevalence of a number of the most frequently occurring congenital defects. About 40% of children with congenital heart disease won't need to be treated because the condition has few or no consequences for the child. For instance a small ventricular septal defect (the most frequent congenital defect) or a slight pulmonary valve stenosis don't need correcting. Children born with these conditions have the same life expectancy and enjoy the same quality of life as healthy children.

In some patients the narrowing valve can be opened up without surgery. Usually this concerns stenoses of the mitral or aortic valve, sometimes the pulmonary valve. This procedure is very similar to coronary artery dilatation, except that the balloon used for valve dilatation is many times bigger. The balloon is slipped into the heart through the veins and inflated at the valve thus stretching it open. It has to be said that this procedure is used only very rarely nowadays.

Arrythmia and conductivity disorders

  • Bradycardia

A normal healthy heart beats between 60 and 80 times a minute. At that rate about 5 litres of blood is pumped through the body. If the heart rate is lower, the heart isn't contracting sufficiently to supply the body with oxygenated blood. This condition is called bradycardia. It occurs mainly in older people and occasionally in young people. Worldwide every year about 60,000 people are treated for a slow heart beat.
Most of the time bradycardia results from a problem with the SA node or a problem with the conduction system. This prevents the heart from making enough pumping motions to meet the needs of the body. It's like a car with a defective petrol pump. Not enough fuel reaches the engine when you press the accelerator and the car jerks. Similarly, your body falters if the heart can't make enough pumping motions.

Treatment of bradycardia

Bradycardia is usually treated by means of a pacemaker. Where necessary, this device will adjust the heartbeat to meet the needs of the body by firing impulses that resemble the heart's normal electrical signals.

Depending on the patient's condition, the pacemaker will:                                    
- replace the SA node impulses that are either too slow or that are not transmitted 
- ensure a normal succession of atrial and ventricular contractions
- ensure that the ventricles always contract at the right rhythm.    

How is a pacemaker implanted?
Implanting a pacemaker is a fairly simple procedure that will take only1 to 2 hours. Before the procedure starts, the patient is given medication to relax. That may cause drowsiness, but the patient will remain conscious.
The anaesthetist numbs the spot where the surgeon is going to locate the pacemaker. The surgeon then prepares a small pocket beneath the skin into which the pacemaker and the leads will be placed, usually just below the collarbone. The leads are slipped into the heart through the vena subclavia and the tips are attached to the lining of the heart.
 Once the pacemaker is in position the doctor will first check by means of an X-ray that the system has been correctly placed and then test the proper functioning of the pacemaker. During this test you may find your heart is beating faster.

  • Tachycardia

Tachycardia is a condition in which the heart beats abnormally fast, often more than 100 times a minute (in extreme cases the heart rate can rise to 240 and more a minute). Because of this, the body doesn't receive enough oxygen and nutrients to function correctly. Everybody, be they young or old, can suffer from tachycardia. Two types occur: supraventricular tachycardia which originates in the atria and ventricular tachycardia which starts in the ventricles.
Supraventricular tachycardia can cause certain symptoms but isn't dangerous or life threatening as the natural barrier between atria and ventricles (the AV node) stops arrythmias spreading from the former to the latter and so they can't influence the heart's pumping function very much. However, ventricular tachycardia can stop the heart pumping altogether and can , in the worst case, lead to sudden cardiac death.

Supraventricular tachycardia is subdivided into subtypes, depending on where it originates:
 - sinus tachycardia
 - atrial flutter
 - atrial fibrillation
 - AV nodal reentrant tachycardia and
 - atrioventricular reentrant tachycardia.

Symptoms and diagnosis
The most frequently occurring symptoms are: palpitations, dizziness, tiredness, temporarily reduced vision, black-outs or syncope. In the worst cases the heart can even stop completely.

Types of tachycardia

Sinus tachycardia
This supraventricular tachycardia originates in the sinus node, the natural pacemaker of the heart. The sinus node (or SA node) is influenced by our autonomous nervous system and, in certain circumstances (stress, physical exercise, emotion etc.) is stimulated to fire impulses faster. In these cases the tachycardia is deemed to be physiological (i.e. the body's normal response). Only rarely does the sinus node begin to work faster for no obvious reason. If it does, we call this a pathological or inappropriate sinus tachycardia.

Atrial flutter
Atrial flutter is a supraventricular tachycardia whereby impulses pass through the atria continuously at a frequency of over 250 a minute. The flutter is the result of a reentrant circuit, usually in the right atrium. The flutter is often spotted as a result of the typical saw-tooth flutter waves on the ECG . Normally the ventricles don't beat as fast as the atria because the AV node acts as a funnel and doesn't let all impulses pass. Although some people can continue to have the flutter for months or even years, often the situation will deteriorate into atrial fibrillation after some time. Atrial flutter is generally treated with ablation (see below), in the same way as atrial fibrillation, because both disorders consist of inefficient contractions of the atria.

Atrial fibrillation
Atrial fibrillation is an arrythmia whereby the atria don't contract normally anymore, but instead do so much too fast and irregularly. This is due to the fact that many foci all fire signals at the AV node at the same time. The number of impulses in the atria usually varies between 300 and 600 in the case of atrial fibrillation. Contrary to what happens with ventricular fibrillation, the heart continues to pump to a large extent because the chambers still contract, albeit in an irregular way. But because pumping is reduced, some blood remains in the atria. If this blood solidifies and clots are formed there is an increased risk of a stroke.

'Does the heart of an atrial fibrillation patient really beat 300 to 600 times a minute?' you may well ask. The answer is no, fortunately not. The AV node restricts the number of impulses that continues to the ventricles. All the same, the heart can end up beating very fast indeed.

Some 5 to 10 % of patients' over-65 suffers from atrial fibrillation. That makes it a condition that occurs fairly frequently, although it is far less acute than ventricular fibrillation. The increased heart rate and the reduced pumping capacity will make the patient short of breath and the oxygen deficit in the heart muscle can cause angina.

The most frequent causes of atrial fibrillation are high blood pressure, a dysfunctional heart valve (in particular mitral valve leakage) and reduced pumping ability of the heart. Other cardial and non-cardial causes that lead to enlargement of the atria have also been linked to atrial fibrillation. And often enough no direct cause can be identified, a condition known as lone atrial fibrillation.

The way to treat atrial fibrillation will depend on the individual patient. Blood thinners (or anti-coagulants) are usually prescribed to stop blood clots forming. Various anti-arrythmic drugs exist that can slow down an excessive heart rate. But often the effect of these medicines doesn't last. Cardioversion is another option. This consists of administering a shock with an external defibrillator to restore a normal heartbeat. Mostly the result is good but in many cases the situation will deteriorate again after some time. Some patients won't benefit from medication at all or suffer serious side effects. That is when a technique known as ablation may be decided upon.

Ablation is a technique that has become widely used only in the last ten years or so. It is a minimally invasive intervention that is carried out in a cathlab.
Catheters are conveyed up into the heart through the patient's groin. That way the electrophysiologist (a cardiologist who specialises in arrythmias and conduction disorders) can establish the cause of the arrythmia. The short circuit that causes it can be 'burnt' by placing the catheter in exactly the right spot and causing a very minor lesion to the heart tissue. Many tachycardias can be cured permanently by means of ablation. A great advantage of this technique is that complications are extremely rare.

AV nodal reentrant tachycardia (AVNRT)
AV nodal reentrant tachycardia (AVNRT) is a circular tachycardia occurring around the AV node. Two conduction pathways with different conduction properties (1 and 2 in drawing below) run by the AV node:
  - pathway 1 with a short refractory period and slow conduction
  - pathway 2 with a long refractory period and fast conduction

After a contraction a muscle cell can't contract again for a while. This interval is called the refractory period. The impulse for a normal sinus rhythm ( image A) reaches the two pathways outside of the refractory period. The signal continues along both pathways, but because conduction is faster on pathway 2, it is the impulse going that way that causes the ventricles to contract. An extrasystole (an impulse fired prematurely) coming from the atria will be blocked by the pathway with the long refractory period and will pass through the pathway with the short refractory period (n° 1). The atrial extrasystole shows up on the ECG because of a longer than normal PR interval.
When the impulse reaches the bundle of His, the fast pathway (n° 2) is no longer refractory. Retrograde conduction may now take place over the fast pathway and can either be blocked or channelled further along the slow pathway again. In the former case we have an AV nodal echo (image B), in the latter the ventricles will contract once more.
When an impulse is continuously being sent down along the slow pathway and returned retrograde along the fast pathway we have AV nodal reentrant tachycardia (imageC).

Atrioventricular reentrant tachycardia
Normally , impulse conduction between the atria and the ventricles is possible in one place only, i.e. in the AV node. But if another pathway exists between the upper and lower half of the heart, a so-called accessory pathway, the reentrant tachycardia will form its loop along there.
The accessory pathway can conduct retrograde only (from the ventricles to the atria) or bi-directionally (retrograde, and antegrade = from atria to ventricles). Atrioventricular tachycardias are subdivided into two types:
the orthodrome type where antegrade conduction goes via the AV node and retrograde conduction along the accessory pathway
the antidrome type with antegrade conduction running along the accessory pathway and retrograde conduction via the AV node.
Ventricular tachycardia
Ventricular tachycardia is a form of tachycardia originating in the lower half of the heart. It can be life-threatening as it can lead to ventricular fibrillation and sudden cardiac death. We have ventricular tachycardia if the ECG reveals more than three successive heartbeats starting in the ventricles, at a rate of more than 100 a minute. Often the frequency isn't as high as with supraventricular tachycardias - usually 130 to 170, but frequencies of over 200 a minute are by no means exceptional. Retrograde activation of the atria is a possibility, but in 50% of cases a retrograde block is observed, leading to AV dissociation. If the tachycardia is relatively slow, with AV dissociation, an atrial impulse may reach the AV node outside of the refractory period, thus activating the ventricles even before they contract as a result of the next ventricular impulse of the tachycardia. Premature ventricle activation due to a supraventricular impulse is called ventricular capture.

From a purely morphological point of view, two kinds of VT's can be distinguished. If all heartbeats have more or less the same shape on the ECG, we refer to a monomorphous VT. In the case of a polymorphous VT almost every heartbeat will look different on the ECG. VT's can also be distinguished according to the duration of the tachycardic period. If the VT goes away by itself within 30 seconds, we call it non-sustained . If it continues beyond that it is a sustained VT.

The cause of the VT is linked to its morphology. The reason why all heartbeats look the same in a monomorphous VT is that the impulse is generated in one single spot in the left or right ventricle or that it always follows the same circuit within the ventricle. The most frequent cause of a monomorphous VT is the scar tissue that develops after a heart attack. Scar tissue has no conductive qualities and so a conduction pathway may develop around it, giving rise to a circular tachycardia.
Polymorphous VT is caused by abnormalities in the electrolytes. The most frequent triggers are a reaction to medication or an oxygen deficit of the heart muscle (after a heart attack or not). Polymorphous VT also consists of a reentry mechanism. It can develop into monomorphous VT or ventricular fibrillation.
The way to treat VT will depend on the individual patient and will be determined among other things by how the patient tolerates the tachycardic episodes and the frequency of the VT. Medication is a solution, but preferably patients who meet the conditions will be given a defibrillator.

  • Sudden cardiac death

Ventricular fibrillation
Ventricular fibrillation (VF) is a tachycardia whereby the ventricular muscle fibres still contract, but not in a co-ordinated way, as a result of which the pumping function cuts out (so the blood ceases to flow and tissues are no longer supplied with oxygen). As a result the patient will lose consciousness within about 10 seconds after the onset of the VF, and, if no assistance is given, irreparable brain damage will occur within 5 minutes. Beyond 10 minutes the victim will almost certainly die.

The only way to treat VF is to apply an electric shock to the heart, a process known as defibrillation. If a patient can be defibrillated within a few minutes, chances of making a full recovery are very high. More information about the implantable defibrillator may be found below in the section on the Brugada syndrome.

The appearance of ventricular fibrillation is the main cause of death in the case of acute myocardial infarction (heart attack) . Heart massage and artificial respiration, when correctly applied, can keep the victim alive till the life-saving shock can be administered.

The Brugada syndrome
In 1987, prof. Dr. Pedro Brugada for the first time spotted a typical deviation in the ECG of a 5-year old boy who'd had to be revived three times because of ventricular fibrillation. When the little sister (who had the same ECG deviation ) died suddenly, the suspicion grew that this was an hereditary disorder. Only a few years later was the Brugada syndrome officially recognised and described as a genetic hereditary hypersensitivity to arrythmias in patients with a characteristic Brugada-ECG (a shark-fin pattern in the right ECG leads).

16 years after the official recognition of this clinical entity, thousands of BS patients have been identified worldwide. Because of the hereditary pattern, patient populations are grouped together geographically (Europe, South-East Asia ...). The striking thing about this disease is that a thorough examination of the heart will reveal no dysfunction as the structure of the heart is totally normal. The defect is located at micro-molecular level. In normal circumstances electrical impulses are transmitted from one heart cell to another via channels in the cell wall or membrane. In the case of the Brugada syndrome a defective gene causes a disorder in one of these channels, the sodium channel, which considerably disturbs the electrical functioning of the heart. In certain circumstances this can lead to dangerous arrythmia originating in the ventricle (ventricular tachycardia, ventricular fibrillation) and sudden cardiac death.

Patients with Brugada syndrome who have been resuscitated or in whom a ventricular arrythmia has been recorded will be given an internal defibrillator (see illustration). This is a small, computerised device (similar to a pacemaker) that is implanted subcutaneously and is connected to the lining of the heart. When an arrythmia happens in the ventricle the defibrillator will recognise this and fire an electrical shock that seeks to restore the normal heart rate (thus saving the patient's life).

When a patient is diagnosed as having the Brugada syndrome, all family members need to be tested, even those not showing symptoms. An ECG will be taken from each and a blood sample for genetic analysis. Recent scientific research has shown that the shark-fin pattern isn't present on the ECG all the time. The ECG can look perfectly normal and display a clear deviation from the normal sinus rhythm a few minutes later. This is why, in order to be sure of the diagnosis, all relatives have to undergo a test whereby a medicine is administered to reveal the hidden shark-fin electrocardiograms. All relatives with a Brugada-ECG have to undergo an electrophysiological study. A catheter is threaded into the heart through the groin and an attempt is made by means of an electrical signal to provoke an arrhythmia. If it occurs, that patient too will need to have the protection of a defibrillator. The ones in whom no arrythmia could be caused are considered to be carriers of the Brugada syndrome (without the risk of sudden cardiac death).

So far no treatment has been found for the Brugada syndrome. Patients can only be offered preventative protection in the form of a defibrillator. Prof. Brugada, in co-operation with his brothers (Dr. Josep Brugada in Barcelona and Dr. Ramon Brugada in Montreal) is continuing his scientific research with the hope of finding a more curative solution.