We are the combination of four hospitals: the General Hospital, the Children’s Hospital, the Women’s Hospital and the Traumatology, Rehabilitation and Burns Hospital. We are part of the Vall d’Hebron Barcelona Hospital Campus: a world-leading health park where healthcare plays a crucial role.
Patients are the centre and the core of our system. We are professionals committed to quality care and our organizational structure breaks down the traditional boundaries between departments and professional groups, with an exclusive model of knowledge areas.
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The heart is made up of four cavities, two atria and two ventricles. The atria are separated from each other by an interatrial wall or septum, and the ventricles by an interventricular wall or septum. Between the atrium and the ventricle there is the atrioventricular valve. The veins arrive into the atria and the major arteries leave the ventricles. Between the ventricle and its artery outlet there is the semilunar valve. The heart is divided into the right and left sides.
Non-oxygenated blood arrives at the right atrium via the venae cavae, from the head and arms (upper vena cava) and from the abdomen and legs (lower vena cava). This blood passes to the right ventricle through the tricuspid valve. The right ventricle pumps this blood, through the pulmonary valve, into the lungs through the pulmonary arteries, which is where the blood gets it oxygen.
This oxygenated blood returns to the left atrium via the pulmonary veins. From the left atrium it is directed to the left ventricle through the mitral valve. The left ventricle pumps the blood to the aorta through the aortic valve to distribute it to all the organs and tissues in the body.
The heart is irrigated by the coronary arteries, right and left. These coronary arteries divide into several branches to carry oxygenated blood throughout the heart tissue.
The heart contracts due to an electric stimulus triggered by the conduction system. The cardiac conduction system is made up of a series of cells that have the capacity to create this stimulus and determine heart rate. This stimulus begins in the sinus node, which is found where the superior vena cava enters the right atrium. This stimulus causes the atrium to contract. This stimulus then propagates the ventricle through another structure called the atrioventricular node. This conduction system is capable of increasing the heart rate when necessary, such as for example during exercise, when you have a fever, when you feel emotions, etc., or decreasing the heart rate when you are sleeping. This system is regulated by the action of different hormones or in response to nervous stimuli in the cardiac plexus.
The cardiac cycle has two phases: systole and diastole. In systole, the heart contracts to send blood to the major arteries and during diastole it relaxes to fill with blood to later be ejected.
Acute myocardial infarction (AMI), commonly known as a heart attack, is the necrosis –the degeneration of tissues due to cell death– of a part of the heart, caused by an interruption in blood flow (ischaemia). The most common cause is the obstruction of a coronary artery (the arteries that supply blood to the heart itself) by a blood clot formed by the rupture or erosion of an atherosclerotic plaque. In the absence of atherosclerosis, there are other, less frequent mechanisms that can cause this condition, such as strokes, dissection, and coronary artery spasms.
The main factor determining the prognosis and initial course of treatment is whether the obstruction of blood flow to the heart is total and persistent or not. The former case is a medical emergency, since the entire myocardial area irrigated by the obstructed artery will die if the blood flow is not quickly restored. The latter, without total and persistent blockage, constitutes a less severe heart attack and treatment is not as urgent.
The clinical presentation, in which the symptoms and initial signs can be characterised, and, most importantly, the electrocardiogram (ECG) results, help distinguish between these two scenarios. AMI is one of the leading causes of death worldwide, since it goes hand-in-hand with a high risk of serious complications, such as malignant arrhythmias, especially in the first few hours following the heart attack. It is also a common cause of long-term disability. Even with the considerable therapeutic advances of the past few decades, it is still a serious condition.
The most common symptom is chest pain, usually described by patients as a kind of pressure in the middle of their chest, which often radiates to the arms, neck, jaw, or back; it starts off as mild pain and progressively increases in intensity. It is sometimes defined as a burning sensation, and it can occur in other parts of the body, such as the stomach area.
Often, it is accompanied by a subjective feeling of weightiness, cold sweats, nausea, and vomiting. Sometimes, especially in the elderly, in women, and in diabetic patients or those with other chronic diseases, the pain is not as obvious or it is accompanied by other symptoms such as shortness of breath, fatigue, or feeling unsteady.
AMI can occur suddenly, as the first sign of ischaemic heart disease, but often, patients have had prior, brief episodes of chest pain, usually upon physical exertion, which should serve as a warning that they may have an unstable coronary injury. Other associated symptoms, such as trouble breathing, fainting, confusion, drowsiness, or extreme weakness usually indicate the presence of serious complications of AMI such as heart failure, arrhythmia, or cardiogenic shock.
Many people, since ischaemic heart disease is the leading cause of death worldwide. According to the WHO, in 2016, it caused close to 10% of deaths overall, surpassing strokes and chronic obstructive pulmonary disease. In Europe, the mortality rates due to ischaemic heart disease and cancer are quite similar. The prevalence of AMI and ischaemic heart disease in general is less in the Mediterranean countries than in the Northern or Eastern European countries.
In Spain, there are some 100,000 cases of AMI per year, a third of which prove to be fatal before the patient reaches the hospital. The prognosis for hospitalised patients has improved greatly in the past few decades; the current hospital mortality rate here is close to 5%.
The prevalence of AMI increases at advanced ages. Although it is commonly believed that AMI is a condition that affects mostly men, its prevalence is similar in both sexes. What happens is that men usually develop this condition starting in their forties, whereas women see an increased incidence of the disease 10-20 years later, almost always after menopause. However, young women can also have an AMI.
Anyone can suffer an AMI, but there are risk factors that are closely associated with a higher risk. The most characteristic of these are those related to any kind of atherosclerosis, such as tobacco use, diabetes, hypertension, and high cholesterol. There are also genetic traits associated with an increased predisposition to the illness.
Lastly, there are factors that can provoke a rupture in the atherosclerotic plaque or a thrombotic response and trigger an AMI, such as:
It is of the utmost importance to identify those patients with complete coronary artery blockage, and who therefore require urgent reperfusion treatment (which restores the blood flow to the blocked arteries), as soon as possible. Every minute counts when it comes to saving myocardial tissue.
In most cases, this identification can be done by assessing the symptoms and analysing the ECG. Therefore, patients with chest pain or other symptoms consistent with an AMI should immediately seek medical attention, and medical staff should perform a clinical evaluation and ECG analysis without delay.
The safest and most effective way to do this is to call 112, as the Spanish Medical Emergency System usually evaluates these patients faster than most accident and emergency departments at health centres and hospitals. In addition, when an AMI requiring immediate catheterisation is detected, the treatment process is initiated at the site where the patient first receives medical attention and they are transferred to a hospital that is equipped for the procedure they need. Moreover, the patient is received directly at the cardiac catheter laboratory, where a team will have already been alerted and will be waiting for them, without losing time having to first go through the emergency department.
In Patients with an ECG that is normal or whose ECG shows ischaemic changes but in whom a complete coronary artery blockage is not suspected, do not require immediate catheterisation and can be evaluated with less urgency at an accident and emergency department. An AMI diagnosis is confirmed by the presence of elevated myocardial necrosis markers in the blood analysis.
From the moment they are diagnosed, AMI patients' heart rate must be continuously monitored to detect and treat serious ventricular arrhythmias, in case they occur. They should be admitted to a cardiovascular intensive care unit or intermediate care unit, depending on their initial risk assessment, and once they are stabilised, they can be transferred to the general ward. The average length of hospital stay due to a non-complicated AMI is 4 to 5 days.
AMI patients require antiplatelet drugs to combat thrombosis and a coronarography is also recommended in all cases. When an acute coronary occlusion is suspected, the coronarography must be performed quickly so than an angioplasty can be carried out to re-open the obstructed artery as soon as possible. Often, a coronary stent, a device that reduces the risk of reobstruction, is simultaneously implanted. If an urgent coronarography cannot be done, for example because the patient is located in an area very far away from a hospital equipped for this procedure, pharmaceuticals can be administered to dissolve the coronary thrombus.
In all other AMI cases, the coronarography and revascularisation are carried out within the first few days of admission. Some patients may require coronary bypass surgery instead of percutaneous revascularisation and stenting, due to the characteristics of their cardiovascular injuries. Apart from this, all patients will receive pharmaceuticals to reduce their cholesterol, and those with severe heart attacks will require specific medications to improve their ventricular dysfunction and prognosis. Participating in cardiovascular rehabilitation programmes after discharge has been shown to improve the prognosis and fosters patient adherence to healthy lifestyle guidelines.
Some patients who experience complications may require implantable electronic devices such as pacemakers or defibrillators, and more severe cases may warrant aggressive interventions such as:
The risk of suffering an AMI can be reduced with preventative health measures, including controlling one's diet. Regular physical exercise and avoiding being overweight are very beneficial to this end. One's diet should be balanced, and following a Mediterranean diet rich in virgin olive oil, vegetables, fruits, legumes, and fish, supplemented with nuts and with a limited intake of red meat and sugar, is the healthiest option. Tobacco consumption should be completely eliminated, and it is wise to avoid heavy exposure to pollution, as well as strenuous activity and high-stress situations.
For patients with cardiovascular risk factors, medications to control cholesterol, hypertension, and diabetes are often recommended, and in very high-risk patients, prophylactic therapy with antiplatelet drugs may be warranted.
Scleroderma is an autoimmune disorder characterised by increased collagen in various body tissues, structural alteration of microcirculation and certain immune abnormalities. The term scleroderma comes from the Greek “skleros”, which means hard, and “derma”, which means skin. This indicates that skin hardening is the most characteristic feature of the condition. As well as the skin, it can also affect the digestive tract, lungs, kidneys and heart. The prognosis varies. There is currently no cure, but the condition can be treated with general measures and treatment of symptoms, depending on the organs affected.
Raynaud syndrome: one of the most characteristic manifestations of the condition (97% of cases), it is the first clinical expression in most patients. It is caused by vasoconstriction of the capillaries. Patients report that with the cold their fingers change colour and turn pale (like wax) first, then turn blue after a while and finally turn reddish. The presence of Raynaud syndrome is not always an indication of scleroderma. In reality, only 5% of people with Raynaud syndrome later develop the condition. Almost half of sufferers may have digital ulcers, as an expression of a severe microcirculatory injury.
The most peculiar manifestation of the disease is the way it affects the skin. It is hard, tight and wrinkle-free (hard to pinch). The extent of the skin condition varies and is related to the prognosis. Two clinical forms are distinguished: limited (distal skin condition to elbows and knees) and diffuse (distal and proximal skin condition to elbows and knees, and torso). The face can be affected equally in both clinical forms. The limited subtype has a better prognosis than the diffuse one. Reduced aperture of the mouth (microstomy) may also be seen. In the skin there are hyperpigmented and coloured areas, telangiectasia (accumulation of small blood vessels) and sometimes subcutaneous calcium deposits can be felt (calcinosis).
Most patients experience joint and muscle pain, and in extreme cases contraction and retraction of the fingers are observed. When the digestive tract is affected, which often happens, the patient complains of a burning sensation and difficulty swallowing, as the oesophagus has lost its ability to move food towards the stomach. Pulmonary disease is the leading cause of death and may occur in the form of fibrosis or pulmonary hypertension; coughing, choking and heart failure are the main manifestations of lung involvement. When the heart is affected, heart rhythm disturbances and in some cases symptoms of angina pectoris are detected, due to the involvement of the small coronary vessels. In a small percentage (about 5%) scleroderma alters the kidney (scleroderma renal crisis) and manifests itself as malignant arterial hypertension and kidney failure.
It should be noted that not all patients with scleroderma present all the manifestations described above. It can also be concluded that there is great, almost individual, variability in the clinical expression of the disease.
Scleroderma is a rare disease with an incidence of 4-18.7/million/year and a prevalence of 31-286/million. It is more common in females, with a variable ratio, depending on the series, ranging from 3:1 to 14:1 (female/male). The age at which it presents is around 30-40 years.
When the above symptomatology is clear, the diagnosis does not offer too much room for doubt. Various complementary tests are helpful in confirming diagnosis and in assessing the degree of involvement of the various organs that may be affected.
“An incurable, but not untreatable condition”. There is currently no treatment for scleroderma that has satisfactory results, but this does not mean that it cannot be treated. Treatment is symptomatic, depending on the organ affected. For Raynaud syndrome: vasodilators, antiplatelets; gastro-oesophageal reflux: proton pump inhibitors; renal crisis: angiotensin converting enzyme inhibitors/dialysis; pulmonary fibrosis: immunosuppressants/lung transplant; pulmonary hypertension: vasodilators/lung transplant. In patients with the diffuse form and less than three years of evolution, immune modulators such as mycophenolate sodium (or mycophenolate mofetil) or methotrexate may be indicated as a basic treatment.
The most common tests to confirm and/or assess the degree of involvement of the various organs are: general analyses and immunological data (specific antinuclear antibodies); capillaroscopy, high-resolution computerised axial tomography scan of the chest, respiratory functional tests, oesophageal manometry and echocardiogram. In the follow-up for these patients, respiratory functional tests and an echocardiogram should be performed annually.
Angina pectoris is characterised by strong, oppressive pain in the chest that spreads to the neck and left arm. It is a sign of lack of oxygen in the heart. It is normally caused by a condition in the coronary arteries, which are the arteries responsible for carrying oxygen to the heart tissue.
Intense pain that appears quickly and intensifies over the course of a few minutes in the chest. It is accompanied by sweating, nausea, vomiting and can spread across the whole chest, the left arm, the neck, and the bottom part of the face.
Angina should be differentiated from the pain that can be caused by pericarditis (inflammation of the membrane surrounding the heart), from hiatal hernia (stomach hernia) and from musculoskeletal pain. It can also be confused with indigestion.
It can affect any age group in adulthood. It is very rare in children. There is a correlation with age (the risk increases as age increases), and there is a slight predominance in males.
Based on clinical observation, electrocardiogram and on determining different blood parameters that show changes in the heart muscle. Diagnosis can be made during an episode of pain, or through a stress test to highlight it, under strict medical control.
The definitive diagnostic test is cardiac catheterisation, which shows blocked areas and often allows the blockage to be cleared with the same catheter.
Electrocardiogram, echocardiogram, nuclear magnetic resonance of the heart, and also cardiac catheterisation which has a diagnostic and therapeutic aim as it can improve blockages in the coronary arteries.
Treatment is aimed at reducing the risk factors, especially tobacco, and improving blood flow in the heart, with the use of various vasodilators.
Health education is essential for those suffering from angina, in order to avoid triggers (quick and intense exercise without warming up) and risk factors (tobacco and alteration of fat content in the blood).
There are numerous coronary vasodilators and various pharmacological families. One thing they all have in common is that they improve coronary blood flow. Controlling arterial hypertension is essential to reduce cardiac effort and overloading of the surrounding vessels.
Cardiac catheterisation consists of inserting a catheter via the arm or leg that reaches the heart and uses contrast to detect coronary obstruction. It thus allows the blockage to be cleared using a dilator or by inserting a stent (an artificial object that allows the flow of blood along the coronary artery to remain open).
Cardiac surgery allows coronary reconstruction with the heart in hand, using artificial arteries or the patient's own vein, which can be taken out of other parts of the body, such as the legs. The advantage is that the reconstruction is better and the disadvantage is that it entails open surgery with the use of extracorporeal circulation.
Tobacco is a big risk factor for developing angina. It should be completed avoided. Controlling fats in the blood and moderate, constant physical exercise are very important.
It is also important to have a healthy diet and regular light or moderate exercise continued over time.
Another important aspect for those who suffer from angina is information relating to how to lead a normal life, over many years, with close monitoring of medication and the relevant tests. Many people have a long life with very few issues after having had angina, as long as the condition is closely controlled.
Cardiology, Cardiac surgery, Haemodynamics and cardiac catheterisation, Intensive care.
Minority diseases, also called rare diseases, are those that affect between 5% and 7% of the population. They are very varied, affecting different parts of the body with a wide range of symptoms that change both between diseases and within the same disease.
It is estimated that some 30 million people in the EU, 3 million in Spain, and around 350,000 in Catalonia suffer from one.
The complexity of most rare diseases requires multidisciplinary care involving expert professionals from different medical specialties, personalized nursing management, psychological support, and social work, among other services.
At Vall d’Hebron, more than 200 specialist professionals care for over 40,000 patients with rare diseases. We are one of the hospitals in Spain that treats the highest number of rare conditions and one of the leading centers in Europe in this field. As of 2025, we are part of 20 European Reference Networks for rare diseases (ERN), 43 Spanish reference centers (CSUR), and the 12 expertise networks of the Department of Health (XUEC). This makes the hospital a highly specialized center for caring for these diseases throughout the entire life journey—from birth to adulthood—through a networked system that allows sharing resources and expertise with other hospitals and centers in the region.
The professionals across the various units and centers aim to improve patient access to diagnosis, information, and personalized care, as well as support research through:
The Rare Diseases Committee aims to establish a common framework for rare disease care at the hospital, identify and align the different initiatives (clinical, training, and research), deploy prioritized action lines, and monitor and evaluate outcomes in order to propose and implement improvements.
The concentration of patients with rare diseases increases knowledge and promotes research. Our Research Institute (VHIR) is a leader in both basic and clinical research. More than 14 basic research groups focus on studying rare diseases to improve diagnosis and develop new therapeutic approaches. We are the center in Spain with the highest number of clinical trials involving orphan drugs, including gene therapies, and we have a leading unit dedicated to the development of advanced therapies.
For more information, you can contact the rare disease team at: minoritaries@vallhebron.cat
Hereditary metabolic diseases (HMDs) are a group of rare genetic disorders. The genetic defect causes a structural alteration in a protein that is involved in one of the metabolic pathways, causing it to block the affected pathway. As a consequence, this causes a build up of substances that may be toxic for the body and a deficiency of others that it needs.
Hereditary metabolic diseases (HMD) are chronic progressive multi-system illnesses that may appear at any age and that in most cases pose diagnostic and therapeutic challenges. Our Unit has been recognised as a leader within Spain (CSUR) and Europe (ERN) for this pathology and takes part in the neonatal screening programme in Catalonia. We are the only centre in Catalonia to offer complete care from paediatrics to adults with particular expertise in lysosomal storage disorders.
HMDs are divided into:
- Intermediary metabolism HMD: usually with acute symptoms.
- HMD related to the organelles (lysosomal storage disorders, peroxisomal diseases, mitochondrial disorders and endoplasmic reticulum storage diseases): chronic presentation with no decompensations (with the exception of some mitochondrial disorders)
Multiple systems in the body are affected and different organs and systems are involved with varying symptoms depending on the disorder and the patient’s age. These disorders require a coordinated approach to care and programmes to manage the transition to adulthood.
Many symptoms become evident during childhood in the form of delayed physical growth and delayed psychomotor development. There may be associated heart problems, kidney conditions, and at times decompensations leading to liver or kidney failure and neurological impairment. In the case of organelle disorders, symptoms are chronic and affect the bones and organs of the senses in greater measure. They are more common in adults than intermediary metabolism disorders.
Diagnosis is carried out by:
They are chronic disorders that need to be treated in specialised centres with multidisciplinary teams to provide support for all related health problems.
The following may be necessary, depending on the type of disorder:
Prevention consists of thorough genetic and reproductive counselling if there is a family history of the disease. Early diagnosis of some diseases through the neonatal screening programme enables effective treatment and improved prognosis.
It is a congenital heart defect characterised by the tricuspid valve sitting lower than normal over the ventricular myocardium, caused by the corresponding atrioventricular ring.
In this case, the right atrium greatly increases its volume and the right ventricle greatly reduces in size and lung flow is not sufficient.
Ebstein’s anomaly encompasses a wide range of defects characterised by different grades of displacement and adherence of the septal valve of the tricuspid valve to the right ventricle chamber. It is a very variable disease that may be severe or mild.
The most serious cases are accompanied by severe cyanosis and congestive heart failure.
In less serious cases, the disease results in a transient period of cyanosis.
This is considered a rare disease and only represents 3% of congenital heart defects. It affects one in every 20,000 live births.
An echocardiogram is used to detect the disease, and to find out if it is associated with anatomical or functional atresia of the pulmonary valve.
The defect is treated with surgery which varies depending on the clinic, the anatomical form of the defect and the age of the patient.
In the case of new-born babies, for example, it is necessary to operate as soon possible. In adolescents or adults with symptoms, it is advisable to repair or replace the tricuspid valve with a prosthetic. If patients have no symptoms the best option is to wait.
Following surgery, 80% of patients diagnosed as teenagers or adults have a very good short to mid term prognosis as their ability to function has improved.
Pulmonary stenosis is a disorder of the heart valve that affects the pulmonary valve, the valve which separates the right ventricle from the pulmonary artery, which is the artery that transports blood to the lungs. Pulmonary stenosis occurs when the valve is unable to open sufficiently and as a result there is less blood flow to the lungs.
Mild stenosis produces no symptoms.
If it is more severe, symptoms may be:
An echocardiogram is the usual way to diagnose the condition. This test assesses the right ventricle, the pulmonary valve, post-stenotic dilatation of the pulmonary artery and pressure gradients through the valve.
Percutaneous pulmonary valvuloplasty is used to treat pulmonary stenosis, and is suitable for patients with a moderate condition over two years old.
In severe cases, percutaneous pulmonary valvuloplasty can be carried out at any age. This procedure is associated with a lower short term morbidity and mortality rate than surgical valvotomy. The procedures have similar long term outcomes.
Valvuloplasty generally attains excellent results. At a 15-year check up, only 4 % of cases need a second procedure. Mild pulmonary valvular insufficiency is well tolerated.
Congenital mitral valve anomalies include a wide range of irregularities in the valves and subvalvular systems. This can cause problems from obstruction to mitral valve insufficiency. Two specific problems can occur: stenosis, which affects children; and congenital mitral insufficiency.
Congenital mitral stenosis tends to appear in the first two years of life,
and congenital mitral insufficiency occurs where there is an excess of liquid in the lung which causes breathing difficulties.
Symptoms of congenital mitral stenosis are:
Congenital mitral insufficiency results in an increase in respiratory infections.
Congenital mitral valve anomalies are rare and make up 0.5% of congenital heart defects.
The disease is detected via echocardiogram, which provides information on the valve’s components. This technique also allows any other associated damage present to be seen.
Congenital mitral stenosis requires different kinds of treatment depending on how severe it is.
Children who have undergone surgery can have a normal life but must be monitored by a cardiologist. However, as the child grows they may need a new procedure to adapt the valve to their growth until they reach adulthood.
In the case of congenital mitral insufficiency, surgical repair or replacement of the valve is necessary in patients with symptoms who have severe mitral insufficiency and do not respond to treatment.
A congenital cyanotic heart defect is a congenital heart disorder in which deoxygenated blood bypasses the lungs and enters the circulatory system, or where there is a mixture of oxygenated and deoxygenated blood entering the system. It is caused by structural defects in the heart such as bidirectional shunting, or the incorrect position of the pulmonary artery or the aorta, or any condition that increases pulmonary vascular resistance. The result is the development of collateral circulation.
Children with this heart condition will have the following symptoms:
Tetralogy of Fallot makes up 10% of all congenital heart disorders and is considered the most common cyanotic heart disease. There are around 400 cases for every million births.
Diagnosis is confirmed via 2D echocardiogram.
Repair is carried out around six months old. If the baby suffers a episode before the defect has been corrected, treatment is started in the form of beta blockers to reduce lung spasms.
If very severe cyanotic episodes persist in babies under six months despite this treatment, then palliative surgery needs to be performed to take blood to the lungs. This surgery consists of making a connection between a systemic artery and the pulmonary arteries (a systemic-pulmonary fistula).
The definitive corrective surgery involves closing the ventricular septal defect with a patch and widening the outlet from the right ventricle.
In cases of severe pulmonary insufficiency there is progressive dilatation of the right ventricle in the long term. If this becomes excessive, it is necessary to replace the valve. Risk of lung valve replacement is around 20% after 25 years.
Unfortunately, there are currently no measures that can be taken to prevent this heart condition.
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