Google+ Link To And Excerpts From StatPearls' "Pulmonary Hypertension" - Tom Wade MD

Link To And Excerpts From StatPearls’ “Pulmonary Hypertension”

Today, I review, link to, and excerpt from StatPearlsPulmonary Hypertension. Sean H. Oldroyd; Gaurav Manek; Abhishek Bhardwaj. Last Update: May 1, 2024.

All that follows is from the above resource.


Pulmonary hypertension encompasses a diverse group of conditions characterized by high pulmonary pressures. The World Health Organization classifies pulmonary hypertension into 5 clinical groups based on pathophysiology, hemodynamic characteristics, clinical features, and management (see Table 1. Clinical Classification of Pulmonary Hypertension).

TABLE 1: Clinical Classification of Pulmonary Hypertension

Group 1: Pulmonary Arterial Hypertension (PAH) Group 2: Pulmonary Hypertension due to left heart disease (PH-LHD) Group 3: Pulmonary Hypertension due to Lung Diseases, Hypoxia, or Both Group 4: Pulmonary Hypertension Due to Pulmonary Artery Obstructions Group 5: Pulmonary Hypertension with Unclear or Multifactorial Mechanisms
1.1 Idiopathic PAH (IPAH)

1.1.1 Non-responders to vasoreactivity testing

1.1.2 Acute responders to vasoreactivity testing

2.1 Heart failure

2.1.1 With preserved ejection fraction

2.1.2 With reduced ejection fraction

3.1 Obstructive lung disease 4.1 Chronic thromboembolic pulmonary hypertension (CTEPH) 5.1 Hematological disorders
1.2 Heritable PAH (HPAH) 2.2 Valvular heart disease 3.2 Restrictive lung disease 4.2 Other pulmonary artery obstructions 5.2 Systemic disorders
1.3 Drug and Toxin induced PAH 2.3 Congenital and acquired cardiovascular conditions leading to postcapillary pulmonary hypertension 3.3 Lung diseases with mixed restrictive and obstructive patterns 5.3 Metabolic disorders
1.4 PAH associated with

1.4.1 Connective tissue disease (CTD)

1.4.2 HIV infection

1.4.3 Portal hypertension

1.4.4 Congenital heart disease (CHD)

1.4.5 Schistosomiasis

3.4 Hypoventilation syndromes 5.4 Chronic renal failure with and without hemodialysis
1.5 PAH with overt features of venous or capillary involvement, ie, pulmonary venoocclusive disease and pulmonary capillary hemangiomatosis 3.5 Hypoxia without lung disease 5.5 Pulmonary tumor thrombotic microangiopathy
1.6 Persistent pulmonary hypertension of the newborn 3.6 Developmental lung disorders 5.6 Fibrosing mediastinitis

From: Pulmonary Hypertension

Besides the above clinical distinctions, pulmonary hypertension has a hemodynamic classification scheme that can aid diagnosis. A mean pulmonary artery pressure (mPAP) greater than 20 mm Hg is above the upper normal limit. However, a mere mPAP elevation is insufficient to define pulmonary hypertension, as this elevation could be due to a cardiac output or pulmonary artery wedge pressure (PAWP) increase. Thus, the 6th World Symposium on Pulmonary Hypertension and the European Society of Cardiology/European Respiratory Society (ESC/ERS) guidelines also classify pulmonary hypertension based on pulmonary vascular resistance (PVR) and PAWP. (see Table 2. Hemodynamic Classification of Pulmonary Hypertension).

TABLE 2: Hemodynamic Classification of Pulmonary Hypertension 

Definition Hemodynamic Characteristics Clinical Groups
Precapillary pulmonary hypertension mPAP >20 mm Hg

PAWP ≤ 15 mm Hg

PVR > 2 Wood units

1, 3, 4, and 5
Isolated postcapillary pulmonary hypertension (IpcPH) mPAP > 20 mm Hg

PAWP > 15 mm Hg

PVR ≤ 2 Wood units

2 and 5
Combined precapillary and postcapillary pulmonary hypertension (CpcPH) mPAP > 20 mm Hg

PAWP > 15 mm Hg

PVR > 2 Wood units

2 and 5

From: Pulmonary Hypertension

Pulmonary vessel measurements are obtained during right heart catheterization (RHC) at rest in the supine position. The latest ESC/ERS guidelines also define exercise pulmonary hypertension as a change in mPAP/cardiac output slope between rest and exercise greater than 3 mm Hg/L/min. However, this definition does not differentiate between precapillary and postcapillary pulmonary hypertension. A PAWP/cardiac output slope change greater than 2 mm Hg/L/min between rest, and exercise may offer such differentiation, but measuring PAWP during exercise is challenging.

As the above table shows, all pulmonary hypertension groups can have precapillary and postcapillary components. Thus, the condition should be classified based on the presumed predominant underlying cause of the increased pulmonary artery pressures. Patients with PAH typically present with precapillary pulmonary hypertension, excluding conditions seen in groups 3 and 4 that can also cause precapillary hypertension.

Pulmonary Circulation Anatomy and Physiology

The pulmonary vasculature comprises the network of blood vessels transporting blood between the heart and lungs. Deoxygenated blood from the heart’s right side is pumped into the pulmonary arteries, which branch into smaller arterioles and eventually into capillaries within the lungs. Gas exchange occurs in the pulmonary arteries, with carbon dioxide diffusing out of the blood and oxygen entering the blood. Oxygenated blood then travels through the pulmonary venules and veins, returning to the left side of the heart via the pulmonary veins. From there, oxygen-rich blood is pumped into the systemic circulation to supply oxygen to tissues throughout the body.

Physiologically, the pulmonary vasculature is characterized by low resistance, allowing efficient blood flow through the lungs. The pulmonary arteries and arterioles are highly compliant and capable of expanding and contracting to accommodate blood flow and pressure changes. Smooth muscle cells within the vessel walls regulate vascular tone, helping to maintain appropriate blood flow distribution and pulmonary artery pressure. Additionally, the pulmonary circulation operates parallel to the systemic circulation, ensuring that blood is oxygenated adequately before being distributed to the body’s tissues. The pulmonary vasculature supports effective gas exchange and oxygenation within the lungs, which is essential for maintaining overall health and function.


Genetic mutations are associated with various pulmonary hypertension types, including IPAH, HPAH, and hereditary hemorrhagic telangiectasia (HHT) associated with PAH. Individuals with HPAH have an inheritable genetic mutation. People with IPAH have a genetic predisposition, but the mutations are sporadic. These groups are clinically indistinguishable. The various mutations associated with IPAH/HPAH are BMPR2 (most common), SMAD1, SMAD9, KCNK3, CAV1, and SOX17, while those associated with HHT are ALK1, ENG, and SMAD4.

The drugs and toxins known to cause PAH include aminorex, fenfluramine, dexfenfluramine, benfluorex, methamphetamines, dasatinib, and toxic rapeseed oil. Some substances that may give rise to PAH include cocaine, phenylpropanolamine, L-tryptophan, St. John’s wort, amphetamines, interferon -α and -β, alkylating agents, bosutinib, direct-acting hepatitis C antivirals, leflunomide, and indirubin. Various CTDs are also known to cause PAH, including systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis, Raynaud disease, and mixed connective tissue disease (MCTD). Among these, systemic sclerosis is the most notorious for causing PAH.

Pulmonary hypertension associated with CHD (PH-CHD) is classified into CHD that causes Eisenmenger syndrome, PAH associated with prevalent systemic-to-pulmonary shunts, PAH with small or coincidental defects, and PAH after defect correction. While PH-CHD is predominantly classified under group 1 pulmonary hypertension, some defects are more appropriately classified under group 2. These conditions include mitral valve disease, left ventricular inflow or outflow obstruction, and left ventricular systolic or diastolic dysfunction that may also result in postcapillary pulmonary hypertension.

Group 3 hypoventilation syndromes comprise conditions causing sleep-disordered breathing. Hypoxia without hypoventilation is seen at high altitudes. Group 4 etiologies include chronic thromboembolic disease, sarcoma, other malignant tumors like renal carcinoma, uterine carcinoma, testicular germ cell tumors, and nonmalignant tumors like leiomyoma, arteritis without CTD, congenital pulmonary artery stenoses, and hydatidosis. These conditions can obstruct the pulmonary artery and cause pulmonary hypertension.

Chronic hemolytic anemia and myeloproliferative disorders are hematological disorders that cause group 5 pulmonary hypertension. Systemic diseases that can cause pulmonary hypertension include pulmonary Langerhans cell histiocytosis, neurofibromatosis type 1, and sarcoidosis. Glycogen storage diseases and Gaucher disease are metabolic disorders that can cause pulmonary hypertension.


Pulmonary hypertension can affect people of any age. Present estimates suggest a prevalence of approximately 1% in the global population. Left heart disease (LHD) is the leading cause, followed by lung disease, particularly chronic obstructive pulmonary disease (COPD). In developing countries, CHD, infectious diseases like schistosomiasis and HIV, and high altitude are significant pulmonary hypertension causes. PAH incidence is approximately 6 cases per million adults, and the prevalence is about 49 to 55 cases per million adults. PAH was initially thought to affect predominantly young women. However, recent data show that the condition is also prevalent in patients aged 65 years and older with cardiovascular comorbidities, leveling the sex distribution.

At least 50% of patients with heart failure with preserved ejection fraction either have IpcPH or CpcPH. The prevalence of pulmonary hypertension increases with disease severity in these patients, with 60 to 70% of patients with severe and symptomatic mitral valve disease and 50% with symptomatic aortic stenosis affected by pulmonary hypertension. Mild pulmonary hypertension is common in patients with advanced COPD and interstitial lung disease (ILD). Only 1% to 5% of patients with advanced COPD were found to have severe pulmonary hypertension. The prevalence increases with increasing severity in patients with idiopathic pulmonary fibrosis and is as high as 60% in patients with end-stage disease. 

Registry data indicate that CTEPH’s incidence and prevalence are 2 to 6 and 26 to 39 cases per million adults, respectively. Pulmonary hypertension in individuals with sarcoidosis is frequent and often associated with increased mortality and morbidity.

History and Physical


The hallmark presenting symptom of pulmonary hypertension is shortness of breath on exertion. Nonspecific symptoms may also be reported, including hemoptysis, fatigue, early exhaustion, palpitations, dizziness, and syncope. As the disease progresses, symptoms of right-sided heart failure manifest, such as weight gain, edema, abdominal distention, and ascites.

Rarely, pulmonary artery enlargement may present with chest pain on exertion from left main coronary artery compression. Hoarseness may manifest from left recurrent laryngeal nerve compression—a condition known as Ortner syndrome. Bronchial compression may present as atelectasis. Pulmonary artery enlargement may also cause wheezing, cough, and frequent lower respiratory tract infections.

Patients may also have symptoms related to their underlying diseases, such as joint pains, skin rashes, cough, daytime somnolence, and a history of blood clots. Family, sexual, and travel history are highly relevant when evaluating a patient with suspected pulmonary hypertension.

Decompensated patients may present with pulselessness, apnea, and unconsciousness. These are signs of cardiorespiratory arrest, warranting immediate resuscitation.

Physical Examination

An increased P2 (pulmonic) component of the second heart sound is usually the initial physical finding. Jugular venous distention with a prominent “a” wave is seen with an eventual prominent “v” wave, signifying tricuspid regurgitation as the disease progresses and right ventricular dysfunction ensues. Tricuspid and pulmonic regurgitation murmurs and right-sided S3 or S4 may be heard. Elevated pulmonary pressures and, eventually, right ventricular failure cause these abnormalities.

Ascites, abdominal distention, hepatomegaly with or without splenomegaly, and dependent edema may also be present. Pallor, delayed capillary refill, and peripheral cyanosis may be seen as right ventricular failure progresses, signifying a low cardiac output state.

Various other physical exam findings may be present in patients with CTD or chronic lung diseases, such as digital clubbing, telangiectasias, Raynaud phenomenon, digital ulceration, gastroesophageal reflux signs like abdominal tenderness, crackles or wheezing on lung auscultation, and joint swelling and erythema.


Basic Concepts in Pulmonary Hypertension Evaluation

Despite technological advances, pulmonary hypertension detection still takes more than 2 years from symptom onset, thus requiring a high index of suspicion. Patients with unexplained shortness of breath or symptoms concerning for pulmonary hypertension should be thoroughly assessed. The evaluation process should include a comprehensive medical and family history, physical examination, monitoring of blood pressure, heart rate, oxygen saturation, and blood tests, including brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) and resting electrocardiogram (ECG). These initial steps help raise suspicion of a cardiopulmonary illness. The next step in the workup involves cardiac assessment with echocardiography. Signs indicative of pulmonary dysfunction warrant pulmonary function tests (PFTs), chest imaging modalities like x-ray and computed tomography (CT), and, in some instances, cardiopulmonary exercise testing (CPET).

The echocardiogram can help assess whether the probability of pulmonary hypertension is low, intermediate, or high. Patients with intermediate-to-high pulmonary hypertension probability on echocardiogram and low-probability patients with PAH or CTEPH risk factors but no other identified causes for their symptoms should be referred to a specialized facility for further comprehensive testing and confirmation of pulmonary hypertension.

PAH risk factors include CTD, HIV, family history of PAH, and portal hypertension. CTEPH risk factors include a history of pulmonary embolism, permanent intravascular devices, malignancy, inflammatory bowel diseases, essential thrombocythemia, and high-dose thyroid replacement.

Warning signs warrant a fast-track referral to a pulmonary hypertension center, including rapidly evolving right ventricular failure symptoms, syncope, low cardiac output signs, hemodynamic decompensation, and poorly tolerated arrhythmias.

Laboratory Testing

Routine hematology studies, renal function tests, liver function tests (LFTs), iron profiles, and thyroid studies should be performed in all patients with clinical signs of pulmonary hypertension. Thyroid dysfunction should always be suspected in individuals with abrupt deterioration, as it is common in PAH and may occur during the disease course.

Routine HIV screening, hepatitis virus serologies, and CTD tests should be performed. Patients with scleroderma have a high PAH prevalence and should be routinely screened with antinuclear antibody immunofluorescence. Clinical findings should determine if other CTD tests, such as anticentromere, antitopoisomerase, anti-RNA polymerase III, double-stranded DNA, anti-Ro, anti-La, and U1-RNP, should be obtained. Patients with CTEPH and those with CTD associated with thrombophilic states should also be screened for coagulopathies and thrombophilias, including lupus anticoagulant, anticardiolipin antibodies, and anti-β2-glycoprotein antibodies. BNP and NT-proBNP levels are independent outcome predictors and may also be considered during evaluation.

Patients may have abnormal LFT values due to congestive hepatopathy from either right heart failure, liver disease, or endothelin receptor antagonist (ERA) therapy. Viral hepatitis should still be ruled out in these individuals by obtaining hepatitis serologies.


A normal ECG does not exclude the diagnosis of pulmonary hypertension. However, an abnormal ECG may indicate severe disease, especially if QRS and QTc are prolonged. ECG abnormalities may include signs of right-sided heart strain and chamber enlargement, including P pulmonale, right axis deviation, right ventricular strain, right ventricular hypertrophy, right bundle branch block, and QTc prolongation. Supraventricular tachycardias, including atrial flutter and fibrillation, can occur in advanced disease, but ventricular arrhythmias are rare.

Chest Radiography

Chest radiography may reveal underlying pulmonary hypertension, such as right atrial enlargement, pulmonary artery enlargement, peripheral vessel pruning, and a water bottle-shaped cardiac silhouette. Signs of left heart disease like Kerley B lines, pleural effusions, and left heart enlargement may also be present. Patients with lung disease may have diaphragmatic flattening, hyperlucency, volume loss, or reticular opacifications on x-ray, depending on their condition. A normal chest X-ray does not rule out pulmonary hypertension.

Pulmonary Function Tests and Arterial Blood Gases

A complete set of PFTs can give diagnostic and prognostic information. Most patients with PAH have decreased carbon monoxide diffusion capacity (DLCO). A DLCO of less than 45% is associated with poor outcomes. Spirometry can help detect obstructive airway disorders. Decreased lung volumes and DLCO may indicate interstitial lung disease.

Patients with PAH usually have a low normal or slightly low partial pressure of oxygen (PaO2). A severely reduced PaO2 should raise suspicion for shunting, as in a patent foramen ovale or hepatic disease. Patients with PAH may also have alveolar hyperventilation, often producing a low or low-to-normal carbon dioxide partial pressure (PaCO2). Unfavorable outcomes have been reported in patients with low PaCO2 at diagnosis and follow-up. An elevated PaCO2 is unusual and should raise suspicion of sleep-disordered breathing or hypoventilation.

Chest CT and Digital Subtraction Angiography

Chest CT is essential for identifying ILDs, helping differentiate between various pulmonary hypertension groups (see Image. Pulmonary Hypertension from Connective Tissue Disease on CT). This modality also provides additional information that may increase suspicion of this condition, such as enlarged pulmonary artery diameter, main pulmonary artery-ascending aorta diameter ratio greater than 0.9, and enlarged right heart chambers. A pulmonary artery diameter of at least 30 mm, right ventricular outflow tract (RVOT) thickness of at least 6 mm, septal deviation greater than 140°, or right-to-left ventricle ratio of at least 1 is highly predictive of pulmonary hypertension.

Contrast CT pulmonary angiography may demonstrate CTEPH signs such as webs, bands, filling defects, enlarged bronchial arteries, and mosaic perfusion. CT pulmonary angiography often has a high diagnostic accuracy for CTEPH when high-quality multi-detector CT images are interpreted by experienced readers. Digital subtraction angiography (DSA) with conventional 2- or 3-planar imaging is used in most centers to confirm CTEPH diagnosis and assess operability for endarterectomy or balloon pulmonary angioplasty.


Transthoracic echocardiography remains the single most crucial noninvasive assessment tool for pulmonary hypertension. However, echocardiographic assessment should only be used to estimate pulmonary hypertension probability. RHC is used for diagnostic confirmation and therapeutic guidance.

Data obtained from normal adults led to the ESC/ERS guidelines for classifying pulmonary hypertension probability into low, intermediate, or high. Tables 3 and 4 provide information about echocardiographic probability and signs suggestive of pulmonary hypertension, respectively.

Table 3: Echocardiographic Pulmonary Hypertension Probability

Peak Tricuspid Regurgitant Velocity (m/s) Presence of Other Pulmonary Hypertension Signs on Echocardiography Echocardiographic Probability of Pulmonary Hypertension
< 2.8 or not measurable No Low
< 2.8 or not measurable Yes Intermediate
2.9-3.4 No Intermediate
2.9-3.4 Yes High
>3.4 Not required High

From: Pulmonary Hypertension

Table 4: Echocardiographic Signs Suggestive of Pulmonary Hypertension 

Ventricles Right-to-left ventricle basal diameter area ratio >1 Interventricular septum flattening (left ventricular eccentricity index > 1.1 in systole, diastole, or both) Tricuspid annular plane systolic excursion-systolic pulmonary artery pressure ratio < 0.55 mm / mm Hg
Pulmonary Artery RVOT acceleration time <105 ms or mid-systolic notching Early diastolic pulmonary regurgitation velocity > 2.2 m/s Pulmonary artery > aortic root  diameter

Pulmonary artery diameter > 25mm

Inferior Vena Cava and Right Atrium Inferior vena cava diameter > 21 mm with decreased inspiratory collapse (<50% with a sniff or <20% with quiet respiration) Right arterial area (end-systole) > 18 cm2

From: Pulmonary Hypertension

RHC should be performed in patients with a high pulmonary hypertension probability on echocardiography, with or without PAH or CTEPH risk factors. In contrast, follow-up imaging should be considered in patients with PAH or CTEPH risk factors and a low pulmonary hypertension probability on echocardiography. However, RHC should be considered in similar patients with a medium pulmonary hypertension probability. An alternative diagnosis should be considered in patients without PAH or CTEPH risk factors and a low pulmonary hypertension probability on echocardiography. Alternative diagnoses or further investigations can be considered in people with medium probability without PAH or CTEPH risk factors.

Besides assessing probability, echocardiography can also detect conditions that may cause pulmonary hypertension, including CHD, valvular heart disease, and left-sided heart dysfunction.

Cardiopulmonary Exercise Testing

Patients with exercise-induced symptoms induced should undergo CPET. In patients with PAH, a low end-tidal partial pressure of carbon dioxide, high ventilatory equivalent for carbon dioxide, low oxygen pulse, and low peak oxygen uptake are typically seen. PAH may be excluded in people with systemic sclerosis with a normal peak oxygen uptake.

Ventilation-Perfusion Scanning

A ventilation-perfusion (V/Q) scan is performed to rule out CTEPH in patients with pulmonary hypertension (see Image. CTEPH Ventilation-Perfusion Scan). This diagnostic test remains the preferred modality since a normal scan can exclude CTEPH with a sensitivity of 90% to 100% and a specificity of 94% to 100%. Recent CT, magnetic resonance imaging (MRI), and single photon emission CT advances have narrowed the gap between V/Q scans and these other modalities. The V/Q-single photon emission CT is superior to planar V/Q scan and should be the preferred modality if available. However, some advanced imaging modalities and the expertise to interpret them may not be widely available. Thus, further studies are needed to establish their clinical utility.

Cardiac Magnetic Resonance Imaging

Cardiac MRI (cMRI) is an incredibly powerful tool that accurately assesses atrial and ventricular function and morphology. This modality can also measure blood flow through the vena cava, pulmonary artery, and aorta, allowing for stroke volume quantification. The test is sensitive for detecting early pulmonary hypertension but does not reliably estimate pulmonary artery pressures. Additionally, cost and availability are considerable barriers to using cMRI.

Abdominal Ultrasound

The main reason for obtaining an abdominal ultrasound is to detect liver abnormalities, portal hypertension, and kidney injury that may arise from chronic pulmonary hypertension. Ultrasonography can help assess the extent of the collateral damage to these organs.

Genetic Testing and Counseling

A trained PAH provider or geneticist should counsel patients with familial PAH, IPAH, HPAH, anorexigenic-associated PAH, pulmonary venoocclusive disease, and pulmonary capillary hemangiomatosis that family members could carry a mutation that increases their PAH risk. Genetic testing can inform the patient and family members to screen for early symptoms and signs to ensure a timely diagnosis. Genetic sequencing technological advancements have led to the development of gene panels that can simultaneously test for several gene mutations. A trained geneticist must provide counseling and help interpret the tests.

The following are nuances regarding RHC measurements:

  • External pressure transducers must be calibrated to zero at the level of the left atrium.
  • PAWP should be measured at the end of normal expiration.
  • Cardiac output should be measured using triplicate thermodilution. However, thermodilution may be inaccurate in patients with intracardiac shunts, warranting direct Fick estimation. The information should be interpreted based on the clinical picture and imaging findings, especially echocardiography.

Vasoreactivity testing is an RHC component that should only be done in patients with IPAH, HPAP, and drug-induced IPAHInhaled nitric oxide at 10 to 20 parts per million is usually preferred, but intravenous epoprostenol, intravenous adenosine, or inhaled iloprost may also be used. The test is deemed positive if there is an mPAP decrease of at least 10 mm Hg, resulting in a final mPAP of 40 mm Hg or less and either unchanged or increased cardiac output. Patients who test positive are suitable for high-dose calcium channel blocker (CCB) treatments.

Other maneuvers, such as a fluid challenge, may be used to discriminate IPAH from left ventricular diastolic dysfunction. However, this technique needs to be further studied before it becomes the standard of care. A left heart catheterization should also be performed in individuals with clinical risk factors for coronary artery disease or echocardiographic signs of left heart systolic or diastolic dysfunction.

RHC contraindications include a recently implanted pacemaker (<1 month), known right atrial or ventricular thrombus, mechanical right heart valve, tricuspid valve clip, and acute infection. The most feared complication of the procedure is pulmonary arterial rupture.

Treatment / Management

The treatment strategy for PAH involves a risk-based approach, considering clinical, functional, exercise, hemodynamic, and right ventricular function parameters. Multiple studies show this treatment approach must be based on baseline methodical risk assessment and follow-up to predict survival or event-free survival.

Patients should be assessed at every visit using a multidimensional approach. Key risk stratification tools include the US Registry to Evaluate Early and Long-term PAH Disease Management (REVEAL) equation and risk score, the 2022 ESC/ERS guidelines risk table categorizing patients as having a low (<5%), intermediate (5 to 20%), or high (>20%) risk based on estimated 1-year mortality, and the French Pulmonary Hypertension Network (FPHN) Registry risk equation. The REVEAL 2.0 risk score calculator refines the original risk assessment tool. However, studies show that the World Health Organization-functional class (WHO-FC), 6-minute walk distance, and BNP (or NT-proBNP) are the strongest survival predictors across all risk scores.

The ESC/ERS risk stratification correlates with the REVEAL 2.0 score: “low risk” has a REVEAL score less than or equal to 6, “intermediate risk” has a REVEAL score of 7 or 8, and “high risk” corresponds to a REVEAL score of at least 9. However, the REVEAL score has many variables and predicts outcomes over a shorter period (1 year), whereas the ESC/ERS system may assign prognostic parameters to multiple risk categories for the same patient. Despite their usefulness, all these stratification systems have limitations. Therefore, a comprehensive risk assessment strategy incorporating clinical judgment is essential for each patient, alongside these scoring tools. The overall treatment goal is to achieve low-risk status.

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