Presentazione a cura del Dottor Carmine Dario Vizza - XII° Congresso Nazionale FIMeG 2018 - The Silver Tsunami: l'anziano fra appropriatezza e farmaeconomia
- The EPHESUS trial randomized over 6,000 patients who had a myocardial infarction with reduced left ventricular ejection fraction (<40%) within 3-14 days to eplerenone or placebo in addition to standard therapy.
- At 16 months follow up, eplerenone reduced the risk of death from any cause by 15% and death from cardiovascular causes by 13% compared to placebo.
- Eplerenone was generally well tolerated but increased the risk of hyperkalemia compared to placebo.
Pliability assessment,pre procedure evaluation-tricks in difficult pbmvMalleswara rao Dangeti
The document discusses techniques for assessing mitral valve pliability and severity of mitral stenosis prior to percutaneous balloon mitral valvuloplasty (PBMV). Key factors include mitral valve area, leaflet thickness, mobility, calcification, and subvalvular involvement. Multiple echocardiography-based scoring systems are described to evaluate valve morphology and predict PBMV outcomes. PBMV is recommended for symptomatic moderate-severe mitral stenosis when the valve is suitable for the procedure based on pre-assessment of pliability and anatomy.
This document discusses strategies to minimize right ventricular pacing, which can have deleterious effects. It summarizes several clinical trials that evaluated ventricular versus atrial or dual-chamber pacing. The trials generally found that atrial or dual-chamber pacing reduced atrial fibrillation compared to ventricular pacing, though effects on other outcomes like mortality were less clear. The document recommends that right ventricular pacing be avoided or minimized when possible, through use of AAI pacing, DDD pacing with long fixed AV delays, search AV hysteresis algorithms, or mode-switching algorithms that favor intrinsic conduction.
This document summarizes a presentation on cardiac resynchronization therapy (CRT) and clinical trials. It discusses:
1) Heart failure is an increasing cardiovascular disease that is disabling, deadly, and costly. Approximately 1 in 3 heart failure patients have ventricular dyssynchrony.
2) Early CRT trials in the 1990s showed feasibility and safety. Larger subsequent trials demonstrated reductions in mortality and morbidity with CRT.
3) The PATH-CHF trial in 1999 was one of the earliest randomized controlled trials of CRT. It found improvements in peak oxygen consumption and quality of life with CRT compared to no pacing or single chamber pacing in heart failure patients.
1. Pulmonary hypertension is defined as a mean pulmonary artery pressure greater than 25 mm Hg at rest as measured by right heart catheterization. Severity is classified as mild, moderate, or severe based on pressure readings.
2. Echocardiography can be used to estimate pulmonary artery pressures and assess right heart structures for signs of pulmonary hypertension. Measurements like tricuspid regurgitation velocity, pulmonary regurgitation pressure gradient, and inferior vena cava size correlate with pulmonary artery pressures.
3. Additional findings on echo that indicate pulmonary hypertension include right ventricular dilation, septal flattening, reduced right atrial emptying, and pulmonary artery acceleration time. Together, echo findings can establish the diagnosis
- The EPHESUS trial randomized over 6,000 patients who had a myocardial infarction with reduced left ventricular ejection fraction (<40%) within 3-14 days to eplerenone or placebo in addition to standard therapy.
- At 16 months follow up, eplerenone reduced the risk of death from any cause by 15% and death from cardiovascular causes by 13% compared to placebo.
- Eplerenone was generally well tolerated but increased the risk of hyperkalemia compared to placebo.
Pliability assessment,pre procedure evaluation-tricks in difficult pbmvMalleswara rao Dangeti
The document discusses techniques for assessing mitral valve pliability and severity of mitral stenosis prior to percutaneous balloon mitral valvuloplasty (PBMV). Key factors include mitral valve area, leaflet thickness, mobility, calcification, and subvalvular involvement. Multiple echocardiography-based scoring systems are described to evaluate valve morphology and predict PBMV outcomes. PBMV is recommended for symptomatic moderate-severe mitral stenosis when the valve is suitable for the procedure based on pre-assessment of pliability and anatomy.
This document discusses strategies to minimize right ventricular pacing, which can have deleterious effects. It summarizes several clinical trials that evaluated ventricular versus atrial or dual-chamber pacing. The trials generally found that atrial or dual-chamber pacing reduced atrial fibrillation compared to ventricular pacing, though effects on other outcomes like mortality were less clear. The document recommends that right ventricular pacing be avoided or minimized when possible, through use of AAI pacing, DDD pacing with long fixed AV delays, search AV hysteresis algorithms, or mode-switching algorithms that favor intrinsic conduction.
This document summarizes a presentation on cardiac resynchronization therapy (CRT) and clinical trials. It discusses:
1) Heart failure is an increasing cardiovascular disease that is disabling, deadly, and costly. Approximately 1 in 3 heart failure patients have ventricular dyssynchrony.
2) Early CRT trials in the 1990s showed feasibility and safety. Larger subsequent trials demonstrated reductions in mortality and morbidity with CRT.
3) The PATH-CHF trial in 1999 was one of the earliest randomized controlled trials of CRT. It found improvements in peak oxygen consumption and quality of life with CRT compared to no pacing or single chamber pacing in heart failure patients.
1. Pulmonary hypertension is defined as a mean pulmonary artery pressure greater than 25 mm Hg at rest as measured by right heart catheterization. Severity is classified as mild, moderate, or severe based on pressure readings.
2. Echocardiography can be used to estimate pulmonary artery pressures and assess right heart structures for signs of pulmonary hypertension. Measurements like tricuspid regurgitation velocity, pulmonary regurgitation pressure gradient, and inferior vena cava size correlate with pulmonary artery pressures.
3. Additional findings on echo that indicate pulmonary hypertension include right ventricular dilation, septal flattening, reduced right atrial emptying, and pulmonary artery acceleration time. Together, echo findings can establish the diagnosis
This document provides an overview of echocardiographic assessment of mitral regurgitation. It describes the anatomy of the mitral valve including the leaflets, annulus, chordae, and papillary muscles. It discusses Carpentier's functional classification system for describing the mechanism of mitral valve dysfunction. Methods for assessing severity are covered, including color flow imaging, continuous wave Doppler, vena contracta width, proximal isovelocity surface area, and volumetric assessment. Key points are made about evaluating jet direction, duration, and velocity in context of blood pressure. The importance of assessing left ventricular and left atrial size and function is also highlighted.
This document discusses Eisenmenger syndrome, a condition where pulmonary hypertension develops due to increased blood flow through defects between the systemic and pulmonary circulations. It provides details on causes, clinical features, pathology findings, and treatments. Key points include:
- Eisenmenger syndrome is caused by defects like VSDs, ASDs, and PDA that allow high blood flow to the lungs and cause pulmonary hypertension over time.
- Common causes of death include hemoptysis from pulmonary artery ruptures, heart failure, and complications from attempted defect repair surgery.
- Pathological findings show thickened pulmonary arteries that resemble the fetal pattern and contribute to high pulmonary vascular resistance.
- Medical treatments are generally ineffective once int
This document discusses heart failure with preserved ejection fraction (HFpEF), formerly known as diastolic heart failure. It provides background on HFpEF versus systolic heart failure and explores the pathophysiology and management of HFpEF. Key points include:
1) HFpEF is a distinct clinical syndrome from heart failure with reduced ejection fraction (HFrEF), with normal ejection fraction but evidence of diastolic dysfunction.
2) Impaired systolic function can be detected in HFpEF patients using strain imaging, despite preserved global ejection fraction.
3) The pathophysiology of HFpEF is complex and multifactorial, involving microvascular inflammation, cardiomyocyte stiff
Echo assessment of Aortic valve disease, Dr Ferdous assistant registrar, Card...Nizam Uddin
This document discusses the echocardiographic evaluation of aortic stenosis. It begins by describing normal aortic valve anatomy and various views used to visualize the aortic valve via 2D echocardiography. It then discusses the classification and causes of aortic stenosis, including calcific, rheumatic, and bicuspid aortic valve stenosis. Evaluation techniques covered include determining aortic valve area using the continuity equation and measuring transaortic jet velocity via continuous-wave Doppler. The document concludes by outlining the anatomical assessment of the aortic valve, methods for determining stenosis severity, and hemodynamic progression of untreated aortic stenosis over time.
COMPARES OPTIMAL MEDICAL THERAPY WITH INVASIVE THERAPY IN A PATIENT WITH STABLE ISCHEMIC HEART DISEASE WITH MODERATE TO SEVERE MYOCARDIAL ISCHEMIA ON NON INVASIVE STRESS TESTING
The document discusses localization of myocardial ischemia, injury, and infarction based on electrocardiogram (ECG) findings. It provides information on interpreting ST segment changes and T-wave abnormalities in different leads to localize occlusion in the left anterior descending, right coronary artery, or left circumflex arteries. Reciprocal changes are also discussed as indicators of occlusion location.
This document discusses sinus node dysfunction (SND), which refers to dysfunction of the sinoatrial node that can cause various electrocardiogram abnormalities like sinus bradycardia, sinus pauses, and inadequate heart rate response to activity. Common causes of SND include sinus node fibrosis, medications that depress sinus node function, infiltrative diseases, inflammatory diseases, and sinus node artery disease. The document recommends permanent pacing for patients with SND who experience symptomatic bradycardia or pauses, as well as those with chronotropic incompetence. It describes various ECG patterns that can occur in SND such as sinus bradycardia, sinus pause/arrest, sinus node exit block, and chronotropic incompetence.
This document discusses fractional flow reserve (FFR), which is a technique used to functionally assess the significance of coronary artery stenosis. FFR is defined as the ratio of maximum blood flow in a stenotic artery to maximum blood flow if there was no stenosis. It is calculated as the ratio of mean distal coronary pressure (Pd) to mean aortic pressure (Pa) during maximal hyperemia induced by pharmacological agents. An FFR value below 0.75 is associated with inducible ischemia, while a value above 0.80 indicates an insignificant stenosis in most cases. FFR has advantages over angiography alone in evaluating stenosis as it accounts for vessel characteristics like length and takes collateral flow into consideration.
The document discusses newer advancements in heart failure device therapy. It summarizes that device therapies have greatly improved outcomes for heart failure patients. Some key devices discussed include implantable cardioverter defibrillators (ICDs) which reduce sudden cardiac death, cardiac resynchronization therapy which improves heart function, and left ventricular assist devices (LVADs) which are increasingly being used as long term support devices or as a destination therapy for end stage heart failure patients. The document provides details on the development, indications, benefits and risks of these various heart failure devices.
This document provides guidance on managing patients who do not respond to cardiac resynchronization therapy (CRT). It discusses that while CRT has been shown to reduce heart failure hospitalizations and mortality, 30-35% of patients do not adequately respond. The document then reviews factors that determine CRT response, including electrical and mechanical dyssynchrony. It also discusses different criteria used to define response and notes lack of agreement. Potential reasons for non-response are explored, including lead placement and individual patient factors. The document concludes by recommending approaches for evaluating and managing CRT non-responders.
A lecture on the echocardiographic evaluation of hypertrophic cardiomyopathy. Starts with an overview of the topic then a systematic approach to diagnosis and then a differential diagnosis followed by take-home messages and conclusion.
This document discusses interventional heart failure therapies including heart transplantation, ventricular assist devices, closure devices for defects, valve repair/replacement procedures, defibrillators, and cardiac resynchronization therapy. It provides details on outcomes of these therapies and notes limitations such as limited organ availability for transplantation. Guidelines for use of defibrillators and cardiac resynchronization therapy are summarized. Ongoing research into treating patients with narrow QRS complexes and those in NYHA class IV is also reviewed.
This document defines and describes different types of aberrancy in ventricular conduction. It discusses mechanisms of aberrancy including premature arrival of supraventricular impulses and refractoriness of conducting tissue. Types of aberrancy include type A from fascicular refractoriness, type B from anomalous activation, and type C from paradoxical critical rate. Ashman phenomenon and acceleration/bradycardia-dependent aberrancy are also summarized.
This document discusses the echocardiographic evaluation of mitral valve prolapse (MVP). It describes the use of M-mode, 2D, and 3D echocardiography to diagnose MVP and assess mitral regurgitation severity. Measurement of the vena contracta and use of the proximal isovelocity surface area method are emphasized for accurate regurgitant quantification. Surgical indications and repair techniques are also summarized.
INOCA, or ischemia with non-obstructive coronary arteries, affects a large proportion of patients undergoing angiography who do not have obstructive coronary artery disease. INOCA can result from heterogeneous mechanisms like coronary vasospasm and microvascular dysfunction and is not benign, as it is associated with increased cardiovascular events and impaired quality of life. The diagnosis of MINOCA, a type of INOCA, requires meeting criteria for an acute myocardial infarction but having non-obstructive arteries on angiography and no other clear cause identified. Further evaluation is then needed to determine the underlying cause of MINOCA.
This document provides an overview of echocardiographic assessment of mitral regurgitation. It describes the anatomy of the mitral valve including the leaflets, annulus, chordae, and papillary muscles. It discusses Carpentier's functional classification system for describing the mechanism of mitral valve dysfunction. Methods for assessing severity are covered, including color flow imaging, continuous wave Doppler, vena contracta width, proximal isovelocity surface area, and volumetric assessment. Key points are made about evaluating jet direction, duration, and velocity in context of blood pressure. The importance of assessing left ventricular and left atrial size and function is also highlighted.
This document discusses Eisenmenger syndrome, a condition where pulmonary hypertension develops due to increased blood flow through defects between the systemic and pulmonary circulations. It provides details on causes, clinical features, pathology findings, and treatments. Key points include:
- Eisenmenger syndrome is caused by defects like VSDs, ASDs, and PDA that allow high blood flow to the lungs and cause pulmonary hypertension over time.
- Common causes of death include hemoptysis from pulmonary artery ruptures, heart failure, and complications from attempted defect repair surgery.
- Pathological findings show thickened pulmonary arteries that resemble the fetal pattern and contribute to high pulmonary vascular resistance.
- Medical treatments are generally ineffective once int
This document discusses heart failure with preserved ejection fraction (HFpEF), formerly known as diastolic heart failure. It provides background on HFpEF versus systolic heart failure and explores the pathophysiology and management of HFpEF. Key points include:
1) HFpEF is a distinct clinical syndrome from heart failure with reduced ejection fraction (HFrEF), with normal ejection fraction but evidence of diastolic dysfunction.
2) Impaired systolic function can be detected in HFpEF patients using strain imaging, despite preserved global ejection fraction.
3) The pathophysiology of HFpEF is complex and multifactorial, involving microvascular inflammation, cardiomyocyte stiff
Echo assessment of Aortic valve disease, Dr Ferdous assistant registrar, Card...Nizam Uddin
This document discusses the echocardiographic evaluation of aortic stenosis. It begins by describing normal aortic valve anatomy and various views used to visualize the aortic valve via 2D echocardiography. It then discusses the classification and causes of aortic stenosis, including calcific, rheumatic, and bicuspid aortic valve stenosis. Evaluation techniques covered include determining aortic valve area using the continuity equation and measuring transaortic jet velocity via continuous-wave Doppler. The document concludes by outlining the anatomical assessment of the aortic valve, methods for determining stenosis severity, and hemodynamic progression of untreated aortic stenosis over time.
COMPARES OPTIMAL MEDICAL THERAPY WITH INVASIVE THERAPY IN A PATIENT WITH STABLE ISCHEMIC HEART DISEASE WITH MODERATE TO SEVERE MYOCARDIAL ISCHEMIA ON NON INVASIVE STRESS TESTING
The document discusses localization of myocardial ischemia, injury, and infarction based on electrocardiogram (ECG) findings. It provides information on interpreting ST segment changes and T-wave abnormalities in different leads to localize occlusion in the left anterior descending, right coronary artery, or left circumflex arteries. Reciprocal changes are also discussed as indicators of occlusion location.
This document discusses sinus node dysfunction (SND), which refers to dysfunction of the sinoatrial node that can cause various electrocardiogram abnormalities like sinus bradycardia, sinus pauses, and inadequate heart rate response to activity. Common causes of SND include sinus node fibrosis, medications that depress sinus node function, infiltrative diseases, inflammatory diseases, and sinus node artery disease. The document recommends permanent pacing for patients with SND who experience symptomatic bradycardia or pauses, as well as those with chronotropic incompetence. It describes various ECG patterns that can occur in SND such as sinus bradycardia, sinus pause/arrest, sinus node exit block, and chronotropic incompetence.
This document discusses fractional flow reserve (FFR), which is a technique used to functionally assess the significance of coronary artery stenosis. FFR is defined as the ratio of maximum blood flow in a stenotic artery to maximum blood flow if there was no stenosis. It is calculated as the ratio of mean distal coronary pressure (Pd) to mean aortic pressure (Pa) during maximal hyperemia induced by pharmacological agents. An FFR value below 0.75 is associated with inducible ischemia, while a value above 0.80 indicates an insignificant stenosis in most cases. FFR has advantages over angiography alone in evaluating stenosis as it accounts for vessel characteristics like length and takes collateral flow into consideration.
The document discusses newer advancements in heart failure device therapy. It summarizes that device therapies have greatly improved outcomes for heart failure patients. Some key devices discussed include implantable cardioverter defibrillators (ICDs) which reduce sudden cardiac death, cardiac resynchronization therapy which improves heart function, and left ventricular assist devices (LVADs) which are increasingly being used as long term support devices or as a destination therapy for end stage heart failure patients. The document provides details on the development, indications, benefits and risks of these various heart failure devices.
This document provides guidance on managing patients who do not respond to cardiac resynchronization therapy (CRT). It discusses that while CRT has been shown to reduce heart failure hospitalizations and mortality, 30-35% of patients do not adequately respond. The document then reviews factors that determine CRT response, including electrical and mechanical dyssynchrony. It also discusses different criteria used to define response and notes lack of agreement. Potential reasons for non-response are explored, including lead placement and individual patient factors. The document concludes by recommending approaches for evaluating and managing CRT non-responders.
A lecture on the echocardiographic evaluation of hypertrophic cardiomyopathy. Starts with an overview of the topic then a systematic approach to diagnosis and then a differential diagnosis followed by take-home messages and conclusion.
This document discusses interventional heart failure therapies including heart transplantation, ventricular assist devices, closure devices for defects, valve repair/replacement procedures, defibrillators, and cardiac resynchronization therapy. It provides details on outcomes of these therapies and notes limitations such as limited organ availability for transplantation. Guidelines for use of defibrillators and cardiac resynchronization therapy are summarized. Ongoing research into treating patients with narrow QRS complexes and those in NYHA class IV is also reviewed.
This document defines and describes different types of aberrancy in ventricular conduction. It discusses mechanisms of aberrancy including premature arrival of supraventricular impulses and refractoriness of conducting tissue. Types of aberrancy include type A from fascicular refractoriness, type B from anomalous activation, and type C from paradoxical critical rate. Ashman phenomenon and acceleration/bradycardia-dependent aberrancy are also summarized.
This document discusses the echocardiographic evaluation of mitral valve prolapse (MVP). It describes the use of M-mode, 2D, and 3D echocardiography to diagnose MVP and assess mitral regurgitation severity. Measurement of the vena contracta and use of the proximal isovelocity surface area method are emphasized for accurate regurgitant quantification. Surgical indications and repair techniques are also summarized.
INOCA, or ischemia with non-obstructive coronary arteries, affects a large proportion of patients undergoing angiography who do not have obstructive coronary artery disease. INOCA can result from heterogeneous mechanisms like coronary vasospasm and microvascular dysfunction and is not benign, as it is associated with increased cardiovascular events and impaired quality of life. The diagnosis of MINOCA, a type of INOCA, requires meeting criteria for an acute myocardial infarction but having non-obstructive arteries on angiography and no other clear cause identified. Further evaluation is then needed to determine the underlying cause of MINOCA.
Presa in carico del paziente con LMC e gestione della terapia a medio e lungo...ASMaD
This document discusses cardiovascular risk management from the perspective of a vascular surgeon. It summarizes the author's experience treating patients with chronic myeloid leukemia who developed vascular complications. The main points are:
1) Patients with chronic myeloid leukemia often have multi-level vascular disease involving the carotid, renal, mesenteric, and lower extremity arteries.
2) Endovascular interventions had high restenosis and failure rates, while open surgeries resulted in better mid-term patency but higher amputation rates.
3) An aggressive surgical approach along with intensive medical management and follow-up is needed for these high-risk patients due to their underlying disease and risk factors. A multidisciplinary team approach
I meccanismi del danno gastrico e la patologia H. Pylori correlataASMaD
Presentazione a cura del Dottor Vincenzo De Francesco - "Malattia da reflussogastroesofageo e infezione da Helicobacter Pylori: old topics?" - Roma 11/05/2019
Ph impedenziometria nella MRGE: quando, come e perchèASMaD
Presentazione a cura della Dottoressa Francesca Galeazzi - "Malattia da reflussogastroesofageo e infezione da Helicobacter Pylori: old topics?" - Roma 11/05/2019
This document discusses the classification of gastroesophageal reflux disease (GERD) and challenges in classifying patients. It notes that while some patients with typical GERD symptoms respond to treatment, they remain unclassified and may not actually have GERD. A single classification system based on symptoms and endoscopy does not capture all clinical conditions related to GERD. Patients who do not respond to PPIs should be referred to a gastroenterologist. Some GERD patients have significant esophageal motility issues. Those who do not respond to PPIs may require an esophageal biopsy. Some PPI responders actually have eosinophilic esophagitis. Some GERD patients have multiple gastrointestinal comor
Cambiamenti di popolazione e flussi migratori: cambiano anche le malattie met...ASMaD
Presentazione a cura della Dottoressa Migneco Maria Giuseppina - "Incontri endocrinologici AME LAzio - L'endocrinologia nel SSN: prospettive e nuove problematiche" - Roma 17/12/2018
Tiroide: chi decide quale intervento e per chi?ASMaD
Presentazione a cura del Dottor Bellotti Carlo - "Incontri endocrinologici AME LAzio - L'endocrinologia nel SSN: prospettive e nuove problematiche" - Roma 17/12/2018
Tiroide: Integrazione tra elementi nutriacetici e farmacologia: utile o inutile?ASMaD
Presentazione a cura del Dottor Roberto Cesareo - "Incontri endocrinologici AME LAzio - L'endocrinologia nel SSN: prospettive e nuove problematiche" - Roma 17/12/2018
L'ecografia tiroidea: strumento cruciale nella gestione clinica?ASMaD
Presentazione a cura del Dottor Guglielmi Rinaldo - "Incontri endocrinologici AME LAzio - L'endocrinologia nel SSN: prospettive e nuove problematiche" - Roma 17/12/2018
Il chirurgo e la tiroide oggi un rapporto in crisi?ASMaD
Presentazione a cura del Dottor Luca Piantoni e del Dottor Francesco Pedicini - "TIROIDE 2018 Nuovi approcci diagnostici e terapeutici" - Roma 24/11/2018
L'ipertensione polmonare:come diagnosticarla e trattarla
1. L’ipertensione polmonare: come
diagnosticarla e trattarla
Carmine Dario Vizza
Centro Ipertensione Polmonare
Primitiva e Forme Associate
Dip. Malattie Cardiovascolari e Respiratorie
Universita’ di Roma “La Sapienza”
Direttore Prof Francesco Fedele
e-mail : dario.vizza@uniroma1.ite-mail : dario.vizza@uniroma1.it
2. Pulmonary Hypertension Unit
La Sapienza University oi Rome
ART POLM ATRIO SIN
ARTERIE VENECAPILLARI
16 mmHg 8 mmHgNormale
PAPm>25 mmHg a riposo
e/o
>30 mmHg durante sforzo (?)
DEFINIZIONE
Condizione fisiopatologica in cui la pressione arteriosa polmonare è aumentata a riposo e/o
durante sforzo
3. Pulmonary Hypertension Unit
La Sapienza University oi Rome
ART POLM ATRIO SIN
ARTERIE VENECAPILLARI
IP postcapillare 30 mmHg 20 mmHg
Classificazione emodinamica
IP Post-capillare
4. Pulmonary Hypertension Unit
La Sapienza University oi Rome
ART POLM ATRIO SIN
ARTERIE VENECAPILLARI
IP precapillare35 mmHg 8 mmHg
Classificazione emodinamica
IP Pre-capillare
5. Pulmonary Hypertension Unit
La Sapienza University oi Rome
1. Pulmonary Arterial Hypertension
• Idiopatic
• Hereditary (BMPR-II ; ALK-1)
•Drug and Toxin induced
• Associated with :
– Connective Tissue Disease
– HIV infection
– Portal hypertension
– Congenital heart diseaswe
– Schistosomiasis
•Persistent PH in the new born
1A
Veno-occlusive disease
3. PH due to lung disease or hypoxia
• COPD
• Interstiial lung disease
• Breathing sleep disorders
• Chronic exposure to high altitude
• Developtmental lung disorders
2. PH due to left heart disease
• Systolic/Diastolic dysfunction
• Valvulopaties
4. Chronic Thromboembolic PH
Pulmonary hypertension: Classification 2013
5. PH with multifactorial mechanisms
H
6. Pulmonary Hypertension Unit
La Sapienza University oi Rome
1. Pulmonary Arterial Hypertension
• Idiopatic
• Hereditary (BMPR-II ; ALK-1)
•Drug and Toxin induced
• Associated with :
– Connective Tissue Disease
– HIV infection
– Portal hypertension
– Congenital heart diseaswe
– Schistosomiasis
•Persistent PH in the new born
1A
Veno-occlusive disease
3. PH due to lung disease or hypoxia
• COPD
• Interstiial lung disease
• Breathing sleep disorders
• Chronic exposure to high altitude
• Developtmental lung disorders
2. PH due to left heart disease
• Systolic/Diastolic dysfunction
• Valvulopaties
4. Chronic Thromboembolic PH
Pulmonary hypertension: Classification 2013
5. PH with multifactorial mechanisms
H
Precapillare
Precapillare
Precapillare
Post-capillare
7. Emodinamica nelle diverse forme
di Ipertensione Polmonare Precapillare
IAP BPCO INT IPCTE
n=44 n=141 n=32 n=12
Pad (mmHg) 11+6 ‡
8+4 8+5 10+5
Pap (mmHg) 62+21 ‡
31+6 34+9 54+14
RVP (WU) 24+11 ‡
5.5+2 8+5 21+9
IC (L/min/m2
) 2.4+0.8 ‡
3.4+0.7 3+0.6 2.7+0.6
FE VD (%) 26+13 ‡
42+11 40+10 28+10
IAP BPCO INT IPCTE
n=44 n=141 n=32 n=12
Pad (mmHg) 11+6 ‡
8+4 8+5 10+5
Pap (mmHg) 62+21 ‡
31+6 34+9 54+14
RVP (WU) 24+11 ‡
5.5+2 8+5 21+9
IC (L/min/m2
) 2.4+0.8 ‡
3.4+0.7 3+0.6 2.7+0.6
FE VD (%) 26+13 ‡
42+11 40+10 28+10
Vizza CD, Chest 1998
‡ p=0.001 IAP e IPCTE vs BPCO e INT
8. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Female 40 yrs
mPAP = 50 mmHg
CI = 2,3 l/m/m2
Male, 35 yrs.
mPAP = 53 mmHg
CI = 2,6 l/m/m2
RV M/V = 0.5 6MWD = 380 m RV M/V = 0.8 6MWD = 540 m
Right ventricular adaptation in severe PH
9. Quando sospettare ipertensione
polmonare (IP)?
Soggetti con cardiopatia o pneumopatia nota con dispnea
sproporzionata al grado di disfunzione cardiaca o
polmonare
Soggetti con dispnea senza storia o evidenza strumentale
di cardiopatia sinistra o pneumopatia (spesso con
ipossiemia marcata)
Pazienti a “rischio” di sviluppare IP:
Ipertensione polmonare cronica trombo-embolica (Embolie
polmonari massive o recidivanti)
Ipertensione arteriosa polmonare (Connettiviti, Epatopatie, HIV,
Cardiopatie congenite…)
10. Quali altri elementi fanno aumentare il
sospetto clinico ?
• Segni obiettivi
II tono rinforzato o sdoppiato,
turgore delle giugulari,
epatomegalia, edemi)
• ECG: P polmonare, prevalenza VD, turbe fase
ripolarizzazione V1-V3
•Rx Torace: dilatazione art.polm dex, ingrandimento
ombra, cardiaca assenza di lesioni parenchimali
11. Eco nella diagnosi di ipertensione polmonare I
Segni indirettiSegni indiretti
Dilatazione sezioni dx e art. polmonareDilatazione sezioni dx e art. polmonare
Tempo di accelerazione flusso polmonareTempo di accelerazione flusso polmonare
Stima della PapStima della Pap
Doppler rigurgito tricuspidale (Paps)Doppler rigurgito tricuspidale (Paps)
Doppler rigurgito polmonareDoppler rigurgito polmonare
Gradiente di pressione = 4 x VGradiente di pressione = 4 x V22
sistolica
media
diastolica
12. Mukerjee D et al. Rheumatology 2004;43:461-466
Relazione tra gradiente tricuspidale al Doppler e
pressione polmonare media cruenta
25
Falsi
positivi
Falsi negativi
14. Eco nella diagnosi di ipertensione polmonare II
Talvolta il segnale Doppler non èTalvolta il segnale Doppler non è
adeguato per una misura accurataadeguato per una misura accurata
Miglioramento del segnaleMiglioramento del segnale
Doppler con mezzo di contrastoDoppler con mezzo di contrasto
Possibilità di sovrastima dellaPossibilità di sovrastima della
pressione per velocità di rigurgitopressione per velocità di rigurgito
elevate. (piccoli errori nellaelevate. (piccoli errori nella
misura della velocitàmisura della velocità
corrispondono a importanticorrispondono a importanti
variazioni nel calcolo della Paps)variazioni nel calcolo della Paps)
LimitiLimiti
P=4xVP=4xV22
15. Eco nella diagnosi di ipertensione polmonare III
Valutazione shuntValutazione shunt
Forame ovale pervioForame ovale pervio
Cardiopatia Congenita (DIA, DIV….)Cardiopatia Congenita (DIA, DIV….)
Diagnosi DifferenzialeDiagnosi Differenziale
Esclusione patologie sezioni sinistreEsclusione patologie sezioni sinistre
Disf ventr sin ,ValvulopatieDisf ventr sin ,Valvulopatie
16. Pulmonary Hypertension Unit
La Sapienza University oi Rome
1. Pulmonary Arterial Hypertension
• Idiopatic
• Hereditary (BMPR-II ; ALK-1)
•Drug and Toxin induced
• Associated with :
– Connective Tissue Disease
– HIV infection
– Portal hypertension
– Congenital heart diseaswe
– Schistosomiasis
•Persistent PH in the new born
1A
Veno-occlusive disease
3. PH due to lung disease or hypoxia
• COPD
• Interstiial lung disease
• Breathing sleep disorders
• Chronic exposure to high altitude
• Developtmental lung disorders
2. PH due to left heart disease
• Systolic/Diastolic dysfunction
• Valvulopaties
4. Chronic Thromboembolic PH
Pulmonary hypertension: Classification 2013
5. PH with multifactorial mechanisms
H
17. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Funzione diastolica: Ecocardiografia..
Zile, M. R. et al. Circulation 2002;105:1387-1393
∂
D
∂
Rapporto E/E’<8 normale Rapporto E/E’>15 WP Alta !!
∂
D
∂
D
18. Iter Diagnostico: diagnosi differenziale
Sospetto clinico
Anamnesi,Rx Torace, ECG
Eco 2D- Doppler
Ipertensione Polmonare
Diagnosi Differenziale
IpertensioneIpertensione
Polmonare sec.Polmonare sec.
PneumpatiePneumpatie
IpertensioneIpertensione
Polmonare CronicaPolmonare Cronica
TromboembolicaTromboembolica IpertensioneIpertensione
ArteriosaArteriosa
PolmonarePolmonare
Invio al centro di riferimento
21. Le prove di funzionalità
respiratoria possono essere utlili
nella diagnostica differenziale?
Nelle forme di IP secondarie a pneumopatia il deficitNelle forme di IP secondarie a pneumopatia il deficit
ventilatorio è severo !ventilatorio è severo !
- FEV1 <20-30% del valore predetto- FEV1 <20-30% del valore predetto
- FVC- FVC 30-40% del valore predetto30-40% del valore predetto
22. Ipertensione Arteriosa Polmonare: PFR
• Riduzione del FVC, FEV1, TLC, VA al di sotto dell’80%
del predetto nel 50% dei pazienti
• VA 96% TLC
• Deficit prevalentemente restrittivo
• Più marcata riduzione del DLCO
• Nelle forme di IP secondarie a pneumopatia il deficitNelle forme di IP secondarie a pneumopatia il deficit
ventilatorio è severo !ventilatorio è severo !
23. Diagnosi Differenziale:
IP sec. Pneumopatie (IP Pneu) vs IAP
TCTC
Alta risoluzioneAlta risoluzione
Prove di funzionalitàProve di funzionalità
respiratorierespiratorie
Nella IAP il deficitNella IAP il deficit
della DLCO>>FVCdella DLCO>>FVC
IP PneuIP Pneu
Deficit ventilatoriDeficit ventilatori
severi con Ipossiemiaseveri con Ipossiemia
IP PneuIP Pneu
Presenza di lesioniPresenza di lesioni
parenchimaliparenchimali
IAP: NormaleIAP: Normale
PVOD: Opacità vetroPVOD: Opacità vetro
smerigliatosmerigliato
Ispessimento setti interlobariIspessimento setti interlobari
24. Quadro TC alta risoluzione nella
IAP con malattia veno-occlusiva
Resten A. Radiology 2002; 222:782–788
5-10% dei pazienti con IAP
26. Ipertensione Polmonare Cronica Tromboembolica
(IPCTE)
Am Resp Crit Care Med 2000
Prossimale Distale
lesioni plessiformi !!!!
27. ScintigrafiaScintigrafia
PerfusionalePerfusionale
Diagnosi Differenziale:
IPCTE prossimale vs IAP
TCTC
SpiraleSpirale
IPCTE: difettiIPCTE: difetti
segmentari multiplisegmentari multipli
IAP: normale oIAP: normale o
difettidifetti “sfumati”“sfumati”
IPCTE: difetti riempimentoIPCTE: difetti riempimento
parziali;parziali;
arterie a coda di topo,arterie a coda di topo,
infarti polmonariinfarti polmonari
IAP: normale oIAP: normale o
trombi stratificatitrombi stratificati
.
28. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Dalla EP alla IPCTE: angio TC
Auger WR. Pulm Circ 2012
Embolia polmonare IP cronica tromboembolica
29. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Scintigrafia Perfusionale
Normale oNormale o
difetti sfumatidifetti sfumati
NormaleNormale TromboemboliaTromboembolia
Funzione respiratoria
Ipert Art PolIpert Art Pol
DeficitDeficit
Mod-severoMod-severo
TC Alta Ris.
PNEUMOPATIEPNEUMOPATIE
Rilievo ECO Doppler diRilievo ECO Doppler di
Ipertensione PolmonareIpertensione Polmonare
NormaleNormale
Difetti segmentaliDifetti segmentali
TC Spirale o Angio
DIA, DIVDIA, DIV
Studio emodinamico
Test Vasoreattività
Ricerca:Ricerca:
Auto-anticorpiAuto-anticorpi
CapillaroscopiaCapillaroscopia
HIVHIV
ECO V PortaECO V Porta
BotalloBotallo
LieveLieve
Polisonno
grafia
OSASOSAS
Funz. VS
Studio ECO contrasto
Normale
AnormaleIP Post-CapillareIP Post-Capillare
31. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Obiettivi studio emodinamico
• la presenza e lla presenza e l’entità di shunt intra/extra cardiaci’entità di shunt intra/extra cardiaci
• salti ossimetricisalti ossimetrici
• le caratteristiche emodinamiche del circolole caratteristiche emodinamiche del circolo
polmonarepolmonare
• misura della WP (pre vs post-capillare)misura della WP (pre vs post-capillare)
• ll’impatto emodinamico della patologia’impatto emodinamico della patologia
• misura PAD e ICmisura PAD e IC
• la presenza di vasocostrizione reversibilela presenza di vasocostrizione reversibile
• test all’ossido nitricotest all’ossido nitrico
32. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Perché è importante fare una
diagnosi precisa ?
Ad ogni tipo, diverse terapie !
35. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Ipertensione polmonare nelle
malattie respiratorie
O2 terapia
BPCO
Sildenafil ?
BPCO
Riociguat ??
36. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Ipertensione polmonare nelle
patologie cuore sinistro
ACEI
Sartani
B-bloccanti
Diuretici
Sildenafil ?
37. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Conclusioni
• L’ipertensione polmonare è una condizione
emodinamica di frequente riscontro nella pratica
clinica
• L’ecocardiogramma è uno strumento utile per
identificare pazienti ad alta probabilità di IP
• E’ necessario un rigoroso approccio diagnostico
per identificare le forme che si possono giovare
di un trattamento terapeutico (IAP e IPCTE)
• La diagnosi va integrata con una stratificazione
prognostica per modulare le terapie
38. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Pulmonary Hypertension Unit
Dept. Cardiovascular and Respiratory Diseases
Sapienza University of Rome
PH clinicians (Cardiology ward, CCU, consultation & outpatients management):
Senior Cardiologists CD. Vizza, R. Badagliacca, S. Papa
Fellows: G. Manzi, A. Pascaretta,
PH Nurse: R Torre
Clinical Study supervisor R. Poscia
Data Manager S. Proietti, F. D’Alessandro
PFTs-CPX Lab
Prof. Palange
Dott.Valli
CT & RNM Lab
Dott. Carbone
Dott. Francone
Reumathologists
Prof Valesini
Prof.Riccieri
Liver Transplant Unit
Prof. Rossi
Prof. Corradini
Lung Transplant Program
Prof. Venuta
HIV clinic
Prof.Vullo
Echo Lab
Dr. Sciomer
Dr. Badagliacca
Right Cath Lab
Dott. Mancone
Dott. Bruno
Pulmonologists
Prof. Palange
Pediatric Cardiology
Prof. B Marino
Prof. P Versacci
39. Pulmonary Hypertension Unit
La Sapienza University oi Rome
PH clinicians (Cardiology ward, CCU, consultation & outpatients management):
Senior Cardiologists Dr Vizza, Dr Badagliacca, , Dr Papa,
Fellows: Dr Manzi
PH Unit
La Sapienza, University of Rome
Coordinator Carmine Dario Vizza
PFTs-CPX Lab
Prof. Palange
Dott.Valli
CT & RNM Lab
Dott. Carbone
Dott. Francone
Reumathologists
Prof Valesini
Prof.Riccieri
Liver Transplant Unit
Prof. Rossi
Prof. Corradini
Lung Transplant Program
Prof.Venuta
HIV clinic
Prof.Vullo
Echo Lab
Dr. Sciomer
Dr. Badagliacca
Right Cath Lab
Dott. Mancone
Dott. Bruno
Pulmonologists
Prof. Parola
41. Pulmonary Hypertension Unit
La Sapienza University oi Rome
ZM 64 aa, sesso F
- Intervento di sostituzione valvolare mitralica 1978 & 1996
- Dispnea progressiva negli ultimi 4 mesi
- Ricovero per IC congestizia refrattaria alla terapia
- ECO: Protesi in sede con normali flussi. Normale FE VS. VD dilatato
Pressioni (mmHg)
Atrio dex 19
Art. Polm. 55
Wedge 6
Indice Card. (l/min/m2) 1,4
RVP tot (WU) 28,2
RVP art (WU) 24,2
19
53
6
1,8
22,1
18,1
NO 20 ppm
Cateterismo cardiaco destro
BaseIpertensione polmonare “reattiva” secondaria a valvulopatia sinistra
42. Pulmonary Hypertension Unit
La Sapienza University oi Rome
PF 72 aa, sesso M
- Ipertensione arteriosa sistemica
- BPCO severa, in trattamento cronico con steroidi e anti-colinergici, NIV
- ECO: VD dilatato, TAPSE 24 mm, PAPs 88 mmHg
EGAEGA Fi02 40%Fi02 40%
pHpH 7,387,38
PaO2,PaO2, mmHgmmHg 6262
PaCO2,PaCO2, mmHgmmHg 6060
HCO3,HCO3, mmol/lmmol/l 30,730,7
BE,BE, mmol/lmmol/l 7,87,8
SatO2%SatO2% 9191
PFRPFR % predetto% predetto
FVCFVC 7373
FEV1FEV1 39,439,4
PEFPEF 49,549,5
FEV1/FVCFEV1/FVC 55%55%
FEF 25-75FEF 25-75 16,516,5
43. Pulmonary Hypertension Unit
La Sapienza University oi Rome
PF 72 aa, sesso M
Pressioni (mmHg)
Atrio dex 13 12
Art. Polm. 40 38
Wedge 8 8
Indice Card. (l/min/m2) 2,7 2,9
RVP tot (WU) 8 6,9
RVP art (WU) 6,4 5,4
NO 20 ppm
Cateterismo cardiaco destro
Base
44. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Ipertensione polmonare “inappropriata”
Thabut, Chest 2005
Escludere altre patologie concomitanti (disfunzione VS, tromboembolia)
45. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Non solo diagnosi…….
Disfunzione VDDisfunzione VD
Valutazione ClinicaValutazione Clinica
ECGECG
ECO 2DECO 2D
EmodinamicaEmodinamica
Neuro-ormoniNeuro-ormoni
RMN ?RMN ?
Adattamento cardiorespiratorioAdattamento cardiorespiratorio
allall’esercizio’esercizio Test del camminoTest del cammino
Test ergospirometricoTest ergospirometrico
Valutare il grado di severità !!
46. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Consigli per il Follow-up
Test del camminoTest del cammino XX XX
ECGECG XX XX
InizialeIniziale MensileMensile SemestraleSemestrale Se indicatoSe indicato
EGAEGA XX XX
PFRPFR XX XX
ECO DopplerECO Doppler XX XX XX
Test ergospirometricoTest ergospirometrico XX XX XX
EmodinamicaEmodinamica XX XX
Valutazione ClinicaValutazione Clinica XX XX
BNP(?)BNP(?) XX XX
XX
48. Pulmonary Hypertension Unit
La Sapienza University oi Rome
Conclusioni
• L’ipertensione arteriosa polmonare è un gruppo
di patologie in cui è disponibile una terapia
efficace nel ridurre la mortalita’
• In caso di dispnea in assenza di cardiopatia o
pneumopatia nota sospettate IP
• L’ecocardiogramma è uno strumento utile per
identificare pazienti ad alta probabilità di IP
• Quando si eseguono esami strumentali (ECO
2D) verificare se è presente dilatazione VD +
PAPs elevata
Editor's Notes
PAPM&gt;= A 25 MMhG
Pw&lt;= A 15 MMhG
Pvr&gt;3 MMhG
Riceve tutta la portata cardiaca
Bassa pressione
Basse resistenze vascolari
(ampio letto capillare 70m2)