Pulmonary hypertension and right ventricular dysfunction in left heart disease (group 2 pulmonary hypertension)

doi:10.1016/j.pcad.2012.07.007

Progress in Cardiovascular Diseases

Volume 55, Issue 2, September–October 2012, Pages 104-118

https://doi.org/10.1016/j.pcad.2012.07.007 Get rights and content

Abstract

Group 2 pulmonary hypertension is most frequently caused by left heart disease, a heterogeneous set of disorders. These processes include left ventricular systolic dysfunction, left ventricular dysfunction with preserved ejection fraction and valvular (mitral and/or aortic) diseases. Left heart disease may cause passive backward transmission of pressure leading to elevated left atrial and pulmonary arterial pressures due to a myriad of processes. Increasingly, it has been recognized that some patients may develop pulmonary arterial pressure out of proportion from what is expected. This is believed to be due to increases in vasomotor tone and/or vascular remodeling. Over time patients may go on to develop progressive right ventricular dysfunction, a marker for poor prognosis. This review will explore the different characteristics of these conditions including the incidence, pathophysiology, clinical implications, prognosis and current state of available medical therapies.

Section snippets

PH due to HFpEF

HFpEF was first described almost 30 years ago in female African American hypertensive patients with normal systolic pump function and evidence for diastolic dysfunction.² Over time a body of literature has accumulated demonstrating that HFpEF is the etiology of half of patients admitted for heart failure symptoms.3, 4, 5, 6 When compared to individuals with impaired systolic function, HFpEF patients have their own set of risk factors but similar morbidity and mortality rates.5, 7, 8 Although

Pathophysiology of HFpEF

Aspects of the pathophysiology of HFpEF are currently unclear, such as whether it is one disease continuum or multiple distinct entities resulting from extra-cardiac alterations and comorbidities. Part of this confusion pertains to the shortcoming of the term HFpEF since patients may be misdiagnosed if the diagnosis if solely based on clinical signs and symptoms of heart failure with exclusion of reduced left ventricular ejection fraction. Additionally, this uncertainty stems from the lack of

Pathophysiology of PH–HFpEF

Our incomplete comprehension of HFpEF limits our understanding for why these patients develop PH. Over time left atrium and ventricular filling pressure from compromised left ventricular and in some, LA, relaxation and distensibility can lead to elevated pulmonary venous pressure triggering vasoconstriction and arterial remodeling.15, 16 Teleologically, development of PH has been considered to be protective of developing pulmonary edema. However, the elevated transpulmonary gradient (TPG)

Pulmonary vascular pathological and cellular changes

At the cellular level, the persistent increased gradient may lead to fracturing of the delicate alveolar–capillary barrier, characterized by endothelium damage and weakening of the extracellular matrix.17, 18, 19 Multiple adaptive processes are triggered as a result of the persistent elevated hydrostatic pressure which may, in part be mediated by proliferating myofibroblasts and/or pericytes which have contractile proteins and secretory capacities and are more abundant on venous and

Prevalence and epidemiology

A common misconception is the prevalence of HFpEF. Many studies have demonstrated that approximately 50% of patients admitted with heart failure have HFpEF.3, 4, 5, 6 Due to the aging population and increasing associated morbidities of HFpEF, the proportion of patients with HFpEF has increased from 38% to 54% over the last two decades.⁴ The high proportion of patients with HFpEF makes it a very common disease, with its prevalence reported in a recent cross-section epidemiological data set to be

Determinants of right ventricular dysfunction in PH–HFpEF

Many masqueraders of right ventricular (RV) dysfunction exist including constrictive pericarditis, restrictive cardiomyopathy, pre-capillary PAH, systolic heart failure and renal disease. When approaching a patient with HFpEF suspected of suffering from right ventricular dysfunction the first step that should be performed is a detailed physical and laboratory examination.

Patients with RV failure often present with the cardinal manifestations of heart failure, fatigue and dyspnea. On physical

Right ventricular dysfunction and prognosis in PH–HFpEF

For many years, early investigators viewed the RV as merely a conduit for blood flow leading to a scarcity in its evaluation. In more recent years the consensus has changed and the importance of a properly functioning RV in the maintenance of overall hemodynamics has been recognized. Comprehensive examination of the RV, the pulmonary circulation and their interactions is crucial in the management of patients. Assessment of the RV can be limited because of the difficulty in quantificating RV

Therapeutic approach to PH and to right ventricular dysfunction in HFpEF

Due to the growing prevalence and increased morbidity and mortality associated with HFpEF and PH–HFpEF there is a heightened focus on potential therapeutic interventions. To date, the focus of HFpEF therapy has been on factors that affect left ventricular end-diastolic pressure—systemic blood pressure, heart rate, circulating volume and ischemia—with disappointing results. To date largely neutral and disappointing outcomes have been reported in randomized drug trials (i.e.,

PH due to systolic left ventricular dysfunction (sLVD)

PH due to left heart disease and, in particular, PH due to sLVD or HFrEF remain one the most common forms of PH.¹¹⁴ Its prevalence is variable, depending on the definition of PH used and on the clinical stage of heart failure studied: notably, in tertiary referral centers up to two thirds of the patients evaluated for heart transplantation have been reported to have PH.54, 89, 115, 116

Pathophysiology of PH due to sLVD

In patients with chronic sLVD, elevation of PAP is usually due to backward transmission of increased left ventricular filling pressure. In a large cohort of patients with sLVD the correlation between PCWP and PASP was found to be highly statistically significant, even though the scatterplot of data around the identity line shows that no correct prediction of PAP is possible once the value of PCWP is known.¹¹⁵ Despite the strong association between wedge pressure and PAP, there is no

PH and the candidacy for heart transplantation

Severe PH is an independent risk factor for mortality after transplantation, since RV failure may occur when a normal donor heart has to face significantly elevated pulmonary vascular resistance in the postoperative period. A precise hemodynamic threshold beyond which RV failure is unacceptably high and below which RV failure never happens cannot be identified; in fact, the risk of death after transplantation increases linearly with the increase in pulmonary vascular resistance (PVR).

Right ventricular dysfunction and prognosis in sLVD

Several studies suggest that RV systolic function is a powerful prognostic marker in patients with heart failure due to sLVD.95, 131, 132, 133 Importantly, the systolic excursion of the tricuspid annular plane turned out to be a significant and independent predictor of mortality after having included in the multivariate model the NYHA class and the well-consolidated echocardiographic predictors such as left ventricular ejection fraction and the deceleration time of the E wave.⁹⁵ Recent data

Determinants of RV dysfunction in sLVD

In patients with heart failure, RV dysfunction could be caused by myocardial disease or by ischemia/infarction of the RV or it could be the direct consequence of the elevated pressure in the pulmonary arteries. The latter hypothesis is the most likely explanation, since, due to its peculiar characteristics, the RV cannot easily tolerate pressure overload; as a matter of fact, the inverse relation between pulmonary artery pressure and RV ejection fraction has been demonstrated in early studies.

Considering both PH and RV dysfunction to stratify prognosis in sLVD

The previous study also showed that RV ejection fraction can be preserved in a substantial number of patients who have PH (possibly due to a more recent onset of PH) and that, conversely, RV dysfunction may be observed in patients with normal pulmonary artery pressure. It is important for clinicians to discriminate such subgroups as the prognosis turned out to be very poor only in patients having both PH and RV dysfunction. In another study looking at patients who underwent a test of

The therapeutic approach to PH and to RV dysfunction in sLVD

There is no specific therapy for PH due to left heart disease. This statement should not be “negatively” viewed as if there is no therapy at all for such patients; on the contrary, it “positively” reminds us the fact that the management of PH due to left heart disease must be aimed at the optimal treatment of the underlying disease. No drug (including diuretics, nitrates, ACE inhibitors, angiotensin enzyme inhibitors, beta-blockers, inotropic agents) and no intervention (such as

The role of left ventricular assist devices

PH unresponsive to an acute vasodilator challenge is considered a contraindication for orthotropic cardiac transplantation, due to the unacceptably high risk of fatal right heart failure after heart transplant. PH which is not rapidly reversible by pharmacological treatment is, in fact, considered the consequence of an irreversible remodeling process of the pulmonary vascular system.²⁹

However, the idea that left ventricular assist devices (LVAD) could play a positive role in the treatment of

PH due to valvular heart disease

The prevalence of PH correlates with severity of valvular disease. Given the aging population, valvular heart disease is becoming an increasingly prevalent disease with some estimates of 10%–15% in patients above 75 years of age.¹³⁸ PH is both an indication for proceeding for surgical or catheter-based interventions and also an operative risk factor for valve interventions. Nearly all patients with severe, symptomatic mitral valve disease have some degree of associated PH and in some surgical

Mitral valve disease and PH

Early reports of the efficacy of closed commissurotomy raised the question of whether the failure to improve PH was due to incomplete valvulotomy coupled with persistence of MR vs. an intrinsic vasculature issue.¹³⁹ Prior to mitral valve replacement (MVR) and more complete repair, pure or predominant MR could not be fixed. Braunwald's landmark report on the efficacy of a Starr-Edwards prosthesis for MS and MR on the pulmonary vasculature in 31 patients (17 male, 14 female) with pulmonary

AS and PH

PH is not as common in the AS surgical cohort as it is in the MV cohort, with reports up to 30%, but more often its prevalence is 10%–15%., However, in the older cohort with comorbidities that we are now addressing with catheter-based interventions it is more prevalent. Traditionally severe PH had been considered uncommon in AS.¹⁴⁶ However, importantly PH has been associated with critical AS including sudden deterioration and sudden death.

Basu et al.¹⁴⁷ reported on 151 cases of aortic valve

Conclusion

Thus, the common stimulus for the development of WHO Group 2 PH in PH–HFpEF, PH–sLVD, PH–aortic or mitral valve disease is LA dysfunction/hypertension, of which an increased LA volume is its hallmark. It is often mediated by increased LVEDP, the further downstream stimulus. What may start as passive pulmonary venous hypertension, particularly with LA pressures > 25 mm Hg may lead to the development of “active” PH with an elevated TPG or PVR in a non-linear relationship due to a combination of

Statement of Conflict of Interest

All authors declare that there are no conflicts of interest.

Acknowledgments

No grant support was used for this work.

References (153)

S. Rosenkranz et al.
Pulmonary hypertension due to left heart disease: updated Recommendations of the Cologne Consensus Conference 2011
Int J Cardiol
(2011)
G.C. Fonarow et al.
Characteristics, treatments, and outcomes of patients with preserved systolic function hospitalized for heart failure: a report from the OPTIMIZE-HF Registry
J Am Coll Cardiol
(2007)
C.W. Yancy et al.
Clinical presentation, management, and in-hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database
J Am Coll Cardiol
(2006)
B.A. Borlaug et al.
Contractility and ventricular systolic stiffening in hypertensive heart disease insights into the pathogenesis of heart failure with preserved ejection fraction
J Am Coll Cardiol
(2009)
B.A. Borlaug et al.
Global cardiovascular reserve dysfunction in heart failure with preserved ejection fraction
J Am Coll Cardiol
(2010)
J. Kjaergaard et al.
Prognostic importance of pulmonary hypertension in patients with heart failure
Am J Cardiol
(2007)
C.S. Lam et al.
Pulmonary hypertension in heart failure with preserved ejection fraction: a community-based study
J Am Coll Cardiol
(2009)
T.T. Phan et al.
Heart failure with preserved ejection fraction is characterized by dynamic impairment of active relaxation and contraction of the left ventricle on exercise and associated with myocardial energy deficiency
J Am Coll Cardiol
(2009)
S.S. Kurdak et al.
Effect of increased duration of high perfusion pressure on stress failure of pulmonary capillaries
Microvasc Res
(1995)
M. Guazzi
Alveolar gas diffusion abnormalities in heart failure
J Card Fail
(2008)

M. Mandegar et al.

Cellular and molecular mechanisms of pulmonary vascular remodeling: role in the development of pulmonary hypertension

Microvasc Res

(2004)

D. Heath et al.

Histological changes in the lung in diseases associated with pulmonary venous hypertension

Br J Dis Chest

(1959)

C.J. Cooper et al.

The influence of basal nitric oxide activity on pulmonary vascular resistance in patients with congestive heart failure

Am J Cardiol

(1998)

M.L. Blitzer et al.

Endothelium-derived nitric oxide regulates systemic and pulmonary vascular resistance during acute hypoxia in humans

J Am Coll Cardiol

(1996)

T. Tsutamoto et al.

Relation between endothelin-1 spillover in the lungs and pulmonary vascular resistance in patients with chronic heart failure

J Am Coll Cardiol

(1994)

R.J. Rodeheffer et al.

Increased plasma concentrations of endothelin in congestive heart failure in humans

Mayo Clin Proc

(1992)

F. Bursi et al.

Pulmonary pressures and death in heart failure: a community study

J Am Coll Cardiol

(2012)

J. Butler et al.

Pulmonary hypertension and exercise intolerance in patients with heart failure

J Am Coll Cardiol

(1999)

J.A. Magana-Serrano et al.

Prevalence of heart failure with preserved ejection fraction in Latin American, Middle Eastern, and North African Regions in the I PREFER study (Identification of Patients With Heart Failure and PREserved Systolic Function: an epidemiological regional study)

Am J Cardiol

(2011)

R.F. Yturralde et al.

Diagnostic criteria for diastolic heart failure

Prog Cardiovasc Dis

(2005)

S.F. Nagueh et al.

Recommendations for the evaluation of left ventricular diastolic function by echocardiography

J Am Soc Echocardiogr

(2009)

N. Nagaya et al.

Plasma brain natriuretic peptide levels increase in proportion to the extent of right ventricular dysfunction in pulmonary hypertension

J Am Coll Cardiol

(1998)

E.A. Sallin

Fiber orientation and ejection fraction in the human left ventricle

Biophys J

(1969)

T.N. James

Anatomy of the crista supraventricularis: its importance for understanding right ventricular function, right ventricular infarction and related conditions

J Am Coll Cardiol

(1985)

R.H. Anderson et al.

Structural-functional correlates of the 3-dimensional arrangement of the myocytes making up the ventricular walls

J Thorac Cardiovasc Surg

(2008)

J.A. Goldstein et al.

Hemodynamic importance of systolic ventricular interaction, augmented right atrial contractility and atrioventricular synchrony in acute right ventricular dysfunction

J Am Coll Cardiol

(1990)

C.T. Gan et al.

Right ventricular diastolic dysfunction and the acute effects of sildenafil in pulmonary hypertension patients

Chest

(2007)

S. Ghio et al.

Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure

J Am Coll Cardiol

(2001)

S. Ghio et al.

Prognostic usefulness of the tricuspid annular plane systolic excursion in patients with congestive heart failure secondary to idiopathic or ischemic dilated cardiomyopathy

Am J Cardiol

(2000)

R. Agarwal et al.

Risk assessment in pulmonary hypertension associated with heart failure and preserved ejection fraction

J Heart Lung Transplant

(2012)

A.F. Hernandez et al.

Clinical effectiveness of beta-blockers in heart failure: findings from the OPTIMIZE-HF (Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure) Registry

J Am Coll Cardiol

(2009)

S. Yusuf et al.

Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction: the CHARM-Preserved Trial

Lancet

(2003)

W.J. Paulus et al.

Treatment of heart failure with normal ejection fraction: an inconvenient truth!

J Am Coll Cardiol

(2010)

E.J. Topol et al.

Hypertensive hypertrophic cardiomyopathy of the elderly

N Engl J Med

(1985)

T.E. Owan et al.

Trends in prevalence and outcome of heart failure with preserved ejection fraction

N Engl J Med

(2006)

C. Tribouilloy et al.

Prognosis of heart failure with preserved ejection fraction: a 5 year prospective population-based study

Eur Heart J

(2008)

R.S. Bhatia et al.

Outcome of heart failure with preserved ejection fraction in a population-based study

N Engl J Med

(2006)

C.M. Yu et al.

Progression of systolic abnormalities in patients with “isolated” diastolic heart failure and diastolic dysfunction

Circulation

(2002)

B.A. Borlaug et al.

Exercise hemodynamics enhance diagnosis of early heart failure with preserved ejection fraction

Circ Heart Fail

(2010)

A. Kerem et al.

Lung endothelial dysfunction in congestive heart failure: role of impaired Ca^2 + signaling and cytoskeletal reorganization

Circ Res

(2010)

W. Huang et al.

Capillary filtration is reduced in lungs adapted to chronic heart failure: morphological and haemodynamic correlates

Cardiovasc Res

(2001)

K. Tsukimoto et al.

Ultrastructural appearances of pulmonary capillaries at high transmural pressures

J Appl Physiol

(1991)

J.B. West et al.

Vulnerability of pulmonary capillaries in heart disease

Circulation

(1995)

J.F. Jasmin et al.

Lung structural remodeling and pulmonary hypertension after myocardial infarction: complete reversal with irbesartan

Cardiovasc Res

(2003)

D. Negrini et al.

Pulmonary interstitial pressure and proteoglycans during development of pulmonary edema

Am J Physiol

(1996)

P. Palestini et al.

Composition, biophysical properties, and morphometry of plasma membranes in pulmonary interstitial edema

Am J Physiol Lung Cell Mol Physiol

(2002)

M.I. Townsley et al.

Pulmonary microvascular permeability. Responses to high vascular pressure after induction of pacing-induced heart failure in dogs

Circ Res

(1995)

J.B. West

Invited review: pulmonary capillary stress failure

J Appl Physiol

(2000)

J.J. Hunter et al.

Signaling pathways for cardiac hypertrophy and failure

N Engl J Med

(1999)

J.T. Berg et al.

Alveolar hypoxia increases gene expression of extracellular matrix proteins and platelet-derived growth factor-B in lung parenchyma

Am J Respir Crit Care Med

(1998)

Cited by (13)

Prognostic impact of right ventricular function affected by pulmonary hypertension in hospitalized heart failure patients
2022, Journal of Cardiology
Citation Excerpt :
RV and LV interactions via common pericardia and myofibers could cause preexisting RV dysfunction [32,33]. Another key determinant of preexisting RV dysfunction is myocardial disease or ischemia/infarction of the right ventricle [34]. However, it is difficult to distinguish between reactive RV dysfunction caused by long-term exposure to PH and preexisting RV dysfunction in patients with HFrEF.
Pulmonary hypertension (PH) may affect right ventricular (RV) function; however, the prognostic implications of RV function in patients with heart failure and PH remain unclear. We aimed to investigate the impact of RV function on the prognosis of hospitalized heart failure patients with and without PH.
This observational study initially included 1,349 consecutive hospitalized heart failure patients. After excluding patients who died in hospital, whose left ventricular (LV) function was preserved, and whose echocardiography data were incomplete, 573 patients with heart failure and reduced LV ejection fractions (HFrEF) were analyzed. The patients were grouped according to RV dysfunction that was defined as an RV-tissue Doppler imaging systolic velocity (RV-TDI s’) of ≤9.5 cm/s. The primary endpoint was a composite of cardiovascular death and rehospitalization as a consequence of heart failure.
Overall, the patients with reduced RV function had significantly higher event rates than those with preserved RV function (log-rank test p = 0.01). This prognostic impact was observed in the patients with PH (p = 0.001) and was not evident among the patients without PH (p = 0.39). In the patients with PH, reduced RV function independently predicted the prognosis after adjusting for the covariates (adjusted hazard ratio: 3.12; 95% confidence interval: 1.44 to 6.73).
RV dysfunction that was estimated during hospitalization using the RV-TDI s’, which is a simply determined index, may predict clinical outcomes in hospitalized patients with HFrEF and PH after discharge, but not in those without PH.
Dynamic Assessment of Pulmonary Artery Pulsatility Index Provides Incremental Risk Assessment for Early Right Ventricular Failure After Left Ventricular Assist Device
2021, Journal of Cardiac Failure
The pulmonary artery pulsatility index (PAPi) has been studied to predict right ventricular failure (RVF) after left ventricular assist device (LVAD) implantation, but only as a single time point before LVAD implantation. Multiple clinical factors and therapies impact RV function in pre-LVAD patients. Thus, we hypothesized that serial PAPi measurements during cardiac intensive care unit (CICU) optimization before LVAD implantation would provide incremental risk stratification for early RVF after LVAD implantation.
Consecutive patients who underwent sequential pulmonary artery catherization with cardiac intensive care optimization before durable LVAD implantation were included. Serial hemodynamics were reviewed retrospectively across the optimization period. The optimal PAPi was defined by the initial PAPi + the PAPi at optimized hemodynamics. RVF was defined as need for a right ventricular assist device or prolonged inotrope use (>14 days postoperatively). Patients with early RVF had significantly lower mean optimal PAPi (3.5 vs 7.5, P < .001) compared with those who did not develop RVF. After adjusting for established risk factors of early RVF after LVAD implantation, the optimal PAPi was independently and incrementally associated with early RVF after LVAD implantation (odds ratio 0.64, 95% confidence interval 0.532–0.765, P < .0001).
Optimal PAPi achieved during medical optimization before LVAD implantation provides independent and incremental risk stratification for early RVF, likely identifying dynamic RV reserve.
Evaluation and management of pulmonary hypertension in the emergency department setting
2020, American Journal of Emergency Medicine
Pulmonary hypertension (PH) is characterized by increased pulmonary vascular resistance and pulmonary arterial pressure and is associated with significant morbidity and mortality.
This narrative review evaluates PH, outlines the complex pathophysiologic derangements, and addresses the emergency department (ED) management of this patient population.
Approximately 10–20% of individuals in the United States suffer from PH. Each year nearly 12,000 PH patients seek care in the ED for a variety of symptoms which may or may not be related to PH. There are 5 classes of PH, some of which respond to particular therapies outlined in this review. As presenting complaints are frequently vague and non-specific, emergency physicians must recognize manifestations of PH and complications related to PH to deliver appropriate care. Early imaging with chest radiograph, bedside echocardiogram, and computed tomography can assist in determining the underlying etiology of PH exacerbation. Restarting oral or intravenous PH medications that may have been discontinued is crucial in initial management. Immense care should be taken to avoid hypoxia and hypercarbia as well as maintaining right ventricular preload support. In addition to correction of underlying precipitants, judicious vasopressor and inotrope use can help to correct pathophysiology and avoid further airway intervention.
An understanding of the pathophysiology of PH and available emergency treatments can assist emergency clinicians in reducing the immediate morbidity and mortality associated with this disease. Restarting maintenance PH medications and proper selection of vasopressors and inotropes will benefit decompensating patients with PH.
Left Heart Disease and Pulmonary Hypertension: Are We Seeing the Full Picture?
2018, Heart Lung and Circulation
Citation Excerpt :
Increased pulmonary venous pressure causes pressure on the alveolar capillary walls and alveolar capillary stress failure due to barotrauma [22]. This damages the endothelial function leading to a decrease in lung diffusion capacity, fluid reabsorption and capillary leakage [23]. Clinically, this causes pulmonary oedema and patients present with shortness of breath.
Pulmonary hypertension (PH) is common, under diagnosed and associated with a high mortality. There are significant delays in the diagnosis of pulmonary hypertension leading to increased morbidity and delays in the initiation of treatment. Once PH is diagnosed, establishing the degree of pulmonary vascular resistance (PVR) enables clinicians to broadly divide the underlying pathology into pre-capillary or post-capillary causes, a crucial step in tailoring management.
Pulmonary hypertension is most commonly due to left heart disease (PH-LHD) and echocardiography (echo) is the most widely accessible investigation in its diagnosis. Regardless of the underlying pathophysiology of LHD, the sequelae lead to pressure overload on the left heart and a reactive increase in pulmonary pressures.
In this review article, we will discuss the prevalence of PH, examine the pathophysiology of PH-LHD, establish how echo can be used to identify patients with PH-LHD and discuss surrogate echo markers of PVR.
Echocardiography does not predict mortality in hemodynamically stable elderly patients with acute pulmonary embolism
2016, Thrombosis Research
The evidence on the prognostic value of transthoracic echocardiography (TTE) in elderly, hemodynamically stable patients with Pulmonary Embolism (PE) is limited.
To evaluate the prevalence of common echocardiographic signs of right ventricular (RV) dysfunction and their prognostic impact in hemodynamically stable patients aged ≥ 65 years with acute PE in a prospective multicenter cohort.
TTE was performed by cardiologists. We defined RV dysfunction as a RV/left ventricular ratio > 0.9 or RV hypokinesis (primary definition) or the presence of ≥ 1 or ≥ 2 of 6 predefined echocardiographic signs (secondary definitions). Outcomes were overall mortality and mortality/non-fatal recurrent venous thromboembolism (VTE) at 30 days, adjusting for the Pulmonary Embolism Severity Index risk score and highly sensitive troponin T values.
Of 400 patients, 36% had RV dysfunction based on our primary definition, and 81% (≥ 1 sign) and 53% (≥ 2 signs) based on our secondary definitions, respectively. Using our primary definition, there was no association between RV dysfunction and mortality (adjusted HR 0.90, 95% CI 0.31–2.58) and mortality/non-fatal VTE (adjusted HR 1.09, 95% CI 0.40–2.98). Similarly, there was no statistically significant association between the presence of ≥ 1 or ≥ 2 echocardiographic signs (secondary definitions) and clinical outcomes.
The prevalence of echocardiographic RV dysfunction varied widely depending upon the definition used. There was no association between RV dysfunction and clinical outcomes. Thus, TTE may not be suitable as a stand-alone risk assessment tool in elderly patients with acute PE.
http://clinicaltrials.gov. Identifier: NCT00973596.
Group 2 Pulmonary Hypertension: Pulmonary Venous Hypertension: Epidemiology and Pathophysiology
2016, Cardiology Clinics
Citation Excerpt :
Medial hypertrophy is the most prominent pathologic finding.56 Smooth muscle cell growth and migration are activated through the induction of endogenous vascular serine elastase, the release of growth factors, and of glycoproteins.2,7,57,58 Intimal fibrosis also develops and is often extensive and severe.59

View all citing articles on Scopus

: Statement of Conflict of Interest: see page 114.

View full text

Pulmonary hypertension and right ventricular dysfunction in left heart disease (group 2 pulmonary hypertension)

Abstract

Section snippets

PH due to HFpEF

Pathophysiology of HFpEF

Pathophysiology of PH–HFpEF

Pulmonary vascular pathological and cellular changes

Prevalence and epidemiology

Determinants of right ventricular dysfunction in PH–HFpEF

Right ventricular dysfunction and prognosis in PH–HFpEF

Therapeutic approach to PH and to right ventricular dysfunction in HFpEF

PH due to systolic left ventricular dysfunction (sLVD)

Pathophysiology of PH due to sLVD

PH and the candidacy for heart transplantation

Right ventricular dysfunction and prognosis in sLVD

Determinants of RV dysfunction in sLVD

Considering both PH and RV dysfunction to stratify prognosis in sLVD

The therapeutic approach to PH and to RV dysfunction in sLVD

The role of left ventricular assist devices

PH due to valvular heart disease

Mitral valve disease and PH

AS and PH

Conclusion

Statement of Conflict of Interest

Acknowledgments

Int J Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

Am J Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

Microvasc Res

J Card Fail

Microvasc Res

Br J Dis Chest

Am J Cardiol

J Am Coll Cardiol

J Am Coll Cardiol

Mayo Clin Proc

J Am Coll Cardiol

J Am Coll Cardiol

Am J Cardiol

Prog Cardiovasc Dis

J Am Soc Echocardiogr

J Am Coll Cardiol

Biophys J

J Am Coll Cardiol

J Thorac Cardiovasc Surg

J Am Coll Cardiol

Chest

J Am Coll Cardiol

Am J Cardiol

J Heart Lung Transplant

J Am Coll Cardiol

Lancet

J Am Coll Cardiol

Hypertensive hypertrophic cardiomyopathy of the elderly

N Engl J Med

Trends in prevalence and outcome of heart failure with preserved ejection fraction

N Engl J Med

Prognosis of heart failure with preserved ejection fraction: a 5 year prospective population-based study

Eur Heart J

Outcome of heart failure with preserved ejection fraction in a population-based study

N Engl J Med

Progression of systolic abnormalities in patients with “isolated” diastolic heart failure and diastolic dysfunction

Circulation

Exercise hemodynamics enhance diagnosis of early heart failure with preserved ejection fraction

Circ Heart Fail

Lung endothelial dysfunction in congestive heart failure: role of impaired Ca2 + signaling and cytoskeletal reorganization

Circ Res

Capillary filtration is reduced in lungs adapted to chronic heart failure: morphological and haemodynamic correlates

Cardiovasc Res

Ultrastructural appearances of pulmonary capillaries at high transmural pressures

J Appl Physiol

Vulnerability of pulmonary capillaries in heart disease

Circulation

Lung structural remodeling and pulmonary hypertension after myocardial infarction: complete reversal with irbesartan

Cardiovasc Res

Lung endothelial dysfunction in congestive heart failure: role of impaired Ca^2 + signaling and cytoskeletal reorganization