scholarly journals Pulmonary Hypertension Due to Left Heart Disease

2016 ◽  
Vol 01 (03) ◽  
pp. 016-019
Author(s):  
S. Basha ◽  
G. Deepthi

AbstractThe most common cause of pulmonary hypertension is left heart disease, arising in response to increased left ventricular or left a trial filling pressures[1,2,3]. During the 5th World Symposium held in Nice, France, in 2013, the consensus was reached to maintain the general scheme of previous clinical classifications, placing the Pulmonary Hypertension due to left heart disease in Group 2 [4]. PH is defined by a mean pulmonary arterial pressure >25 mmHg. In the case of PH associated with LHD, this is associated with a pulmonary capillary wedge pressure >15 mmHg or left ventricular end-diastolic pressure (LVEDP) > 18 mm Hg [1,5]. Pulmonary hypertension due to left-sided heart disease is associated with higher morbidity and mortality [6,7,8]. This study is done to know the pattern of clinical presentation of pulmonary hypertension and to see the gender difference.

2015 ◽  
Vol 24 (138) ◽  
pp. 665-673 ◽  
Author(s):  
Harrison W. Farber ◽  
Simon Gibbs

Pulmonary hypertension (PH) associated with left heart disease (PH-LHD) is the most common type of PH, but its natural history is not well understood. PH-LHD is diagnosed by right heart catheterisation with a mean pulmonary arterial pressure ≥25 mmHg and a pulmonary capillary wedge pressure >15 mmHg. The primary causes of PH-LHD are left ventricular dysfunction of systolic and diastolic origin, and valvular disease. Prognosis is poor and survival rates are low. Limited progress has been made towards specific therapies for PH-LHD, and management focuses on addressing the underlying cause of the disease with supportive therapies, surgery and pharmacological treatments. Clinical trials of therapies for pulmonary arterial hypertension in patients with PH-LHD have thus far been limited and have provided disappointing or conflicting results. Robust, long-term clinical studies in appropriate target populations have the potential to improve the outlook for patients with PH-LHD. Herein, we discuss the knowledge gaps in our understanding of PH-LHD, and describe the current unmet needs and challenges that are faced by clinicians when identifying and managing patients with this disease.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
B Janssen ◽  
P Trujillo ◽  
J Grignola Rial

Abstract Background The proportion of patients (pts) diagnosed with pulmonary arterial hypertension (PAH) at a more advanced age and/or with more risk factors for left ventricular diastolic dysfunction is increasing. Therefore, it can be challenging to differentiate PH associated with left heart disease (PH-LHD, PHpost) from other precapillary forms of PH (PHpre). Purpose We analyzed the performance of the Opotowsky (OS), D'Alto (DS), and simplified D'Alto (sDS) echocardiographic scores according to the pretest probability (before right heart catheterization – RHC) of PH-LHD in pts with suspected PH submitted to RHC to identify the hemodynamic phenotype. Methods 37 consecutive stable pts (3/2018–3/2020) with a tricuspid regurgitation peak velocity >2.8 m/s were prospectively included (21F, 49±17 yrs). Blinded transthoracic echocardiography was performed within 2 hours of RHC. We assessed OS (−2 to 2 points) and DS/sDS (0 to 34/7 points). We estimated cardiac index (thermodilution) and hemodynamic parameters using standard formulas. If PA occlusion pressure (PAOP) cannot properly be measured at end-expiration, we assessed left ventricular end-diastolic pressure (LVEDP). PH was defined as a mean PA pressure (mPAP) ≥25 mmHg. PAOP/LVEDP >15 mmHg defined PHpost. If the PAOP/LVEDP was between 13–15 mmHg in an I pt, a volume challenge was done. We categorized pts according to the pretest probability of PH-LHD proposed in the 6th WSPH based on the combination of 7 noninvasive variables (age, presence of CV comorbidities, presence of current or paroxysmal atrial fibrillation, prior cardiac intervention, presence of structural LHD, presence of left bundle branch/LV hypertrophy or RV strain in ECG, presence of left atrial dilatation/grade >2 mitral flow in Echo). The individual average probability was calculated by assigning a score of 1, 2, and 3 for each variable (1 = low (L), 2 = intermediate (I), and 3 = high (H) probability) rounding the average of the sum of values allocated for each variable to the nearest integer. Nonparametric ROC plots assessed the performance of echo-scores. Results All pts had PH. 19 pts showed PHpost, 10/19 with PVR >3Wu (Combined PHpost). All scores were lower in PHpost compared to PHpre pts (p<0.05) (Table 1). ROC area was >0.9 with a similar Youden index (0.83) among the three scores (p<0.05) (Figure 1). 17 PHpost with H pts were correctly identified by all scores (94–100%). In 15 PHpre with L pts OS performed better than DS/sDS (93 vs. 80%). In 3 PHpre and 2 PHpost with I pts, DS/sDS performed better than OS (100 vs. 80%). Conclusion The use of simple echo-scores could facilitate the screening of the hemodynamic phenotype in pts with PH, regardless of the pretest probability of PH-LHD. D'Alto scores might have some advantage compared to OS to classify the intermediate pretest probability of PH pts correctly. FUNDunding Acknowledgement Type of funding sources: Public hospital(s). Main funding source(s): Centro Cardiovascular Universitario. Hospital de Clínicas. Facultad de Medicina. Universidad de la República Table 1. Echo & Hemodynamic Data Figure 1. ROC curves of Echo scores


2015 ◽  
Vol 14 (2) ◽  
pp. 70-78 ◽  
Author(s):  
Christopher F. Barnett ◽  
Van N. Selby

Background: Left heart disease (LHD) is the most common cause of pulmonary hypertension (PH) and is associated with poor patient outcomes, especially among patients undergoing heart transplant evaluation. Implications for clinicians: Left heart disease should be considered in all patients undergoing an evaluation for PH. Correct management of PH from LHD is to optimize treatment of LHD. Pulmonary vasodilators used to treat pulmonary arterial hypertension should not be used in patients with PH from LHD. Conclusions: Additional research is needed to better understand how PH develops in patients with LHD and to investigate the role for treatment targeting PH in these patients.


2018 ◽  
Vol 9 (1) ◽  
pp. 204589401881543 ◽  
Author(s):  
Doron Aronson ◽  
Emilia Hardak ◽  
Andrew J. Burger

The diastolic pressure gradient (DPG) has been proposed as the metric of choice for the diagnosis of pulmonary vascular changes in left heart disease. We tested the hypothesis that this metric is less sensitive to changes in left atrial pressure and stroke volume (SV) than the transpulmonary gradient (TPG). We studied the effect of dynamic changes in pulmonary capillary wedge pressure (PCWP), SV, and pulmonary artery capacitance (PAC) on DPG and TPG in 242 patients with acute heart failure undergoing decongestive therapy with continuous hemodynamic monitoring. There was a close impact of PCWP reduction on TPG and DPG, with a 0.13 mmHg (95% confidence interval [CI] 0.07–0.19, P < 0.0001) and 0.21 mmHg (95% CI 0.16–0.25, P < 0.0001) increase for every 1 mmHg decrease in PCWP, respectively. Changes in SV had a negligible effect on TPG and DPG (0.19 and 0.13 mmHg increase, respectively, for every 10-mL increase in SV). Heart rate was positively associated with DPG (0.41-mmHg increase per 10 BPM [95% CI 0.22–0.60, P < 0.0001]). The resistance-compliance product was positively associated with both TPG and DPG (2.65 mmHg [95% CI 2.47–2.83] and 1.94 mmHg [95% CI 1.80–2.08] for each 0.1-s increase, respectively). In conclusion, DPG is not less sensitive to changes in left atrial pressure and SV compared with TPG. Although DPG was not affected by changes in PAC, the concomitant increase in the resistance-compliance product increases DPG.


2018 ◽  
Vol 9 (1) ◽  
pp. 204589401879680 ◽  
Author(s):  
Greta M. Krafsur ◽  
Joseph M. Neary ◽  
Franklyn Garry ◽  
Timothy Holt ◽  
Daniel H. Gould ◽  
...  

The obesity epidemic in developed societies has led to increased cardiovascular diseases including pulmonary hypertension associated with left heart disease (PH-LHD), the largest and fastest-growing class of PH. Similar to obese humans, PH and heart failure (HF) are increasingly recognized in North American fattened beef cattle. We hypothesized that PH and HF in fattened beef cattle are novel, phenotypically distinct manifestations of bovine PH arising from left ventricular (LV) dysfunction similar to obesity-related PH-LHD in humans. We conducted a semi-quantitative histopathological assessment of cardiopulmonary tissues obtained from fattened beef cattle suffering end-stage HF compared to asymptomatic cattle of equivalent age undergoing the same fattening regimens. In HF animals we observed significant LV fibrosis, abundant cardiac adipose depots, coronary artery injury, and pulmonary venous remodeling recapitulating human obesity-related PH-LHD. Additionally, striking muscularization, medial hypertrophy, adventitial fibrosis, and vasa vasorum hyperplasia in the pulmonary arterial circulation were associated with sequela of pathologic right ventricular (RV) remodeling suggesting combined pulmonary venous and arterial hypertension. The association between obesity, pathologic cardiopulmonary remodeling, and HF in fattened beef cattle appears to recapitulate the complex pathophysiology of obesity-associated PH-LHD in humans. This novel, naturally occurring, and large animal model may provide mechanistic and translational insights into human disease.


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