Association of the Metabolic Syndrome With Pulmonary Venous Hypertension

Robbins, Ivan M.; Newman, John H.; Johnson, Roger F.; Hemnes, Anna R.; Fremont, Richard D.; Piana, Robert N.; Zhao, David; Byrne, Daniel W.

doi:10.1378/chest.08-2008

Cited by 158 publications

(148 citation statements)

References 29 publications

(30 reference statements)

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“…An emerging body of evidence suggests that the metabolic syndrome and insulin resistance may predispose to pulmonary vascular disease (17)(18)(19)(20). An apolipoprotein E-deficient mouse model on a highfat diet developed insulin resistance, pulmonary vascular remodeling, and right ventricular hypertrophy, changes that were reversed by rosiglitazone, an insulin-sensitizer drug (17).…”

mentioning

confidence: 99%

Plasma Levels of High-Density Lipoprotein Cholesterol and Outcomes in Pulmonary Arterial Hypertension

Heresi¹,

Aytekin²,

Newman³

et al. 2010

Am J Respir Crit Care Med

113

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Rationale: High-density lipoprotein cholesterol (HDL-C) promotes healthy vascular function, and it is decreased in insulin resistance. Insulin resistance predisposes to pulmonary vascular disease. Objectives: We hypothesized that HDL-C is associated with clinical outcomes in pulmonary arterial hypertension (PAH). Methods: Plasma HDL-C concentrations were measured in 69 patients with PAH (age, 46.7 6 12.9 yr; female, 90%) and 229 control subjects (age, 57 6 13 yr; female, 48%). Clinical outcomes of interest included hospitalization for PAH, lung transplantation, and all-cause mortality. Survival and time to clinical worsening curves were derived by the Kaplan-Meier method. Cox regression modeling of outcome versus HDL-C with individual covariate adjustments was performed. Measurement and Main Results: HDL-C was low in subjects with PAH compared with control subjects (median, interquartile range: PAH: 36, 29-40 mg/dl; control subjects: 49, 40-60 mg/dl; P , 0.001). An HDL-C level of 35 mg/dl discriminated survivors from nonsurvivors, with a sensitivity of 100% and specificity of 60%. After a median follow-up of 592 days, high HDL-C was associated with decreased mortality (hazard ratio for every 5-mg/dl increase in HDL-C, 0.643; 95% confidence interval, 0.504-0.822; P 5 0.001) and less clinical worsening (hazard ratio for every 5-mg/dl increase in HDL-C, 0.798; 95% confidence interval, 0.663-0.960; P 5 0.02). HDL-C remained a significant predictor of survival after adjusting for cardiovascular risk factors, C-reactive protein, indices of insulin resistance, and severity of PAH (all P , 0.05). Conclusions: Low plasma HDL-C is associated with higher mortality and clinical worsening in PAH. This association does not appear to be explained by underlying cardiovascular risk factors, insulin resistance, or the severity of PAH.

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mentioning

confidence: 99%

Plasma Levels of High-Density Lipoprotein Cholesterol and Outcomes in Pulmonary Arterial Hypertension

Heresi¹,

Aytekin²,

Newman³

et al. 2010

Am J Respir Crit Care Med

113

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“…54,55 In two small studies of symptomatic patients, metabolic syndrome was found to be associated with both PAH 56 and pulmonary venous hypertension. 49 Recently, Gopal et al 57 have demonstrated that metabolic syndrome is associated with RV diastolic dysfunction, increased pulmonary artery diameter, and raised PAP (10 mmHg higher than in controls). These findings persisted even when the increased LV diastolic dysfunction found in the group with metabolic syndrome was accounted for.…”

Section: Risk Factorsmentioning

confidence: 99%

Pulmonary Hypertension in Patients with Heart Failure and Preserved Ejection Fraction: Differential Diagnosis and Management

et al. 2016

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Abstract:The most common cause of pulmonary hypertension (PH) due to left heart disease (LHD) was previously rheumatic mitral valve disease. However, with the disappearance of rheumatic fever and an aging population, nonvalvular LHD is now the most common cause of group 2 PH in the developed world. In this review, we examine the challenge of investigating patients who have PH and heart failure with preserved ejection fraction (HF-pEF), where differentiating between pulmonary arterial hypertension (PAH) and PH-LHD can be difficult, and also discuss the entity of combined precapillary and postcapillary PH. Given the proven efficacy of targeted therapy for the treatment of PAH, there is increasing interest in whether these treatments may benefit selected patients with PH associated with HF-pEF, and we review current trial data.Keywords: pulmonary arterial hypertension, combined pre-and postcapillary pulmonary hypertension, heart failure with preserved ejection fraction, diastolic dysfunction. (Table 1) by a mean pulmonary arterial pressure (PAP) of ≥25 mmHg at right heart catheterization (RHC), with the most recent classification identifying 5 groups (Fig. 1): 2 group 1, pulmonary arterial hypertension (PAH), which can be idiopathic (IPAH) or associated with other conditions (most frequently systemic sclerosis and congenital heart disease); group 2, PH owing to left heart disease (PH-LHD); group 3, PH owing to lung disease (PH-Lung); group 4, chronic thromboembolic PH (CTEPH); and group 5, PH owing to unclear or multifactorial mechanisms. Accurate classification of disease is important in identifying the most appropriate form of therapy 3 and defining prognosis. 4 This requires a systematic approach to the evaluation of the breathless patient and an awareness of conditions associated with particular forms of PH. Pulmonary hypertension (PH) is definedThe most commonly encountered form of PH is related to left heart disease (LHD). 5,6 PH may be seen in heart failure with preserved ejection fraction (HF-pEF) and heart failure with reduced ejection fraction (HF-rEF), and its presence in HF-rEF is known to convey a poor prognosis. 7 HF-pEF accounts for approximately half of all new heart failure (HF) diagnoses. 8,9 While HF-pEF was initially believed to confer a better outcome than HF-rEF, the two conditions have equivalent morbidity and mortality. [10][11][12] The prevalence of PH-HF-pEF is unclear and varies with diagnostic criteria. Studies quote rates of between 53% and 83% (based on an echocardiographic systolic PAP [sPAP] > 35 mmHg or mean PAP > 25 mmHg at RHC). 13-15 A recent study 16 found that only 7% of heart failure (HF) patients had PH (but used an sPAP cutoff of ≥45 mmHg at echocardiography). PATHOPHYSIOLOGY OF PH-LHDPAH, PH-Lung, and CTEPH are precapillary in nature, caused by obstruction or destruction of the pulmonary arterial bed, whereas PH-LHD is thought to be primarily due to postcapillary abnormalities. 5 In patients with LHD, an increase in left ventricular (LV) and left atrial (LA) filling pressu...

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“…11 mm for a diagnosis of PAH. [13][14][15][16] Patients with PVH had no other cause of PH identifi ed after evaluation and had a PAOP . 15 mm Hg at rest, increased PAOP .…”

Section: Setting and Populationmentioning

confidence: 99%

End Tidal CO 2 Tension

Hemnes

Pugh

Newman

et al. 2011

Chest

Self Cite

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Background: CO 2 excretion is impaired in pulmonary arterial hypertension (PAH) due to underlying vascular obstruction and increased dead space. Our aim was to determine whether resting end tidal CO 2 (E TCO 2 ) could differentiate patients with PAH from those with pulmonary venous hypertension (PVH) or patients without pulmonary hypertension (PH) and whether successful treatment of PAH resulted in higher E TCO 2 values. Methods: We performed E TCO 2 measurements for fi ve breaths at rest and after a 6-min walk test (6MWT) in patients seen at our pulmonary vascular center. Mean E TCO 2 values were correlated with 6-min walk distance and right-sided heart catheterization data. Results: We enrolled 84 patients with PAH, 17 with PVH without left ventricular systolic dysfunction, and seven with no PH and no severe alterations in pulmonary function testing. E TCO 2 was signifi cantly lower in patients with PAH than in those with no PH and PVH ( P , .0001 PAH vs both groups). E TCO 2 correlated with the pulmonary artery diastolic pressure-to-pulmonary artery occlusion pressure gradient ( r 5 2 0.50, P 5 .0002) and pulmonary vascular resistance ( r 5 2 0.44, P 5 .002). E TCO 2 after 6MWT correlated with walk distance ( r 5 0.34, P 5 .003). In patients with prostaglandin therapy escalation, E TCO 2 increased in those who had clinical improvement, whereas in patients who did not improve clinically, E TCO 2 failed to rise ( P 5 .04). Conclusions: E TCO 2 is a promising tool to differentiate patients with PAH from those with PVH or no PH, correlates with diagnostic and prognostic hemodynamic indicators, and may increase with successful treatment of PAH. CHEST 2011; 140(5):1267-1273Abbreviations: 6MWT 5 6-min walk test; E tco 2 5 end tidal CO 2 ; mPAP 5 mean pulmonary artery pressure; PAd 5 diastolic pulmonary artery pressure; PAH 5 pulmonary arterial hypertension; PAOP 5 pulmonary artery occlusion pressure; PH 5 pulmonary hypertension; PVH 5 pulmonary venous hypertension; PVR 5 pulmonary vascular resistance; RHC 5 right-sided heart catheterization

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Association of the Metabolic Syndrome With Pulmonary Venous Hypertension

Cited by 158 publications

References 29 publications

Plasma Levels of High-Density Lipoprotein Cholesterol and Outcomes in Pulmonary Arterial Hypertension

Plasma Levels of High-Density Lipoprotein Cholesterol and Outcomes in Pulmonary Arterial Hypertension

Pulmonary Hypertension in Patients with Heart Failure and Preserved Ejection Fraction: Differential Diagnosis and Management

End Tidal CO 2 Tension

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