Impaired Right Ventricular Hemodynamics Indicate Preclinical Pulmonary Hypertension in Patients With Metabolic Syndrome

Abstract

BackgroundMetabolic disease can lead to intrinsic pulmonary hypertension in experimental models. The contributions of metabolic syndrome (MetS) and obesity to pulmonary hypertension and right ventricular dysfunction in humans remain unclear. We investigated the association of MetS and obesity with right ventricular structure and function in patients without cardiovascular disease.Methods and ResultsA total of 156 patients with MetS (mean age 44 years, 71% women, mean body mass index 40 kg/m2), 45 similarly obese persons without MetS, and 45 nonobese controls underwent echocardiography, including pulsed wave Doppler measurement of pulmonary artery acceleration time (PAAT) and ejection time. Pulmonary artery systolic pressure was estimated from PAAT using validated equations. MetS was associated with lower tricuspid valve e′ (right ventricular diastolic function parameter), shorter PAAT, shorter ejection time, and larger pulmonary artery diameter compared with controls (P<0.05 for all). Estimated pulmonary artery systolic pressure based on PAAT was 42±12 mm Hg in participants with MetS compared with 32±9 and 32±10 mm Hg in obese and nonobese controls (P for ANOVA <0.0001). After adjustment for age, sex, hypertension, diabetes, body mass index, and triglycerides, MetS remained associated with a 20‐ms–shorter PAAT (β=−20.4, SE=6.5, P=0.002 versus obese). This association persisted after accounting for left ventricular structure and function and after exclusion of participants with obstructive sleep apnea.ConclusionsMetS is associated with abnormal right ventricular and pulmonary artery hemodynamics, as shown by shorter PAAT and subclinical right ventricular diastolic dysfunction. Estimated pulmonary artery systolic pressures are higher in MetS and preclinical metabolic heart disease and raise the possibility that pulmonary hypertension contributes to the pathophysiology of metabolic heart disease.

Impact of Body Mass Index >50 on Cardiac Structural and Functional Characteristics and Surgical Outcomes After Bariatric Surgery

“…Several studies support the impact of increased weight on the development of breathing disorders and pulmonary hypertension [32]. It is well known that obesity-induced LV hypertrophy can promote LV diastolic dysfunction leading to pulmonary hypertension, but there is increasing evidence that metabolic syndrome, regardless of the presence of obstructive sleep apnea, can alter pulmonary hemodynamics [33]. Intravascular volume expansion through activation of the renin-angiotensin-aldosterone system is a characteristic of obesity [34] and can provoke passive increase in LA pressure as well [35].…”

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“…Observational studies over the last years have established that at least in the USA severe PAH is increasingly diagnosed in obese, menopausal or post-menopausal women (81,82). A large and growing literature backs up the concept of adiposity as an inflammatory state and a connection has been made between PAH and the metabolic syndrome (83,84). As adipose tissue expands, there is an increase in chronic smoldering inflammation due to infiltration of cytokine producing macrophages, T -and B lymphocytes and eosinophiles (85, 86).…”

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“…apelin) in pulmonary endothelial cells (83). Cohort participants with metabolic syndrome, albeit asymptomatic for cardiovascular disease, present subclinical pulmonary hypertension and right ventricular diastolic dysfunction (84), also observed in experimental models (85). In obesity-induced insulin resistance model, treatment with NO 2 -FAs improves right ventricular function (86).…”