Plasma aldosterone levels are elevated in patients with pulmonary arterial hypertension in the absence of left ventricular heart failure: a pilot study

Introduction: Pulmonary arterial hypertension (PAH) is an acknowledged independent prognostic factor in patients with heart failure (HF). Beyond a “passive” component due to the increased left ventricular pressure, an “active” component due to pulmonary vascular reactivity is frequently observed. However, the mechanism behind pulmonary vasoconstriction is not fully understood. Hypothesis: We hypothesized that central apneas (Cheyne-Stokes respiration [[Unable to Display Character: –]] CSR) through chemoreflex stimulation may contribute to PAH in HF. Methods: we studied 56 HF patients (left ventricular ejection fraction <50%), on stable optimal pharmacological treatment, without increased left ventriculare pressure (excluding patients with severe mitral disease and severe diastolic dysfunction). All patients underwent echocardiographic and neurohormonal assessment, 24-hour cardiorespiratory screening for CSR (patients with obstructive events were excluded) and chemoreflex test for hypoxic (HVR) and hypercapnic (HCVR) ventilatory responses (by rebreathing technique) . Results: Thirteen patients (23%) showed CSR, as defined by a 24 hour AHI > of 15. HF patients with CSR compared with patients with normal breathing, presented higher systolic arterial pulmonary pressure (SPAP: 40.1±7.6 vs 33.1±5.9, p<0.01) at echocardiography, despite similar systolic and diastolic function (data not shown). Furthermore, patients with central apneas also presented with enhanced HVR (median 0.78, interquartile range -IR 0.48-1.22 vs 0.43, IR 0.19-0.69 L/min/%, p<0.05) and HCVR (1.18, IR 0.98-1.35 vs 0.75, IR 0.51-0.95 L/min/mmHg, p<0.01) as well as increased plasma norepinephrine levels (546, IR 371-732 vs 393, IR 229-538 pg/mL, p<0.05). SPAP was indeed correlated with AHI (Spearman’s Rho, R=0.44, p<0.01), HCVR (R=0.48, p<0.001), HVR (R=0.33, p<0.05) and norepinephrine levels (R=0.31, p<0.05). Conclusions: In patients with systolic HF, the presence of diurnal-nocturnal CSR, likely via recurrent hypoxia and hypercapnia cycles, may determine a chemoreflex mediated adrenergic discharge and a consequent pulmonary vasoconstriction, responsible of the undesirable increase in pulmonary arterial pressure.

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673 Impedance Cardiography Is Inaccurate in the Assessment of Cardiac Output in Pulmonary Arterial Hypertension in Comparison to Left Ventricular Heart Failure

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2011.01.687 ◽

2011 ◽

Vol 30 (4) ◽

pp. S224

Author(s):

P. Lesny ◽

B. Liska ◽

M. Luknar ◽

E. Goncalvesova

Keyword(s):

Heart Failure ◽

Cardiac Output ◽

Pulmonary Arterial Hypertension ◽

Arterial Hypertension ◽

Impedance Cardiography ◽

Left Ventricular ◽

Pulmonary Arterial

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Elevated pulmonary arterial and systemic plasma aldosterone levels associate with impaired cardiac reserve capacity during exercise in left ventricular systolic heart failure patients: A pilot study

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2015.10.019 ◽

2016 ◽

Vol 35 (3) ◽

pp. 342-351 ◽

Cited By ~ 6

Author(s):

Bradley A. Maron ◽

Thomas E. Stephens ◽

Laurie A. Farrell ◽

William M. Oldham ◽

Joseph Loscalzo ◽

...

Keyword(s):

Heart Failure ◽

Pilot Study ◽

Systolic Heart Failure ◽

Left Ventricular ◽

Plasma Aldosterone ◽

Reserve Capacity ◽

Heart Failure Patients ◽

Cardiac Reserve ◽

Pulmonary Arterial

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Abstract 17289: A Baffling Heart: a 30 Year-old Man with Biventricular Heart Failure and Severe Pulmonary Hypertension

Circulation ◽

10.1161/circ.130.suppl_2.17289 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Lucas S Zier ◽

Christopher Barnett ◽

Elyse Foster

Keyword(s):

Heart Failure ◽

Congenital Heart Disease ◽

Heart Disease ◽

Pulmonary Arterial Hypertension ◽

Arterial Hypertension ◽

Congenital Heart ◽

Left Ventricular ◽

Lv Dysfunction ◽

Pulmonary Arterial

A thirty year-old man with an unknown surgery for congenital heart disease presented with intermittent chest pain and progressive decline in his exercise tolerance. Cardiovascular examination revealed a soft S1, loud S2 without splitting, right ventricular heave, a sustained and laterally displaced apical impulse and clubbing of his fingers. An echocardiogram showed d-transposition of the great arteries (d-TGA), a dilated, sub-pulmonic left ventricle (LV) with reduced function, smaller than expected sub-aortic right ventricle with reduced function, and elevated sub-pulmonic left ventricular systolic pressure without LV outflow tract obstruction. Cardiac MRI revealed d-TGA status post Senning repair, biventricular dysfunction without baffle obstruction, no evidence of repaired atrial or ventricular septal defect or delayed gadolinium enhancement. Cardiac catheterization showed a suprasystemic pulmonary artery pressure, a pulmonary vascular resistance of 18.4 Wood units and a small right to left shunt due to a baffle leak. No coronary disease was found on angiography. The patient was diagnosed with severe pulmonary arterial hypertension and biventricular dysfunction. This pattern of heart failure was discordant from the expected sequelae of palliated congenital heart defects as pulmonary arterial hypertension and LV dysfunction are both uncommon long-term complications after atrial switch. Systematic evaluation for a unifying cause of the patient’s pattern of heart failure was unrevealing until the patient presented with decompensated heart failure and evidence of stimulant withdrawal. Urine toxicology was positive for methamphetamine and the patient was diagnosed with methamphetamine induced pulmonary arterial hypertension and subpulmonic LV dysfunction. This case demonstrates the importance of understanding the common, long-term patterns of heart failure in repaired congenital heart disease and the need to search for alternative etiologies when the pattern is inconsistent. This case further shows the toxic effects of methamphetamine on the pulmonary vasculature and myocardium, which in our patient resulted in a highly unique pattern of sub-pulmonic LV dysfunction and pulmonary arterial hypertension.

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Cardiac sympathetic dysfunction in pulmonary arterial hypertension: lesson from left-sided heart failure

Pulmonary Circulation ◽

10.1177/2045894019868620 ◽

2019 ◽

Vol 9 (3) ◽

pp. 204589401986862 ◽

Cited By ~ 2

Author(s):

Valentina Mercurio ◽

Teresa Pellegrino ◽

Giorgio Bosso ◽

Giacomo Campi ◽

Paolo Parrella ◽

...

Keyword(s):

Heart Failure ◽

Nervous System ◽

Pulmonary Arterial Hypertension ◽

Left Ventricular Ejection Fraction ◽

Arterial Hypertension ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Ventricular Ejection Fraction ◽

Pulmonary Arterial ◽

Sympathetic Nervous

Sympathetic nervous system hyperactivity has a well-recognized role in the pathophysiology of heart failure with reduced left ventricular ejection fraction. Alterations in sympathetic nervous system have been related to the pathophysiology of pulmonary arterial hypertension, but it is unclear whether cardiac sympathetic nervous system is impaired and how sympathetic dysfunction correlates with hemodynamics and clinical status in pulmonary arterial hypertension patients. The aim of this study was to evaluate the cardiac sympathetic nervous system activity by means of123Iodine-metaiodobenzylguanidine nuclear imaging in pulmonary arterial hypertension patients and to explore its possible correlation with markers of disease severity. Twelve consecutive pulmonary arterial hypertension patients (nine women, median age 56.5 (17.8), eight idiopathic and four connective tissue-associated pulmonary arterial hypertension) underwent cardiac123Iodine-metaiodobenzylguanidine scintigraphy. The results were compared with those of 12 subjects with a negative history of cardiovascular or pulmonary disease who underwent the same nuclear imaging test because of a suspected paraganglioma or pheochromocytoma, with a negative result (controls), and 12 patients with heart failure with reduced left ventricular ejection fraction. Hemodynamics, echocardiography, six-minute walking distance, cardiopulmonary exercise testing, and N-terminal pro brain natriuretic peptide were collected in pulmonary arterial hypertension patients within one week from123Iodine-metaiodobenzylguanidine scintigraphy. Cardiac123Iodine-metaiodobenzylguanidine uptake, assessed as early and late heart-to-mediastinum ratio, was significantly lower in pulmonary arterial hypertension compared to controls (p = 0.001), but similar to heart failure with reduced left ventricular ejection fraction. Myocardial123Iodine-metaiodobenzylguanidine turnover, expressed as washout rate, was similar in pulmonary arterial hypertension and heart failure with reduced left ventricular ejection fraction and significantly higher compared to controls (p = 0.016). In the pulmonary arterial hypertension group, both early and late heart-to-mediastinum ratios and washout rate correlated with parameters of pulmonary arterial hypertension severity including pulmonary vascular resistance, right atrial pressure, tricuspid annular plane systolic excursion, N-terminal pro brain natriuretic peptide, and peak VO2. Although we evaluated a small number of subjects, our study showed a significant impairment in cardiac sympathetic nervous system in pulmonary arterial hypertension, similarly to that observed in heart failure with reduced left ventricular ejection fraction. This impairment correlated with indices of pulmonary arterial hypertension severity. Cardiac sympathetic dysfunction may be a contributing factor to the development of right-sided heart failure in pulmonary arterial hypertension.

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