Role of cardiopulmonary exercise test in the prediction of hemodynamic impairment in patients with pulmonary arterial hypertension.

Periodic repetition of right heart catheterization (RHC) in pulmonary arterial hypertension (PAH) can be challenging. We evaluated the correlation between RHC and cardiopulmonary exercise test (CPET) aiming at CPET use as a potential noninvasive tool for hemodynamic burden evaluation. One hundred and forty-four retrospective PAH patients who had performed CPET and RHC within 2 months were enrolled. The following analyses were performed: (a) CPET parameters in hemodynamic variables tertiles; (b) position of hemodynamic parameters in the peak end-tidal carbon dioxide pressure (PETCO2) versus ventilation/carbon dioxide output (VE/VCO2) slope scatterplot, which is a specific hallmark of exercise respiratory abnormalities in PAH; (c) association between CPET and a hemodynamic burden score developed including mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), cardiac index, and right atrial pressure. VE/VCO2 slope and peak PETCO2 significantly varied in mPAP and PVR tertiles, while peak oxygen uptake (peak VO2) and O2 pulse varied in the tertiles of all hemodynamic parameters. PETCO2 versus VE/VCO2 slope showed a strong hyperbolic relationship (R 2 = 0.7627). Patients with peak PETCO2 > median (26 mmHg) and VE/VCO2 slope < median (44) presented lower mPAP and PVR (p < 0.005) than patients with peak PETCO2 < median and VE/VCO2 slope > median. Multivariate analysis individuated peak VO2 (p = 0.0158) and peak PETCO2 (p = 0.0089) as hemodynamic score independent predictors; the formula 11.584 - 0.0925 × peak VO2 - 0.0811 × peak PETCO2 best predicts the hemodynamic score value from CPET data. A significant correlation was found between estimated and calculated scores (p < 0.0001), with a precise match for patients with mild-to-moderate hemodynamic burden (76% of cases). The results of the present study suggest that CPET could allow to estimate the hemodynamic burden in PAH patients.

Pathophysiology of cardiorenal syndrome in decompensated heart failure: role of lung-right heart-kidney interaction.

Cardiorenal syndrome (CRS) is defined as an interaction of cardiac disease with renal dysfunction that leads to diuretic resistance and renal function worsening, mainly with heart failure (HF) exacerbation. Hemodynamic variables linking heart and kidney are renal blood flow (cardiac output) and perfusion pressure, i.e., the aortic - renal venous pressure gradient. CRS has traditionally been interpreted as related to defective renal perfusion and arterial underfilling and, more recently, to elevation in central venous pressure transmitted back to renal veins. Our suggestion is that in a setting where aortic pressure is generally low, due to heart dysfunction and to vasodrepressive therapy, the elevated central venous pressure (CVP) contributes to lower the renal perfusion pressure below the threshold of kidney autoregulation (≤80mm Hg) and causes renal perfusion to become directly pressure dependent. This condition is associated with high neurohumoral activation and preglomerular vasoconstriction that may preserve pressure, but may decrease filtration fraction and glomerular filtration rate and enhance proximal tubular sodium absorption. Thus, congestion worsens and drives the vicious cycle of further sodium retention and HF exacerbation. Lowering CVP by targeting the lung-right heart interaction that sustains elevated CVP seems to be a more rational approach rather than reducing intravascular volume. This interaction is crucial and consists of a cascade with stepwise development of pulmonary post-capillary hypertension, precapillary arteriolar hypertone, right ventricular overload and enlargement with tricuspid incompetence and interference with left ventricular filling (interdependence). The resultant CVP rise is transmitted to the renal veins, eventually drives CRS and leads to a positive feedback loop evolving towards HF refractoriness.

Prognostic value of lymph node status and number of removed nodes in patients with squamous cell carcinoma of the vulva treated with modified radical vulvectomy and inguinal-femoral lymphadenectomy.

PURPOSE OF INVESTIGATION: To assess the outcome of patients with squamous cell vulvar carcinoma treated with deep partial or total vulvectomy and inguinal-femoral lymphadenectomy. MATERIALS AND METHODS: The authors assessed 87 patients who underwent primary surgery. RESULTS: Tumor recurred in 34 patients, and the first relapse was local in 19, inguinal in ten, and distant in five. Five-year disease-free survival was 56.7% and was related to Stage (p < 0.0001), grade (p = 0.023), and node status (p < 0.0001). Groin failure occurred in 4.9% of node-negative patients compared with 29.6% of node-positive patients (p = 0.0096). Distant recurrences only developed in women with positive nodes. Among the 47 patients who underwent bilateral lymphadenectomy and who had negative nodes, groin recurrence occurred in 12% of those who had < or = 15 nodes removed and 0% of those who had > 15 nodes removed. CONCLUSIONS: Stage and node status were the most important prognostic variables. There was a trend favoring a better groin control in patients with node-negative disease who underwent extensive lymphadenectomy.