Atrial flutter regression in HIV-associated pulmonary arterial hypertension after treatment with bosentan

Pulmonary arterial hypertension (PAH) is a rare condition characterized by an increase in pulmonary arterial resistance leading to right heart failure and death. Arrhythmias are a growing problem in PAH; therefore, maintenance of sinus rhythm is considered to be an important treatment aim in these patients. We described the case of a 46-year-old woman with HIV-associated pulmonary arterial hypertension who developed atrial flutter. After treatment with bosentan, it was observed a significant improvement in clinical and haemodynamic parameters. In addition, the AFL, which had previously persisted to both antiarrhythmic drug therapy and electrical stimulation, and had recurred after transthoracic electrical cardioversion, disappeared in absence of any antiarrhythmic drug. Though the precise factors responsible for supraventricular arrhythmogenesis are still largely obscure, it is likely that initiation and maintenance of AFL may depend on all the conditions that can lead to increase in right atrial pressure, size, and wall stress, such as PAH. In our case, bosentan reduced both mean pulmonary artery pressure (mPAP) value and right heart chambers pressures. Therefore, it is conceivable that with the anatomical substrate needed for the maintenance of AFL being disappeared, sinus rhythm was restored.</p

Using PaCO2 values to grade obesity-hypoventilation syndrome severity: a retrospective study

Background: To date, an important aspect that has still not been clarified is the assessment of OHS severity. The purpose of this retrospective study was to evaluate whether grading OHS severity according to PaCO2 values may be useful in order to provide a more definite characterization and targeted management of patients. In this regard, baseline anthropometric and sleep polygraphic characteristics, treatment options, and follow up outcomes, were compared between OHS patients with different degree of severity (as assessed according to PaCO2 values). Methods: Patients were classified into three groups, according to PaCO2 values: 1) mild (46 mmHg ≤ PaCO2 ≤ 50 mmHg), moderate (51 mmHg ≤ PaCO2 ≤ 55 mmHg), severe (PaCO2 ≥ 56 mmHg). Therefore, differences among the groups in terms of baseline anthropometric, and sleep polygraphic characteristics, treatment modalities and follow up outcomes were retrospectively evaluated. Results: Patients with more severe degree of hypercapnia were assessed to have increased BMI and bicarbonate levels, worse diurnal and nocturnal hypoxemia, and a more severe impairment in pulmonary mechanics compared to milder OHS. CPAP responders rate significantly decreased from mild to severe OHS. After follow up, daytime sleepiness (as measure by the ESS), PaO2, and PaCO2 significantly improved with PAP therapy in all three groups. Discussion and Conclusions: Classification of OHS severity according to PaCO2 levels may be useful to provide a more defined characterization and, consequently, a more targeted management of OHS patients. Further studies are needed to confirm our findings

Obstructive Sleep Apnea, Hypertension, and Their Additive Effects on Atherosclerosis

Background and Aims. It is widely accepted that obstructive sleep apnea (OSA) is independently associated with atherosclerosis. Similar to OSA, hypertension (HTN) is a condition associated with atherosclerosis. However, to date, the impact of the simultaneous presence of OSA and HTN on the risk of atherosclerosis has not been extensively studied. The aim of this study was to evaluate the consequences of the coexistence of OSA and HTN on carotid intima-media thickness (IMT) and on inflammatory markers of atherosclerosis (such as interleukin- [IL-] 6 and pentraxin- [PTX-] 3). Methods. The study design allowed us to define 4 groups: (1) controls (n=30); (2) OSA patients without HTN (n=30); (3) HTN patients without OSA (n=30); (4) patients with OSA and HTN (n=30). In the morning after portable monitoring (between 7 am and 8 am), blood samples were collected, and carotid IMT was measured. Results. Carotid IMT, IL-6, and PTX-3 in OSA normotensive patients and in non-OSA HTN subjects were significantly higher compared to control subjects; in addition, in OSA hypertensive patients they were significantly increased compared to OSA normotensive, non-OSA HTN, or control subjects. Conclusions. OSA and HTN have an additive role in the progression of carotid atherosclerosis and in blood levels of inflammatory markers for atherosclerosis, such as interleukin-6 and pentraxin-3