Multimodality Imaging of Purulent Pericarditis: Hints to Speed up Diagnosis and Promote Healing.

Purulent pericarditis is rare and usually associated with pneumonia, bacteremia, immunosuppression, and thoracic surgery. A timely diagnostic pericardiocentesis with dedicated maneuvers to improve the effectiveness of drainage and pericardial fibrinolytic rinsing can improve prognosis and prevent a surgical pericardiectomy. Imaging offers useful clues for a more aggressive approach.

Cardiac Arrest in a 31-Year-Old Man With Noonan Syndrome.

A 31-year-old man with Noonan syndrome who suffered an out-of-hospital cardiac arrest presented at our institution with severe postanoxic coma (Glasgow coma scale 3), but normalized electrocardiogram and stable hemodynamics. Coronary angiography documented a giant right coronary artery supplying collateral flow to the left coronary artery, which presented a left main functional occlusion.

Rapid rule-out of suspected acute coronary syndrome in the Emergency Department by high-sensitivity cardiac troponin T levels at presentation.

The reliability of initial high-sensitivity cardiac troponin T (hs-cTnT) under limit-of-detection in ruling-out short- and long-term acute coronary events in subjects for suspected non-ST-segment elevation acute coronary syndrome (NSTE-ACS) is not definitely settled. In a retrospective chart review analysis, 1001 subjects with hs-cTnT ≤ 14 ng/L out of 4053 subjects with hs-cTnT measured at Emergency Department (ED) presentation were recruited. The main outcome measure is fatal or non-fatal myocardial infarction (MI) within 30 days; secondary outcomes are MI or major acute coronary events (MACE) as a combination of MI or re-hospitalization for unstable angina within 1 year. In subjects with hs-cTnT < 5 ng/L [32.6% of cases, mean age 63 years (interquartile range 23)], no cases (0%, NPV 100%) had MI within 30 days, 2 cases (0.6%, NPV 99.4%) MI at 1-year, and 11 cases (3.4%, NPV 96.6%) MACE at 1-year. Patients with hs-cTnT < 5 ng/L would have benefited from a shortened decision (9.30 h and 53% overnight ED stay saved). Hs-cTnT < 5 ng/L is confirmed as safe for patients and comfortable for physicians in ruling out MI or MACE both at short and long term, suggesting that a sizable number of patients can be rapidly discharged without unnecessary diagnostic tests and ED observation.

Combining bosentan and sildenafil in pulmonary arterial hypertension patients failing monotherapy: real-world insights.

Pulmonary arterial hypertension is a severe disease with a complex pathogenesis, for which combination therapy is an attractive option.This study aimed to assess the impact of sequential combination therapy on both short-term responses and long-term outcomes in a real-world setting.Patients with idiopathic/heritable pulmonary arterial hypertension, or pulmonary arterial hypertension associated with congenital heart disease or connective tissue disease and who were not meeting treatment goals on either first-line bosentan or sildenafil monotherapy, were given additional sildenafil or bosentan and assessed after 3-4 months. Double combination therapy significantly improved clinical and haemodynamic parameters, independent of aetiology or the order of drug administration. Significant improvements in functional class were observed in patients with idiopathic/heritable pulmonary arterial hypertension. The 1-, 3- and 5-year overall survival estimates were 91%, 69% and 59%, respectively. Patients with pulmonary arterial hypertension associated with connective tissue disease had significantly poorer survival rates compared to other aetiologies (p<0.003).The favourable short-term haemodynamic results and good survival rates, observed in patients receiving both bosentan and sildenafil, supports the use of sequential combination therapy in patients failing on monotherapy in a real-world setting.

[Pulmonary arterial hypertension. Part II: Medical and surgical treatment]. / L'ipertensione arteriosa polmonare. Parte II: Terapia medica e chirurgica.

Treatment of pulmonary arterial hypertension (group 1 of clinical classification) has been recently characterized by important progresses, particularly in pharmacological therapy. Only until few years ago, patients with pulmonary arterial hypertension were treated with non-specific drugs, such as diuretics and digoxin for right heart failure and calcium-channel blockers in the minority of cases, responders to the acute vasoreactivity test. In addition, use of oral anticoagulant treatment was supported by uncontrolled studies. In the last 15 years (in particular in the last 8 years) different randomized controlled trials assessing the functional, clinical and hemodynamic efficacy of three classes of targeted drugs (prostanoids, endothelin receptor antagonists and phosphodiesterase type 5 inhibitors) with pulmonary vascular dilating and antiproliferative effects have been performed. This information has allowed the proposal of an evidence-based treatment algorithm. Treatment starts with general measures (physical activity, fertility control, respiratory tract infection, etc.) and supportive therapy (anticoagulant therapy, diuretics, oxygen, digoxin). Patients who respond to the acute vasoreactivity test (10% of idiopathic form) are treated with high doses of calcium-channel blockers, non-responders with targeted therapies either on monotherapy or combination. Usually an oral active drug is initiated and a second compound of a different class is combined in case of non-satisfactory response to the first treatment. Combination therapy should be performed only in specialized centers with large experience on use of targeted therapies and their relevant side effects. In case of failure of medical therapy, possible options are balloon atrial septostomy and/or listing for lung or heart-lung transplantation. As available treatments do not constitute a cure for pulmonary arterial hypertension, further progresses are expected in the near future.

[Pulmonary arterial hypertension. Part I: pathobiologic, pathophysiologic, clinical and diagnostic aspects]. / L'ipertensione arteriosa polmonare. Parte I: patobiologia, fisiopatologia, aspetti clinici e diagnostici.

Pulmonary hypertension is a pathophysiologic condition characterized by the increase of mean pulmonary arterial pressure > or =25 mmHg. A concomitant increase of pulmonary wedge pressure >15 mmHg may be present (post-capillary pulmonary hypertension) or not (precapillary pulmonary hypertension). The increase of pulmonary arterial pressure and of pulmonary vascular resistance and consequent elevation of the right ventricular afterload lead to right ventricular failure after variable periods of time. Pulmonary hypertension is present in multiple clinical conditions which have been classified in five groups. Pulmonary arterial hypertension (group 1) includes the familial and the idiopathic form and the forms associated with anorexigen drug use, connective tissue diseases, congenital heart diseases, HIV infection and portal hypertension. Group 2 includes all left heart diseases characterized by the increase of left atrial pressure and pulmonary wedge pressure (post-capillary pulmonary hypertension). Group 3 includes parenchymal lung diseases (chronic obstructive lung disease, lung fibrosis, ecc). Chronic thromboembolic pulmonary hypertension (group 4) is characterized by the obstruction of elastic pulmonary arteries at different levels by organized thromboembolism. Group 5 includes heterogeneous conditions such as sarcoidosis and histiocytosis X. These clinical groups are characterized by different pathobiologic and pathophysiologic mechanisms and therapeutic strategies. The exact pathobiologic mechanisms leading to pulmonary arterial hypertension (group 1) are unknown. Genetic factors (inheritable forms), predisposing factors (female gender) and exogenous factors (drugs, antibodies, viruses, congenital heart disease, etc). Endothelial dysfunction of lung microcirculation is invariably present and is characterized by the reduction of vasodilator and antiproliferative substances (prostacyclin, nitric oxide) and by the increase of vasoconstrictor and mitogenic factors (endothelin, thromboxane A2). Current approved therapies are targeted to the correction of this imbalance, which leads to the progressive increase of pulmonary vascular resistance. Different therapeutic strategies that are effective in diverse groups require an appropriate diagnostic algorithm in order to identify the precise group and specific conditions within the group. Evaluation of vasoreactivity and assessment of the severity of functional and hemodynamic changes are also required in pulmonary arterial hypertension for an appropriate therapeutic decision-making and estimate of results.