On the bright side of market concentration in a mixed-oligopoly healthcare industry.

We describe the healthcare industry as a mixed oligopoly, where a public and two private providers compete, and examine the effects of a merger between the two private healthcare providers on prices, quality, and welfare. When the price and (eventually) quality of the public provider are regulated, the cost synergies required for the merger to increase consumer welfare are less significant than in a setting with only profit-maximizing providers. When, instead, the public provider can adjust its policy to the rivals' behavior and maximizes a weighted sum of profits and consumer surplus (i.e., it has 'semi-altruistic' preferences), the merger is consumer surplus increasing if the public provider is sufficiently altruist, in some cases even absent efficiencies. These results suggest that ignoring the role and objectives of the public sector in the healthcare industry may lead agencies to reject mergers that, while would decrease consumer welfare in fully privatized industries, would increase it in mixed oligopolies.

Infective endocarditis or myxoma? Description of a patient with new diagnosis of congestive heart failure.

Infective endocarditis (IE) is an inflammatory disease which interests heart endothelium and mostly heart valves. IE is not a uniform disease, but presents in a variety of different forms that makes the diagnosis difficult. Echocardiography is a crucial diagnostic tool for the diagnosis, especially in those patients who have no typical symptoms as in the case here presented, in which the possibility of a myxoma was also considered.

Prognostic factors of mid-term clinical outcome in congestive heart failure patients discharged after acute decompensation.

INTRODUCTION: Risk stratification in congestive heart failure (CHF) patients is based on a variety of clinical and laboratory variables. We analysed renal function, BNP, water composition, echocardiographic and functional determinations in predicting mid-term outcome in CHF patients discharged after decompensation. MATERIAL AND METHODS: All subjects with NYHA class II-IV were enrolled at hospital discharge. NYHA class, BNP, water body composition, non-invasive cardiac output and echocardiogram were analysed. Death, cardiac transplantation and hospital readmission for CHF were scheduled. RESULTS: Two-hundred and thirty-seven (64.5% males, age 71.1±10.1) patients were discharged after obtaining normal hydration; left ventricular ejection fraction (LVEF) was 43.2±16.2%, cardiac output was 3.8±1.1 l/min and BNP at discharge resulted 401.3±501.7 pg/ml. During the 14-month follow-up 15 patients (6.3%) died, 1 (0.4%) underwent cardiac transplantation and 18 (7.6%) were readmitted for CHF (event group); in 203 (85.6%) no events were observed (no-event group). Higher NYHA class (2.1±0.7 vs. 1.9±0.4, p=0.01), BNP at discharge (750.2±527.3 pg/ml vs. 340.7±474.3 pg/ml, p=0.002) and impaired LVEF (33.7±15.7% vs. 44.5±15.8%, p=0.0001) and creatinine (1.7±0.6 vs. 1.2±0.8 mg/dl, p=0.004) were noticed in the event group. At multivariate Cox analysis LVEF (p=0.0009), plasma creatinine (p=0.006) and BNP at discharge (p=0.001) were associated with adverse mid-term outcome. Kaplan-Meier survival curves demonstrated that adding cut-off points for creatinine 1.5 mg/dl and discharged BNP of 250 pg/ml discriminated significantly prognosis (p=0.0001; log rank 21.09). CONCLUSIONS: In predicting mid-term clinical prognosis in CHF patients discharged after acute decompensation, BNP at discharge ≥ 250 pg/ml added with plasma creatinine > 1.5 mg/dl are strong adverse predictors.

Effects of levosimendan/furosemide infusion on plasma brain natriuretic peptide, echocardiographic parameters and cardiac output in end-stage heart failure patients.

BACKGROUND: Acute decompensation heart failure (ADHF) remains a cause of hospitalization in patients with end-stage congestive HF. The administration of levosimendan in comparison with a standard therapy in CHF patients admitted for ADHF was analysed. MATERIAL/METHODS: Consecutive patients admitted for ADHF (NYHA class III-IV) were treated with levosimendan infusion 0.1 µg/kg/min or with furosemide infusion 100-160 mg per day for 48 hours (control group). All subjects underwent determination of brain natriuretic peptide (BNP), non-invasive cardiac output (CO), and echocardiogram at baseline, at the end of therapy and 1 week after therapy. RESULTS: Seven patients admitted for 20 treatments in 16 months (age 66 years; mean admission/year 5.4) were treated with levosimendan and compared with 7 patients admitted for 15 treatments (age 69.1 years; mean admission/year 6.1). At the end of levosimendan therapy, BNP decreased (from 679.7 ± 512.1 pg/ml to 554.2 ± 407.6 pg/ml p = 0.03), and 6 MWT and LVEF improved (from 217.6 ± 97.7 m to 372.2 ± 90.4 m p = 0.0001; from 22.8 ± 9.1% to 25.4 ± 9.8% p = 0.05). Deceleration time, E/A, E/E', TAPSE, pulmonary pressure and CO did not change significantly after levosimendan therapy and after 1 week. At follow-up, only 6-min WT and NYHA class showed a significant improvement (p = 0.0001, p = 0.001 respectively). The furosemide infusion reduced NYHA class and body weight (from 3.4 ± 0.6 to 2.3 ± 0.5 p = 0.001; from 77.5 ± 8.6 kg to 76 ± 6.6 kg p = 0.04), but impaired renal function (clearances from 56.3 ± 21.9 ml/min to 41.2 ± 10.1 ml/min p = 0.04). CONCLUSIONS: Treating end-stage CHF patients with levosimendan improved BNP and LVEF, but this effect disappeared after 1 week. The amelioration of 6 MWT and NYHA class lasted longer after levosimendan infusion.

[Antianginal efficacy of ivabradine in a very old patient with aortic stenosis: effects on cardiac output and transvalvular aortic gradients]. / Efficacia antianginosa dell'ivabradina in un grande anziano con stenosi aortica: analisi dell'effetto sulla portata cardiaca e sui gradienti transvalvolari.

Ivabradine is a selective I(f) current inhibitor in the sinus node that decreases heart rate without negative inotropic effects. We report the case of an 88-year-old diabetic patient with arterial hypertension and peripheral arterial disease who experienced an antero-lateral non-ST-elevation myocardial infarction following post-surgical anemia. After admission, the patient complained of anginal pain at rest with ischemic alterations of ST-T at the ECG and mild increase in troponin T levels. According to the clinical status, the association of ivabradine with beta-blockers was started. The addition of ivabradine reduced heart rate, improved symptoms (CCS class I-II) without modifying the main hemodynamic (non-invasively measured cardiac output, stroke volume and cardiac index) and echocardiographic parameters (left ventricular ejection fraction and aortic transvalvular gradients). In conclusion, the antianginal effect of ivabradine seems to be sure in very old ischemic patients with aortic stenosis.