Electrocardiographic modifications induced by breast implants.

BACKGROUND: Echocardiography realization can be challenging in the presence of breasts implants (BI). It is less known if electrocardiograms (ECG) may be modified in the presence of BI. METHODS: ECG from women with BI (and without any known cardiac structural disease) were sent and analyzed by two experienced electrophysiologists (EP1 and EP2) who were blinded and completely unaware of the context of the patients (Group 1). ECG from a control matched-group of female women without BI (Group 2) were also blindly sent for analysis. RESULTS: ECG were collected from 28 women with BI (42 ± 8 years) without any acute medical condition. A proportion of 42% of the ECG were considered abnormal by EP1 and 46% by EP2. The abnormalities were for EP1: negative T waves (5), ST depression in inferolateral leads (2), absence of R wave progression from V1 to V4 (4), left ventricular (LV) hypertrophy (1), long QT(1), early repolarization (1), short PR (1); For EP2: negative T waves (6), ST depression in inferolateral leads (2), absence of R wave progression from V1 to V4 (4), LV hypertrophy(3), long QT (1), early repolarization (1). ECG from group 2 were considered abnormal in only 1 patient (5%) for EP1, and normal in all for EP2 (P = 0.0002 between the groups). CONCLUSIONS: ECG from women with BI were considered abnormal in 42% to 46% of the cases by expert readers. ECG interpretation can thus be misleading in these women.

Outcome of patients with right heart thrombi: the Right Heart Thrombi European Registry.

Our aim was the assessment of the prognostic significance of right heart thrombi (RiHT) and their characteristics in pulmonary embolism in relation to established prognostic factors.138 patients (69 females) aged (mean±sd) 62±19 years with RiHT were included into a multicenter registry. A control group of 276 patients without RiHT was created by propensity scoring from a cohort of 963 contemporary patients. The primary end-point was 30-day pulmonary embolism-related mortality; the secondary end-point included 30-day all-cause mortality. In RiHT patients, pulmonary embolism mortality was higher in 31 patients with systolic blood pressure <90 mmHg than in 107 normotensives (42% versus 12%, p=0.0002) and was higher in the 83 normotensives with right ventricular dysfunction (RVD) than in the 24 normotensives without RVD (16% versus 0%, p=0.038). In multivariable analysis the simplified Pulmonary Embolism Severity Index predicted mortality (hazard ratio 2.43, 95% CI 1.58-3.73; p<0.0001), while RiHT characteristics did not. Patients with RiHT had higher pulmonary embolism mortality than controls (19% versus 8%, p=0.003), especially normotensive patients with RVD (16% versus 7%, p=0.02).30-day mortality in patients with RiHT is related to haemodynamic consequences of pulmonary embolism and not to RiHT characteristics. However, patients with RiHT and pulmonary embolism resulting in RVD seem to have worse prognosis than propensity score-matched controls.

Pulmonary hypertension in patients with neurofibromatosis type I.

Neurofibromatosis type I (NF1) is a rare genetic disease caused by mutations in the NF1 gene, which codes for tumor suppressor neurofibromin. NF1 is transmitted as an autosomal dominant and fully penetrant trait with no sex predominance. Precapillary pulmonary hypertension (PH) is a severe complication of NF1, initially described in patients with advanced parenchymal lung disease, which may complicate the course of NF1. We conducted this study to describe clinical, functional, radiologic, and hemodynamic characteristics and outcome of patients with NF1-associated PH. We identified 8 new cases of NF1-associated PH in patients carrying a NF1 gene mutation. No bone morphogenic protein receptor 2 (BMPR2) point mutation or large size rearrangements were identified. Seven female patients and 1 male patient were reported, suggesting a possible female predominance. PH occurred late in the course of the disease (median age, 62 yr; range, 53-68 yr). Dyspnea and signs of right heart failure were the major symptoms leading to the diagnosis of PH. At diagnosis, patients had severe hemodynamic impairment with low cardiac index (median, 2.3 L/min per m2; range, 1.9-4.7) and elevated indexed pulmonary vascular resistance (median, 15.1 mm Hg/L/min per m2; range, 4.5-25.9). All patients were in New York Heart Association functional class III with severe exercise limitation (median 6-min walk distance, 180 m; range, 60-375 m). Most patients had associated parenchymal lung disease, but some had no or mild lung involvement with disproportionate pulmonary vascular disease. Overall, the impact of PH therapy was limited and outcomes were poor. In conclusion, PH represents a rare but severe complication of NF1, characterized by female predominance, late onset in the course of NF1, and severe functional and hemodynamic impairment. Because of poor outcome and limited impact of specific PH therapy, eligible patients require early referral for lung transplantation. Further studies are needed to better understand the pathophysiology and the role, if any, of neurofibromin in NF1-associated PH.