BACKGROUND: Patients with congestive heart failure or COPD may share an increased response in minute ventilation (V̇ _E ) to carbon dioxide output (V̇ CO ₂ ) during exercise. The goal of this study was to ascertain whether the V̇ _E /V̇ CO ₂ slope and V̇ _E /V̇ CO ₂ intercept can discriminate between subjects with congestive heart failure and those with COPD at equal peak oxygen uptake (V̇ O ₂ ). METHODS: We studied 46 subjects with congestive heart failure (mean age 61 ± 9 y) and 46 subjects with COPD (mean age 64 ± 8 y) who performed a cardiopulmonary exercise test. RESULTS: The V̇ _E /V̇ CO ₂ slope was significantly higher in subjects with congestive heart failure compared with those with COPD (39.5 ± 9.5 vs 31.8 ± 7.4, P < .01) at peak V̇ O ₂ < 16 mL/kg/min, but not ≥ 16 mL/kg/min (28.3 ± 5.3 vs 28.9 ± 6.6). The V̇ _E /V̇ CO ₂ intercept was significantly higher in both subgroups of subjects with COPD compared with the corresponding values in the subjects with congestive heart failure (3.60 ± 1.7 vs −0.16 ± 1.7 L/min, P < .01; 3.63 ± 2.7 vs 0.87 ± 1.5 L/min, P < .01). According to receiver operating characteristic curve analysis, when all subjects with peak V̇ O ₂ < 16 mL/kg/min were considered, subjects with COPD had a higher likelihood to have the V̇ _E /V̇ CO ₂ intercept > 2.14 L/min (0.92 sensitivity, 0.96 specificity). Regardless of peak V̇ O ₂ , the end-tidal pressure of CO ₂ (P ETCO ₂ ) at peak exercise was not different in subjects with congestive heart failure ( P = .42) and was significantly higher in subjects with COPD ( P < .01) compared with the corresponding unloaded P ETCO ₂ . CONCLUSIONS: The ventilatory response to V̇ CO ₂ during exercise was significantly different between subjects with congestive heart failure and those with COPD in terms of the V̇ _E /V̇ CO ₂ slope with moderate-to-severe reduction in exercise capacity and in terms of the V̇ _E /V̇ CO ₂ intercept regardless of exercise capacity.

The Anderson-Fabry disease (AFD, or simply Fabry Disease, FD; MIM #301500) is a rare X-linked lysosomal storage disorder (Xq22.1) characterized by progressive renal failure, leading to morbidity through cardio- and cerebro-vascular involvement. Despite the classic phenotype, only cardiac involvement (cardiac variant of AFD; MIM 301500) is frequent in about 40% of male and 28% of female AFD patients, as reported by the Fabry Registry ( https://www.registrynxt.com ). Morphologically, the cardiac characteristic of the disease, occurs as left ventricular hypertrophy, is accompanied by myocardial fibrosis. Cardiologists may come across these patients during clinical and instrumental evaluation in individuals with non-specific symptoms such as chest pain and arrhythmias, or after instrumental evidence of left ventricular hypertrophy/hypertrophic cardiomyopathy (HCM; MIM 192600). A comprehensive cardiological work-up, including a cardiological visit, a baseline electrocardiogram (ECG) and imaging by both echocardiography (ECHO) and magnetic resonance (MRI) enables identification of the cardiac involvement in patients with a proven diagnosis of AFD. The heart involvement is present in up to 75% of AFD patients irrespective of their sex. Involvement includes ECG and echocardiography features which suggest AFD and not HCM. Cardiac imaging plays an important role in detecting this sub-type of cardiomyopathy, which, since 2001, has benefited from the introduction of the enzyme replacement therapy (ERT) in symptomatic and pre-symptomatic patients.

Electric external cardioversion (EEC) for permanent atrial fibrillation (AF) carries a risk of thromboembolic events (TE). The use of transesophageal echocardiography (TEE) to guide the management of atrial fibrillation may be considered a clinically effective alternative strategy to conventional therapy for patients in whom elective cardioversion is planned. Therapeutic anticoagulation with novel oral anticoagulants (NOAC) is recommended for 3 to 4 weeks before and an anticoagulation life-long therapy is recommended after EEC to reduce TE, in patients with high CHA2DS2-VASc score; however, only few data are currently available about safety of shortterm anticoagulation with NOAC in the setting of EEC. Patients with increased risk of thromboembolism have not been adequately studied and the monitoring of anticoagulant effects can also have important benefits in case of drug interactions. We report a case of a 68-year old man with AF from September 2014. Moderate depression of global left ventricular systolic function was detected by echocardiographic exam. On the basis of a high thromboembolic risk, an anticoagulant therapy with rivaroxaban, at the dose of 20 mg/day, was started. TEE showed a thrombus in the left atrial appendage. This case demonstrates the utility of performing TEE prior than EEC in patients with hypokinetic cardiomyopathy other than AF in therapy with NOAC. We underline the presence of significant pharmacodynamic interference of rivaroxaban with other drugs such as oxcarbazepine.