Detection of Mechanical Prosthetic Valve Dysfunction.

The long-term outcome of mechanical aortic and mitral prosthetic valve (A-PV, M-PV) dysfunction (PVD) remains a serious complication associated with high morbidity and mortality. We sought to evaluate the incremental diagnostic value of combined transthoracic echocardiography (TTE) and fluoroscopy (F) in patients with suspected PVD. A total of 354 patients (178 A-PV, 176 M-PV) were imaged by TTE and F within 5 days of hospital admission. PVD was confirmed by transesophageal echocardiography, computed tomography, effective thrombolysis, or surgical inspection. PVD was confirmed in 101 patients (57%) with M-PV and 99 (55%) with A-PV. Regardless of the mechanism of PVD, TTE shows good sensitivity and specificity, with accuracy of 80% for M-PV and 91% for A-PV. F shows high specificity, but low sensitivity with accuracy of 68% for M-PV and 78% for A-PV. The integration of TTE + F significantly improved accuracy both for M-PV (83%) and A-PV (96%). At ROC analysis, the combined model of TTE + F showed the highest area under the curve for the detection of PVD compared with TTE and F alone (p < 0.001). In conclusion, in patients with a clinical suspicion of PVD, the combined model of TTE + F offers incremental value over TTE or F alone. This multimodality imaging approach overcomes limitations of TTE or F alone and provides prompt identification of patients who may require further imaging assessment and/or closer follow up.

Cardiac output changes during exercise in heart failure patients: focus on mid-exercise.

AIMS: Peak exercise oxygen uptake (VO2 ) and cardiac output (CO) are strong prognostic indexes in heart failure (HF) but unrelated to real-life physical activity, which is associated to submaximal effort. METHODS AND RESULTS: We analysed maximal cardiopulmonary exercise test with rest, mid-exercise, and peak exercise non-invasive CO measurements (inert gas rebreathing) of 231 HF patients and 265 healthy volunteers. HF patients were grouped according to exercise capacity (peak VO2  < 50% and ≥50% pred, Groups 1 and 2). To account for observed differences, data regarding VO2 , CO, stroke volume (SV), and artero-venous O2 content difference [ΔC(a-v)O2 ] were adjusted by age, gender, and body mass index. A multiple regression analysis was performed to predict peak VO2 from mid-exercise cardiopulmonary exercise test and CO parameters among HF patients. Rest VO2 was lower in HF compared with healthy subjects; meanwhile, Group 1 patients had the lowest CO and highest ΔC(a-v)O2 . At mid-exercise, Group 1 patients achieved a lower VO2 , CO, and SV [0.69 (interquartile range 0.57-0.80) L/min; 5.59 (4.83-6.67) L/min; 62 (51-73) mL] than Group 2 [0.94 (0.83-1.1) L/min; 7.6 (6.56-9.01) L/min; 77 (66-92) mL] and healthy subjects [1.15 (0.93-1.30) L/min; 9.33 (8.07-10.81) L/min; 87 (77-102) mL]. Rest to mid-exercise SV increase was lower in Group 1 than Group 2 (P = 0.001) and healthy subjects (P < 0.001). At mid-exercise, ΔC(a-v)O2 was higher in Group 2 [13.6 (11.8-15.4) mL/100 mL] vs. healthy patients [11.6 (10.4-13.2) mL/100 mL] (P = 0.002) but not different from Group 1 [13.6 (12.0-14.9) mL/100 mL]. At peak exercise, Group 1 patients achieved a lower VO2 , CO, and SV than Group 2 and healthy subjects. ΔC(a-v)O2 was the highest in Group 2. At multivariate analysis, a model comprising mid-exercise VO2 , carbon dioxide production (VCO2 ), CO, haemoglobin, and weight predicted peak VO2 , P < 0.001. Mid-exercise VO2 and CO, haemoglobin, and weight added statistically significantly to the prediction, P < 0.050. CONCLUSIONS: Mid-exercise VO2 and CO portend peak exercise values and identify severe HF patients. Their evaluation could be clinically useful.

Contribution of central and peripheral factors at peak exercise in heart failure patients with progressive severity of exercise limitation.

BACKGROUND: A reduced cardiac output (CO) response during exercise is a major limiting factor in heart failure (HF). Oxygen consumption (VO2) is directly proportional to CO. Peripheral mechanisms via arteriovenous oxygen difference (Δ(a-v)O2) play a pivotal role in chronic HF. We hypothesized a weak correlation between peak VO2 and peak CO with a greater Δ(a-v)O2 variability in most severe HF. METHODS: We analyzed 278 HF patients (NYHA II-III) who performed maximal cardiopulmonary exercise test with non-invasive CO measurement by inert gas rebreathing. RESULTS: Median peakVO2, CO and Δ(a-v)O2 were 0.96 (0.78-1.28) L/min, 6.3 (5.1-8.0) L/min and 16.0 (14.2-18.0) mL/100mL respectively, with a linear relationship between VO2 and CO: CO=5.3×VO2+1.13 (r2=0.705, p<0.001). Patients were grouped according to exercise limitation. Group 1 (101 patients) peakVO2<50% pred: peakVO2 0.80 (0.67-0.94) L/min, peakCO 5.6 (4.7-6.5) L/min, peakΔ(a-v)O2 14.8 (12.9-17.1) mL/100mL. Group 2 (89 patients) peakVO2≥50-<65% pred: peakVO2 1.02 (0.84-1.29) L/min, peakCO 6.4 (5.1-8.0) L/min, peakΔ(a-v)O2 16.7 (15.0-18.5) mL/100mL. Group 3 (88 patients) peakVO2≥65% pred: peakVO2 1.28 (0.93-1.66) L/min, peakCO 8.0 (6.2-9.7) L/min, peakΔ(a-v)O2 16.8 (14.6-18.3) mL/100mL. A peakVO2 and peakCO linear relationship was observed in Group 1 (r2=0.381, p<0.001), Group 2 (r2=0.756, p<0.001) and Group 3 (r2=0.744, p<0.001). CONCLUSIONS: With worsening HF we observed a progressive reduction of peak CO and peak VO2. However in most compromised patients also peripheral mechanisms play a role as indicated by reduced Δ(a-v)O2.

ANMCO Position Paper: long-term follow-up of patients with pulmonary thromboembolism.

Venous thromboembolism (VTE), including pulmonary embolism and deep venous thrombosis, is the third most common cause of cardiovascular death. The management of the acute phase of VTE has already been described in several guidelines. However, the management of the follow-up (FU) of these patients has been poorly defined. This consensus document, created by the Italian cardiologists, wants to clarify this issue using the currently available evidence in VTE. Clinical and instrumental data acquired during the acute phase of the disease are the cornerstone for planning the FU. Acquired or congenital thrombophilic disorders could be identified in apparently unprovoked VTE during the FU. In other cases, an occult cancer could be discovered after a VTE. The main targets of the post-acute management are to prevent recurrence of VTE and to identify the patients who can develop a chronic thromboembolic pulmonary hypertension. Knowledge of pathophysiology and therapeutic approaches is fundamental to decide the most appropriate long-term treatment. Moreover, prognostic stratification during the FU should be constantly updated on the basis of the new evidence acquired. Currently, the cornerstone of VTE treatment is represented by both the oral and the parenteral anticoagulation. Novel oral anticoagulants should be an interesting alternative in the long-term treatment.

Reference Values for Peak Exercise Cardiac Output in Healthy Individuals.

BACKGROUND: Cardiac output (Q˙) is a key parameter in the assessment of cardiac function, its measurement being crucial for the diagnosis, treatment, and prognostic evaluation of all heart diseases. Until recently, Q˙ determination at peak exercise has been possible through invasive methods, so that normal values were obtained in studies based on small populations. METHODS: Nowadays, peak Q˙ can be measured noninvasively by means of the inert gas rebreathing (IGR) technique. The present study was undertaken to provide reference values for peak Q˙ in the normal general population and to obtain a formula able to estimate peak exercise Q˙ from measured peak oxygen uptake (V˙o2). RESULTS: We studied 500 normal subjects (age, 44.9 ± 1.5 years; range, 18-77 years; 260 men, 240 women) who underwent a maximal cardiopulmonary exercise test with peak Q˙ measurement by IGR. In the overall study sample, peak Q˙ was 13.2 ± 3.5 L/min (men, 15.3 ± 3.3 L/min; women, 11.0 ± 2.0 L/min; P < .001) and peak V˙o2 was 95% ± 18% of the maximum predicted value (men, 95% ± 19%; women, 95% ± 18%). Peak V˙o2 and peak Q˙ progressively decreased with age (R2, 0.082; P < .001; and R2, 0.144; P < .001, respectively). The V˙o2-derived formula to measure Q˙ at peak exercise was (4.4 × peak V˙o2) + 4.3 in the overall study cohort, (4.3 × peak V˙o2) + 4.5 in men, and (4.9 × peak V˙o2) + 3.6 in women. CONCLUSIONS: The simultaneous measurement of Q˙ and V˙o2 at peak exercise in a large sample of healthy subjects provided an equation to predict peak Q˙ from peak V˙o2 values.

[ANMCO Position paper: Recommendations for the follow-up of patients with pulmonary thromboembolism]. / Position paper ANMCO: Raccomandazioni per il follow-up del paziente con tromboembolia polmonare.

Venous thromboembolism (VTE), including deep venous thrombosis and pulmonary embolism, is the third most common cause of cardiovascular death. The management of the acute phase of VTE is well described in several papers and guidelines, whereas the management of the follow-up of the patients affected from VTE is less defined. This position paper of the Italian Association of Hospital Cardiologists (ANMCO) tries to fill the gap using currently available evidence and the opinion of the experts to suggest the most useful way to manage patients in the chronic phase.The clinical and laboratory tests acquired during the acute phase of the disease drives the decision of the following period. Acquired or congenital thrombophilic factors may be identified to explain an apparently not provoked VTE. In some patients, a not yet clinically evident cancer could be the trigger of VTE and this could lead to a different strategy. The main target of the post-acute management is to prevent relapse of the disease and to identify those patients who could worsen or develop chronic thromboembolic pulmonary hypertension. The knowledge of the etiopathogenetic ground is important to address the therapeutic approach, choosing the best antithrombotic strategy and deciding how long therapy should last. During the follow-up period, prognostic stratification should be updated on the basis of new evidences eventually acquired.Treatment of VTE is mainly based on oral or parenteral anticoagulation. Oral direct inhibitors of coagulation represent an interesting new therapy for the acute and extended period of treatment.