Roberto Baglini

Six-Month Echocardiographic Study in Patients With Submassive Pulmonary Embolism and Right Ventricle Dysfunction: Comparison of Thrombolysis With Heparin

Introduction:The aim of this study was to assess the effect of thrombolysis versus heparin treatment on echocardiographic parameters and clinical outcome, during hospitalization and within the first 180 days after admission, in patients with first episode of submassive pulmonary embolism (SPE) and right ventricle dysfunction (RVD). Methods:Consecutive patients (age, 18–75 years) with a first episode of SPE, symptoms onset since no more than 6 hours, normal blood pressure (>100 mm Hg), echocardiographic evidence of RVD and positive lung spiral computed tomography were double-blind randomized: 1 group received 100 mg of alteplase (10-mg bolus, followed by a 90-mg intravenous infusion over a period of 2 hours), while the other group received matching placebo. In addition to alteplase or placebo, both groups received an unfractionated heparin treatment. Echocardiogram was performed at admission, at 24, 48 and 72 hours, at discharge and at 3 and at 6 months after randomization. Results:Seventy-two patients were included into the study; 37 were assigned to thrombolysis and 35 to placebo. Both groups were well matched with regard to features and clinical presentation. Thrombolysis group showed a significant early improvement of RV function compared with heparin group, and this improvement was observed also during the follow-up (180 days). The same group also showed significant reduction in clinical events during the hospitalization and follow-up. Conclusions:Our data suggest that, in hemodynamically stable patients with SPE, thrombolysis shows an earliest reduction of RVD and a more favorable trend in clinical outcome, so, it could merit consideration in SPE.

Haemodynamic predictors of a penetrating atherosclerotic ulcer rupture using fluid-structure interaction analysis.

We present preliminary data on the flow-induced haemodynamic and structural loads exerted on a penetrating atherosclerotic aortic ulcer (PAU). Specifically, one-way fluid-structure interaction analysis was performed on the aortic model reconstructed from a 66-year-old male patient with a PAU that evolved into an intramural haematoma and rupture of the thoracic aorta. The results show that elevated blood pressure (117 mmHg) and low flow velocity at the aortic wall (0.15 m/s(2)) occurred in the region of the PAU. We also found a low value of time-averaged wall shear stress (1.24 N/m(2)) and a high value of the temporal oscillation in the wall shear stress (oscillatory shear index = 0.13) in the region of the PAU. After endovascular treatment, these haemodynamic parameters were distributed uniformly on the luminal surface of the stent graft. These findings suggest that wall shear stress could be considered one of the major haemodynamic factors indicating the structural fragility of the PAU wall, which ultimately lead to PAU growth and rupture.

Can learning to interpret pump messages help lead to an early diagnosis of HeartWare ventricular assist device thrombosis

Left ventricular assist device thrombosis is a detrimental complication that, if not properly diagnosed and treated, can lead to low output syndrome and death. When ongoing thrombus formation is caused by inappropriate anticoagulation, timely identification is possible, and could perhaps be the key to successful treatment.

Computational fluid dynamics simulation to evaluate aortic coarctation gradient with contrast-enhanced CT.

Coarctation of aorta (CoA) is a narrowing of the aorta leading to a pressure gradient (ΔP) across the coarctation, increased afterload and reduced peripheral perfusion pressures. Indication to invasive treatment is based on values of maximal (systolic) trans-coarctation ΔP. A computational fluid dynamic (CFD) approach is herein presented for the non-invasive haemodynamic assessment of ΔP across CoA. Patient-specific CFD simulations were created from contrast-enhanced computed tomography (CT) and appropriate flow boundary conditions. Computed ΔP was validated with invasive intravascular trans-CoA pressure measurements. Haemodynamic indices, including pressure loss coefficient (PLc), time-averaged wall shear stress (TAWSS) and oscillatory shear index (OSI), were also quantified. CFD-estimated ΔP values were comparable to the invasive ones. Moreover, the aorta proximal to CoA was exposed to altered TAWSS and OSI suggesting hypertension. PLc was found as a further geometric marker of CoA severity. Finally, CFD-estimated ΔP confirmed a significant reduction after percutaneous balloon dilatation and stenting of the CoA in one patient (e.g. from ΔP∼52 mmHg to ΔP∼3 mmHg). The validation of the ΔP computations with catheterisation measurements suggests that CFD simulation, based on CT-derived anatomical data, is a useful tool to readily quantify CoA severity.

Left Main Coronary In‐Stent Intimal Hyperplasia and Hemodynamics as Detected by Contrast‐Enhanced Transesophageal Echocardiography

Patients and methods: In‐stent hemodynamics were studied by transesophageal echocardiography (TEE) in a group of 54 patients after left main coronary artery stenting, during a 6‐month follow‐up. TEE was performed within 24 hours after stenting and at 1‐ and 3‐month follow‐up. Pulsed wave and color Doppler signals were enhanced by IV administration of Levovist. Results: Angiographic immediate success was obtained in all patients. No in‐hospital death occurred. Ten patients (18.4%) complained of recurrent angina at the follow‐up of 4.8 ± 1.2 months. Both TEE and coronary angiography confirmed in‐stent restenosis in all. Thirty‐nine patients (68.5%) remained symptoms free. Mean late loss in these patients was 0.69 ± 0.20 mm. A linear significant positive relation between mean late loss values and diastolic coronary velocity (r: 0.89, P < 0.001) was found. After 3‐ and 6‐month follow‐up, PDV showed a significant increase in comparison with basal values (0.7 ± 0.3 and 0.6 ± 0.26 vs. 0.32 ± 0.2 cm/sec, P < 0.01). All patients with restenosis showed a significant increase of diastolic coronary velocity in comparison with basal values (2.89 ± 0.25 cm/sec, P < 0.001). Conclusion: TEE can predict the development of in‐stent intimal hyperplasia in patients with unprotected left main coronary artery stenting.

Percutaneous treatment of aortic coarctation to manage severe hypertension in a 66-year-old patient.

Percutaneous treatment of aortic coarctation to manage severe hypertension in a 66-year-old patient

Use of bivalirudin for heparin-induced thrombocytopaenia after thrombolysis in massive pulmonary embolism: a case report.

A 68-year-old man was referred to the emergency department 6xa0h after onset of sudden acute dyspnoea. Immediate ECG showed sinus tachycardia with the typical S1-Q3-T3 pattern and incomplete right bundle branch block. The echocardiogram showed the presence of mobile thrombus in the right atrium, a distended right ventricle with free wall hypokinesia and displacement of the interventricular septum towards the left ventricle. Lung spiral computed tomography (CT) showed bilateral pulmonary involvement and confirmed the picture of a thrombotic system in the right atrium and caval vein. Thrombolytic treatment with recombinant tissue plasminogen activator (rt-PA) and heparin (alteplase 10xa0mg bolus, then 90xa0mg over 2xa0h) was administered. Six hours after thrombolysis bleeding gums and significant reduction in platelet count (around 50,000) were observed. Heparin was discontinued and bivalirudin (0.1xa0mg/kg bolus and 1.75xa0mg/kg per h infusion) plus warfarin was initiated and continued for 5xa0days until the international normalised ratio (INR) was within the therapeutic range (2.0–3.0) for 2 consecutive days, with concomitant platelet count normalisation. Lung spiral and lower abdominal CT before discharge did not show the presence of clots in the pulmonary arteries of the right and left lung. This case suggests that bivalirudin could offer promise for use in patients with heparin-induced thrombocytopaenia (HIT) after thrombolysis for massive pulmonary embolism.