Clinical impact of portal vein pulsatility on the prognosis of hospitalized patients with acute heart failure.

BACKGROUND: Heart failure (HF) causes extracardiac organ congestion, including in the hepatic portal system. Reducing venous congestion is essential for HF treatment, but evaluating venous congestion is sometimes difficult in patients with chronic HF. The portal vein (PV) flow pattern can be influenced by right atrial pressure. Ultrasound images of the PV are quite easy to obtain and are reproducible among sonographers. However, the association between PV pulsatility and the condition of HF remains unclear. We hypothesize that PV pulsatility at discharge reflects the condition of HF. AIM: To evaluate the usefulness of PV pulsatility as a prognostic marker for hospitalized patients with acute HF. METHODS: This observational study was conducted from April 2016 to January 2017 and April 2018 to April 2019 at Shinko Hospital. We enrolled 56 patients with acute HF, and 17 patients without HF served as controls. PV flow velocity was measured by ultrasonography on admission and at discharge. We calculated the PV pulsatility ratio (PVPR) as the ratio of the difference between the peak and minimum velocity to the peak velocity. The primary endpoint was cardiac death and HF re-hospitalization. The observation period was 1 year from the first hospitalization. The Kaplan-Meier method was used to determine the stratified composite event-free rates, and the log-rank test was used for comparisons between groups. RESULTS: On admission, the PVPR was significantly higher in patients with acute HF than controls (HF: 0.29 ± 0.20 vs controls: 0.08 ± 0.07, P < 0.01). However, the PVPR was significantly decreased after the improvement in HF (admission: 0.29 ± 0.20 vs discharge: 0.18 ± 0.15, P < 0.01) due to the increase in minimum velocity (admission: 12.6 ± 4.5 vs discharge: 14.6 ± 4.6 cm/s, P = 0.03). To elucidate the association between the PVPR and cardiovascular outcomes, the patients were divided into three groups according to the PVPR tertile at discharge (PVPR-T1: 0 ≤ PVPR ≤ 0.08, PVPR-T2: 0.08 < PVPR ≤ 0.21, PVPR-T3: PVPR > 0.21). The Kaplan-Meier analysis showed that patients with a higher PVPR at discharge had the worst prognosis among the groups. CONCLUSION: PVPR at discharge reflects the condition of HF. It is also a novel prognostic marker for hospitalized patients with acute HF.

Recurrent myocardial infarction associated with vasculo-Behçet's disease: a case report.

A 39-year-old Japanese man presented with chest oppression in February 2017. Electrocardiogram showed ST-elevation myocardial infarction (MI), and cardiac catheterisation revealed thrombotic occlusion of the right coronary artery (RCA), which was treated with thrombectomy, and he received warfarin. Three days after discharge, he complained of chest oppression again, and re-cardiac catheterisation showed thrombi occlusion of the circumflex artery (LCX) and 90% stenosis with thrombosis in the proximal site of the anterior descending artery (LAD) and RCA. Drug eluting stent was implanted in the LAD and RCA; aspirin and prasugrel hydrochloride were added to warfarin. Before discharge, coronary computed tomography angiography (CTA) found new thrombi in the RCA, LAD, and LCX, and he was referred to our hospital on suspicion of Behçet's disease (BD). Past medical history was notable for recurrent aphthous stomatitis, a pudendal ulcer, and Crohn's disease, for which he had been taking infliximab (5 mg/kg) every 8 weeks until December 2016. Notably, his C-reactive protein (CRP) level increased before and after each MI, suggesting that the thrombi were caused by inflammation. Consequently, we concluded that his abnormalities were manifestations of vasculo-BD. After 3 days of hospitalisation, treatment with prednisolone and colchicine was started. His CRP and D-dimer levels decreased, and coronary CTA after 8 days showed disappearance of the thrombi. We tapered the prednisolone dose, and cardiovascular events have not been observed for 7 months after the treatment initiation. In summary, we report a rare case of MI associated with vasculo-BD and review the relevant literature.

Acute pulmonary edema in patients with reduced left ventricular ejection fraction is associated with concentric left ventricular geometry.

Although acute pulmonary edema (APE) is common in patients with heart failure (HF) with preserved ejection fraction (EF), its pathogenesis in patients with HF with reduced EF (HFrEF) is not completely understood. The purpose of our study was to explore the contributions of left ventricular (LV) geometry to understand the difference between HFrEF patients with or without APE. We studied 122 consecutive acute decompensated HF patients with HFrEF (≤40%). APE was defined as acute-onset dyspnea and radiographic alveolar edema requiring immediate airway intervention. LV geometry was determined from a combination of the LV mass index and relative wall thickness (RWT). Long-term unfavorable outcome events were tracked during a follow-up of a median of 21 months (interquartile range, 10-28 months), during which APE was observed in 29 patients (24%). Compared to those without APE, hospitalized patients with APE had a higher systolic blood pressure, RWT, and LVEF and lower end-diastolic dimension. Among echocardiographic variables, a multivariate logistic regression analysis identified RWT as the only independent determinant of APE (hazard ratio: 2.46, p < 0.001). Those with concentric geometry (n = 25; RWT > 0.42) had a higher incidence of APE relative to those with non-concentric geometry. Furthermore, among patients with APE, mortality was significantly higher among those with concentric geometry (log-rank, p = 0.008). Compared with non-concentric geometry, concentric geometry (increased RWT, not LV mass) was strongly associated with APE onset and a poorer outcome among APE patients. An easily obtained echocardiographic RWT index may facilitate the risk stratification of patients.

Dasatinib-Induced Pulmonary Arterial Hypertension Treated with Upfront Combination Therapy.

Pulmonary arterial hypertension (PAH) is a rare complication of dasatinib that was approved as a first-line therapy for chronic myelocytic leukemia (CML). A 24-year-old man presenting dyspnea at rest and leg edema was admitted to our hospital. He had been diagnosed with CML and prescribed dasatinib for 4 years. Chest X-ray showed significant bilateral pleural effusion and heart enlargement. Echocardiography revealed interventricular septal compression and elevated peak tricuspid regurgitation pressure gradient of 66.7 mmHg indicating severe pulmonary hypertension. After the other specific diseases to provoke PAH were excluded, he was diagnosed with dasatinib-induced PAH. Despite discontinuation of dasatinib and intravenous administration of diuretic for two weeks, World Health Organization (WHO) functional class was still II and mean pulmonary arterial pressure (PAP) was high at 37 mmHg. Therefore, we administered sildenafil and bosentan together as an upfront combination therapy three weeks after dasatinib discontinuation. Six months later, his symptoms improved to WHO functional class I and mean PAP was decreased to 31 mmHg. Although PAH is a rare complication of dasatinib, symptomatic patients prescribed with dasatinib should have an echocardiogram for PAH screening. Moreover, the upfront combination therapy would be a useful option for symptomatic patients after discontinuation of dasatinib.

An Unusual Case of Inferior Vena Cava Thrombosis in a Healthy Male Bodybuilder.

Inferior vena cava (IVC) thrombosis is very rare, particularly in the absence of an apparent congenital caval abnormality or hypercoagulable state. We herein report an unusual case of a healthy and active 62-year-old male bodybuilder with a mass-like IVC thrombus. We placed an IVC filter and began treatment with rivaroxaban. The patient recovered successfully, and the IVC thrombus completely disappeared three months later. This case suggested that extrinsic compression of IVC by a tightened weightlifting belt around the abdomen is a triggering factor of IVC thrombosis, and rivaroxaban, a new oral anticoagulant, may be a useful option for treatment.