Tohru Watanabe

Anomalous reduction in thrust/reaction of water jets issuing from microapertures

Thrusts and reactions of water jets issuing through small orifices and thin slots were measured and compared with the predictions from numerical solutions of the Navier-Stokes equations. Reasonable agreements were obtained between the experimental and numerical results for orifices and slots with openings of the order of 1mm size, but not with those of 10μm or less. The experimental results were found to be well below the predictions for apertures of the order of 10μm. The difference between the numerically calculated and the measured thrusts/reactions for the small apertures was found to be proportional to the square of the mean velocity. Several possible causes for the observed reduction in jet thrust/reaction in small apertures were examined, but none of them could adequately explain the flow anomaly.

Liver Congestion in Heart Failure Contributes to Inappropriately Increased Serum Hepcidin despite Anemia

Hepcidin is a key regulator of mammalian iron metabolism and mainly produced by the liver. Hepcidin excess causes iron deficiency and anemia by inhibiting iron absorption from the intestine and iron release from macrophage stores. Anemia is frequently complicated with heart failure. In heart failure patients, the most frequent histologic appearance of liver is congestion. However, it remains unclear whether liver congestion associated with heart failure influences hepcidin production, thereby contributing to anemia and functional iron deficiency. In this study, we investigated this relationship in clinical and basic studies. In clinical studies of consecutive heart failure patients (n = 320), anemia was a common comorbidity (41%). In heart failure patients without active infection and ongoing cancer (n = 30), log-serum hepcidin concentration of patients with liver congestion was higher than those without liver congestion (p = 0.0316). Moreover, in heart failure patients with liver congestion (n = 19), the anemia was associated with the higher serum hepcidin concentrations, which is a type of anemia characterized by induction of hepcidin. Subsequently, we produced a rat model of heart failure with liver congestion by injecting monocrotaline that causes pulmonary hypertension. The monocrotaline-treated rats displayed liver congestion with increase of hepcidin expression at 4 weeks after monocrotaline injection, followed by anemia and functional iron deficiency observed at 5 weeks. We conclude that liver congestion induces hepcidin production, which may result in anemia and functional iron deficiency in some patients with heart failure.

A Case of Aortic Regurgitation Presenting with Recurrent Detachment of a Prosthetic Valve, as the First Presenting Symptom of Cardiovascular Behçet's Disease

A 33-year-old man with severe aortic regurgitation underwent initial aortic valve replacement (AVR). During the 2 years after AVR, 3 reoperations for prosthetic valve detachment were required. During hospitalization, he had no typical clinical findings, with the exception of a persistent inflammatory reaction; a pseudo-aneurysm around the Bentall graft developed 27 days after the 4th operation. This unique clinical course suggested the possibility of Behçets disease. In the 8 years of follow-up after the administration of prednisolone, the pseudo-aneurysm did not become enlarged and the detachment of the prosthetic valve was not observed. We herein present a case of cardiovascular Behçets disease, with a review of the literature.

Failing Left Ventricles Have an Enhanced Post-Stimulation Potentiation Despite Their Impaired Force Frequency Relationship.

The left ventricular contractile force (LV dP/dtmax) of patients with left ventricular systolic dysfunction does not increase effectively with an increase in heart rate. In other words, their force-frequency relationship (FFR) is impaired. However, it is unknown whether a longer coupling interval subsequent to tachycardia causes a stronger contraction (poststimulation potentiation, PSP) in a rate-dependent manner.In 16 patients with idiopathic dilated cardiomyopathy (DCM) (48 ± 2 years old, LVEF 30 ± 10%) and 6 control patients (58 ± 4 years old, LVEF 70 ± 7%), FFR was assessed by right atrial pacing using a micro-manometer-tipped catheter. At each pacing rate, the increase of LV dP/dtmax over basal LV dP/dt (ΔFFR) and the increase of LV dP/dtmax of the first beat after pacing cessation over LV dP/dtmax during pacing (ΔPSP) were evaluated.Patients with DCM had smaller LV dP/dtmax at baseline (872 ± 251 versus 1370 ± 123 mmHg/second, P = 0.0002) and developed smaller ΔFFR (eg, at 120/minute, 77 ± 143 versus 331 ± 131 mmHg/second, P = 0.0011). In contrast, they showed a rate-dependent increase of LV dP/dtmax of PSP and had greater ΔPSP (eg, at 120/minute, 294 ± 173 versus -152 ± 131 mmHg/second, P < 0.0001).Failing left ventricles develop little contractile force during tachycardia despite their rate-dependent enhancement in post-stimulation potentiation, suggesting that refractoriness of contractile force underlies impaired FFR.

Cibenzoline Abolished Pulsus Alternans in a HOCM Patient

A 50-year-old man with hypertrophic obstructive cardiomyopathy (HOCM) underwent cardiac catheterization to evaluate the hemodynamic effects of cibenzoline, a class 1a antiarrhythmic agent. Initially, the pressure gradient between the left ventricle (LV) and aorta (Ao) was more than 100 mm Hg (Picture A). During atrial pacing at 110/min, the LV contraction was enhanced, as judged by an increase in LV dP/dt, and LV pulsus alternans appeared (Picture B). After the patient received intravenous cibenzoline (1.4 mg/kg) therapy, his LV dP/dt decreased, the pressure gradient was abolished (Picture C), and the atrial pacing no longer caused pulsus alternans (Picture D). Pulsus alternans is a sign of compromised systemic perfusion (1) and suppression of an LV contraction may augment this condition. However, in this case of HOCM, cibenzoline therapy suppressed the LV contraction and abolished LV pulsus alternans, thus indicating that pulsus alternans is not always caused by impaired LV contractility but may also be related to other cardiac burdens, such as tachycardia and changes in the LV afterload (2).