Osahiko Sunagawa

Rescue Balloon Pulmonary Angioplasty Under Veno-Arterial Extracorporeal Membrane Oxygenation in a Patient With Acute Exacerbation of Chronic Thromboembolic Pulmonary Hypertension

We describe a case of a 41-year-old woman with acute exacerbation of chronic thromboembolic pulmonary hypertension (CTEPH) complicated by rapidly progressive respiratory failure and right heart failure with cardiogenic shock. A computed tomography (CT) showed thrombi in the right main pulmonary artery and bilateral peripheral pulmonary arteries, and echocardiography showed right ventricular dilatation and tricuspid regurgitation, with an estimated pressure gradient of 80 mmHg. The patient was initially diagnosed with acute pulmonary thromboembolism, and thrombolytic therapy was administered. Her condition subsequently deteriorated, however, necessitating mechanical ventilation and veno-arterial extracorporeal membrane oxygenation (VA-ECMO). We performed emergency catheter-directed thrombectomy and thrombus aspiration. Pulmonary hypertension (PH) temporarily improved, but subsequently worsened, and the patient was diagnosed with CTEPH. Pulmonary endarterectomy (PEA) was performed. After PEA, we were unable to wean the patient off VA-ECMO, and rescue balloon pulmonary angioplasty (BPA) to the middle and inferior lobe branches of the right lung was performed. Five days after BPA, the patient was removed from VA-ECMO and on the 57th day of hospitalization, she was weaned off the ventilator. The patient was discharged after 139 days of hospitalization. Rescue BPA represents a useful intervention for improving PH and weaning off VA-ECMO in a patient with acute exacerbation of CTEPH.

Low-sodium diet and alpha-adrenoceptors of renal basolateral membrane in spontaneously hypertensive rats.

To clarify the effect of dietary sodium restriction on the mechanism regulating sodium and water in the development of hypertension, we determined the number of the alpha-adrenoceptors in renal basolateral membrane in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The rats had been fed a low-sodium (0.5%) or normal-sodium (0.4%) diet from 3 weeks of age. The experiments were performed at 6, 8 and 20 weeks of age in both rat groups. Renal basolateral membranes were prepared using Percoll and radioligand binding studies were performed using 3H-prazosin and 3H-rauwolscine. Systolic blood pressure in SHR was already elevated at 6 weeks of age compared with that in WKY rats and rose to hypertensive levels at 8 weeks of age. The sodium balance in WKY rats on both diets decreased at 8 weeks of age, but that of SHR decreased at 20 weeks of age. The maximum number (Bmax) for the alpha 1-adrenoceptor did not differ in any groups of the WKY rats or SHR. Bmax for the alpha 2-adrenoceptors increased at 8 weeks of age in the low-sodium SHR compared with normal-sodium SHR, but did not increase in WKY rats. The data show that the increases in blood pressure in the SHR occur prior to significant increases in the alpha 2-adrenoceptor density of renal basolateral membrane, and that the modulation of alpha 2-adrenoceptor density in SHR differs from that in WKY rats under sodium restriction. The results suggest that renal alpha 2-adrenoceptors in SHR could relate the regulatory mechanism to sodium reabsorption under sodium restriction rather than to the primary cause of the development of hypertension in SHR. There may be the possibility of an abnormality in renal alpha 2-adrenoceptor mechanism in SHR.

Alpha2-Adrenoceptors in Brain and Kidney during Development of Hypertension in Dahl-Iwai Salt-Sensitive Rats

Background: Both renal and extrarenal factors have been considered to contribute to the development of hypertension in Dahl salt-sensitive rats, but contents of both factors have not been established precisely.Aim: To clarify the role of those factors in the sympathetic nervous system, we examined the regulation of alpha2-adrenoceptors in the lower brainstem and the renal tubular basolateral membranes simultaneously during the development of salt-induced hypertension in Dahl-lwai salt-sensitive rats.Methods: Dahl-lwai salt-sensitive or resistant rats were fed a high (8.0 % NaCI)- or low (0.3 %)- salt diet from 4 to 6 or 10 weeks of age. At 4, 6 and 10 weeks of age, the plasma membranes of the lower brainstem and the renal tubular basolateral membranes were obtained simultaneously and alpha2-adrenoceptors were quantified by a radioligand binding assay using 3H-rauwolscine.Results: In the salt-sensitive rats, systolic blood pressure was significantly higher in those fed a high-salt diet than in those fed a ...

A Case of Refractory Heart Failure in Becker Muscular Dystrophy Improved With Corticosteroid Therapy

The patient was a 26 year-old man who was referred to our hospital in June 2011 because of severe heart failure. At age 24 years, he was found to have Becker muscular dystrophy. He received enalapril for cardiac dysfunction; however, he had worsening heart failure and was thus referred to our hospital. Echocardiography showed enlargement of the left ventricle, with a diastolic dimension of 77 mm and ejection fraction of 19%. His condition improved temporarily after an infusion of dobutamine and milrinone. He was then administered amiodarone for ventricular tachycardia; however, he subsequently developed hemoptysis. Amiodarone was discontinued and corticosteroid pulse therapy was administered followed by oral prednisolone (PSL). His creatinine phosphokinase (CPK) level and cardiomegaly improved after the corticosteroid therapy. The PSL dose was reduced gradually, bisoprolol was introduced, and the catecholamine infusion was tapered. A cardiac resynchronization device was implanted; however, the patients condition gradually worsened, which necessitated dobutamine infusion for heart failure. We readministered 30 mg PSL, which decreased the CPK level and improved the cardiomegaly. The dobutamine infusion was discontinued, and the patient was discharged. He was given 7.5 mg PSL as an outpatient, and he returned to normal life without exacerbation of the heart failure. There are similar reports showing that corticosteroids are effective for skeletal muscle improvement in Duchenne muscular dystrophy; however, their effectiveness for heart failure has been rarely reported. We experienced a case of Becker muscular dystrophy in which corticosteroid therapy was effective for refractory heart failure.

Tolvaptan Improves Prognosis in Responders with Acute Decompensated Heart Failure by Reducing the Dose of Loop Diuretics

It is unknown whether a response to tolvaptan (TLV) is related to prognosis in patients with acute decompensated heart failure (ADHF). We selected 25 patients as responders by their urinary response to TLV and by reduction of loop diuretics from 37 consecutive ADHF patients treated with TLV. As a control group, we selected 25 patients from 100 consecutive ADHF patients who were not treated with TLV by propensity score matching for age, serum sodium level, serum creatinine level, plasma B-type natriuretic peptide (BNP) level, systolic blood pressure, heart rate, and dose of loop diuretics. The primary outcome was defined as a composite endpoint of mortality and/or hemodialysis. The amount of loop diuretics administered to responders was reduced by TLV from 68.8 ± 26.2 mg to 30.4 ± 18.6 mg of furosemide equivalents per day, whereas the loop diuretic dose administered to non-responders was increased. The event-free survival of the TLV responders during 20 months was significantly better than that of the control group (95.8% versus 68.4%, P = 0.0406). The TLV responders, plasma BNP level, and estimated glomerular filtration rate were significantly related to the events in the Cox proportional hazard analysis. Patients with ADHF who respond to TLV may have a better prognosis than propensity-matched patients not receiving TLV treatment. In TLV responders, it may be possible to improve the patients prognosis if the dose of loop diuretics can be reduced with TLV therapy.

Amiodarone-Induced Hyponatremia Masked by Tolvaptan in a Patient with an Implantable Left Ventricular Assist Device

A 43-year-old man was referred to our hospital in June 2014 because of severe heart failure. He was diagnosed with familial dilated cardiomyopathy and was administered oral tolvaptan and amiodarone for atrial and ventricular tachycardia. Since up-titration of carvedilol had failed and he was dependent on dobutamine, a left ventricular assist device (LVAD) was implanted. Tolvaptan and furosemide were both discontinued after LVAD implantation and he was discharged from the hospital. Thirteen months later, he was hospitalized for lethargy and hyponatremia of 108 mEq/L, with an antidiuretic hormone level of 2.5 pg/mL, which suggested syndrome of inappropriate antidiuretic hormone secretion (SIADH). We discontinued amiodarone and administered fludrocortisones. However, hyponatremia persisted for a few more days, eventually resulting in delirium and damage to the LVAD driveline. He received an urgent pump exchange and hyponatremia was gradually improved. We considered the possibility that amiodarone-induced SIADH was masked by tolvaptan therapy before LVAD implantation.