うっ血性心不全に対するIsosorbide dinitrate持続静注の臨床的，血行力学的検討

Clinical and hemodynamic effects of continuous intravenous injection of isosorbide dinitrate in patients with congestive heart failure

　1975年，Johnson^1），Ziffer^2）らによって，nitroglycerinのうっ血性心不全に対する有効性が報告されて以来，血管拡張療法は，ジギタリス剤，利尿剤，カテコールアミン剤と並んで，心不全に対する重要な位置をしめるにいたった。特に1971年，Majid^3）らが，虚血性心疾患に基づく重症左心不全患者に，α-blockerであるphentolami—neを静注し，心拍出量の増大と，臨床症状の改善を報告して以来，各種血管拡張剤について，その有効性が多く報告されてきた^4〜13）。

　今回我々は，Isosorbide dinitrate （ISDN）の持続静注の心不全に対する急性効果を臨床的ならびに血行力学的に観察し，その有効性を示唆する知見を得たので文献的考案を加え報告する。

We studied the hemodynamic effects of isosorbide dinitrate administered by continuous i.v. infusion to10 patients with refractory pump failure. Patients entered the study only if mean pulmonary capillary wedge pressure was higher than 20mmHg and systolic arterial pressure 90mmHg or above. The etiology was valvular heart disease in 5 patients, hypertensive and/or arteriosclerotic heart disease in 3 patients, di-lated cardiomyopathy in 1 patient and acute myo-cardial infarction in 1 patient. The initial dosage of 3mg/hr was increased to the maintenance dose until PCWP was reduced to 18 mmHg or less.

After two hours injection of ISDN in a dose range of 5-8mg/hr, mean pulmonary capillary wedge pres-sure decreased from 33mmHg to 15mmHg (P< 0.001), mean pulmonary arterial pressure 41mmHg to 23mmHg (P<0.001), mean right atrial pressure 14mmHg to 5mmHg (P<0.001). There were no deleterious effects on heart rate, blood pressure, cardiac index, stroke volume index, stroke work index, double product, systemic vascular resistance or pulmonary vascular resistance. But the change in cardiac index correlated positively with the initial SVR levels (r=0.71, P<0.01) and inversely with the control cardiac index (r=-0.85, P<0.01). During these studies, the clinical signs of left ventricular failure disappeared in all patients and there was only one untoward effect of slight headache.

These data indicate that i.v. ISDN is a potent vas-odilator with acting as preload reduction and useful for the treatment of congestive heart failure as a de-loading agent.