心筋梗塞症に対するCa拮抗薬の心機能におよぼす影響—心エコー図，血行力学による検討

Comparative effects of three calcium antagonists (nifedipine, verapamil and diltiazem) on hemodynamics in recent myocardial infarction

　近年，Caイオンと心筋虚血との関係が注目され，虚血時の心筋細胞へのCaイオンの流入を防止することが，虚血心筋の障害を緩和することが報告されている^1）。そのため心筋興奮に際しておこるCaイオンの細胞内流入を抑制するCa拮抗薬が，心筋梗塞急性期において虚血巣の拡大防止など虚血心筋保護効果を有することが期待される。しかしながら心筋梗塞急性期にCa拮抗薬を投与する場合，心機能，房室伝導におよぼす影響をも考慮されねばならない。

　そこで我々は心筋梗塞急性期にCa拮抗薬投与の安全性を検討する目的で，急性心筋梗塞回復期の症例に対して同一量のnifedipine,diltiazem, verapamilを1回投与し，心機能におよぼす影響を比較検討した。なお，薬剤の効果は症例の投薬前の病態により影響されるので，薬剤の作用をより正確に比較するため同一症例においてcrossover法によりnifedipineの他にdiltiazemあるいはverapamilのいずれか一方を投与し，右心カテーテル法ならびに心エコー図法により両薬剤の心機能におよぼす影響を比較する方法を用いた。

Hemodynamic effects of diltiazem and verapamil were compared with those of nifedipine in 11 patients with recent myocardial infarction by crossover method. Right heart catheterization and echocardiography were performed in 5 patients (Group A) with an oral dose of 10 mg of nifedipine followed by an intravenous injection of 10 mg of diltiazem, and in 6 patients (Gruop B) with nif-edipine followed by an intravenous injection of 10 mg of verapamil.

After the administration of nifedipine, systemic vascular resistance (SVR) decreased by 13.4%and cardiac output (CO) increased by 11.0%without the change of heart rate (HR). Ejectionfraction (EF), which was measured by echocardio-graphy, tended to increase. This vasodilator effect (JSVR) was proportional to SVR in control state and accompanied with an increase of CO.

Vasodilator effect of three calcium antagonists was not different significantly (ΔJSVR : verapamil -10.0±2.9%, nifedipine -13.4±3.0%, diltiazem -20.0±6.4%). But EF tended to decrease with verapamil and diltiazem, and HR was unchanged following the administration of both drugs. Vera-pamil and diltiazem increased pulmonary artery pressure and suppressed atrioventricular (AV) nodal conduction with a prolongation of P-R interval, but nifedipine did not show these changes.

Therefore, it is concluded that among three calcium antagonists nifedipine can be used as a vasodilator with the least untoward effects on AV conduction and cardiac contractility in patients with recent myocardial infarction.