Low-molecular-weight dextran in acute myocardial infarction.

In spite of vasopressor agents, anti-arrhythmic drugs, early ambulation, and anticoagulant therapy the mortality among patients with acute myocardial infarction is almost 40%/,O . Intensive-care units may reduce this figure, but other attempts to lower the mortality should be sought. Langsjoen et al. (1963) reported the beneficial effect of low-molecular-weight dextran (mean molecular weight 40,000) in acute infarction, the mortality being reduced from 46.6 to 17.6%. Two years later Langsjoen (1965) confirmed his favourable impression of this treatment. Linden (1964) reported a reduction of the mortality from 33 to 15% in a small series of patients with myocardial infarction receiving low-molecular-weight dextran. Both these stud-es were, however, carried out without proper controls and therefore do not admit of definite conclusions. Theoretically, low-molecuiar-weight dextran has many advantages. It has antithrombotic properties (Bryant et al., 1963) ; it increases plasma volume (Gelin et al., 1961) and may thus prevent shock; it improves blood-flow (Gelin and Thoren, 1961) by reducing viscosity and may therefore improve circulation at the border of the infarction, thereby limiting its extension. It has an antisludging effect (Long et al., 1962), which will improve microcirculation. Sludging of the red cells is a frequent finding in myocardial infarction (Bloch, 1955), and it can itself produce myocardial infarction (Long et al., 1962). Theoretically, 500 ml. of 10% low-molecular-weight dextran binds 1,000 ml. of water. The increase in plasma volume will depend on the injected amount, on the infusion-time, and on the renal function. Dextran molecules of less than 50,00060,000 are cleared by the kidney (Arturson and Wallenius, 1963). The effect on plasma volume, which may be beneficial by preventing shock, may have an opposite effect on the already strained left ventricle, thus causing pulmonary congestion. On the other hand, Asfrog and Fossaberg (1965) used lowmolecular-weight dextran in the treatment of pulmonary oedema, caused by overloading of the circulation, in patients with apparently normal hearts. Severe congestive heart frilure is said by the manufacturer to be a contraindication to lowmolecular-weight dextran therapy. Weighing the possible advantages against the disadvantages, we believed treatment with low-molecufar-weight dextran to be encouraging enough to warrant clinical trial. With our selection of patients and with the method of administration we have been unable to demonstrate any beneficial effect of low-molecularweight dextran on mortality in patients with acute myocardial infarction.