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Myocardial infarction (MI, heart attack) is the deterioration of heart tissue due to cessation of the heart's blood supply, which may result from a blood clot obstructing the coronary arteries, the major blood vessels supplying the heart. Heparin is a polysaccharide, or glucose compound, that prevents the coagulation of blood and the formation of blood clots. The effects of heparin on the development of coronary collaterals (small blood vessels that supplement circulation to the heart when a coronary artery is blocked) and on the function of the heart were examined in 18 patients recovering from an MI. Collateral development was greater in patients receiving heparin than in patients without this treatment. Heart function was indicated by measurements of left ventricular ejection fraction, or the amount of blood emptied from the left ventricle during contraction, and muscle shortening of the infarcted heart tissue. These characteristics improved to a greater extent in patients receiving heparin treatment, compared with patients receiving no treatment. The results demonstrate that heparin preserves left ventricular function as a result of collateral development in patients who have sustained an MI. (Consumer Summary produced by Reliance Medical Information, Inc.)

Klassen, Christopher L., Jay H. Traverse, and Robert J. Bache. Nitroglycerin dilates coronary collateral vessels during exercise after blockade of endogenous NO production. Am. J. Physiol. 276 (Heart Circ. Physiol. 45): H918--H923, 1999.--In a previous study nitroglycerin failed to dilate coronary collateral vessels during exercise. This study tested the hypothesis that failure of nitroglycerin to increase collateral flow occurred because endogenous nitric oxide (NO) had activated the guanylate cyclase vasodilator pathway so that additional NO from nitroglycerin could have no additional effect. Six dogs were collateralized using intermittent 2-min occlusions of the left anterior descending coronary artery followed by permanent occlusion. One week after permanent coronary occlusion, dogs were exercised on a treadmill (heart rate 202 [+ or -] 5 beats/rain), while blood flow was measured with radioactive microspheres. Blood flow to the collateral zone during control exercise was 1.90 [+ or -] 0.11 ml [multiplied by] [min.sup.-1] [multiplied by] [g.sup.-1] compared with 2.28 [+ or -] 0.15 ml [multiplied by] [min.sup-1] in the normal zone (P [is less than] 0.05); systolic wall thickening was 23 [+ or -] 3% in the collateral zone compared with 27 [+ or -] 2% in the normal zone. When [N.sup.G]-nitro-L-arginine (L-NNA; 20 mg/kg iv) was administered to block NO production, collateral zone flow during exercise decreased to 1.43 [+ or -] 0.20 ml [multiplied by] [min.sup.-1] [multiplied by] [g.sup.-1] (P [is less than] 0.05), and systolic wall thickening decreased to 12 [+ or -] 14% (P [is less than] 0.05). A subsequent infusion of nitroglycerin (2 [micro]g [multiplied by] [min.sup.-1] iv) increased collateral zone blood flow to 1.65 [+ or -] 0.16 ml [multiplied by] [min.sup.-1] [g.sup.-1] (p [is less than] 0.05) and increased systolic wall thickening to 22 [+ or -] 5% (P [is less than] 0.05). These findings demonstrate that endogenous NO contributes to collateral zone blood flow during exercise. If endogenous NO synthesis is blocked, then nitroglycerin is effective in improving collateral zone blood flow and contractile function during exercise. angiogenesis; blood flow; collateral circulation; endothelium-derived factors