Alleviation of cocaine-induced coronary vasoconstriction by nitroglycerin

.JACCVol. 17.No. 2 February 1991: 174A

ABSTRACTS

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500 ALLEVIATION OF COCAINE-INDUCED CORONARY VASOCONSTRICTION Walter C. Brogan, Richard A. Lange, BY NITROGLYCERIN. Anatole L, David Hillis, -_- - S. - Kim. David J. Moliterno, u of Texas Southwestern Medical Center, Dallas, TX. We have previously shown that cocaine induces vasoconstriction of epicardial coronary arteries in pdtients with coronary artery disease (CAD), and this cocaineinduced vasoconstriction is especially intense in the This study was done to assess the diseased seylnents. influence of nitroglycerin (NTG) on cocaine-induced vasoconstriction. In 19 patients (16 men, 3 women, aged 43-65 yrs) with CAD, computer-assisted quantitative analysis was performed on nondiseased and diseased coronary arterial segments (a) at base1 ine (BL),(b)after intranasal saline (n=5) or cocaine, 2 mg/kg (n=14), and (c) after sublingual placebo (n=6) or NTG, 0.4-0.8 mg (n=8). Epicardial coronary artery cross-sectional area was not altered by saline. In responst. to cocaine, coronary artery cross-sectional area fell by 2327% (mean *SD) in nondiseased segments (4.6~2.4 mm2 at BL, 3.621.9 mm2 after cocaine; ~~0.05) and by 41215% in diseased segments (1.720.6 mm2 at BL, 1.020.3 mm2 after cocaine; The magnitude of cocaine-induced vasoconstricpcO.05). tion was greater (~~0.05) in the diseased segments. Cocaine-induced vasoconstriction was unaffected by sublingual placebo. In contrast, sublingual NTG reversed cocaine-induced vasoconstriction in both nondiseased (5.7t1.7 r(m2 after NTG, 38248% above BL) and diseased segments (2.lkO.7 mm2 after NTG, 28232% above BL). The magnitude of NTG-induced vasodilatation was similar in nondiseased and diseased segments. Thus, nitroglycerin alleviates cocaine-inducr:d vasoconstriction in nondiseased and diseased arterial segments in patients with coronary artery disease.

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TACHYCARDIA

Paul J. Wang, Kaoru Okishige, and Peter R Foster. Brigham a2d Women8~gkpital, Boston, . 02115 Selective bolus intracoronary (IC) injection of 96% ethanol (ETOH) into the A-V nodal (AVN) artery has been used to abolish AVX conduction. This method causes abrupt occlusion of the AVN artery with reflux of ETOX into the distal circulation and can sometimes lead to unintmded myocardial infarction In order to avoid method of chemical this complication a ablation or modification of AVN function by slow selective IC infusicn of ETOHwas studied in 9 patients with uncontrolled ventricular rates during supraventricular tachycardiz Twenty-five percent ETOHwas infused into the AVN artery at 0.5 to 1.0 cc/min for 5 to 15 minutes. ETOH infusion caused modification of AVN conduction without complete AVN block in 5 patients and resulted in complete AVN block in 4 patients. Ventricular rates in all SVT patients became controlled without Abrupt vessel occlusion after 25% ETOH of non-targeted regions did not occur. This method of PC chemical ablation of the AV node is safer than bolus IC injection of 96% ETOH. Since acute occlusion of the AVN artery does not occur this method also al.lows one to administer repeated doses of ETOH, a necessary step in establishing a dose-response relationship. (SW

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