Intravenous nitroglycerin suppresses exercise-induced arrhythmias in patients with ischaemic heart disease: implications for long-term treatment

We studied 20 patients with ischaemic heart disease, who consistentlydeveloped complex ventricular arrhythmias during exercise testing.Treadmill exercise was performed twice, both during the placeboinfusion and then during intravenous administration of nitroglycerin,titrated to reduce systolic blood pressure by 10 mmHg. Exerciseduration in those administered placebo was 7·8 ±1·7 and 7·9 ± 1·5 min, respectively(ns): angina developed in five patients and ischaemic ST changesin 10. In those administered nitroglycerin, exercise durationincreased to 8·4 ± 2 mm (P<0·05). DiagnosticST segment depression was observed in only two patients andonly one had angina. Ventricular arrhythmias, consistently presentduring both tests on those administered placebo, were dramaticallyreduced by nitroglycerin in all 20 patients. There were 455(mean 35·8± 16·8) and 4l8 (mean 34·4±11·1)ventricular ectopic beats in the two exercise tests on thoseadministered placebo and 11 in those receiving the nitroglycerininfusion (mean 0·6 ± 0·1 (P<0·001).There were 28 and 29 couplets in those receiving placebo (ns)and none in those receiving nitroglycerin (P<0·001).Ventricular tachycardia was present in six and eight patientswho received placebo but in none in those administered nitroglycerin(P<0·001). Abolition of exercise-induced arrhythmiaswas maintained during chronic treatment with oral coronary vasodilators.Prevention of exercise-related arrhythmias by nitroglycerinappears a good indicator of their ischaemic origin and may providevaluable information for long-term prophylaxis with oral vasodilators,thus avoiding antiarrhythmic agents with their potential sideeffects.     

Intravenous nitroglycerin suppresses exercise-induced arrhythmias in patients with ischaemic heart disease: implications for long-term treatment

We studied 20 patients with ischaemic heart disease, who consistentlydeveloped complex ventricular arrhythmias during exercise testing.Treadmill exercise was performed twice, both during the placeboinfusion and then during intravenous administration of nitroglycerin,titrated to reduce systolic blood pressure by 10 mmHg. Exerciseduration in those administered placebo was 7·8 ±1·7 and 7·9 ± 1·5 min, respectively(ns): angina developed in five patients and ischaemic ST changesin 10. In those administered nitroglycerin, exercise durationincreased to 8·4 ± 2 mm (P<0·05). DiagnosticST segment depression was observed in only two patients andonly one had angina. Ventricular arrhythmias, consistently presentduring both tests on those administered placebo, were dramaticallyreduced by nitroglycerin in all 20 patients. There were 455(mean 35·8± 16·8) and 4l8 (mean 34·4±11·1)ventricular ectopic beats in the two exercise tests on thoseadministered placebo and 11 in those receiving the nitroglycerininfusion (mean 0·6 ± 0·1 (P<0·001).There were 28 and 29 couplets in those receiving placebo (ns)and none in those receiving nitroglycerin (P<0·001).Ventricular tachycardia was present in six and eight patientswho received placebo but in none in those administered nitroglycerin(P<0·001). Abolition of exercise-induced arrhythmiaswas maintained during chronic treatment with oral coronary vasodilators.Prevention of exercise-related arrhythmias by nitroglycerinappears a good indicator of their ischaemic origin and may providevaluable information for long-term prophylaxis with oral vasodilators,thus avoiding antiarrhythmic agents with their potential sideeffects.     

Preserved Vasodilator Response to Acetylcholine in Atherosclerotic Coronary Arteries Before and After PTCA

The vascular response to local administration of acetylcholine is used, clinically, to assess endothelial function in vivo. However, whether this response predominantly reflects the functional state of the vascular endothelium, or rather results from smooth muscle reactivity per se is not clear. In 15 patients with chronic stable angina and angiographically significant coronary disease, we studied the effects of increasing doses of intracoronary acetylcholine (5, 10, 30, 50, and 80 μg) and nitroglycerin (200 μg) on coronary vascular tone. In three patients the protocol was perfrnned at the time of diagnostic coronary angiographv and 7 and 24 hours after angioplasty. The remaining five underwent acetylcholine administration before and after percutaneous transluminl coronary angioplasty (PTCA). We quantitatively assessed the diameter of 54 coronary arterial segments; 12 stenotic segments, 13 post-PICA segments with residual irregularities, 18 reference segments of the ranee arteries taken proximal to the stenosis or to the dilatation site, and II remote segments ofnonstenotic vessels. They all showed a bimodal response to acetylcholine. At the lowest concentration (5 μg) the agent invariably caused dilatation (9.22 ± 6.55%), which was not significantly different in the various segments and was always less than that induced by nitroglycerin (24.56 ± 12.82%, P < 0.0001). At the highest doses (50 or 80 μg) acetylcholine always induced vasoconstriction, which was significantly more pronounced in the post-PTCA (-31.54 ± 10.65%) and stenotic segments (-23.08 ± 11.88%) than in the reference and remote segments (respectively, -14.88 + 7.63% and - 18.67 + 8.37%, P < 0.05). We conclude that: (l) some degree of endothelial dependent vasodilatation is preserved even in the presence of atheroma and intimal injury induced by angioplasty; (2) atheroma and especially acute intimal injury augment the vasoconstrictor response to high dose acetylcholine, the effect being most probably mediated by primary smooth muscle supersensivity: (3) since acetylcholine has direct and endothelium-mediated vasoactive effects, this agent may not be the ideal one for testing endothelial integrity. (J Interven Cardiol 1994; 7:57–64)     

Non Q-wave myocardial infarction following hyperventilation test

We report a case of acute myocardial infarction following ahyperventilation test performed at coronary angiography. Thepotential pathophysiological mechanisms and clinical implicationsare discussed.