Yutaka Horio

Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm.

We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 micrograms ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of the 25 of the 27 patients. The injection of 20 to 100 micrograms ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm.

Multivessel coronary spasm in patients with variant angina: a study with intracoronary injection of acetylcholine.

Multivessel coronary spasm has been described but its incidence in patients with variant angina still remains unclear. Thirty-three patients with variant angina were studied during coronary angiographic examination with selective intracoronary injection of acetylcholine (ACh). In all but three patients, the location of ischemia during attack was determined by the electrocardiographic findings, by exercise 201Tl myocardial scintigraphy, and by two-dimensional echocardiography during a hyperventilation test, and the coronary artery (or arteries) responsible for the attack was predicted before the study. ACh induced spasm of at least one coronary artery in all but one patient. ACh induced spasm of both the left and right coronary arteries (i.e., multivessel coronary spasm) in 24 patients: in two of the four patients who were predicted to have spasm of the left coronary artery, in six of the 11 predicted to have spasm of the right coronary artery, in 13 of the 15 predicted to have spasm of both the left and right coronary arteries, and in three of the three in whom coronary artery responsible for attack had not been predicted. This ACh-induced spasm of the left and right coronary arteries occurred separately and no patients showed hemodynamic instability during attack. In one patient in whom multivessel coronary spasm had been predicted and ACh failed to induice coronary spasm, ergonovine maleate (0.2 mg) induced spasm of both the left and right coronary arteries simultaneously, resulting in severe prolonged hypotension. Nineteen of the 25 patients in whom multivessel coronary spasm was documented showed angiographically normal or nearly normal coronary arteries after administration of nitroglycerin.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of intracoronary injection of acetylcholine on coronary arterial diameter

The effects of intracoronary injection of acetylcholine on coronary arterial diameter was examined by coronary arteriography in 30 adult patients (13 men, 17 women), aged 23 to 67 years (mean 51), with normal or almost normal coronary arteriographic findings. Patients with angina pectoris, myocardial infarction and other severe cardiac diseases were excluded. Two minutes after injection of 30 to 100 micrograms of acetylcholine into the left coronary artery, significant diffuse narrowing (more than 25% reduction in diameter) of the left main trunk, the proximal, mid- and distal left anterior descending artery, and the proximal, mid- and distal left circumflex artery occurred in 1 (4%), 5 (20%), 3 (12%), 9 (36%), 6 (24%), 8 (32%) and 3 (12%) of 25 patients, respectively. After injection of 30 to 50 micrograms of acetylcholine into the right coronary artery, significant diffuse narrowing of the proximal, mid- and distal right coronary artery occurred in 5 (25%), 7 (35%) and 10 (50%) of 20 patients, respectively. However, significant diffuse dilatation (more than 25% increment in diameter) appeared in the left main trunk, left anterior descending, left circumflex and right coronary arteries in a few patients. These results indicate that acetylcholine induces coronary vasoconstriction in a significant number and coronary vasodilatation in a small number of adult humans, and that response of the coronary artery to acetylcholine varies along the course of the coronary artery.

Effects of intracoronary injection of acetylcholine on coronary arterial hemodynamics and diameter.

To examine the effects of intracoronary injection of acetylcholine on coronary blood flow and on coronary arterial diameter in humans, acetylcholine was injected into the left coronary artery in 32 adult patients (21 men and 11 women with a mean age of 54 years, range 37 to 65) with normal or almost normal coronary arteriographic findings. Patients with angina pectoris, myocardial infarction and severe cardiac diseases were excluded. Temporary right ventricular pacing was set at a rate of 60 beats/min to prevent transient bradyarrhythmias during intracoronary injection of acetylcholine. Measurements of coronary sinus blood flow and coronary vascular resistance and quantification of coronary arterial diameters using a computer-assisted technique were performed before and after each injection of 20, 50 and 100 micrograms of acetylcholine. Significant increase in coronary sinus blood flow and significant decrease in coronary vascular resistance occurred after intracoronary injection of acetylcholine. In contrast, mean diameter of normal epicardial coronary artery tended to decrease and that of irregular epicardial coronary artery decreased significantly after intracoronary injection of acetylcholine. Intracoronary injection of acetylcholine increases coronary blood flow, suggesting vasodilation in the coronary arteriolar bed, while it induces vasoconstriction in most of epicardial coronary arteries in adult humans.

Effects of propranolol and nifedipine on exercise-induced attack in patients variant angina: assessment by exercise thallium-201 myocardial scintigraphy with quantitative rotational tomography

To examine the effects of propranolol and nifedipine on exercise-induced attack in patients with variant angina, exercise 201Tl myocardial scintigraphy with quantitative analysis by emission-computed tomography was performed in 20 patients with variant angina after oral propranolol (80 mg), nifedipine (20 mg), and placebo. Exercise-induced attack occurred in 11 patients on placebo, in 14 on propranolol, and in none on nifedipine. The exercise duration was significantly shorter in those on propranolol (p less than .05), but significantly longer in patients on nifedipine (p less than .05) than in those on placebo. The peak rate-pressure product was significantly lower in patients on propranolol (p less than .01), but did not change in those on nifedipine, as compared with that in patients on placebo. The size of the perfusion defect as measured by 201Tl tomography was significantly greater in patients on propranolol (p less than .05), but significantly less in those on nifedipine (p less than .01) than in those on placebo. In conclusion, propranolol does not suppress but rather may aggravate exercise-induced attack in patients with variant angina, while nifedipine suppresses it. This unfavorable effect of propranolol on exercise-induced attack in patients with variant angina is likely to be due to a reduction of regional myocardial blood flow.

Increase of human atrial natriuretic polypeptide in response to cardiac pacing

6 weeks, but in a few, as in the subject of this report, the only identifiable precipitant is major surgery.8 In the 8 days between coronary artery bypass surgery and the onset of symptoms, there was no sign of viral illness in this patient, nor was there a history of viral infection in the weeks preceding his surgery. There was a pericardial reaction after operation manifest as a transient rub, and probably contributing to supraventricular arrhythmias. Such a reaction is common, and more likely to be due to trauma than to occult viral illness. There was no pleurisy, arthralgia, coryza, headache, or rash. The incidence of Guillain-Barre syndrome after coronary artery bypass grafting is low, and it is unlikely that bypass surgery or cardiopulmonary bypass represent a special stress or trigger to this process. However, one should be alert to unexplained weakness occurring after any major operative procedure, including cardiac surgery.

Blocking effect of verapamil on conduction over a catecholamine-sensitive bypass tract in exercise-induced Wolff-Parkinson-White syndrome

By intravenous administration of isoproterenol, 0.5 micrograms/min, a catecholamine-sensitive bypass tract was confirmed in two patients with exercise-induced Wolff-Parkinson-White syndrome. In a 24 year old woman, an intravenous bolus injection of 5 mg of verapamil suddenly blocked conduction over a catecholamine-sensitive bypass tract. In a 62 year old man, the exercise-induced Wolff-Parkinson-White syndrome disappeared after 3 days of oral administration of verapamil (120 mg/day). These observations suggest that a slow inward calcium current plays an important role in conduction over a catecholamine-sensitive bypass tract in exercise-induced Wolff-Parkinson-White syndrome.

Effects of phentolamine and atropine on angina pectoris induced by handgrip test in patients with variant angina

In 19 patients with variant angina, handgrip test as an isometric exercise was performed in 3 conditions on different successive days in the early morning: in the control, after administration of phentolamine (0.3 mg/kg) and after administration of atropine sulfate (0.04 mg/kg). Angina associated with ST-segment elevation on the electrocardiogram was induced in 5 patients (26%) in the control condition, in 14 (74%) after phentolamine and in 5 of 16 (31%) after atropine. All anginal events but 1 occurred after the cessation of the exercise and were not associated with the significant increase of rate-pressure products. These attacks were considered to be due to coronary spasm. The frequency of the induction of angina was significantly higher after phentolamine than in the other 2 conditions (p less than 0.01). It is concluded that the attack can be induced by the handgrip exercise in a sizable number of patients with variant angina, and that the administration of phentolamine increases the incidence of angina induced by handgrip exercise. The mechanism or mechanisms by which coronary spasm is induced by handgrip exercise remains to be elucidated.

AN AUTOPSY CASE OF CHRONIC CHAGAS' DISEASE

慢性Chagas病は本邦にて,未だその報告を見なかつたが,最近,我々は本病の1例を経験したので,ここに報告する.症例は62才,男性で, 21才時ブラジルに移住し農薬に從事していた.数年前より動悸,呼吸困難を自覚し,強心剤,利尿薬の投与を受けていた.入院前1週間頃より,夜間呼吸困難,動悸を自覚し,昭和52年7月20日に入院した.入院時は,毎分100の絶対性不整脈,心拡大,肺野ラ音,頚部静脈怒張,肝腫大,下腿浮腫を認め,重症うつ血性心不全の状態であつた.心電図上は,心房細動,右脚ブロック型心室内伝導障害を有しており,ジギタリス薬投与にて多源性心室性期外収縮の頻発を認めたので,電気的除細動を行ない洞調律に復した.心臓超音波検査にても,左心室後壁のAkinesiaと低心拍出性心不全の状態を呈していた.ブラジルでのMachado-Guerreiro補体結合反応陽性にて,慢性Chagas病と診断した.本例の重症うつ血性心不全はジギタリス薬,利尿薬などに抵抗性であつた.死亡前日より,心室頻拍の発作が頻回出現し, 38病日には,心室細動にて死亡した.死後剖検にて,心重量は740gであつた.組織学的には慢性間質性心筋炎と心筋線維内にTrypanosoma cruziのleishmaniaの巣が認められた.

Transient Left Atrial Mobile Thrombus in Acute Myocardial Infarction—A Case Report

The authors report a fifty-year-old woman with acute inferior myocardial infarction in whom left atrial mobile thrombus was found by echocardiography. They believe this to be the first echocardiographic documentation of such a thrombus after acute myocardial infarction. The combination of the stagnant flow in the left atrium due to atrial ischemia, the low output state due to left ventricular dysfunction, and the hemoconcentric tendency from use of diuretics might have played a role in the present thrombus formation. The thrombus was safely lysed without complication after intravenous urokinase.