Increased susceptibility of angiographically smooth left anterior descending coronary artery to an impairment of vasoresponse to acetylcholine, and the relation between impaired vasoresponse and low-density lipoprotein cholesterol level.

In the present study, we demonstrated that the angiographically smooth LAD is more susceptible than the LC to an impairment of vasoresponse to acetylcholine, suggesting the more severe endothelial dysfunction in the LAD. We also showed that levels of LDL play a partial but important role on endothelial dysfunction.

A case in which coronary spasms were induced by ergonovine provocation at the sites of coronary artery ectasia.

We experienced a patient in whom coronary spasms were induced by an ergonovine provocation test during coronary angiography at the sites of coronary artery ectasia. The patient was a 45-year-old male with chest pain at rest, which promptly disappeared when given sublingual nitroglycerin. Similar attacks occurred frequently even with the administration of drugs after admission, but no significant changes were observed in electrocardiography (ECG) during the attacks or by repeated Holter ECG. The results of exercise ECG and provocation tests such as Valsalva maneuver, hyperventilation, and cold pressor test were negative. Coronary angiography showed ectatic changes in the left coronary artery, and the coronary spasms were induced by ergonovine administration at the ectatic portion of the left anterior descending artery and left circumflex artery, and right coronary artery with chest symptoms similar to those observed during spontaneous attacks. However, there were no significant changes in ECG. This rare case suggests an involvement of spasms in the pathogenic mechanism of myocardial ischemia in coronary artery ectasia.

Sustained-release nifedipine (nifedipine-L) suppresses plasma thromboxane B2 and 6-keto prostaglandin F1 alpha in both young male smokers and nonsmokers.

Sustained-release nifedipine (nifedipine-L) (40 mg twice a day) was administered orally to healthy young adult male smokers and nonsmokers for 10 days, and its effects on platelet aggregation, beta-thromboglobulin and platelet factor 4 levels, and plasma thromboxane B2 (TxB2) and 6-ketoprostaglandin F1 alpha (6-Keto-PGF1 alpha) concentrations were studied. The plasma nifedipine-L concentration in smokers (46.0 +/- 7.4 ng/ml) was significantly lower than that in nonsmokers (88.2 +/- 1.2 ng/ml). Nifedipine-L did not affect platelet aggregation induced by adenosine diphosphate, collagen, or epinephrine in either smokers or nonsmokers. The plasma beta-thromboglobulin level on the tenth day of nifedipine-L administration in nonsmokers was lower than that in smokers, but there were no significant differences either with or without nifedipine-L or between nonsmokers and smokers. Nifedipine-L had no effect on the concentration of platelet factor 4 in either smokers or nonsmokers. On the other hand, nifedipine-L significantly decreased the plasma TxB2 and 6-keto-PGF1 alpha concentrations in both smokers and nonsmokers. Thus we concluded that nifedipine-L suppressed the production of plasma TxB2 from platelets and also subsequently suppressed the production of 6-keto-PGF1 alpha and that this action was not affected by cigarette smoking.

[A case of intermittent ventricular pre-excitation syndrome with a Mahaim fiber].

A 61 year-old woman with intermittent ventricular pre-excitation syndrome using a Mahaim fiber was reported. The electrocardiogram showed QRS-complex with small delta wave (100 msec in QRS width) or without small delta wave (80 msec in QRS width). On electrophysiological study, during sinus rhythm, A-H interval was 100 msec. H-V intervals were 25 msec in QRS-complex with small delta wave and 45 msec in QRS-complex without small delta wave. From these findings, it was considered that the small delta wave was produced by a Mahaim fiber.

Comparison of serum lipid values in variant angina pectoris and fixed coronary artery disease with normal subjects.

Lipid and apolipoprotein (apo) levels in patients with variant angina were examined and compared with patients with coronary artery disease (CAD) and normal subjects (control). Cholesterol and triglyceride levels in plasma, lipoprotein fractions and several apolipoproteins were measured in 108 men (90 of whom had undergone coronary angiography): 22 had variant angina, 56 had fixed CAD (effort angina and old myocardial infarction) and 30 were normal subjects. Patients with variant angina showed more severe atherosclerotic lesions than the control group, but less severe lesions than the patients with fixed CAD. In comparison with lipid and apolipoprotein, high density lipoprotein cholesterol, apo AI and apo AII decreased significantly in control, variant angina and fixed CAD groups, respectively. Additionally, stepwise discriminant analysis revealed that apo AI was the best discriminator among the 3 groups or between variant angina or fixed CAD and the control group. Variant angina and fixed CAD patients could be discriminated from the control subjects by an apo AI level of 135 and 126 mg/dl, with 71% (p less than 0.025) and 73% (p less than 0.005) accuracy, respectively. By these criteria 77% of the patients with variant angina and 73% of the patients with fixed CAD were precisely discriminated. Discrimination between variant angina and fixed CAD patients, however, was not practical, even if the best discriminator was used. Thus, the apo AI level is useful in discriminating patients with variant angina and fixed CAD from normal subjects. Therefore, symptomatic patients with low apo AI levels should be aggressively examined.

The study of a case of single coronary artery using stress 201thalium single photon emission computed tomogram.

A 48-year-old female, who had been having episodes of chest discomfort and oppression lasting for several minutes for 15 years was diagnosed as having a single left coronary artery by coronary angiography. The electrocardiogram taken during a chest pain attack demonstrated the depression of the ST-segment in leads II, III, aVF, and V4-6. The chest pain was relieved, and the ischemic change in ECG was improved by sublingual nitroglycerine. 201Thalium single photon emission computed tomography under stress indicated poor uptake in both the anterior and infero-posterior myocardium, which was compatible with the change in ECG either during the attack or during exercise. The anterior myocardial ischemia was reduced by propranolol and the chest pain was successfully relieved by propranolol. The chest pain in this case might have partly been due to the myocardial ischemia in the anterior and infero-posterior myocardium, under stress, which could have been the steal phenomenon to lateral myocardium due to the anatomical anomaly, besides other possible mechanisms for chest pain proposed in the case of single coronary artery. Our findings suggested that 201Thalium stress single photon emission computed tomography is a useful method for detecting the myocardial ischemia in patients with single coronary artery and those suffering from chest pain without any coronary stenosis.