Toshinori Utsunomiya

Mental stress test is an effective inducer of vasospastic angina pectoris: comparison with cold pressor, hyperventilation and master two-step exercise test

BACKGROUND Cold pressor, hyperventilation and exercise stress tests were usually used for inducing an angina attack in patients with vasospastic angina pectoris. We induced vasospastic angina attack using the mental calculation stress test, and compared the results with those using other stress tests. SUBJECTS AND METHODS Subjects were 29 patients with vasospastic angina pectoris. Their ages were 60.8+/-8.4 years. Coronary vasospasm was induced by an acetylcholine infusion test during coronary angiography. The mental stress test was performed as follows; after memorizing six digits numbers, they repeated these numbers in reverse for 5 min, and performed serial subtraction of 17 from 1000 for 5 min. Blood pressure, heart rate and ECG were recorded every 1-5 min during the mental stress test. The serum concentrations of epinephrine and norepinephrine were measured before and during the mental stress test. We compared these results with those obtained using cold pressor, hyperventilation and the Master two-step exercise stress test. RESULTS (1) Eight of the 29 patients (28%) showed ischemic ST-T change, which was caused by the mental stress test. (2) The increase in norepinephrine was greater in patients with an ST-T change than without an ST-T change (0.11+/-0.06 vs. 0.04+/-0.04 ng/ml, P<0.01). (3) The incidence of the ST-T change caused by the mental stress test (28%) was similar to the cold pressor test (27%) and greater than that caused by the hyperventilation test (13%). The incidence of ST-T change caused by the Master two-step test was 55%. CONCLUSIONS The mental stress test is an effective inducer of vasospastic angina attack, and attack may be induced by neurohumoral vasoconstrictive reflex and/or increased left ventricular afterload.

Effect of ticlopidine on exercise-induced Platelet aggregation and exercise tolerance time in patients with ischemic heart disease

Platelet aggregation is one of the most important mechanisms for acute myocardial infarction during exercise. We sought to evaluate the effect of ticlopidine (TP) on platelet aggregation (PA) during exercise in patients with ischemic heart disease (IHD). We studied 38 patients with IHD, 26 patients with effort angina pectoris, and 12 patients with a previous myocardial infarction. In protocol I, subjects were divided into two groups. Drugs altering platelet aggregation were withheld 2-4 weeks before the study in 25 patients (control group). TP (200 mg/day) was administered for 7 days in 13 patients (ticlopidine group). A symptom-limited modified Bruce protocol treadmill exercise test was performed. PA was measured at rest and after exercise by using optical densitometry induced by adenosine diphosphate (ADP). PA ratio (percentage of maximum) was compared. In protocol II, in 12 patients, treadmill exercise test and PA measurement were performed with and without TP. PA significantly increased after exercise in control (from 51.7+/-23.3% to 64.4+/-27.7%, p < 0.01) and ticlopidine (from 31.9+/-10.5% to 42.0+/-20.4%, p < .01) groups; however, its grade was lower in the ticlopidine group than in the control group. After exercise, PA was lower in the ticlopidine group than in control group (42.0+/-20.4% vs. 64.4+/-27.7%; p < 0.01). In the same patients, PA was lower with TP than without TP after exercise. Treadmill exercise-tolerance time was greater in the ticlopidine group than in the control group, but not statistically significant (762.3+/-139.2 vs. 711.6+/-169.6 s; NS). Exercise-tolerance time was significantly greater with TP than without TP in same patient (791.7+/-98.9 vs. 733.3+/-152.8 s; p < .05). TP suppressed the increase of PA during exercise and increased the exercise-tolerance time in patients with IHD.

Short- and long-term effects of nisoldipine on cardiac function and exercise tolerance in patients with hypertrophic cardiomyopathy

Nisoldipine is a second generation dihydropyridine calcium antagonist having characteristics of strong coronary artery dilating effect and less negative inotropic action. The purpose of this study was to evaluate the effect of nisoldipine on the cardiac function (systolic and diastolic) and the exercise tolerance in patients with hypertrophic cardiomyopathy (HCM).Subjects: Twenty-three patients with HCM were studied.Methods: We measured the following indices using M-mode and pulsed wave Doppler echocardiography before and after nisoldipine therapy; left ventricular fractional shortening (LVFS), isometric relaxation time (IRT), deceleration half-time (DHT) of early diastolic mitral (E) flow, late diastolic mitral (A) flow and A/E ratio. Symptomlimited treadmill exercise test was performed. Exercise tolerance (EX) time was measured. Nisoldipine of 10mg/day was orally administered. Same tests were repeated on day 14 and after 6 months.Results: 1) Short-term effects; LVFS did not change (55.9±5.9%→57.0±7.4%, NS) after 2 weeks. However, LV diastolic function significantly improved (IRT; 92.1±7.7 ms→85.2±11.6 ms, p<0.05, DHT; 70.7±16.2 ms→63.3±3.7 ms, p<0.05). EX time increased (8.9±2.6 min→ 10.0±3.3 min, p<0.05). 2) Long-term effects; LV diastolic function had a tendency toward improvement, but is statistically not significant (IRT; 91.1±7.6→83.8±11.6 ms, DHT; 73.1±23.4→61.0±11.4 ms, A/E; 1.26±0.29→1.11±0.36) after 6 months. EX time was significantly increased (9.4±1.7→ 10.1±1.7 min, p<0.05).Conclusions: Nisoldipine improved LV diastolic dysfunction and exercise tolerance in patients with HCM. These effects were similar to the first generation calcium antagonists. LV diastolic dysfunction may be improved due to the reduction of intracellular calcium concentration and the relief of myocardial ischemia by strong coronary artery dilating effect. However, nisoldipine did not affect the LV systolic function because of its less negative inotropic effect.

A case of benign asbestos pleurisy as pleural bloody effusion

50才男性でアスベストにより血性胸水を生じた1例である.症例は30年間のアスベスト暴露歴を有し,昭和58年12月胸部写真で胸水貯留を無症候性に認め,昭和59年2月胸水が増加して入院精査した.胸水は血性滲出液で細胞診や細菌培養は陰性.喀痰中や気管支肺胞洗浄液中に多数のアスベスト小体が証明され,悪性腫瘍や結核などを否定し,無治療で経過観察をした. 6カ月後に胸水が減少し,胸膜肥厚や肺の線維化が認められ, 2年6カ月後の現在も悪性腫瘍の発生はなく,アスベストによる良性胸水貯留と考えられた.アスベストによる良性胸水貯留と診断しえた症例の報告は,本邦において少なく,その診断に気管支肺胞洗浄が有用と思われた.