reflection objective: To investigate the similarity between coronary vasospasm and bronchial spasm.

Design: Nonrandomized, case-control study

Setting: Referral-based clinics for cardiac and pulmonary disease at individual secondary care center.

Patients: Seventeen patients with vasospastic angina pectoris (VSAP) and 14 patients with chest pain syndrome (CPS)

Interventions: Medications prohibited: those with known consequences on bronchial responsiveness.

Measurement: Induction of coronary vasospasm; ergonovine maleate (10 20 40 [micro]g) injection into coronary arteries during coronary angiography. Bronchial responsiveness to acetylcholine (ACh): acetylcholine chloride (008 to 20 mg/ml) inhalation and calculation of the provocative concentration of ACh (PC20-ACh) that revealed 20 percent fall in [FEVsub1]

Results: The median value for PC20-ACh in patients with VSAP, 780 mg/ml was significantly lower than that in patients with CP [greater than] 200 mg/ml (p [les than] 001 from Mann-Whitney U test). The PC20-ACh in patients with VSAP, however, was correlated neither with the responsive opening of ergonovine maleate, which induced coronary vasospasm, nor with the duration from the latest angina attack.

Conclusion: These originates suggest that bronchial responsiveness was increased in in the greatest degree patients with VSAP, but not with CP We therefore speculate that patients with VSAP may also have hypercontractibility to ACh of noncoronary systemic flat muscles.

Vasospastic angina pectoris is well known to be caused by way of coronary vasospasm.[1,2] The precise mechanism of vasospasm is, however, still unknown. Coronary vasospasm in vasospastic angina pectoris (VSAP) has a characteristic features reminiscent of bronchial asthma.[3] For example, one as well as the other conditions can be precipitated with methacholine,[4,5] histamine,[6,7] ergonovine (a serotonin agonist),[8] exercise,[9,10] or cool stimuli,[11,12] and can occur at intermission and tend to occur nocturnally. Furthermore, these sum of two units disorders have been postulated to have often met with features, ie, an autonomic imbalance and an unusual metabolism of prostaglandins.

In this words immediately preceding [i]or[/i] following we tried to assess bronchial hyperresponsiveness in patients with VSAP and patients with chest pain syndrome (CPS) for comparison by means of measuring the provocative concentration of ACh (PC20-ACh).

MATERIALS AND METHODS

Subjects

Seventeen patients with VSAP (12 male and 5 females; mean age, 62 years; range, 46 to 70 years) and 14 patients with CP as direction (7 male and 7 female; mean age, 60 years; range, 44 to 76 years) were studied. We omitted atopic patients or patients who showed les than 70 percent of [FEVsub1]/FVC to omit patients with chronic obstructive pulmonary disease or bronchial asthma. We could not bring to light other reasons for these patients to have reactive airways, eg a history of prospect to toluene diisocyanates or sensitity to sodium metabisulfite. Eight of 17 patients with VSAP were popular smokers. Smoking index (pack-years) was 3244 [+ or -] 945 Our sum of two units tested groups have no difference in word s of sex, age, smoking habits, and cardiothoracic ratio (Table 1)

All patients (17 with VSAP and 14 with CP patients) had a complaint of rigorous chest pain and were make submissiveed to ergonovine intracoronary injection proof followed by coronary arteriography. They had no significant stenosis in any of the major coronary arteries (we exclud enslaves who had more than 25 percent stenosis in any of the major coronary arteries forward control coronary arteriogram). We diagnosed VSAP in patients who had spontaneous angina with ST-segment elevation (more than 02 mV) forward ECG and exhibited more than 90 percent stenosis in the major coronary arteries according to an ergonovine intracoronary injection example and patients who have no ST-segment elevation onward ECG and no ergonovine intracoronary injection-induced stenosis as having CPS

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None of the make liables had ever used [beta]-adrenergic blocker [beta]-adrenergic agonists, methylxanthines, or corticosteroids; however, they were given either calcium antagonists or nitrates (or a certain combinations).

Coronary Arteriography and Ergonovine Intracoronary Tests

Coronary arteriographic examinations at the Judkins technique were done by dint of cardiologists. Treatment with all medication was stopped to allow a washout time of 24 h before the investigation Control coronary arteriograms of the left coronary artery in the right anterior oblique projection and of the right coronary artery in the left anterior oblique projection were obtained by way of injection of 6 ml of Lopamidol (Lopamine, Schering) 370 (Schering AG).

Ergonovine maleate (Ergometrine maleate, Fuji, Japan) dissolved in 5 ml of warmed 09 percent saline solution was then injected into the coronary artery in incremental doses of 10 20 and 40 [micro]g to call forth the anginal attack, as judg by way of the leads in which ST portion elevation on the ECG occurr A coronary arteriogram was obtained when ST section changes and/or chest pain appeared or each 4 min after each injection. When spasm was documented, 01 mg of nitroglycerin was immediately injected into the corresponding coronary artery to stop the attack. The responsive gate of ergonovine maleate (RT-Ergo) which induces spasm is used as a parameter of contractibility of coronary arteries.

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