Three-vessel coronary artery spasm in a patient with variant angina and normal coronary arteries

Variant angina with two or more electrocardiographic or angiographic localizations has seldom been reported [1-4]. We present a case of variant angina pectoris and normal coronary arteries with three different and independent electrocardiographic localizations.     

Prevalence of migraine and Raynaud's phenomenon in Japanese patients with vasospastic angina

The prevalence of migraine and Raynaud's phenomenon in Japanese patients with vasospastic angina (group I) were compared with those in 2 control groups: one with effort angina (group II) and the other group without known ischemic heart disease (group III). There were no significant differences among the 3 groups with respect to age and sex. The prevalence of migraine in group I was 23 of 100, as compared with 4 of 100 in group II (p<0.01) and 11 of 100 in group III (p<0.05). The prevalence of Raynaud's phenomenon in group I was 9 of 100, as compared with 3 of 100 in group II and 4 of 100 in group III. Thus, in Japan, the prevalence of migraine in patients with vasospastic angina was higher than those in the 2 control groups, whereas the prevalence of Raynaud's phenomenon did not differ significantly among the 3 groups. The prevalence of Raynaud's phenomenon in Japanese patients with vasospastic angina was different from that reported from North America, although the prevalence of migraine was the same. This may be partially explained by racial differences.     

Supersensitivity of coronary arteries in variant angina to spasm induced by intracoronary acetylcholine

Acetylcholine (20 to 100 micrograms) was infused directly into coronary arteries in 10 patients with variant angina (group A), 13 subjects without coronary artery disease (group B) and 8 patients with significant organic coronary artery stenosis (greater than or equal to 50%) but without variant angina (group C) during coronary arteriography, to clarify the action of this agent on coronary arteries. Temporary pacing was performed at a demand heart rate of 40 beats/min while bradyarrhythmia developed. Coronary arteriography after administration of acetylcholine showed coronary vasoconstriction in all 10 patients (100%) of group A. Angina accompanied by electrocardiographic ischemic changes in 9 of 10 (90%, 7 ST-segment elevation and 2 depression) was provoked during this test. In the patients of group B, acetylcholine also induced vasoconstriction in 8 of 22 (36%) coronary arterial systems examined, chest pain in 3 (14%) and ST-segment deviation in none (0%). In the patients of group C, acetylcholine induced vasoconstriction in 3 of 9 (33%), chest pain in 2 (22%) and ST-segment depression in 1 (11%). No definite coronary artery dilation induced by acetylcholine was noted. Coronary vasoconstriction (p less than 0.05), electrocardiographic ischemic findings (p less than 0.01) and chest pain (p less than 0.01) were induced significantly more frequently in group A than in both groups B and group C. No significant difference was found between group B and group C. The coronary arteries in the patients with variant angina seem to be more susceptible to acetylcholine than those of patients without variant angina irrespective of the presence of significant atherosclerosis.     

Inflammation of the coronary arteries in patients with unstable angina

During surgery, 21 patients undergoing coronary artery bypass for unstable angina were found to have "red lines" overlying one or more coronary arteries. Adventitial biopsies showed vascular distention and inflammatory cells. The group was followed for an average of 54 months (14 to 68 months). There were no operative deaths. Recurrent myocardial ischemia developed in 38.1% (8/21); recurrent angina developed in 23.8% (5/21) and are being treated medically; myocardial infarction occurred in 9.5% (2/21); and reoperation was required in 4.8% (1/21). There was also one late death from a brain tumor. We suggest that the presence of adventitial inflammation may represent an aggressive, variant form of atherosclerosis and a less favorable clinical prognosis.     

Myocardial metabolism in angina with angiographically normal coronary arteries

Myocardial metabolism was studied during rapid atrial pacing in 22 patients with angina and angiographically normal coronary arteries. Pyruvate, non esterified fatty acid and lactate levels were measured in the coronary arteries and veins under basal conditions, at the peak of atrial pacing and during the recovery phase. A control group of 8 patients had neither angina, ST depression, or lactate production during atrial pacing. A correlation was observed between the coronary arterio-venous difference and arterial pyruvate and non esterified fatty acid levels in the 22 patients during the 3 periods of study. The control patients did not differ significantly from the rest of the population. There was a correlation between the coronary arterio-venous difference and arterial lactate levels under basal conditions in all of the study and control groups. This correlation remained significant during atrial pacing and the recovery period only in the control group. It was possible to distinguish a group of 14 patients (64 p. 100) (Group A) with a correlation coefficient of lactate production similar to the control group (+/- 2 standard deviations) during atrial pacing, from a second group of 8 patients (36 p. 100) (Group B) with abnormal myocardial metabolism. The arterial lactate concentrations were similar in both groups in the 3 periods of study. A coefficient of lactate extraction less than 10 p. 100 was observed in 2 patients in Group A and in 7 patients in Group B (88 p. 100, p less than 0.01). One patient in Group B had a coefficient of lactate extraction greater than 10 p. 100 (+ 13 p. 100).(ABSTRACT TRUNCATED AT 250 WORDS)     

Raynaud's phenomenon of the lung

To determine if pulmonary vessels develop vasospasm during Raynaud's phenomenon, digital vasospasm was induced by hand immersion in 15 degrees C water (cold pressor test) in 17 subjects, and pulmonary function was measured during the subsequent 120 minutes. Five healthy persons were control subjects, seven subjects had well documented systemic disorders associated with Raynaud's phenomenon (secondary Raynaud's), and five subjects had a history of Raynaud's phenomenon but no evidence of an associated disorder (primary Raynaud's). The only measure of pulmonary function that changed significantly following cold pressor testing was carbon monoxide diffusing capacity. Subjects with primary Raynaud's phenomenon had normal baseline carbon monoxide diffusing capacity (23.7 +/- 4.6 ml/minute/mm Hg) but demonstrated significant decreases (p less than 0.05) at 15 minutes (21.2 +/- 3.5 ml/minute/mm Hg), 45 minutes (19.5 +/- 3.7 ml/minute/mm Hg), and 120 minutes (17.1 +/- 2.1 ml/minute/mm Hg) after cold pressor testing. Subjects with secondary Raynaud's phenomenon had low baseline carbon monoxide diffusing capacity (71 percent predicted) and showed no significant change following cold pressor testing. These findings indicate that digital vasospasm in patients with primary Raynaud's phenomenon is part of a systemic vascular response that includes a decrease in the size of the pulmonary capillary bed.     

Diffuse intimal thickening of coronary arteries in patients with coronary spastic angina

OBJECTIVES: The purpose of this study was to evaluate the extent of atherosclerotic changes in angiographically normal coronary arteries using intravascular ultrasound (IVUS) technique in patients with coronary spastic angina. BACKGROUND: Nitric oxide activity was shown to be decreased in coronary arteries of patients with coronary spastic angina (CSA). Decrease in nitric oxide causes arterial intimal hyperplasia or thickening. However, it remains unclear whether intimal thickening is diffusely present in coronary arteries of patients with CSA. METHODS: The IVUS study was performed in 26 patients with CSA and with normal coronary angiograms and in 31 control subjects in whom age and gender was matched with those in patients with CSA. RESULTS: Compared with control subjects, patients with CSA had significantly larger percent intima + media area (%I + M area), intima + media area and maximal intima + media thickness in all of proximal, middle and distal segments (p<0.01, respectively). Lumen area was comparable between these groups. The presence of spasm was the most powerful independent predictor of increase in percent intima + media area, in multiple-regression analysis with the traditional risk factors as covariates. CONCLUSIONS: Intimal thickening existed entirely in a coronary artery in patients with CSA and with normal angiograms, independently of other traditional risk factors. The diffuse intimal thickening in the spasm coronary arteries is intimately related with coronary spasm.     

Evaluation of coronary reserve in angina pectoris with angiographically normal coronary arteries

Coronary reserve was studied: 1) during rapid atrial pacing and then, 2) during dipyridamole infusion (0.6 mg/Kg/4 min) in 3 groups of subjects: 13 patients with angina pectoris and angiographically normal coronary arteries (ANC) with proven myocardial ischaemia during atrial pacing, 15 patients with coronary artery disease (COR) and 17 normal controls with normal coronary angiography and atrial pacing. Coronary sinus flow (QCS) was measured by thermodilution and myocardial metabolism studied by the coefficient of lactate extraction (K). At maximal pacing rates, K remained 15 p. 100 in the control group (average 24 +/- 7 p. 100) but was inversed in the ANC (-3 +/- 10 p. 100) and COR groups (-27 +/- 38 p. 100). The risk in QCS was low in the COR group (+60 +/- 33 p. 100) p less than 0.02, but significant in the ANC group (+104 +/- 57 p. 100) and normal controls (+107 +/- 41 p. 100). Coronary reserve, calculated as the percentage increase in QCS with dipryridamole, was found to be the same in the ANC group (+225 +/- 79 p. 100) as in normal subjects (+191 +/- 81 p. 100) but was low in the COR group (74 +/- 42 p. 100, p less than 0,001). Therefore, no reduction in coronary reserve was shown in patients with angina and normal coronary arteries whilst the myocardial ischaemia in coronary disease does seem to be related to an amputation of the coronary reserve.     

An unusual association with Raynaud's phenomenon

A 36-yr-old lady with a year of typical Raynaud's and polyarthralgiahad a normal examination other than cold peripheries and bloodpressure of     

An unusual association with Raynaud's phenomenon

SIR, We read with interest the report by AL-Deiri et al. [1].There is little doubt that the clinical scenario suggests anassociation of possible Raynauds phenomenon (RP) and pituitaryinsufficiency. It again raises     

Pathogenesis of Raynaud's phenomenon

The pathogenesis of Raynaud's phenomenon is not fully understood. However, the last 20 yr have witnessed enormous increases in our understanding of different mechanisms which, singly or in combination, may contribute. A key point is that Raynaud's phenomenon can be either primary (idiopathic) or secondary to a number of underlying conditions, and that the pathogenesis and pathophysiology vary between these conditions. This review concentrates upon those subtypes of Raynaud's phenomenon of most interest to rheumatologists: systemic sclerosis-related Raynaud's phenomenon, primary Raynaud's phenomenon and Raynaud's phenomenon secondary to hand-arm vibration syndrome. In this review, I shall discuss the main mechanisms thought to be important in pathophysiology under the three broad headings of 'vascular', 'neural' and 'intravascular'. While these are false distinctions because all interrelate, they facilitate discussion of the key elements: the blood vessel wall (particularly the endothelium), the neural control of vascular tone, and the many circulating factors which can impair blood flow and/or cause endothelial injury. Vascular abnormalities include those of both structure and function. Neural abnormalities include deficiency of the vasodilator calcitonin gene-related peptide (released from sensory afferents), alpha(2)-adrenoreceptor activation (possibly with up-regulation of the normally 'silent' alpha(2C)-adrenoreceptor) and a central nervous system component. Intravascular abnormalities include platelet activation, impaired fibrinolysis, increased viscosity and probably oxidant stress. As our understanding of the pathophysiology of Raynaud's phenomenon increases, so do our possibilities for identifying effective treatments.     

Comparative results of coronary intervention in patients with variant angina versus those with non-variant angina

Coronary angioplasty is reported to be feasible and safe in patients with coronary spasm and fixed stenosis. However, the long-term results are not positive. We compared the results of coronary angioplasty in 20 patients with variant angina versus 17 patients with non-variant angina among 231 consecutive patients with vasospastic angina. Coronary angioplasty was performed successfully in all 37 patients without any complications. Stenting for coronary dissection or recoil was performed in 8 patients, directional coronary atherectomy was selected for ostial lesion of left anterior descending coronary artery stenosis in 2 patients, and standard balloon angioplasty was performed in 27 patients. There were no clinical differences between the two groups. The restensois rate in patients with variant angina was similar to that in patients with non-variant angina (30% vs 29%, ns). There was no relationship between the provoked spasm and restenosis. During the follow-up period, no major complications were observed in patients with variant angina or those with non-variant angina. In conclusion, full medication with calcium channel antagonists and isosorbide dinitrate, and treatment by coronary angioplasty including the use of new devices, were useful treatments for patients with coronary vasospasm and significant organic stenosis. There was no difference concerning the results of coronary intervention between the patients with variant angina and those with non-variant angina.