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Tl-201 scintigraphy in multivessel exercise-induced variant angina.

A 53-year-old man presented for evaluation of nocturnal chest pain, consistent with angina pectoris. An exercise stress test reproduced his symptoms, however, exercise electrocardiograms were nondiagnostic. An exercise-thallium perfusion study confirmed vasospasm as the cause. This knowledge guided subsequent successful medical therapy.

Angina Pectoris, Variant↗

Relation of basal coronary tone and vasospastic activity in patients with variant angina.

OBJECTIVE: To examine the vasoconstrictor response to ergonovine and the vasodilator response to isosorbide dinitrate in spastic and non-spastic coronary segments from 31 patients undergoing serial angiographic follow up of variant angina. METHODS: Coronary angiograms and ergonovine provocation tests were repeated at an interval of 45 (SD 15) months apart. While all 31 patients showed a positive response to ergonovine initially, vasospastic responsiveness persisted in only 16 patients at follow up (group 1) and not in the other 15 patients in whom symptoms of variant angina had resolved (group 2). Mean luminal diameter of 170 normal or near normal entire coronary segments (American Heart Association classification) were measured (a) at baseline, (b) after the administration of ergonovine, and (c) after the administration of isosorbide dinitrate, during both the initial and follow up angiograms using a computer based quantitative angiography analysis system (CAAS II). RESULTS: In vasospastic patients (initial and follow up angiograms in group 1, and initial angiogram in group 2), basal tone was significantly higher in spastic segments compared to adjacent segments or segments in non-spastic vessels. The diagnostic sensitivity and specificity at 20% increase in basal coronary tone for the prediction of vasospasm were 77% and 73%, respectively. CONCLUSIONS: Coronary artery tone may change in proportion to the activity of variant angina over several years. Contrary to some previous reports, the estimation of basal coronary tone may be useful in the assessment of vasospastic activity in patients with variant angina.

Angina Pectoris, Variant↗

Coronary spasm, variant angina, and recurrent myocardial infarctions.

A 24-year-old male student had three myocardial infarctions, one prior to and two following the angiographic documentation of normal coronary arteries. A spontaneous episode of variant angina prompted repeat coronary angiography, during which intravenous ergonovine caused spasm of the left anterior descending coronary artery, transient ST-segment elevation, and ischemic chest pain; the previously normal right coronary artery was found to be occluded proximally. This constellation of clinical and angiographic findings suggests that coronary spasm can cause acute myocardial infarction as well as variant angina.

Adult↗

Peripheral vascular reactivity in patients with variant angina.

Previous studies have suggested a high prevalence of migraine headache and Raynaud's phenomenon in patients with variant angina. These findings suggest increased reactivity to vasoconstrictor stimuli in the extremities in these patients. In this study we examined forearm vascular responses to a cold pressor test and intra-arterially infused norepinephrine and angiotensin II in patients with variant angina (mean age 60 +/- 4 years, n = 6) and those with other forms of ischemic heart disease or atypical chest pain (mean age 59 +/- 5 years, n = 8). Arm blood flow was measured by strain gauge plethysmography and forearm vascular resistance was calculated. There was no difference in forearm vasoconstrictive responses to a cold pressor test, norepinephrine or angiotensin II between the two groups of patients. Minimal forearm vascular resistance after 10 min of arterial occlusion was also similar between the two groups. Thus our study suggests that peripheral vasoconstrictive reactivity is not increased in patients with variant angina.

Aged↗

Frequency of systemic microvascular dysfunction in syndrome X and in variant angina.

In addition to coronary vascular abnormalities, patients with syndrome X and variant angina often have systemic vascular symptoms. To determine whether these patients exhibit a generalized abnormality of vasoreactivity, we used high-resolution ultrasound to compare flow responses and endothelial function in the brachial artery in 21 patients with syndrome X, 15 patients with variant angina, and 20 healthy controls. Arterial diameter was measured at rest, after reactive hyperemia (endothelium-dependent flow-mediated vasodilation), and after sublingual glyceryl trinitrate (endothelium-independent vasodilation). The magnitude of hyperemic flow response was measured after transient forearm occlusion. Flow-mediated dilation in the brachial artery did not differ among patients with syndrome X, variant angina, and controls (2.7 +/- 2.3%, 3.8 +/- 3.5%, and 4.2 +/- 3.0%). Endothelium-independent vasodilation in the brachial artery was similar in the 3 groups (16.0 +/- 7.2%, 12.7 +/- 4.6%, and 14.8 +/- 4.9%). Despite a considerable overlap, reactive hyperemia was lower in patients with syndrome X than in patients with variant angina and controls (342+/-86% vs 466+/-184% and 452+/-104%; p < 0.05). These findings indicate that a substantial proportion of patients with syndrome X have a systemic microvascular abnormality, whereas variant angina is predominantly a segmental disorder of conduit vessels.

Angina Pectoris, Variant↗