Provocation of coronary artery spasm by the cold pressor test. Hemodynamic, arteriographic and quantitative angiographic observations.

Abstract

In this study we attempted to determine if the cold pressor test, a known sympathetic reflexogenic stimulus, could precipitate coronary artery spasm. Thirty-five patients undergoing coronary arteriography for evaluation of chest pain syndromes were given the cold pressor test. During 1 minute of cold pressor stimulation, aortic systolic pressure increased 18.1 ± 9.7 mm Hg (mean ± SD) and heart rate did not change significantly. Focal coronary artery spasm was provoked in seven patients, each of whom had an atheromatous plaque at the site of spasm. Four of six patients with a precatheterization clinical diagnosis of variant angina (group 1) had coronary artery spasm, and two of the four had associated ischemic manifestations. Of 14 patients in whom classic angina (group 2) was diagnosed before cardiac catheterization, two manifested focal coronary spasm. One of 15 patients thought to have atypical chest pain (group 3) manifested spasm. There were no significant differences in baseline variables (aortic systolic or diastolic pressure, heart rate, double product and left ventricular end-diastolic pressure) or hemodynamic response (aortic systolic pressure, heart rate or double product) to cold pressor stimulation between patients in each group and between those who manifested spasm and those who did not. Ventricular ectopy and ventricular tachycardia developed in one patient but were readily reversed with intravenous nitroglycerin. Quantitative angiography showed that the luminal diameter of normal coronary segments significantly decreased in each group of patients in response to cold pressor stimulation, but this response was most pronounced in the variant angina group (-12.7 ± 11.5% from control in group 1, -5.1 ± 10.2% in group 2, and -7.9 ± 9.6% in group 3; p < 0.001 for each group). Patients who are prone to coronary spasm may represent one extreme of a spectrum of reactivity to a coronary vasoconstrictive stimulus. The cold pressor test can provoke focal coronary artery spasm in certain patients and may be a useful nonpharmacologic provocative screening test to aid in the diagnosis of this phenomenon.CORONARY ARTERY SPASM has become the focus of increasing attention. Its role in variant angina is well documented,'-' and it has been observed in patients with classic angina,6 7 unstable angina8 9 and myocardial infarction.10 The transience of coronary artery spasm makes it difficult to diagnose. Consequently, various interventions, primarily pharmacologic, have been used to provoke coronary artery spasm during coronary arteriography. These pharmacologic interventions include the administration of ergot aklaloids,", 12 epinephrine in combination with propranolol,13 and methacholine.14 Thirty-five patients (34 males and one female), mean age of 50.1 years (range 30-62 years), undergoing routine cardiac catheterization and coronary arteriography for evaluation of chest pain syndromes were included in this study. The patients were categorized according to their precatheterization clinical presentation. Group 1 consi...

Coronary artery constriction caused by the cold pressor test in human hypertension.

“…Although some studies have reported that cold pressor stimulation induced constriction of normal coronary arteries, 23 -24 the control subjects were not selected to have completely smooth coronary arteries without intraluminal irregularities. It has since been demonstrated that the cold pressor test dilates the epicardial coronary arteries in the absence of stenosis or luminal irregularities.…”

The effect of generalized alpha-receptor stimulation on regional myocardial blood flow distal to a severe coronary artery stenosis.

“…After control recording of hemodynamics (heart rate, systemic arterial and left atrial pressure) and determination of regional myocardial blood flow, i.v. norepinephrine, [6][7][8][9][10][11][12][13][14] ,ug/min, was infused to increase mean arterial pressure approximately 20 mm Hg above control levels so as to mimic the blood pressure increase (15-20 mm Hg) in humans subjected to cold pressor stress.5 6 After 10 minutes, hemodynamics were recorded, a second injection of radiolabeled microspheres was performed, and the infusion was then discontinued. After the pig had recovered for 20-30 minutes, hemodynamics were again recorded and microspheres again injected to determine regional myocardial blood flow.…”

The paradox of adrenergic coronary vasoconstriction.

“…77' 78, 80 The region of decreased flow has even been localized to the region of atherosclerotic narrowing in some patients.79 81 Administration of the a-receptor-blocking agent phentolamine blunts the coronary vasoconstriction in patients with angina.77 fl-Receptor blockade with propranolol potentiates the cold pressor vasoconstrictor response.80 Although the cold pressor test can elicit spasm in some patients with variant angina, narrowing of coronary stenoses in patients not thought to have variant angina was observed in several cases. 82 Taken together, these studies suggest that placing a patient's hand in ice water elicits a reflex a-receptor-mediated coronary vasoconstriction that in some patients results in supercritical narrowing of a stenotic arterial segment, which can lead to reduced flow despite tachycardia and an increase in blood pressure. a-Blockade.…”

“…No. 4, October 1987 with coronary sinus thermodilution during cold pressor tests, and in patients without significant coronary artery disease the expected increase in coronary blood flow secondary to the increase in myocardial metabolism is observed.77 81 Angiographic analysis of normal segments of arteries during a cold pressor test indicates there is a generalized vasoconstrictor response in large 82 coronary arteries.…”