|
| CASE REPORT |
|
| Year : 2009 | Volume
: 10
| Issue : 2 | Page : 70-73 |
 |
|
Multivessel coronary vasospasm in a young patient with acute coronary syndrome
Panduranga Prashanth, Abdullah Amour Riyami, Mohammed Mukhaini, Said Abdurrahman
Department of Cardiology, Royal hospital, Muscat, Oman
| Date of Web Publication | 17-Jun-2010 |
Correspondence Address:
Panduranga Prashanth
Department of Cardiology, Royal hospital, PB 1331, Muscat-111
Oman
 Source of Support: None, Conflict of Interest: None  | Check |
How to cite this article:
Prashanth P, Riyami AA, Mukhaini M, Abdurrahman S. Multivessel coronary vasospasm in a young patient with acute coronary syndrome. Heart Views 2009;10:70-3 |
How to cite this URL:
Prashanth P, Riyami AA, Mukhaini M, Abdurrahman S. Multivessel coronary vasospasm in a young patient with acute coronary syndrome. Heart Views [serial online] 2009 [cited 2023 Jun 7];10:70-3. Available from: https://www.heartviews.org/text.asp?2009/10/2/70/63750 |
 Introduction | |  |
Coronary vasospasm (variant angina) is a transient abnormal contraction of an epicardial coronary artery that results in myocardial ischemia. Vasospasm frequently occurs at the site of coronary atheroma, implicating endothelial dysfunction in the pathogenesis of this phenomenon. In patients without coronary stenosis abnormalities of nitric oxide synthase and reduced bioavailability of nitric oxide has been implicated.
Definitive diagnosis is made after angiographic evidence of coronary vasoconstriction that reverses with the administration of intravenous or intra-arterial nitroglycerin. Medical therapy involves the use of high-dose calcium channel blockers and/or nitrates.
Long-term prognosis of treated patients is excellent but is dependent on the severity of vasospastic episodes and the degree of underlying coronary artery disease and left ventricular dysfunction.
We reported a case of severe vasospasm that localized to the mid left anterior descending artery and ostial obtuse marginal but with diffuse right coronary artery involvement and which was successfully treated with vasodilators. The pathophysiology, diagnosis and management of coronary vasospasm are also reviewed.
| Case report | | |
A 23-year-old Omani female with a history of asthma and no cardiac risk factors presented to a local hospital with severe retrosternal chest pain waking her from sleep in the early morning hours. Electrocardiogram (ECG) done at that time showed normal sinus rhythm with 1-2mm ST elevation in II, III, AVF with ST depression of 2-4 mm in V1 to V4, AVL. She was given sublingual Nitroglycerin (NTG) with repeat ECG showing normalization of ST changes. She was diagnosed as acute coronary syndrome and treated with aspirin, oral nitrates, and enoxaparin. On the same day of admission she developed severe chest pain at rest with transient hypotension and the ECG showed 5-6 mm ST elevation in II, III, AVF, V4-6 with 5-10 mm ST depression in V1-V3, I, AVL [Figure 1], which normalized after sublingual nitrates [Figure 1]a. She was referred to our centre for coronary angiography.
Cardiovascular examination was normal. Blood chemistry was normal including cholesterol levels except for Troponin I, which was elevated at 8 ng/ml (normal < 0.04 ng/ml). Echocardiogram was normal. Her coronary angiogram showed tight focal spasm of ostial obtuse marginal artery (OM) and mid left anterior descending artery (LAD) [Figure 2] and spasm of the right coronary artery (RCA) [Figure 3]. There was no organic coronary stenosis. After 50 micgm of nitroglycerin intracoronary injection there was immediate relief of spasm with return of coronary diameter to normal size [Figure 2]a and [Figure 3]a. She had 3 more episodes of rest anginal pains with ST changes and finally settled on high doses of nitrates and diltiazem.
| Discussion | | |
In 1959, Prinzmetal et al. [1] first described a syndrome of chest pain at rest secondary to myocardial ischemia with ST-segment elevation. This syndrome, known as Prinzmetal or variant angina, is due to focal coronary artery vasospasm and may be associated with acute myocardial infarction, serious ventricular arrhythmias, and sudden death. Variant angina is defined by the angiographic demonstration of spontaneous or induced coronary spasm in patients with rest pain. A Japanese variant of variant angina (termed vasospastic angina) may constitute a more diffuse disorder of large vessel vasomotor reactivity. In the United States estimates are that 2-3% of all patients undergoing diagnostic cardiac catheterization for chest pain will subsequently be classified as having variant angina.
Variant angina is characterized by a pressure-like, squeezing retrosternal chest discomfort associated with transient ST-segment elevation or depression which resolve spontaneously or with administration of nitroglycerin. Episodes usually occur at night or early morning hours and tend to occur in young females.
Variant angina is caused by focal coronary artery vasospasm, and a generalized abnormality of coronary artery vasomotor reactivity is not present. Focal coronary artery spasm typically occurs at the site of or adjacent (within 1cm) to a fixed atheromatous stenosis, implicating endothelial dysfunction in the pathogenesis of this phenomenon Elevated serum low-density lipoprotein cholesterol, especially the oxidized form of this lipid moiety, is responsible for the decreased production of nitric oxide due to down-regulation of endogenous nitric oxide synthase and the oxidative inactivation of nitric oxide by oxygen free radicals. A substantial number of patients have normal coronary angiogram results, in whom abnormalities of nitric oxide synthase and reduced bioavailability of nitric oxide has been implicated [2] . This may result in increased basal vascular tone, vasoconstriction, vasospasm, and in activation, adhesion, and aggregation of platelets with release of additional vasoconstrictors. Nakayama et al. [3] found mutations in the eNOS (endothelial nitric oxide synthase) gene in 30% of Japanese patients with coronary spasm, which regulates the production of nitric oxide. The second most predictive risk factor was cigarette smoking. Other associations with coronary vasospasm have included hyperinsulinemia, magnesium deficiency, carcinoid crisis, pseudoephedrine, anticholinesterase medications, vitamin E and estrogen deficiency. In rare cases it appears to be a manifestation of generalized vasospastic disorder along with migraine headache and Raynaud phenomenon; it has also been reported with aspirin-induced asthma [2] .
Coronary angiography is the criterion standard for the diagnosis of variant angina. Focal spasm of the proximal portion of a major coronary artery not preceded by an increase in heart rate or blood pressure that is followed by chest pain, ST-segment elevation, and ventricular dysfunction is pathognomonic [2] . Definitive diagnosis is made after angiographic evidence of coronary vasoconstriction that reverses with the administration of intravenous or intra-arterial nitroglycerin. Right coronary artery is commonly involved followed by left anterior descending artery. Some have migratory spasm involving different sites on two different occasions as in our patient. It is also interesting to note that in our patient there were both focal spasms (OM/LAD) as well as diffuse vasospastic element (RCA).
If minimal or no angiographic evidence of coronary artery disease is found in a patient who has recently had angina at rest with transient ST-segment elevation, variant angina is the likely diagnosis, and further testing is unnecessary. In some patients, it may be necessary to perform provocative testing to induce coronary artery spasm. Of the provocative test agents shown to induce coronary artery spasm in susceptible patients, ergonovine maleate, methylergonovine maleate, acetylcholine, or hyperventilation are the most useful but rarely done in catheterization labs presently.
Variant angina, which is associated with ventricular dysrhythmia and sudden cardiac death, may be detected during inpatient telemetry observation or ambulatory Holter monitoring along with ST-segment changes. Approximately 25-50% of hospitalized patients with variant angina have been reported to have ventricular ectopy during spontaneous coronary spasm including ventricular tachycardia or fibrillation, high-grade atrioventricular block and sinus arrest.
Exercise tolerance testing is controversial and of questionable utility. The results of exercise testing in patients with variant angina therefore are highly variable, and approximately equal numbers of patients show ST-segment depression, elevation, or no change during exercise testing. Thallium scintigraphy has been used to localize the myocardial perfusion defect to an area perfused by a coronary artery in which spasm can be demonstrated by angiography.
Medical therapy initially should include intravenous or sublingual nitroglycerin and an oral calcium channel antagonist. Long-acting oral nitrates are appropriate for the prevention of recurrent episodes and may be used in combination with the calcium channel antagonist for long-term prophylaxis. If the patient does not respond to one calcium-channel blocker, switching to a different agent has been recommended. If effective, calcium antagonists should not be discontinued, particularly in those patients with episode of angina-linked cardiac arrest, recurrent attacks or multivessel coronary spasm. However, if the patient does not have a recurrence after 12 months, drug therapy can be withdrawn, provided there was no history of cardiac arrest. Approximately 20% of coronary spasm patients will not respond to treatment with two calcium-channel blockers plus a long-acting nitrate. Prazosin and nicorandil are useful. Recently, intravenous magnesium has been shown to suppress acetylcholine-induced coronary spasm in patients with vasospastic angina [4] . Beta-adrenergic blockers should be avoided in coronary vasospasm because of their propensity to increase the frequency and duration of attacks. Treatment of ventricular arrhythmias that accompany attacks should be aimed at treating the coronary spasm. Angioplasty/stenting and bypass grafting are useful in patient with variant angina and discrete, proximal fixed obstructive lesions.
Many patients pass through an acute, active phase, with frequent episodes of angina and cardiac events during the first 3-6 months after diagnosis. In a large series of 277 patients with a median follow-up of 7.5 years, recurrent angina occurred in 39% of patients but cardiac death and myocardial infarction was relatively low at 3.6 and 6.5 percent of patients respectively [5] . The long- term survival at 5 years is excellent (89 to 97 percent). Factors found to adversely affect long-term prognosis in variant angina include extent and severity of coronary artery disease, ST-segment elevation in both anterior and inferior leads without myocardial infarction and left ventricular dysfunction.
In conclusion, coronary vasospasm has to be suspected in young patients without any coronary risk factors who present with acute coronary syndrome and have to be investigated with coronary angiography and treated with vasodilators.
| References | | |
| 1. | Prinzmetal M, Kennamar R, Merliss R. A variant form of angina pectoris. Am J Med 1959; 27:375-388.  |
| 2. | Gersh BJ, Braunwald E, Bonow RO: Chronic Coronary Artery Disease, Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Disease, 6th ed. Philadelphia, WB Saunders; 2001: 1324-1328. |
| 3. | Nakayama M, Yasue H, Yoshimura M.T-786 C mutation in the 5th-flanking region of the endothelial nitric oxide synthase gene is associated with coronary spasm. Circulation 1999; 99:2864-2870. |
| 4. | Teragawa H, Kato M, Yamagata T, Matsuura H, Kajiyama G. The preventive effect of magnesium on coronary spasm in patients with vasospastic angina. Chest 2000; 118:1690-1695. |
| 5. | Bory M, Pierron F, Panagides D, Bonnet JL, Yvorra S, Desfossez L. Coronary artery spasm in patients with normal or near normal coronary arteries. Long-term follow-up of 277 patient's. Eur Heart J 1996; 17:1015-1021. |
[Figure 1], [Figure 2], [Figure 3]
|
