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PubMed2004

Endothelial dysfunction and coronary artery spasm.

Coronary spasm plays an important role in the pathogenesis of not only variant angina but also coronary heart disease in general including acute coronary syndromes. The incidence of coronary spasm in Japanese patients with angina pectoris was about 40%. The total number of patients with angina pectoris increases with old age. The patients' age distribution was relatively younger in the coronary spasm than in the stable effort angina. The vascular endothelium has been reported to be a multifunctional organ whose integrity is essential to normal vascular physiology, and whose dysfunction can be a critical factor in the pathogenesis of vascular disease. Acetylcholine and methacholine cause vasodilation by endothelium-derived relaxing factor when endothelium is functioning normal, whereas they cause vasoconstriction when endothelium is removed or damaged. Coronary spasm can be induced by acetylcholine and methacholine. The patients with coronary spasm may have a disturbance in the endothelial function of the coronary arteries.

Angina Pectoris↗
PubMed1977

Cerebral perfusion, vascular spasm, and outcome in patients with ruptured intracranial aneurysms.

In a retrospective study of 44 patients with verified ruptured intracranial aneurysms, the results of radionuclide cerebral perfusion scintigraphy (dynamic brain scanning) and the presence or absence of arteriographic spasm were correlated with the clinical outcome. The data indicated that patients with normal dynamic scans had a better outcome as a group and following intracranial surgery than those in whom perfusion was reduced. Patients with normal perfusion had a higher incidence of preoperative rebleeding from their aneurysms, while patients with reduced perfusion had a higher incidence of infarction, especially after intracranial surgery. There was no correlation between the presence or absence of arteriographic spasm and the results of the dynamic scans, and nor correlation between the presence of absence of spasm and the outcome of the group as a whole. However, in some individual cases with severe spasm, reduced perfusion on the dynamic scan and a poor outcome were noted. It was concluded that the results of the dynamic scan correlated better with eventual patient outcome than the presence or absence of arteriographic spasm. It is therefore suggested that patients in Grades I and II with normal dynamic scans be operated on promptly to prevent rebleeding, and that surgery in patients in Grades I and II with abnormal dynamic scans be delayed until the dynamic scan returns to normal.

Adolescent↗
PubMed1981

Subarachnoid hemorrhage and cerebrovascular spasm. Morphological study of intracranial arteries based on animal experiments and human autopsies.

Artificial subarachnoid hemorrhage (SAH) produced by injection of autologous blood into the cisterna magna in dogs gave rise to considerable narrowing or spasm of the basilar artery and its branches, including the posterior cerebral arteries, as demonstrated by cerebral angiography. Repeated cisternal injections of blood at various intervals produced more severe spasm than a single injection. After perfusion-fixation of the brain, the cerebral arteries were examined by light and electron microscopy. None of the animals showed abnormalities in the intima or media of the vessel walls. Previously reported findings of morphological changes due to spasm could not be confirmed. Postmortem examination of brain vessels from nine patients with SAH and arterial spasm showed no specific changes that could be ascribed to spasm.

Angiography↗
PubMed1992

Posttraumatic cerebral arterial spasm: transcranial Doppler ultrasound, cerebral blood flow, and angiographic findings.

Thirty patients admitted after suffering closed head injuries, with Glasgow Coma Scale scores ranging from 3 to 15, were evaluated with transcranial Doppler ultrasound monitoring. Blood flow velocity was determined in the middle cerebral artery (MCA) and the intracranial portion of the internal carotid artery (ICA) in all patients. Because proximal flow in the extracranial ICA declines in velocity when arterial narrowing becomes hemodynamically significant, the extracranial ICA velocity was concurrently monitored in 19 patients. To assess cerebral perfusion, cerebral blood flow (CBF) measurements obtained with the intravenous 133Xe technique were completed in 16 patients. Vasospasm, designated as MCA velocity exceeding 120 cm/sec, was found in eight patients (26.7%). Severe vasospasm, defined as MCA velocity greater than 200 cm/sec, occurred in three patients, and was confirmed by angiography in all three. Subarachnoid hemorrhage (SAH) was documented by computerized tomography in five (62.5%) of the eight patients with vasospasm. All cases of severe vasospasm were associated with subarachnoid blood. The time course of vasospasm in patients with traumatic SAH was similar to that found in patients with aneurysmal SAH; in contrast, arterial spasm not associated with SAH demonstrated an uncharacteristically short duration (mean 1.25 days), suggesting that this may be a different type of spasm. A significant correlation (p less than 0.05) was identified between the lowest CBF and highest MCA velocity in patients during the period of vasospasm, indicating that arterial narrowing can lead to impaired CBF. Ischemic brain damage was found in one patient who had evidence of cerebral infarction in the territories supplied by the arteries affected by spasm. These findings demonstrate that delayed cerebral arterial spasm is a frequent complication of closed head injury and that the severity of spasm is, in some cases, comparable to that seen in aneurysmal SAH. This experience suggests that vasospasm is an important secondary posttraumatic insult that is potentially treatable.

Adolescent↗
PubMed1990

[Value of negative U waves in coronary artery spasm].

The significance of U-wave inversion during coronary arterial spasm was investigated in 188 consecutive ergometric tests performed in 69 patients. All patients had previously undergone coronary arteriography which had clearly shown coronary spasm either at rest or after a single 0.4 mg injection of ergometrine. The ergometrine tests were then performed at the patient's bedside using a standard protocol with injection of incremental doses of ergometrine: 0.05, 0.1, 0.2 and 0.4 mg every 5 minutes with 12-lead ECG recordings every minute. Fifty of the 59 patients with positive tests had classical signs of spasms: ST elevation or depression and/or T wave inversion; the other 9 patients had inversion of the U wave alone (2 cases) or associated with classical ST segment changes in the remaining cases. The 10 other patients had no ECG changes although 2 of them suffered typical anginal pain. Negative U waves were observed in 4 of the 12 patients with spasm of the left anterior descending artery, accompanied by ST elevation in the anterior wall leads. A negative U wave would appear to be a sign of less ischaemia than the classical ECG changes because anginal pain is less common: 4 out of 9 cases in which U wave inversion was a very early change, 8 out of 9 cases in which it was the first or only abnormality. The recognition of a negative U wave increases the sensitivity of the electrocardiogram during resting angina and allows earlier treatment of coronary spasm with nitrate derivatives after an ergometrine test.

Adult↗
PubMed1989

Cocaine-induced small vessel spasm in isolated rat hearts.

Cocaine abuse has been associated with pathologic cardiovascular events including acute myocardial infarction (AMI) and sudden death. Although coronary vasospasm has been proposed as a possible mechanism, the ability of cocaine to induce coronary spasm has not been conclusively demonstrated. In these studies, isolated rat hearts were perfused with cocaine (100 micrograms to 500 micrograms/ml) for 1 minute, perfusion-fixed with glutaraldehyde, and histologically assessed for evidence of coronary spasm through light and electron microscopy. Light micrographs revealed that cocaine induced spasm in coronary arterioles up to 65 microns in diameter, whereas larger caliber vessels did not constrict. Ultrastructurally, vacuolation was observed in the endothelial and smooth muscle cells of constricted arterioles. Endothelial integrity was maintained and interendothelial junctions remained intact. Morphologic evidence of constriction was supported by data obtained from Langendorff-heart preparations in which cocaine reduced myocardial flow rate under constant pressure conditions and increased aortic perfusion pressure under constant flow conditions. Spasm induced by cocaine was prevented by the calcium entry blocker nitrendipine, but not by phentolamine, an alpha-adrenergic antagonist. The finding of small vessel spasm in this study may explain the significant number of clinical cases of cocaine-associated AMI in which the main coronary arteries appear angiographically normal.

Animals↗
PubMed1987

A review of medical therapy for coronary artery spasm.

This article reviews controlled trials of medical therapy for coronary artery spasm. The calcium antagonists, either alone or in combination with long-acting nitrates, are effective therapy for patients with coronary artery spasm. These drugs definitely decrease angina and the frequency of ischemic ST shifts recorded during continuous electrocardiographic monitoring. Therapy is still relatively nonspecific, however, since the mechanism(s) that lead to spasm remain unknown. Interestingly, the initial response to therapy is similar regardless of the presence or absence of severe coronary artery disease accompanying spasm. Drugs that block adrenergic or serotonin receptors or that alter platelet aggregability or prostaglandin production have been ineffective in relieving angina or decreasing the frequency of ischemic ST shifts. Patients with resting angina syndromes are a heterogeneous group; many do not have coronary spasm since other mechanisms also precipitate ischemic episodes at rest. Prevention of angina or ischemic ST shifts may not necessarily prevent acute myocardial infarction and sudden cardiac death. Both initial and long-term therapies should be individualized according to a detailed clinical and angiographic assessments of each patient.

Adrenergic beta-Antagonists↗
PubMed1987

[Pure coronary spasm: autonomic disease or form of onset of atheroma? Contribution of repeat coronarography in 23 patients].

Coronary spasm has often been blamed for facilitating the development of atheroma, but some authors regard it as a separate disease. In order to form an opinion on these two theories, we performed repeat coronary arteriography at an interval of 4 years on average in 23 patients: 19 men and 4 women aged from 38 to 62 years (mean: 49,4 years). At the initial examination the coronary vessels were normal in 11 patients and showed irregular arterial walls without significant stenosis in 12 patients. Coronary spasm was demonstrated directly in 17 cases (6 spontaneous spasms during arteriography and 11 induced spasms) and indirectly in 6 cases (ECG signs of ischaemia during the anginal attack). At the second coronary arteriography we found that the spasms persisted, with positive response to a challenge test in 17 out of the 19 patients tested. The challenge test was not performed in 4 patients who had developed significant lesions. The vessels themselves were altered in 6 patients, with images of occlusion (2 cases), stenosis (2 cases), parietal irregularities (1 case) and aneurysm (1 case) appearing on spastic arteries, and images of stenosis in 2 patients with apparently non-spastic arteries. There was no difference in age, sex, risk factors, initial coronary status and time interval between arteriographies between these 6 patients and the 17 patients whose coronary arteries had remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

The diagnosis of coronary artery spasm in the cardiac catheterization laboratory.

Coronary artery spasm can now be well documented in the cardiac catheterization laboratory. At present, reliable criteria are available for the diagnosis of severe episodes that are characteristic of patients with Prinzmetal's variant angina. Newer criteria for the diagnosis of milder episodes of spasm are gradually being developed. Optimal criteria may become available with further progress of quantitative angiography. Provocation techniques for the induction of an attack of spasm in the cardiac catheterization laboratory are widely available. Of these, ergonovine testing is the most popular. The tests can usually be performed by experienced angiographers with impressive safety and provide a high degree of sensitivity and specificity when used in patients with the clinical diagnosis of variant angina. Although the research applications of such techniques are extremely broad, their practical clinical indications are somewhat limited to the work-up of patients with infrequent chest pains and normal or near-normal coronary arteriograms. There are other indirect methods for the diagnosis of coronary spasm, but the ideal technique is not available yet. Further expansion of newer modalities for the diagnosis of coronary artery spasm will certainly enhance our understanding of myocardial ischemia and will improve our ability to manage patients with ischemic heart disease.

Angina Pectoris, Variant↗
PubMed1984

[Rest and exercise angina caused by spasm of the left coronary artery. Apropos of a case with angiographically normal coronary arteries].

A 42 year old woman presented with resting and effort angina. During an attack of chest pain, ST-T wave depression was recorded in the anterior chest leads. Coronary angiography showed spontaneous spasm of the left main stem, relieved by nitrate derivatives. The coronary arteries were angiographically normal between attacks of angina. Thallium 201 myocardial scintigraphy showed anterior wall hypofixation at maximal effort. A good therapeutic result was obtained with calcium antagonists. The site of coronary spasm is the special feature of this case, which may be grouped with other rare reported cases of spontaneous spasm or spasm on effort. We confirm that spasm-induced myocardial ischaemia may cause ST depression on the surface ECG.

Adult↗
PubMed1983

Calcium channel blockers for the treatment of coronary artery spasm: rationale, effects, and nursing responsibilities.

Coronary artery spasm is recognized as a cause of ischemic heart disease, producing a syndrome of the variant form of angina that occurs at rest. Spasm also may play a role in other types of rest angina (unstable angina) and exertional angina. Calcium is essential for the basic tonus of vascular smooth muscle. The accentuated contraction that occurs in coronary artery spasm is the result of an increase in intracellular calcium ions. Current therapy is aimed at blocking the slow calcium currents that are responsible for electrical activation and contraction of smooth muscle cells. A marked coronary vasodilatation is produced with calcium channel blockers, thus demonstrating effective therapy for coronary artery spasm. A similar effect is achieved by nitrates, and these agents will continue to have a role in the therapy of spasm. Calcium channel blockers produce beneficial effects on myocardial oxygen supply and demand and, therefore, are also useful in the prevention of classic exertional angina caused by fixed obstruction. Verapamil and diltiazem possess electrophysiologic effects and have, in addition, proved useful in the treatment of supraventricular dysrhythmias.

Calcium↗
PubMed1982

Coronary arterial spasm.

Coronary arterial spasm has been postulated to be a cause of myocardial ischemia for over 100 years. It was not until the work of Prinzmetal et al in 1959, however, that major clinical attention and research began to be addressed to the role of vasospasm in the manifestations of ischemic heart disease. It is now known that spasm may be clinically important in patients with significant underlying atherosclerotic coronary artery disease as well as in patients with anatomically normal or subcritically stenosed coronary vessels. Research has suggested that spasm may be associated with symptoms of stable resting and/or exertional angina pectoris and that it almost certainly plays a role in the pathogenesis of unstable angina pectoris and acute myocardial infarction. Symptomatic arrhythmias, including sinus bradycardia, heart block, and ventricular tachyarrhythmias, have been documented to complicate coronary vasospasm. Given the potential importance of coronary arterial spasm in so many different ischemic heart disease syndromes, the development of therapeutic agents that may prevent spasm has obvious clinical importance.

Adult↗
PubMed1981

Coronary artery spasm: recognition and treatment.

Coronary artery spasm may produce angina, major arrhythmias, syncope, myocardial infarction, and death in patients with normal or nearly normal coronary arteriograms. The clinical picture in patients with symptomatic coronary artery spasm is characterized by: (1) predominant angina at rest, with little or no exertional angina; (2) changes of myocardial ischemia, especially ST segment elevation, on the electrocardiogram during pain: and (3) major arrhythmias and syncope during angina. A complete electrocardiogram during pain, or at least a Holter monitor recording, is important in establishing a diagnosis. The ergonovine maleate provocative test is a reliable method of establishing the diagnosis, but it is associated with some risks. Calcium flux antagonists are more effective than nitrates or beta blockers in the treatment of coronary spasm. Coronary bypass surgery is generally ineffective in the treatment of coronary spasm unless the spasm is superimposed on a fixed severe coronary obstruction.

Arrhythmias, Cardiac↗
PubMed1981

The role of coronary arterial spasm in ischemic heart disease.

With the arteriographic demonstration of coronary arterial spasm, fundamental questions have been raised concerning the role of spasm in myocardial ischemia and infarction. It is now clear that coronary arterial spasm is the cause of Prinzmetal's variant angina pectoris in patients with and without coronary atherosclerosis. In most patients with coronary heart disease, major ischemic events frequently result from increased myocardial oxygen demand or coronary thrombosis. However, recent evidence suggests that coronary arterial spasm may initiate or contribute to the development of unstable angina pectoris, acute myocardial infarction, and sudden death in these patients. Thus, episodes of myocardial ischemia and infarction are induced by factors, acting singly or in combination, that augment myocardial oxygen demand or diminish myocardial oxygen supply, and the latter alteration can result from thrombotic coronary occlusion or a dynamic increase in coronary arterial tone (that is, coronary arterial spasm).

Angina Pectoris↗
PubMed1982

Coronary artery spasm with sinus node dysfunction and syncope.

In a 55-year-old man, attacks of spontaneous angina were associated with dizziness and syncope. Holter ECG monitoring disclosed evidence of sinus node dysfunction. Dizziness and syncope were corrected by a permanent ventricular demand pacemaker. Coronary cineangiography showed spontaneous, severe, diffuse spasm in a dominant left coronary artery and localized spasm in a nondominant right coronary artery. The patient died of pump failure shortly after cardiac catheterization. An autopsy disclosed only minimal coronary atherosclerosis. This patient's condition shows that (1) coronary spasm may cause sinus node dysfunction, dizziness, and syncope, (2) severe spasm that involves all the coronary artery branches may be fatal, and (3) severe spasm occur in minimally diseased coronary arteries confirmed by pathologic examination.

Arrhythmia, Sinus↗
PubMed1982

[Spasm of the coronary arteries].

Spontaneous spasm and methylergometrine maleate-provoked spasm are defined, the latter being observed in nearly all cases of so-called Prinzmetal angina, in approximately one out of three cases of angina at rest, and a certain number of cases of unstable angina: it has even been demonstrated during effort tests with coronarography. Several studies have demonstrated its possible implication in myocardial infarction. Continuous electrocardiogram recordings and isotopic studies have also shown the frequency of silent spasms, or those associated with other ECG modifications than an increased STT latency period. It is now well-established that this type of angina is provoked by reduction in myocardial oxygen supply. To explain the triggering mechanism of the spasm, various factors have been successively evoked: alpha- and beta-receptor disequilibrium, a vagal effect, the very important role played by thromboxane A2 of platelet origin. Emphasis is also placed on circadian variations observed during the spasm, but the course of spastic angina is often unpredictable, leading to necrosis or sudden death in a fairly large number of cases. Medical treatment is essentially by long-acting nitrate derivatives and calcium inhibitors (beta-blockers are considered, according to different teams, as being useless or even dangerous). Surgical treatment may be by aortocoronary shunt or transluminal angioplasty in cases that are stable with trinitrate compounds; associated plexectomy has given good results according to teams in Lille; while heart transplantation has been performed in rare cases. Choice of therapy is difficult in cases with apparently non-surgical moderate stenosis and recurrent spastic angina.

Angina Pectoris, Variant↗
PubMed1982

[Spasm of the cranio-cerebral vascular system].

A definition of spasm of the cranio-encephalic vascular system is followed by a study of problems of angiographic diagnosis. The main differential diagnosis are illustrated. A review of the regulation of the cerebral circulation is followed by a summary of the physiopathology of spasm. The importance of spasm in cerebral vascular pathology is discussed, whether manifestations of ischaemia, hypertensive encephalopathy or subarachnoid haemorrhage. The relations between spasm and trauma are then described, together with the metabolic and pharmacodynamic aetiologies. The study ends with a review of the principal methods for the prevention of spasm during general anaesthesia.

Cerebral Angiography↗
PubMed1995

Association of lipoprotein levels with atherosclerotic changes in patients with coronary artery spasm and insignificant coronary artery stenosis.

BACKGROUND: Coronary artery spasm readily occurs at sites of atheromatous plaque. Some lipid profiles are related to the genesis of coronary artery spasm. In Korean patients, it is frequently observed in grossly normal coronary arteries, in contrast to the situation in western patients, who frequently have coronary artery spasm superimposed on significant coronary artery stenosis. Intravascular ultrasound examination has shown that mild or diffuse atherosclerotic changes in patients with focal vasospasm, even in the absence of angiographic coronary disease. OBJECTIVES: We studied prospectively 104 patients in order to find out which lipid profiles were associated with atherosclerotic changes in patients with coronary artery spasm. METHODS: Patients were grouped as follows: group I, control, 50 patients (34 men, 16 women); group II, 35 patients (26 men, 9 women) with significant coronary artery disease; group III, 19 patients (13 men, six women) with significant coronary artery spasm and either no coronary artery stenosis or insignificant stenosis. There was no significant difference in age (group I 55 +/- 1 years, group II 56 +/- 2 years, group III 54 +/- 2 years) or sex among the groups. The following parameters were evaluated: hypertension, cigarette smoking, diabetes mellitus, and lipid profile. RESULTS: The incidence of hypertension in group II patients was higher than in group I or III (P < 0.05). No significant difference was found in the percentage of cigarette smokers and patients with diabetes mellitus among three groups. The lipid profiles of each group were analysed. Group II patients had higher lipoprotein (a) levels (39 +/- 6 mg/dl) than those in group I (21 +/- 3 mg/dl) or group III (13 +/- 3 mg/dl) (P < 0.05). Other lipid profiles were not significantly different among the groups. CONCLUSION: Our results indicate that the atherosclerotic changes in the coronary arteries of group III patients were not associated with lipid profiles, including lipoprotein (a).

Constriction, Pathologic↗