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At least 1,603 records · Page 89Linked to original sources
PubMed1982

Intracoronary nitroglycerin reversal of life-threatening ergonovine maleate-induced coronary artery spasm.

Ergonovine maleate was given to a patient suspected as a case of Prinzmetal's variant angina following demonstration of normal coronary arteries by angiography. Profound shock, heart block, and severe pain accompanied marked spasm of the left coronary artery. Direct infusion of nitroglycerin into the left coronary artery reversed the spasm when sublingual and intraaortic nitroglycerin failed to prevent further hemodynamic and clinical deterioration.

Angina Pectoris, Variant↗
PubMed1984

Mitral valve prolapse and spasm of normal coronary arteries: report of four cases and review of the literature.

The association between mitral valve prolapse (MVP) and atypical chest pain has been well-described. Numerous theories have been proposed to explain this association. A number of lines of evidence suggest that underlying ischemia may cause chest pain in some patients with MVP. We have recently evaluated 4 patients with chest pain syndromes who had angiographic evidence of MVP and spasm of angiographically normal coronary arteries. The possibility that coronary spasm is the underlying etiology of chest pain in some patients with mitral valve prolapse raises a theoretical argument against beta-blockade in these patients. Three of our patients were successfully treated with calcium channel blockers.

Adult↗
PubMed1988

The interdependence of hypertension, calcium overload, and coronary spasm in the development of myocardial infarction.

It is a well-known fact that systemic hypertension is one of the major risk factors for myocardial infarction (MI). Extensive studies on hypertensive rats revealed that calcium is excessively elevated in the myocytes, as well as in the coronary artery wall of these animals, which results in a higher resting tension and a stronger contractile response of those muscle strips. Over many years coronary spasm has been claimed by various authors to be greatly involved in the pathophysiology of early phase of acute MI (AMI). It can be shown that thrombocytes that aggregate at the injured vessel wall next to atherosclerotic plaques release vasoconstrictive factors that induce series of severe spasms at the sites with defective endothelium that end up in myocardial infarction; the pathophysiologic pathway is called the thrombo-ischemic reentry mechanism. This local contractile response may be enhanced in the presence of systemic hypertension since intracellular calcium is elevated in the coronary smooth muscle. On the other hand, it has been shown that heart muscle fibers undergo severe alterations finally resulting in necrotization, as soon as free calcium ions penetrate excessively through the sarcolemma membrane into the myoplasm so that the capacities of the calcium binding or extrusion processes become overpowered; this is especially the case during ischemia. Since free intracellular calcium is already ten times elevated in the myocytes in systemic hypertension, the myocardium may be more vulnerable to further calcium overload owing to the ischemia and necrotization is augmented. The elevation of intracellular Ca of the myocytes of the cardiovascular system in systemic hypertension enhances the pathologic response of the coronary arteries and the myocardium. This work gives a complete overview of the pathophysiologic principles involved in AMI occurring with systemic hypertension.

Animals↗
PubMed1996

Guide wire-induced coronary artery spasm during percutaneous transluminal coronary angioplasty. A case report.

Coronary artery spasm induced by a guide wire is a very rare complication of percutaneous transluminal coronary angioplasty (PTCA). The authors describe a patient who developed coronary vasoconstriction distal to the dilated lesion during PTCA, which was refractory to intracoronary nitroglycerin and intravenous calcium antagonist injection and balloon angioplasty but responded promptly and completely to withdrawal of the guide wire from the coronary artery, suggesting that the spasm had been induced by the guide wire.

Aged↗
PubMed1995

Microvascular decompression by the retrosigmoid approach for idiopathic hemifacial spasm: experience with 300 cases.

Three hundred patients with idiopathic hemifacial spasm who underwent microvascular decompression through the retrosigmoid approach are reported. Vascular compression was found in every patient on operation. The results of 1 to 6 years of follow-up show that 276 patients are free of the symptom, 4 patients have markedly diminished spasms and a decreased episode rate, 10 patients have no significant relief from the operation, and 9 have had recurrences of the symptom since the operation. The cure rate in this group is 92%. Complications were sensorineural hearing loss in 13 patients (7 temporary cases, 6 permanent), tinnitus in 7 (4 temporary cases, 3 permanent), temporary postoperative facial weakness in 16, and postoperative meningitis in 10 (9 cases were controlled with antibiotics and 1 patient died).

Adult↗
PubMed2006

Vasodilator resistant lethal spasm after uncomplicated off-pump coronary surgery.

We report a case of lethal spasm of non-grafted coronary arteries after an uncomplicated off-pump coronary artery bypass grafting in a patient with no predisposing factors other than smoking. Transcatheter intraluminal injection of several vasodilators failed to relieve the spasm. The patient remained in profound cardiogenic shock due to broad acute myocardial infarction and died of multiple organ failure.

Aged↗
PubMed1980

Attempted prevention or treatment of intracranial arterial spasm: a survey.

Published accounts of attempts at prevention or treatment of intracranial arterial spasm have been reviewed. These data are summarized in a table according to the agent tested, the dosage used, the route of administration, and the animal species used. Precautions are given concerning the organization and assessment of such studies. The best current management of patients with cerebral vasospasm involves promoting cerebral perfusion and avoiding detrimental factors. It may be possible in the future to identify those patients at risk of developing cerebral vasospasm, perhaps by assessing the location and amount of subarachnoid blood by computerized tomography. This would aid the development of measures to prevent intracranial arterial spasm, which seems to be a more promising approach to the problem than is treatment.

Animals↗
PubMed1981

Microsurgical treatment of intractable hemifacial spasm.

Ten patients with intractable hemifacial spasm were treated by posterior fossa exploration and microsurgical technique. These patients have been followed 1 to 5 years. The spasmodic motor disorder was related to compression of the 7th nerve or its exit zone at the brain stem by a dolichoectatic anterior inferior cerebellar artery in eight patients and to kinking and ectasia of the basilar or vertebral artery in two patients. In five patients, there were prominent arachnoidal adhesions in the cerebellopontine angle, and an arachnoid cyst was a component of the lesion in another patient. Additional conditions associated with hemifacial spasm included geniculate neuralgia, facial paresis, vertigo, hearing loss, and trigeminal neuralgia. The surgical morbidity and postoperative results are discussed.

Adult↗
PubMed2006

Stent deformity caused by coronary artery spasm.

Previous studies have shown that coronary stents have radial strength above the pressure induced by coronary artery spasm. This case report describes a stent deformity caused by coronary artery spasm during percutaneous coronary intervention.

Angioplasty, Balloon, Coronary↗
PubMed1983

Arteriographic features of angina pectoris associated with ST segment depression during coronary arterial spasm.

To examine the angiographic features of vasospastic angina associated with ST segment depression, we attempted to analyze the coronary arteriograms of 12 patients who exhibited ST segment depression during the ergonovine provocative test. Right and left coronary arteriograms were obtained successively within a short period when the ergonovine administration revealed ST segment depression. Eight out of 12 patients showed non-total spastic obstructions in one of the major coronary arteries. Among them, a collateral augmentation was found only in one patient. Two cases exhibited the well-developed collateral channels during non-anginal periods and in one case a collateral blood supply was reduced by the spasm occurred in the donating artery. In another one, the collateral circulation did not change during anginal period. Three out of 4 patients who showed total spastic obstructions demonstrated transiently augmented collateral circulation which was supplied by the non-spastic artery. These findings may indicate that ST segment depression during coronary artery spasm could attribute to a subendocardial ischemia caused by an incomplete occlusion of large coronary artery and transient reduction or augmentation of collateral blood flow.

Adult↗
PubMed1985

Coronary spasm, prostaglandin and HLA factors.

To elucidate the contribution of prostanoids in coronary spasm, plasma levels of thromboxane B2 (TXB2) and 6-keto PGF1 alpha at the coronary sinus and ascending aorta in 21 patients with variant angina were measured, as compared with findings in 20 with effort angina and 13 subjects with normal coronaries. In the coronary sinus blood, plasma TXB2 in patients with effort angina exhibited statistically significant high levels, as compared with data in the controls. On the contrary, the data obtained from patients with variant angina were not statistically significant. However, eight patients whose coronary angiogram revealed more than 50% of coronary stenoses had statistically significant high levels of TXB2 and other patients with normal coronaries or less than 50% of narrowing showed almost the same levels of TXB2 as the controls. In contrast to TXB2, the plasma levels of 6-keto PGF1 alpha in patients with variant angina were very low in both groups with variant angina. These data suggest that high levels of TXB2 observed in patients with atherosclerotic coronaries may be an accelerating factor while low levels of prostacyclin may be an essential factor leading to spasm. HLA analysis of 23 patients with variant angina was performed to search for genetic factors, under the hypothesis that such may contribute to the low levels in prostacyclin. This preliminary study revealed statistically significant high frequencies of Bw52 and B-40 in the patients, as compared with frequencies among 152 normal Japanese. Genetic studies are ongoing in our clinic.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Clinical characteristics and possible role of coronary artery spasm in syncope and/or aborted sudden death.

We investigated the clinical and pathophysiologic characteristics in patients with vasospastic angina who developed syncope and/or experienced aborted sudden death (SD). Vasospastic angina was diagnosed using the methylergonovine test. Syncope was found in 32 (10.4%) patients among 309 who were admitted to our institute in a one-year period. The most frequent cause of syncope was ventricular tachycardia which was found in 10 (31.2%) of the 32 patients. The next important cause of syncope was vasospastic angina which was found in 7 patients (21.8%). Among the 7 patients with vasospastic angina who experienced one or more syncopal episodes, there were 3 patients with aborted SD, 3 with syncope and one with shock. Cardiovascular collapse was observed in 4. Interior wall ischemia was found in 5 and anterior wall ischemia in 2 during the methylergonovine test. None of the 7 patients had significant coronary stenosis. Two patients had no prodromal symptom such as chest pain. Our results suggest that coronary artery spasm may be one of the most frequent cardiovascular diseases that causes syncope which is not always accompanied by a prodromal symptom. Therefore, coronary spasm should be distinguished in patients with unexplained syncope or aborted SD.

Coronary Angiography↗
PubMed1998

Left coronary artery-left ventricle fistula with right coronary artery spasm.

A 72-year-old woman was admitted to our hospital for evaluation of chest pain. Coronary angiography showed a left coronary artery-left ventricle fistula. An acetylcholine provocation test induced vasoconstriction of the right but not the left coronary artery. Her chest pain was not relieved by combined therapy with isosorbide dinitrate, diltiazem and nicorandil. Because of the coronary spasm, beta-blockers could not be used. However, her chest pain was relieved after the administration of a minor tranquilizer. Thus, the patient's chest pain was unlikely to be associated with either the fistula or the coronary spasm.

Acetylcholine↗
PubMed1999

Coronary spasm and cardiac arrest from carcinoid crisis during laser bronchoscopy.

Bronchoscopic manipulation of an endobronchial carcinoid can precipitate a carcinoid crisis. Coronary artery spasm is an uncommon manifestation of carcinoid crisis, and has never been reported as a complication of flexible bronchoscopy. We report a case of a 10-year-old girl who developed coronary artery spasm and cardiac arrest during neodymiumyttrium aluminum garnet (Nd-YAG) laser photoresection of an endobronchial carcinoid. Recognition of this unusual presentation of a carcinoid crisis is important as the treatment approach differs from standard resuscitation protocols.

Bronchial Neoplasms↗
PubMed1984

Coronary artery spasm--1984.

Coronary artery spasm was virtually unknown not long ago, but the intense, ongoing interest it has generated in the past decade has produced a number of specific diagnostic techniques and therapeutic approaches, as well as considerable insight into mechanisms of coronary vascular tone and various coronary syndromes. There is growing evidence that coronary artery spasm is involved in unstable angina, stable angina, myocardial infarction, and sudden death. It is by no means a benign process and is associated with significant morbidity or mortality if misdiagnosed or untreated. It seems clear that what started as a mere clinical curiosity involving a minority of patients with the so-called Prinzmetal's variant angina is snowballing into a major arena for research, diagnosis, and treatment in the field of ischemic coronary artery disease.

Arrhythmias, Cardiac↗
PubMed1987

Diffuse triple-vessel coronary artery spasm complicated by idioventricular rhythm and syncope.

A 70-year-old man presented with diffuse triple-vessel coronary arterial spasm accompanied by ST segment elevation in the inferior and anterior leads when the severity of pain moderated. At the beginning, he noted throat and chest pain followed by syncope. Atropine, norepinephrine, and lidocaine were administered therapeutically. The initial electrocardiogram showed an idioventricular rhythm without ST segment deviations, which made the prompt diagnosis of coronary arterial spasm difficult.

Aged↗