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Platelet activation during provocation of coronary artery spasm by ergonovine and cold pressor testing in patients with angina pectoris.

The role of coronary spasm in variant angina is well established. We have studied the time course of platelet activation during Ergonivine provocation to determine one significance of platelet indices for spasm testing. The results showed that spontaneous platelet aggregates and beta-thromboglobulin levels in patients with coronary vasospasm were increased during provocation and that platelet activation during a positive Ergonivine test precede ECG changes and chest pain.

Adenosine Diphosphate↗

Cerebral arterial spasm after subarachnoid hemorrhage. A case report with SPECT and iodine-123 HIPDM.

Cerebral arterial spasm following subarachnoid hemorrhage can be responsible for secondary neurological deficits and can influence history, prognosis, and results of surgical treatment. The demonstration of vasospasm can be important for therapy. The use of I-123 HIPDM and SPECT in evaluating regional cerebral blood flow showed the effects on cerebral perfusion of diffuse arterial spasm in a case of subarachnoid hemorrhage and its recovery. There was a parallel with clinical neurological status.

Female↗

Increased sarcolemmal permeability in the cerebral artery during chronic spasm: an assessment using DNA-binding dyes and detection of apoptosis.

Alteration of sarcolemmal permeability was evaluated in the cerebral artery after subarachnoid hemorrhage. Significance of membrane dysfunction in the pathogenesis of chronic spasm and contribution of apoptosis were investigated in a canine model. Permeability of the smooth muscle cell (SMC) membrane was assessed by double staining with a hydrophilic (ethidium bromide [EB]) and a lipophilic (Hoechst 33342) DNA-binding dye. Quantitative observations were made with a ultraviolet-fluorescence microscope and a ultraviolet-laser confocal microscope. Occurrence of apoptosis was studied using electrophoresis and TUNEL method. In the normal arteries, nuclei of SMC were stained with Hoechst 33342 but not with EB. In the spastic arteries, SMC in the inner layer of the tunica media were stained with EB. The incidence of EB-positive cells reached maximum on day 7 (45 +/- 19%) and decreased in 2 to 4 weeks (13 +/- 5.2% and 5.0 +/- 2.1%, respectively), in parallel with amelioration of spasm. Electron and light microscopic observations revealed increased density of SMC cytoplasm with widening of the extracellular space. Necrosis was not evident. Apoptosis was not detected by the two methods. These results demonstrate that an augmentation in sarcolemmal permeability takes place during the course of chronic vasospasm and suggest its close correlation to pathogenesis.

Animals↗

Prevention of coronary spasm by nicorandil: comparison with nifedipine.

The efficacy of nicorandil was compared with that of nifedipine in 13 patients with vasospastic angina enrolled in a randomized, placebo-controlled, crossover study. All patients had a coronary spasm during coronary arteriography, either spontaneously or ergometrine-induced. During two consecutive periods of 2 days, patients received active drugs or placebo in a randomized order. Each patient received single oral doses of 30 mg nicorandil, 10 mg nifedipine, and, on 2 days, a placebo. One hour after drug intake, patients underwent an ergometrine test with increasing doses of Methergin (ergometrine) (0.05, 0.10, 0.20, and 0.40 mg every 5 min). After placebo, the tests always were positive, and the ECG changes occurred at the same +/- 1 dose of ergometrine in 10 cases, showing good reproducibility. After nicorandil, the tests were negative in nine patients and positive for a higher or lower dose of ergometrine in three and one patient, respectively (p = 0.0034 vs. placebo). After nifedipine, the tests were negative in five patients and positive for a higher or the same dose of ergometrine in four and four patients, respectively (p = 0.0039 vs. placebo). Nifedipine (10 mg) and nicorandil (30 mg) were equally effective in eight patients; in the remaining five patients, nicorandil had better results (p = 0.06). Nicorandil (30 mg) prevents ergometrine-induced coronary spasm. This compound may be beneficial in patients with vasospastic angina.

Administration, Oral↗

Coronary artery spasm induced by trigeminal nerve stimulation and vagal reflex during intracranial operation.

This report describes a case of ventricular fibrillation resulting from coronary vasospasm during intracranial operation under general anesthesia. An autonomic response associated with the intracranial procedure caused a coronary spasm, which was worsened by alpha-agonists. Nitroglycerin effectively resolved the coronary spasm and co-complications persisted.

Adrenergic alpha-Agonists↗

Role of coronary spasm in different anginal syndromes.

Angina pectoris is a clinical syndrome caused by transient myocardial ischaemia due to an imbalance between myocardial oxygen demand and supply. It is now evident that coronary artery spasm plays an important role in the pathogenesis of various forms of angina pectoris. Angina pectoris that is mainly caused by coronary artery spasm (coronary spastic angina) has one or more of the following characteristics: 1) the attack occurs at rest, 2) the attack is associated with ST-segment elevation in the ECG, 3) the attack has a variable exercise threshold, and 4) the attack is suppressed by Ca-antagonists but not by beta-adrenergic blocking agents. On the other hand, angina pectoris that is caused by increased myocardial oxygen demand in the presence of severe and extensive organic stenosis (organic angina) has the following characteristics: 1) the attack is induced by constant amount of exertion irrespective of hour and day and is relieved by rest, 2) the attack is associated with ST-segment depression in the ECG, and 3) the attack is suppressed by beta-adrenergic blocking agents, which decrease myocardial oxygen demand.

Angina Pectoris↗

Torsade de pointes ventricular tachycardia following coronary artery spasm during general anaesthesia.

We present a patient who suffered two episodes of torsade de pointes ventricular tachycardia during general anaesthesia for abdominal surgery. The first occurred on suctioning of the tracheobronchial tree and the second while anaesthesia was light. Since ST segment elevation was in each case noted before the onset of torsade de pointes, coronary artery spasm was suspected to be the cause. An intravenous infusion of nitroglycerine was effective in treating and preventing these episodes. These findings suggest that coronary artery dilators such as nitroglycerine are indicated for initial treatment of torsade de pointes following coronary artery spasm in order to facilitate recovery from myocardial ischaemia.

Anesthesia, General↗

Facial spasm.

There are many varieties of abnormal facial movement. This paper discusses hemifacial spasm and blepharospasm in particular. A technique found useful for the symptomatic relief of idiopathic hemifacial spasm is described, and experience with its use on 15 patients also described. Experiences in the operative treatment of 6 patients with essential blepharospasm are recounted.

Blepharospasm↗

Acute myocardial infarction during pregnancy caused by coronary artery spasm.

A 33-year-old pregnant woman suffered from acute anteroseptal myocardial infarction at the 19th gestational week. Despite periodic attacks of myocardial ischaemia after admission, the coronary arteriograms under the use of nitroglycerin were normal. Thereafter, she remained free from the ischaemic events with diltiazem hydrochloride and delivered a healthy baby. The coronary arteriography at puerperium also showed no organic narrowing. However, the provocative test with acetylcholine chloride caused severe spasm of the left anterior descending coronary artery. These findings strongly suggest that acute myocardial infarction in this pregnant woman was caused by coronary artery spasm.

Adult↗

The transient appearance of collateral circulation during coronary spasm.

This article reports a case of transient augmentation of collateral circulation due to spontaneous coronary arterial spasm during angiography. The patient's electrocardiogram revealed ST-segment depression during vasospastic attack; this depression differs from the typical change of the ST-segment elevation in coronary spasm without collateral circulation.

Collateral Circulation↗

Myoclonic spasms during treatment with high doses of intravenous morphine in renal failure.

Myoclonic spasms occurred in a patient suffering from renal failure after high doses of continuous intravenous morphine (100 mg/h). The concentrations of morphine, morphine-6-glucuronide and morphine-3-glucuronide (mumol/l) in plasma were: 1.93, 52.06 and 381.8, and in cerebrospinal fluid were: 1.02, 5.86 and 61.82, respectively. The role of morphine and morphine glucuronides in myoclonic spasms is discussed.

Acute Kidney Injury↗

A possible relationship between migraine and coronary artery spasm.

Five patients, all women in their 50s and all with a documented history of migraine headaches, had ischemic chest pains investigated. Four patients had angina primarily occurring at rest, with documented ischemic electrocardiographic changes during pain in all five. Three subjects sustained myocardial infarction, one shortly after taking ergotamine tartrate for an acute attack of migraine. Subsequent coronary angiography in all five subjects revealed no evidence of atherosclerotic coronary artery disease, suggestive of spasm as the cause of ischemia. In subjects with known migraine, the occurrence of chest pain may represent coronary artery spasm, and should be investigated with concurrent electrocardiographs, as these two clinical entities may be related as part of a generalised vasospastic disorder. The use of ergot preparations should be contraindicated in such patients, as exacerbation of chest pain and frank myocardial infarction may result. These chest pains responded favourably to calcium channel blockers.

Coronary Disease↗

Arterial stenosis in migraine: spasm or arteriopathy?

Segmental arterial narrowing has rarely been angiographically demonstrated in patients with migraine. One new case is reported and 12 previous cases are reviewed. Though often referred to as vasospasm, arteriographic stenosis may result from edema of the vessel wall, arterial dissection, the effects of puerperium or arteritis. A biphasic course of spasm, similar to the pattern noted with subarachnoid hemorrhage, has been recorded in some migraineurs. The current neurogenic and biochemical concepts of "spasm" developed for subarachnoid hemorrhage are reviewed. Arterial narrowing may be important in several phenomena associated with migraine. It may account for migrainous cerebral infarction or hemorrhage. Vasoconstriction has also been invoked to explain the aura and other features of migraine. But the site of stenosis does not always correlate with the headache or focal neurologic features in location or timing. The angiographic changes are probably an epiphenomena rather than a primary mechanism of migraine. These changes may result from altered sympathetic neuronal activity; factors supporting that concept are reviewed.

Adolescent↗

Disturbed calcium and phosphate homeostasis during treatment with ACTH of infantile spasms.

Kidney histology of five infants who died during or immediately after treatment with adrenocorticotrophic hormone (ACTH) showed severe tubular and interstitial calcinosis. We therefore studied serum concentrations of calcium, inorganic phosphate, and parathormone, serum activities of alkaline phosphatase, and urinary excretion of calcium, inorganic phosphate, and cyclic adenosine monophosphate (cAMP) in 16 other children with infantile spasms before, during, and after 6 weeks of treatment with ACTH. During the treatment the following observations were made: hypocalcaemia developed in three infants; the mean daily urinary excretion of calcium in the group increased threefold and seven infants had hypercalciuria; the excretion of phosphate increased but its tubular reabsorption remained stable; and in most infants serum parathormone and urinary cAMP excretion increased, and in four infants they increased to supranormal concentrations. These biochemical changes were reversible in most infants. Radiographs suggested loss of bone mass by 3-4 weeks of treatment, with rapid recovery after treatment. We conclude that infants treated with ACTH for infantile spasms are at risk of suffering disturbance in calcium and phosphate homeostasis, which leads to nephrocalcinosis.

Adrenocorticotropic Hormone↗

Intracarotid phenoxybenzamine for cerebral arterial spasm.

Phenoxybenzamine was injected into the carotid artery of 23 patients after operations on their cerebral arterial aneurysms. Rapid improvement was seen in three cases with pronounced neurological disability. The other 20 were treated prophylactically in an attempt to prevent the onset of spasm. These results would appear to indicate that intracarotid phenoxybenzamine may be of value in the treatment of cerebral arterial spasm, provided that it is given before irreversible infarction of the brain has occurred. Until more is known about its action it would be best to give the drug only after operation.

Adult↗

Supersensitivity to pentagastrin in diffuse oesophageal spasm.

A 38-year-old patient, complaining of dysphagia and substernal pain of nine months' duration, was found by manometric studies to have diffuse oesophageal spasm. As has similarly been reported for cholinergic agents in achalasia and in some cases of diffuse oesophageal spasm the oesophageal body responded in a hypersensitive fashion to subcutaneous and intravenous injections of pentagastrin. This effect was inhibited by the intravenous administration of atropine and completely abolished by nitroglycerine. When pentagastrin was subcutaneously injected before a barium examination a distortion of the oesophageal contour, described as curling or corkscrew oesophagus, regularly appeared.

Adult↗

Angiographic documented coronary arterial spasm in absence of critical coronary artery stenoses in a patient with variant angina episodes during exercise and dobutamine stress echocardiography.

Dobutamine stress echocardiography is widely performed as a useful diagnostic tool in patients with known or suspected coronary artery disease. Dobutamine induced myocardial ischaemia is frequently associated with ST segment depression. ST segment elevation is uncommon and is almost always associated with prior myocardial infarction or transient total coronary occlusion. Dobutamine induced ST segment elevation in absence of significant coronary artery disease is a rare condition and is supposed to be a consequence of severe coronary artery spasm. The case of a 58 year old man with variant angina episodes at rest, during exercise test, and dobutamine stress echocardiography is reported, in whom coronary spasm without significant coronary artery stenoses was documented angiographically.

Angina Pectoris, Variant↗

Coronary artery spasm induced by carotid sinus massage.

A 60 year old man with a history of frequent episodes of chest pain and dizziness was referred for evaluation of coronary artery disease. He had no significant coronary artery stenosis at baseline coronary angiography. A carotid sinus massage was performed for evaluation of carotid sinus hypersensitivity in the patient. Both heart rate and blood pressure decreased a little, and returned to baseline level immediately after carotid sinus massage. However, 2.5 minutes after carotid sinus massage, ECG showed ST segment elevation in leads II, III, and aVF. Four minutes after carotid sinus massage, he had chest pain with a progressive elevation in the ST segment in the same leads, when he had 99% focal spasm in the right coronary artery. The vasospasm induced by carotid sinus massage was reproducible over several minutes and resolved spontaneously. Coronary artery spasm may be provoked by the enhanced vagal activation due to carotid sinus massage.

Carotid Sinus↗