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At least 703 records · Page 39Linked to original sources
PubMed1988

[Coronary spasm immediately following coronary revascularization].

Of 2,600 coronary operations performed from August 1983, to December 1988, two ischemic reactions of the inferior wall immediately after operation were observed. In both patients the right coronary artery was either dissected or revascularized intraoperatively. Under the diagnosis of postoperative spasm both patients had reangiography three hours after surgery. Right coronary artery spasm was demonstrated in both patients. After intracoronary injection of calcium channelblockers the spasm resolved completely. Patient 1 demonstrated a small inferior infarction during control angiography, patient 2 remained free of a myocardial infarction. The possible causes of coronary spasm during or after surgery are discussed. The diagnosis and an approach to therapy are outlined.

Coronary Artery Bypass↗
PubMed1987

Use of nimodipine for prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage.

The chemistry, pharmacology, pharmacokinetics, adverse effects, dosage, and availability of nimodipine are discussed, and the clinical use of nimodipine in preventing and treating cerebral arterial spasm in patients with subarachnoid hemorrhage is reviewed. Nimodipine is a highly lipid-soluble dihydropyridine derivative that readily crosses the blood-brain barrier. In animal studies, nimodipine has been shown to be effective in increasing cerebral blood flow; preventing vasoconstriction attributable to sympathetic stimulation, hypocapnia, and hypertension; and improving neurological outcome after cerebral ischemia. Nimodipine is reported to be 90% protein bound; its half-life is approximately 13 hours, with substantial interpatient variability. Nimodipine has been studied in the prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. In four open trials, in which nimodipine was administered orally, intravenously, topically during surgery, or by intracarotid injection, and in two double-blind, placebo-controlled trials, neurological outcomes were improved in patients receiving the drug. However, in both sets of trials nimodipine had limited effects on cerebral arterial spasm. Although nimodipine can cause hypotension, no serious adverse reactions to the drug were reported in clinical trials in patients with subarachnoid hemorrhage. Based on limited data currently available, nimodipine appears to improve neurological outcome in patients with subarachnoid hemorrhage. However, its efficacy in preventing or treating cerebral arterial spasm in these patients seems to be limited.

Humans↗
PubMed1985

Prevention with molsidomine of coronary artery spasm caused by alkalosis.

A provocative test of coronary artery spasm caused by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of anginal pain and significant, transient ischemic changes of the ST segment resulting from alkalosis-induced coronary spasm. A second provocative test was performed under the same conditions, 24 hours later, after the administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.

Alkalosis↗
PubMed1985

[Spasm of organically altered coronary arteries].

The paper is concerned with 11 patients with an angiographically recorded spasm at the site of the coronary artery stenosis. In the 2 patients, the spasm was spontaneous, whereas in the 9, it was provoked by ergometrine. None of the patients had a typical clinical picture of Prinzmetal's angina pectoris, but all the cases were characterized by exacerbation of coronary heart disease, which was manifested by repetition and increase of the intensity of attacks of angina pectoris at rest. The data of the repeated ergometrine tests, during which the ECG was recorded indicate that in the majority of the patients, the ability to respond by spasms toward ergometrine administration disappeared as the clinical condition was stabilized, but some of the patients preserved this ability despite therapy with calcium antagonists. If 2 or 3 coronary vessels were involved, spasm developed but in one of the vessels. This is indirect evidence for the fact that during multiple stenosing of the coronary arteries, the reactivity of one of the stenoses plays the leading part in the genesis of the disease exacerbation.

Adult↗
PubMed1979

[Muscle spasms in patients with amyotrophic lateral sclerosis (clinico-electromyographnic analysis)].

The diagnostic importance and electromyographic characteristics of the muscular spasms were studied in patients with lateral amyotrophic sclerosis at various stages of the disease. It has been shown that the muscular spasms are a typical symptom of this disease, and may be an early manifestation of the latter. The clinical and electromyographic characteristics of the spasms depend on the depth of the pathological process. Of importance in the origin of the muscular spasms in the lateral amyotrophic sclerosis is involvement of many levels of the cortico-muscular path, however, distrubances of the intraspinal mechanisms are, probably, the leading cause.

Amyotrophic Lateral Sclerosis↗
PubMed1983

[Early coronary spasm after myocardial revascularization surgery].

Six cases of early post-operative coronary artery spasm were observed in a series of 460 consecutive patients who underwent myocardial revascularization. This is a rare accident, only quite recently described. The spasm involves the coronary arterial network or the graft and is reflected in an elevated ST segment accompanied by collapse and ventricular dysrhythmia. The condition may be lethal or may result in myocardial infarction. Treatment consists of calcium inhibitors. The cause of the spasm is unknown, but it seems to be encouraged by trauma of the coronary arteries during surgery and by metabolic changes (production of thromboxane A2) induced by the cardio-pulmonary bypass. This particular spasm must be watched by heart surgeons and their team in order to avoid some deaths and peroperative necroses, as it appears that we are only confronted with its more severe forms.

Coronary Vasospasm↗
PubMed1983

[Molsidomine prevention of coronary artery spasm caused by alkalosis].

A test provocation of coronary artery spasm by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of angina pain and significant, transient ischaemic changes of the ST segment, due to alkalosis induced coronary spasm. A second provocation test was performed under the same conditions, 24 hours later, after the prior administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.

Alkalosis↗
PubMed1981

[Clinical application of the alkalosis induction test for coronary artery spasm].

Alkalosis was used for stress testing for coronary artery spasm in 70 patients (average age: 56 years) with resting angina. A rapid intravenous infusion of an alkaline buffer (THAM) immediately followed by 5 minutes' maximal ventilation increased the arterial pH to 7.67 +/- 0.5. Anginal pain and ECG changes were observed in 24 Patients, with ST elevation in 10 cases and ST depression in 14 cases. The ischaemic changes occurred during hyperventilation in 16 cases and in the 3 minutes following the test in 8 cases. The heart rate increased from 66 +/- II to 71 +/- 14 bpm (p less than 0,01) but systolic blood pressure fell from 139 +/- 12 to 130 +/- 12 mm Hg during hyperventilation; there was no significant change in the rate-pressure product (1130 +/- 1750 to 8990 +/- 2690). In all cases, the angina and ischaemic changes regressed after intravenous Trinitrin. Coronary angiography was performed in 56 patients: in the 24 patients with positive responses (Group I) and in 30 of the 46 patients with negative responses (Group II). Significant coronary artery narrowing (greater than 70%) was observed in 21 patients of Group I: in the 3 patients without coronary lesions an intravenous injection of 0.4 mg methylergometrine provoked coronary spasm. In Group II, significant narrowing was demonstrated in 18 patients: in the 12 other patients, coronary spasm could not be induced by methylergometrine. Therefore, in the absence of organic coronary lesions, an excellent correlation has been shown between the alkalosis and methylergometrine tests. This stress test was repeated in 16 of the 24 patients in Group I one hour after administration of 20 mg of Nifedepine: the test was negative in all cases. We conclude that the alkalosis test could be useful in the coronary care unit as a stress test for coronary spasm to determine the antianginal treatment of choice and to evaluate its efficacity.

Coronary Angiography↗
PubMed1982

[Treatment of a severe coronary artery spasm, refractory to complete denervation of the heart (autotransplantation)].

The case reported is that of a 49 year old man with very severe Prinzmetal angina due to spasm of the left circumflex artery. Despite intensive medical treatment he continued to suffer frequent attacks with atrioventricular block. As plexectomy was not possible in this case, complete cardiac denervation was performed. After surgery, he had no further attacks and continuous ECG monitoring showed no ischemic phenomena. Nevertheless, a stress test was still able to induce spasm of the same artery which was painless but associated with ECG changes. Eighteen months postoperatively, resting angina recurred with positive stress tests giving painful attacks. Four hypotheses are discussed: 1) the local factor was very important, with a zone of hyperactivity on the left circumflex artery, 2) one of the mechanisms of coronary artery spasm could be the nervous stimulation of this zone, 3) this zone was insensitive to nervous stimulation after autotransplantation but remained sensitive to methylergometrine, 4) the recurrence of resting angina and painful symptoms on stress testing suggests the possibility of reinnervation of the heart, as has been shown after cardiac transplantation, the autonomic nervous system does not play the role generally attributed to it in the genesis of spasm.

Aged↗
PubMed1981

[Trigeminal neuralgia and hemifacial spasm caused by the compression of tortuous vertebro-basilar system--a case report (author's transl)].

A 63-year-old man was admitted to our clinic on August 14, 1980 with the chief compliant of left-sided intermittent facial pain. He had been suffering from twitching of the left facial muscles since 1972. During two years before admission, severe pain of the left face, starting in the left upper jaw and radiating to the left periorbital region, occurred intermittently. The pain aggravated by eating, talking and face-washing, gradually worsened and he became unable to take meals. On admission, he was alert. No sensory disturbance was seen. Muscle twitching was seen in the left orbicularis oculi, orbicularis oris and sometimes in the platysma. Mild facial palsy was recognized on the left side and other cranial nerves were intact. Computed tomogram with contrast enhancement revealed shift of the basilar artery to the left side. Markedly enlarged and tortuous vertebrobasilar system kinking at the left cerebello-pontine angle, was seen on the left vertebral angiogram. This tortuous vertebrobasilar system was presumed to be the cause of the trigeminal neuralgia and hemifacial spasm. The neuralgia disappeared after a controlled thermocoagulation of the left Gesserian ganglion, and the frequency of hemifacial spasm was reduced too. He was discharged with mild hemifacial spasm. The combination of trigeminal neuralgia and hemifacial spasm caused by direct compression of tortuous vertebro-basilar system on the nerve roots is rare. A case was reported and the literature were reviewed.

Basilar Artery↗
PubMed1995

Endothelin-1 is not involved in serotonin-induced coronary spasm in a swine model.

OBJECTIVES: The role of endothelin-1 (ET-1) in the pathogenesis of coronary artery spasm is not well understood. We aimed to determine if ET-1 is involved in serotonin-induced coronary spasm in the swine model. METHODS: In 10 miniature pigs, a segment of the left anterior descending coronary artery was denuded and irradiated with X-ray. Three months after endothelial denudation, coronary vasomotion was assessed in vivo by quantitative arteriography. RESULTS: Intracoronary serotonin at 10 micrograms/kg provoked coronary spasm (augmented narrowing of the luminal diameter) at the denuded site (diameter reduction 93 +/- 4%) but not at the non-denuded control site (19 +/- 4%, P < 0.01) associated with ST segment elevation in the region perfused by the denuded artery. Intracoronary administration of ET-1 at 25 ng/kg caused mild vasoconstriction of the denuded (26 +/- 4) and non-denuded site (16 +/- 3%, n.s.), but provoked ST segment elevation in the regions perfused by both the denuded and non-denuded arteries. The treatment with an endothelin antagonist (BQ123 0.1 mg/kg) significantly attenuated coronary vasoconstriction and ST segment elevation evoked with ET-1, but did not alter serotonin-induced vasoconstriction either at the denuded or control site. CONCLUSIONS: The results of this study suggest that endogenous ET-1 may not be involved in the pathogenesis of serotonin-induced coronary spasm in our swine model.

Animals↗
PubMed1995

Perioperative coronary artery spasm in modified Bentall's operation for annulo-aortic ectasia in Marfan's syndrome. A case report of perioperative chordal rupture of the mitral valve.

We experienced a rare case of Marfan's syndrome with annulo-aortic ectasia, aortic regurgitation and Prinzmetal's variant angina. In a modified Bentall's operation (button technique), perioperative severe coronary artery spasm occurred in spite of the preventive use of nitroglycerin infusion, which resulted in profound ventricular fibrillation and subsequent chordal rupture of the mitral valve with Sellers IV regurgitation. Use of nicardipine contained in cardioplegia, continuous infusion of nicardipine and nitroglycerin after aortic declamping completely prevented coronary spasm throughout the course of a second surgery for mitral valve replacement. It is worthy to report this case because of rarities such as Marfan's syndrome accompanied by Prinzmetal's variant angina, perioperative coronary artery spasm in modified Bentall's operation, and perioperative chordal rupture of the mitral valve and progression of mitral valve regurgitation. We also stress the efficacy of a new calcium antagonist, nicardipine, to prevent coronary artery spasm during open heart surgery.

Angina Pectoris, Variant↗
PubMed1994

[Prevention of coronary spasm during and shortly after coronary revascularization in patients with variant angina].

From June 1990 to March 1993, 9 patients undergoing coronary artery bypass grafting (CABG), 4.4% of all CABG cases at our hospital during this period, had significant perioperative coronary spasm. For 4 patients who underwent CABG before May 1992 (Group 1), preventive and suppressive procedures for the coronary spasm were the addition of diltiazem in the cardioplegic solution and the continuous intravenous infusion of nitroglycerin. Perioperative myocardial infarction (PMI) occurred in all 4 patients in Group 1, with the mean peak MB-CPK of 356 +/- 197 IU/l. One patient had delayed sternal closure because of his unstable hemodynamic status. Thereafter, we changed our protocol as follows: 1) Ergometrine loading (intracoronary infusion) test was performed in all candidates for CABG, aiming at finding out patients with a high risk. And for the high-risk patients, in addition to the measures done in Group 1, 2) intraaortic balloon pumping was performed through the perioperative period, and 3) a pig-tail catheter was dwelled in the Valsalva sinus, through which bolus doses of isosorbide dinitrate were injected frequently in this period. 4) Additionally nifedipine was periodically administered through the nasogastric tube. With these intensive preventive/suppressive measures, the perioperative spasm in 5 patients (Group 2) with variant angina were successfully managed, with no resultant PMI nor operative death (The occurrence of PMI was significantly less frequent in Group 2 than in Group 1, with the p value < 0.05). For patients with variant angina undergoing CABG, combined intensive preventive/suppressive measures for perioperative coronary spasm as listed above proved effective.

Adult↗
PubMed1993

Successful treatment of coronary artery spasm following coronary artery bypass grafting.

A case of coronary artery spasm developed 6 hours after myocardial revascularization inducing both hemodynamic and electrocardiographic changes, is reported. The spasm was documented by coronary angiography, and it was not reversed by intracoronary infusion of isosorbide dinitrate. Intravenous infusion of nifedipine (initial dose of 0.0104 mg/min to final dose of 0.0208 mg/min), along with infusion of glyceronitrate (1.0 micrograms/kg/min) was able to significantly improve hemodynamic impairment and to reverse electrocardiographic changes in 12 hours. Coronary angiography, repeated in postoperative day 3, after 48 hours of continuous nifedipine infusion, showed a resolution of coronary spasm. There was no evidence of myocardial infarction as resulted from total CPK and MB isoenzyme release. Nifedipine infusion was gradually reduced as oral administration of slow release nifedipine (40 mg twice daily) was started. The combined intravenous infusion of glyceronitrate and nifedipine seems to be able to control and overcome coronary artery spasm following coronary surgery.

Coronary Angiography↗
PubMed1995

[Current views on the clinical significance of coronary artery spasm].

Current views about etiology, pathogenesis, diagnostics and treatment of coronary artery spasm have been presented. A lot of researches show complexity of factors, which are responsible for coronary artery spasm. The most important are: a local hypersensitivity of vessels wall, neurogenic factors and humoral factors. The lack of magnesium plays also important role. Clinical manifestations of coronary artery spasm are: Printzmetal's angina, arrhythmia, acute myocardial infarction, atypical chest pain and cardiac sudden death. Among diagnostic examination the main importance have provocative tests with ergonovine and acetylcholine, rarely hyperventilation and cold are used. Calcium channel blockers, nitrate, molsidomine are employed in treatment patients with coronary artery spasm. There are taken modern examinations of new drugs like beta-1 adrenergic agonists and derived molsidomine agents. Beta-adrenergic blocking agents are contraindicated. It has been emphasized, that early diagnostics and pharmacologic treatment improve long-term prognosis in this group of patients.

Coronary Vasospasm↗
PubMed1996

[A case of coronary artery spasm during burr hole opening for craniotomy].

We report a rare case of coronary artery spasm during burr hole opening for craniotomy in a patient with no past history of coronary artery disease. A 52-year-old man was scheduled for the removal of the brain tumor under general anesthesia. Anesthesia was induced with fentanyl, thiamylal, and vecuronium, and maintained with sevoflurane plus nitrous oxide in oxygen. When burr holes were made for the craniotomy, the heart rate decreased suddenly and the ECG in lead II demonstrated the elevation of the ST segment (0.3mV). After about 1 min, the ST segment elevation returned to normal without any treatment. The dura mater was rather tense with inspection. Despite many reported cases of coronary artery spasm during general anesthesia, coronary artery spasm during burr hole opening for craniotomy has not been reported. In the present case, since the heart rate decreased and the elevation of the ST segment occurred at the time of the burr hole opening for craniotomy, the activated vagal tone reflex induced by the stimulation of the dura mater seemed to have caused the coronary artery spasm.

Anesthesia, General↗
PubMed1997

[Reproducibility of spasm in patients with long-term remission of vasospastic angina by medical treatment].

The reproducibility of coronary vasospasm was assessed in nine patients with complete remission of vasospastic angina by medical treatment by reexamination at intervals of mean [+/-SD] 5.7 +/- 0.9 years. Twenty-one segments were defined as spastic, demonstrating more than 90% narrowing after acetylcholine injection at the initial angiography. The degree of spasticity, type of spasm (diffuse or focal) and coronary artery diameter in these segments at the initial and follow-up studies were compared. Of the 21 segments, 17 (81%) still had some spasticity (> 25%) at the follow-up study and 8 (38%) of these 17 showed spasticity with greater than 90% narrowing. On the other hand, spasm was not reprovoked in 4 (19%) segments. Luminal diameter of the spastic segments decreased significantly at the follow-up study (2.52 +/- 0.83 vs 2.26 +/- 0.62 mm, p = 0.01), but percentage stenosis was not different between the initial and follow-up studies (9.1 +/- 7.2 vs 10.3 +/- 8.0%, NS). The reproducibility of the type of spasm provoked was 83%. Coronary vasospasticity persists to some extent in spite of complete remission of angina by medical treatment, and the type of spasm provoked has high reproducibility. Therefore, the cessation of drug treatment should be done carefully.

Acetylcholine↗
PubMed1998

[Pathophysiology of coronary spasm].

There is a deficiency in both basal and stimulated NO release in the spasm arteries of patients with coronary spastic angina. The deficient NO release may lead to the supersensitivity of the artery to the vasodilator effect of nitroglycerin and to the vasoconstrictor effect of acetylcholine in patients with coronary spastic angina. Flow-dependent coronary dilation of proximal LAD was found to be less in spasm arteries than in control arteries. The infusion of L-NMMA in the proximal site of LAD suppressed the flow-dependent dilation in control arteries, while L-NMMA did not have significant effect in spasm arteries. The results indicate that flow-dependent coronary dialtion is impaired in spasm arteries partly due to deficiency in endothelial NO bioactivity, which in turn may possibly contribute to increase in coronary tone during the physiological stress in patients with coronary spastic angina.

Acetylcholine↗