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PubMed1999

Coronary artery spasm after coronary artery bypass grafting.

We report a case of a 62-year-old man with severe manifestations of postoperative coronary artery spasm following effective coronary artery bypass grafting. The coronary artery spasm was manifested by ST segment elevation, hypotension and wall motion abnormalities on echocardiography. Urgent angiography confirmed the diagnosis and intracoronary infusion of nitroglycerine and verapamil relieved the coronary spasm.

Cardiac Catheterization↗
PubMed1996

Hemifacial spasm associated with external carotid artery compression of the facial nerve.

We report a unique case of hemifacial spasm due to compression of the facial nerve by the main trunk of the external carotid artery within the parotid space. Decompression of the facial nerve as well as partial section of the proximal trunk of the nerve, caused the hemifacial spasm to disappear. Our case gives support to the theory that hemifacial spasm can be caused by pressure on the facial nerve along all its course and not only in its intra-cranial portion.

Carotid Artery, External↗
PubMed2004

Vaginal spasm, pain, and behavior: an empirical investigation of the diagnosis of vaginismus.

This study investigated the roles of vaginal spasm, pain, and behavior in vaginismus and the ability of psychologists, gynecologists, and physical therapists to agree on a diagnosis of vaginismus. Eighty-seven women, matched on age, relationship status, and parity, were assigned to one of three groups: vaginismus, dyspareunia resulting from vulvar vestibulitis syndrome (VVS), and no pain with intercourse. Diagnostic agreement was poor for vaginismus; vaginal spasm and pain measures did not differentiate between women in the vaginismus and dyspareunia/VVS groups; however, women in the vaginismus group demonstrated significantly higher vaginal/pelvic muscle tone and lower muscle strength. Women in the vaginismus group also displayed a significantly higher frequency of defensive/avoidant distress behaviors during pelvic examinations and recalled past attempts at intercourse with more affective distress. These data suggest that the spasm-based definition of vaginismus is not adequate as a diagnostic marker for vaginismus. Pain and fear of pain, pelvic floor dysfunction, and behavioral avoidance need to be included in a multidimensional reconceptualization of vaginismus.

Adult↗
PubMed1997

The comparison of the responsiveness of human isolated internal mammary and gastroepiploic arteries to levcromakalim: an alternative approach to the management of graft spasm.

AIMS: We studied the effectiveness of levcromakalim, a potassium channel opener (KCO), in the prevention and reversal of spasm in arterial grafts used in coronary artery bypass operations, namely, internal mammary artery (IMA) and gastroepiploic artery (GEA). METHODS: Spasm was mimicked in vitro in arterial rings from 109 patients by increasing the vascular tension with noradrenaline, the thromboxane analogue U46619, endothelin-1 and K+. RESULTS: GEA displayed considerably higher contractile force to these agents than IMA. Pretreatment with levcromakalim depressed significantly the maximal contractile responses (either absolute or relative) to noradrenaline and U46619 but did not affect those of endothelin-1 and K+ in both of the arteries. Sensitivities (to all agents, except to endothelin-1) decreased significantly after levcromakalim. In experiments evaluating the antispasmodic activity of levcromakalim, a higher relaxant capacity was observed in GEA than IMA (for K+ contraction; IMA: 31.32 +/- 3.83%, n= 13 vs GEA: 98.01 +/- 0.71%, n=7, P<0.05). This different activity of levcromakalim between two arterial grafts was apparent even when GEA rings were contracted to higher force (g) than that of IMA (for K+ contraction; GEA: 72.56 +/- 4.96%, n = 7). Responses to levcromakalim were similar in IMA and GEA when endothelin-1 was used as the spasmogenic agent (IMA: 80.98 +/- 4.85%, n=10 vs GEA: 91.93 +/- 3.17%, n=7, P>0.05). CONCLUSIONS: Our results provide evidence that levcromakalim may have a therapeutic value in the treatment of spasm of coronary artery bypass grafts, especially GEA.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1998

Low prevalence of coronary artery spasm in patients with normal coronary angiograms and unexplained ventricular fibrillation.

AIMS: The aetiology of ventricular fibrillation in patients without identifiable structural heart disease is unknown. Recently, high prevalence of silent ischaemia due to coronary artery spasm has been reported in such patients. However, in at least one report, all patients had non-critical coronary artery lesions. Identification of coronary artery spasm as the underlying aetiology of ventricular fibrillation has important therapeutic implications. METHODS AND RESULTS: We performed ergonovine provocation tests in 18 patients (14 males, and four females; mean age, 36 years) with documented ventricular fibrillation in the absence of identifiable structural heart disease who had undergone aborted sudden death. In group I (n = 7) ergonovine provocation tests were performed at a mean interval of 31 months (range 21-42 months) after the index episode. These patients had already received an implantable cardioverter defibrillator, after failed electrophysiologically guided antiarrhythmic therapy. In group II (n = 11) the ergonovine provocation test was performed prospectively as part of the diagnostic evaluation. All patients were off antiarrhythmic drugs, calcium entry or beta-adrenoceptor blockers at the time of the ergonovine provocation test. Ergonovine was administered intravenously as a bolus injection, beginning with 0.05 mg followed every 3 min by incremental doses up to a cumulative maximum dose of 0.45 mg. Predefined end-points were (1) recording of ischaemic ST segment shifts of > or = 1 mm in at least two corresponding leads of the 12-lead electrocardiogram; (2) induction of ventricular tachycardia or ventricular fibrillation; and (3) administration of a cumulative dose of 0.45 mg. A positive response to ergonovine was seen in only one patient (5%) in group I in whom there developed ST segment elevation without angina and a short burst of rapid ventricular tachycardia. CONCLUSIONS: This study found a low prevalence of coronary artery spasm in patients with aborted sudden death resulting from documented ventricular fibrillation and non-apparent underlying heart disease. All patients had normal coronary angiograms and a negative history for spontaneous episodes of chest pain. The mechanism of arrhythmogenesis in such patients remains largely unknown.

Adult↗
PubMed2004

[Rest angina caused by coronary spasm].

HISTORY AND PHYSICAL EXAMINATION: A 70-year-old woman with recurrent angina at rest and dyspnea was admitted for coronary angiography. Prior to the admission an ECG showed new negative T-waves in the precordial leads, which have completely disappeared the day after. Clinical examination revealed a low systolic murmur over the aortic valve and a low murmur over the left groin artery. The other examination findings were normal. INVESTIGATIONS: Exercise ECG revealed no signs of ischemia. In the coronary angiography a plaque in the left circumflex artery without significant lumen reduction could be detected. Intracoronary administration of acetylcholine induced a spasm in the left circumflex artery with total lumen occlusion with reproduction of intense chest pain. After injection of nitroglycerin coronary spasm and chest pain were reversible TREATMENT AND CLINICAL COURSE: After the diagnosis of vasospastic angina pectoris medical treatment with isosorbide dinitrate and amlodipine was initiated. Additionally ACE- and CSE-inhibitors were prescribed to improve endothelial dysfunction. After one year the patient was free of symptoms. CONCLUSION: Coronary spasm can cause angina at rest. After confirmation of diagnosis an appropriate medical therapy could be applied and other unnecessary examinations including further coronary angiographies could be prevented.

Aged↗
PubMed1995

[Acute myocardial ischemia in spontaneous coronary artery spasm].

AIM OF STUDY: To discover what factors indicate spontaneous coronary artery spasms as a cause of myocardial ischaemia. PATIENTS AND METHOD: In a retrospective analysis 15 of 1407 consecutive patients who had undergone coronary arteriography (six women and nine men; mean age 47 +/- 11 years) had acute ischaemia due to spontaneous coronary artery spasms. The clinical findings at the time of first investigation and during the follow-up period (mean of 29 [3-65] months) were evaluated. RESULTS: The most common risk factors were hypercholesterolaemia (> or = 200 mg/dl) in ten patients (66%) and heavy nicotine consumption > or = 20 cigarettes per day) in eight patients (55%). Of the patients with angina at rest nine had reversible ST elevations, six had terminal T negativity in the ECG and an increased incidence of ventricular arrhythmias (n = 6). At time of hospitalization ten patients had acute myocardial ischaemia and five had signs of acute myocardial infarction (maximal creatine kinase concentration: 121-2980 U/l). Acute coronary angiography revealed circumscribed coronary artery constriction, reversible with nitroglycerin, with stenosis of < 70% in five patients and of > or = 70% in six, as well as intermittent vessel occlusion in four patients. Angiography showed smooth coronary artery walls in almost all instances. Angiographic evidence of circumscribed arteriosclerotic lesion with maximally 50% narrowing was present in six patients. CONCLUSION: Especially in younger, male patients with hypercholesterolaemia and heavy smoking recurrent anginal pectoris at rest, with reversible ECG signs of myocardial ischaemia but without advanced coronary sclerosis, speaks for spontaneous coronary artery spasms as the cause.

Acute Disease↗
PubMed1992

A new paradiscal injection technique for the relief of back spasm after chemonucleolysis.

Back spasm, or spasm of the back muscles, is the commonest adverse reaction encountered after chemonucleolysis. In order to overcome this troublesome complication, the authors present a new 'paradiscal injection technique'. After the injection of chymopapain into the affected disc, the needle is withdrawn to just outside the annulus. Bupivacaine is injected into the paradiscal 'space' which acts upon the paravertebral muscles. Eighty consecutive patients have been treated by chemonucleolysis with paradiscal injection for pain relief. All patients were discharged the same day or the following day and no immediate complications occurred. When reviewed 3 weeks later, only three (3.8%) patients complained of back pain (which was different in character to that present before the injection or was exacerbated by the injection). Pain persisted in the same patients until 6 months after the injection but was negligible. None of the remaining patients had developed back pain as a result of chymopapain. The authors suggest that the addition of paradiscal injection of bupivicaine after cymopapain injection can reduce the incidence of spasm of the back muscles. This technique is a major contribution to increasing the efficacy of chemonucleolysis for the treatment of herniated lumbar disc.

Adult↗
PubMed1989

Hydrostatic distention and pharmacological treatment of epinephrine-induced microarterial spasm.

The efficacy of using hydrodistention and vasodilatory drugs to relieve spasm in arteries was investigated. The femoral arteries of 64 rabbits (divided into five groups) were placed in spasm by the topical application of epinephrine (1 mg/ml). In group A (controls) vasospasm was induced without further treatment. In group B vasospasm was induced, and the arteries were hydrodistended with normal saline. In three additional groups vasospasm was induced and either 10% lidocaine hydrochloride (group C), verapamil hydrochloride (group D), or chlorpromazine hydrochloride (group E) was applied. Thirty minutes later the vessels were hydrodistended. All vessels were measured at set intervals, and some specimens were retained for light and electron microscopy. All methods of spasm relief were successful, although to varying degrees. Hydrodistention alone produced the widest dilation for the longest time. Lidocaine was the most successful drug treatment alone. Verapamil followed by hydrodistention was the most successful combination regimen, but did not produce better results than hydrodistention alone. Hydrodistention alone produced significant arterial wall damage, resulting in permanent structural modifications. Prior vasodilatory drug treatment reduced but did not eliminate hydrodistention damage. Although hydrodistention dilates for longer periods than vasodilatory drugs, the arterial wall damage associated with hydrodistention indicates that it should be used only when all other methods of vasodilation have failed.

Animals↗
PubMed1984

Spasm and dynamic coronary stenoses.

Spasm is only one type of dynamic stenosis typically responsible for variant angina; spasm with or without transient intraluminal plugging, superimposed on a wide range of old or fresh, fixed stenoses, is largely responsible for unstable angina; physiological changes of tone around pliable coronary stenoses probably account for the variable exercise tolerance and for spontaneous attacks in patients with stable angina. Sustained spasms, not responsive to nitrates and thrombosis, are likely to be involved at different times or simultaneously in acute coronary occlusion causing myocardial infarction. Acute or worsening phases of coronary diseases are largely caused by dynamic stenoses, whereas stable, fixed-threshold, predictable angina may be the only feature of quiescent phases of coronary disease.

Angina Pectoris↗
PubMed2003

Synergistic interaction of T-786-->C polymorphism in the endothelial nitric oxide synthase gene and smoking for an enhanced risk for coronary spasm.

OBJECTIVE: We previously reported that a T-786-->C polymorphism in the 5'-flanking region of the endothelial nitric oxide synthase gene and smoking were independently associated with coronary spasm; however, the interaction between this polymorphism and smoking remains to be elucidated. METHODS: We analyzed 209 men and 238 women who were admitted consecutively at our institution; all subjects received an intracoronary injection of acetylcholine (ACh) while undergoing coronary angiography for evaluation of chest pain: all subjects had no significant coronary stenosis. We divided these subjects into four groups: non-smokers with T/T genotype (Control Group A); non-smokers with C/T or C/C genotype (Group B); smokers with T/T genotype (Group C); and smokers with C/T or C/C genotype (Group D). We further examined quantitative coronary angiographies of the left anterior descending coronary artery in a subset of 54 consecutive men and 53 consecutive women. RESULTS: The frequencies of coronary spasm in Group B (male: 61%, female: 78%), Group C (62%, 59%) and Group D (91%, 92%) were significantly higher than in Group A (30%, 38%). In the males, ACh-induced vasoconstriction was greatest in Group D, and the change was weakest in Group A. In the females, ACh-induced vasoconstrictions were significantly greater in Groups B, C and D than in Group A. The T-786-->C polymorphism and smoking combine to increase the risk of coronary spasm.

Acetylcholine↗
PubMed1994

Facilitation of coronary spasm by propranolol in Prinzmetal's angina: fact or unproven extrapolation?

BACKGROUND: Alpha-adrenergic activation enhances coronary vascular tone; beta-blockade leaves alpha-adrenergic vasoconstriction unopposed. Whether beta-adrenergic blockade facilitates coronary spasm in patients with Prinzmetal's angina is unknown. METHODS: Using quantitative angiography, we evaluated the response of normal and narrowed coronary arteries to intravenous propranolol, a cold pressor test (an alpha-stimulus), and the combination of the two in 15 patients with Prinzmetal's (group 1) and in 19 with classic (group 2) angina. From measurements of heart rate, systemic and pulmonary arterial pressures, and left and right ventricular ejection times, we derived the tension-time index per minute as a measure of the oxygen need (O2 demand) of the whole heart. RESULTS: In group 1, cold invariably constricted normal and diseased vessels, and in two patients elicited spasm at sites of significant lesions; these changes did not correlate with those in O2 demand. In group 2, the vasomotor reaction of normal and narrowed vessels in response to cold correlated with the modifications in O2 demand. After propranolol administration, (1) in normal vessels in both groups, the baseline luminal diameter varied in parallel with the changes in myocardial O2 demand; (2) narrowings in group 1 patients invariably dilated and in group 2 the caliber varied according to changes in O2 demand; (3) during cold stimulation, luminal narrowing in group 1 varied in parallel with O2 demand, and, in group 2, vessels were uniformly constricted. CONCLUSION: These results do not support the facilitation of coronary spasm by propranolol in Prinzmetal's angina and support the hypothesis that the contractility of coronary vessels in patients with this form of angina is different from that in the classic form.

Adult↗
PubMed1983

Coronary artery spasm during non-cardiac surgical procedure.

A case of coronary artery spasm during a non-cardiac surgical procedure is presented. Two paroxysmal episodes of ST segment elevation in lead 11 and aVF without changes in V5 developed during general anaesthesia. These changes were not preceded by increases in heart rate or arterial pressure. The second episode was associated with a ventricular bigeminal rhythm. This case demonstrates the importance of monitoring several leads in patients likely to develop peroperative spasm of the coronary arteries. Intravenous nitroglycerin was effective in treating the second episode of coronary artery spasm. However, this episode occurred in spite of nitroglycerin administered intravenously at a rate of 0.25 microgram/kg min.

Aorta, Abdominal↗
PubMed1977

Effects of (+) and (-)-propranolol on the responses of the human isolated basilar artery to cerebrospinal fluid obtained from patients with subarachnoid haemorrhage and cerebral arterial spasm.

1. The human isolated basilar artery has been used as a model to investigate the aetiology of cerebral arterial spasm associated with rupture of intracranial aneurysms. 2. The isolated artery is contracted by 5-hydroxytryptamine, noradrenaline, six prostaglandins and cerebrospinal fluid from patients with ruptured aneurysms and cerebral arterial spasm. 3. These contractions are reversed by (+/-)--, (+)-- and (--)-propranolol in concentrations known to produce local anaesthetic effects on isolated frog sciatic nerve; the (+) isomer was 2.5 to 10 times more potent (-)-propranolol in antagonising all contractions. 4. As the two isomers are known to have similar local anaesthetic potency but (-)-propranolol has greater beta-adrenoreceptor blocking effects we conclude that the antagonistic effects described do not involve beta-adrenoreceptor blockade. 5. The data indicate that propranolol may be of clinical use in reversing cerebral arterial spasm.

Basilar Artery↗
PubMed1986

Acute myocardial infarction: an episodic event of several coronary spasms followed by dilatation?

Acute myocardial infarction (AMI) can no longer be considered as a single event, but as a series of episodes. In most of the cases, the initial event may be the induction of a severe spasm of the coronary artery by vasoconstrictive substance released from aggregated platelets. These spasms are followed by dilatation, which is caused by substances set free from the ischemic tissue. Dilatation then results in a washing-out of vasoactive mediators (as well as myoglobin) and platelets, which is reflected as a peak in the blood myoglobin concentration-time curve. The local depletion of vasodilative metabolites allows a further contraction of the coronary vessel. A new accumulation of platelets then stimulates another spasm. This vicious circle (thrombo-ischemic re-entry-mechanism) is repeated several times and can be interrupted by the systemic administration of thrombolytic drugs (streptokinase).

Coronary Vasospasm↗
PubMed1990

Spasm index in subarachnoid haemorrhage: consequences of vasospasm upon cerebral blood flow and oxygen extraction.

A spasm index, defined as transcranial Doppler detected flow velocity in the middle cerebral artery divided by regional cortical cerebral blood flow (CBF), was used on 24 patients with subarachnoid haemorrhage (SAH). The aim was to estimate degree and time course of vasospasm, even in cases with great day-to-day variation in CBF, and correlate to CBF and oxygen extraction. All patients showed increase in spasm indices with peak index in the second or third week. The index seemed stable in spite of day-to-day fluctuations in CBF. Severe vasospasm were associated with poor clinical condition, reduced CBF (less than 30) and high AVDO2. The same picture could be seen with minor degree of vasospasm, probably, in some cases, due to high intracranial pressure. The results suggest that the spasm index is useful in monitoring patients with subarachnoid haemorrhage, and that severe vasospasm has a negative influence on clinical condition, CBF and oxygen extraction.

Blood Flow Velocity↗
PubMed1985

Efficacy of diltiazem for coronary artery spasm.

The introduction of calcium entry blockers which caused marked vascular smooth muscle relaxation with minimal effects on myocardial contractility have provided a new approach to the patient with angina due to coronary artery spasm. Multiple, double-blinded, randomized studies of diltiazem versus placebo have demonstrated that this agent results in reduction in angina frequency and nitroglycerin consumption by 30% to 70% with a demonstrated dose response. A long-term, open label follow-up study of 18 patients who participated in a 44-week prospective, double-blind crossover trial of 240 mg of diltiazem versus placebo for prophylaxis of angina in patients with coronary artery spasm demonstrated a 75% decrease in angina attacks during the first five months of the study and an 80% decrease compared to the placebo period during the second six months. Both the short- and long-term studies have demonstrated very few adverse side effects, less than 7%. A recent long-term study of 43 patients who took diltiazem regularly and were followed in the Coronary Artery Spasm Clinic at Stanford University Medical Center for a mean of 19.6 months (range 6 to 28.5 months) was analyzed for cardiovascular events in the 19.6 months prior to therapy and the 19.6 months after the initiation of therapy. Cardiovascular events on diltiazem, including sudden cardiac death, myocardial infarction, and hospitalization to rule out myocardial infarction utilizing a binomial distribution showed over a 90% reduction compared to the pre-diltiazem period. Adverse effects were reported in six patients who reported minimal to mild pedal oedema.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Cerebral artery spasm--a possible mechanism of TIA?

The pathogenetic transitory ischemic attacks (TIA) is usually ascribed to emboli although in some 25% of TIA patients there is no source of embolism to be found in either the heart or neck vessels and angiographically visible carotid lesions are present only in about half the patients with carotid distribution TIA. A case is reported with repeated attacks of amaurosis fugax without remaining neurological symptoms in this very sensitive area. This and similar case histories raise the possibility of spasm in the cerebral arteries as the underlying cause of certain forms of TIA. As certain Ca-blocking agents, such as nifedipine and especially nimodipine, can relieve spasm, there are reasons to conduct a controlled study in man to find out if and to what extent a Ca-blocker with a verified effect on cerebral artery spasm in animal experiments has a beneficial effect on TIA in man.

Animals↗