Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spasm”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,495 records · Page 83Linked to original sources
PubMed1985

Role of coronary spasm in the genesis of myocardial infarction: study of a case treated by isosorbide dinitrate in situ then by transluminal angioplasty.

We report the observation of a 62-year-old patient who was admitted for unstable angina. A prolonged chest pain (more than two hours) with a major electrocardiographic lesion in the posterior leads needed an urgent coronary arteriography in order to attempt a recanalization. Antecedents of arteriopathy of the lower limbs with aortobifemoral bypass required an axillary artery right side approach. A selective right coronary opacification showed complete occlusion at the junction of segments 1 and 2. An intracoronary injection of isosorbide dinitrate relieved a coronary spasm and allowed a complete visualization of the right coronary artery. This appeared to be very atherosclerotic with several severe narrowings, and a subocclusive lesion at the site of the initial occlusion. Percutaneous transluminal coronary angioplasties (PTCA) were performed and led to real 'restructuring' of the right coronary artery. The clinical outcome was excellent without recurrent angina pectoris. An angiographic control performed 6 months after PTCA demonstrated the persistence of the coronary recanalization and an evident improvement of the segmental contractility. This report emphasizes the role of coronary spasm in the genesis of myocardial infarction and shows that PTCA may be performed as a first approach at the acute phase of myocardial infarction; to our knowledge it is the first PTCA performed by an axillary approach at the acute stage of myocardial infarction.

Angina Pectoris, Variant↗
PubMed1986

Recurrence of coronary artery spasm after successful percutaneous transluminal coronary angioplasty.

A 47-year-old man presented with angina, and coronary angiograms showed a significant organic stenosis with spasm in the left anterior descending coronary artery. Percutaneous transluminal coronary angioplasty was successfully performed for the organic lesion in the left anterior descending coronary artery. Symptom of angina due to coronary artery spasm recurred, even without restenosis at the site of successful angioplasty.

Angina Pectoris↗
PubMed2001

Detection of the "midband" lipoprotein in patients with coronary artery spasm.

BACKGROUND: Dyslipidemia in patients with coronary vasospasm has been characterized by a low level of high-density lipoprotein (HDL) cholesterol without elevation of low-density lipoprotein (LDL) cholesterol, distinct from patients with organic coronary artery disease. HYPOTHESIS: Disordered triglyceride-rich lipoprotein metabolism may be linked to the genesis of coronary artery spasm. METHODS: The incidence of the "midband" lipoprotein observed between very low-density lipoprotein (VLDL) and LDL bands in the polyacrylamide disc gel electrophoretic analysis was determined in 48 patients with coronary spastic angina (CSA), in 50 patients with stable effort angina and a significant fixed coronary stenosis (SEA), and in 40 control subjects without coronary artery disease (Control). RESULTS: The incidence was significantly (p<0.05) higher in CSA (71%) than in SEA (50%) and Control (25%). Smoking was significantly (p < 0.05) more prevalent in CSA (77%) than in SEA (50%) and Control (50%). In SEA, serum levels of triglyceride and apoproteins C-II, C-III, and E were all significantly higher, and the serum level of HDL cholesterol was significantly lower in the midband-positive than in the midband-negative subgroup. In CSA, no significant differences were found in these serum levels between the midband-positive and -negative subgroups, except for a significantly (p < 0.05) lower level of HDL cholesterol in the former. However, a significantly (p < 0.05) higher incidence of diabetes mellitus or impaired glucose tolerance was noted in the midband-positive (41%) than in the midband-negative subgroup (7%) in CSA. The incidence of the detected midband lipoprotein was significantly decreased in the blood samples obtained from 20 of CSA after a > 6-month angina-free period (70-->25%, p < 0.05). CONCLUSIONS: The midband lipoprotein was frequently detected in patients with coronary vasospasm, suggesting that dyslipidemia with disordered triglyceride-rich lipoprotein metabolism may be linked to the genesis of coronary artery spasm.

Adult↗
PubMed1980

'Variant' angina: evidence for small vessel coronary artery spasm?

A unique case of 'variant' angina pectoris has been observed in a patient with normal coronary arteries and typical chest pain appearing spontaneously at rest, and repeatedly provoked by ergonovine maleate (0.1 mg iv) associated with large transmural perfusion defects on 201Tl-imaging (after ergonovine) and a marked increase in T wave voltage despite no demonstrable spasm of a major coronary artery after the same doses of ergonovine. While saline solution could not provoke chest pain and treatment with a beta-blocking agent increased the frequency of ischemic attacks, a calcium antagonist therapy reduced and eventually eliminated the attacks. Thus, this case provides evidence for yet another aspect of a 'variant' form of angina pectoris: small vessel coronary artery spasm.

Adult↗
PubMed1982

Electrocardiographic alterations in subarachnoid haemorrhage. Correlation between spasm of the arteries of the left side on the brain and T inversion and QT prolongation.

In a retrospective study of 89 patients with subarachnoid haemorrhage (SAH), the frequency and specificity of changes in the electrocardiogram (ECG) were determined, as well as electrocardiographically established arrhythmias. The ECG changes were correlated with neurological as well as angiographic findings (localization of the aneurysm and vascular spasm). Abnormal ECGs were found in about 80% of the patients. The following abnormalities were found with decreasing frequency: depression and elevation of the ST segment, prolongation of the QT interval, flattening and inversion of the T wave, U waves and TU fusion waves, and arrhythmias (sinus tachycardia and bradycardia, extrasystole). A verified correlation (chi-square test) was shown between angiographically demonstrated spasm of the brain arteries of the left side and negative T waves as well as a prolongation of the QT interval. These results are related to the causal role of the left stellate ganglion in the generation of ECG changes and arrhythmias (animal experiments, and the success by blockade or surgical removal of the stellate ganglion in hereditary QT prolongation.

Adolescent↗
PubMed1998

[Coronary spasm--a clinically relevant problem?].

Coronary spasms are defined as reversible coronary stenosis, which limits coronary blood flow under resting conditions. The demonstration of either spontaneous or provoked coronary spasm proves coronary hypercontractility and thus the diagnosis of variant angina. Several stimuli can provoke coronary vasospasm, but the highest sensitivity and specificity has been shown with ergonovine. Alternatively acetylcholine or with less sensitivity, but high specificity, hyperventilation may be employed. Typically coronary vasospasm presents with angina pectoris at rest; the manifestation with myocardial infarction or syncope are of great clinical importance. The prevalence of the disease is unknown due to the rarely performed provocation tests in Western countries. The incidence of positive test results strongly depends on the symptoms of the patients; from 0% in patients without any evidence for myocardial ischemia up to 54% in patients with typical angina at rest have been observed. Coronary vasospasm is closely related to atherosclerotic coronary artery disease, since intravascular ultrasound studies reveal atherosclerotic plaques in almost any spastic segment. Risk factors for coronary artery disease and coronary vasospasm, however, differ profoundly. For the latter cigarette smoking is the only established risk factor. Although several candidates and predisposing factors (serotonin, histamine, thromboxane, endothelin) have been described, the mediators and the pathogenesis of the disease remains unknown. Endothelial dysfunction alone is not sufficient to explain the features of variant angina. Some evidence supports the hypothesis of local inflammation. The mortality in variant angina depends on the extent of the coronary artery disease. Pure coronary vasospasm does not lead to increased mortality; patients with highly active disease presenting with syncope may have an increased risk. Medical treatment should include long-acting calcium antagonists or nitrates, beta-blockers may even favor the occurrence of ischemic attacks. Although the benefit has not been proven, the use of aspirin may considered in highly active disease.

Coronary Vasospasm↗
PubMed2002

[Spontaneous coronary spasm as a rare cause of survived sudden cardiac death].

CASE REPORT: A 39-year-old man was admitted to our intensive care unit after successful resuscitation because of ventricular fibrillation with clinical and electrographic signs of acute myocardial infarction. Coronary angiography showed normal coronary arteries. MINC syndrome (myocardial infarction with angiographically normal coronary arteries) was due to a severe proximal spontaneous spasm of the left anterior descending artery (LAD). Intracoronary ultrasound imaging demonstrated an eccentric fibrous plaque in the proximal segment of LAD and a fibrofatty plaque distal to the spastic segment. At the time of electrophysiologic study, the patient was noninducible. After starting therapy with calcium antagonist, nitrate and molsidomine, the patient was stable and symptom-free. CONCLUSION: Coronary spasm without significant organic stenosis is an important cause of sudden cardiac arrest and MINC syndrome. Because of the good prognosis under adequate treatment, exact diagnosis is important in the prevention of sudden death.

Adult↗
PubMed2003

Characterization of basal hepatic bile flow and the effects of intravenous cholecystokinin on the liver, sphincter, and gallbladder in patients with sphincter of Oddi spasm.

The major objectives of this project were to establish the pattern of basal hepatic bile flow and the effects of intravenous administration of cholecystokinin on the liver, sphincter of Oddi, and gallbladder, and to identify reliable parameters for the diagnosis of sphincter of Oddi spasm (SOS). Eight women with clinically suspected sphincter of Oddi spasm (SOS group), ten control subjects (control group), and ten patients who had recently received an opioid (opioid group) were selected for quantitative cholescintigraphy with cholecystokinin. Each patient was studied with 111-185 MBq (3-5 mCi) technetium-99m mebrofenin after 6-8 h of fasting. Hepatic phase images were obtained for 60 min, followed by gallbladder phase images for 30 min. During the gallbladder phase, 10 ng/kg octapeptide of cholecystokinin (CCK-8) was infused over 3 min through an infusion pump. Hepatic extraction fraction, excretion half-time, basal hepatic bile flow into the gallbladder, gallbladder ejection fraction, and post-CCK-8 paradoxical filling (>30% of basal counts) were identified. Seven of the patients with SOS were treated with antispasmodics (calcium channel blockers), and one underwent endoscopic sphincterotomy. Mean (+/-SD) hepatic bile entry into the gallbladder (versus GI tract) was widely variable: it was lower in SOS patients (32%+/-31%) than in controls (61%+/-36%) and the opioid group (61%+/-25%), but the difference was not statistically significant. Hepatic extraction fraction, excretion half-time, and pattern of bile flow through both intrahepatic and extrahepatic ducts were normal in all three groups. Gallbladder mean ejection fraction was 9%+/-4% in the opioid group; this was significantly lower (P<0.0001) than the values in the control group (54%+/-18%) and the SOS group (48%+/-29%). Almost all of the bile emptied from the gallbladder refluxed into intrahepatic ducts; it reentered the gallbladder after cessation of CCK-8 infusion (paradoxical gallbladder filling) in all eight patients with SOS, but in none of the patients in the other two groups. Mean paradoxical filling was 204% (+/-193%) in the SOS group and less than 5% (P<0.05) in both the control and the opioid group. After treatment, six of the SOS patients had complete pain relief and one, partial pain relief. The basal tonus of the sphincter is variable in patients with SOS, and allows relatively more of the hepatic bile to enter the GI tract than the gallbladder. Due to simultaneous contraction of the sphincter and gallbladder in response to CCK-8, most of the bile emptied from the gallbladder refluxes into intrahepatic ducts, and reenters the gallbladder immediately after cessation of hormone infusion. The characteristic features of gallbladder filling, emptying, and paradoxical refilling with cholecystokinin provide objective parameters for noninvasive diagnosis of SOS by quantitative cholescintigraphy.

Adult↗
PubMed2006

Right coronary artery spasms triggered by mechanical compression during off-pump coronary artery bypass grafting surgery.

In this case report, we describe recurrent spasms of the right coronary artery with no apparent preexisting abnormal angiogram that caused second-degree atrioventricular (AV) block and inferior wall hypokinesis. These hemodynamic changes were induced by mechanical compression of the right coronary artery by a pericardium drain tube. From our experience, we should be aware that mechanical compression may trigger an exaggerated vasomotor response, leading to severe coronary artery spasms.

Aged↗
PubMed2006

Esophageal motility disorders (distal esophageal spasm, nutcracker esophagus, and hypertensive lower esophageal sphincter): modern management.

The group of hypercontractile esophageal motility disorders includes distal esophageal spasm (DES), nutcracker esophagus (NE), and hypertensive lower esophageal sphincter (LES). The clinical relevance of these abnormalities identified during esophageal manometry is debated, and their management can be challenging. Hypercontractile esophageal motility abnormalities are defined through specific manometric criteria. Current pathophysiologic concepts for these abnormalities include defects in the nitronergic neural pathways and imbalances between the cholinergic and nitronergic pathway. Proposed treatments for NE, DES, and hypertensive LES include proton-pump inhibitors, nitrates, calcium channel blockers, phosphodiasterase inhibitors, and tricyclic antidepressants or serotonin reuptake inhibitors. Small case series reported benefits after botulinum toxin injections, dilatations, and myotomies. The optional management of esophageal spasm, NE, and hypertensive LES is still debated. Treatment recommendations are based on controlled studies with small numbers of patients or on case series. Medical treatment, including acid suppression, smooth muscle relaxants, and visceral analgesics, should be tried first. In nonresponding patients, botulinum toxin injections or balloon dilatations can be tried. Pneumatic dilatations or myotomies should be regarded as last-option treatments for nonresponding patients.

Journal Article↗
PubMed2004

Hemifacial Spasm.

Hemifacial spasm (HFS) is a peripheral movement disorder caused by direct or indirect compression or distortion of the root exit zone of the seventh cranial nerve, which is most commonly compressed by an arterial loop, but also may be compressed by a tumor, cyst, or aneurysm. All patients with HFS should undergo magnetic resonance imaging, with particular attention to the seventh cranial nerve. For patients with HFS who want treatment, there are three options. Oral medications, particularly anticonvulsants, may be useful, but the response rate is low and evidence is almost exclusively anecdotal. Local injection of botulinum toxin into the overactive muscles has a very high rate of success and virtually no serious side effects. Backed by controlled clinical trials, the authors consider it the treatment of choice. Microvascular surgical decompression has the advantage of being potentially curative, and obviates the need for chronic injections with botulinum toxin. However, surgery carries much greater risk than botulinum toxin and the spasm may recur. It is important that surgery is carried out by an experienced neurosurgeon to reduce the risk.

Journal Article↗
PubMed1981

Histamine provocation of clinical coronary artery spasm: implications concerning pathogenesis of variant angina pectoris.

Twelve patients with nonexertional chest pain and nonobstructive fixed coronary disease (less than 50% luminal diameter narrowing) were given histamine to investigate the potential role (coronary artery H1 receptor agonism) of the endogenous agent in producing coronary artery spasm (CAS). Histamine, at intravenous dose of 0.5 to 1.0 microgram/kg/min, provoked CAS in four patients. In six patients neither histamine nor ergonovine provoked spasm, and these patients were considered by chronic follow-up evaluation to have noncardiac etiology for their chest pain syndrome. In one patient CAS was provoked with ergonovine but not by histamine, and one ergonovine-positive patient had an equivocally positive histamine result. Pretreatment with cimetidine (H2 receptor antagonism) was necessary to avoid unpleasant side effects of histamine. Thus these observations indicate that histamine should be included among the specific agents capable of inducing CAS and provide new insight concerning the mechanism(s) causing variant angina pectoris.

Adult↗
PubMed1981

Platelet activation in clinical coronary artery disease and spasm.

Current concepts of atherogenesis, based on animal models, suggest a role for platelets in the development of atherosclerotic lesions, possibly through the release of alpha granule constituents. Platelets may also contribute to the development of vascular spasm through thromboxane A2 production. Platelet activation in the coronary circulation in patients with coronary artery disease (CAD) should occur if these hypotheses apply clinically. We measured aortic and coronary sinus plasma levels of the platelet alpha granule constituent beta-thromboglobulin (B-TG) and thromboxane B2 (TX B2) by radioimmunoassay in 15 patients with severe atherosclerotic CAD, seven patients with angiographically normal coronaries, and five patients undergoing evaluation for coronary artery spasm (CAS). Compared with the controls, CAD patients had significantly greater transmyocardial release of B-TG (11.1 +/- 8.1 ng/ml, mean +/- SEM vs 62.5 17.2, p less than 0.05 by rank sum test); TX B2 gradients showed a similar trend but the difference was not statistically significant (-0.08 +/- 0.03 ng/ml vs 0.22 +/- 0.02, 0.05 less than p less than 0.10). Three of the five patients studied developed CAS which was associated with acute elevation in coronary sinus TX B2; the two non-CAS patients with drug provocation had undetectable coronary sinus TX B2. We conclude that abnormal platelet activation takes place in the coronary circulation of CAD patients, and that production of acute myocardial ischemia by CAS occurs with increased coronary sinus TX B2.

Angina Pectoris↗
PubMed1981

Clinical course of patients following the demonstration of coronary artery spasm by angiography.

The clinical course of 25 patients was determined during an average of 2.7 years following the angiographic demonstration of coronary artery spasm (CAS). Seventeen patients received medical treatment after the demonstration of coronary spasm and six patients had cardiac surgery. Twenty-three patients were living and two patients had died at the time of follow-up. Twenty-one of the 23 surviving patients has either no chest pain or markedly reduced symptoms. However, the demonstration of CAS by angiography was associated with a high incidence of subsequent cardiac complications, which included myocardial infarct (four patients), cardiac arrest (four patients), and death (two patients). We concluded from this study that after the demonstration of CAS by angiography: (1) the clinical course was variable, with most patients (21 of 25 patients, 84%) having improvement of symptoms at the time of follow-up; (2) major cardiac complications were frequent (11 out of 25 patients, 44%) and; (3) although clinical and coronary angiographic features were of limited use in predicting major cardiac complications, most of the patients who had an uncomplicated course (11 of 14 patients, 79%) had either less than 50% fixed coronary artery luminal diameter narrowing (CAN) or coronary artery bypass graft operations, the majority of patients with less than 50% CAN (8 of 11 patients, 73%) had no major cardiac complications, and myocardial infarction or death usually occurred during periods of increased angina pectoris.

Adult↗
PubMed1982

Randomized double-blind comparison of nifedipine and isosorbide dinitrate therapy in variant angina pectoris due to coronary artery spasm.

Twelve patients were entered prospectively into a randomized double-blind study comparing the efficacy of nifedipine and isosorbide dinitrate (ISDN) in the treatment of variant angina pectoris due to coronary artery spasm. Using the diary technique, both anginal episodes and nitroglycerin tablets consumed were recorded during the pretrial, no drug period, and both active drug phases. During the baseline pretrial period, an average of 1.1 anginal episodes/day occurred with reduction to 0.28/day during nifedipine treatment and 0.39/day during ISDN treatment. Headache was the major side effect during ISDN treatment, occurring in 9 of 11 (81%) patients; and nonheart failure related pedal edema during nifedipine treatment, occurring in 4 of 12 (33%) patients. Intolerable side effects necessitating cessation of treatment occurred in two patients during nifedipine treatment and in three patients during ISDN treatment. Patients preferred nifedipine over ISDN because of increased efficacy and fewer uncomfortable side effects. We conclude that both nifedipine and ISDN are effective therapy for coronary spasm, but that nifedipine was more effective and was preferred by the majority of patients.

Adult↗
PubMed1983

Arterial and coronary sinus catecholamines in the course of spontaneous coronary artery spasm.

We studied plasma catecholamine levels in 10 patients with frequent spontaneous episodes of coronary artery spasm to evaluate the role of the sympathetic nervous system. Peripheral venous norepinephrine in supine and upright postures, urinary excretion of catecholamines, and functional testing of the sympathetic nervous system did not differ from the same measurements in control subjects. Arterial and coronary sinus levels of norepinephrine and epinephrine drawn early in ischemia were not elevated over baseline; coronary sinus norepinephrine levels were higher than those in arterial samples and rose from 315 +/- 32 (pg/ml +/- SE) at the onset of ST elevation to 490 +/- 49 pg/ml late in ischemia (p less than 0.05). Plasma epinephrine levels, higher in arterial than coronary sinus samples, also rose significantly only late in ischemia, from 44 +/- 14 pg/ml to 148 +/- 35 pg/ml (p less than 0.05) in arterial blood and from 33 +/- 10 pg/ml to 108 +/- 29 pg/ml in coronary sinus samples (p less than 0.05). Generalized sympathetic nervous system activation is not likely to be the sole cause of coronary artery spasm.

Adult↗
PubMed1983

Myocardial infarction in patients with coronary artery spasm demonstrated by angiography.

Twelve cases of myocardial infarction (MI) were documented in 11 of 39 patients who had coronary artery spasm (CAS) that was observed by angiography either before MI (3 patients), after MI (5 patients), or both before and after MI (3 patients). MI corresponded in location to sites of ECG changes of myocardial ischemia during spontaneous angina pectoris in 7 of 7 patients and to the region of myocardium supplied by the vessel in which CAS was observed by angiography in each patient. MI occurred in the distribution of the right coronary artery in 8 patients and of the left coronary artery in 4 patients. Of 12 vessels that supplied infarcted regions of myocardium, 7 vessels had greater than or equal to 50% diameter fixed coronary artery narrowing (CAN), but the remaining 5 vessels had minimal (10%) or no fixed CAN. In those patients who were studied after MI, coronary angiography demonstrated that only 3 of 9 vessels in the distribution of infarcted regions of myocardium were completely occluded. Clinical follow-up for an average of 1.3 years after MI showed that 7 patients continued to have chest pain, 2 patients were asymptomatic, and 2 patients died suddenly 9 weeks and 1 year, respectively, after MI. Therefore, among our patients with CAS demonstrated by angiography, MIs (1) were frequent (28%), (2) occurred in the distribution of observed coronary spasm, (3) were frequently (5 of 12 arteries) in the distribution of vessels having minimal or no fixed narrowing, and (4) were often (6 of 9 arteries) in the distribution of vessels that were demonstrated to be patient after MI.

Adult↗