Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate coronary vasospastic activity after percutaneous transluminal coronary angioplasty (PTCA), we performed intracoronary injection of acetylcholine in 55 patients, mean 3.3 months after successful PTCA. Coronary spasm was defined as transient total or subtotal occlusion of the PTCA sites. Sixty-nine lesions of the 55 patients were examined to determine whether spasm was provoked by incremental doses of acetylcholine. Restenosis was defined as coronary luminal narrowing of > or = 50% after nitroglycerin or isosorbide dinitrate. Twenty of the 55 patients (36%) and 23 of the 69 lesions (33%) had coronary spasm. There was no correlation between the incidence of coronary spasm and the interval from PTCA to the acetylcholine test. The spasm was provoked in 17 lesions of the 50 non-restenotic lesions (34%) and was also provoked in 6 of the 19 restenotic lesions (32%). On the other hand, restenoses occurred in 6 of the 23 spastic lesions (26%) and in 13 of the 43 non-spastic lesions (28%). There was no correlation between the incidence of coronary spasm and the occurrence of restenoses. Twenty-four patients had undergone acetylcholine provocative test before PTCA. Among these 24 patients, 11 had coronary spasm before PTCA, and 7 had coronary spasticity after PTCA. Four patients who had positive evidence of coronary spasm before PTCA did not show negative spasm after PTCA. On the other hand, 3 patients who did not show evidence of coronary spasm showed positive evidence of coronary spasm after PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiol 1991
PMID:[Coronary vasospastic activity at sites of percutaneous transluminal coronary angioplasty: evaluation using intracoronary acetylcholine administration]. 184 42

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.
J Cardiol 1997 May
PMID:[Reproducibility of spasm in patients with long-term remission of vasospastic angina by medical treatment]. 917 79

Native coronary artery spasm is a very rare complication during off-pump coronary artery bypass grafting. We report the case of a 74-year-old man who experienced angiographically documentated right coronary artery spasm while undergoing off-pump coronary artery bypass grafting on the diseased left coronary system. Despite two episodes of ventricular fibrillation and persistent ST segment elevation of the posterior wall, the off-pump procedure was successfully completed by grafting the left internal thoracic artery to the left anterior descending artery and a saphenous vein graft to the Ramus intermedius. The immediate postoperatively performed coronary angiography demonstrated patent anastomoses and two areas of significant spasticity within the course of the right coronary artery. Intracoronary nitroglycerin infusion into the ostium of the right coronary artery resolved the spasms of this nondiseased vessel as well as the associated ST segment elevations.
Clin Res Cardiol 2006 Feb
PMID:Coronary artery spasm of the native right coronary artery during off-pump coronary surgery of the left coronary artery system. 1659 21

We discuss the case of a 71-year-old female patient who presented with findings suggestive of an acute myocardial infarction. Subsequent evaluation revealed an extrinsic cardiac mass encasing the left circumflex and right coronary arteries (RCA) which caused compression and spasticity of the RCA. Biopsy findings were consistent with a hematologic malignancy. Reports of extrinsic compression of epicardial coronary arteries are uncommon. Neoplasms, either primary cardiac tumors or metastatic disease, are a rare cause of extrinsic compression of coronary arteries.
J Invasive Cardiol 2008 Nov
PMID:Cardiac mass presenting as ST-elevation myocardial infarction: case report and review of the literature. 1898 5

Stroke is the second leading cause of death and the leading cause of disability in Western countries. More than 60% of patients remain disabled, 50% of patients suffer from hemiparesis and 30% remain unable to walk without assistance. The skeletal muscle is the main effector organ accountable for disability in stroke. This disability is primarily attributed to the brain lesion; however less attention is paid to structural, metabolic and functional alterations of muscle tissue after stroke. Hemiparetic stroke leads to various muscle abnormalities: A combination of denervation, disuse, inflammation, remodelling and spasticity accounts for a complex pattern of muscle tissue phenotype change and atrophy. The molecular mechanisms of muscle degradation after stroke are only incompletely understood. Reinnervation, fibre-type shift, disuse atrophy, and local inflammatory activation are only some of the key features yet to be explained. Only limited data is available today on clinical muscle changes after stroke that results from few studies in a mere 500 patients. Despite its importance for optimum post stroke recovery, stroke-related sarcopenia is not considered in current guidelines for stroke therapy or rehabilitation and measurement tools to address sarcopenia are infrequently used. This lack of robust evidence on muscle pathology after stroke and on treatment strategies needs to be addressed in an interdisciplinary integrated approach. This review provides an overview on current pathophysiologic insights and on clinical relevance of sarcopenia in stroke patients and on measurement tools to address the problem in the clinical setting.
Int J Cardiol 2013 Dec 10
PMID:Stroke induced Sarcopenia: muscle wasting and disability after stroke. 2423 Oct 58