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Vasospastic Angina (vasospastic + angina)
Selected AbstractsLeft Atrial Catheter Ablation Promotes Vasoconstriction of the Right Coronary ArteryPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2007EIJI YAMASHITA M.D. Background: Multiple cardiac ganglia are present in the left atrial (LA) region, and marked changes in autonomic nervous activity can occur after left atrial catheter ablation (CA) for atrial fibrillation (AF). Vasospastic angina involving the inferior wall of the left ventricle has been reported as a complication shortly after LACA. Methods: We studied 20 patients with drug-refractory AF who underwent LACA, performed to encircle the left- and right-sided pulmonary veins, 1 to 2 cm from their ostia under fluoroscopic guidance. Quantitative coronary angiography was performed before and after LACA, and we analyzed the minimal lesion diameter (MLD) of the proximal segment of the coronary arteries, and the basal tone, the baseline percent constriction versus maximal dilation after nitroglycerin administration. Results: No significant difference was observed in MLD or basal tone of the left coronary arteries after LACA. However, in the right coronary artery (RCA), the basal MLD was smaller (P < 0.01) and the basal tone was greater (P< 0.05) after than before LACA. No correlation was found between the baseline MLD or tone of the RCA and total amount of radiofrequency energy delivered or procedure duration. In 75% of RCA, the baseline MLD was smaller after than before LACA, which was significantly higher (P < 0.01) than observed in the left coronary arteries (38%). Conclusion: Vasoconstriction was promoted in the RCA shortly after LACA, which may explain the variant angina reported after LACA. [source] Stent implantation in variant angina refractory to medical treatmentCLINICAL CARDIOLOGY, Issue 12 2006Dr Vicens Martí M.D. Abstract Background Vasospastic angina usually responds well to medical treatment. Hypothesis The present study describes our experience in patients who received a coronary stent because of recurrent variant angina refractory to medical treatment and evaluates stent implantation as an alternative treatment. Materials and methods Between March 1998 and February 2005, recurrent variant angina was diagnosed in 22 patients admitted to our coronary care unit. Of these, five patients (22.7%), were refractory to pharmacologic treatment. Coronary angiography and coronary stents were indicated. Clinical follow-up was 29 ± 6 months. Results Stenting was performed during diagnostic coronary angiography in two patients. In the other three patients, the stent was implanted 24,48 h later. We observed coronary spasm recurrences proximal or distal to the stent in four patients,two during the stent implantation procedure and the other two in the coronary care unit within 48 h post angioplasty. Three patients where treated with additional stenting and the fourth patient improved with pharmacologic treatment. During follow-up three patients remained asymptomatic. The fourth patient had diffuse in-stent restenosis in the third month, and the fifth patient showed a de novo lesion in the treated segment 2 years later. Conclusions Stent implantation in patients with recurrent variant angina refractory to medical treatment may be an alternative treatment in carefully selected, clinically unstable patients. Spasm recurrences may occur in other segments of the treated artery, probably due to the diffuse nature of the disease. Immediate and continued surveillance is recommended because of the risk of adverse clinical events. Copyright © 2006 Wiley Periodicals, Inc. Wiley Periodicals, Inc. [source] Outpatient Intravenous Dihydroergotamine for Refractory Cluster HeadacheHEADACHE, Issue 3 2004E. Magnoux MD Objective.,To evaluate the efficacy and safety of outpatient intravenous dihydroergotamine (DHE) for treatment of refractory cluster headache. Method.,Medical records were retrospectively reviewed of all patients with cluster headache who received outpatient intravenous DHE for treatment of refractory cluster headache between January 1992 and May 2000. Results.,One hundred four treatments were identified in 70 patients. There were 7 dropouts. Of the 97 completed treatments, 60 were for episodic cluster headache and 37 were for chronic cluster headache. Results for all treatments showed complete resolution of pain during the intravenous phase at 1 month in 61 (63%) of 97 cases, partial resolution in 13 cases (15%), and failure in 23 cases (24%). For the treatment of episodic cluster headache, there was complete resolution in 44 (73%) of 60 cases, partial resolution in 9 cases (13%), and failure in 7 cases (12%). For treatment of chronic cluster headache, there was complete resolution in 17 (46%) of the 37 cases, partial resolution in 4 cases (11%), and 16 failures (43%). As regards side effects and safety, the treatment triggered chest pain suspected of being vasospastic angina in 1 patient on day 7 of the treatment, when she was in the subcutaneous phase. Two patients dropped out due to fear of the injection, 1 because of palpitations, 1 because of chest tightness, and 2 others because of leg cramps, nausea, and diarrhea. Conclusions.,Outpatient intravenous DHE is a safe treatment. It is useful for refractory cluster headache, is more effective for the episodic form than the chronic form, and has a rapid onset of action. It did not change the evolution of the episodic form, but it did appear to induce remission in the chronic form or transform it to the episodic form. We advance a hypothesis to explain this. [source] Cardiotoxicity with 5-fluorouracil and capecitabine: more than just vasospastic anginaINTERNAL MEDICINE JOURNAL, Issue 4 2010T. Stewart Abstract In this case series we present a variety of different cardiac toxicities with 5-fluorouracil and its pro-drug capecitabine, including myocardial infarction, cardiomyopathy, sinoatrial and atrioventricular node dysfunction, tako-tsubo cardiomyopathy and QT prolongation with torsade-de pointes ventricular tachycardia. We stress the fact that while vasospasm is a well-recognized side-effect of this class of chemotherapeutic agent, broader cardiotoxicity is commonly seen and an increased awareness of the range of toxicity is necessary if repeat toxicity is to be avoided. [source] Occurrence of "J Waves" in 12-Lead ECG as a Marker of Acute Ischemia and Their Cellular BasisPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2007SHINDE RITUPARNA M.D. The "J wave" (also referred to as "the Osborn wave,""the J deflection," or "the camel's hump") is a distinctive deflection occurring at the QRS-ST junction. In 1953, Dr. John Osborn described the "J wave" as an "injury current" resulting in ventricular fibrillation during experimental hypothermia. Although "J Wave" is supposed to be pathognomonic of hypothermia, it is seen in a host of other conditions such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from over sedation, the Brugada syndrome, vasospastic angina, and idiopathic ventricular fibrillation. However, there is paucity of literature data as regards to ischemic etiology of "J Wave." In this article, we present a case where "J waves" were probably induced by ischemia. We also discuss the mechanism of ischemia-induced "J wave" accentuation and its prognostic implications. [source] | ||||||||||