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Changing features of anginal pain after PTCA suggest a stenosis on a different artery rather than restenosis
No full textBackground We recently found that patients who had had two myocardial infarctions in different myocardial regions frequently reported different locations of infarct pain, whereas patients who had had two infarcts at the same site had a similar distribution of pain. The aim of this study was to assess whether a different location of anginal pain may help identify patients with a new stenosis on an artery perfusing another myocardial region as opposed to those with restenosis after coronary angioplasty (PTCA). Methods and Results We studied 38 patients (59 +/- 11 years old) who underwent PTCA for single-vessel disease, with recurrence of symptoms requiring repeat coronary angiography during a 3-year follow-up. According to our inclusion criteria, angiography showed either a significant restenosis of the dilated lesion, with no evidence of lesions in the other vessels (n = 26), or a new stenosis in either of the other coronary arteries, with no restenosis in the dilated vessel (n = 12). Before each procedure, patients reported the location and radiation of anginal pain. There was no relation between location of pain and site of the coronary stenosis. However, none of the patients viith restenosis reported a different location of pain after angioplasty, compared with 5 patients with new stenosis (0% versus 42%, P = .002). Radiation of pain involved different areas of the body in 1 patient with restenosis and in 6 with new stenosis (4% versus 50%, P = .002). Overall, location or radiation of pain in a different body area had a specificity of 96% and a sensitivity of 58% in detecting a stenosis an a new artery. Conclusions A different location of anginal pain may distinguish patients with a new coronary stenosis from those with restenosis after PTCA for single-vessel disease. These findings suggest that in individual patients, differences in the location of cardiac pain may be indicative of the occurrence of ischemia in different myocardial regions
Changing features of anginal pain after PTCA suggest a stenosis on a different artery rather than restenosis
No full textPrevention of myocardial damage during coronary intervention
No full textMyocardial injury during coronary intervention occurs in 10-40% of cases and is often characterized by a slight increase of markers of myocardial necrosis, without symptoms, electrocardiographic changes or impairment of cardiac function. However, even small increases of creatine kinase-MB levels are expression of a true and detectable infarction, and may be associated with higher follow-up mortality. The cause of CK-MB elevation in case of procedural complications (dissection, transient vessel closure, no reflow, side branch occlusion etc.) is obvious; however, most cases of minor CK-MB elevation occur in patients with uncomplicated procedure with excellent final angiographic results. It has been suggested that the main mechanism explaining occurrence of myocardial necrosis during otherwise successful coronary interventions may be distal microembolization of plaque components, an enhanced inflammatory state or due to total plaque burden and/or to plaque instability. Different treatments have been proposed to prevent myocardial injury during coronary intervention, including nitrate infusion, intracoronary beta-blockers, adenosine, clopidogrel and IIb/IIIa inhibitors, but none of those (apart from the use of IIb/IIIa inhibitors) has been routinely introduced in clinical practice. We performed the ARMYDA (Atorvastatin for Reduction of MYocardial Damage during Angioplasty) trial, i.e. the first prospective, randomised, placebo controlled study to evaluate effects of 7 days of pre-treatment with a fixed dose of atorvastatin (40 mg/day) on post-procedural release of markers of myocardial damage in patients with stable angina undergoing percutaneous intervention. In this study therapy with atorvastatin has been associated with 80% risk reduction on the occurrence of peri-procedural myocardial infarction, as well as with significant reduction of post-intervention peak levels of all markers of myocardial damage. The mechanisms underlying the beneficial effects of atorvastatin may be an inflammatory action reducing myocardial necrosis due to microembolization, an improvement of endothelial function on microcirculation, and direct protection of myocardium
Contributors to survival benefit of dual versus single antithrombotic therapy in chronic coronary syndrome: Survival benefit of dual antithrombotic therapy in CCS
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