Iatrogenic takotsubo cardiomyopathy induced by locally applied epinephrine and cocaine.

A 67-year-old man underwent surgery under general anaesthesia to obtain a biopsy from a tumour in the left maxillary sinus. Before the procedure a mucosal detumescence containing epinephrine and cocaine was applied onto the nasal mucosa. Shortly after termination of anaesthesia the patient developed tachycardia and an abrupt rise in blood pressure followed by a drop to critical levels. The patient turned pale and clammy but denied chest pain at any time. An ECG showed inferolateral ST-segment elevation, and troponin T was elevated at 0.773 ng/mL. An acute coronary angiography demonstrated normal coronary arteries; however, left ventriculography showed apical ballooning of the left ventricle, and the diagnosis of takotsubo cardiomyopathy was made. This was confirmed by a subsequent transthoracic echocardiography. Four days later the patient had complete resolution of the symptoms, and a new echocardiography showed normalisation of the left ventricular systolic function with no signs of apical ballooning.

Platelet response to aspirin and clopidogrel in patients with peripheral atherosclerosis.

Aspirin and clopidogrel are important drugs in the secondary prevention of ischemic events. A considerable individual variation in platelet response to these drugs has, however, been reported, and high residual platelet reactivity despite treatment may be an independent risk factor for ischemic events. Most studies have been undertaken in patients with coronary heart disease, but patients with peripheral artery disease (PAD) may exhibit greater residual platelet reactivity, possibly because of platelet activation by a larger area of diseased endothelium. It is yet unsettled which method that best measures platelet reactivity and an eventual lack of response to aspirin. Several instruments are promoted to measure platelet response and low-response to platelet inhibitors, but it is questionable if they measure this in comparable ways. We studied the comparability of three tests of platelet reactivity for the assessment of low-response to aspirin and clopidogrel in patients with PAD. In 263 patients, platelet function was assessed twice, 3 months apart, by the Platelet Function Analyzer-100 (PFA), light transmission aggregometry (LTA), and whole blood impedance aggregometry (IA). In a subgroup of 43 patients, we studied the effect of a single dose of 600 mg clopidogrel on platelet function. Low-response to aspirin assessed by analyses targeting cyclooxygenase-1 activity (LTA, IA) was rare (≤ 8.1%). With the PFA, we found 17% with low response at both visits, and 60% who were consistently responsive, whereas 23% were categorized differently at the two visits. Low response to clopidogrel, occurred in 0-23%, depending on the method and the criteria used. A low-response to aspirin, defined by lack of COX-1 inhibition, is a rare phenomenon whereas high residual platelet reactivity as determined by PFA may be a rather frequent finding but is not consistent over time in all patients. A low-response to clopidogrel depends very much on the method and definition used.

Long-term aspirin and clopidogrel response evaluated by light transmission aggregometry, VerifyNow, and thrombelastography in patients undergoing percutaneous coronary intervention.

BACKGROUND: A reduced response to aspirin and clopidogrel predicts ischemic events, but reliable tests are needed to identify low responders. We compared 3 platelet-function tests during long-term dual treatment with aspirin and clopidogrel. METHODS: Patients who underwent a percutaneous coronary intervention and were receiving a combination of 325 mg/day aspirin and 75 mg/day clopidogrel were followed for 1 year. Blood was sampled 5 times during this period for 3 tests: light transmission aggregometry (LTA) assay, with 5.0 micromol/L ADP or 1.0 mmol/L arachidonic acid (AA) used as an agonist; VerifyNow assay, with the P2Y(12) or aspirin cartridge (Accumetrics); and thrombelastography (TEG), stimulated by 2.0 micromol/L ADP or 1.0 mmol/L AA. RESULTS: Twenty-six of 33 patients completed all scheduled visits. A low response to clopidogrel was found in a few patients at variable frequencies and at different visits, depending on the method and criteria used. We found a moderate correlation between the LTA (ADP) and VerifyNow (P2Y(12) cartridge) results, but the TEG (ADP) results correlated poorly with the LTA and VerifyNow results. A low response to aspirin was found with the VerifyNow (aspirin cartridge) and TEG (AA) methods on 6 and 2 occasions, respectively, but not with the LTA (AA) method, except for 1 occasion caused by probable noncompliance. CONCLUSIONS: Detecting a low response to clopidogrel depends largely on the method used. Which method best predicts ischemic events remains uncertain. A low response to aspirin is rare with AA-dependent methods used at the chosen cutoffs. In some patients, the response to clopidogrel or aspirin may be classified differently at different times, even with the same method.

The ELAPSE (Evaluation of Long-Term Clopidogrel Antiplatelet and Systemic Anti-Inflammatory Effects) study.

OBJECTIVES: This study was designed to evaluate the effects of long-term clopidogrel and aspirin administration on platelet aggregation, activation, and inflammation. BACKGROUND: Clopidogrel resistance was described in 15% to 30% of patients with short-term therapy, but its antiplatelet effects with long-term therapy is unknown. METHODS: We performed a prospective study of patients undergoing coronary stenting who were on aspirin for > or =5 days but not previously on clopidogrel. Clopidogrel 600 mg was given before stenting. Clopidogrel 75 mg/day and aspirin 325 mg/day were continued for 1 year. Light-transmittance aggregometry with 5-micromol/l adenosine diphosphate and 1-mmol/l arachidonic acid stimulation; VerifyNow clopidogrel and aspirin assays; platelet activation receptor expression of CD40L, CD62P, and PAC-1 (antibody against activated glycoprotein IIb/IIIa); and inflammatory markers of soluble CD40L and P-selectin, high-sensitivity C-reactive protein, interleukin-10, and interleukin-18 were measured at baseline; 1 day; and 1, 6, and 12 months. Our primary analysis compared light-transmittance aggregometry aggregation at 1 versus 12 months. RESULTS: We enrolled 26 patients who completed a 1-year follow-up. Maximal platelet adenosine diphosphate-stimulated aggregation was 61.8 +/- 25.9% at baseline, 22.1 +/- 18.3% at 1 day, 30.6 +/- 16.8% at 1 month, 29.0 +/- 13.3% at 6 months, and 26.7 +/- 13.6% at 12 months (p = 0.099 for 12 months vs. 1 month). VerifyNow clopidogrel platelet inhibition was similar at 12 months versus 1 month (38.9 +/- 19.7% vs. 45.6 +/- 26.7%, p = 0.578). Likewise, there was no difference in aspirin's effects on platelet aggregation at 12 months versus 1 month. In contrast, platelet activation receptor expression of CD40L, CD62P, and PAC-1 were higher at 12 months versus 1 month. CONCLUSIONS: Our pilot study showed no attenuation of clopidogrel's effects on platelet aggregation with long-term administration. However, platelet activation receptor expression increased with time and should be further evaluated.

Acute coronary artery thrombosis and a giant coronary artery aneurysm: an atypical combination and an unconventional catheter-based intervention.

Coronary artery aneurysm is an unusual finding at coronary arteriography. We present a case of acute myocardial infarction and a giant aneurysm of the left circumflex coronary artery (CX) in a 70-year-old male with hypertension. The culprit lesion was a thrombus occupying the aneurysm and the distal CX. By an unconventional manoeuvre the thrombus was aspirated via the 7 French guiding catheter. After stent implantation in the distal CX a thrombolysis in myocardial infarction 3 flow was achieved and still present at 2-month follow-up. The patient was prescribed aspirin and clopidogrel as a life-long therapy.