Safety of enoxaparin versus unfractionated heparin during percutaneous coronary intervention.

We sought to determine the safety and efficacy of enoxaparin versus unfractionated heparin during percutaneous coronary intervention (PCI). Four hundred ninety-three consecutive patients undergoing elective or emergency PCI received unfractionated heparin (70 U/kg, intravenously) or enoxaparin (1 mg/kg, intravenously). Patients who had received subcutaneous enoxaparin in the emergency department were given a supplementary 0.3-mg/kg intravenous dose. There was no crossover of therapies. All patients received oral antiplatelet therapy and eptifibatide. Primary safety outcomes were bleeding and a postprocedural hemoglobin decrease of >or=3 g/dL. Troponin I levels were considered a marker for myocardial injury.Two hundred twenty-two patients received enoxaparin, and 271 received unfractionated heparin. There were no thrombotic events or in-hospital deaths. Multivariate logistic regression analysis showed that, compared with unfractionated heparin, enoxaparin yielded a lower risk of bleeding (odds ratio [OR]=0.47; 95% confidence interval [CI], 0.21-1.05) and significantly fewer >3-g/dL decreases in hemoglobin (OR=0.45; 95% CI, 0.22-0.94). Enoxaparin also produced less of a decrease in mean platelet count (41 +/- 34 vs 55 +/- 63 x10(9)/L; P = 0.02) and in platelets >30% from baseline (OR=0.56; 95% CI, 0.31-0.99). After elective PCI, fewer enoxaparin patients had troponin I levels >or=3 times the upper limit of normal (OR=0.40; 95% CI, 0.028-0.66).Compared with unfractionated heparin, enoxaparin entailed less bleeding during both elective and emergent PCI and less cardiac enzyme elevation in patients undergoing elective PCI. Therefore, we believe that intravenous enoxaparin is a safe alternative to unfractionated heparin in both settings.

Spontaneous closure of an iatrogenic circumflex coronary artery-to-coronary vein fistula.

Coronary artery fistulae are rare and usually discovered as incidentally during coronary angiography. They may be congenital or acquired secondary to trauma or cardiac intervention, and usually involve the left anterior descending or right coronary artery, with the circumflex artery much less often affected. They have been reported in transplanted hearts, usually as a secondary complication to right ventricular biopsies, and typically drain into the right ventricle. We hereby report a case of circumflex coronary artery to the great cardiac vein fistula that we believe occurred after transplantation and spontaneously closed while we were assessing the patient for percutaneous closure of the fistula.

Monitoring of enoxaparin level using citrated clotting time during percutaneous coronary intervention.

OBJECTIVES: To evaluate the use of citrated clotting time (CCT) during percutaneous coronary intervention (PCI) in both emergent and elective scenarios and using intravenous (IV) or subcutaneous (SC) dosing. BACKGROUND: Monitoring of enoxaparin during PCI had limitations in the past due to lack of point-of-care testing. Introduction of the CCT enables the determination of the degree of anticoagulation by enoxaparin. METHODS AND RESULTS: An analysis on 51 consecutive patients revealed that after three SC doses (1 mg/kg twice a day) or a single IV bolus (1 mg/kg) of enoxaparin, the CCT was consistently in the therapeutic range of > or =260 seconds (475 +/- 105 and 565 +/- 151 sec, respectively). Patients who received < 3 SC doses of enoxaparin were subtherapeutic for PCI. A supplemental IV bolus of 0.3 mg/kg was found always to raise the CCT to therapeutic level (499 +/- 178 sec). CONCLUSIONS: Enoxaparin was found to be effective and safe during PCI with low vascular complication rate (9.3%). Patients who received < 3 SC doses of enoxaparin benefit most from using CCT monitoring. IV dosing consistently achieved adequate anticoagulation.

Profound sinus bradycardia due to diltiazem, verapamil, and/or beta-adrenergic blocking drugs.

Both beta-adrenergic receptor antagonist drugs (beta-blockers) and non-dihydropyridine calcium-channel blockers (non-DHP CCBs), ie, diltiazem and verapamil, can cause sinus arrest or severe sinus bradycardia, and when drugs from the two classes are used together, these effects may be more than additive. We report nine patients in whom a beta-blocker (one patient), a non-DHP CCB (one patient), or the combination (seven patients) caused sinus arrest or severe sinus bradycardia which resulted in hospitalization in six of the nine. Although this combination of drugs always has the potential for causing profound bradycardia, certain aspects of the history, such as age, the presence of renal or hepatic disease, and the number and types of other medications, are further predictors of marked bradycardia with hypotension.