Percutaneous Repair of Postoperative Mitral Regurgitation After Left Ventricular Assist Device Implant.

Mitral regurgitation commonly improves after implantation of a left ventricular assist device without concomitant valvular repair owing to the mechanical unloading of the left ventricle. However, the development (or persistence) of significant mitral regurgitation after implantation of a left ventricular assist device is associated with adverse clinical events. We present a case of a left ventricular assist device patient who successfully underwent a percutaneous MitraClip procedure for repair of persistent late postoperative mitral insufficiency with demonstrable clinical and hemodynamic improvement.

The State of the Absorb Bioresorbable Scaffold: Consensus From an Expert Panel.

Significant progress has been made in the percutaneous coronary intervention technique from the days of balloon angioplasty to modern-day metallic drug-eluting stents (DES). Although metallic stents solve a temporary problem of acute recoil following balloon angioplasty, they leave behind a permanent problem implicated in very late events (in addition to neoatherosclerosis). BRS were developed as a potential solution to this permanent problem, but the promise of these devices has been tempered by clinical trials showing increased risk of safety outcomes, both early and late. This is not too dissimilar to the challenges seen with first-generation DES in which refinement of deployment technique, prolongation of dual antiplatelet therapy, and technical iteration mitigated excess risk of very late stent thrombosis, making DES the treatment of choice for coronary artery disease. This white paper discusses the factors potentially implicated in the excess risks, including the scaffold consideration and deployment technique, and outlines patient and lesion selection, implantation technique, and dual antiplatelet therapy considerations to potentially mitigate this excess risk with the first-generation thick strut Absorb scaffold (Abbott Vascular, Abbott Park, Illinois). It remains to be seen whether these considerations together with technical iterations will ultimately close the gap between scaffolds and metal stents for short-term events while at the same time preserving options for future revascularization once the scaffold bioresorbs.

Characterization of circulating endothelial cells in acute myocardial infarction.

Acute myocardial infarction (MI), which involves the rupture of existing atheromatous plaque, remains highly unpredictable despite recent advances in the diagnosis and treatment of coronary artery disease. Accordingly, a clinical measurement that can predict an impending MI is desperately needed. Here, we characterize circulating endothelial cells (CECs) using an automated and clinically feasible CEC three-channel fluorescence microscopy assay in 50 consecutive patients with ST-segment elevation MI and 44 consecutive healthy controls. CEC counts were significantly elevated in MI cases versus controls, with median numbers of 19 and 4 cells/ml, respectively (P = 1.1 × 10(-10)). A receiver-operating characteristic (ROC) curve analysis demonstrated an area under the ROC curve of 0.95, suggesting near-dichotomization of MI cases versus controls. We observed no correlation between CECs and typical markers of myocardial necrosis (ρ = 0.02, creatine kinase-myocardial band; ρ = -0.03, troponin). Morphological analysis of the microscopy images of CECs revealed a 2.5-fold increase (P < 0.0001) in cellular area and a twofold increase (P < 0.0001) in nuclear area of MI CECs versus healthy controls, age-matched CECs, as well as CECs obtained from patients with preexisting peripheral vascular disease. The distribution of CEC images that contained from 2 to 10 nuclei demonstrates that MI patients were the only subject group to contain more than 3 nuclei per image, indicating that multicellular and multinuclear clusters are specific for acute MI. These data indicate that CEC counts may serve as a promising clinical measure for the prediction of atherosclerotic plaque rupture events.

Prognostic significance of post-clopidogrel platelet reactivity assessed by a point-of-care assay on thrombotic events after drug-eluting stent implantation.

AIMS: The aim of this study was to determine whether platelet reactivity on clopidogrel therapy, as measured by a point-of-care platelet function assay, is associated with thrombotic events after percutaneous coronary intervention (PCI) with drug-eluting stents (DESs). METHODS AND RESULTS: Platelet reactivity on clopidogrel (post-treatment reactivity) was measured with the VerifyNow P2Y12 assay (Accumetrics Inc., San Diego, CA, USA) in 380 patients undergoing PCI with sirolimus-eluting stents. Receiver-operating characteristic curve analysis was used to derive the optimal cut-off value for post-treatment reactivity in predicting 6 month out-of-hospital cardiovascular (CV) death, non-fatal MI, or stent thrombosis. The mean post-treatment reactivity was 184 +/- 85 PRU (P2Y12 reaction units). The optimal cut-off for the combined endpoint was a post-treatment reactivity > or =235 PRU [area under the curve 0.711 (95% confidence interval 0.529-0.893), P = 0.03], which was similar to the threshold of the upper tertile (231 PRU). Patients with post-treatment reactivity greater than the cut-off value had significantly higher rates of CV death (2.8 vs. 0%, P = 0.04), stent thrombosis (4.6 vs. 0%, P = 0.004), and the combined endpoint (6.5 vs. 1.0%, P = 0.008). CONCLUSION: High post-treatment platelet reactivity measured with a point-of-care platelet function assay is associated with post-discharge events after PCI with DES, including stent thrombosis. Investigation of alternative clopidogrel dosing regimens to reduce ischaemic events in high-risk patients identified by this assay is warranted.

Efficacy and safety of triple antiplatelet therapy with and without concomitant anticoagulation during elective percutaneous coronary intervention (the REMOVE trial).

Adjunctive glycoprotein IIb/IIIa inhibition decreases ischemic events after percutaneous coronary intervention (PCI) but is associated with increased bleeding. We hypothesized that maximal antiplatelet therapy with aspirin, a thienopyridine, and a glycoprotein IIb/IIIa inhibitor without unfractionated heparin (UFH) would result in fewer bleeding complications and maintain efficacy in elective PCI. A total of 159 patients undergoing elective PCI were randomized to intraprocedural eptifibatide alone or eptifibatide plus UFH. Patients received aspirin 325 mg and clopidogrel 300 mg before the procedure. The primary end point was the Landefeld bleeding index. Secondary end points included the composite clinical outcome of in-hospital death, myocardial infarction, urgent target vessel revascularization, and Thrombolysis In Myocardial Infarction major bleeding, and a composite bleeding outcome of major, minor, and nuisance bleeding. The Landefeld bleeding index was significantly lower in the eptifibatide-only group compared with the eptifibatide-plus-UFH group (3.0 vs 3.9, p = 0.03). There was no significant difference in the composite clinical end point between groups (eptifibatide only 17% vs eptifibatide plus UFH 15%, p = 0.7). There was a trend toward a decrease in the composite bleeding end point in the eptifibatide-only compared with the eptifibatide-plus-UFH group (43% vs 56%, p = 0.10). In conclusion, during elective PCI, a strategy of aggressive antiplatelet therapy using aspirin, clopidogrel, and eptifibatide without anticoagulant therapy appears to decrease bleeding complications.

Utility of three-dimensional reconstruction of coronary angiography to guide percutaneous coronary intervention.

OBJECTIVE: The goal of this study was to determine whether three-dimensional (3D) reconstruction of traditional coronary angiography could optimize the choice of drug-eluting stent (DES) length and number during percutaneous coronary intervention (PCI). BACKGROUND: Coronary angiography is subject to significant foreshortening artifact that limits the ability of the operator to accurately determine lesion length. METHODS: The angiographic images of the target vessels of consecutive PCI procedures were postprocessed using a 3D reconstruction algorithm. The appropriate length and optimal number of DES to span each target lesion were calculated and compared with the number and length of DES actually chosen by the operator. RESULTS: A total of 42 target vessels were analyzed, and 3D reconstruction was successful in 38/42 (90.5%) of cases. The results of 3D analysis would have changed operator decision making in six cases (16%): in four cases, the stent chosen by the operator was too short requiring an additional DES; in two cases, the chosen DES was too long and exchanged for a shorter one. In each of these six cases, 3D analysis would have determined the correct stent length prior to stent selection. The optimal stent number derived by 3D reconstruction was significantly less than the actual number of stents per lesion used by the operator (1.31 +/- 0.47 versus 1.54 +/- 0.68, P = 0.01), and the optimal stent length trended less than the actual stented length (27.5 +/- 12.8 mm versus 28.7 +/- 14.7 mm, P = 0.23). CONCLUSIONS: 3D reconstruction algorithm of standard coronary angiography is a promising technique to improve DES utilization during PCI.

Early- and medium-term outcomes after paclitaxel-eluting stent implantation for sirolimus-eluting stent failure.

The optimal treatment for sirolimus-eluting stent (SES) restenosis is not known. This study evaluated the safety and clinical outcome of paclitaxel-eluting stent (PES) implantation for SES restenosis. From March 2004 to July 2005, PESs were implanted in 125 patients with 140 lesions with SES restenosis. Acute and 6-month clinical outcomes were determined through review of the medical record and/or telephone interview. In-hospital major adverse cardiac events (death, nonfatal myocardial infarction, or repeat revascularization) occurred in 14 patients (11.2%), driven entirely by postprocedure non-Q-wave myocardial infarction. At a mean clinical follow-up of 7.2 +/- 1.8 months, the incidence of target lesion revascularization (TLR) was 14.0%, and the rate of major adverse cardiac events was 17.2%. Subacute thrombosis occurred in 2 patients (1.6%). Length of PES implanted, postprocedure diameter stenosis, and total occlusion of the target lesion were independent predictors of TLR. In patients with de novo SES restenosis, TLR was only 8.7%. In conclusion, at medium-term follow-up, PES implantation for SES failure appears to be safe and effective, although efficacy is decreased in the setting of total occlusions, greater residual diameter stenosis, and longer PESs.

Left ventricular cardiac tamponade in the setting of cor pulmonale and circumferential pericardial effusion. Case report and review of the literature.

Circumferential pericardial effusion typically results in biventricular tamponade and equalization of intracardiac and pericardial pressure during diastole. However, tamponade may involve the right or left ventricle. While isolated left ventricular cardiac tamponade (LVCT) can occur as a postoperative complication from localized posterior pericardial effusions, circumferential pericardial effusions leading to LVCT are rare. We report a case of a patient with severe pulmonary hypertension, a large nonloculated pericardial effusion, and LVCT, which was probably due to a chronic undifferentiated connective tissue disorder. This case illustrates that when evaluating patients with circumferential pericardial effusions and associated pulmonary hypertension, the typical findings of cardiac tamponade (pulsus paradoxus, right ventricular diastolic compression and hypotension) may be masked. The echocardiogram must be reviewed carefully as it may reveal left ventricular diastolic compression, the hallmark of LVCT, which may significantly compromise left ventricular filling and cardiac output.

Aspirin sensitivity: implications for patients with coronary artery disease.

CONTEXT: Although acetylsalicylic acid (aspirin) is commonly used for patients with chronic cardiovascular disease, a minority of patients have a sensitivity to acetylsalicylic acid and other nonsteroidal anti-inflammatory drugs. OBJECTIVE: To provide a diagnostic strategy for evaluating and treating patients with aspirin sensitivity, with additional consideration for issues specific to patients with coronary artery disease (CAD). EVIDENCE ACQUISITION: Published articles were identified through a search of MEDLINE and the Cochrane databases using the dates 1966 to June 2004 and the search terms aspirin allergy, coronary artery disease, aspirin desensitization, and aspirin sensitivity. References of retrieved articles were also reviewed for pertinent studies. Articles were included in this review if they were controlled studies, published in the English language, and appeared in a peer-reviewed journal. EVIDENCE SYNTHESIS: The prevalence of aspirin-exacerbated respiratory tract disease is approximately 10% and for aspirin-induced urticaria the prevalence varies from 0.07% to 0.2% of the general population. Aspirin sensitivity is most often manifested as rhinitis and asthma or urticaria/angioedema induced by cross-reacting nonsteroidal anti-inflammatory drugs that inhibit cyclooxygenase 1. The primary mechanism of sensitivity is less often related to drug-specific IgE antibody production leading to urticaria/angioedema and rarely to anaphylaxis. Most patients with acetylsalicylic acid sensitivity are able to undergo desensitization therapy safely and successfully except in cases of chronic idiopathic urticaria. However, there have not been any randomized trials that specifically focus on the efficacy of aspirin desensitization. Furthermore, experience with acetylsalicylic acid desensitization in patients with CAD is very limited. After successful desensitization, acetylsalicylic acid therapy must be indefinitely continued to prevent resensitization. CONCLUSIONS: Acetylsalicylic acid sensitivity is common and desensitization can be performed safely in many patients. Large-scale trials are warranted to determine the safety and efficacy of acetylsalicylic acid desensitization therapy in patients with concomitant CAD because data are currently limited to small case series.