Posttraumatic Stress Disorder After Spontaneous Coronary Artery Dissection: A Report of the International Spontaneous Coronary Artery Dissection Registry.

BACKGROUND: Myocardial infarction secondary to spontaneous coronary artery dissection (SCAD) can be traumatic and potentially trigger posttraumatic stress disorder (PTSD). In a large, multicenter, registry-based cohort, we documented prevalence of lifetime and past-month SCAD-induced PTSD, as well as related treatment seeking, and examined a range of health-relevant correlates of SCAD-induced PTSD. METHODS AND RESULTS: Patients with SCAD were enrolled in the iSCAD (International SCAD) Registry. At baseline, site investigators completed medical report forms, and patients reported demographics, medical/SCAD history, psychosocial factors (including SCAD-induced PTSD symptoms), health behaviors, and health status via online questionnaires. Of 1156 registry patients, 859 patients (93.9% women; mean age, 52.3 years) completed questionnaires querying SCAD-induced PTSD. Nearly 35% (n=298) of patients met diagnostic criteria for probable SCAD-induced PTSD in their lifetime, and 6.4% (n=55) met criteria for probable past-month PTSD. Of 811 patients ever reporting any SCAD-induced PTSD symptoms, 34.8% indicated seeking treatment for this distress. However, 46.0% of the 298 patients with lifetime probable SCAD-induced PTSD diagnoses reported never receiving trauma-related treatment. Younger age at first SCAD, fewer years since SCAD, being single, unemployed status, more lifetime trauma, and history of anxiety were associated with greater past-month PTSD symptom severity in multivariable regression models. Greater past-month SCAD-induced PTSD symptoms were associated with greater past-week sleep disturbance and worse past-month disease-specific health status when adjusting for various risk factors. CONCLUSIONS: Given the high prevalence of SCAD-induced PTSD symptoms, efforts to support screening for these symptoms and connecting patients experiencing distress with empirically supported treatments are critical next steps. REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04496687.

The initial U.S. experience with the Tempo active fixation temporary pacing lead in structural heart interventions.

OBJECTIVES: This multicenter retrospective study of the initial U.S. experience evaluated the safety and efficacy of temporary cardiac pacing with the Tempo® Temporary Pacing Lead. BACKGROUND: Despite increasing use of temporary cardiac pacing with the rapid growth of structural heart procedures, temporary pacing leads have not significantly improved. The Tempo lead is a new temporary pacing lead with a soft tip intended to minimize the risk of perforation and a novel active fixation mechanism designed to enhance lead stability. METHODS: Data from 269 consecutive structural heart procedures were collected. Outcomes included device safety (absence of clinically significant cardiac perforation, new pericardial effusion, or sustained ventricular arrhythmia) and efficacy (clinically acceptable pacing thresholds with successful pace capture throughout the index procedure). Postprocedure practices and sustained lead performance were also analyzed. RESULTS: The Tempo lead was successfully positioned in the right ventricle and achieved pacing in 264 of 269 patients (98.1%). Two patients (0.8%) experienced loss of pace capture. Procedural mean pace capture threshold (PCT) was 0.7 ± 0.8 mA. There were no clinically significant perforations, pericardial effusions, or sustained device-related arrhythmias. The Tempo lead was left in place postprocedure in 189 patients (71.6%) for mean duration of 43.3 ± 0.7 hr (range 2.5-221.3 hr) with final PCT of 0.84 ± 1.04 mA (n = 80). Of these patients, 84.1% mobilized out of bed with no lead dislodgment. CONCLUSION: The Tempo lead is safe and effective for temporary cardiac pacing for structural heart procedures, provides stable peri and postprocedural pacing and allows mobilization of patients who require temporary pacing leads.

Two cases of pericardial tamponade due to nitinol wire fracture of a gore septal occluder.

Percutaneous patent foramen ovale (PFO) closure is recommended for secondary prevention of paradoxical embolism through a PFO. In the United States, two Food and Drug Administration-approved PFO closure devices are currently available, and the choice depends on operator preference and PFO anatomy. Although these devices are easy to implant, there are several potential complications. As opposed to the Amplatzer PFO Occluder, there has been no published case of atrial erosion with Gore closure devices. This report describes two cases of pericardial tamponade due to perforation of the atrial wall induced by a wire frame fracture of the Gore Helex and Cardioform devices.

A new ST-segment elevation myocardial infarction equivalent pattern? Prominent T wave and J-point depression in the precordial leads associated with ST-segment elevation in lead aVr.

Certain acute coronary syndrome electrocardiographic (ECG) patterns, which do not include ST-segment elevation, are indicative of acute coronary syndrome caused by significant arterial occlusion; these patterns are, of course, associated with significant risk to the patient and mandate a rapid response from the health care team. One such high-risk ECG pattern includes the association of the prominent T wave and J-point depression producing ST-segment depression seen in the precordial leads coupled with ST-segment elevation in lead aVr. This ECG presentation is associated with significant left anterior descending artery obstruction. We report the case of a patient with this ECG presentation who progressed over a very short time to ST-segment elevation myocardial infarction of the anterior wall.

Timing and correlates of very early major adverse clinical events following percutaneous coronary intervention.

We attempted to determine the incidence, timing and correlates of very early (< 24 hours) major adverse clinical events in patients undergoing contemporary percutaneous coronary intervention (PCI). Early discharge following PCI may offer significant advantages to patient and practitioner, but the timing of, and risk factors for, very early (< 24 hours) major adverse clinical events following PCI are not well characterized. A retrospective analysis of the CREDO trial was performed. A total of 1,815 patients underwent a PCI procedure and 139 patients (7.7%) experienced a major adverse clinical event (death, myocardial infarction or urgent target vessel revascularization) within the first 28 days. The majority of these events (111 patients) occurred within the first 24 hours, with the greatest risk of an event within the first 6 hours. Multivariable predictors of very early events were age, AHA lesion grade, history of peripheral vascular disease, preprocedural TIMI flow grade and no. of vessels with stenosis > 50%. These data show a very low and constant risk of adverse events 6 hours following PCI.

Can N-acetylcysteine reverse the antiplatelet effects of clopidogrel? An in vivo and vitro study.

BACKGROUND: The active metabolite of clopidogrel binds the P2Y12 ADP receptor on the platelet surface via a disulfide bond. N-Acetylcysteine (NAC) is able to reduce disulfide bonds. We postulated that NAC might reverse clopidogrel's effect on platelets. METHODS: Two groups of patients were investigated. Group 1 included 11 patients with stable coronary disease who, after discontinuation of aspirin, received 14 days of clopidogrel, 75 mg/day. Bleeding time and whole-blood platelet aggregometry (with 5 micromol/L ADP) were compared before and after the 14 days. Patients were then treated with 6 g of NAC orally, followed by repeat measurement of bleeding time and aggregometry. In group 2, 14 patients were treated with clopidogrel (300 mg) and aspirin before a percutaneous coronary intervention. Blood was drawn 22 +/- 3 hours later and divided into 2 samples. One was sent immediately for platelet-rich plasma aggregometry (using 5 and 2 micromol/L ADP, collagen, and arachidonic acid as agonists), thromboelastography, and aggregometry using the Plateletworks assay (Helena Laboratories, Beaumont, Tex). The other sample was treated with NAC (500 mg/L), after which these same platelet function tests were performed. RESULTS: In group 1, NAC therapy did not significantly change the bleeding time or results of aggregometry. In group 2, neither aggregometry nor the Plateletworks assay suggested reversal of inhibition by NAC. CONCLUSIONS: These studies reveal that a large dose of NAC does not reduce inhibition of platelet aggregation by clopidogrel in vitro or in vivo.

Outcome of patients undergoing balloon angioplasty in the two months prior to noncardiac surgery.

We report on the incidence of adverse cardiac events in 350 patients who underwent noncardiac surgery within 2 months of successful balloon angioplasty (BA) at our institution between 1988 and 2001. Three patients died perioperatively (n = 1) or had myocardial infarction (n = 2) (0.9%, 95% confidence interval [CI] 0.2% to 2.5%), which is a lower incidence than that reported for patients undergoing noncardiac surgery after stenting (3.9% to 32%). One patient died, and 2 had a nonfatal myocardial infarction. All 3 (1.6%, 95% CI 0.3% to 4.6%) were among the 188 patients who underwent surgery within 2 weeks of BA. Repeat target vessel revascularization was performed in 10 patients (2.9%, 95% CI 1.4% to 5.2%): in 3 (1.6%, 95% CI 0.3% to 4.6%) of 188 patients who underwent surgery within 2 weeks of BA and in 7 (5.1%, 95% CI 2.1% to 10.2%) of 138 patients who underwent surgery within 3 to 7 weeks of BA. Therefore, in patients in whom percutaneous coronary revascularization is required before noncardiac surgery, BA appears to be safe, especially in patients who need to undergo surgery early after percutaneous coronary intervention.

Differences in human antioxidized LDL autoantibodies in patients with stable and unstable angina.

BACKGROUND: Autoantibodies to oxidized LDL (anti-oxLDL) have been found in the serum of patients with coronary artery disease (CAD). This study was designed to compare the differences in anti-oxLDL titers and isotypes in unstable and stable angina patients and to correlate these results with known markers of active inflammation in CAD. METHODS: Thirty patients from a tertiary referral general hospital with documented CAD were studied. Anti-oxLDL IgG titers and its isotypes, high sensitivity C-reactive protein (hsCRP) and serum amyloid A (SAA) were measured. RESULTS: The anti-oxLDL IgG titer was lower (p=0.03) in the unstable angina group compared to the stable angina patients (0.084+/-0.102 OD versus 0.195+/-0.149 OD, respectively). The predominant IgG isotype in both groups was IgG2. IgG4 was significantly higher (0.270+/-0.146 OD, p=0.04) in the unstable angina group versus patients with stable angina (0.198+/-0.019 OD). There was a significant inverse correlation between anti-oxLDL and hsCRP and SAA in this sample population (R=0.37, p<0.05 and R=0.36, p<0.05, respectively). CONCLUSION: Patients with unstable angina have lower levels of anti-oxLDL IgG in the acute setting of CAD. Plaque instabilization does not seem to acutely modify the isotype subsets of anti-oxLDL IgG in these patients.

Routine intravascular ultrasound scanning guidance of coronary stenting is not associated with improved clinical outcomes.

PURPOSE: The purpose of the current study was to determine whether there is any incremental benefit to routine intravascular ultrasound (IVUS) guidance of percutaneous coronary intervention. METHODS AND RESULTS: We compared the outcome of 796 patients who underwent an IVUS study (IVUS group) during the index stent procedure with 8274 patients who did not have an IVUS study (angiography group). The primary end point was the composite end point of death, myocardial infarction, or ischemia-driven target vessel revascularization within 9 months of the index stent procedure. There were statistically significant differences in multiple procedural characteristics. Most importantly, those patients who underwent an IVUS study had a larger postprocedural minimal lumen diameter and smaller postprocedural percent diameter stenosis. However, there was no significant difference between the IVUS group and the angiography group with respect to the primary end point (RR 1.10, 95% CI 0.91, 1.32) or any of the individual clinical end points. Adjustment for multiple clinical and procedural characteristics did not significantly alter these findings. CONCLUSIONS: These data suggest that the routine performance of IVUS during stent placement influences the performance of the procedure, as judged by differences in procedural characteristics, but does not improve clinical outcome at 9 months.

Cutting balloon angioplasty vs. conventional balloon angioplasty in patients receiving intracoronary brachytherapy for the treatment of in-stent restenosis.

The objective of this study was to evaluate the safety and efficacy of cutting balloon angioplasty (CBA) for the treatment of in-stent restenosis prior to intracoronary brachytherapy (ICB). Cutting balloon angioplasty may reduce the incidence of uncontrolled dissection requiring adjunctive stenting and may limit "melon seeding" and geographic miss in patients with in-stent restenosis who are subsequently treated with ICB. We performed a retrospective case-control analysis of 134 consecutive patients with in-stent restenosis who were treated with ICB preceded by either CBA or conventional balloon angioplasty. We identified 44 patients who underwent CBA and ICB, and 90 control patients who underwent conventional percutaneous transluminal coronary angioplasty (PTCA) and ICB for the treatment of in-stent restenosis. Adjunctive coronary stenting was performed in 13 patients (29.5%) in the CBA/ICB group and 41 patients (45.6%; P < 0.001) in the PTCA/ICB group. There was no difference in the injury length or active treatment (ICB) length. The procedural and angiographic success rates were similar in both groups. There were no statistically significant differences in the incidence of death, myocardial infarction, recurrent angina pectoris, subsequent target lumen revascularization, or the composite endpoint of all four clinical outcomes (P > 0.05). Despite sound theoretical reasons why CBA may be better than conventional balloon angioplasty for treatment of in-stent restenosis with ICB, and despite a reduction in the need for adjunctive coronary stenting, we were unable to identify differences in clinical outcome.

Modulating thrombotic potential in catheter-based percutaneous coronary and peripheral vascular interventions.

Thrombosis is an obligatory consequence of all percutaneous vascular interventions. Balloon angioplasty, intravascular stents and other devices routinely used to facilitate dilatation of critical vascular stenoses result in fracture of the intima and exposure of the thrombogenic subendothelium with initiation and perpetuation of platelet activation and aggregation. This not uncommonly results in thrombus formation that may lead to abrupt vessel closure, distal ischemia and tissue infarction, and target organ dysfunction. Fortunately, advances in our understanding of the mechanisms that underlie vascular thrombosis have led to advances in the use of adjunctive pharmacological agents that modulate this pathophysiological response and have led to important reductions in the incidence and severity of thrombotic complications of percutaneous transluminal interventions.

Transport and centralization of acute coronary syndrome care.

Primary percutaneous coronary intervention (PCI) is the optimal treatment for patients presenting with ST-elevation myocardial infarction (STEMI). But PCI facilities are not widely available, and the majority of patients who receive reperfusion therapy are treated with thrombolytic therapy. However, with significant improvements in the procedural success of PCI, there has been a concomitant reduction in the need for emergency bypass surgery and there is evidence to support primary PCI without on-site cardiac surgical facilities. Others have proposed immediate transfer to a suitable hospital for immediate primary PCI. An alternative treatment strategy is facilitated PCI, which might combine the early benefits of thrombolysis with the higher patency rates and superior clinical outcomes of primary PCI, although this remains unproven. Finally, rescue PCI remains a reasonable treatment option for patients with failed thrombolysis, but there is insufficient evidence to support this option as a preferred treatment strategy for patients with STEMI.

Increased Th1 activity in patients with coronary artery disease.

BACKGROUND: Atherosclerotic lesions are mainly composed of macrophages and T lymphocytes. Specific T helper type 1 (Th1) cytokines and interferon gamma (IFN-gamma) inducible chemokines have been shown to be present in these lesions, modulating the local immunologic response. To explore whether this increase in Th1 activity could also be detected in circulating cells indicating a systemic activation, we studied the peripheral expression of Th1 cytokines and chemokines in patients with coronary artery disease and controls. METHODS AND RESULTS: Fifty patients with coronary artery disease (25 with unstable angina and 25 with stable angina) and 10 controls were studied. Serum interleukin (IL)-12 and IFN-gamma and the expression of IFN-gamma inducible chemokines IP-10, Mig and their receptor CXCR3 in peripheral cells were analyzed. Serum IL-12 and intracellular expression of IFN-gamma were significantly elevated in patients with unstable angina. An enhanced expression of IFN-gamma chemokines IP-10, Mig and CXCR3 in patients with stable angina was also observed. CONCLUSIONS: This study demonstrates an increased systemic inflammatory activity in patients with coronary heart disease with a predominant Th1 response, particularly in patients with unstable angina, suggesting an important role played by this polarization in plaque formation and rupture.

Routine intravascular ultrasound guidance of percutaneous coronary intervention: a critical reappraisal.

Intravascular ultrasound (IVUS) has played an integral role in the evolution of interventional cardiology. However, routine IVUS guidance of coronary stent implantation is not supported by a critical reappraisal of the available evidence. Although there is a trend toward a benefit with respect to target lumen revascularization favoring IVUS-guided coronary stent implantation, it is likely that this effect is driven by improved outcomes in small vessels, long coronary stenoses, and possibly saphenous vein graft interventions. No consistent trend in the incidence of death or myocardial infarction is apparent. Furthermore, the safety, efficacy, and effectiveness of IVUS should be taken into account when considering the goals, risks, benefits, and alternatives to such a treatment strategy.

Safety and efficacy of aspirin, clopidogrel, and warfarin after coronary stent placement in patients with an indication for anticoagulation.

BACKGROUND: Dual antiplatelet therapy with aspirin and clopidogrel has replaced aspirin and systemic anticoagulation with warfarin as the preferred antithrombotic therapy after percutaneous coronary intervention (PCI) with stent placement. However, a number of patients have indications for all 3 drugs. We sought to determine the frequency and type of hemorrhagic complications in patients who undergo systemic anticoagulation with warfarin while receiving aspirin and clopidogrel after a PCI with stent placement. METHODS: We performed a retrospective analysis of the Mayo Clinic PCI database and identified 66 consecutive patients who were discharged from hospital after PCI between January 2000 and August 2002 (inclusive) receiving a combination of dual antiplatelet therapy (aspirin and clopidogrel) and systemic anticoagulation (warfarin) to determine the incidence of bleeding and other clinical events during the treatment period. RESULTS: Six patients (9.2%; 95% CI, 3.5-19.0) reported a bleeding event; 2 patients required a blood transfusion. No patient died or sustained a myocardial infarction or stent thrombosis. CONCLUSIONS: The risk of bleeding may be increased in patients treated with aspirin, a thienopyridine, and warfarin early after PCI with stent placement.

Incidence, correlates, management, and clinical outcome of coronary perforation: analysis of 16,298 procedures.

BACKGROUND: Coronary perforation is a serious but uncommon complication of percutaneous coronary intervention (PCI) and is associated with significant morbidity and mortality. METHODS: We performed an analysis of the Mayo Clinic PCI database. Clinical records, procedural reports, and angiographic studies were reviewed. Multiple logistic regression analysis was performed to identify clinical, procedural, anatomic, and angiographic correlates of coronary perforation. RESULTS: A total of 16,298 PCI procedures were performed between January 1990 and December 2001. We identified 95 coronary perforations (0.58%; 95% CI, 0.47-0.71). The incidence of coronary perforation varied with time. Correlates of coronary perforation included the use of an atheroablative device and female sex. Twelve patients (12.6%) sustained an acute myocardial infarction, and cardiac tamponade developed in 11 patients (11.6%). Management strategies included reversal of heparin, pericardiocentesis, placement of a covered stent, and surgical repair. Seven patients died (7.4%). CONCLUSIONS: Coronary perforation during PCI is rare, but is associated with significant morbidity and mortality. The variable frequency of perforation may be explained by temporal variations in the use of atheroablative devices.

Does clopidogrel increase the degree of platelet inhibition when a platelet glycoprotein IIb/IIIa inhibitor has been given? Insights from an optical platelet aggregometry study.

INTRODUCTION: While the CURE trial demonstrated the benefits of clopidogrel in acute coronary syndromes, patients receiving glycoprotein IIb/IIIa antagonists were excluded. Given the frequent coadministration of these two medications, we sought to examine their interaction and their combined effect on platelet inhibition. METHODS: Ten patients admitted to the hospital with stable or unstable angina underwent phlebotomy prior to, three hours and six hours after administration of a standard oral loading dose of clopidogrel. The samples were then treated in vitro with incremental concentrations of tirofiban (0, 10, 20, 40, 60, and 80 ng/mL), and optical platelet aggregometry was performed utilizing ADP and TRAP as agonists. We analyzed the combined effects of these agents using a mixed effects model with time and tirofiban concentration as fixed effects, and subject and timing of phlebotomy as random effects. RESULTS: There was no evidence of additional inhibition of platelet aggregation due to clopidogrel regardless of the concentration of tirofiban or the study agonist (ADP 20 muM or iso-TRAP). Specifically, there was no difference in the tirofiban dose-response curves with either platelet agonist for any of the three time points (before, and three and six hours after, clopidogrel administration). DISCUSSION: There is no evidence that the combination of clopidogrel and tirofiban achieves greater inhibition of platelet aggregation than tirofiban alone.