Douglas Ing

Decreased complication rates using the transradial compared to the transfemoral approach in percutaneous coronary intervention in the era of routine stenting and glycoprotein platelet IIb/IIIa inhibitor use: A large single-center experience

BACKGROUND Studies evaluating the efficacy and safety of the transradial approach for percutaneous coronary intervention (PCI) were carried out mainly before the widespread use of stents and glycoprotein (GP) IIb/IIIa inhibitors. We sought to determine the association between the choice of the vascular access site and procedural complications after PCI performed with routine stenting and GP IIb/IIIa inhibition. METHODS The data source was a prospective registry of 13,499 consecutive cases of PCI at the University Health Network, Toronto, Canada, from April 2000 to September 2006. Logistic regression was used to calculate the probability of selection to the radial access group. Using propensity score methodology, 3,198 patients with femoral access were randomly matched to 3,198 patients with radial access based on clinical, angiographic, and procedural characteristics. Multivariable logistic regression analysis was used to identify the independent predictors of access site-related complications. Major adverse cardiac event was defined as death, myocardial infarction, abrupt vessel closure, or coronary artery bypass surgery. RESULTS Use of the transradial approach was associated with fewer vascular access complications (1.5% vs 0.6%, P<.001) and a shorter length of hospital stay. Multivariable analysis revealed transradial access (OR 0.39, 95% CI 0.2-0.7) to be an independent predictor of lower risk, whereas primary PCI (OR 4.36, 95% CI 1.4, 13), recent myocardial infarction (OR 2.0 95% CI 1.2, 3.4), age (per 10 years increase: OR 1.37, 95% CI 1.1-1.7) and female gender (0R 2.78 95% CI 1.7, 4.6) were independent predictors of a higher risk of access site complications. CONCLUSIONS Use of transradial access for PCI is safe and is independently associated with a reduced rate of in-hospital access site complications and reduced length of hospital stay.

The Adverse Long-Term Impact of Renal Impairment in Patients Undergoing Percutaneous Coronary Intervention in the Drug-Eluting Stent Era

Background—An observational study determining the long-term impact of chronic kidney disease (CKD) on patients undergoing percutaneous coronary intervention at a tertiary cardiac referral center. CKD is associated with poor in-hospital outcomes after percutaneous coronary intervention, but its effect beyond 1 year, particularly in the drug-eluting stent (DES) era, has not been reported. Methods and Results—Baseline creatinine was available for 11 953 patients entered into a prospective registry (April 2000 to September 2007). Patients were stratified: those with or without at least moderate CKD (creatinine clearance, <60 mL/min). Follow-up data were obtained through linkage to a provincial registry. Kaplan–Meier analysis was performed. Cox multiple-regression analysis identified independent predictors of late mortality and major adverse cardiac events (MACE) and examined the association between DES use and late outcomes in the presence or absence of CKD. CKD was present in 3070 patients (25.7%). In-hospital mortality and MACE were significantly increased in CKD (3.34% versus 0.44%, P<0.001 and 5.73% versus 2.2%, P<0.001). Survival and MACE-free survival at 7 years were reduced (64.5±1.4% versus 89.4±0.5%, P<0.001; 44.0±1.4% versus 63.4±0.8%, P<0.001). CKD was an independent predictor of late mortality and MACE (hazard ratio [HR]: 2.18, CI: 1.90 to 2.49, P<0.0001; HR: 1.37, CI: 1.25 to 1.49, P<0.0001). DES use was associated with a significant reduction in both (HR: 0.71, CI: 0.60 to 0.83, P<0.0001; HR: 0.70, CI: 0.63 to 0.78, P<0.0001). In patients with CKD, DES use was associated with reduced revascularization (HR: 0.68, CI: 0.53 to 0.88, P=0.004) and reduced MACE (HR: 0.81, CI: 0.69 to 0.95, P=0.011) but not reduced mortality (HR: 0.85, CI: 0.69 to 1.05, P=0.1). Conclusion—In a large registry of “all comers” for percutaneous coronary intervention, CKD was an independent predictor of adverse late outcomes. DES use may be associated with improved long-term outcomes in this high-risk cohort, but further prospective studies are required.

Impact of renal insufficiency on angiographic, procedural, and in-hospital outcomes following percutaneous coronary intervention.

Patients with chronic renal insufficiency (RI) have higher in-hospital mortality and major adverse cardiac event (MACE) rates after percutaneous coronary intervention (PCI). The mechanisms of this adverse course are not well understood. It was hypothesized that this worse outcome may be caused by inadequate PCI results secondary to more complex coronary anatomy in patients with RI. Baseline, procedural, and outcome variables of all PCI cases at the University Health Network are entered prospectively in the PCI Registry. All PCI cases between April 1, 2000, and October 31, 2005, excluding patients in shock, who had preprocedural creatinine clearance (CrCl) measured were included in this study (n = 10,821 of 11,023 patients). Moderate RI (CrCl <60 ml/min) was evaluated as an independent predictor of procedural outcomes, death, and MACE (defined as death, myocardial infarction, abrupt closure, or coronary artery bypass grafting). Moderate RI (CrCl <60 ml/min) independently predicted the procedural outcomes of worse residual stenosis >20% (p = 0.03), number of undeliverable stents (p = 0.003), and smallest stent diameter (p <0.001). Worst residual stenosis >20% and any undeliverable stent were significantly associated with in-hospital MACEs (odds ratio [OR] 3.97, 95% confidence interval [CI] 3.0 to 5.3, p <0.001 and OR 1.89, 95% CI 1.2 to 2.9, p = 0.002) and mortality (OR 3.82, 95% CI 2.2 to 6.7, p <0.001 and OR 3.0, 95% CI 1.6 to 5.9, p = 0.002). These risks were independent of all other measured variables. In conclusion, moderate to severe RI was a strong predictor of worse procedural results during PCI, which, in turn, were independent predictors of in-hospital MACE and mortality and independent contributors to the higher risk of in-hospital adverse events observed after PCI in patients with RI.

Antithrombotic Therapy After Coronary Stenting in Patients With Nonvalvular Atrial Fibrillation

BACKGROUND The safety and efficacy of triple therapy (TT; warfarin with dual antiplatelet therapy [DAPT]) in post-percutaneous coronary intervention (PCI) patients with atrial fibrillation (AF) are unclear. We aimed to determine whether TT is associated with a decreased stroke rate and an acceptable bleeding rate in this population. METHODS This was a single-centre, retrospective study. Primary composite outcome was death, ischemic stroke, or transient ischemic attack. Secondary outcomes included components of primary outcome, bleeding, and blood transfusion rates. RESULTS Of 602 post-PCI patients with AF between 2000 and 2009, 382 received TT, 220 DAPT. Mean follow-up post PCI was 5.9 ± 5.0 months. The TT group had a higher CHADS(2) score (2.6 vs 2.1, P < 0.001), older age (72.9 vs 70.5 years, P = 0.039), more heart failure (72.3% vs 36.9%, P = 0.010), and more strokes (14.4% vs 6.4%, P = 0.010). Neither primary outcome, major bleeding, nor blood transfusion rates differed between treatment groups, but more gastrointestinal bleeding occurred with TT use (2.6% vs 0.5%, P = 0.045). Net clinical benefit was -5.2 (CHADS(2) ≤ 2), 0.9 (CHADS(2) > 2), and -3.2 (overall) per 100 patient-years. CONCLUSIONS Although we found no association with TT usage and a reduction in cerebrovascular ischemic or major bleeding events in post-PCI patients with AF regardless of CHADS(2) score vs DAPT, the study was likely underpowered to demonstrate a clinically relevant reduction. TT was associated with a 5-fold increase in gastrointestinal bleeding vs DAPT. Net clinical benefit calculations suggest benefits of TT in patients with CHADS(2) > 2. Stratification with CHADS(2) might be useful to determine the optimal antithrombotic therapy post PCI.

The sPLA2 Inhibition to Decrease Enzyme Release After Percutaneous Coronary Intervention (SPIDER-PCI) Trial

Background— Secretory phospholipase A2 (sPLA2) may play a role in myonecrosis after elective percutaneous coronary intervention (PCI). Inhibition of this enzyme may have a beneficial effect. The central hypothesis of this study was that treatment with varespladib, a small-molecule inhibitor of sPLA2 would reduce postprocedural release of cardiac biomarkers after elective percutaneous coronary intervention. Methods and Results— Between October 2007 and June 2009, 144 stable patients were randomized in a phase II trial to receive varespladib 500 mg PO BID or placebo 3 to 5 days before and for 5 days after elective percutaneous coronary intervention. The primary end point was elevation of troponin I or creatine kinase-MB above the upper limit of normal at 6 to 8 or 18 to 24 hours after percutaneous coronary intervention. Mean age was 63±10 and 64±10 years, with 38% and 42% with diabetes mellitus and 29% and 28% with prior myocardial infarction for the varespladib and placebo groups, respectively. The primary end point occurred in 75% of varespladib and 63% of placebo patients (P=0.14). Troponin I 3 times the upper limit of normal was observed in 57% and 50% (P=0.39) and creatine kinase-MB 2 times the upper limit of normal in 14% and 3% (P=0.018). Median (first and third quartiles) change in high-sensitivity C-reactive protein in these 2 groups was 0.65 mg/L (−0.18 and 1.48) and 0.70 mg/L (0.00 and 1.50) at 18 to 24 hours (P=0.81) and 0.20 mg/L (−0.70 and 1.40) and 0.60 mg/L (−0.12 and 1.72) at 3 to 5 days (P=0.23), whereas change in sPLA2 activity at 3 to 5 days in a subset was −2.85 ng/ml (−3.40 and −1.85) and 0.25 ng/ml (−0.20 and 0.85) (P<0.001). Conclusions— Inhibition of sPLA2 by varespladib administered for 3 to 5 days before the procedure does not reduce periprocedural myonecrosis associated with elective percutaneous coronary intervention. Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00533039.

Long-term outcomes using a two-stent technique for the treatment of coronary bifurcations

BACKGROUND The crush and culotte are probably the most common two-stent techniques utilized for percutaneous coronary intervention (PCI) of complex bifurcation lesions. Long-term outcome associated with the utilization of these techniques is unknown. Our objective was to evaluate the long-term outcomes after bifurcation PCI utilizing these 2 techniques with a prospective PCI registry. METHODS Between 11/1/2003 and 12/31/2007, 360 patients were treated with either crush (n=304) or culotte (n=56). Primary outcome was the occurrence of major adverse cardiac events (MACE) defined as the composite of death, myocardial infarction and target vessel revascularization. The major secondary outcome measure was MACE or occurrence of CCS Class ≥ 2 angina. RESULTS After a median follow-up of 4.1 years (3.0-5.1), the occurrence of MACE was 23.9%. MACE or CCS Class ≥ 2 angina occurred in 27.5% of patients. Multivariable analysis revealed that creatinine clearance <60 ml/min (odds-ratio [OR]=1.71, 95% CI 1.08-2.71; p=0.022) and left ventricular ejection fraction <40% (OR=2.14, 95% CI 1.21-3.79; p=0.008) were independent predictors of MACE or CCS Class ≥ 2 angina. A larger main vessel reference diameter (OR=0.57, 95% CI 0.61-0.92), bifurcation angle <50% (OR=0.59, 95% CI 0.35-0.92) and a final kissing-balloon inflation (OR=0.75, 95% CI 0.35-0.99) were associated with a lower risk of MACE or CCS Class ≥ 2 angina. CONCLUSIONS Application of the crush and culotte techniques is associated with efficacy and safety at long-term follow-up. Bifurcation angle, a final kissing balloon inflation and vessel reference diameter are important variables that impact on very long-term outcomes.

Choice of stent and outcomes after treatment of drug-eluting stent restenosis in highly complex lesions.

Our aim was to compare the outcomes of a same versus different drug‐eluting stent (DES) implantation strategy for the treatment of DES instent restenosis (ISR).

Right ventricular perforation by a passive-fixation pacemaker lead

La perforación ventricular subaguda es una complicación rara del implante de marcapasos o desfibrilador cardioversor implantable (DCI). Entre tanto, puede ser potencialmente fatal. El desarrollo de cables electrodos de fijación activa de pequeños diámetros puede estar asociado al aumento de riesgo de perforación tardía ventricular. Además de eso, el tratamiento de esa complicación ha sido poco descripto. Reportamos un caso poco usual de perforación subaguda de ventrículo derecho, causada por un cable electrodo de fijación pasiva. Perforación del Ventrículo Derecho por Cable de Marcapasos de Fijación PasivaPalavras-chave Ventrículos do coração/lesões; ventrículo direito/lesões, ferimentos e lesões; ferimentos perfurantes. Perfuração ventricular subaguda é uma complicação rara do implante de marca-passo ou desfibrilador cardioversor implantável (DCI). Entretanto, ela pode ser potencialmente fatal. O desenvolvimento de cabos-eletrodos de fixação ativa de pequenos diâmetros pode estar associado com o aumento de risco de perfuração tardia ventricular. Além disso, o tratamento dessa complicação tem sido pouco descrito. Reportamos um caso pouco usual de perfuração subaguda de ventrículo direito, causada por um cabo-eletrodo de fixação passiva. Subacute ventricular perforation is a rare complication of pacemaker or implantable-cardioverter defibrillator implantation. However, it can be life threatening. The development of small-diameter active fixation leads may be associated with increased risk for delayed right ventricular perforation. Additionally, the management of this complication has been poorly described. We report an unusual case of subacute right ventricular perforation caused by a passive fixation lead. Perfuração do Ventrículo Direito por Cabo de Marca-passo de Fixação Passiva

Inhibition of sPLA2 and Endothelial Function: A Substudy of the SPIDER-PCI Trial

BACKGROUND Inflammation plays an important role in the pathophysiology of atherosclerosis and endothelial dysfunction, and occurs after percutaneous coronary intervention (PCI). We evaluated whether endothelial function is attenuated after PCI and if inhibition of secretory phospholipase A2 (sPLA2) activity augments endothelial function and coronary flow reserve (CFR) in these patients. METHODS In the sPLA2 Inhibition to Decrease Enzyme Release After Percutaneous Coronary Intervention (SPIDER-PCI) study, patients undergoing elective PCI were randomized to receive Varespladib (Anthera Pharmaceuticals Inc, San Mateo, CA), an inhibitor of sPLA2, or placebo 3-5 days prior to PCI and for 5 days after PCI. In this substudy, endothelial function was assessed in 31 patients by flow-mediated dilation (FMD) before treatment and on the day after PCI, while taking study medication. During the PCI procedure, CFR was assessed using a Doppler guide wire. RESULTS Baseline and procedural characteristics were comparable in both groups and sPLA2 activity was similar at baseline. After PCI, sPLA2 activity decreased only in the Varespladib group (2.9 ± 0.9 to 0.5 ± 0.4 ng/mL), and high-sensitivity C-reactive protein (hsCRP) increased by more than 100% in both groups. FMD at baseline was 3.66 ± 2.45% (Varespladib) and 3.37 ± 1.73% (placebo) with nonsignificant increase in both groups after PCI. The effect of Varespladib on FMD, adjusted for pre-PCI FMD by linear regression, was -1.16 ± 1.68%; P = 0.5. CFR was 2.45 ± 0.66 and 2.77 ± 0.85 in the Varespladib and placebo groups, respectively (P = 0.36). CONCLUSIONS Systemic endothelial function is not reduced after elective PCI despite eliciting acute inflammatory response. Acute inhibition of sPLA2 activity with Varespladib does not affect endothelial or microvascular function after PCI.

Tachycardias: one or two?

A 71-year-old patient presented with a 3-year history of paroxysmal, rapid regular palpitations despite trials of sotalol and diltiazem. A previous Holter study had documented a narrow QRS tachycardia (Fig. 1). The patient underwent an electrophysiology study (EPS) during which a tachycardia was inducible with programmed atrial stimulation (Fig. 2). What is the diagnosis? The Holter rhythm strips A and B (Fig. 1) document a narrow QRS tachycardia. The tachycardia is initiated by an atrial premature beat (APB) (third beat in Panel I) without a P wave to R wave interval (PR) jump. After the first four cycles, atrial but not ventricular activity becomes regular. The irregularity in RR cycle length (CL) persists until the end of Panel II, at which time it too becomes regular. The CL of the tachycardia in Panel III is 340 msec (shorter than in Panel II by 20 msec). The relationship between the ventricular and atrial excitation is not constant in Panels I and II. In Panel III, there is a constant and short RP relationship favoring atrioventricular nodal reentrant tachycardia (AVNRT). The irregularity in the RP relationship in Panels I and II could potentially be explained by AVNRT with variable block to the ventricle. An alternative explanation would be an atrial