Sanjaya Khanal

Prevalence, Predictors, and Outcomes of Premature Discontinuation of Thienopyridine Therapy After Drug-Eluting Stent Placement Results From the PREMIER Registry

Background— Although drug-eluting stents (DES) significantly reduce restenosis, they require 3 to 6 months of thienopyridine therapy to prevent stent thrombosis. The rate and consequences of prematurely discontinuing thienopyridine therapy after DES placement for acute myocardial infarction (MI) are unknown. Methods and Results— We used prospectively collected data from a 19-center study of MI patients to examine the prevalence and predictors of thienopyridine discontinuation 30 days after DES treatment. We then compared the mortality and cardiac hospitalization rates for the next 11 months between those who stopped and those who continued thienopyridine therapy. Among 500 DES-treated MI patients who were discharged on thienopyridine therapy, 68 (13.6%) stopped therapy within 30 days. Those who stopped were older, less likely to have completed high school or be married, more likely to avoid health care because of cost, and more likely to have had preexisting cardiovascular disease or anemia at presentation. They were also less likely to have received discharge instructions about their medications or a cardiac rehabilitation referral. Patients who stopped thienopyridine therapy by 30 days were more likely to die during the next 11 months (7.5% versus 0.7%, P<0.0001; adjusted hazard ratio=9.0; 95% confidence interval=1.3 to 60.6) and to be rehospitalized (23% versus 14%, P=0.08; adjusted hazard ratio=1.5; 95% confidence interval=0.78 to 3.0). Conclusions— Almost 1 in 7 MI patients who received a DES were no longer taking thienopyridines by 30 days. Prematurely stopping thienopyridine therapy was strongly associated with subsequent mortality. Strategies to improve the use of thienopyridines are needed to optimize the outcomes of MI patients treated with DES.

Association of a Continuous Quality Improvement Initiative With Practice and Outcome Variations of Contemporary Percutaneous Coronary Interventions

Background— The objective of this study was to evaluate the association of a continuous quality improvement program with practice and outcome variations of percutaneous coronary intervention (PCI). Methods and Results— Data on consecutive PCI were collected in a consortium of 5 hospitals; 3731 PCIs reflected care provided at baseline (January 1, 1998, to December 31, 1998), and 5901 PCIs reflected care provided after implementation of a continuous quality improvement intervention (January 1, 2002, to December 31, 2002). The intervention included feedback on outcomes, working group meetings, site visits, selection of quality indicators, and use of bedside tools for quality improvement and risk assessment. Postintervention data were compared with baseline and with 10 287 PCIs from 7 hospitals added to the consortium in 2002. Quality indicators included use of preprocedural aspirin or clopidogrel, use of glycoprotein IIb/IIIa receptor blockers and postprocedural heparin, and amount of contrast media per case. Outcomes selected included emergency CABG, contrast nephropathy, myocardial infarction, stroke, transfusion, and in-hospital death. Compared with baseline and the control group, the intervention group at follow-up had higher use of preprocedural aspirin and glycoprotein IIb/IIIa blockers, lower use of postprocedural heparin, and a lower amount of contrast media per case (P<0.05). These changes were associated with lower rates of transfusions, vascular complications, contrast nephropathy, stroke, transient ischemic attack, and combined end points (all P<0.05). Conclusions— Our nonrandomized, observational data suggest that implementation of a regional continuous quality improvement program appears to be associated with enhanced adherence to quality indicators and improved outcomes of PCI. A randomized clinical trial is needed to determine whether this is a “causal” or a “casual” relationship.

Continuous Aortic Flow Augmentation A Pilot Study of Hemodynamic and Renal Responses to a Novel Percutaneous Intervention in Decompensated Heart Failure

Background— Diminished aortic flow may induce adverse downstream vascular and renal signals. Investigations in a heart failure animal model have shown that continuous aortic flow augmentation (CAFA) achieves hemodynamic improvement and ventricular unloading, which suggests a novel therapeutic approach to patients with heart failure exacerbation that is inadequately responsive to medical therapy. Methods and Results— We studied 24 patients (12 in Europe and 12 in the United States) with heart failure exacerbation and persistent hemodynamic derangement despite intravenous diuretic and inotropic and/or vasodilator treatment. CAFA (mean±SD 1.34±0.12 L/min) was achieved through percutaneous (n=19) or surgical (n=5) insertion of the Cancion system, which consists of inflow and outflow cannulas and a magnetically levitated and driven centrifugal pump. Hemodynamic improvement was observed within 1 hour. Systemic vascular resistance decreased from 1413±453 to 1136±381 dyne · s · cm−5 at 72 hours (P=0.0008). Pulmonary capillary wedge pressure decreased from 28.5±4.9 to 19.8±7.0 mm Hg (P<0.0001), and cardiac index (excluding augmented aortic flow) increased from 1.97±0.44 to 2.27±0.43 L · min−1 · m−2 (P=0.0013). Serum creatinine trended downward during treatment (overall P=0.095). There were 8 complications during treatment, 7 of which were self-limited. Hemodynamics remained improved 24 hours after CAFA discontinuation. Conclusions— In patients with heart failure and persistent hemodynamic derangement despite intravenous inotropic and/or vasodilator therapy, CAFA improved hemodynamics, with a reduction in serum creatinine. CAFA represents a promising, novel mode of treatment for patients who are inadequately responsive to medical therapy. The clinical impact of the observed hemodynamic improvement is currently being explored in a prospective, randomized, controlled trial.

R-wave amplitude changes measured by electrocardiography during early transmural ischemia.

BACKGROUND Changes in the amplitude of the R wave (RWA) on the electrocardiogram (ECG) have been described during acute myocardial ischemia and infarction. However, this has not been well studied in a controlled setting. We hypothesized that significant increase in RWA occurs during early transmural myocardial ischemia. METHODS We prospectively evaluated changes in RWA in 50 patients during brief episodes of transmural ischemia induced by first balloon occlusion (mean, 38 seconds at 6-10 atmospheric pressures) during elective percutaneous coronary intervention. We recorded 12-lead ECGs at 20-second intervals before and during balloon inflation in 16 right coronary arteries, 14 left circumflex arteries, and 20 left anterior descending arteries. R wave amplitude was digitally measured in each of the 12 leads in every ECG using the ECG interval editor (General Electric HC, Menomonee Falls, WI). Intracoronary (IC) ECGs were also recorded in 4 patients. The mean of the RWA in each lead before balloon inflation was compared to the mean RWA during balloon inflation. RESULTS R wave amplitude significantly increased during balloon inflation from baseline in limb leads I, II, aVL, and all the precordial leads with the exception of lead V(1). The RWA increase did not reach statistical significance in leads III, aVF, and V(1). Mean RWA increase was consistent in all leads except aVR during the brief episodes of ischemia during initial balloon inflation because of the inverse polarity of this lead. The increase in RWA was seen in most patients (mean, 75%) in whom transmural ischemia was induced by first balloon inflation. Besides, the RWA showed an increase from baseline in 3 patients who had IC-lead recordings. CONCLUSION R wave amplitude increases significantly in precordial leads (V(2)-V(6)) and limb leads (I, II, aVL) of the surface ECG during brief episodes of transmural ischemia. The increase in RWA might be consistent with the expansion of the left ventricular cavity during ischemia and/or alterations in conduction that are intrinsic to the myocardium.

Rapid Progression of Native Renal Artery Fibromuscular Dysplasia Following Kidney Donation

Fibromuscular dysplasia is the second commonest anatomical abnormality apart from multiple renal arteries in the potential live donors. Pretransplant evaluation of the donors may include an angiography to evaluate the renal arteries, and failure to recognize renal arterial stenosis, particularly fibromuscular dysplasia, by noninvasive methods may eventually lead to hypertension and ischemic renal failure. We report a case of fibromuscular dysplasia that was undetected by computed tomographic angiography prior to donation. One year after kidney donation, it rapidly progressed to severe symptomatic stenosis with hypertension and acute renal failure. Following renal artery angioplasty, her blood pressure normalized over a period of 2 weeks without any need for antihypertensive medications and the serum creatinine returned to her baseline. The acceptability of renal donors with fibromuscular dysplasia depends on the age, race and the availability of the other suitable donors. Mild fibromuscular dysplasia in a normotensive potential renal donor cannot be considered a benign condition. Such donors need regular follow‐up postdonation for timely detection and treatment.

Intracoronary electrocardiographic deflections during transmural ischemia induced by percutaneous transluminal coronary angioplasty.

Patient 1 Baseline 0.68 0 16.93 0 1.12 2.88 B1 0.34 1.22 71.88 0 13.90 56.60 Patient 2 Baseline 1.41 17.03 149.76 0 3.75 −12.44 B1 1.22 15.37 159.38 0 5.22 −17.08 Patient 3 Baseline 0.16 0 94.13 60.46 1.36 23.96 B1 0.13 0 101.99 37.13 13.61 48.75 Patient 4 Baseline 3.80 2.87 32.84 51.58 3.56 19.86 B1 1.14 8.10 103.84 12.73 16.10 50.11 Intracoronary electrocardiographic deflections during transmural ischemia induced by percutaneous transluminal coronary angioplasty