Thirty-Day Readmission Rate and Costs After Percutaneous Coronary Intervention in the United States: A National Readmission Database Analysis.

BACKGROUND: The association of short-term readmissions after percutaneous coronary intervention (PCI) on healthcare costs has not been well studied. METHODS AND RESULTS: The Healthcare Cost and Utilization Project National Readmission Database encompassing 722 US hospitals was used to identify index PCI cases in patients ≥18 years old. Hierarchical regression analyses were used to examine the factors associated with risk of 30-day readmission and higher cumulative costs. We evaluated 206 869 hospitalized patients who survived to discharge after PCI from January through November 2013 and analyzed readmissions over 30 days after discharge. A total of 24 889 patients (12%) were readmitted within 30 days, with rates ranging from 6% to 17% across hospitals. Among the readmitted patients, 13% had PCI, 2% had coronary artery bypass surgery, and 3% died during the readmission. The most common reasons for readmission included nonspecific chest pain/angina (24%) and heart failure (11%). Mean cumulative costs were higher for those with readmissions ($39 634 versus $22 058; P<0.001). The multivariable analyses showed that readmission increased the log10 cumulative costs by 45% (ß: 0.445; P<0.001). There was no significant difference in cumulative costs by the type of insurance. CONCLUSIONS: In a national sample of inpatient PCI cases, 30-day readmissions were associated with a significant increase in cumulative costs. The majority of readmissions were because of low-risk chest pain that did not require any intervention. Ongoing effort is warranted to recognize and mitigate potentially preventable post-PCI readmissions.

Reperfusion therapy of acute ischaemic stroke and acute myocardial infarction: similarities and differences.

The evolution of reperfusion therapy in acute myocardial infarction and acute ischaemic stroke has many similarities: thrombolysis is superior to placebo, intra-arterial thrombolysis is not superior to intravenous (i.v.), facilitated intervention is of questionable value, and direct mechanical recanalization without thrombolysis is proven (myocardial infarction) or promising (stroke) to be superior to thrombolysis-but only when started with no or minimal delay. However, there are also substantial differences. Direct catheter-based thrombectomy in acute ischaemic stroke is more difficult than primary angioplasty (in ST-elevation myocardial infarction [STEMI]) in many ways: complex pre-intervention diagnostic workup, shorter time window for clinically effective reperfusion, need for an emergent multidisciplinary approach from the first medical contact, vessel tortuosity, vessel fragility, no evidence available about dosage and combination of peri-procedural antithrombotic drugs, risk of intracranial bleeding, unclear respective roles of thrombolysis and mechanical intervention, lower number of suitable patients, and thus longer learning curves of the staff. Thus, starting acute stroke interventional programme requires a lot of learning, discipline, and humility. Randomized trials comparing different reperfusion strategies provided similar results in acute ischaemic stroke as in STEMI. Thus, it might be expected that also a future randomized trial comparing direct (primary) catheter-based thrombectomy vs. i.v. thrombolysis could show superiority of the mechanical intervention if it would be initiated without delay. Such randomized trial is needed to define the role of mechanical intervention alone in acute stroke treatment.

Enhanced sensitivity to drug-induced QT interval lengthening in patients with heart failure due to left ventricular systolic dysfunction.

Patients with heart failure (HF) are at increased risk for drug-induced torsades de pointes (TdP) due to unknown mechanisms. Our objective was to determine if sensitivity to drug-induced QT interval lengthening is enhanced in patients with HF. In this multicenter, prospective study, 15 patients with atrial fibrillation or flutter requiring conversion to sinus rhythm were enrolled: 6 patients with New York Heart Association class II to III HF (mean ejection fraction [EF], 30% ± 9%), and 9 controls (mean EF, 53% ± 6%). Patients received ibutilide 1 mg intravenously. Blood samples and 12-lead electrocardiograms were obtained prior to and during 48 hours postinfusion. Serum ibutilide concentrations at 50% maximum effect on Fridericia-corrected QT (QT(F)) intervals (EC(50)) were determined, and areas under the effect (QT(F) interval vs time) curves (AUECs) were calculated. Ibutilide concentration-QT(F) relationships were best described by a sigmoidal E(max) model with a hypothetical effect compartment. Median [interquartile range] AUEC from 0 to 4 hours was larger in the HF group than in controls (1.86 [1.86-1.93] vs 1.82 [1.81-1.84] s·h; P = .04). Median EC(50) was lower in the HF group (0.48 [0.46-0.49] vs 1.85 [1.10-3.23] µg/L; P = .008). Sensitivity to drug-induced QT interval lengthening is enhanced in patients with systolic HF, which may contribute to the increased risk of drug-induced TdP.

Pharmacokinetics of ibutilide in patients with heart failure due to left ventricular systolic dysfunction.

STUDY OBJECTIVE: To assess whether the increased risk of ibutilide-induced torsade de pointes in patients with heart failure may be due to increased ibutilide exposure, we sought to determine if the pharmacokinetics of ibutilide are altered in patients with heart failure due to left ventricular systolic dysfunction. DESIGN: Multicenter, prospective pharmacokinetic study. SETTING: Four academic medical centers in the United States. PATIENTS: Sixteen adult patients with atrial fibrillation or atrial flutter requiring conversion to normal sinus rhythm: six patients who had New York Heart Association (NYHA) class II or III heart failure due to left ventricular dysfunction (mean +/- SD left ventricular ejection fraction [LVEF] 30 +/- 9%); 10 patients who did not have left ventricular dysfunction (mean +/- SD LVEF 54 +/- 5% in six of these 10 patients) served as controls. INTERVENTION: All patients received a single dose of ibutilide 1.0 mg administered intravenously over 10 minutes. Blood samples were obtained through an indwelling catheter in the contralateral arm before ibutilide administration, at the end of the infusion, and at 5, 15, 30, 45 minutes and 1, 1.5, 2, 3, 4, 6, 8, 10, 12, 24, and 48 hours after the infusion. MEASUREMENTS AND MAIN RESULTS: Serum ibutilide concentrations were determined by using high-performance liquid chromatography and mass spectrometry. No significant differences were noted between the heart failure and normal left ventricular function groups in the following parameters: maximum serum ibutilide concentration (median [interquartile range] 3.8 [2.3-5.7] vs 5.8 [3.1-14.4] microg/L, p=0.31), area under the serum concentration-time curve from time zero extrapolated to infinity (mean +/- SD 11.0 +/- 9.4 vs 13.2 +/- 10.6 microg*hr/L, p=0.88), steady-state volume of distribution (1380 +/- 334 vs 1390 +/- 964 L, p=0.99), systemic clearance (129 +/- 60 vs 125 +/- 81 L/hr, p=0.92), or half-life (12.5 +/- 10.7 vs 12.4 +/- 8.6 hrs, p=0.99). CONCLUSION: The pharmacokinetics of ibutilide do not appear to be altered in patients with NYHA class II or III heart failure due to left ventricular systolic dysfunction. Therefore, the increased risk of ibutilide-induced torsade de pointes in patients with heart failure does not appear to be due to increased ibutilide exposure.

Percutaneous intervention through a Cabrol composite graft.

Similar to other surgical techniques, ascending thoracic aortic repair has evolved through a series of modifications, each with improvement in longevity, morbidity, and mortality. Until recently, most, if not all, aortic composite graft-coronary ostial anastamotic complications have been addressed with repeat surgery. Due to this, most interventional cardiologists have little to no experience in approaching postsurgical aortic composite graft-coronary ostial anastamotic lesions percutaneously when the anatomy is altered by a Cabrol interposition graft. Nevertheless, it is important that operators are aware of the various surgical techniques used to repair the ascending aorta and reimplant the coronary arteries. Furthermore, in the present era of addressing more and more stenotic lesions percutaneously, it is important to have knowledge into which type of lesion lends itself to a percutaneous approach. Our review of the literature reveals that there have been no reported cases of percutaneous interventions of the native coronary arteries through a Cabrol composite graft. We report the first case of percutaneous intervention of an unprotected left main anastamotic stenosis through a Cabrol composite graft.