Rate versus rhythm control in patients with newly diagnosed atrial fibrillation: Effects of the treatment timing on health status outcomes.

BACKGROUND: Recent randomized clinical trials have demonstrated that applying rhythm control during the early stage of atrial fibrillation (AF) may lead to improved clinical outcomes. However, the effects of this modality on health-related quality of life (HRQoL) have not been fully investigated. We aimed to assess the association between the AF stage, determined by the time between AF diagnosis and referral to the cardiology clinic, and HRQoL outcomes. METHODS: Using an outpatients-based multicenter AF registry (n = 3,313), we analyzed 2,070 patients with AF diagnosed within 5 years. The patients were divided into 2 groups according to AF stage: early and late AF (AF duration ≤1 and >1 year, respectively). All patients had HRQoL information collected at baseline and 1 year after their initial treatment (assessed via the Atrial Fibrillation Effect on Quality-of-Life-overall summary [AFEQT-OS] score, with higher scores reflecting better HRQoL). The change in AFEQT-OS was adjusted for patient characteristics using a generalized linear mixed model. RESULTS: The early AF group (n = 1,644) was older (early, 68.5 ± 11.1, late, 64.4 ± 10.6 years, P < .001) and had more heart failure (early, 19.9%, late, 12.7%, P < .001) than the late AF group (n = 426). At 1 year after treatment, the adjusted changes in AFEQT-OS were similar in patients with rhythm (adjusted difference [SE], early, 8.4 [1.2], late, 7.2 [1.4], P = .15) or rate (early, 4.0 [0.7], late, 2.3 [1.4], P = .16) control, regardless of AF stage. Furthermore, the improvement in HRQoL was similar between early and late AF in patients undergoing catheter ablation (early, 10.2 [2.1], late, 9.8 [2.4], P = .78), whereas a significant difference was observed in those receiving antiarrhythmic drug therapy alone (early, 10.2 [1.4], late, 3.5 [2.2], P < .001). CONCLUSIONS: Rhythm control therapy provided clinically meaningful improvements in HRQoL, regardless of AF stage. For patients with impaired HRQoL, AF duration should not be a deterrent to treatment, especially catheter ablation.

Incidence of periprocedural myocardial infarction and cardiac biomarker testing after percutaneous coronary intervention in Japan: results from a multicenter registry.

Periprocedural myocardial infarction (pMI) is an important complication associated with percutaneous coronary intervention (PCI). However, data on the frequency of biomarker testing and the incidence of pMI remain unclear. Using the multicenter Japan Cardiovascular Database, we identified 2182 patients who underwent PCI without preprocedural cardiac biomarker elevation (silent ischemia, stable angina, or unstable angina without biomarker elevation) from September 2008 to August 2011. Of these, 550 patients (25.2 %) underwent cardiac biomarker testing within 6-24 h after PCI. The incidence of pMI was 2.7 % among all identified patients and 7.5 % among those who underwent cardiac marker testing. Of note, cardiac biomarker testing was performed more frequently than no testing in patients with a higher risk profile such as unstable angina (32.7 vs 24.7 %, P < 0.001), higher symptom scaling (28.2 vs 22.5 %, P = 0.008), urgent or emergent procedures (19.3 vs 15.0 %, P = 0.022 or 4.2 vs 1.0 %, P < 0.001, respectively), and type C lesion (31.3 vs 25.2 %, P = 0.006). Presentation with silent ischemia (odds ratio = 1.51, 95 % confidence interval (CI) 1.16-1.97) and nonemergent PCIs (odds ratio = 3.45, 95 % CI 1.79-6.67) were associated with no postprocedural cardiac biomarker testing. The real-world multicenter PCI registry in Japan revealed an incidence of 2.7 % for pMI; however, cardiac biomarkers were assessed in only 25.2 % of patients after PCI. The results suggest an underuse of postprocedural biomarker testing and room for procedural quality improvement, particularly in cases of silent ischemia and nonemergent cases.

Conventional medical therapy in heart failure patients eligible for the PARADIGM-HF, DAPA-HF, and SHIFT trials.

BACKGROUND: Recent trials on novel heart failure (HF) treatments (angiotensin receptor-neprilysin inhibitor, sodium-glucose cotransporter 2 inhibitor, and ivabradine) emphasize the use of conventional medical therapy (angiotensin-converting enzyme inhibitors, beta-blockers [BB], and mineral corticosteroid receptor antagonists). We aimed to evaluate the prescription rate of conventional medical therapy and its association with long-term outcomes in patients eligible for recent trials. METHODS: We examined 1295 consecutive patients with HF with reduced ejection fraction (HFrEF) from a multicenter registry (WET-HF registry). We assessed conventional medical therapy implementation among patients meeting the PARADIGM-HF/DAPA-HF and SHIFT enrollment criteria. We also examined the association between conventional medical therapy use and long-term outcomes within each enrollment criterion. RESULTS: Overall, 62.2% and 35.3% of HFrEF patients met the enrollment criteria of the PARADIGM-HF/DAPA-HF and SHIFT trials. Only 33.9% and 31.9% received full conventional medical therapy within each patient subset. Notably, 84.2% of patients who met the SHIFT enrollment criteria were on BB, and only 23.0% and 4.4% were on ≥50% or the full recommended dose, respectively. Implementation of full conventional medical therapy use was associated with lower 2-year mortality and HF readmission rates in the PARADIGM-HF/ DAPA-HF eligible group (HR 0.68, 95% CI 0.50-0.92). The use of BB at ≥50% of the recommended dose was associated with lower 2-year mortality and HF readmission rates in the SHIFT-eligible group (HR 0.50, 95% CI 0.30-0.84). CONCLUSIONS: Conventional medical therapy was underutilized among patients eligible for novel trials within a Japanese HF registry. Further efforts to optimize conventional medical therapy are needed.

Adenosine triphosphate-sensitive potassium channels prevent extension of myocardial ischemia to subepicardium during hemorrhagic shock.

Cardiac dysfunction during hemorrhagic shock (HS) is associated with myocardial ischemia, during which adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channels can be activated. We investigated the role of K(ATP) channels in HS-induced myocardial ischemia. Canine HS was induced using an aortic reservoir to maintain the aortic pressure at a constant 40 mmHg. To visualize the myocardial ischemia as a nicotinamide adenine dinucleotide (NADH) - fluorescent area, the beating hearts were rapidly cross-sectioned (120 ms) and freeze-clamped (-190 degrees C) using a sampling device after 10 min of HS. The effect of a K(ATP) channel blocker, glibenclamide (1 mg/kg, i.v.), on myocardial ischemia was also quantified. Regional myocardial blood flow was measured using heavy element-loaded nonradioactive microspheres. Myocardial ischemia developed in the subendocardium in the HS alone group, whereas it extended through all the cardiac layers in the glibenclamide-treatment group. The coadministration of a K(ATP) channel opener, cromakalim (50 microg/kg, i.v.), with glibenclamide prevented the extension of myocardial ischemia to the subepicardium. Glibenclamide decreased the myocardial ATP concentration selectively in the subepicardium during HS. The HS decreased myocardial blood flow transmurally, and following the administration of glibenclamide, further decreased the blood flow selectively in the subepicardium. These results suggest that K(ATP) channels are activated during HS, enabling selective subepicardial coronary dilatation and protecting the myocardium from the extension of myocardial ischemia to the subepicardium.

A rare case of fungal endocarditis caused by Candida glabrata after completion of antibiotic therapy for Streptococcus endocarditis.

We present the rare case of a 76-year-old female with infective endocarditis (IE) caused by Candida glabrata. Immediately before developing the present infection, she developed IE with vegetation on the mitral annular calcification, which was caused by Streptococcus mitis and successfully treated with penicillin-G and gentamicin. However, her fever recurred, and she developed disseminated intravascular coagulation. Blood culture revealed C. glabrata, and echocardiography revealed new vegetation on the mitral valve. After 4 weeks of treatment with micafungin, prosthetic valve replacement was performed, followed by additional administration of micafungin for 4 weeks (total of 8 weeks). No relapse at 9 months after surgery has been observed. C. glabrata endocarditis is extremely rare and difficult to manage. Our case and review of past reported cases suggest that early diagnosis and initiation of treatment contribute to good prognosis of C. glabrata endocarditis.

Significance of echocardiographic assessment for right ventricular function after balloon pulmonary angioplasty in patients with chronic thromboembolic induced pulmonary hypertension.

Balloon pulmonary angioplasty (BPA) may improve hemodynamics and exercise tolerance in patients with chronic thromboembolic pulmonary hypertension (CTEPH). We studied consecutive 25 patients with CTEPH who underwent BPA and evaluated hemodynamics by right-sided heart catheterization. Right ventricular (RV) function was assessed before and after BPA by echocardiography including speckle-tracking echocardiography and 3-dimensional echocardiography. BPA improved the mean pulmonary artery pressure, pulmonary vascular resistance, and cardiac index. BPA also ameliorated the 3-dimentional RV volume, RV ejection fraction, and RV systolic peak strain, all of which were significantly correlated with hemodynamic parameters. The changes in cardiac index were significantly correlated with those in 3-dimentional RV volume index. Furthermore, RV dyssynchrony quantified by the RV strain analyses was ameliorated after BPA even in patients with mild pulmonary hypertension, implicating the merit of BPA in this patient population with CTEPH. BPA not only improved the hemodynamics in patients with CTEPH, but also ameliorated RV remodeling and dyssynchrony as assessed by 3-dimensional echocardiography or speckle-tracking echocardiography. Thus, the assessment of RV function may provide valuable information about the appropriate indication for BPA, its efficacy, and the therapeutic goal for patients with CTEPH.

Impact of periprocedural bleeding on incidence of contrast-induced acute kidney injury in patients treated with percutaneous coronary intervention.

OBJECTIVES: This study sought to evaluate the association between contrast-induced acute kidney injury (CI-AKI) after percutaneous coronary intervention and severity of bleeding estimated from periprocedural hemoglobin (Hb) measurement. BACKGROUND: The relationship between CI-AKI and bleeding in contemporary practice remains controversial. METHODS: In a retrospective analysis of the prospectively maintained Japan Cardiovascular Database-Keio Interhospital Cardiovascular Studies (JCD-KICS) multicenter registry, we divided 2,646 consecutive patients into 5 groups according to the change of Hb level after compared with before percutaneous coronary intervention: patients without a decrease in Hb level (group A) and patients with a decreased Hb level: <1 g/dl (group B); 1 to <2 g/dl (group C); 2 to <3g/dl (group D); and >3 g/dl (group E). CI-AKI was defined as an increase in serum creatinine level ≥ 0.5 mg/dl or ≥ 25% above baseline values at 48 h after administration of contrast media. Procedure and outcome variables were compared. RESULTS: The mean patient age was 67 ± 11 years. Of the 2,646 patients, CI-AKI developed in 315 (11.9%). The CI-AKI incidence was 6.2%, 7.5%, 10.7%, 17.0%, and 26.2%, in groups A through E, respectively (p < 0.01), whereas the incidence of major bleeding was 0.7%, 1.3%, 2.0%, 4.1%, and 28.3%, respectively (p < 0.01). CI-AKI was associated with higher rates of mortality (5.4% vs. 0.6%, p < 0.01) and of composite of heart failure, cardiogenic shock, and death (16.5% vs. 2.8%, p < 0.01). CONCLUSIONS: Periprocedural bleeding was significantly associated with CI-AKI, with CI-AKI incidence correlating with bleeding severity.

Primary stenting for left-main shock syndrome.

AIMS: Acute myocardial infarction (AMI) complicated by unprotected left-main shock (LMS) remains a highly morbid event among acute coronary syndromes. Whether early percutaneous coronary intervention (PCI) in the stent era improves the clinical outcome remains poorly defined. METHOD AND RESULTS: 25 consecutive patients who presented with LMS were treated by primary stenting of bare metal stents for the unprotected left main lesion with an aid of conventional supportive measures. Mean age of the patients was 67 (range, 46-89), 84% were male, with an initial mean systolic BP of 88mmHg (range, 40-120), HR of 82 bpm (range, 38-130), and symptom onset to reperfusion of 4.8hours (range, 1.5-17). An initial TIMI grade 0 flow was noted on the emergent CAG among 56% of the patients, but after PTCA and stenting, TIMI grade 3 flow was obtained among 84%. 30-day mortality was 32%, while one patient underwent emergent CABG for subacute stent thrombosis and 3 patients required elective CABG for residual disease during admission. Among 11 patients who were discharged alive, one required further institutionalization for ischemic brain injury, and the 2 required target vessel revascularization for restenoses. The major adverse cardiac events (death, re-infarction, stroke, and target vessel revascularization) occurred in 68% (17/25) over a 12-month follow-up, including 40% of mortality. CONCLUSIONS: AMI complicated by unprotected LMS could be treated effectively with a prompt application of stenting and result in an acceptable mortality and morbidity.

Flow-independent myocardial ischemia induced by endothelin-1: an NADH fluorescence analysis.

The endothelin-1 (ET-1) is known to cause myocardial ischemia; however, whether this effect is entirely dependent on vasoconstriction is uncertain. The aim of this study was to characterize the myocardial ischemia after the intracoronary administration of endothelin-1, and compare it with that induced by coronary stenosis. In the left anterior descending coronary artery of 15 dogs, a mild inflow reduction (30%) was produced for 10 minutes using intracoronary endothelin-1 (46 +/- 33 pmol/min) or coronary stenosis. The hearts were rapidly cross-sectioned at short axial plane and freeze-clamped within 120 milliseconds using a specially developed device to visualize and quantify the area of ischemia (%IA) with NADH fluorescence photography. The %IA was larger in the endothelin-1 group than in the stenosis group (66 +/- 23 versus 18 +/- 18, P = 0.0005); furthermore, the ischemia was transmural in the ET-1 group, but limited to subendocardium in the stenosis group. ET-1 increased the coronary arterial resistance especially in subepicardial region and produced smaller ischemic foci in microcirculation. The mechanism of larger ischemia produced by ET-1 might depend on pro-ischemic effects on myocytes and vasoconstriction of the coronary microcirculation, predominantly in the subepicardium in vivo.