The impact of atrial fibrillation on clinical outcomes in heart failure with mid-range and preserved ejection fraction patients.

BACKGROUND: The combined effect of left ventricular ejection fraction (LVEF) and atrial fibrillation (AF) on clinical outcomes in heart failure (HF) remains complex. OBJECTIVE: In this post hoc analysis of the TOPCAT trial, we aimed to evaluate the impact of AF on clinical outcomes in patients with HF stratified by LVEF range. METHODS: A total of 3442 patients were included, stratified into 3 groups according to LVEF range-HF with mid-range ejection fraction (HFmrEF), LVEF of 45%-50% (n = 823); HF with preserved ejection fraction (HFpEF), LVEF of 51%-60% (n = 1682); and HF with normal ejection fraction (HFnEF), LVEF >60% (n = 937)-and subdivided according to the presence of AF at enrollment. Cox regression analysis was used to define independent associations between AF and clinical outcomes. RESULTS: AF was prevalent in 38.6% in HFmrEF, 34.6% in HFpEF, and 33.7% in HFnEF (P = .07). AF was associated with worse primary outcome in each subgroup and with HF hospitalizations and worse cardiovascular mortality in HFpEF and HFnEF. The hazard ratio for the primary outcome in those with AF compared with sinus rhythm (SR) was 1.11 (1.01-1.22; P = .03) in HFmrEF, 1.20 (1.11-1.29; P < .001) in HFpEF, and 1.16 (1.05-1.28; P = .004) in HFnEF. When LVEF was treated as a continuous variable, there was a linear negative association between LVEF and the effect of AF vs SR for the primary end point and HF hospitalizations and a linear positive association for cardiovascular mortality. CONCLUSION: Compared with SR, AF was independently associated with worse outcomes across all LVEF ranges.

Association between atrial fibrillation and heart failure patient reported outcomes across the ejection fraction spectrum.

BACKGROUND: Atrial fibrillation (AF) is common in patients with heart failure (HF) and is associated with worse clinical outcomes. We evaluated the relationship between AF and longitudinal changes in health-related quality of life (HRQoL) measured by Kansas City Cardiomyopathy Questionnaire (KCCQ) in both HF with preserved (HFpEF) and reduced ejection fraction (HFrEF). METHODS: This is a post-hoc analysis of the TOPCAT and HF-ACTION trials. The effect of AF on KCCQ overall summary scores (OSS), in both trials, was examined using a mixed effects regression model. Patients were divided into 3 groups according to AF status at baseline: patients with a history of AF but no AF detected on ECG at enrollment (Hx AF group), patients with history of AF and AF detected on ECG at enrollment (ECG AF group) and patients with post-randomization new-onset AF (New AF group). RESULTS: In TOPCAT, among 1,710 patients with KCCQ data available, AF was associated with a significantly lower KCCQ-OSS (-3.98; 95% CI -7.21: -0.74) at 48 months, with a significant AF status by time interaction (P = .03). In HF-ACTION, among 1,814 patients with available KCCQ data, AF was associated with a significantly lower KCCQ-OSS (-3.67; 95% CI -6.21: -1.41) at 24 months but there was no significant AF status by time interaction. In both trials, the type of AF was not associated with significant changes in KCCQ-OSS score. CONCLUSION: Ιn patients with both HFpEF and HFrEF, AF was independently associated with worse HRQoL measured by KCCQ.

Does spotty calcification attenuate the response of nonculprit plaque to statin therapy?: A serial optical coherence tomography study.

OBJECTIVES: The aim of this study was to determine if spotty calcification decreases the response of plaque progression to statin therapy. BACKGROUND: Previous studies showed that the presence of spotty calcification is a marker of vulnerable plaque. However, the relationship between spotty calcification and plaque progression is not clear. METHODS: Ninety-six nonculprit lipid-rich plaques in 69 patients who received serial optical coherence tomography (OCT) imaging were included. Plaques were divided into three groups: spotty calcification (n = 38), calcified (n = 12) and noncalcified (n = 46) plaques. Spotty calcification was identified by the presence of a lesion <4 mm in length with an arc of calcification <90°. Changes in plaque characteristics and fibrous cap thickness (FCT) at 6 and 12 months under statin therapy were analyzed by OCT. RESULTS: The increase of FCT was sustained from baseline to 6 and 12 months in three groups: spotty calcification (62.8 ± 20.9, 126.4 ± 84.9, and 169.2 ± 81.6 µm, respectively; P < .001), calcified (59.8 ± 17.0, 93.4 ± 51.4, and 155.2 ± 61.7 µm, respectively; P < .001) and noncalcified (60.0 ± 17.2, 125.5 ± 62.1, and 161.0 ± 80.5 µm, respectively; P < .001). Intensive statin induced a greater change in FCT at 12 months than moderate statin in the spotty calcification group (P = 0.034). The mean lipid arc decreased significantly at 12 months from baseline in the three groups (P = 0.004, P = 0.023, and P < .001, respectively). CONCLUSIONS: Statin therapy was effective for plaque stabilization in plaques with and without spotty calcification. Patients with spotty calcification benefitted more from intensive statin than from moderate statin therapy.

Impact of statins therapy on morphological changes in lipid-rich plaques stratified by 10-Year framingham risk score: A serial optical coherence tomography study.

The aim of the study was to investigate the impact of statins therapy on morphological changes of lipid-rich plaques by OCT (optical coherence tomography) in patients with known CHD (coronary heart disease), stratified by FRS. Ninety-seven lipid-rich plaques from sixty-nine patients who received statins therapy and underwent serial OCT images (baseline, 6-month and 12-month) were divided into 2 groups according to the FRS (framingham risk score): low risk group A (FRS<10%, N=35, n=45), moderate to high risk group B (FRS≥10%, N=34, n=52). Fibrous cap thickness (FCT) was measured at its thinnest part 3 times. Baseline characteristics were not different between the 2 groups. FCT sustained increased from baseline to 6-month and 12-month follow up in both group A (59.8±20.4µm, 118.3±62.5µm, and 158.8±83.4µm respectively, P<0.001) and group B (62.2±16.8µm, 125.1±78.7µm, 163.8±75.5µm respectively, P<0.001). Lipid index was significantly decreased in both group A (1862.1±1164.5, 1530.3±1108.7, 1322.9±1080.4, P<0.001) and group B (1646.6±958.5, 1535.1±1049.1, 1258.6±1045, P=0.016). The incidence of TCFA was decreased statistically in both group A (P <0.001) and group B (P <0.001). The patients with known CHD can equivalently benefit from statins therapy by stabilizing the lipid-rich plaques. Patients with moderate to high FRS might benefit more within the first year from event time.

Chronic total occlusion is associated with a higher incidence of malapposition and uncovered stent struts: OCT findings at 6 months following DES implantation.

OBJECTIVES: To compare stent coverage and malapposition in patients with chronic total occlusion (CTO) lesions and non-CTO lesions (including lipid-rich plaque [LRP] and non-lipid-rich plaque [non-LRP]) after drug-eluting stent (DES) implantation by optical coherence tomography (OCT). BACKGROUND: Different initial lesion characteristics may be related to heterogeneous vessel responses after DES implantation. However, the vessel response in patients with CTO and non-CTO lesions after stenting is unclear. Methods We retrospectively enrolled 64 patients with 68 target lesions. All of the patients underwent OCT imaging immediate after stenting and 6 months after stenting. LRP was defined as the plaque with lipid content in ≥2 quadrants. Non-LRP consisted of fibrous, fibrocalcific plaque, and lipid plaque with less than 2 quadrants lipid content. RESULTS: The malapposition (3.0%, 2.6% vs. 0.6%, P = 0.022), tissue protrusion (15.0% vs. 11.0% vs. 6.4%, P < 0.001), and intrastent thrombus (3.8% vs. 2.4% vs. 1.1%, P = 0.012) were more frequent in the CTO and LRP groups. At 6-month follow-up, malapposition (5.0% vs. 1.0% and 0.4%, P = 0.002) and cross sections with uncovered struts (23.4% vs. 8.2% and 6.6%, P < 0.001) were most frequently observed in the CTO group. Although the incidence of stent thrombosis was non-significantly higher in the CTO group than the other two groups, no events were observed in patients with CTO. CONCLUSIONS: Patients with CTO lesions showed unfavorable responses to DES in the acute phase as well as at the 6-month follow-up, indicating the important pathological link between the original lesion morphology underneath the stents and heterogeneous artery healing. © 2017 Wiley Periodicals, Inc.