Electrophysiological characteristics of non-pulmonary vein triggers excluding origins from the superior vena cava and left atrial posterior wall: Lessons from the self-reference mapping technique.

BACKGROUND: The detailed electrophysiological characteristics of atrial fibrillation (AF) initiating non-pulmonary vein (PV) triggers excluding origins from the superior vena cava (SVC) and left atrial posterior wall (LAPW) (Non-PV-SVC-LAPW triggers) remain unclear. This study aimed to clarify the detailed electrophysiological characteristics of non-PV-SVC-LAPW triggers. METHODS: Among 446 AF ablation procedures at 2 institutions, patients with reproducible AF initiating non-PV-SVC-LAPW triggers were retrospectively enrolled. The trigger origin was mapped using the self-reference mapping technique. The following electrophysiological parameters were evaluated: the voltage during sinus rhythm and at the onset of AF at the earliest activation site, coupling interval of the trigger between the prior sinus rhythm and AF trigger, and voltage change ratio defined as the trigger voltage at the onset of AF divided by the sinus voltage. RESULTS: Detailed electrophysiological data were obtained at 28 triggers in 21 patients. The median trigger voltage at the onset of AF was 0.16mV and median trigger coupling interval 182msec. Normal sinus voltages (≧0.5mV) were observed at 16 triggers and low voltages (<0.5mV) at 12 triggers. The voltage change ratio was significantly lower for the normal sinus voltage than low sinus voltage (0.20 vs. 0.60, p = 0.002). The trigger coupling intervals were comparable between the normal sinus voltage and low sinus voltage (170ms vs. 185ms, p = 0.353). CONCLUSIONS: The trigger voltage at the onset of AF was low, regardless of whether the sinus voltage of the trigger was preserved or low.

Clinical Significance of B-Type Natriuretic Peptide Levels at 3 Months after Atrial Fibrillation Ablation.

The role of B-type natriuretic peptide (BNP) levels as a predictor of arrhythmia recurrence (AR) after atrial fibrillation (AF) ablation remains unclear. In this study, we investigated the association of BNP levels before and 3 months after ablation with the risk of AR. A total of 234 patients undergoing their first session of AF ablation were included (68% male, mean age of 69 years). The cut-off value for discriminating AR was determined based on the maximum value of the area under the receiver operating characteristic (ROC) curve. The impact of BNP levels on AR was evaluated using Cox regression analysis. ROC curve analysis showed that the area under the curve for BNP at 3 months after the procedure was larger (0.714) compared to BNP levels before ablation (0.593). Elevated levels of BNP 3 months after the procedure (>40.5 pg/mL, n = 96) was associated with a higher risk of AR compared to those without elevated levels (34.4% vs. 10.9%, p < 0.01). Multivariate Cox regression analysis revealed that elevated BNP levels were associated with an increased risk of AR (hazard ratio 2.43; p = 0.014). Elevated BNP levels 3 months after AF ablation were a significant prognostic factor in AR, while baseline BNP levels were not.

Clinical impact of a self-reference mapping technique to detect non-pulmonary vein triggers: A multi-center study.

BACKGROUND: The method to perform a precise mapping of non-pulmonary vein (PV) triggers has not been fully investigated. The purpose of this study was to assess the efficacy of self-reference mapping for eliminating non-PV triggers in a large series of patients including the long-term outcomes. METHOD: Among 446 atrial fibrillation (AF) ablation procedures in 431 patients at 2 institutions, we prospectively enrolled patients who had reproducible non-PV triggers. Non-PV triggers from the left atrial posterior wall (LAPW) and superior vena cava (SVC) were excluded. Ablation procedure and long-term clinical outcomes were evaluated. The origin of non-PV triggers were detected using a self-reference mapping technique, which does not require any other reference catheters. Instead of using signals obtained from a fixed intracardiac catheter as the reference, an operator repeatedly moved a multi-electrode catheter to the earliest site creating a new reference each time to map the non-PV trigger. RESULTS: A total of 32 non-PV triggers excluding origins from the LAPW and SVC were induced in 23 patients. All triggers were mapped using a self-reference mapping technique with 11.0 ± 10.2 min and eliminated by radiofrequency ablation with 10.7 ± 10.0 points application. No major complications were observed. During the follow-up (529 ± 270 days), 18 patients (77%) were free from atrial tachyarrhythmias after a 3-month blanking period. Three patients received additional ablation procedures. No non-PV triggers ablated during the previous procedure were observed. CONCLUSIONS: A novel self-reference mapping technique is useful for eliminating non-PV triggers for the short- and long-term outcomes.

Longitudinal Stent Elongation of a Tapered Lesion during Percutaneous Coronary Intervention: A Case Report.

The therapeutic strategy for percutaneous coronary intervention (PCI) of a tapered lesion is still being developed. Herein, we describe a 67-year-old man with stable angina who underwent elective PCI of a tapered lesion. The coronary angiogram showed diffuse, severe stenosis in the tapered left anterior descending artery. A third-generation sirolimus-eluting stent (2.5 × 24-mm Ultimaster, Terumo, Tokyo, Japan) was deployed, and the distal side was selected as the reference. Postdilatation with a balloon diameter 2.0 mm larger than the stent was needed because of the tapered lesion. We performed postdilatation from the distal side to the proximal side of the stent with a noncompliant balloon (4.5 × 8-mm Powered Lacrosse2, Goodman, Aichi, Japan). The final angiogram showed that the total stent length was 6 mm longer than the original length. Therefore, physicians should be aware of longitudinal stent elongation of a tapered lesion during PCI to ensure appropriate treatment.

A decline in activities of daily living due to acute heart failure is an independent risk factor of hospitalization for heart failure and mortality.

BACKGROUND: Although activities of daily living (ADL) are recognized as being pertinent in averting relevant readmission of heart failure (HF) and mortality, little research has been conducted to assess a correlation between a decline in ADL and outcomes in HF patients. METHODS: The Kitakawachi Clinical Background and Outcome of Heart Failure Registry is a prospective, multicenter, community-based cohort of HF patients. We categorized the patients into four types of ADL: independent outdoor walking, independent indoor walking, indoor walking with assistance, and abasia. We defined a decline in ADL (decline ADL) as downgrade of ADL and others (non-decline ADL) as preservation of ADL before discharge compared with admission. RESULTS: Among 1253 registered patients, 923 were eligible, comprising 98 (10.6%) with decline ADL and 825 (89.4%) with non-decline ADL. Decline ADL exhibited a higher risk of hospitalization for HF and mortality compared with non-decline ADL. A multivariate analysis revealed that decline ADL emerged as an independent risk factor of hospitalization for HF [hazard ratio (HR), 1.42; 95% confidence interval (CI): 1.01-1.96; p=0.046] and mortality (HR, 1.95; 95% CI: 1.23-2.99; p<0.01). Although 66.3% of patients with decline ADL were registered for long-term care insurance, few received daycare services (32.7%) or home-visit medical services (8.2%). CONCLUSIONS: Decline in ADL is a predictor of hospitalization for HF and mortality in HF patients.

The utility of atrial overdrive pacing during catheter ablation of premature ventricular contractions originating from the posterior-superior process of the left ventricle.

A 76-year-old man presented with frequent premature ventricular contractions (PVCs). The electrophysiological findings revealed the origin of the PVCs was in the posterior-superior process of the left ventricle (PSP-LV), which is anatomically adjacent to the infero-medial aspect of the right atrium (RA). After a failed ablation from the LV, ablation in the RA eliminated the PVCs. During additional ablation, the atrio-his (AH) interval was monitored by atrial overdrive pacing, and ablation was terminated immediately after the AH interval prolonged to 174 ms. We believe that the atrial overdrive pacing was useful for monitoring the AH interval to prevent atrioventricular block during ablation of PVCs from the PSP-LV. .

Atrial tachycardia related to local abnormal atrial activity.

A 42-year-old woman without a history of catheter ablation or cardiac surgery was referred to our institution for a paroxysmal atrial tachycardia (AT). Programed stimulation could not induce any AT. The AT spontaneously initiated during a continuous isoproterenol infusion. The earliest activation during the AT was recorded at the cavo-tricuspid isthmus, and local abnormal atrial activity (LAATA) was recorded during sinus rhythm at that same site. When rapid atrial activity was recorded at the cavo-tricuspid isthmus where the LAATA was recorded, an AT was induced. Radiofrequency ablation was performed over the entire area where the LAATA was recorded during sinus rhythm, rendering the AT non-inducible.

The usefulness of ventricular pacing during atrial fibrillation ablation in a persistent left superior vena cava: A case report.

A 69-year-old woman with palpitations was referred to our hospital for a second session of atrial fibrillation (AF) catheter ablation. She had a history of AF ablation including pulmonary vein (PV) isolation and persistent left superior vena cava (PLSVC) isolation. Electrophysiologic studies showed the veno-atrial connections that had recovered. After PV isolation was performed, AF was induced by atrial premature contraction (APC) from the PLSVC, and AF storm occurred. During PLSVC isolation, AF was not induced by APC from the PLSVC. PLSVC isolation continued during sinus rhythm. The elimination of the PLSVC potential was difficult to confirm because of the far-field potential of the left ventricle. Then, we performed right ventricular pacing. The remaining PLSVC potential was identified. After that, the PLSVC isolation was successful during right ventricular pacing. Complications were not observed. The patient had no recurrence of AF thereafter.

Clinical Impact of Ventricular Tachycardia and/or Fibrillation During the Acute Phase of Acute Myocardial Infarction on In-Hospital and 5-Year Mortality Rates in the Percutaneous Coronary Intervention Era.

BACKGROUND: The aim of this study was to investigate the prognostic impact of acute-phase ventricular tachycardia and fibrillation (VT/VF) on ST-segment elevation myocardial infarction (STEMI) patients in the percutaneous coronary intervention (PCI) era. METHODS AND RESULTS: Using the database of the Osaka Acute Coronary Insufficiency Study (OACIS), we studied 4,283 consecutive patients with STEMI who were hospitalized within 12 h of STEMI onset and underwent emergency PCI. Acute-phase VT/VF, defined as ≥3 consecutive ventricular premature complexes and/or VF within the 1st week of hospitalization, occurred in 997 (23.3%) patients. In-hospital mortality risk was significantly higher in patients with acute-phase VT/VF than inthose without (14.6% vs. 4.3%, adjusted hazard ratio (HR) 1.83, P=0.0013). Among patients discharged alive, 5-year mortality rates were comparable between patients with and without acute-phase VT/VF. Subgroup analysis showed that acute-phase VT/VF was associated with increased 5-year mortality after discharge in high-risk patients (GRACE Risk Score ≥115; adjusted HR 1.60, P=0.043), but not in intermediate- or low-risk patients. CONCLUSIONS: Even in the PCI era, acute-phase VT/VF was associated with higher in-hospital deaths of STEMI patients. However, the 5-year prognostic impact of acute-phase VT/VF was limited to high-risk patients. (Circ J 2016; 80: 1539-1547).

Reduced risk of recurrent myocardial infarction in homozygous carriers of the chromosome 9p21 rs1333049 C risk allele in the contemporary percutaneous coronary intervention era: a prospective observational study.

OBJECTIVES: Chromosome 9p21 single nucleotide polymorphism (SNP) is a susceptibility variant for acute myocardial infarction (AMI) in the primary prevention setting. However, it is controversial whether this SNP is also associated with recurrent myocardial infarction (ReMI) in the secondary prevention setting. The purpose of this study is to evaluate the impact of chromosome 9p21 SNP on ReMI in patients receiving secondary prevention programmes after AMI. DESIGN: A prospective observational study. SETTING: Osaka Acute Coronary Insufficiency Study (OACIS) in Japan. PARTICIPANTS: 2022 patients from the OACIS database. INTERVENTIONS: Genotyping of the 9p21 rs1333049 variant. PRIMARY OUTCOME MEASURES: ReMI event after survival discharge for 1 year. RESULTS: A total of 43 ReMI occurred during the 1 year follow-up period. Although the rs1333049 C allele had an increased susceptibility to their first AMI in an additive model when compared with 1373 healthy controls (OR 1.20, 95% CI 1.09 to 1.33, p=2.3*10(−4)), patients with the CC genotype had a lower incidence of ReMI at 1 year after discharge of AMI (log-rank p=0.005). The adjusted HR of the CC genotype as compared with the CG/GG genotypes was 0.20 (0.06 to 0.65, p=0.007). Subgroup analysis demonstrated that the association between the rs1333049 CC genotype and a lower incidence of 1 year ReMI was common to all subgroups. CONCLUSIONS: Homozygous carriers of the rs1333049 C allele on chromosome 9p21 showed a reduced risk of 1 year ReMI in the contemporary percutaneous coronary intervention era, although the C allele had conferred susceptibility to their first AMI.

Association of lifestyle-related factors with circadian onset patterns of acute myocardial infarction: a prospective observational study in Japan.

OBJECTIVE: The onset of acute myocardial infarction (AMI) shows characteristic circadian variations involving a definite morning peak and a less-defined night-time peak. However, the factors influencing the circadian patterns of AMI onset and their influence on morning and night-time peaks have not been fully elucidated. DESIGN, SETTING AND PARTICIPANTS: An analysis of patients registered between 1998 and 2008 in the Osaka Acute Coronary Insufficiency Study, which is a prospective, multicentre observational study of patients with AMI in the Osaka region of Japan. The present study included 7755 consecutive patients with a known time of AMI onset. MAIN OUTCOMES AND MEASURES: A mixture of two von Mises distributions was used to examine whether a circadian pattern of AMI had uniform, unimodal or bimodal distribution, and the likelihood ratio test was then used to select the best circadian pattern among them. The hierarchical likelihood ratio test was used to identify factors affecting the circadian patterns of AMI onset. The Kaplan-Meier method was used to estimate survival curves of 1-year mortality according to AMI onset time. RESULTS: The overall population had a bimodal circadian pattern of AMI onset characterised by a high and sharp morning peak and a lower and less-defined night-time peak (bimodal p<0.001). Although several lifestyle-related factors had a statistically significant association with the circadian patterns of AMI onset, serum triglyceride levels had the most prominent association with the circadian patterns of AMI onset. Patients with triglyceride ≥150 mg/dL on admission had only one morning peak in the circadian pattern of AMI onset during weekdays, with no peaks detected on weekends, whereas all other subgroups had two peaks throughout the week. CONCLUSIONS: The circadian pattern of AMI onset was characterised by bimodality. Notably, several lifestyle-related factors, particularly serum triglyceride levels, had a strong relation with the circadian pattern of AMI onset. TRIAL REGISTRATION NUMBER: UMIN000004575.

Renin-angiotensin-aldosterone system polymorphisms and 5-year mortality in survivors of acute myocardial infarction: a report from the Osaka Acute Coronary Insufficiency Study.

This study sought to evaluate whether genetic variants in the renin-angiotensin-aldosterone system (RAAS) have an impact on long-term mortality after acute myocardial infarction (AMI) in the percutaneous coronary intervention (PCI) era. We investigated the impacts of individual and combinations of 4 major RAAS genetic variants, angiotensinogen (AGT) T1311C, angiotensin-converting enzyme (ACE) insertion/deletion (I/D), angiotensin 2 type 1 receptor A1166C, and aldosterone synthase T4660C on 5-year mortality in 3149 post-AMI patients using multivariate Cox regression analysis. The predictive accuracy of all possible RAAS genetic combinations was evaluated using Cox regression analysis, and the best combination that affected prognosis was determined based on the minimal Akaike Information Criterion. There were 220 deaths during a median follow-up of 4.9 years. Independent analyses of any single RAAS variant did not show significant impacts on 5-year mortality. However, analyses in combination revealed that absence of both AGT CC genotype and ACE D allele was associated with lower 5-year mortality (log-rank P = 0.005). Patients with at least either of the AGT CC or ACE D allele had increased mortality with adjusted hazard ratios of 2.07 (95% confidence interval 1.18-3.65, P = 0.012), compared with those with neither the AGT CC nor ACE D allele. Among the 4 RAAS genetic variants examined, a combination of AGT and ACE polymorphisms was associated with 5-year mortality after AMI.

Comparison of 5-year survival after acute myocardial infarction using angiotensin-converting enzyme inhibitor versus angiotensin II receptor blocker.

Few studies have investigated whether angiotensin II receptor blocker (ARB) is a practical alternative to angiotensin-converting enzyme inhibitor (ACEI) for long-term use after acute myocardial infarction (AMI) in real-world practice in the percutaneous coronary intervention era. We compared 5-year survival benefits of ACEI and ARB in patients with AMI registered in the Osaka Acute Coronary Insufficiency Study. Study subjects were divided into 3 groups: ACEI (n = 4,425), ARB (n = 2,158), or patients without either drug (n = 2,442). A total of 661 deaths were recorded. Cox regression analysis revealed that treatment with either ACEI or ARB was associated with reduced 5-year mortality (adjusted hazard ratio [HR] 0.70, 95% confidence interval [CI] 0.58 to 0.83, p <0.001 and HR 0.79, 95% CI 0.64 to 0.98, p = 0.03, respectively). However, Kaplan-Meier estimates and Cox regression analyses based on propensity score revealed that ACEI was associated with better survival than ARB from 2 to 5 years after survival discharge (adjusted HR 0.53, 95% CI 0.38 to 0.74, p <0.001). These findings were confirmed in a propensity score-matched population. In conclusion, treatment with ACEI was associated with better 5-year survival after AMI.

Clinical impact of acute hyperglycemia on development of diabetes mellitus in non-diabetic patients with acute myocardial infarction.

BACKGROUND: Acute hyperglycemia (AH) after the onset of acute myocardial infarction (AMI) is a manifestation of transient abnormal glucose metabolism that may reflect AMI severity, and thus be a predictor of poor prognosis. However, it remains unknown whether AH may predict development of de novo diabetes mellitus (dn-DM) in non-diabetic AMI patients. METHODS AND RESULTS: Among AMI patients registered in the Osaka Acute Coronary Insufficiency Study between 1998 and 2007, we investigated hospital records of 1493 patients who had an admission glycated hemoglobin A1c (HbA1c) level of ≤6.0% and were subjected to glycometabolic profiling after survival discharge. dn-DM was defined as initiation of diabetic medication or documentation of an HbA1c level of ≥6.5% during the 5-year follow-up period. AH, defined as an admission serum glucose level of ≥200mg/dl, was observed in 133 (8.9%) patients. dn-DM development was more frequent in post-AMI patients with AH than those without [24.8% vs 12.0%, adjusted hazard ratio (HR) 1.776, p=0.021], particularly among patients with an HbA1c of <5.6% on admission. Treatment with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers was associated with a reduced incidence of dn-DM in patients with AH (adjusted HR 0.397, p=0.031). CONCLUSION: Admission AH was a predictor of dn-DM in non-diabetic post-AMI patients. Renin-angiotensin system inhibitors were associated with reduced incidence of dn-DM in post-AMI patients with AH.

Living alone and risk of cardiovascular events following discharge after acute myocardial infarction in Japan.

BACKGROUND: Little is known about the long-term risk of cardiovascular events after discharge among acute myocardial infarction (AMI) survivors living alone in Japan. METHODS AND RESULTS: A large-scale prospective, observational study in the Osaka region involved consecutive patients with AMI from January 2002 through December 2010. We evaluated the association between living alone and longitudinal risk of cardiovascular events following discharge after AMI. A Cox proportional-hazards model was used to assess the association between living alone and the primary composite endpoint consisting of major adverse cardiovascular events and total deaths. During the study period, 5845 patients (4415 male patients, 1430 female patients) were registered. Living alone was found to be independently associated with a higher risk of composite endpoint consisting of major adverse cardiovascular events and total deaths [adjusted hazard ratio (HR) 1.32; 95% confidence interval (CI): 1.11-1.58]. Multivariate-adjusted HRs of composite endpoint were 1.34 (95% CI: 1.08-1.68) among male patients and 1.31 (95% CI: 0.95-1.81) in the female patients. AMI survivors living alone tend to have a higher adjusted HR of composite endpoint than those not living alone irrespective of age and gender groups. CONCLUSIONS: From this large AMI registry in Osaka, AMI survivors living alone after discharge had a higher risk of cardiovascular events and total deaths than those not living alone.

Circulating p53-responsive microRNAs are predictive indicators of heart failure after acute myocardial infarction.

RATIONALE: Despite a recent decline of in-hospital mortality attributable to acute myocardial infarction (AMI), the incidence of ischemic heart failure (HF) in post-AMI patients is increasing. Although various microRNAs have been proposed as diagnostic indicators for AMI, no microRNAs have been established as predictors of ischemic HF that develops after AMI. OBJECTIVE: We attempted to identify circulating microRNAs that can serve as reliable predictors of ischemic HF in post-AMI patients. METHODS AND RESULTS: Using sera collected a median of 18 days after AMI onset, we screened microRNAs in 21 patients who experienced development of HF within 1 year after AMI and in 65 matched controls without subsequent cardiovascular events after discharge. Among the 377 examined microRNAs, the serum level of only miR-192 was significantly upregulated in AMI patients with development of ischemic HF. Because miR-192 is reported to be p53-responsive, the serum levels of 2 other p53-responsive microRNAs, miR-194 and miR-34a, also were investigated. Interestingly, both microRNAs were coordinately increased with miR-192, particularly in exosomes, suggesting that these microRNAs function as circulating regulators of HF development via the p53 pathway. Furthermore, miR-194 and miR-34a expression levels were significantly correlated with left ventricular end-diastolic dimension 1 year after AMI. CONCLUSIONS: In the sera of post-AMI patients who experienced development of de-novo HF within 1 year of AMI onset, the levels of 3 p53-responsive microRNAs had been elevated by the early convalescent stage of AMI. Further investigations are warranted to confirm the usefulness of these circulating microRNAs for predicting the risk of development of ischemic HF after AMI.

Decreased mortality associated with statin treatment in patients with acute myocardial infarction and lymphotoxin-alpha C804A polymorphism.

AIMS: We previously reported the association of single nucleotide polymorphisms in the lymphotoxin alpha (LTα) gene with susceptibility to acute myocardial infarction (AMI) and increased mortality after discharge. In the present study, we investigated whether the adverse effect of LTα C804A polymorphism on mortality could be pharmacologically modified by statin treatment after AMI. METHODS AND RESULTS: We conducted a multicenter study that included 3486 post-AMI patients between 1998 and 2008. During a median follow-up period of 1775 days, 247 deaths were recorded. The mortality rate was significantly higher in LTα 804A allele carriers compared to non-804A allele carriers (7.9% vs. 5.7%, p = 0.011). The LTα 804A allele was significantly associated with increased mortality for post-AMI patients not receiving statins (hazard ratio [HR]: 1.48, 95% confidence interval [CI]: 1.03-2.12, p = 0.034), but not for those receiving statins (HR: 1.22, 95% CI: 0.70-2.10, p = 0.486). In-vitro experimental analyses demonstrated that the LTα 804A polymorphic protein, 26Asn-LTα3, induced monocyte-endothelial interaction and endoplasmic reticulum (ER) stress in cardiomyocytes more strongly than the LTα3 804C polymorphic protein 26Thr-LTα3. However, the effects of both LTα3 proteins were decreased and became comparable by the pretreatment of cells with pravastatin. CONCLUSION: LTα C804A polymorphism was associated with an increased risk of mortality for AMI patients, although this effect was masked in patients treated with statins. This finding is supported by the observed attenuation of 26Asn-LTα3-mediated monocyte-endothelial interaction and ER stress in cardiomyocytes treated with pravastatin. LTα C804A polymorphism may have potential as a novel therapeutic target for secondary prevention after AMI.

Elevated serum heart-type fatty acid-binding protein in the convalescent stage predicts long-term outcome in patients surviving acute myocardial infarction.

BACKGROUND: Little is known about the prognostic significance of elevated serum heart-type fatty acid-binding protein (H-FABP) in post-acute myocardial infarction (post-AMI) patients. METHODS AND RESULTS: A total of 1,283 post-AMI patients with available serum samples collected in the convalescent stage were studied. During a median follow-up period of 1,785 days, 176 patients (14%) had adverse events (all-cause mortality, n=81; non-fatal MI, n=44; readmission for heart failure [HF], n=51). Patients were divided into 2 groups according to a serum H-FABP level of 6.08ng/ml, which was determined to be the optimal cut-off for discriminating all-cause mortality based on the maximum value of the area under the receiver operating characteristic curve. Patients with elevated H-FABP (>6.08ng/ml, n=224) had a significantly higher incidence of death (18.3% vs. 3.8%, P<0.001) and readmission for HF (10.3% vs. 2.6%, P<0.001), but not of non-fatal MI (4.5% vs. 3.2%, P=0.187), compared to those with H-FABP <6.08ng/ml. Multivariate Cox regression analysis indicated that elevated serum H-FABP was associated with an increased risk of mortality (hazard ratio [HR], 1.91; 95% confidence interval [CI]: 1.03-3.51, P=0.039) and readmission for HF (HR, 2.49; 95% CI: 1.15-5.39, P=0.020). CONCLUSIONS: Elevated serum H-FABP during the convalescent stage of AMI predicted long-term mortality and readmission for HF after survival discharge in the post-AMI patients.

Low levels of serum n-3 polyunsaturated fatty acids are associated with worse heart failure-free survival in patients after acute myocardial infarction.

BACKGROUND: Intake of long-chain n-3 polyunsaturated fatty acids (n-3 PUFA), including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), is associated with a lower risk of atherosclerotic cardiovascular events, particularly acute myocardial infarction (AMI). However, limited data are available regarding the association between serum n-3 PUFA levels and heart failure (HF) events in survivors of AMI. METHODS AND RESULTS: We evaluated whether serum DHA and EPA levels were associated with HF-free survival and HF hospitalization rates after AMI. A total of 712 patients were divided into 3 groups according to their tertile serum levels of DHA and EPA (Low, Middle, and High). Propensity-score-stratified Cox regression analysis revealed that DHA- and EPA-Low groups presented statistically significant worse HF-free survival (hazard ratio (HR) 1.68, 95% confidence interval (CI) 1.03-2.72, P=0.0358, and HR 1.69, 95% CI 1.05-2.72, P=0.0280, respectively), with the EPA-Low group having a higher risk of HF hospitalization (HR 2.40, 95% CI 1.21-4.75, P=0.0097) than the DHA-Low group (HR 1.72, 95% CI 0.86-3.45, P=0.1224). The relationship between a low DHA or EPA level and decreased HF-free survival was almost common to all subgroups; however, the effect of low serum EPA on HF hospitalization was prominent in male patients, and those with low levels of high-density lipoprotein cholesterol or without statin therapy. CONCLUSIONS: Low levels of circulating n-3 PUFA are associated with decreased HF-free survival in post-AMI patients.