Heart Failure-Smart Life: a randomized controlled trial of a mobile app for self-management in patients with heart failure.

BACKGROUND: It is an important strategy for healthcare providers to support heart failure patients with comprehensive aspects of self-management. A practical alternative to a comprehensive and user-friendly self-management program for heart failure patients is needed. This study aimed to develop a mobile self-management app program for patients with heart failure and to identify the impact of the program. METHODS: We developed a mobile app, called Heart Failure-Smart Life. The app was to provide educational materials using a daily health check-up diary, Q & A, and 1:1 chat, considering individual users' convenience. An experimental study was employed using a randomized controlled trial to evaluate the effects of the program in patients with heart failure from July 2018 to June 2019. The experimental group (n = 36) participated in using the mobile app that provided feedback on their self-management and allowed monitoring of their daily health status by cardiac nurses for 3 months, and the control group (n = 38) continued to undergo their usual care. The differences in the physical, psychosocial, and behavioral factors between the two groups over time were analyzed using the analysis of covariance. RESULTS: After 3 months of intervention, significant differences between experimental and control groups were shown in the New York Heart Association functional class (p = 0.003) and cardiac diastolic function (p = 0.024). The improvements over time in the experimental group tended to be higher than those in the control group in considered variables. However, no changes in psychosocial and behavioral variables were observed between the groups over time. CONCLUSIONS: This study provides evidence that the mobile app program may provide benefits to its users, specifically improvements of symptom and cardiac diastolic function in patients with heart failure. Healthcare providers can effectively and practically guide and support patients with heart failure using comprehensive and convenient self-management tools such as smartphone apps.

Association between self-management behaviour and quality of life in people with heart failure: a retrospective study.

BACKGROUND: The purpose of this study was to investigate the variables that significantly associated with the quality of life in people with heart failure, and particularly, to identify the association between self-management behaviour and the quality of life. METHODS: This retrospective study used data from heart failure outpatient clinics at two large tertiary medical centres in Seoul and Suwon, South Korea. We enrolled 119 participants who completed echocardiography and stress tests and responded to questionnaires on self-management behaviour and quality of life. We collected more data on sociodemographic and clinical characteristics and anthropometric and serum blood test results through electronic medical record review. We analysed data using multiple linear regression and the classification and regression tree (CART) method to explore the associated factors with the quality of life in participants with heart failure. RESULTS: Participants' mean age was 74.61 years, and women represented 52.1% of the sample. It showed that cardiac systolic function (ß = 0.26, p = .013) and self-management behaviour (ß = 0.20, p = .048) were two major associated factors with the quality of life in participants with heart failure in the multiple linear regression analysis. Also, cardiac systolic function and self-management behaviour were shown to be the primary determinants for the quality of life in those with heart failure in the CART analysis. Therefore, self-management behaviour of the participants with heart failure was a significant modifiable factor that can improve their quality of life. CONCLUSIONS: Healthcare providers should be aware of the importance of self-management in people with heart failure and help promote their quality of life by enhancing their self-management behaviour as own efforts to properly maintain and monitor the health status and prevent further worsening of heart failure.

Predictive Model for Quality of Life in Patients With Heart Failure.

BACKGROUND: Although many studies have been conducted to examine predictors of quality of life (QoL), little information exists on the real-world application of Rector's conceptual model for QoL related to heart failure (HF). OBJECTIVES: In this study, we aimed to examine a hypothetical model of QoL based on Rector's conceptual model for QoL in relation to HF and the existing literature on patients with HF. METHODS: Using a cross-sectional survey, 165 patients with HF were recruited from an outpatient clinic in Korea. Data were collected based on Rector's model constructs, such as cardiac function, symptoms, functional limitation, depression, distress, and QoL. Left ventricular ejection fraction for cardiac function was measured using echocardiography. RESULTS: Functional limitation, depression, and distress, but not symptoms, had a direct effect on QoL (all Ps < .001). Cardiac function and symptoms directly affected functional limitation (ß = 0.186, P = .004, and ß = -0.488, P = < .001, respectively), whereas cardiac function, symptoms, and depression affected QoL through functional limitation and distress. CONCLUSIONS: These results confirm that the Rector's model is suitable for predicting QoL in patients with HF. These findings have potential to guide and inform intervention programs designed to alleviate symptoms in patients with HF, enhance their physical functioning, and moderate their psychological distress with the ultimate goal of improving their QoL.

Anti-Inflammatory and Neuroprotective Mechanisms of GTS-21, an α7 Nicotinic Acetylcholine Receptor Agonist, in Neuroinflammation and Parkinson's Disease Mouse Models.

Neuroinflammation is crucial in the progression of neurodegenerative diseases. Thus, controlling neuroinflammation has been proposed as an important therapeutic strategy for neurodegenerative disease. In the present study, we examined the anti-inflammatory and neuroprotective effects of GTS-21, a selective α7 nicotinic acetylcholine receptor (α7 nAChR) agonist, in neuroinflammation and Parkinson's disease (PD) mouse models. GTS-21 inhibited the expression of inducible nitric oxide synthase (iNOS) and proinflammatory cytokines in lipopolysaccharide (LPS)-stimulated BV2 microglial cells and primary microglia. Further research revealed that GTS-21 has anti-inflammatory properties by inhibiting PI3K/Akt, NF-κB, and upregulating AMPK, Nrf2, CREB, and PPARγ signals. The effects of GTS-21 on these pro-/anti-inflammatory signaling molecules were reversed by treatment with an α7 nAChR antagonist, suggesting that the anti-inflammatory effects of GTS-21 are mediated through α7 nAChR activation. The anti-inflammatory and neuroprotective properties of GTS-21 were then confirmed in LPS-induced systemic inflammation and MPTP-induced PD model mice. In LPS-injected mouse brains, GTS-21 reduced microglial activation and production of proinflammatory markers. Furthermore, in the brains of MPTP-injected mice, GTS-21 restored locomotor activity and dopaminergic neuronal cell death while inhibiting microglial activation and pro-inflammatory gene expression. These findings suggest that GTS-21 has therapeutic potential in neuroinflammatory and neurodegenerative diseases such as PD.

The phosphodiesterase 10 inhibitor papaverine exerts anti-inflammatory and neuroprotective effects via the PKA signaling pathway in neuroinflammation and Parkinson's disease mouse models.

BACKGROUND: Neuroinflammation plays a pivotal role in the pathogenesis of Parkinson's disease (PD). Thus, the development of agents that can control neuroinflammation has been suggested as a promising therapeutic strategy for PD. In the present study, we investigated whether the phosphodiesterase (PDE) 10 inhibitor has anti-inflammatory and neuroprotective effects in neuroinflammation and PD mouse models. METHODS: Papaverine (PAP) was utilized as a selective inhibitor of PDE10. The effects of PAP on the expression of pro-inflammatory molecules were examined in lipopolysaccharide (LPS)-stimulated BV2 microglial cells by ELISA, RT-PCR, and Western blot analysis. The effects of PAP on transcription factors were analyzed by the electrophoretic mobility shift assay, the reporter gene assay, and Western blot analysis. Microglial activation and the expression of proinflammatory molecules were measured in the LPS- or MPTP-injected mouse brains by immunohistochemistry and RT-PCR analysis. The effect of PAP on dopaminergic neuronal cell death and neurotrophic factors were determined by immunohistochemistry and Western blot analysis. To assess mouse locomotor activity, rotarod and pole tests were performed in MPTP-injected mice. RESULTS: PAP inhibited the production of nitric oxide and proinflammatory cytokines in LPS-stimulated microglia by modulating various inflammatory signals. In addition, PAP elevated intracellular cAMP levels and CREB phosphorylation. Treatment with H89, a PKA inhibitor, reversed the anti-inflammatory effects of PAP, suggesting the critical role of PKA signaling in the anti-inflammatory effects of PAP. We verified the anti-inflammatory effects of PAP in the brains of mice with LPS-induced systemic inflammation. PAP suppressed microglial activation and proinflammatory gene expression in the brains of these mice, and these effects were reversed by H89 treatment. We further examined the effects of PAP on MPTP-injected PD model mice. MPTP-induced dopaminergic neuronal cell death and impaired locomotor activity were recovered by PAP. In addition, PAP suppressed microglial activation and proinflammatory mediators in the brains of MPTP-injected mice. CONCLUSIONS: PAP has strong anti-inflammatory and neuroprotective effects and thus may be a potential candidate for treating neuroinflammatory disorders such as PD.

Impact of new-onset diabetes on clinical outcomes after ST segment-elevated myocardial infarction.

Objective. Patients with diabetes have higher mortality rate than patients without diabetes after ST-segment elevated myocardial infarction (STEMI). Prognosis of patients with new onset diabetes (NOD) after STEMI remains unclear. The aim of this study was to evaluate the prognosis of patients with NOD compared to that of patients without NOD after STEMI. Design. This study was a retrospective observational study. We enrolled 901 STEMI patients. Patients were divided into diabetic and non-diabetic groups at index admission. Non-diabetic group was divided into NOD and non-NOD groups. Kaplan-Meier analysis and Cox's proportional hazard regression models were used to compare major adverse cardiac events (MACE) free survival rate and hazard ratio for MACE between NOD and non-NOD groups. Results. Mean follow-up period was 59 ± 28 months. Diabetes group had higher MACE than non-diabetes group (p = .038). However, MACE was not different between NOD and non-NOD groups (p = 1.000). After 1:2 propensity score matching, incidence of MACE was not different between the two groups. In Kaplan-Meier survival curves, MACE-free survival rates were not statistically different between NOD and non-NOD groups either (p = .244). Adjusted hazard ratios of NOD for MACE, all-cause of death, recurrent myocardial infarction, and target vessel revascularization were 0.697 (95% confidence interval [CI]: 0.362-1.345, p = .282), 0.625 (95% CI: 0.179-2.183, p = .461), 0.794 (95% CI: 0.223-2.835, p = .723), and 0.506 (95% CI: 0.196-1.303, p = .158), respectively. Conclusion. This retrospective observational study with a limited statistical power did not show a different prognosis in patients with and without NOD.

Sulforaphane rescues amyloid-ß peptide-mediated decrease in MerTK expression through its anti-inflammatory effect in human THP-1 macrophages.

BACKGROUND: Mer tyrosine kinase (MerTK) activity necessary for amyloid-stimulated phagocytosis strongly implicates that MerTK dysregulation might contribute to chronic inflammation implicated in Alzheimer's disease (AD) pathology. However, the precise mechanism involved in the regulation of MerTK expression by amyloid-ß (Aß) in proinflammatory environment has not yet been ascertained. METHODS: The objective of this study was to determine the underlying mechanism involved in Aß-mediated decrease in MerTK expression through Aß-mediated regulation of MerTK expression and its modulation by sulforaphane in human THP-1 macrophages challenged with Aß1-42. We used protein preparation, Ca2+ influx fluorescence imaging, nuclear fractionation, Western blotting techniques, and small interfering RNA (siRNA) knockdown to perform our study. RESULTS: Aß1-42 elicited a marked decrease in MerTK expression along with increased intracellular Ca2+ level and induction of proinflammatory cytokines such as IL-1ß and TNF-α. Ionomycin A and thapsigargin also increased intracellular Ca2+ levels and production of IL-1ß and TNF-α, mimicking the effect of Aß1-42. In contrast, the Aß1-42-evoked responses were attenuated by depletion of Ca2+ with ethylene glycol tetraacetic acid. Furthermore, recombinant IL-1ß or TNF-α elicited a decrease in MerTK expression. However, immunodepletion of IL-1ß or TNF-α with neutralizing antibodies significantly inhibited Aß1-42-mediated downregulation of MerTK expression. Notably, sulforaphane treatment potently inhibited Aß1-42-induced intracellular Ca2+ level and rescued the decrease in MerTK expression by blocking nuclear factor-κB (NF-κB) nuclear translocation, thereby decreasing IL-1ß and TNF-α production upon Aß1-42 stimulation. Such adverse effects of sulforaphane were replicated by BAY 11-7082, a NF-κB inhibitor. Moreover, sulforaphane's anti-inflammatory effects on Aß1-42-induced production of IL-1ß and TNF-α were significantly diminished by siRNA-mediated knockdown of MerTK, confirming a critical role of MerTK in suppressing Aß1-42-induced innate immune response. CONCLUSION: These findings implicate that targeting of MerTK with phytochemical sulforaphane as a mechanism for preventing Aß1-42-induced neuroinflammation has potential to be applied in AD therapeutics.

Anti-inflammatory and anti-oxidant mechanisms of an MMP-8 inhibitor in lipoteichoic acid-stimulated rat primary astrocytes: involvement of NF-κB, Nrf2, and PPAR-γ signaling pathways.

BACKGROUND: Recent evidence suggests that reactive astrocytes play an important role in neuroinflammation and neurodegenerative diseases. Thus, controlling astrocyte reactivity has been suggested as a promising strategy for treating neurodegenerative diseases. In the present study, we investigated whether a matrix metalloproteinase (MMP)-8 inhibitor, M8I, could control neuroinflammation in lipoteichoic acid (LTA)-stimulated rat primary astrocytes. METHODS: The effects of M8I on the expression of inducible nitric oxide synthase, cytokines, and MMPs were examined in LTA-stimulated rat primary astrocytes by ELISA, RT-PCR, and Western blot analysis. The effects of M8I on reactive oxygen species (ROS) generation and phase II antioxidant enzyme expression were examined by the DCF-DA assay, RT-PCR, and Western blot analysis. The detailed molecular mechanisms underlying the anti-inflammatory and antioxidant effects of M8I were analyzed by the electrophoretic mobility shift assay, the reporter gene assay, Western blot, and RT-PCR analysis. RESULTS: Treatment with LTA, a major cell wall component of Gram-positive bacteria, led to astrocyte activation and induced the expression of inflammatory molecules such as iNOS, COX-2, and pro-inflammatory cytokines. In addition, LTA induced the expression of MMPs such as MMP-1, MMP-3, MMP-8, MMP-9, and MMP-13 in rat primary astrocytes. Based on previous reports showing that MMP-8 plays a role as a proinflammatory mediator in microglia, we investigated whether MMP-8 is also involved in inflammatory reactions of reactive astrocytes. We found that treatment of astrocytes with M8I significantly inhibited LTA-induced expression of iNOS, TNF-α, IL-1ß, IL-6, and TLR-2. In addition, M8I inhibited LTA-induced NF-κB, MAP kinase, and Akt activities, while it increased the anti-inflammatory PPAR-γ activities. Moreover, M8I showed antioxidant effects by suppressing ROS production in LTA- or H2O2-stimulated astrocytes. Interestingly, M8I increased the expression of phase II antioxidant enzymes such as hemeoxygenase-1, NQO1, catalase, and MnSOD by modulating the Nrf2/ARE signaling pathway. CONCLUSIONS: The data collectively suggest the therapeutic potential of an MMP-8 inhibitor in neuroinflammatory disorders that are associated with astrocyte reactivity.

Myocardial Mass Contributes to the Discrepancy Between Anatomic Stenosis Severity Assessed by Intravascular Ultrasound and Fractional Flow Reserve in Intermediate Lesions of the Coronary Artery.

OBJECTIVES: The present study investigated the major contributors to the discrepancy between the minimal lumen area (MLA) and fractional flow reserve (FFR). BACKGROUND: There was considerable discrepancy between MLA or diameter stenosis (DS) and FFR. METHODS: We enrolled 744 patients with intermediate stenoses of the left anterior descending artery (LAD). Summed epicardial coronary artery length distal to the target stenosis was obtained from each longest view of the vessels on the coronary angiograms. Mismatching was defined as a lesion with FFR of >0.80 and MLA smaller than the best cut-off value (BCV) for predicting FFR of ≤0.80. Reverse mismatching was defined as a lesion with FFR of ≤0.80 and MLA larger than the BCV. RESULTS: Summed epicardial coronary artery length was longer at the lesions of proximal LAD than that of middle LAD (380 mm ± 82 mm vs. 341 mm ± 80 mm, P < 0.001). Reverse mismatching was found more frequently in the proximal than middle LAD (28.3% vs. 5.5%, P < 0.001). Independent predictors of FFR ≤ 0.80 were age, male, multi-vessel disease, proximal LAD lesion, MLA, DS, plaque burden at distal reference, lesion length and summed epicardial coronary artery length. Proximal LAD lesion was an independent predictor of reverse mismatching (hazard ratio 3.162, 1.858-5.382, P < 0.001). CONCLUSIONS: Myocardial mass subtended by a lesion is an important factor predicting FFR ≤0.80 and discrepancy between FFR and MLA. Myocardial mass subtended by a lesion should be considered when determining the revascularization therapy by intravascular ultrasound parameters. © 2017 Wiley Periodicals, Inc.

Normal reference values of diastolic strain rate in healthy individuals: Chronological trends and the comparison according to genders.

PURPOSE: Recently, the diastolic strain rate (DSR) utilizing speckle-tracking echocardiography has been proposed as a novel parameter for left ventricular diastolic function. We aimed to present normal reference data for those in a large-sized, selected group of healthy individuals. METHODS: The current study was a part of the Normal echOcardiogRaphic Measurements in KoreAn popuLation (NORMAL), a prospective nationwide survey from 23 centers in Korea. We analyzed 447 subjects (age 48 ± 15 years, 234 females) without any history of cardiovascular disease and presented the early and late DSRs (SRe and SRa , respectively) in a total and gender-/age-specified groups. RESULTS: Among the total subjects, the mean SRe and SRa were 1.6 ± 0.4 S-1 and 0.8 ± 0.3 S-1 , respectively. With increasing age, there were significant trends of decreasing SRe and increasing SRa . Although both gender groups showed comparable age, the female group presented significantly higher SRe compared to male subjects with age of 20-59 years, which diminished after the age of 60 years. However, the SRa was comparable between genders in all age groups. On multiple linear regression, age showed independent associations with both SRe (ß = -0.132, P = .010) and SRa (ß = 0.440, P < .001), whereas gender did not show any association with SRe or SRa . CONCLUSION: We present normal reference data of a novel parameter, DSR, in a large-sized selected group with healthy Korean subjects. Additionally, we present significant age-related changes both in SRe and SRa without the impact of their gender.

Suppression of neuroinflammation by matrix metalloproteinase-8 inhibitor in aged normal and LRRK2 G2019S Parkinson's disease model mice challenged with lipopolysaccharide.

Microglial priming is caused by aging and neurodegenerative diseases, and is characterized by an exaggerated microglial inflammatory response to secondary and sub-threshold challenges. In the present study, we examined the effects of the matrix metalloproteinase-8 (MMP-8) inhibitor (M8I) on the brain of aged normal and leucine-rich repeat kinase 2 (LRRK2) G2019S Parkinson's disease (PD) model mice systemically stimulated with lipopolysaccharide (LPS). The results indicated that Iba-1 positive microglia and GFAP-positive astrocytes, which were increased by LPS, significantly decreased by M8I in aged normal and PD model mice. M8I also decreased the expression of pro-inflammatory markers in the hippocampus and midbrain of aged normal and PD model mice challenged with LPS, while it also improved the motor coordination of aged normal mice after LPS challenge in rotor rod test and the general crossing locomotor activities of LPS-treated LRRK2G2019S PD mice after LPS challenge in open field test. To assess the effects of M8I in an in vitro priming model, BV2 microglia were pretreated with macrophage colony-stimulating factor (CSF)-1 or interleukin (IL)-34, and subsequently stimulated with LPS or polyinosinic-polycytidylic acid (poly[I:C]). M8I inhibited the LPS- or poly(I:C)-induced production of the tumor necrosis factor-α and nitric oxide, alone or in combination with CSF-1 or IL-34. Collectively, the data suggested that M8I has a therapeutic potential in treating neurodegenerative diseases that are aggravated by systemic inflammation.

Anti-inflammatory mechanism of lonchocarpine in LPS- or poly(I:C)-induced neuroinflammation.

Neuroinflammation plays an important role in the progression of various neurodegenerative diseases. In this study, we investigated the anti-inflammatory effects of lonchocarpine, a natural compound isolated from Abrus precatorius, under in vitro and in vivo neuroinflammatory conditions induced by challenge with lipopolysaccharide (LPS)- or polyinosinic-polycytidylic acid (poly(I:C)). Lonchocarpine suppressed the expression of iNOS and proinflammatory cytokines in LPS or poly(I:C)-stimulated BV2 microglial cells. These anti-inflammatory effects were verified in brains of mice with systemic inflammation induced by administration of LPS or poly(I:C). Lonchocarpine reduced the number of Iba-1-positive activated microglia, and suppressed the mRNA expression of various proinflammatory markers in the cortex of LPS- or poly(I:C)-injected mice. Molecular mechanistic experiments showed that lonchocarpine inhibited NF-κB activity by reducing the phosphorylation and degradation of IκBα in LPS- or poly(I:C)-stimulated BV2 cells. Analysis of further upstream signaling pathways in LPS-stimulated microglia showed that lonchocarpine inhibited the phosphorylation of IκB kinase and TGFß-activated kinase 1 (TAK1). Moreover, lonchocarpine suppressed the interaction of myeloid differentiation factor 88 (MyD88) and intereleukin-1 receptor-associated kinase 4 (IRAK4). These data suggest that toll-like receptor 4 downstream signals such as MyD88/IRAK4-TAK1-NF-κB are at least partly involved in the anti-inflammatory mechanism of lonchocarpine in LPS-stimulated microglia. Its strong anti-inflammatory effects may make lonchocarpine an effective preventative drug for neuroinflammatory disorders that are associated with systemic inflammation.

Echocardiographic epicardial fat thickness is a predictor for target vessel revascularization in patients with ST-elevation myocardial infarction.

BACKGROUND: The amount of epicardial adipose tissue (EAT) has been demonstrated to correlate with the severity of coronary artery disease (CAD) and the CAD activity. The aim of this study is to assess the impact of EAT on long term clinical outcomes in patients with ST elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI). METHODS: We analyzed the data and clinical outcomes of 761 patients (614 males, 57 ± 12 year-old) with STEMI who underwent successful primary PCI from 2003 to 2009. All patients were divided into two groups: thick EAT group, EAT ≥ 3.5 mm and thin EAT group, EAT < 3.5 mm. The primary end points were all-cause death, recurrent MI, target vessel revascularization (TVR) and major cardiac adverse events (MACEs), composite of all-cause death, recurrent MI and TVR, within 5 years. RESULTS: Median and mean EAT of 761 patients were 3.3 mm and 3.6 ± 1.7 mm, respectively. Mean follow up period was 46 ± 18 months. MACE-free survival rate in the thick EAT group was significantly lower than in the thin EAT group (log-rank P = 0.001). The event-free survival rate of all-cause death of the thick EAT group was significantly lower than that of the thin EAT group (log-rank P = 0.005). The TVR-free survival rate in the thick EAT group was significantly lower than in the thin EAT group (log-rank P = 0.007). The event-free survival rate of recurrent MI were not significantly different between the groups (log-rank P = 0.206). In the Cox's proportional hazard model, the adjusted hazard ratio of thick EAT thickness for TVR was 1.868 (95% confidence interval 1.181-2.953, P = 0.008). CONCLUSION: This study demonstrates that the EAT thickness is related with long term clinical outcome in patients with STEMI. The EAT thickness might provide additional information for future clinical outcome, especially TVR.

Percutaneous Pericardial Effusion Drainage under Ultrasonographic and Fluoroscopic Guidance for Symptomatic Pericardial Effusion: A Single-Center Experience in 93 Consecutive Patients.

PURPOSE: To evaluate the safety and efficacy of ultrasound-guided and fluoroscopically guided percutaneous pericardial effusion drainage as performed by interventional radiologists in patients with symptomatic pericardial effusion. MATERIALS AND METHODS: From July 2002 to December 2013, 93 patients were treated with percutaneous pericardial effusion drainage. Pericardial effusion drainage was performed via 3 routes: apical, subxiphoid, and transhepatic routes. After puncturing the pericardial sac with a 22-gauge needle under ultrasound guidance, a drainage catheter was inserted under fluoroscopic guidance. Pericardial effusion was categorized according to its distribution in the pericardial cavity: "circumferential even," "circumferential uneven" (predominant site specified), and "loculated." Technical success, recurrence, and complication rates were assessed. RESULTS: The technical success rate was 99%. Pericardial effusion drainage was performed via the subxiphoid approach in 54 procedures, transhepatic approach in 30 procedures, and apical approach in 13 procedures. The transhepatic approach was mainly performed in cases where the effusion was distributed posteriorly to the heart (80%). One patient died of uncontrolled hypotension without evidence of hemopericardium. CONCLUSIONS: Ultrasound-guided and fluoroscopically guided pericardial effusion drainage is a safe and effective procedure for patients with symptomatic pericardial effusion. The transhepatic approach may be preferable for posteriorly distributed pericardial effusion that would otherwise be inaccessible by a traditional subxiphoid or apical approach.

ß-Blocker Therapy in the Era of Primary Percutaneous Intervention for ST Elevation Myocardial Infarction.

OBJECTIVES: With the present therapeutic advances in the era of primary percutaneous coronary intervention (PCI), the role of ß-blockers in ST elevation acute myocardial infarction (STEMI) has remained contentious. METHODS: We analyzed the data and clinical outcomes of 901 STEMI patients who had undergone primary PCI. We classified the patients into ß-blocker (n = 598) and non-ß-blocker groups (n = 303). RESULTS: The cumulative incidence of all-cause death was 10.0% in the ß-blocker group and 25.4% in the non-ß-blocker group (p < 0.001). The incidence of major adverse cardiac events (MACE) was 22.1% in the ß-blocker group and 34.3% in the non-ß-blocker group (p < 0.001). The relative hazard ratio (HR) of ß-blockers for all-cause death and MACE with low left ventricle ejection fraction (LVEF; <50%) was 0.55 [95% confidence interval (CI) 0.35-0.86, p = 0.009] and 0.75 (95% CI 0.51-1.09, p = 0.125), respectively. In patients with normal LVEF (≥50%), the relative HR of ß-blockers for death and MACE were 0.50 (95% CI 0.29-0.88, p = 0.016) and 0.75 (95% CI 0.51-1.12, p = 0.162), respectively. After propensity score matching of the difference of the baseline characteristics, the Kaplan-Meier survival curve demonstrated lower mortality in the ß-blocker group than in the non-ß-blocker group with both low LVEF and normal LVEF (p = 0.02 and p = 0.001, respectively). CONCLUSIONS: ß-Blockers have beneficial clinical outcomes in the era of primary PCI for STEMI, regardless of the LVEF. © 2015 S. Karger AG, Basel.

Independent risk factors for mortality in patients with chronic obstructive pulmonary disease who undergo comprehensive cardiac evaluations.

BACKGROUND: Cardiovascular disease is the most common cause of death in chronic obstructive pulmonary disease (COPD). However, the impact of cardiovascular comorbidities on the prognosis of COPD is not well known. OBJECTIVES: This study was performed to investigate the effects of cardiovascular comorbidities on the prognosis of COPD. METHODS: We enlisted 229 patients with COPD who underwent comprehensive cardiac evaluations including coronary angiography and echocardiography at Ajou University Hospital between January 2000 and December 2012. Survival analyses were performed in this retrospective cohort. RESULTS: Kaplan-Meier analyses showed that COPD patients without left heart failure (mean survival = 12.5 ± 0.7 years) survived longer than COPD patients with left heart failure (mean survival = 6.7 ± 1.4 years; p = 0.003), and the survival period of nonanemic COPD patients (mean survival = 13.8 ± 0.8 years) was longer than that of anemic COPD patients (mean survival = 8.3 ± 0.8 years; p < 0.001). The survival period in COPD with coronary artery disease (CAD; mean survival = 11.37 ± 0.64 years) was not different from that in COPD without CAD (mean survival = 11.98 ± 0.98 years; p = 0.703). According to a multivariate Cox regression model, a lower hemoglobin level, a lower left ventricular ejection fraction, and the forced expiratory volume in 1 s (FEV1) were independently associated with higher mortality in the total COPD group (p < 0.05). CONCLUSIONS: Hemoglobin levels and left ventricular ejection fraction along with a lower FEV1 were identified as independent risk factors for mortality in COPD patients who underwent comprehensive cardiac evaluations, suggesting that multidisciplinary approaches are required in the care of COPD.

Left ventricular hypertrophy on long-term cardiovascular outcomes in patients with ST-elevation myocardial infarction.

BACKGROUND: Left ventricular hypertrophy (LVH) had been associated with increased adverse cardiovascular events in hypertensive patients. Prognostic significance of LVH in patients with ST-elevation myocardial infarction (STEMI) is not established. This study aimed to investigate prognostic impact of LVH on the patients with STEMI. METHODS: We analyzed the data and clinical outcomes of 30-day survivors with STEMI who underwent successful coronary intervention from 2003 to 2009. Definition of LVH was LV mass index (LVMI) >115 g/m(2) in male and >95 g/m(2) in female. Patients were classified into a LVH group and a non-LVH group. Occurrence of major adverse cardiovascular events (MACE; death, recurrent MI, target vessel revascularization (TVR)) within 5 years was evaluated. RESULTS: We enrolled 418 patients and mean follow-up duration was 43 ± 17 months. Two hundred and fourteen patients (51%) had LVH. The survival of the patients with LVH was significantly worse than the patients without LVH (log-rank p = 0.024). In a multivariate regression model, the presence of LVH was independently associated with increased risk for all-cause mortality (OR, 2.37; 95% CI, 1.096-5.123, p = 0.028). When the end points were analyzed based on LVH severity, all-cause mortality was significantly correlated with LVH severity (p = 0.011). The severe LVH was independently associated with increased risk for all-cause mortality (OR, 5.110; 95% CI, 1.454-17.9, p = 0.001). CONCLUSION: LVH was associated with increased rate of adverse clinical outcomes in 30-day survivors after STEMI, who underwent successful coronary intervention.