Modulators of Mortality Benefit From Peri-Angioplasty Adjunctive Tirofiban in Patients With ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention.

BACKGROUND: Studies investigating the modulators of mortality benefit conferred by peri-angioplasty glycoprotein IIb/IIIa inhibitors in ST-elevation myocardial infarction (STEMI) are still lacking.Methods and Results:A prospective database (n=1,025) of consecutive cases undergoing primary percutaneous coronary intervention for STEMI was retrospectively analyzed. For patients in Killip class I, II or III, IV, the multivariate-adjusted hazard ratios of 30-day all-cause mortality associated with adjunctive tirofiban were 3.873 (95% CI 0.504-29.745; P=0.193), 0.550 (95% CI 0.188-1.609; P=0.275), and 0.264 (95% CI 0.099-0.704; P=0.008), respectively. The P value for a linear trend was 0.032. Patients who had a body mass index (BMI) within 22.9-25.0 kg/m2had a significant benefit from tirofiban (adjusted HR 0.344; 95% CI 0.145-0.814; P=0.015) compared to other BMI groups. The P value for a quadratic trend was 0.012. A novel Killip-BMI score (KBS = 2.5 × Killip category - | BMI - 24 |) was calculated to select the beneficial population. A KBS ≥2 was associated with significant mortality benefit, whereas a KBS <0 predicted increased 30-day mortality with tirofiban use. CONCLUSIONS: Survival benefit from peri-angioplasty tirofiban therapy for STEMI was positively correlated with the Killip class. Tirofiban should be used cautiously in either underweight or overweight patients. The novel KBS used in this study can guide peri-angioplasty use of adjunctive tirofiban in patients with STEMI undergoing primary angioplasty.

Elevated serum uric acid is associated with incident hypertension in the health according to various contemporary blood pressure guidelines.

BACKGROUND AND AIMS: Elevated serum uric acid (SUA) is associated with hypertension according to its traditional definition. We investigated the association between SUA and incident hypertension according to the European Society of Cardiology (ESC) and American Society of Cardiology (ACC) guidelines. METHODS AND RESULTS: In this retrospective cohort study, we enrolled 10,537 healthy individuals ≥30 years old who underwent a routine annual health examination with office blood pressure recorded at our hospital in 2016; of the participants, 7349 repeated the exam in 2017. According to the ESC and ACC guidelines, hypertension was defined as office BP ≥ 140/90 mmHg or ≥130/80 mmHg. Hyperuricemia (HUA) was defined as SUA ≥7 mg/dL in men and ≥6 mg/dL in women. The hypertension incidence was 5.8% among 6378 individuals in the ESC cohort and 19% among 4330 individuals in the ACC cohort. Incident hypertension was significantly more common in the hyperuricemic group than in the normouricemic group (ESC: 8.6% vs. 4.7%, P < 0.001; ACC: 25.5% vs. 16.9%, P < 0.001). In the fully adjusted multivariate logistic regression analyses, each increase in SUA was associated with an increase in incident hypertension risk (ESC: adjusted OR: 1.167, 95% CI: 1.061-1.284, P = 0.001; ACC: adjusted OR: 1.125, 95% CI: 1.044-1.213, P = 0.002). The association can be explained by a significant correlation of baseline SUA with the BP in the following year (r = 0.24, P < 0.001 for baseline SUA and SBP in the following year; r = 0.239, P < 0.001 for baseline SUA and DBP in the following year). CONCLUSION: Elevated SUA was associated with incident hypertension in healthy individuals according to various contemporary BP guidelines (ClinicalTrials.gov: NCT03473951). CLINICAL TRIALS: ClinicalTrials.gov with the identification number of NCT03473951.

miR-26a attenuates cardiac apoptosis and fibrosis by targeting ataxia-telangiectasia mutated in myocardial infarction.

Apoptosis and fibrosis play a vital role in myocardial infarction (MI) induced tissue injury. Although microRNAs have been the focus of many studies on cardiac apoptosis and fibrosis in MI, the detailed effects of miR-26a is needed to further understood. The present study demonstrated that miR-26a was downregulated in ST-elevation MI (STEMI) patients and oxygen-glucose deprivation (OGD)-treated H9c2 cells. Downregulation of miR-26a was closely correlated with the increased expression of creatine kinase, creatine kinase-MB and troponin I in STEMI patients. Further analysis identified that ataxia-telangiectasia mutated (ATM) was a target gene for miR-26a based on a bioinformatics analysis. miR-26a overexpression effectively reduced ATM expression, apoptosis, and apoptosis-related proteins in OGD-treated H9c2 cells. In a mouse model of MI, the expression of miR-26a was significantly decreased in the infarct zone of the heart, whereas apoptosis and ATM expression were increased. miR-26a overexpression effectively reduced ATM expression and cardiac apoptosis at Day 1 after MI. Furthermore, we demonstrated that overexpression of miR-26a improved cardiac function and reduced cardiac fibrosis by the reduced expression of collagen type I and connective tissue growth factor (CTGF) in mice at Day 14 after MI. Overexpression of miR-26a or ATM knockdown decreased collagen I and CTGF expression in cultured OGD-treated cardiomyocytes. Taken together, these data demonstrate a prominent role for miR-26a in linking ATM expression to ischemia-induced apoptosis and fibrosis, key features of MI progression. miR-26a reduced MI development by affecting ATM expression and could be targeted in the treatment of MI.

Systemic lupus erythematosus is associated with poor outcome after acute myocardial infarction.

BACKGROUND: Systemic lupus erythematosus (SLE) is associated with a higher risk of cardiovascular disease. However, it is not clear whether or not SLE is associated with poor outcomes after acute myocardial infarction (AMI). METHODS AND RESULTS: Using the Taiwan National Health Insurance Database, we identified the SLE group as patients with AMI who have a concurrent discharge diagnosis of SLE. We also selected an age-, sex-, hospital level-, and admission calendar year-matched non-SLE group at a ratio of 1:3 from the total non-SLE group. One hundred fifty-one patients with SLE, 113,791 patients without SLE, and 453 matched patients without SLE were admitted with a diagnosis of AMI. Patients with SLE were significantly younger, predominantly female, and more likely to have chronic kidney disease than those without SLE. The in-hospital mortality rates were 12.6%, 9.0%, and 4.2% in the SLE, total non-SLE, and matched non-SLE groups, respectively. The in-hospital mortality was significantly higher in the SLE group than in the total non-SLE group (OR = 1.98; 95% CI = 1.2-3.26) and the matched non-SLE group (mortality OR = 2.20; 95% CI = 1.06-4.58). In addition, the SLE group was associated with a borderline significant risk of prolonged hospitalization when compared with the non-SLE group. CONCLUSION: SLE is associated with a higher risk of in-hospital mortality and a borderline significantly higher risk of prolonged hospitalization after AMI.

SYNTAX Score of Infarct-Related Artery Other Than the Number of Coronary Balloon Inflations and Deflations as an Independent Predictor of Contrast-Induced Acute Kidney Injury in Patients with ST-Segment Elevation Myocardial Infarction.

BACKGROUND: Although remote ischemic post-conditioning (RIPC) has been shown to prevent contrast-induced acute kidney injury (CIAKI) in patients with acute coronary syndrome, its efficacy in patients with ST-segment elevation myocardial infarction (STEMI) remains unclear. We examined the relationship among balloon inflations and deflations (BID) times, SYNTAX score of infarction-related artery (SI), periprocedural complications, and CIAKI in STEMI patients undergoing primary percutaneous coronary intervention (pPCI). METHODS: Patients with STEMI undergoing pPCI with Mehran risk score (MRS) ≥ 5 were enrolled between February 2007 and September 2012. The study end point was the development of CIAKI. RESULTS: Of 206 patients, the median age was 65 years [interquartile range (IQR): 55-77] with 72.8% male and Mehran risk score (MRS) 8 (IQR: 6-12). Receiver operating characteristic curve showed that BID times > 9 times or SI > 10 was the best cut-off associated with CIAKI. In univariate analysis, significant association with CIAKI existed in BID > 9 times [odds ratio (OR): 3.106, 95% confidence interval (CI): 1.284-7.513, p = 0.012] and SI > 10 (OR: 3.909, 95% CI: 1.570-9.735, p = 0.003). Other variables associated with CIAKI included creatinine, hemoglobin, angiotensin converting enzyme inhibitor or angiotensin receptor blocker use at discharge. In multivariate analysis, SI > 10 remained an independent predictor of CIAKI in different adjustment model, even on top of MRS (adjusted OR: 3.498, 95% CI: 1.086-11.268, p = 0.036). CONCLUSIONS: Vascular complexity of infarct-related artery rather than higher BID times (> 9) was the major determinant of the development of CIAKI after pPCI in STEMI patients.

Endovascular therapy for a patient with chronic mesenteric ischemia.

Percutaneous transluminal angioplasty is now used widely in the revascularization of peripheral artery disease. We report the case of a 75-year-old woman with chronic mesenteric ischemia, who presented with postprandial abdominal pain, food fear, and weight loss for 6 months. Mesenteric angiography showed critical stenosis in the celiac trunk, and superior and inferior mesenteric arteries. Instead of surgical revascularization, balloon angioplasty and stenting was performed on the celiac trunk and superior mesenteric artery. The patient had improved appetite and weight gain after the procedure. This case report demonstrates the clinical benefit of multiple vessel intervention with stenting in the treatment of chronic mesenteric ischemia.

Associated factors and impacts of sedentary behaviour in patients with heart failure: A longitudinal study.

BACKGROUND: Sedentary behaviours may be related to factors such as self-efficacy, mood and social support. However, there is a paucity of longitudinal follow-up studies examining factors related to sedentary behaviour from physical-psychosocial perspectives in patients with heart failure. AIMS: The purpose of this study was to explore the multidimensional associated factors and impacts of sedentary behaviour in heart failure patients. METHODS: A longitudinal design was used. A convenience sample of 128 heart failure patients recruited from two large medical centres in northern Taiwan was obtained. Patients were interviewed with structured questionnaires to assess physical activity, symptom distress, exercise self-efficacy, anxiety and depression, social support, sleep quality and quality of life before discharge and at 3 and 6 months after discharge. RESULTS: Heart failure patients reported low physical activity and tended to be sedentary. Sedentary behaviour was gradually reduced from hospitalization to 6 months after discharge. Sleep quality, quality of life, analgesic use, symptom distress and exercise self-efficacy were significant associated factors that explained 42.1-51% of the variance in sedentary behaviour. Patients with high sedentary behaviour had significantly greater depression and poorer sleep and quality of life than those with low sedentary behaviour at hospitalization and showed a significant improvement in depression at 3 and 6 months after discharge. CONCLUSION: Sedentary behaviour is common in heart failure patients and has impacts on depression and quality of life. An appropriate physical activity programme focusing on disease self-management and enhancing self-efficacy is needed for heart failure patients to improve their sedentary behaviour and quality of life.

Implementation of extracorporeal membrane oxygenation before primary percutaneous coronary intervention may improve the survival of patients with ST-segment elevation myocardial infarction and refractory cardiogenic shock.

BACKGROUND: The mortality of patients with ST-segment elevation myocardial infarction (STEMI) and refractory cardiogenic shock (RCS) is high. Extracorporeal membrane oxygenation (ECMO) before percutaneous coronary intervention (PCI) has shown some favorable results, but this may delay door-to-balloon (D2B) time. Whether the benefit surpasses the risk of longer D2B time remains controversial. METHODS: From January 2005 to December 2014, there were 46 patients with STEMI RCS who received ECMO and PCI. Comparison was made between patients whose ECMO were setup before (n = 12) and after (n = 34) the coronary angiography. RESULTS: There were no significant differences on the baseline characteristics. The ECMO before PCI group had significantly better six-month survival (58.3% vs. 14.7%, p = 0.006), and the benefit persisted to the end of two-year follow-up (41.7% vs. 11.8%, p = 0.045). The rates of neurological, vascular, or bleeding complications were not different between the groups. ECMO before PCI was associated with a nonsignificant increase of median D2B time (30 min) and decrease of patients achieving D2B time < 90 min (9.1% vs. 32.0%). After adjusting for GRACE score, gender, D2B time, complete revascularization, ECMO before PCI and shock index < 0.8 before PCI were significantly associated with six-month survival. CONCLUSIONS: In STEMI RCS patients, ECMO before PCI improves both short- and long-term outcomes, even if it nonsignificantly increases the D2B time. Our data suggests that ECMO before PCI is a reasonable and safe strategy in this particularly-ill population.

Relationship of serum uric acid and Killip class on mortality after acute ST-segment elevation myocardial infarction and primary percutaneous coronary intervention.

BACKGROUND: There is conflicting information regarding the association between hyperuricemia and survival in STEMI patients. Our study examined the interaction between hyperuricemia and Killip class on mortality of STEMI patients. METHODS: We analyzed 951 consecutive STEMI patients between February 2006 and September 2012. Hyperuricemia was defined as SUA of at least 7mg/dL in males and 6mg/dL in females. Killip class I patients were divided into hyperuricemia and normouricemia groups. RESULTS: The Killip class I hyperuricemia and normouricemia groups had similar baseline and procedural characteristics, but the hyperuricemia group had significantly greater BMI, serum creatinine, and SUA, and a lower TIMI risk score (2, IQR: 1-4 vs. 3, IQR: 2-4, p=0.019). The hyperuricemia group also had greater 30-day and 1-year mortality rates (2.9% vs. 0.3%, p=0.022; 6.5% vs. 1.1%, p=0.002, respectively). However, hyperuricemia was not associated with mortality of patients in Killip classes II-IV or in the overall study population. Hyperuricemia was associated with increased mortality in subgroups of patients who were at least 65years-old, male, had BMI of 25kg/m2 or less, were in Killip class I, without diabetes, and who did not receive intra-aortic balloon pump support. Hyperuricemia interacted with Killip class I in increasing the risk for 1-year mortality (p for interaction=0.038). CONCLUSIONS: Hyperuricemia increased the 1-year mortality of STEMI patients in Killip class I, but not of patients in Killip classes II-IV. An interaction of hyperuricemia and Killip class significantly affects the mortality of STEMI patients.

Rapid Early Triage by Leukocytosis and the Thrombolysis in Myocardial Infarction (TIMI) Risk Score for ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention: An Observational Study.

The clinical utility of leukocytosis in risk assessment for ST-elevation myocardial infarction (STEMI) is still unclear. We aim to demonstrate the prognostic value of leukocyte counts independent from traditional risk factors and the TIMI risk score (TRS) for STEMI and to propose a practical model comprising leukocyte count for early triage in STEMI undergoing primary angioplasty. A prospective database (n = 796) of consecutive STEMI cases receiving primary angioplasty at a tertiary medical center was retrospectively analyzed in the period from February 1, 2007 through December 31, 2012. Primary endpoints were 30-day and 1-year mortality. Propensity score-adjusted Cox regression models and subdivision analysis were performed. Leukocytosis group (n = 306) had higher 30-day mortality (5.9% vs 3.1%, P = 0.048) and 1-year mortality (9.2% vs 5.1%, P = 0.022). After adjustment by propensity score and TRS, leukocyte count (per 10/µL) was an independent predictor of 1-year mortality (HR: 1.086, 95% CI: 1.034-1.140, P = 0.001). Subdivision analysis demonstrated the correlation between leukocytosis and higher 1-year mortality within both high and low TRS strata (divided by 4, the median of TRS). Additionally, 24% (191 out of 796) of patients were characterized by nonleukocytosis and TRS < 4, having 0% of mortality rate at 1-year follow-up. In conclusion, leukocyte count is an independent prognostic factor adding incremental value to TRS for STEMI. Nonleukocytosis in conjunction with TRS < 4 identifies a large patient group at extremely low risk and thus provides rapid early triage for STEMI patients undergoing primary PCI. This finding is worth validation in the future.