Pen-Chih Liao

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.

AbstractThe 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 103/&mgr;L) 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.

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.

Hyperuricemia as an Outcome Predictor in Patients with ST-Segment Elevation Myocardial Infarction: Too Good to be True?

Hyperuriacemia has been reported as an independent predictor of short- and long-term prognosis in patients with acute coronary syndrome.1,2 In the recent issue of Acta Cardiologica Sinica, Akgul et al. advocated that uric acid > 5.7 mg/dl was associated with increased in-hospital and six-month cardiovascular death in Turkish patients with ST-segment elevation myocardial infarction (STEMI) undergoing angioplasty.3 The level of uric acid upon hospital admission is a powerful predictor of six-month mortality, with a hazard ratio as high as 5.57. However, one aspect of the study must be noted. Although the enrollment of consecutive patients was stated, most patients in the study were at Killip’s class I (91.9%), which is not a common condition of general practice.

P-1 Remodeling of Myocardial Gap Junctions and its Correlation with Cardiac Contractility in Diabetic Rats

not available at time of printing. Poster Sessions 1: Heart Failure/Myocardial Diseases P-1 Remodeling of Myocardial Gap Junctions and its Correlation with Cardiac Contractility in Diabetic Rats Dong-Feng Yeih1, Pen-Chih Liao1, Ho-Tsung Hsin1, Kuo-Chin Chen1, Ai-Hsian Li1, Yung-Zu Tseng2. 1Department of Cardiology, Far-Eastern Memorial Hospital, Taiwan, 2Department of Cardiology, National Taiwan University, Taiwan Introduction: Gap junctions play an essential role in coupling adjacent cardiomyocytes, ensuring organized propagation of action potential and synchronizing beating in cardiomyocytes. However, it remains unclear that temporal remodeling of myocardial gap junctions and its relation to cardiac contractility in diabetic rats. Methods: Male Wistar rats, weighing 250 to 300 grams, were randomized to injection with either vehicle or streptozotocin (50mg, IP). Invasive hemodynamic studies with simultaneous recordings of left ventricular pressure and aortic flow signals were done at 4, 8 and 12 weeks after injection. Maximal systolic elastance (Emax) and maximum theoretical flow (Qmax) were assessed by curve fitting techniques; protein expression of non-phosphorylated Cx43 (P0) and total amount of Cx43 (T) in the left ventricle by western blotting analysis. Results: Emax was significantly lower in diabetic rats than in controls and Emax was significantly depressed with time in diabetic groups. On the other hand, Qmax was preserved and cardiac output was maintained in diabetic rats. Protein expression of total Cx43 was persistently attenuated in diabetic groups, while P0 was enhanced at 8 and 12 weeks after injection. The ratio of P0 to T was significantly increased with time, which correlated well with the declines in Emax in diabetic rats. Conclusions: Temporal remodeling of myocardial gap junctions, with persistently lower total Cx43 and gradually increased non-phosphorylated Cx43 and the ratio of P0 to T, occurred in the evolution of systolic dysfunction in diabetic rats. P-2 Quantification of Left Ventricular Diastolic Dynamics in Normal and Diseased Myocardium by Speckle-Tracking Echocardiography Kaoru Dohi1, Katsuya Onishi2, Takeshi Takamura1, Emiyo Sugiura1, Hiroshi Nakajima1, Kazuhide Ichikawa1, Masaki Tanabe1, Hiroya Tamada1, Masatoshi Miyahara1, Mashio Nakamura1, Masaaki Ito1. 1Department of Cardiology, Mie University Graduate School of Medicine, Japan, 2Department of Molecular and Laboratory Medicine, Mie University Graduate School of Medicine, Japan Background: The present study aimed to quantify left ventricular (LV) diastolic dynamics and to elucidate their relations to systolic properties in normal and diseased myocardium. Methods: 50 patients with hypertensive LV hypertrophy (LVH: EF 61±8%, QRS 96±16ms), 50 patients with dilated cardiomyopathy (DCM: EF 31±10%, QRS 121±32ms), and 50 normal controls (Control: EF 5±6%, QRS 89±9ms) had echo-study with speckle-tracking strain and strain rate imaging. To quantify LV diastolic relaxation and segmental synchrony, global peak relaxation rate (PRR) during early diastole and standard deviation (SD) of the 18 segmental time-to-PRR (TPRR-SD) were calculated from apical 4-, 2-, and long axis views. To elucidate the relations between diastolic and systolic properties, global peak systolic strain (PSS) and SD of the segmental time-to-peak PSS (TPSS-SD) were also evaluated. Results: LV relaxation and diastolic synchrony were significantly impaired in LVH and was more prominent in DCM (PRR: 0.8±0.3* 1/s in LVH, 0.5±0.2*# 1/s in DCM, and 1.2±0.3 1/s in Control, TPRR-SD: 55±16*ms in LVH, 79±35*# ms in DCM, and 42±13ms in Control, *p < 0.05 vs. Control and #p < 0.05 vs. LVH, respectively). There were strong correlations between PSS and PRR, and TPRR-SD and TPSS-SD (r = 0.83 and r = 0.83, p < 0.05, respectively). Conclusion: Speckle-tracking echocardiography quantified LV diastolic dynamics and exhibited the strong relation to systolic properties.