Myung Hwan Bae

White Blood Cell, Hemoglobin and Platelet Distribution Width as Short-Term Prognostic Markers in Patients with Acute Myocardial Infarction

The aim of this study was to assess the prognostic value of combined use of white blood cell (WBC), hemoglobin (Hb), and platelet distribution width (PDW) in patients with acute myocardial infarction (AMI). This study included 1,332 consecutive patients with AMI. Patients were categorized into complete blood cell (CBC) group 0 (n=346, 26.0%), 1 (n=622, 46.7%), 2 (n=324, 24.3%), and 3 (n=40, 3.0%) according to the sum of the value defined by the cut-off levels of WBC (1, ≥14.5×103/µL; 0, <14.5×103/µL), Hb (1, <12.7 g/dL; 0, ≥12.7 g/dL), and PDW (1, ≥51.2%; 0: <51.2%). In-hospital death occurred in 59 (4.4%) patients. Patients who died during index hospitalization had higher WBC and PDW and lower Hb. The patients could be stratified for in-hospital mortality according to CBC group; 1.2%, 2.7%, 9.0%, and 22.5% in CBC groups 0, 1, 2, and 3 (P<0.001), respectively. In multivariate logistic regression analysis, CBC group≥2 (odds ratio, 3.604; 95% confidence interval, 1.040-14.484, P=0.043) was an independent predictor for in-hospital death. The prognostic impact of the combined use of CBC markers remained significant over 12 months. In conclusions, combination of WBC, Hb, and PDW, a cheap and simple hematologic marker, is useful in early risk stratification of patients with AMI.

Impact of Multivessel Coronary Disease With Chronic Total Occlusion on One-Year Mortality in Patients With Acute Myocardial Infarction

Background and Objectives The impact of multivessel coronary disease (MVD) with chronic total occlusion (CTO) on one-year mortality in patients with acute myocardial infarction (AMI) is not clearly known. We investigated the impact of MVD with concurrent CTO lesion on one-year mortality in patients with AMI. Subjects and Methods We studied 1008 consecutive patients who underwent coronary angiography between November 2005 and December 2008 with a diagnosis of AMI. Results Among 1008 patients, 432 patients (43%) had MVD, and 88 patients (8.7%) had CTO lesion. The one-year overall mortality was higher in patients with MVD than in patients with single vessel disease (SVD) (10.2% vs. 5.9%, p=0.012). However, the one-year overall mortality was not significantly higher in patients with CTO lesion than in patients without that lesion (12.5% vs. 7.3%, p=0.080). In multivariate analysis, independent predictors of one-year overall mortality were age older than 65 years {hazard ratio (HR) 2.41, 95% confidence interval (CI): 1.43 to 4.08}, Killip class ≥III (HR 3.59, 95% CI: 2.24 to 5.77), ST-elevation myocardial infarction (HR 2.45, 95% CI: 1.49 to 4.05) and MVD (HR 1.76, 95% CI: 1.07 to 2.89). Conclusion Patients with MVD showed higher one-year mortality than patients with SVD. However, the presence of CTO was not an independent predictor of one-year mortality in this study that included patients with successfully revascularized CTO lesion.

Genetic Analysis of SCN5A in Korean Patients Associated with Atrioventricular Conduction Block

Recent several studies have shown that the genetic variation of SCN5A is related with atrioventricular conduction block (AVB); no study has yet been published in Koreans. Therefore, to determine the AVB-associated genetic variation in Korean patients, we investigated the genetic variation of SCN5A in Korean patients with AVB and compared with normal control subjects. We enrolled 113 patients with AVB and 80 normal controls with no cardiac symptoms. DNA was isolated from the peripheral blood, and all exons (exon 2-exon 28) except the untranslated region and exon-intron boundaries of the SCN5A gene were amplified by multiplex PCR and directly sequenced using an ABI PRISM 3100 Genetic Analyzer. When a variation was discovered in genomic DNA from AVB patients, we confirmed whether the same variation existed in the control genomic DNA. In the present study, a total of 7 genetic variations were detected in 113 AVB patients. Of the 7 variations, 5 (G87A-A29A, intervening sequence 9-3C>A, A1673G-H558R, G3578A-R1193Q, and T5457C-D1819D) have been reported in previous studies, and 2 (C48G-F16L and G3048A-T1016T) were novel variations that have not been reported. The 2 newly discovered variations were not found in the 80 normal controls. In addition, G298S, G514C, P1008S, G1406R, and D1595N, identified in other ethnic populations, were not detected in this study. We found 2 novel genetic variations in the SCN5A gene in Korean patients with AVB. However, further functional study might be needed.

Hyponatremia in acute heart failure: a marker of poor condition or a mediator of poor outcome?

See Article on Page 460-470 n nHeart failure is a growing issue around the world; there are currently more than 20 million affected patients. Hospitalization for acute heart failure (AHF) is associated with poor prognosis; the 1-year mortality rate for AHF patients is roughly 10 times that for healthy individuals [1]. n nAmong various predictors known to correlate with clinical outcomes, hyponatremia is a common electrolyte disturbance that has been associated with high mortality and rehospitalization in Western AHF studies [2,3,4]. However, little is known about the prognostic value of hyponatremia in Asian AHF patients. In the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF), low sodium levels were associated with high in-hospital mortality [3], and the Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) showed that low serum sodium levels were an independent predictor of prolonged hospitalization and increased mortality 60 days after discharge [4]. In the Korean Heart Failure (KorHF) registry, hyponatremia was associated with a poor clinical outcome [5]. n nThere are several explanations for the association between hyponatremia and prognosis in patients with AHF. However, whether hyponatremia is a marker of poor patient condition or a mediator of poor patient outcome has yet to be determined. Low cardiac output due to reduced left ventricular systolic function activates several neurohormonal systems to preserve blood volume and pressure. Activation of the renin-angiotensin-aldosterone pathway and the non-osmotic release of arginine vasopressin (AVP) result in decreased water and sodium delivery to the kidneys, decreased water excretion, water retention by the kidneys, and, ultimately, hyponatremia [6,7]. Due to these factors, hyponatremia may be a marker of neurohormonal activation. n nA recent study reported that low serum sodium levels were associated with increased mortality in oligoanuric patients receiving maintenance hemodialysis [8]. Patients with end-stage renal disease do not have the ability to concentrate urine in response to circulating AVP, and the removal of water and sodium is determined by dialysis. This suggests that hyponatremia itself can be seen as directly toxic rather than as a result of neurohormonal activation caused by low cardiac output. n nFew studies have examined the prognostic impact of hyponatremia correction during hospitalization, and the results are conflicting. In a single-center study by Madan et al. [9], serum sodium levels increased in 68.9% of patients during hospitalization, and patients with increased serum sodium concentrations had markedly improved long-term outcomes. This suggests that optimal treatment can be effective in increasing serum sodium levels, and that patients who respond to optimizing therapy have better outcomes than those who do not. However, in the KorHF registry [5], improved hyponatremia during hospitalization was not associated with better outcomes. n nIn a multinational, multicenter study published in the current issue of this journal, 1,470 patients hospitalized for AHF at eight centers in South Korea, Taiwan, and China were analyzed [10]. Hyponatremia at admission was defined as a serum sodium level < 135 mmol/L, and was present in 247 patients (16.8%). Patients with hyponatremia had poor baseline characteristics such as older age, higher frequency of chronic kidney disease, lower systolic blood pressure, and a lower prescription rate of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, β-blockers, and/or spironolactone. Hyponatremia was an independent predictor of 12-month mortality after adjusting for these confounding variables by a multivariate analysis and propensity score matching. Moreover, the postdischarge clinical outcomes of the patients with hyponatremia at admission were not improved by hyponatremia correction. n nThis study shows that hyponatremia at hospital admission is common, and that it is an independent predictor of a worse clinical outcome in hospitalized Asian heart failure patients. However, there are several limitations to this study. First, this was not a prospective study. As discussed by the authors, unmeasured confounding variables could have affected the results even though propensity score matching for unbalanced variables was performed. Second, the distribution of the patients serum sodium concentrations and the technical details of sodium measurement at each center or in each nation were not presented. This study included eight centers from three nations. Although the measurement of serum sodium is standardized, we do not know the systems, calibration data, and normal values used at each center. Third, although hyponatremia was defined as a serum sodium level < 135 mmol/L, the optimal cut-off level for predicting a poor clinical outcome in AHF patients may differ for each study population, center, or country. If 140 mmol/L, the level at which mortality was the lowest, was used as the cut-off level, the authors may have obtained different, and probably better, results. Finally, differences in socioeconomic status, medical resources, and treatment patterns at each center were not controlled in this study. n nHowever, since this study demonstrates an association between hyponatremia and poor prognosis in Asian AHF patients, it is worth considering, despite the limitations.

Catecholaminergic Polymorphic Ventricular Tachycardia in a Patient With Recurrent Exertional Syncope

A 16-year-old male with a prior history of recurrent syncope was referred to our hospital after being resuscitated from cardiac arrest developed while playing volleyball. His electrocardiogram (ECG) demonstrated ventricular fibrillation at a local emergency department. After referral, an ECG showed bidirectional ventricular tachycardia (VT) and nonsustained Torsade de Pointes. Two days later, his heart rate became regular, and no additional episodes of VT were observed. His ECG showed sinus rhythm with a corrected QT interval of 423 msec, and two-dimensional echocardiography was unremarkable. We made the diagnosis of a catecholaminergic polymorphic VT. However, only premature ventricular complex bigeminy was induced on exercise ECG and epinephrine infusion tests, and the patient showed no episodes of syncope. His father and mother had different missense mutations in the cardiac ryanodine receptor on genetic testing. The proband had both mutations in different alleles and was symptomatic. It was recommended that the patient avoid competitive physical activities, and a β-blocker was prescribed.

Angiotensin II type 1 receptor blockers as a first choice in patients with acute myocardial infarction

Background/Aims: Angiotensin II type 1 receptor blockers (ARBs) have not been adequately evaluated in patients without left ventricular (LV) dysfunction or heart failure after acute myocardial infarction (AMI). Methods: Between November 2005 and January 2008, 6,781 patients who were not receiving angiotensin-converting enzyme inhibitors (ACEIs) or ARBs were selected from the Korean AMI Registry. The primary endpoints were 12-month major adverse cardiac events (MACEs) including death and recurrent AMI. Results: Seventy percent of the patients were Killip class 1 and had a LV ejection fraction ≥ 40%. The prescription rate of ARBs was 12.2%. For each patient, a propensity score, indicating the likelihood of using ARBs during hospitalization or at discharge, was calculated using a non-parsimonious multivariable logistic regression model, and was used to match the patients 1:4, yielding 715 ARB users versus 2,860 ACEI users. The effect of ARBs on in-hospital mortality and 12-month MACE occurrence was assessed using matched logistic and Cox regression models. Compared with ACEIs, ARBs significantly reduced in-hospital mortality(1.3% vs. 3.3%; hazard ratio [HR], 0.379; 95% confidence interval [CI], 0.190 to0.756; p = 0.006) and 12-month MACE occurrence (4.6% vs. 6.9%; HR, 0.661; 95% CI, 0.457 to 0.956; p = 0.028). However, the benefit of ARBs on 12-month mortality compared with ACEIs was marginal (4.3% vs. 6.2%; HR, 0.684; 95% CI, 0.467 to 1.002; p = 0.051). Conclusions: Our results suggest that ARBs are not inferior to, and may actually be better than ACEIs in Korean patients with AMI.

Prediction of improvement in cardiac function by high dose dobutamine stress echocardiography in patients with recent onset idiopathic dilated cardiomyopathy

The prognosis of patients with recent onset idiopathic dilated cardiomyopathy (DCM) is grave and highly variable [1]. Dobutamine stress echocardiography (DSE) has been used to assess contractile reserve in patients with ischemic and idiopathic DCM. Several studies have suggested that contractile reserve assessed by DSE can be of prognostic value inpatientswith idiopathic DCM [2–5]. In this study,we investigated whether contractile reserve on DSE could predict late improvement of cardiac function and had incremental prognostic value for future cardiac events in recent onset idiopathic DCM. Between December 2004 and May 2011, forty-one patients were enrolled in this study. The study population consisted of patients with idiopathic DCMwho had symptom durations of less than 6 months. All study subjects underwent coronary angiography to exclude ischemic heart disease, and endomyocardial biopsies were performed in 35 patients (85%) to exclude reversible causes, such as myocarditis. Patients with chronic kidney disease (estimated glomerular filtration rate b60 ml/min/1.73 m) were also excluded. All patients had a complete echocardiographic study and follow-up echocardiogram was performed after 6 month and 12 month, then when any clinical events occurred. The interval between the time of DSE and last follow-up echocardiogramwas 16±15 months. Dobutamine was infused in 5-min dose increments, starting from 5 μg/kg/min and increasing to 10, 20, 30, and finally, to the maximal dose of 40 μg/kg/min. The infusion was discontinued before the maximal dose was reached if 85% of the maximal predicted heart rate for the age group was achieved, or if symptomatic complex ventricular arrhythmias, defined as the presence of multiform or repetitive ventricular extrasystoles, were observed. Beta-blockers were stopped 48 h before dobutamine testing in all patients taking these agents. The institutional committee of Kyungpook National University Hospital approved the study protocol. Informed consent was obtained in all patients. Cardiac death and hospitalization were combined end-point. The mean age of the patients was 50±14.8 years, and 24 patients (59%)weremale. During themean follow-up period of 30±24 months, 14 patients (34%) experienced cardiac events, and 5 (12%) of them died. Three (7%) of themwere sudden cardiac death, and two (4%) were low cardiac output death. Of the remaining patients, 9 (21%) were rehospitalized due to aggravation of heart failure. During dobutamine infusion, no significant complications occurred. Tenpatientsdidnot reachapeakdoseof dobutamine. Sixpatients reached maximal heart rates before thepeakdose of dobutamine, and in 4patients the test was stopped before the peak dose due to frequent premature complex. The mean value of the maximal dobutamine dose given was 35.6±8.7 μg/kg/min. We investigated the correlation between follow-up LVEFand clinical and echocardiographic parameters (Table 1). The followup LVEF correlated with baseline LVEDV (r=−0.519, p=0.001), LVESV (r=−0.499, p=0.001), LVEDV at peak dose (r=−0.509, p=0.001), LVEFat peakdose (r=0.692, pb0.001), and the changeof LVEF (r=0.515, p=0.001) from baseline to peak dose of dobutamine. Among them, LVEF at the peak dose of dobutamine was the most significant predictor of follow-up LVEF. Follow-up LVEFwas predicted by LVEF at the peak dose of DSE (y=1.033×−0.979, r=0.465, p=0.001). Receiver-operating characteristic analysis was used to determine the optimal cutoff value for predicting cardiac events with respect to the change of LVEF. The optimal change in LVEFwas 9.8%, The Kaplan–Meier survival estimates were stratified according to the results of baseline to peak LVEF variation during dobutamine administration (Fig. 1). The presence of inotropic response after dobutamine infusion, identified in this study as a change of LVEF≥9.8%, showed a significantly better outcome than little inotropic response (pb0.001). In the Cox-proportional hazard model, the change of LVEF from peak to baseline (hazard ratio [HR] 0.834, 95% confidence interval [CI] 0.713–0.976, p=0.024), in addition to age (HR 0.921, 95% CI 0.863– 0.984, p=0.015), log NT-ProBNP (HR 0.261, 95% CI 0.091–0.749, p=0.013), deceleration time (HR 0.964, 95% CI 0.932–0.998, p=0.039) and E/E′ ratio (HR 1.177, 95% CI 1.046–1.325, p=0.007) was also a significant independent predictor of cardiac event (Table 2). Moreover, the LVEF change in DSE had incremental prognostic value to

A Hypereosinophilic Syndrome with Cardiac Involvement from Thrombotic Stage to Fibrotic Stage

Cardiac involvement is a major cause of morbidity and mortality in hypereosinophilic syndrome (HES). It is classified into 3 stages by the degree of eosinophils-mediated heart injury; acute necrotic stage, thrombotic stage, and fibrotic stage. Nonetheless, definitive evidence that each patient passes sequentially through these stages is lacking. We present a case of 48-year-old male patient with dyspnea and peripheral edema who underwent valve replacement surgery due to severe mitral regurgitation. After the valve replacement, HES with cardiac involvement in the thrombotic stage was diagnosed. In the follow-up study, the patient progressed into fibrotic stage of HES.

Effect of renin-angiotensin system blockade in patients with severe renal insufficiency and heart failure

BACKGROUNDnRenin-angiotensin system blockade (RAB) is the cornerstone in the management of patients with heart failure. However, the benefit of RAB in patients with accompanying severe renal impairment is not clear. We aimed to examine the effect of RAB and the differential effect of RAB depending on renal replacement (RR) in patients with severe renal insufficiency and acute heart failure.nnnMETHODS AND RESULTSnAmong 5625 patients from the Korean Acute Heart Failure registry, 673 in-hospital survivors (70.9u202f±u202f12.8u202fyears, 376 men) who had left ventricular ejection fractionu202f<u202f40% and estimated glomerular filtration rateu202f<u202f30u202fmL/min/1.73u202fm2 during hospitalization were analyzed. The inverse probability of treatment weighting (IPTW)-adjusted survival analysis was used to compare the composite of all-cause mortality and rehospitalization between patients with and without pre-discharge RAB. A total of 334 (49.6%) adverse events were observed during the 1-year follow-up. The IPTW-adjusted Kaplan-Meier survival analysis showed that the 1-year event rate was 48.7% and 53.8% for patients with RAB and those without, respectively (log rank pu202f=u202f0.048). RAB was significantly related to better prognosis in patients receiving RR therapy (hazard ratio [HR]u202f=u202f0.436 [0.269-0.706], pu202f=u202f0.001), but not in patients not receiving RR therapy (HR 0.956 [0.731-1.250], pu202f=u202f0.742) in a weighted cohort (p for interactionu202f=u202f0.005).nnnCONCLUSIONSnEarly RAB treatment in patients with heart failure and severe renal insufficiency was related to better prognosis. The benefit of RAB was particularly prominent in patients receiving RR therapy.

Tachycardia-Induced Right Heart Failure and Severe Tricuspid Regurgitation That Improved with Medication

Secondary tricuspid regurgitation (TR) primarily develops due to left heart failure or primary pulmonary diseases. Tricuspid annular dilation, which is commonly caused by right ventricular volume and pressure overload followed by right ventricle dilation, is believed to be the main mechanism underlying secondary TR. It is reported that once the tricuspid annulus is dilated, its size cannot spontaneously return to normal, and it may continue to dilate. These reports also suggest the use of an aggressive surgical approach for secondary TR. In the present report, we describe a case of tachycardia-induced severe TR that was completely resolved without the need for surgery.