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Furosemide Monotherapy Aggravates Worsening Renal Function in Patients With Acute Heart Failure
The 14th Annual Scientific Meeting of Bio-Informational Pharmacology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan Background: The most important causes responsible for sudden cardiac death in patients with heart failure (HF) are attributed to lethal cardiac arrhythmias, which are in part due to a complex remodeling of cardiac ion channels. It has been reported that a gain of function in KCNH2 encoding the rapid component of the delayed rectifier current (IKr) is associated with an increased risk of arrhythmia that can cause sudden death. Meanwhile some chemical agents under study enhance the KCNH2 channel, no intrinsic activator of KCNH2 channel have yet been reported. Methods and Results: Study subjects were 7 patients with non-ischemic HF (!50%) who had a history of documented ventricular tachyarrhythmias (ventricular tachycardia 6 and ventricular fibrillation 1) and 4 normal controls. We investigate the effects of the patient’s serum on recombinant IKr recorded from human embryonic kidney (HEK) 293 cells stably expressing KCNH2 by using the whole-cell patchclamp technique. Overnight treatment with the 2% serum obtained from the patient resulted in a significant enhancement in the peaks of IKr tail currents compared to the serum from normal controls (64.862.8 pA/pF vs 56.361.9 pA/pF, p!0.05) without the shift of voltage-dependence of the activation. Conclusion: The present study describes the existence of intrinsic KCNH2 channel activator in serum of HF with severe ventricular tachyarrhythmia.
079 Lo¨ffler’s Endocarditis With Severely Impaired Left Ventricular Function and Thrombus TAKAYUKI TSUJI, HIDEKAZU TANAKA, AKIHIRO KANEKO, KEIKO RYO, KOUHEI YAMAWAKI, KAZUHIRO TATSUMI, KENSUKE MATSUMOTO, HIROYA KAWAI, KEN-ICHI HIRATA Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.Kobe, Japan A 47-year-old male was admitted to our hospital because of dyspnea. Since laboratory examinations revealed hypereosinophilia (O10000/ml) at a local hospital, he had been treated with corticosteroids. Transthoracic echocardiography showed dilated left ventricle and severely impaired left ventricular function of ejection fraction 20%. The left ventricular walls were thickened by an abnormal mass that differed from the myocardium, suggesting left ventricular thrombus (Figure). The patient had hypereosinophilia-related complications such as asthma, neuropathy, purpura and angiitis. Thus, the diagnosis was Lo¨ffler’s endocarditis in the fibrotic stage associated with Churg-Strauss syndrome. The patient was given conservative medical treatment including anticoagulants for heart failure and left ventricular thrombus immediately on admission. His symptoms obviously improved after medical treatment, and the patient was discharged 82 days after admission.
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080 Furosemide Monotherapy Aggravates Worsening Renal Function in Patients With Acute Heart Failure MEGUMI KUNISHIGE, SHUICHI ISHIZUKA, KUNIYASU IKEOKA, AKIKO MATSUO, MINORU ICHIKAWA, AKIRA NISHIBE, YUSUKE NAKAGAWA, YOSHIYUKI KIJIMA, TAKESHI HATA The Department of Cardiology, Higashi-osaka City General Hospital, Osaka, Japan Background: Worsening renal function (WRF) during treatment of patients with acute heart failure (AHF) often occurs within days of hospitalization and is an independent predictor of adverse outcomes. However, causes of WRF are incompletely understood. Methods and Results: A total of 90 consecutive patients with AHF admitted at our hospital were analyzed. WRF was defined as the occurrence of both a O 25% and a O 0.3mg/dl increase in serum creatinine (s-Cr) during hospitalization. In this study cohort (age 70614 years, left ventricular ejection fraction 44616 %, s-Cr on entry 1.0060.34 mg/dl, peak s-Cr 1,3360.54 mg/dl), 55 patients (61%) developed WRF. Eighty percent of the patients received furosemide treatment, 53% of them received vasodilators, and 27% of them received inotropic agents at the early phase of AHF. Furthermore, 41% of the patients received monotherapy. Patients were followed for 8036603 days. Eight patients died and 29 were rehospitalized for heart failure. Kaplan-Meier analyses revealed that the group with WRF marked higher event rate than the group without WRF (log-rank, p!0.05). The independent predictors of WRF evaluated using multivariable logistic regression, were s-Cr level on entry (p!0.0001), peak s-Cr level (p!0.0001) and furosemide monotherapy (p! 0.05). Conclusions: WRF is a frequent finding in patients with AHF and is associated with a poor prognosis. Furosemide monotherapy is an important predictor of developing WRF.
081 A Case of Heart Failure Due to Tachycardia-Induced Cardiomyopathy TAKESHI WADA, YASUNOBU KAWANO, YUJI NAKAZATO Department of Cardiology, Juntedo University Urayasu hospital, Chiba, Japan A 61 year-old female without previous illness was admitted our hospital with the complaints of dyspnea, orthopnea and palpitation. Her ECG showed atrial fibrillation (AF) with rapid ventricular response with the heart rate around 150 beats per minute. On echocardiogram, ejection fraction (EF) was 0.26. Under the diagnosis of congestive heart failure, digitalis, diuretics and ACE-I were started. Carvedilol was also titrated from low dose. Her symptoms were improved by those medications, but AF persisted and EF unchanged. Coronary angiography revealed no atherosclerotic heart disease. Although the onset of AF was unknown, left atrial dimension was 42 mm and we administered amiodarone for aiming the pharmacological sinus conversion before DC cardioversion. After 4 months, AF was restored to sinus rhythm and EF improved 0.64. After the maintenance of sinus rhythm for 1 year, all the medication was discontinued and she is doing well without recurrence. Tachycardia-induced Cardiomyopathy is a well-recognized cause of cardiac dysfunction. The clinicians should consider the diagnosis in patients with unexplained cardiac dysfunction with any form of tachyarrhythmias.
082 Serial Changes in Creatinine Reflect the Types of Acute Heart Failure MASAKI YAMATO1, HIROKAZU KITADA1, MASAO KOIDE1, NORIKO SASAKI1, KEIJI HIROOKA1, YOSHIHIRO KAWAGUCHI1, YOSHIO YASUMURA1, YUKIHIRO KORETSUNE2, HIDEO KUSUOKA1 1 The Division of Cardiology, Osaka National Hospital, Osaka, Japan, 2The Clinical Research Center, Osaka National Hospital, Osaka, Japan Objectives: We studied whether changing pattern of renal function in response to the therapy is different between two categories of acute heart failure (AHF); acutely decompensated heart failure (ADHF) characterized by fluid accumulation and acute vascular failure (AVF) by central volume shift. Methods: Consecutive 29 patients with AHF who were administrated carperitide (CAR) with/without furosemide and inotropic agents. Creatinine (Cr(mg/dl)) at five phases were recorded: 1) on admission (Cr-ad), 2) minimum value for a week after admission (Cr-MIN), 3) Cr at the end of CAR administration (Cr-end), 4) maximal value after the end of CAR (Cr-MAX), 5) at discharge (Cr-dis). Patients were divided into 2 groups by the change (dCr) from Cr-ad to Cr-MIN: GpA; dCr!5-0.1, GpB; dCrO-0.1. BP on admission (BPad(mmHg)), LV fractional shortening(FS), bilirubin (T-bil(mg/dl)), and minimal diameter of IVC(minIVC(mm)) were compared between 2 groups. Results: Changing pattern of Cr was different between 2 groups. dCr in GpA was -0.2760.16 and GpB was -0.0360.03mg/dl. FS and BPad were lower and T-bil and minIVC were larger in GpA than in GpB. Cr significantly increased from Cr-MIN to Cr-MAX in both groups. Conclusion: AHF in GpA was considered to be cardiac failure with fluid accumulation. Rapid decrease in Cr-ad in response to therapy implies the increase in Cr in the course of cardiac failure before therapy.
079 Lo¨ffler’s Endocarditis With Severely Impaired Left Ventricular Function and Thrombus TAKAYUKI TSUJI, HIDEKAZU TANAKA, AKIHIRO KANEKO, KEIKO RYO, KOUHEI YAMAWAKI, KAZUHIRO TATSUMI, KENSUKE MATSUMOTO, HIROYA KAWAI, KEN-ICHI HIRATA Division of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.Kobe, Japan A 47-year-old male was admitted to our hospital because of dyspnea. Since laboratory examinations revealed hypereosinophilia (O10000/ml) at a local hospital, he had been treated with corticosteroids. Transthoracic echocardiography showed dilated left ventricle and severely impaired left ventricular function of ejection fraction 20%. The left ventricular walls were thickened by an abnormal mass that differed from the myocardium, suggesting left ventricular thrombus (Figure). The patient had hypereosinophilia-related complications such as asthma, neuropathy, purpura and angiitis. Thus, the diagnosis was Lo¨ffler’s endocarditis in the fibrotic stage associated with Churg-Strauss syndrome. The patient was given conservative medical treatment including anticoagulants for heart failure and left ventricular thrombus immediately on admission. His symptoms obviously improved after medical treatment, and the patient was discharged 82 days after admission.
JHFS
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080 Furosemide Monotherapy Aggravates Worsening Renal Function in Patients With Acute Heart Failure MEGUMI KUNISHIGE, SHUICHI ISHIZUKA, KUNIYASU IKEOKA, AKIKO MATSUO, MINORU ICHIKAWA, AKIRA NISHIBE, YUSUKE NAKAGAWA, YOSHIYUKI KIJIMA, TAKESHI HATA The Department of Cardiology, Higashi-osaka City General Hospital, Osaka, Japan Background: Worsening renal function (WRF) during treatment of patients with acute heart failure (AHF) often occurs within days of hospitalization and is an independent predictor of adverse outcomes. However, causes of WRF are incompletely understood. Methods and Results: A total of 90 consecutive patients with AHF admitted at our hospital were analyzed. WRF was defined as the occurrence of both a O 25% and a O 0.3mg/dl increase in serum creatinine (s-Cr) during hospitalization. In this study cohort (age 70614 years, left ventricular ejection fraction 44616 %, s-Cr on entry 1.0060.34 mg/dl, peak s-Cr 1,3360.54 mg/dl), 55 patients (61%) developed WRF. Eighty percent of the patients received furosemide treatment, 53% of them received vasodilators, and 27% of them received inotropic agents at the early phase of AHF. Furthermore, 41% of the patients received monotherapy. Patients were followed for 8036603 days. Eight patients died and 29 were rehospitalized for heart failure. Kaplan-Meier analyses revealed that the group with WRF marked higher event rate than the group without WRF (log-rank, p!0.05). The independent predictors of WRF evaluated using multivariable logistic regression, were s-Cr level on entry (p!0.0001), peak s-Cr level (p!0.0001) and furosemide monotherapy (p! 0.05). Conclusions: WRF is a frequent finding in patients with AHF and is associated with a poor prognosis. Furosemide monotherapy is an important predictor of developing WRF.
081 A Case of Heart Failure Due to Tachycardia-Induced Cardiomyopathy TAKESHI WADA, YASUNOBU KAWANO, YUJI NAKAZATO Department of Cardiology, Juntedo University Urayasu hospital, Chiba, Japan A 61 year-old female without previous illness was admitted our hospital with the complaints of dyspnea, orthopnea and palpitation. Her ECG showed atrial fibrillation (AF) with rapid ventricular response with the heart rate around 150 beats per minute. On echocardiogram, ejection fraction (EF) was 0.26. Under the diagnosis of congestive heart failure, digitalis, diuretics and ACE-I were started. Carvedilol was also titrated from low dose. Her symptoms were improved by those medications, but AF persisted and EF unchanged. Coronary angiography revealed no atherosclerotic heart disease. Although the onset of AF was unknown, left atrial dimension was 42 mm and we administered amiodarone for aiming the pharmacological sinus conversion before DC cardioversion. After 4 months, AF was restored to sinus rhythm and EF improved 0.64. After the maintenance of sinus rhythm for 1 year, all the medication was discontinued and she is doing well without recurrence. Tachycardia-induced Cardiomyopathy is a well-recognized cause of cardiac dysfunction. The clinicians should consider the diagnosis in patients with unexplained cardiac dysfunction with any form of tachyarrhythmias.
082 Serial Changes in Creatinine Reflect the Types of Acute Heart Failure MASAKI YAMATO1, HIROKAZU KITADA1, MASAO KOIDE1, NORIKO SASAKI1, KEIJI HIROOKA1, YOSHIHIRO KAWAGUCHI1, YOSHIO YASUMURA1, YUKIHIRO KORETSUNE2, HIDEO KUSUOKA1 1 The Division of Cardiology, Osaka National Hospital, Osaka, Japan, 2The Clinical Research Center, Osaka National Hospital, Osaka, Japan Objectives: We studied whether changing pattern of renal function in response to the therapy is different between two categories of acute heart failure (AHF); acutely decompensated heart failure (ADHF) characterized by fluid accumulation and acute vascular failure (AVF) by central volume shift. Methods: Consecutive 29 patients with AHF who were administrated carperitide (CAR) with/without furosemide and inotropic agents. Creatinine (Cr(mg/dl)) at five phases were recorded: 1) on admission (Cr-ad), 2) minimum value for a week after admission (Cr-MIN), 3) Cr at the end of CAR administration (Cr-end), 4) maximal value after the end of CAR (Cr-MAX), 5) at discharge (Cr-dis). Patients were divided into 2 groups by the change (dCr) from Cr-ad to Cr-MIN: GpA; dCr!5-0.1, GpB; dCrO-0.1. BP on admission (BPad(mmHg)), LV fractional shortening(FS), bilirubin (T-bil(mg/dl)), and minimal diameter of IVC(minIVC(mm)) were compared between 2 groups. Results: Changing pattern of Cr was different between 2 groups. dCr in GpA was -0.2760.16 and GpB was -0.0360.03mg/dl. FS and BPad were lower and T-bil and minIVC were larger in GpA than in GpB. Cr significantly increased from Cr-MIN to Cr-MAX in both groups. Conclusion: AHF in GpA was considered to be cardiac failure with fluid accumulation. Rapid decrease in Cr-ad in response to therapy implies the increase in Cr in the course of cardiac failure before therapy.