Clinical Utility of Reduced Heart Rate Recovery After Exercise in Elderly Patients With Chronic Heart Failure

S72 Journal of Cardiac Failure Vol. 23 No. 10S October 2017 P5-3 A Case of Cardiac Amyloidosis Showing Diagnostic Usefulness of Cardiac Magnetic Resonance T1 Imaging Haruka Sato1, Koichiro Sugimura1, Tatsuo Aoki1, Shunsuke Tatebe1, Saori Yamamoto1, Toru Shimizu1, Kimio Satoh1, Noriko Fukuhara2, Hideki Ota3, Hiroaki Shimokawa1; 1 Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan; 2Department of Hematology and Rheumatology, Tohoku University Graduate School of Medicine, Sendai, Japan; 3Department of Diagnostic Radiology, Tohoku University Graduate School of Medicine, Sendai, Japan Novel cardiac magnetic resonance T1 imaging technique enables us to quantitatively assess diffuse myocardial disease. We here report a case where native T1 was useful to diagnose cardiac amyloidosis. A 73 years-old man was admitted to our hospital for the treatment of his multiple myeloma. He had been treated with bortezomib and dexamethasone without any relapses since 2012. However, in 2017, serum level of BNP was elevated (from 12.2 to 243.4 pg/mL) and Holter ECG showed an increase in the number of premature ventricular contractions. He did not have shortness of breath or other subjective symptoms. Echocardiography showed that left ventricular ejection fraction was 60%, interventricular septum 10 mm, transmitral peak early (E) and late (A) flow velocity was 0.68 m/s and 0.52 m/s, respectively. Cardiac magnetic resonance imaging showed that although there was no late gadolinium enhancement, interventricular wall thickness was increased and native T1 was elevated. Then, we performed cardiac catheterization and myocardial biopsy to examine possible chemotherapyinduced cardiotoxicity and cardiac amyloidosis. Histological examination showed that cardiac tissues had amyloid fibrils with apple-green birefringence under polarized light, making the final diagnosis of cardiac amyloidosis. We thus changed bortezomib to melphalan because the former has been reported to cause cardiac dysfunction and ventricular arrhythmias. In this case, native T1 was useful to diagnose cardiac amyloidosis.

P5-4 Usefulness of Multidetector Computed Tomography and Magnetic Resonance Imaging on Diagnosing Left Ventricular Noncompaction Shun Hasegawa, Yoichi Ajiro, Ryozo Maeda, Kazuyuki Hamada, Ko Sugiyama, Masahiro Watanabe, Takashi Saito, Fumiaki Mori, Kazunori Iwade; National Hospital Organization Yokohama Medical Center, Kanagawa, Japan Introduction: Left ventricular nonconpaction (LVNC) is classified as primary cardiomyopathy. Because of its poor outcome, the diagnosis of LVNC is important. However, not all LVNC patient could be diagnosed only by echocardiography mostly due to the limitation in obtaining reliable apex image. We experienced a LVNC patient who could be diagnosed using the multidetector computed tomography (MDCT) and magnetic resonance imaging (MRI) in addition to echocardiography. Case: A 48 year-old male was admitted to our hospital because of left paralysis and NYHA 4 exertional breathlessness. He was diagnosed cerebral infarction (CI) and acute heart failure (AHF) accompanying tachycardiac atrial fibrillation (AF). AHF was compensated by carvedilol, enalapril with LV ejection fraction improvement from 22% to 61%. Echocardiography revealed dilated cardiomyopathy like heart and non-compacted layer in lateral side of apex even though the diagnostic image for LVNC could not be obtained. We conducted MDCT and MRI to obtain clear tangent image at apex; and diagnosed LVNC with the non-compaction/compaction ratio of 2.8, 3.5 respectively. The anticoagulant therapy and optical medical therapy were continued even after AF eradication by pulmonary vein isolation, this patient has spent 6 months free from any adverse cardiovascular events. Conclusion: MDCT and MRI should be considered when echocardiography cannot provide diagnostic image for LVNC.

P5-5 Left Ventricular Noncompaction With Multiple Thrombi in Apical Aneurysm Daisuke Yakabe, Shouji Matsushima, Takeo Fujino, Kisho Ohtani, Tomomi Ide, Taiki Higo, Hiroyuki Tsutsui; Department of Cardiovascular Medicine, Kyushu University Hospital, Fukuoka, Japan Left ventricular noncompaction (LVNC) is a rare form of cardiomyopathy caused by the failure of myocardial compaction during embryogenesis. Its clinical features are variable ranging from asymptomatic to cardiac dysfunction, heart failure (HF), arrhythmias, and systemic thromboembolism. However, there have been only few reports regarding its coexistence with LV aneurysm. A 44-year-old man with no significant cardiopulmonary history was admitted to our hospital because of heart failure. The chest radiography exhibited pulmonary congestion. The laboratory data was unremarkable except for elevated brain-type natriuretic peptide and troponin T. Transthoracic echocardiography demonstrated global hypokinesis with an ejection fraction of 32%, prominent trabeculation and deep intertrabecular recesses, and apical aneurysm with multiple thrombi (10 × 13 mm in inferior wall, 15 × 8 mm in anteriol wall). Cardiac magnetic resonance imaging showed increased noncompacted (NC) endomyocardial layer depth compared to the compacted (C) epicardial layer (NC/C ratio > 2.3) and thrombi in apical aneurysm. Coronary angiography revealed no significant obstructive stenosis. Pathological analysis demonstrated no evidence of myocarditis, sarcoidosis, amyloidosis or hemochromatosis. Based on these findings, he was diagnosed as LVNC complicated with apical aneurysm. Carvedilol, enalapril, furosemide and warfarin were started to manage HF and prevent stroke or systemic thromboembolism. Four weeks after starting anticoagula-

tion, apical thrombi disappeared without clinical signs of embolism. Here, we report the patient who have LVNC with multiple thrombi in apical aneurysm.

P6-1 Protein Acetylation in Skeletal Muscle Impairs Mitochondrial Fatty Acid Oxidation and Limits Exercise Capacity in Post-Infarct Heart Failure in Mice Katsuma Yamanashi, Masaya Tsuda, Arata Fukushima, Shingo Takada, Takaaki Furihata, Junichi Matsumoto, Satoshi Maekawa, Takashi Katayama, Takashi Yokota, Shintaro Kinugawa; Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan Background: Exercise intolerance is a major clinical manifestation in heart failure (HF) patients, due largely to skeletal muscle (SKM) abnormalities. Lysine Acetylation is a reversible post-translational modification involved in regulating mitochondrial metabolic enzymes. We investigated whether mitochondrial acetylation in SKM could contribute to impaired fatty acid oxidation and exercise intolerance associated with HF. Methods and Results: MI was created in male C57BL/6J mice by ligating the left coronary artery (n = 7), and a sham operation was performed in other mice (n = 7). After 4 weeks, the work and peak oxygen uptake (VO2) was significantly reduced in MI mice compared to sham mice (work 11 ± 1 vs 23 ± 1 J; peak VO2 143 ± 5 vs 159 ± 3 mL·kg−1·min−1). Mitochondrial proteins that include TCA cycle enzymes, electron transport chain, and fatty acid β-oxidation enzymes such as enoyl-CoA hydratase and 3-ketoacyl-CoA thiolase were hyperacetylated in SKM from MI mice, in conjunction with a decrease in mitochondrial fatty acid respiratory capacity rates. In addition, metabolomic analysis revealed that plasma N6-acetyl-lysine level was increased in HF patients compared to controls (15.0 ± 3.2 × 10−5 vs 9.8 ± 2.4 × 10−5, P < .01) and negatively correlated with peak VO2 measured by cardiopulmonary exercise test (r2 = 0.52, P < .01). Conclusions: Mitochondrial acetylation is associated with impaired fatty acid oxidation and reduced exercise capacity in HF. These results provide a novel pathophysiological insight into the mechanism of exercise intolerance in HF.

P6-2 Clinical Utility of Reduced Heart Rate Recovery After Exercise in Elderly Patients With Chronic Heart Failure Kenichiro Okada1, Yasuji Doi2, Hiroshi Sawabe1, Akiya Sakatani1, Koichi Miyazaki1, Keiji Okuda1, Kiyoshi Kume1, Mayu Nishio1, Keiji Hirooka1, Toru Hayashi1; 1Division of Cardiology, Saiseikai Senri Hospital, Osaka, Japan; 2Health Administration Center, Takeda Pharmaceutical Company Limited, Osaka, Japan Background: Peak oxygen uptake (peak VO2) has been known to be a strong predictor of mortality. Reduced heart rate recovery (HRR) has also been shown to predict mortality. However, little is known about the significance of reduced HRR in elderly patients with chronic heart failure (CHF). Methods and Results: We evaluated 152 elderly patients with CHF (mean age 73 ± 5.4 years, 82% men) who in cardiac rehabilitation program and underwent cardiopulmonary exercise testing between April 2013 and March 2016. HRR1 was defined as the difference in heart rate between peak exercise and 1 minute later; a value less than or equal to 12 beats per minute was considered abnormal. All cause of death and hospitalization due to cardiovascular events were followed up as the primary end points (adverse events). Of 152 patients, 35 had an abnormal HRR1. Among patients with an abnormal HRR1, four were hospitalized. None of the patients with a normal HRR1 died or was hospitalized (P < .05). Multivariate analysis demonstrated that peak VO2 and an abnormal HRR1 were predictors of adverse events, suggesting importance of exercise capacity and cardiac parasympathetic activity. Conclusions: Reduced HRR1 could be a predictor of adverse events in elderly CHF patients who participated in cardiac rehabilitation.

P6-3 Exercise-Induced Pulmonary Arterial Wedge Pressure Elevation in Subjects Who Had SOB Unknown Reason Ayumi Goda, Kaori Takeuchi, Hanako Kikuchi, Takumi Inami, Toru Satoh, Hideaki Yoshino; Department of Cardiology, Kyorin Unversity Hospital, Tokyo, Japan Background: Exercise-induced elevation of pulmonary arterial wedge pressure (PAWP) may show preclinical or exercise-induced left ventricular diastolic dysfunction. The aim of this study was to compare the CPX parameters, that can be available noninvasively, between elevation and normal exercise PAWP in subjects with SOB unknown reason. Methods: Fourteen subjects who had SOB unknown reason (55 ± 14 y/o, 13 female, mean pulmonary arterial pressure (PAP) 16 mmHg, PAWP 8 mmHg) with normal PAWP (under 15 mmHg) at rest underwent symptom-limited exercise test using supine cycle ergometer with right heart catheter. Exercise-induced elevation in PAWP of more than 20 mmHg was defined as elevation group. Results: Among 14 subjects, exerciseinduced PAWP elevation was shown in 5 subjects. In the elevation group, age was tend to be older, δPAWP (after legs raise—rest) was higher (4.2 ± 4.6 vs 1.7 ± 4.1 mmHg) after legs raise approximately 30 degrees for cycle ergometer exercise. In the CPX parameters, peak oxygen consumption was tend to be lower (14.0 ± 8.1 vs 18.9 ± 7.7 mL·min−1·kg−1, and VE vs VCO2 slope (44.3 ± 22.9 vs 32.1 ± 7.6) was tend to be higher compared with in the non-elevation group. Conclusion: Exerciseinduced PAWP elevation is often seen in subjects who had SOB unknown reason, even if normal PAWP pressure at rest. Exercise intolerance and higher ventilator efficiency