The prognostic impact of the serum heart-type fatty acid-binding protein level in patients with sepsis who were admitted to the non-surgical intensive-care unit.

Ongoing myocardial damage at the acme of the sepsis status has not been sufficiently evaluated. The clinical data of 160 sepsis patients who require intensive care and 127 outpatients with chronic heart failure (HF) were compared as a retrospective cohort study. Thereafter, the sepsis patients were divided into 3 groups according to the serum heart-type fatty acid-binding protein (H-FABP) quartiles [low H-FABP = Q1 (n = 39), middle H-FABP = Q2/Q3 (n = 81), and high H-FABP = Q4 group (n = 40)]. The H-FABP level was measured within 15 min of admission. The serum H-FABP levels in the sepsis patients [26.6 (9.3-79.0) ng/ml] were significantly higher than in the choric HF patients [6.6 (4.6-9.7) ng/ml]. A Kaplan-Meier curve showed that the survival rate of the high-H-FABP group was significantly lower than that of the middle- and low-H-FABP groups. The multivariate Cox regression analysis for the 365-day mortality showed that the high-H-FABP group (hazard ratio: 6.544, 95% confidence interval [CI] 2.026-21.140; p = 0.002) was an independent predictor of the 365-day mortality. The same trend in the prognostic impact was significantly (p = 0.015) observed in the cohort that had not been suffering from the cardiac disease before admission. The serum H-FABP level was an independent predictor of the 365-day mortality in the patients who were emergently hospitalized in the intensive-care unit due to sepsis. Ongoing myocardial damage was detected in the majority of patients with sepsis, suggesting that ongoing myocardial damage might be a candidate predictor of adverse outcomes in sepsis patients.

Characteristics of Patients with an Abnormally Decreased Plasma Xanthine Oxidoreductase Activity in Acute Heart Failure Who Visited the Emergency Department.

BACKGROUND: The factors associated with a low plasma xanthine oxidoreductase (XOR) activity were not elucidated in patients with acute heart failure (AHF). METHODS: Two-hundred and twenty-nine AHF patients who visited the emergency department were prospectively analyzed. AHF patients were divided into 3 groups according to the plasma XOR quartiles (Q1 = low-XOR group [n = 57], Q2/Q3 = middle-XOR group [n = 115], and Q4 = high-XOR group [n = 57]). The prognostic nutritional index (PNI) and the controlling nutritional status (CONUT) score were evaluated. RESULTS: The multivariate logistic regression model showed that the nutritional status (PNI: OR 1.044, 95% CI 1.000-1.088; CONUT: OR 3.805, 95% CI 1.158-12.498), age, and serum creatinine level were independently associated with a low plasma XOR activity. The Kaplan-Meier curve showed a significantly lower incidence of heart failure events in the low-XOR group than in the middle + high-XOR group (hazard ratio, HR 1.648, 95% CI 1.061-2.559). In particular, a low XOR activity with an increased serum creatinine level (>1.21 mg/dL) was independently associated with heart failure events (HR 1.937, 95% CI 1.199-3.130). CONCLUSION: A low plasma XOR activity was associated with malnutrition, renal dysfunction, and aging in AHF. A low XOR activity complicated with renal dysfunction leads to adverse long-term outcomes.

Plasma xanthine oxidoreductase (XOR) activity in patients who require cardiovascular intensive care.

Hyperuricemia is known to be associated with adverse outcomes in cardiovascular intensive care patients, but its mechanisms are unknown. A total of 569 emergency department patients were prospectively analyzed and assigned to intensive care (ICU group, n = 431) or other departments (n = 138). Uric acid (UA) levels were significantly higher in the intensive care patients (6.3 [5.1-7.6] mg/dl vs. 5.8 [4.6-6.8] mg/dL). The plasma xanthine oxidoreductase (XOR) activity in the ICU group (68.3 [21.2-359.5] pmol/h/mL) was also significantly higher than that in other departments (37.2 [15.1-93.6] pmol/h/mL). Intensive care patients were divided into three groups according to plasma XOR quartiles (Q1, low-XOR, Q2/Q3, normal-XOR, and Q4, high-XOR group). A multivariate logistic regression model showed that lactate (per 1.0 mmol/L increase, OR 1.326; 95%, CI 1.166-1.508, p < 0.001) and the Acute Physiology and Chronic Health Evaluation II score (per 1.0 point increase, OR 1.095, 95% CI 1.034-1.160, p = 0.002) were independently associated with the high-XOR group. In-hospital mortality was significantly higher in the high-XOR group (n = 28, 26.2%) than in the normal- (n = 11, 5.1%) and low- (n = 9, 8.3%) XOR groups. The high-XOR group (vs. normal-XOR group) was independently associated with the in-hospital mortality (OR 2.934; 95% CI 1.170-7.358; p = 0.022). Serum UA levels and plasma XOR activity were high in patients admitted to intensive care. The enhanced XOR activity may be one of the mechanisms under which hyperuricemia was associated with adverse outcomes in patients requiring cardiovascular intensive care.

Mechanisms of Urgently Presenting Acute Heart Failure.

The mechanisms of urgently presenting acute heart failure (AHF) are not clear. We evaluated the serum catecholamine values of AHF patients immediately after admission. A total of 1,475 AHF patients were screened, and 484 who were admitted from their homes and in whom serum catecholamine could be evaluated immediately after admission were analyzed. The patients were divided into three groups according to the time interval from the onset of symptoms to admission (OA): < 3 hours (early-OA group; n = 283), 3-24 hours (middle-OA group; n = 142), and ≥24 hours (late-OA group; n = 59). In the early-OA group, the systolic blood pressure (SBP) was significantly higher, orthopnea was more frequent, the pH value was significantly decreased, and the use of noninvasive positive-pressure ventilation was required significantly more often than in the other groups. The serum noradrenaline level was significantly increased in the early-OA group (1.96 [1.02-3.60] ng/mL) than in the middle-OA (1.49 [0.73-3.41] ng/mL) and late-OA (1.40 [0.91-2.42] ng/mL) groups, and the adrenaline level was significantly increased in the early-OA group (0.36 [0.13-1.17] ng/mL) than in the late-OA (0.22 [0.09-0.52] ng/mL) group. A multivariate logistic regression model indicated the early-OA group was independently associated with the SBP > 140 mmHg (odds ratio [OR]: 2.219, 95% CI: 1.375-3.581), midnight/early morning admission (OR: 3.158, 95% CI: 2.048-4.868), and high serum catecholamine value (adrenaline > 0.96 ng/mL, noradrenaline > 3.39 ng/mL, and dopamine > 0.21 ng/mL) (OR 2.091, 95% CI: 1.161-3.767). In conclusion, urgently presented AHF might be induced by an endogenous catecholamine surge, which causes an excessive rise in blood pressure leading to increased after-overload and volume-shift lung congestion.

Features and Outcomes of Patients with Calcified Nodules at Culprit Lesions of Acute Coronary Syndrome: An Optical Coherence Tomography Study.

OBJECTIVES: We sought to clarify clinical features and outcomes related to calcified nodules (CN) compared with plaque rupture (PR) and plaque erosion (PE) detected by optical coherence tomography (OCT) at the culprit lesions in patients with acute coronary syndrome (ACS). METHODS: Based on OCT findings for culprit lesion plaque morphologies, ACS patients with analyzable OCT images (n = 362) were classified as CN, PR, PE, and other. RESULTS: The prevalence of CN, PR, and PE was 6% (n = 21), 45% (n = 163), and 41% (n = 149), respectively. Patients with CN were older (median 71 vs. 65 years, p = 0.03) and more diabetic (71 vs. 35%, p = 0.002) than those without CN. In OCT findings, the distal reference lumen cross-sectional area (median 4.2 vs. 5.2 mm2, p = 0.048) and the postintervention minimum lumen cross-sectional area (median 4.5 vs. 5.3 mm2, p = 0.04) were smaller in lesions with CN than in those without. Kaplan-Meier estimate survival curves showed that the 500-day survival without target lesion revascularization (TLR) was lower (p = 0.011) for patients with CN (72.9%) than for those with PR (89.3%) or PE (94.8%). CONCLUSIONS: ACS patients with CN at the culprit lesion had more TLR compared to those with PR or PE.

The prognostic impact of malnutrition in patients with severely decompensated acute heart failure, as assessed using the Prognostic Nutritional Index (PNI) and Controlling Nutritional Status (CONUT) score.

Patients with heart failure (HF) are sometimes classified as malnourished, but the prognostic value of nutritional status in acute HF (AHF) remains largely unstudied. 1214 patients who were admitted to the intensive care unit between January 2000 and June 2016 were screened based on their serum albumin, lymphocyte count, and total cholesterol measures. A total of 458 HF patients were enrolled in this study. The Prognostic Nutritional Index (PNI) is calculated as 10 × serum albumin (g/dL) + 0.005 × lymphocyte count (per mm3) (lower = worse). The Controlling Nutritional Status (CONUT) score is points based, and is calculated using serum albumin, total cholesterol, and lymphocyte count (range 0-12, higher = worse). Patients were divided into three groups according to PNI: high-PNI (PNI < 35, n = 331), middle-PNI (35 ≤ PNI < 38, n = 50), and low-PNI (PNI ≥ 38, n = 77). They were also divided into four groups according to CONUT score: normal-CONUT (0-1, n = 128), mild-CONUT (2-4, n = 179), moderate-CONUT (5-8, n = 127), and severe-CONUT (≥9, n = 24). The PNI, which exhibited a good balance between sensitivity and specificity for predicting in-hospital mortality [66.1 and 68.4%, respectively; area under the curve (AUC) 0.716; 95% confidence interval (CI) 0.638-0.793), was 39.7 overall, while the CONUT score was 5 overall (61.4 and 68.4%, respectively; AUC 0.697; 95% CI 0.618-0.775). A Kaplan-Meier curve indicated that the prognosis, including all-cause death, was significantly (p < 0.001) poorer in low-PNI patients than in high-PNI groups and was also significantly poorer in severe-CONUT patients than in normal-CONUT and mild-CONUT groups. A multivariate Cox regression model showed that the low-PNI and severe-CONUT categories were independent predictors of 365-day mortality [hazard ratio (HR) 2.060, 95% CI 1.302-3.259 and HR 2.238, 95% CI 1.050-4.772, respectively). Malnutrition, as assessed using both the PNI and the CONUT score, has a prognostic impact in patients with severely decompensated AHF.

Prognostic benefit of maintaining the hemoglobin level during the acute phase in patients with severely decompensated acute heart failure.

The optimum method of managing anemia during the acute phase of acute heart failure (AHF) remains to be elucidated. The data from 1109 AHF patients were enrolled in present study. The hemoglobin (Hb) levels were evaluated in all patients at admission (day 1) and 3 days after admission (day 3), and in survival discharge patients (n = 998) before discharge (pre-discharge). The serum hemoglobin levels were significantly lower on day 3 (11.2 (9.6-12.9) g/dl) than on day 1 (12.4 (10.4-14.2) g/dl) and at pre-discharge (11.6 (10.1-13.2) g/dl). A multivariate Cox regression model showed that mild anemia (11.0 ≤ Hb ≤ 12.9 g/dl, n = 316) and severe anemia (Hb ≤ 10.9 g/dl, n = 517) on day 3 were independent predictors of HF event (hazard ratio (HR) 1.542, 95% confidence interval (CI)1.070-2.221, HR 2.026, 95% CI 1.439-2.853), and severe anemia on day 3 were independent predictors of 365-day mortality (HR 2.247, 95% CI 1.376-3.670). The prognosis, including all-cause death and HF events, in patients with non-anemia on day 1 was significantly poorer in severe new-anemia patients on day 3 (n = 44) than in mild new-anemia patients on day 3 (n = 153) and non-anemia patients on day 3 (n = 252). In patients with anemia on day 1, the prognosis was significantly poorer in patients with severe anemia on day 3 (n = 190) than in those with non-anemia or mild anemia on day 3 (n = 482). The hemoglobin level after the initial treatment might be easily influenced by clinical decongestion. Successfully treated decongestion can help maintain the hemoglobin levels. It, therefore, leads to a prognostic benefit in patients with AHF. These findings might underscore the importance of hemoglobin management of the acute phase of AHF.

Prognostic benefit of acute heart failure associated with atherosclerosis: the importance of prehospital medication in patients with severely decompensated acute heart failure.

Atherosclerotic diseases sometimes contribute to acute heart failure (AHF). The aim of the present study is to elucidate the prognostic impact of AHF with atherosclerosis. A total of 1226 AHF patients admitted to the intensive care unit were analyzed. AHF associated with atherosclerosis was defined by the etiology: atherosclerosis-AHF group (n = 708) (patients whose etiologies were ischemic heart disease or hypertensive heart disease) or AHF not associated with atherosclerosis (non-atherosclerosis-AHF) group (n = 518). Kaplan-Meier curves showed that the survival rate of the atherosclerosis-AHF group was significantly better than that of the non-atherosclerosis-AHF group within 730 days of follow-up. Regarding pre-hospital medications, atherosclerosis-AHF patients were more likely to be administered nitroglycerin (20.3 vs. 13.7%, p = 0.003), nicorandil (18.8 vs. 7.5%, p < 0.001), angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II receptor blocker (ARB) (46.5 vs. 38.6%, p = 0.006), ß-blocker (33.2 vs. 26.6%, p = 0.014) and statin (30.1 vs. 22.4%, p = 0.003) because of a previous coronary event or atherosclerotic diseases. In sub-group analysis of medication including administered ≥ 3 drugs within 5 medications and ACE-I/ARB, atherosclerosis-AHF significantly decreased the rate of all-cause death within 180 days (hazard ratio (HR) 0.215, 95% CI 0.078-0.593 and HR 0.395, 95% CI 0.244-0.641, respectively) with a significant interaction (p value for interaction 0.022 and 0.005, respectively). Kaplan-Meier curves showed that the 180-days survival rate of the atherosclerosis-AHF group with ACE-I/ARB and ≥ 3 drugs were significantly better than other groups. The AHF patients associated with atherosclerosis lead to be a good long-term outcome. A relationship may exist between efficient treatment including ACE-Is before admission and a good outcome in mid-term.

Decreased blood glucose at admission has a prognostic impact in patients with severely decompensated acute heart failure complicated with diabetes mellitus.

The prognostic impact of a decreased blood glucose level in acute heart failure (AHF) has not been sufficiently clarified. The data from 1234 AHF patients were examined in the present study. The blood glucose (BG) levels were evaluated at admission. The patients were divided into groups based on the following: with or without diabetes mellitus (DM), and BG level ≥ 200 mg/dl (elevated BG) or < 200 mg/dl (decreased BG). The elevated and decreased BG patients were further divided into another three groups: 200 mg/ml ≤ BG < 300 mg/dl (mild-elevated), 300 mg/ml ≤ BG < 400 mg/dl (moderate-elevated) and BG ≥ 400 mg/ml (severe-elevated); and 150 mg/ml ≤ BG < 200 mg/dl (mild-decreased), 100 mg/ml ≤ BG < 150 mg/dl (moderate-decreased) and BG < 100 mg/ml (severe-decreased), respectively. The DM patients had a significantly poorer mortality than the non-DM patients. The prognosis was different between patients with elevated or decreased BG. In DM patients with elevated BG, the severe-elevated patients had a significantly poorer prognosis than moderate- and mild-elevated patients. In the DM patients with decreased BG, the severe-decreased patients had a significantly poorer prognosis than those moderate- and mild-decreased patients. The multivariate Cox regression model showed that a severe-decreased [hazard ratio (HR) 3.245, 95% confidence interval (CI) 1.271-8.282] and severe-elevated (HR 2.300, 95% CI 1.143-4.628) status were independent predictors of 365-day mortality in AHF patients with DM. The mortality was high among AHF patients with DM. Furthermore, both severe hyperglycemia and hypoglycemia were independent predictors of the mortality in patients with AHF complicated with DM.

Are atherosclerotic risk factors associated with a poor prognosis in patients with hyperuricemic acute heart failure? The evaluation of the causal dependence of acute heart failure and hyperuricemia.

Atherosclerosis induces the elevation of uric acid (UA), and an elevated UA level is well known to lead to a poor prognosis in patients with acute heart failure (AHF). However, the prognostic value of atherosclerotic risk factors in hyperuricemic AHF patients remains to be elucidated. The data from 928 patients who were admitted to the intensive care unit (ICU) at Nippon Medical School Chiba Hokusoh Hospital between January 2001 and December 2014, and whose serum UA levels were measured were screened. A total of 394 AHF patients with hyperuricemia were enrolled in this study. The patients were assigned to a low-risk group (≤1 atherosclerosis risk factor) and a high-risk group (≥2 atherosclerosis risk factors) according to their number of risk factors. The patients in the low-risk group were more likely to have dilated cardiomyopathy, clinical scenario 3 than those in the high-risk group. The serum total bilirubin, blood urea nitrogen, C-reactive protein, and brain-type natriuretic peptide levels were significantly higher in the low-risk group than the high-risk group (p < 0.001, p = 0.005, p = 0.003, and p = 0.008, respectively). A multivariate Cox regression model revealed that the number of risk factors (number = 1, HR (hazard ratio) 0.243, 95 % CI 0.096-0.618, p = 0.003; number = 2, HR 0.253, 95 % CI 0.108-0.593, p = 0.002; number ≥3, HR 0.209, 95 % CI 0.093-0.472, p < 0.001), eGFR (per 1.0 mmol/l increase) (HR 0.977, 95 % CI 0.961-0.994, p = 0.007), and serum UA level (per 1 mg/dl increase) (HR 1.270, 95 % CI 1.123-1.435, p < 0.001) was an independent predictor of 1-year mortality. The prognosis, including all-cause death and HF events, was significantly poorer among the low-risk patients than among the high-risk patients. Atherosclerotic risk factors were not associated with a poor prognosis in patients with hyperuricemic AHF.

Association between the body mass index and the clinical findings in patients with acute heart failure: evaluation of the obesity paradox in patients with severely decompensated acute heart failure.

Obesity is known to be associated with the development of heart failure (HF). However, the relationship between the body mass index (BMI) and acute HF (AHF) remains to be elucidated. Eight hundred and eight AHF patients were enrolled in this study. The patients were assigned to four groups according to their BMI values: severely thin (n = 11, BMI <16), normal/underweight (n = 579, 16 ≤ BMI <25), overweight (n = 178, 25 ≤ BMI <30) and obese (n = 40, BMI ≥30). The patients in the severely thin group were more likely to be female, have systolic blood pressure (SBP) <100 mmHg and have valvular disease than normal/underweight patients. The patients in the overweight group were significantly younger than those in the normal/underweight, and those in the overweight group were more likely to have SBP ≥140 mmHg and hypertensive heart disease and less likely to have valvular disease than the patients in the normal/underweight group. The prognosis, including all-cause death, was significantly poorer among patients who were severely thin than those who were normal/underweight, overweight and significantly better among those who were overweight than those who were normal/underweight, severely thin and obese patients. A multivariate Cox regression model identified that severely thin [HR: 3.372, 95% confidence interval (CI) 1.362-8.351] and overweight (HR: 0.615, 95% CI 0.391-0.966) were independent predictors of 910-day mortality as the reference of normal/underweight. Overweight patients tended to have SBP ≥140 mmHg and be relatively young, while severely thin patients tended to have SBP <100 mmHg and be female. These factors were associated with a better prognosis of overweight patients and adverse outcomes in severely thin patients. These factors may contribute to the "obesity paradox" in severely decompensated AHF patients.

Matrix Metalloproteinase-9 as a Marker for Plaque Rupture and a Predictor of Adverse Clinical Outcome in Patients with Acute Coronary Syndrome: An Optical Coherence Tomography Study.

OBJECTIVES: The present study sought to clarify the relationship between matrix metalloproteinase-9 (MMP-9) levels and plaque morphology demonstrated by optical coherence tomography (OCT), and to examine their prognostic impacts in patients with acute coronary syndrome (ACS). METHODS: MMP-9 levels were measured for patients with ACS (n = 249). Among 249 patients, 120 with evaluable OCT images were categorized into patients with ruptured plaques (n = 65) and those with nonruptured plaques (n = 55) on the basis of culprit lesion plaque morphology demonstrated by OCT. RESULTS: MMP-9 levels on admission were significantly higher in the rupture group than in the nonrupture group (p = 0.029). Although creatine kinase-MB (CK-MB) on admission was comparable between the groups, peak CK-MB was higher in the rupture group than in the nonrupture group (p < 0.001). By receiver operating characteristic curve analysis, the optimal cut-off value of MMP-9 to detect ruptured plaques was 65.5 ng/ml (p = 0.029). There was a nonstatistically significant trend toward increased cardiac death at 2 years (5.9 vs. 1.0%, p = 0.059) in patients with high MMP-9 (≥65.5 ng/ml) compared to those with low MMP-9 (<65.5 ng/ml). CONCLUSIONS: MMP-9 can differentiate ACS with ruptured plaques from nonruptured plaques, and MMP-9 may be a valuable predictor of long-term cardiac mortality in patients with ACS reflecting plaque rupture.

The serum heart-type fatty acid-binding protein (HFABP) levels can be used to detect the presence of acute kidney injury on admission in patients admitted to the non-surgical intensive care unit.

BACKGROUND: No cardiac biomarkers for detecting acute kidney injury (AKI) on admission in non-surgical intensive care patients have been reported. The aim of the present study is to elucidate the role of cardiac biomarkers for quickly identifying the presence of AKI on admission. METHODS: Data for 1183 patients who underwent the measurement of cardiac biomarkers, including the serum heart-type fatty acid-binding protein (s-HFABP) level, in the emergency department were screened, and 494 non-surgical intensive care patients were enrolled in this study. Based on the RIFLE classification, which was the ratio of the serum creatinine value recorded on admission to the baseline creatinine value, the patients were assigned to a no-AKI (n = 349) or AKI (Class R [n = 83], Class I [n = 36] and Class F [n = 26]) group on admission. We evaluated the diagnostic value of the s-H-FABP level for detecting AKI and Class I/F. The mid-term prognosis, as all-cause death within 180 days, was also evaluated. RESULTS: The s-H-FABP levels were significantly higher in the Class F (79.2 [29.9 to 200.3] ng/mL) than in the Class I (41.5 [16.7 to 71.6] ng/mL), the Class R (21.1 [10.2 to 47.9] ng/mL), and no-AKI patients (8.8 [5.4 to 17.7] ng/mL). The most predictive values for detecting AKI were Q2 (odds ratio [OR]: 3.743; 95 % confidence interval [CI]: 1.693-8.274), Q3 (OR: 9.427; 95 % CI: 4.124-21.548), and Q4 (OR: 28.000; 95 % CI: 11.245-69.720), while those for Class I/F were Q3 (OR: 5.155; 95 % CI: 1.030-25.790) and Q4 (OR: 22.978; 95 % CI: 4.814-109.668). The s-HFABP level demonstrating an optimal balance between sensitivity and specificity (70.3 and 72.8 %, respectively; area under the curve: 0.774; 95 % CI: 0.728-0.819) was 15.7 ng/mL for AKI and 20.7 ng/mL for Class I/F (71.0 and 83.1 %, respectively; area under the curve: 0.818; 95 % CI: 0.763-0.873). The prognosis was significantly poorer in the high serum HFABP with AKI group than in the other groups. CONCLUSIONS: The s-H-FABP level is an effective biomarker for detecting AKI in non-surgical intensive care patients.

JAK2 mutation and acute coronary syndrome complicated with stent thrombosis.

Acute coronary syndrome (ACS) could be a precious opportunity for patients to reveal concealed diseases other than conventional risk factors for ACS, such as hypertension, dyslipidemia, diabetes mellitus, etc. In the setting of ACS, the intracoronary and systemic prothrombotic environment has led to an increase in the risk of stent thrombosis of which mortality was higher among patients with ACS, especially with the highest mortality in patients with ST elevation myocardial infarction. The some specific conditions which were concealed beyond the cardiovascular pathophysiology except well-known risk factors for ACS and stent thrombosis might involve the onset of ACS. We describe a case of a 64-year-old man who was admitted to intensive care unit for chest pain. This case found the possibility that polycythemia vera with Janus kinase 2 (JAK2) V617F mutation might be a underlying disease of ACS with stent thrombosis, and highlighted the importance of recognizing polycythemia vera with JAK2 V617F mutation as concealed disease for cardiologists. We would like to report and review the relationship between ACS and polycythemia vera with JAK2 V617F mutation.

Preventable effects of bare-metal stent on restenosis after everolimus-eluting stent deployment.

This case report describes a patient who underwent implantation of a bare-metal stent (BMS) for the treatment of everolimus-eluting stent (EES) restenosis caused by chronic stent recoil, and the BMS successfully escaped from duplicate restenosis and target lesion revascularization (TLR).

Different characteristics of cardiac biomarkers to decide and predict the culprit lesions in patients with suspicious acute coronary syndrome.

This multicenter prospective study was conducted to assess high-sensitivity troponin T (hs-TnT) and other biomarkers to decide and predict culprit lesions indicated for emergency percutaneous coronary intervention (PCI) in patients with suspicious acute coronary syndrome (ACS). We have reported Hs-TnT is the most sensitive biomarker for earlier diagnosis and decision making in patients with suspected ACS. In this study, we had conducted subanalysis investigating the usefulness for prediction of ACS culprit lesion. The patients with suspicious ACS and initially negative whole-blood rapid troponin T test, who underwent coronary angiogram (CAG), were enrolled (n = 74). Hs-TnT, quantitative assay for conventional troponin T (c-TnT), creatine kinase MB isozyme (CK-MB), and heart-type fatty acid-binding protein (H-FABP) were simultaneously measured. ACS culprit lesion was described as total occlusion, subtotal occlusion, and/or angiographical unstable lesion such as thrombosis, ulceration or irregularity. The CAG revealed that 49 cases had ACS lesions to be indicated for emergency PCI. The areas under the ROC curves and ROC-optimized cut-off of hs-TnT, c-TnT, CK-MB, and H-FABP were 0.75, 0.67, 0.68, and 0.75, respectively, and 18, 11, 2.0, and 4.6 ng/ml, respectively. In patients with total occlusion and 90-99 % of diameter stenosis (TIMI 2 or 3), hs-TnT could predict emergency PCI with significantly higher sensitivity compared with H-FABP (hs-TnT >14 ng/ml; 71 %, and H-FABP >6.2 ng/dl; 51 %, p = 0.021) and other biomarkers. Meanwhile, H-FABP displayed significant correlations with number of diseased vessels and presence of thrombotic lesion. The present study first revealed different characteristics of correlation between the angiographic culprit lesions and each cardiac biomarker. For prediction of ACS lesions requiring emergency PCI, hs-TnT had the highest sensitivity with satisfied analytical precision.

Blunted renal vasoconstriction in patients with subclinical contrast-induced renal injury.

Contrast media are considered to cause acute kidney injury by activating various factors that induce renal vasoconstriction. We analysed the renal microvascular haemodynamic response using the Doppler flow wire method. Then changes in urinary liver-type fatty acid-binding protein levels following contrast medium administration were compared between groups with or without a micro-injury of the kidney. In the group without renal micro-injury, the average peak velocity (APV) decreased significantly, whereas the renal artery resistance index (RI) increased significantly following contrast medium administration. In contrast, there was no significant change in either the APV or RI in the group with a renal micro-injury. A blunted microvascular response was found in the micro-injury group, whereas microvascular resistance increased in the non-micro-injury group.

Geographical predisposition influences on the distribution and tissue characterisation of eccentric coronary plaques in non-branching coronary arteries: cross-sectional study of coronary plaques analysed by intravascular ultrasound.

BACKGROUND: We investigated the influence of geographical predisposition on the spatial distribution and composition of coronary plaques. METHODS: Thirty coronary arteries were evaluated. A total of 1441 cross-sections were collected from intravascular ultrasound (IVUS) and radio-frequency signal-based virtual histology (VH-IVUS) imaging. To exclude complex geographical effects of side branches and to localise the plaque distribution, we analysed only eccentric plaques in non-branching regions. The spatial distribution of eccentric plaques in the coronary artery was classified into myocardial, lateral, and epicardial regions. The composition of eccentric plaques was analysed using VH-IVUS. RESULTS: The plaque was concentric in 723 sections (50.2%) and eccentric in 718 (49.9%). Eccentric plaques were more frequently distributed towards the myocardial side than towards the epicardial side (46.7 ± 7.5% vs. 12.5 ± 4.2%, p = 0.003). No significant difference was observed between the myocardial and lateral sides (46.7 ± 7.5% vs. 20.8 ± 5.0%) or between the lateral and epicardial sides. Eccentric thin-capped fibroatheromas were more frequently distributed towards the myocardial side than towards the lateral side (p = 0.024) or epicardial side (p = 0.005). CONCLUSION: Geographical predisposition is associated with distribution, tissue characterisation, and vulnerability of plaques in non-branching coronary arteries.

Serum heart-type fatty acid-binding protein level can be used to detect acute kidney injury on admission and predict an adverse outcome in patients with acute heart failure.

BACKGROUND: Different mechanisms of acute kidney injury (AKI) may exist for acute heart failure (AHF) patients compared with other patients. METHODS AND RESULTS: We analyzed data from 282 patients with AHF. The biomarkers were measured within 30 min of admission. Patients were assigned to a no-AKI (n=213) or AKI group (Class R (n=49), Class I (n=15) or Class F (n=5)) using the RIFLE classifications on admission. We evaluated the relationships between the biomarkers and AKI, in-hospital mortality, all-cause death and HF events (HF re-admission, all-cause death) within 90 days. The serum heart-type fatty acid-binding protein (s-HFABP) levels were significantly higher in the AKI than in the no-AKI group, and the predictive biomarker for AKI was s-HFABP (odds ratio: 6.709; 95% confidence interval: 3.362-13.391). s-HFABP demonstrated an optimal balance between sensitivity and specificity (71.0%, 79.3%; area under the receiver-operating characteristic curve [AUC]=0.790) at 22.8 ng/ml for AKI, at 22.8 ng/ml for Class I/F (90.0%, 71.4%; AUC=0.836) and at 21.0 ng/ml for in-hospital mortality (74.3%, 70.0%; AUC=0.726). The Kaplan-Meier survival curves showed a significantly poorer prognosis in the high s-HFABP group (≥22.9 ng/ml) than in other groups. CONCLUSIONS: The s-HFABP level can indicate AKI on admission, and a high s-HFABP level is associated with a poorer prognosis for AHF patients.

Seasonal variation in patients with acute heart failure: prognostic impact of admission in the summer.

There have been few reports discussing the clinical significance of the season of admission of acute heart failure (AHF) patients. The data of 661 patients with AHF admitted to the intensive care unit were analyzed. Patients were assigned to a summer admission (Group-S, n = 113, between July and September), a winter admission (Group-W, n = 214, between December and February), or to the other seasons admission group (Group-O, n = 334). We evaluated the relationships between the seasonal variations and the clinical profiles, and the long-term prognosis. There were significantly more patients with cardiomyopathy and New York Heart Association class 4, and the serum levels of total bilirubin were significantly higher in Group-S (85.8, 24.8 %, and 0.60 [0.50-0.90]) than in Group-W (75.2, 15.4 %, and 0.60 [0.40-0.78]). The left ventricular ejection fraction on admission was significantly reduced and intravenous administration of dobutamine was used more frequently in Group-S (30.0 [25.0-46.0], 31.9 %) than in Group-W (34.4 [25.2-48.0], 20.6 %) and Group-O (35.0 [25.0-46.0], 19.8 %). The multivariate Cox regression model found that summer admission was independently associated with cardiovascular death (HR: 1.58, 95 % CI 1.01-2.48; p = 0.044) and heart failure (HF) events (HR: 1.55, 95 % CI 1.05-2.28; p = 0.028). The Kaplan-Meier curves showed that the cardiovascular death rate was significantly higher in Group-S than in Group-W and Group-O, and the HF events were significantly higher in Group-S than in Group-O. The summer admission AHF patients included sicker patients, and the prognosis in these patients was worse than in the patients admitted at other times.