Neutrophil gelatinase-associated lipocalin (NGAL) for the early detection of contrast-induced nephropathy after percutaneous coronary intervention.

BACKGROUND: Contrast-induced acute kidney injury (CI-AKI) occurs in up to 13% of patients undergoing percutaneous coronary intervention (PCI). Neutrophil gelatinase-associated lipocalin (NGAL) is an early biomarker for renal impairment. We investigated whether increased urinary NGAL concentrations were predictive of CI-AKI within 2 days after PCI or of a higher re-hospitalization rate within 9 months. METHODS: Consecutive patients (n = 128), with stable coronary heart disease and eGFR ≥ 30 mL/min/1.73 m(2), undergoing PCI were included. Venous serum samples for measurement of creatinine, blood urea nitrogen, and cystatin C and urine samples for NGAL measurement were collected 4 hours and 1 and 2 days after contrast medium application. Patients were followed over 9 months to determine clinical endpoints. RESULTS: CI-AKI was observed in 14 patients (10.9%) after PCI. NGAL concentrations before PCI were significantly higher in patients with subsequent CI-AKI (19.8 ng/mL [14.4-35.8] vs. 11.6 ng/mL [5.6-28.2]; p = 0.04). There was no significant difference in NGAL concentrations 4 h after PCI between patients with and without CI-AKI. One day after PCI, NGAL concentrations were significant higher in patients developing CI-AKI (100.1 ng/mL [41.5-129.2] vs. 16.6 ng/mL [9.1-28.1]; p < 0.001). Compared to common biomarkers, NGAL best predicted CI-AKI (AUC 0.939 [95% CI 0.89-0.99; p < 0.001]). The re-hospitalization rate due to progressive renal insufficiency within 9 months was higher in the group with CI-AKI than the group without (4 [28.6%] vs. 4 [3.5%], p < 0.01). CONCLUSION: Urinary NGAL is a biomarker for predicting CI-AKI when measured 1 day after PCI.

Release kinetics of copeptin in patients undergoing transcoronary ablation of septal hypertrophy.

BACKGROUND: The release kinetics of copeptin in patients with acute myocardial infarction (AMI) have been difficult to establish. METHODS: We analyzed the release kinetics of copeptin in patients with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH) as a model of AMI. We included 21 consecutive patients who underwent TASH. Blood samples were collected before and at 15, 30, 45, 60, 75, 90, and 105 min, and at 2, 4, 8, and 24 h after TASH. Serum copeptin was quantified by a sandwich immunoluminometric assay. RESULTS: All patients had copeptin concentrations below the 99th percentile at baseline. The median copeptin concentration was significantly increased at 30 min [16.0 pmol/L; interquartile range (IQR), 13.4-20.2 pmol/L], compared with the median baseline concentration (6.6 pmol/L; IQR, 5.3-8.3 pmol/L; P = 0.002). The copeptin concentration peaked 90 min after induction of myocardial infarction and returned to baseline concentrations (median, 8.2 pmol/L; IQR, 6.3-10.1) after 24 h, compared with the above baseline values (P = 0.06). Serum creatine kinase (CK) activities were significantly increased above baseline values by 1 day after TASH [median maximal postprocedural CK activity, 935.0 U/L (IQR, 545.5-1115.0 U/L); median baseline CK activity, 80.0 U/L (IQR, 63.5-109.0 U/L); P < 0.001]. CONCLUSIONS: Our results provide additional evidence that early rule-out of suspected AMI is possible by using the copeptin concentration in combination with cardiac troponin T.

Influence of renal sympathetic denervation on quality of life.

BACKGROUND: Therapy-resistant arterial hypertension causing psychosocial stress and is associated with cardiovascular morbidity and mortality. The aim of the study was to evaluate the effect on quality of life (QoL) in patients with resistant hypertension undergoing renal sympathetic denervation (RSD). METHODS AND RESULTS: We analyzed responses to the SF-36 Quality of Life Questionnaire provided by patients with resistant arterial hypertension after RSD. Thirty consecutive patients from 2 centers were included in this study, from October 2011 until February 2012. The phone interview was performed after the 3-month follow-up. A significant reduction (26 ± 13.5 mmHg) in systolic blood pressure (BP) was detected at the 3-month follow-up (142.0 ± 15.1 mmHg vs 168.0 ± 13.7 mmHg; P < 0.001). Seventy-five percent of the patients indicated that their health situation was a lot better (better, 21%; equal to, 4%) 3 months after RSD compared to the time before the therapeutic procedure. Furthermore, the majority of patients felt full of pep (always, 29%; mostly, 58%; quite often, 8%; sometimes, 4%), and full of energy (always, 25%; mostly, 54%; quite often, 16.7%; sometimes, 4.2%) after the procedure. Recipients of RSD indicated that they felt more light and healthy, and nearly all recipients (93%) described a loss of anxiety and indisposition. CONCLUSIONS: This investigation revealed that sufficient BP reduction by RSD and time following therapeutic success lead to significant improvements in patient QoL.

Mechanisms of stress (takotsubo) cardiomyopathy.

Stress cardiomyopathy is a form of reversible systolic dysfunction of the mid and apical left ventricle with pathologic changes of the electrocardiogram in the absence of an obstructive coronary artery disease. The prevalence of stress cardiomyopathy among patients with symptoms suggestive of myocardial infarction is 0.7% to 2.5%, and it is found predominantly in postmenopausal women (90%). No large studies have confirmed the cause of stress cardiomyopathy. Published data suggest that substantially elevated plasma catecholamine levels, due to emotional or physical stress, may be relevant.

Release kinetics of cardiac biomarkers in patients undergoing transcoronary ablation of septal hypertrophy.

BACKGROUND: The release kinetics of cardiac troponin T measured with conventional vs high-sensitivity cardiac troponin T (hs-cTnT) assays in patients with acute myocardial infarction (AMI) is difficult to establish. METHODS: We analyzed the release kinetics of cTnT measured by fourth generation and high-sensitivity assays, creatine kinase-MB (CK-MB), and myoglobin in patients with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy (TASH), a model of AMI. Consecutive patients (n = 21) undergoing TASH were included. Serum and EDTA-plasma samples were collected before and at 15, 30, 45, 60, 75, 90, and 105 min, and 2, 4, 8, and 24 h after TASH. RESULTS: cTnT concentrations measured by the hs assay were significantly increased at 15 min [21.4 ng/L, interquartile range (IQR) 13.3-39.7 ng/L vs 11.3 ng/L, IQR 6.0-18.8 ng/L at baseline; P = 0.031]. In comparison, cTnT concentrations measured by the conventional fourth generation assay increased significantly at 60 min (30.0 ng/L, IQR 20.0-30.0 ng/L vs <10.0 ng/L, IQR <10.0-10.0 ng/L; P < 0.01), CK-MB at 90 min (8.4 µg/L, IQR 6.9-14.4 µg/L vs 0.9 µg/L, IQR 0.4-1.1 µg/L; P < 0.01), and myoglobin at 30 min (188.0 µg/L, IQR 154.0-233.0 µg/L vs 38.0 µg/L, IQR 28.0-56.0; P < 0.01). CONCLUSIONS: cTnT concentrations measured by the hs assay were significantly increased after TASH at all of the time points, with a doubling at 15 min after induction of AMI, confirming earlier evidence of myocardial injury compared to the fourth generation cTnT assay and CK-MB and myoglobin.

Mobile left ventricular thrombus in left ventricular dysfunction: case report and review of literature.

INTRODUCTION: Left ventricular (LV) thrombi carry a high risk of embolization. Therapeutic recommendations like treatment with low molecular heparin and intravenous unfractionated heparin (UFH), thrombolysis or surgical thrombectomy have failed to reach a consensus. CASE DESCRIPTION: A 56-year-old female patient presented in cardiogenic shock to the emergency department. Echocardiography demonstrated a dilated LV with a severely depressed global systolic function and a large LV apical thrombus. Treatment with UFH was initiated as well as a treatment with catecholamines for stabilizing the patient's hemodynamic situation. On the follow-up echocardiographic examination, extensive free-floating parts of the thrombus could be documented. Given the high risk of embolization in a now hemodynamically stable situation, emergency surgical embolectomy was performed. DISCUSSION: A conservative procedure might be useful for bridging till surgical treatment is available and/or the risk due to surgery is acceptable. CONCLUSION: In absence of evidence-based guidelines for the treatment of LV thrombi, individualized management options concerning surgical, embolization and bleeding risk must be taken into account.

Door-to-implantation time of extracorporeal life support systems predicts mortality in patients with out-of-hospital cardiac arrest.

OBJECTIVE: This study aimed to identify predictors of mortality in patients with out-of-hospital cardiac arrest (OHCA) undergoing in-hospital extracorporeal life support system (ECLS) treatment. METHODS: We retrospectively studied the characteristics and clinical outcomes of 28 patients (January 2010 and December 2011) with OHCA and veno-arterial ECLS implemented during ongoing cardiopulmonary resuscitation (CPR) upon admission to the cath lab. Baseline left ventricular ejection fraction (LVEF) was determined after ECLS implantation and then every 24 h during and after successful weaning from ECLS. RESULTS: Overall 30-day survival rate was 39.3 % (11 of 28 patients). Baseline characteristics, initial laboratory measurements, and LVEF on admission were not significantly different between survivors and non-survivors. There was no difference regarding median CPR duration [survivors 44.0 min (IQR 31.0-45.0) vs. non-survivors 53.0 min (IQR 40.0-61.3); P = 0.23]. Door-to-ECLS implantation time was significantly longer in non-survivors [42.5 min (IQR 28.0-56.5) vs. 25.0 min (IQR 21.0-30.0); P < 0.01]. ECLS treatment duration was not significantly different between the two groups [survivors: 4.0 days (IQR 1.5-7.5) vs. non-survivors 6.5 days (IQR 1.0-8.0); P = 0.69]. LVEF significantly improved in survivors during ECLS treatment (mean ± SD survivor 47.5 ± 14.7 % vs. non-survivor 23.3 ± 14.9 %; P < 0.01). The door-to-ECLS implantation time was the only significant and independent predictor of 30-day mortality in multivariate Cox regression analysis (P = 0.04). Kaplan-Meier survival analysis showed a benefit favouring patients with a door-to-ECLS implantation time <30 min (log rank 6.29; P = 0.01). CONCLUSION: A door-to-ECLS implantation time <30 min significantly improves 30-day outcomes in patients with OHCA.

Release kinetics of circulating muscle-enriched microRNAs in patients undergoing transcoronary ablation of septal hypertrophy.

OBJECTIVES: This study sought to evaluate exact release kinetics of microRNAs (miRNAs) in acute myocardial infarction (AMI). BACKGROUND: miRNAs may be useful as novel biomarkers in patients with cardiovascular disease, although it is difficult to establish the detailed release kinetics of miRNAs in patients with AMI. METHODS: We analyzed the release kinetics of circulating cardiac-specific (miR-21, miR-208a) and muscle-enriched (miR-1, miR-133a) miRNAs using the TaqMan polymerase chain reaction in patients with hypertrophic obstructive cardiomyopathy who were undergoing transcoronary ablation of septal hypertrophy (TASH), a procedure mimicking AMI. Consecutive patients (n = 21) undergoing TASH were included. Serum samples were collected prior to and at 15, 30, 45, 60, 75, 90, and 105 min and 2, 4, 8, and 24 h after TASH. RESULTS: Circulating concentrations of miR-1 were significantly increased (>3-fold; p = 0.01) after 15 min, with a peak after 75 min (>60-fold; p < 0.001). The miR-21 concentrations were not increased at any time point. Concentrations of miR-133a were significantly increased at 15 min (2.9-fold; p < 0.001) and reached a plateau between 75 and 480 min (>50-fold change). The miR-208a concentrations were elevated at 105 min (>2-fold; p = 0.01), without a further increase. CONCLUSIONS: miR-1, miR-133a, and miR-208a were continuously increased during the first 4 h after the induction of MI. In particular, miR-1 and miR-133a were significantly increased at early time points. These results demonstrate the release kinetics of miRNAs, which are helpful for developing their potential use as biomarkers in patients with acute coronary syndromes.

Bone marrow-derived cells contribute to cell turnover in aging murine hearts.

The paradigm that cardiac myocytes are non-proliferating, terminally differentiated cells was recently challenged by studies reporting the ability of bone marrow-derived cells (BMCs) to differentiate into cardiomyocytes after myocardial damage. However, little knowledge exists about the role of BMCs in the heart during physiological aging. Twelve-week-old mice (n=36) were sublethally irradiated and bone marrow from littermates transgenic for enhanced green fluorescent protein (eGFP) was transplanted. After 4 weeks, 18 mice were sacrificed at the age of 4 months and served as controls (group A); the remaining mice were sacrificed at the age of 18 months (group B). Group A did not exhibit a significant number of eGFP+ cells, whereas 9.4±2.8 eGFP+ cells/mm2 was documented in group B. In total, only five eGFP+ cardiomyocytes were detected in 20 examined hearts, excluding a functional role of BM differentiation in cardiomyocytes. Similarly, a relevant differentiation of BMCs in endothelial or smooth muscle cells was excluded. In contrast, numerous BM-derived fibroblasts and myofibroblasts were observed in group B, but none were detected in group  A. The present study demonstrates that BMCs transdifferentiate into fibroblasts and myofibroblasts in the aging murine myocardium, suggesting their contribution to the preservation of the structural integrity of the myocardium, while they do not account for regenerative processes of the heart.