A Rare Case of Postoperative Extradural Hematoma in the Posterior Fossa Complicated by Both Stunned Myocardium and Neurogenic Pulmonary Edema.

Acute neurological insult can trigger a cascade of events in other organ systems such as the heart and lung. Neurogenic stunned myocardium (NSM) and Neurogenic pulmonary edema (NPE) are mostly reported after stroke, subarachnoid hemorrhage, or seizures whenever sympathetic storm and autonomic dysregulation occurs. We report here for the first time, a case of postoperative infratentorial extradural hematoma in a patient triggering NSM and NPE at the same time. The challenges involved in the management of such a patient are described in this case report. The patient was successfully managed and discharged home with no new neurological deficits.

Impact of hibernating and viable myocardium on improvement in perfusion and left ventricular ejection fraction after coronary artery bypass graft.

OBJECTIVES: The association between the extent and degree of perfusion-metabolism mismatch and improvement in perfusion and left ventricular ejection fraction (LVEF) after revascularization was assessed. The secondary aim was to identify the best precoronary artery bypass graft surgery (pre-CABG) PET parameter, if any, to predict the improvement in the perfusion and LVEF after CABG. METHODS AND RESULTS: Overal, 31 patients (mean age: 58+8.3 years) with ischemic left ventricle dysfunction underwent NH3 and F-FDG PET for the assessment of myocardial viability. CABG was performed in these patients and after a mean interval of 3 months, NH3 PET was repeated. The percentages of viable myocardium (VM), hibernating myocardium, degree of mismatch, and LVEF in pre-CABG PET were calculated. These were compared, the median [INCREMENT]LVEF and percent increase in perfusion being 5 (interquartile range: 3-9) and 78.7 (interquartile range: 51.3-100), respectively. No significant association was observed between the severity or extent of perfusion defect/mismatch and improvement in perfusion or LVEF after CABG. Patients with at least 65% VM predicted a 5-unit increase in LVEF at 88.9% sensitivity (P=0.1). CONCLUSION: There was no significant relation between the severity and extent of perfusion-metabolism mismatch with improvement in perfusion and LVEF after CABG. After CABG for ischemic left ventricle dysfunction, VM shows a tendency toward better improvement in LVEF.

Prevalence and Localization of Hibernating Myocardium Among Patients with Left Ventricular Dysfunction.

OBJECTIVE: This study evaluated how much of the myocardium was hibernating in patients with left ventricle dysfunction and/or comorbidities who planned to undergo either surgical or interventional revascularization. Furthermore, this study also identified which irrigation areas of the coronary arteries presented more scar and hibernating tissue. METHODS: At rest, Tc-99m MIBI SPECT and cardiac F-18 FDG PET/CT images collected between March 2009 and September 2016 from 65 patients (55 men, 10 women, mean age 64±12) were retrospectively analyzed in order to evaluate myocardial viability. The areas with perfusion defects that were considered metabolic were accepted as hibernating myocardium, whereas areas with perfusion defects that were considered non-metabolic were accepted as scar tissue. RESULTS: Perfusion defects were observed in 26% of myocardium, on average 48% were associated with hibernation whereas other 52% were scar tissue. In the remaining Tc-99m MIBI images, perfusion defects were observed in the following areas in the left anterior descending artery (LAD; 31%), in the right coronary artery (RCA; 23%) and in the Left Circumflex Artery (LCx; 19%) irrigation areas. Hibernation areas were localized within the LAD (46%), LCx (54%), and RCA (64%) irrigation areas. Scar tissue was also localized within the LAD (54%), LCx (46%), and RCA (36%) irrigation areas. CONCLUSION: Perfusion defects are thought to be the result of half hibernating tissue and half scar tissue. The majority of perfusion defects was observed in the LAD irrigation area, whereas hibernation was most often observed in the RCA irrigation area. The scar tissue development was more common in the LAD irrigation zone.

Hyperinsulinaemic euglycaemic therapy use in neurogenic stunned myocardium following subarachnoid haemorrhage.

We present a 62-year-old female who collapsed with a subarachnoid haemorrhage. This was complicated by profound shock secondary to neurogenic stunned myocardium. As the patient demonstrated life-threatening catecholamine-resistant shock that was unresponsive to conventional treatment measures, hyperinsulinaemic euglycaemic therapy was utilised as a rescue therapy. To our knowledge this has not previously been described in the literature. The patient proceeded to stabilise and made a good recovery.

Myocardial stunning-induced left ventricular dyssynchrony on gated single-photon emission computed tomography myocardial perfusion imaging.

OBJECTIVES: Myocardial stunning provides additional nonperfusion markers of coronary artery disease (CAD), especially for severe multivessel CAD. The purpose of this study is to assess the influence of myocardial stunning to the changes of left ventricular mechanical dyssynchrony (LVMD) parameters between stress and rest gated single-photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI). PATIENTS AND METHODS: A total of 113 consecutive patients (88 males and 25 females) who had undergone both stress and rest Tc-sestamibi gated SPECT MPI were retrospectively enrolled. Suspected or known patients with CAD were included if they had exercise stress MPI and moderate to severe myocardial ischemia. Segmental scores were summed for the three main coronary arteries according to standard myocardial perfusion territories, and then regional perfusion, wall motion, and wall thickening scores were measured. Myocardial stunning was defined as both ischemia and wall dysfunction within the same coronary artery territory. Patients were divided into the stunning group (n=58) and nonstunning group (n=55). RESULTS: There was no significant difference of LVMD parameters between stress and rest in the nonstunning group. In the stunning group, phase SD and phase histogram bandwidth of contraction were significantly larger during stress than during rest (15.05±10.70 vs. 13.23±9.01 and 46.07±34.29 vs. 41.02±32.16, P<0.05). Phase SD and phase histogram bandwidth of relaxation were also significantly larger during stress than during rest (21.21±13.91 vs. 17.46±10.52 and 59.03±37.82 vs. 52.38±36.89, P<0.05). CONCLUSION: Both systolic and diastolic LVMD parameters deteriorate with myocardial stunning. This kind of change may have incremental values to diagnose CAD.

Exploring the Pathophysiology of Takotsubo Cardiomyopathy.

PURPOSE OF REVIEW: The purpose of this review is to explore the pathophysiology of Takotsubo cardiomyopathy by appraising the interplay between myocardial perfusion, function, metabolism, and, particularly, sympathetic innervation. RECENT FINDINGS: A number of hypotheses have been proposed to explain the pathogenesis of Takotsubo cardiomyopathy, which include (1) catecholamine cardiac toxicity, (2) myocardial sympathetic innervation disruption, (3) coronary vasospasm, (4) myocardial microvascular dysfunction, and (5) aborted myocardial infarction. These proposals are primarily derived from findings of nuclear myocardial perfusion, metabolism, and cardiac sympathetic innervation imaging. Although data in the literature are not necessarily uniform, the two most plausible working postulates for explaining the phenomenon are (1) regional myocardial stunning (due to coronary vasospasm, microvascular dysfunction, or aborted myocardial infarction) and (2) cardiac sympathetic innervation disruption or toxicity. Current data suggest that disturbances of both coronary circulation and neural innervation are associated with the Takotsubo cardiomyopathy: myocardial stunning from transient ischemic attack and sympathetic innervation disruption. It remains to be determined, however, whether the observed leading mechanistic explanations that have gained momentum are merely the sequelae of the disease rather than its primary etiology.

Atorvastatin can ameliorate left atrial stunning induced by radiofrequency ablation for atrial fibrillation.

The objective of this study was to study the functional changes of the left atrium after radiofrequency ablation treatment for atrial fibrillation and the therapeutic effect of atorvastatin. Fifty-eight patients undergoing radiofrequency ablation for atrial fibrillation were randomly divided into non-atorvastatin group and atorvastatin group. Patients in the atorvastatin group were treated with atorvastatin 20 mg p.o. per night in addition to the conventional treatment of atrial fibrillation; patients in the non-atorvastatin group received conventional treatment of atrial fibrillation only. Echocardiography was performed before radiofrequency ablation operation and 1 week, 2 weeks, 3 weeks, and 4 weeks after operation. Two-dimensional ultrasound speckle tracking imaging system was used to measure the structural indexes of the left atrium. Results indicated that there was no significant change for indexes representing the structural status of the left atrium within a month after radiofrequency ablation (P > 0.05); however, there were significant changes for indexes representing the functional status of the left atrium. There were also significant changes in indexes reflecting left atrial strain status: the S and SRs of atorvastatin group were higher than those of non-atorvastatin group (P < 0.05). In summary, atorvastatin could improve left atrial function and shorten the duration of atrial stunning after radiofrequency ablation of atrial fibrillation.

Hibernating substrate of ventricular tachycardia: a three-dimensional metabolic and electro-anatomic assessment.

PURPOSE: Hibernating myocardium (HM) is associated with sudden cardiac death (SCD). Little is known about the electrophysiological properties of HM and the basis of its association with SCD. We aimed to electrophysiologically characterize HM in patients with ventricular tachycardia (VT). METHODS: Endocardial voltage mapping, metabolic 18FDG-positron emission tomography (PET) and perfusion 82Rb, 201Tl, or 99mTc scans were performed in 61 ischemic heart disease patients with VT. Hibernating areas were identified which was followed by three-dimensional PET reconstructions and integration with voltage maps to allow hybrid metabolic-electro-anatomic assessment of the arrhythmogenic substrate. RESULTS: Of 61 patients with ischemic heart disease and refractory VT, 7 were found to have hibernating myocardium (13%). A total of 303 voltage points were obtained within hibernating myocardium (8.2 points per 10 cm2) and displayed abnormal voltage in 48.5 and 78.3% of bipolar and unipolar recordings, respectively, with significant heterogeneity of bipolar (p < 0.0001) and unipolar voltage measurements (p = 0.0004). Hibernating areas in 6 of 7 patients contained all three categories of bipolar voltage-defined scar (<0.5 mV), border zone (0.5-1.5 mV), and normal myocardium (>1.5 mV). The characteristics of local electrograms were also assessed and found abnormal in most recordings (76.6, 10.2% fractionated, 5.3% isolated potentials). Exit sites of clinical VTs were determined in 6 patients, of which 3 were located within hibernating myocardium. CONCLUSIONS: Hibernating myocardium displays abnormal and heterogeneous electrical properties and seems to contribute to the substrate of VT. These observations may underlie the vulnerability to reentry and SCD in patients with hypoperfused yet viable myocardium.

Neurogenic stunned myocardium in subarachnoid hemorrhage.

"Stunned myocardium," characterized by reversible left ventricular dysfunction, was first described via animal models using transient coronary artery occlusion. However, this phenomenon has also been noted with neurologic pathologies and collectively been labeled "neurogenic stunned myocardium" (NSM). Neurogenic stunned myocardium resulting from subarachnoid hemorrhage (SAH) is a challenging pathology due to its diagnostic uncertainty. Traditional diagnostic criteria for NSM after SAH focus on electrocardiographic and echocardiographic abnormalities and troponemia. However, tremendous heterogeneity still exists. Traditional pathophysiological mechanisms for NSM encompassed hypothalamic and myocardial perivascular lesions. More recently, research on pathophysiology has centered on myocardial microvascular dysfunction and genetic polymorphisms. Catecholamine surging as a mechanism has also gained attention with particular focus placed on the role of adrenergic blockade in both the prehospital and acute settings. Management remains largely supportive with case reports acknowledging the utility of inotropes such as dobutamine and milrinone and intra-aortic balloon pump when NSM is accompanied by cardiogenic shock. Neurogenic stunned myocardium that follows SAH can result in many complications such as arrhythmias, pulmonary edema, and prolonged intubation, which can negatively impact long-term recovery from SAH and increase morbidity and mortality. This necessitates the need to accurately diagnose and treat NSM.

Noninvasive epicardial and endocardial electrocardiographic imaging of scar-related ventricular tachycardia.

BACKGROUND: The majority of life-threatening ventricular tachycardias (VTs) are sustained by heterogeneous scar substrates with narrow strands of surviving tissue. An effective treatment for scar-related VT is to modify the underlying scar substrate by catheter ablation. If activation sequence and entrainment mapping can be performed during sustained VT, the exit and isthmus of the circuit can often be identified. However, with invasive catheter mapping, only monomorphic VT that is hemodynamically stable can be mapped in this manner. For the majority of patients with poorly tolerated VTs or multiple VTs, a close inspection of the re-entry circuit is not possible. A noninvasive approach to fast mapping of unstable VTs can potentially allow an improved identification of critical ablation sites. METHODS: For patients who underwent catheter ablation of scar-related VT, CT scan was obtained prior to the ablation procedure and 120-lead body-surface electrocardiograms (ECGs) were acquired during induced VTs. These data were used for noninvasive ECG imaging to computationally reconstruct electrical potentials on the epicardium and on the endocardium of both ventricles. Activation time and phase maps of the VT circuit were extracted from the reconstructed electrograms. They were analyzed with respect to scar substrate obtained from catheter mapping, as well as VT exits confirmed through ablation sites that successfully terminated the VT. RESULTS: The reconstructed re-entry circuits correctly revealed both epicardial and endocardial origins of activation, consistent with locations of exit sites confirmed from the ablation procedure. The temporal dynamics of the re-entry circuits, particularly the slowing of conduction as indicated by the crowding and zig-zag conducting of the activation isochrones, collocated well with scar substrate obtained by catheter voltage maps. Furthermore, the results indicated that some re-entry circuits involve both the epicardial and endocardial layers, and can only be properly interpreted by mapping both layers simultaneously. CONCLUSIONS: This study investigated the potential of ECG-imaging for beat-to-beat mapping of unstable reentrant circuits. It shows that simultaneous epicardial and endocardial mapping may improve the delineation of the 3D spatial construct of a re-entry circuit and its exit. It also shows that the use of phase mapping can reveal regions of slow conduction that collocate well with suspected heterogeneous regions within and around the scar.

Sudden QRS morphology change during ventricular pacing in a scar-related isthmus What is the mechanism?

We present an example of sudden modification in QRS morphology during ventricular pacing inside a scar-related isthmus. This is explained by a "concealed" sudden block in both the orthodromic and antidromic wavefront directions, allowing then the activation to proceed through a now overt antidromic conduction.

Takotsubo cardiomyopathy in the setting of acute hydrocephalus secondary to neurocysticercosis.

We report the case of a 45-year-old male who presented with transient neurogenic stunned myocardium, or takotsubo cardiomyopathy, secondary to acute hydrocephalus caused by obstruction of the third ventricle by neurocysticercosis.

Prolonged Cardiac Dysfunction After Intraparenchymal Hemorrhage and Neurogenic Stunned Myocardium.

Cardiac dysfunction occurring secondary to neurologic disease, termed neurogenic stunned myocardium, is an incompletely understood phenomenon that has been described after several distinct neurologic processes. We present a case of neurogenic stunned myocardium, discovered intraoperatively after anesthetic induction, in a patient who presented to our operating room with a recent intraparenchymal hemorrhage. We discuss the longitudinal cardiac functional course after neurogenic stunned myocardium. Finally, we discuss the pathophysiology of neurogenic stunned myocardium, as well as its implications for anesthesiologists caring for neurosurgical patients.

Sex differences in the mechano-energetic effects of genistein on stunned rat and guinea pig hearts.

Although the phytoestrogen genistein (Gen) is considered protective in cardiovascular diseases, its direct effects on stunned hearts after transient ischemia-reperfusion (I/R) are unknown. This report studied the effects of 20 µmol/L Gen on the mechano-calorimetric behaviour during I/R of rat and guinea pig hearts to evaluate the energetics of Ca(2+) homeostasis. Isolated beating hearts were perfused with control Krebs solution inside a calorimeter with or without perfusion of Gen before a transient period of I/R. Left ventricular pressure development (P) and total heat rate (Ht) were continuously measured. At 37°C, Gen did not change post-ischemic contractile recovery (PICR), but it increased the relaxation rate. However, PICR was reduced in hearts of male rats and guinea pigs at 30°C. Total muscle economy (P/Ht) showed the same behaviour as P at each temperature. Inhibition of phosphatases with orthovanadate during Gen perfusion prevented a decrease in PICR in male rat hearts, suggesting that this effect is due to tyrosine kinase inhibition. Reperfusing ischemic hearts with 10 mmol/L caffeine-36 mmol/L Na(+)-Krebs induced contracture dependent on the sarcoreticular Ca(2+) content. Contracture relaxation depends on mitochondrial Ca(2+) uptake and Gen reduced the relaxation rate. Moreover, Gen prevented the increase in Rhod-2 fluorescence (free [Ca(2+)]m) of rat cardiomyocytes. In guinea pig hearts, Gen maintained ischemic preconditioning, but was reduced by 5-hydroxydecanoate, suggesting the participation of mitochondrial adenosine triphosphate (ATP)-dependent K channels. Results suggest that Gen acts on several mechanisms that regulate myocardial calcium homeostasis and energetics during I/R, which differ in a temperature- and sex-dependent manner.

Aturdimiento miocárdico neurogénico en Pediatría. A propósito de un caso / Neurogenic stunned myocardium in Pediatrics. A case report

El aturdimiento miocárdico neurogénico es una entidad poco frecuente que semeja un síndrome coronario agudo, con alteraciones electrocardiográficas, disfunción cardiaca y aumento de enzimas cardiacas, pero sin evidencia de lesión coronaria. Puede ocurrir en el posoperatorio de neurocirugía. Se presenta el caso de un paciente pediátrico que a las 24 h de ser intervenido de un meduloblastoma de fosa posterior desarrolló un aturdimiento miocárdico neurogénico que evolucionó a taquicardia nodal con repercusión hemodinámica. La evolución fue satisfactoria, aunque precisó tratamiento antiarrítmico, con resolución bioquímica, ecográfica y clínica en menos de una semana (AU)

Neurogenic stunned myocardium is an unusual clinical entity. It mimics an acute coronary syndrome with electrocardiographic abnormalities, cardiac dysfunction and elevated cardiac enzymes with absence of obstructive coronary disease. It may occur after a neurosurgical procedure. A case is presented of neurogenic stunned myocardium occurring in a child after removal of a posterior fossa medulloblastoma. The patient developed nodal tachycardia with hemodynamic impairment. The clinical course was satisfactory due to antiarrhythmic therapy, with biochemical, echocardiographic, and clinical improvement within a week (AU)

Specificity for each of the 46 criteria of the Selvester QRS score for electrocardiographic myocardial scar sizing in left bundle branch block.

BACKGROUND: The Selvester QRS score consists of a set of electrocardiographic criteria designed to identify, quantify and localize scar in the left ventricle using the morphology of the QRS complex. These criteria were updated in 2009 to expand their use to patients with underlying conduction abnormalities, but these versions have thus far only been validated in small and carefully selected populations. AIM: To determine the specificity for each of the criteria of the left bundle branch block (LBBB) modified Selvester QRS Score (LB-SS) in a population with strict LBBB and no myocardial scar as verified by cardiovascular magnetic resonance imaging with late gadolinium enhancement (CMR-LGE). METHODS: We identified ninety-nine patients with LBBB without scar on CMR-LGE, who underwent a clinically indicated CMR scan at three different centers. The ECG recording date was any time prior to or <30days after the CMR scan. The LB-SS was applied and specificity for detection of scar in each of the 46 separate criteria was determined. RESULTS: The specificity ranged between 41% and 100% for the 46 criteria of LB-SS and 27/46 (59%) met ≥95% specificity. The mean±SD specificity was 90%±14%. CONCLUSION: Several of the criteria in the LB-SS lack adequate specificity. Elimination or modification of these nonspecific QRS morphology criteria may improve the specificity of the overall LB-SS.

[Fragmented QRS. Relevance in clinical practice]. / Fragmentierter QRS-Komplex. Bedeutung in der klinischen Praxis.

The QRS complex represents the electrical depolarization of ventricular myocardium. In the case of an undisturbed depolarization, the QRS complex has a normal configuration and duration, but abnormal electrical conduction leads to widening of the QRS complex. The block of one of the Tawara branches results in a typical bundle branch block pattern. A QRS complex that cannot be classified as bundle branch block due to an atypical configuration and contains notched R or S waves is called a fragmented QRS. The underlying pathophysiologies are manifold and include myocardial scars induced by ischemic heart disease, myocardial fibrosis due to other diseases, primary cardiac pathologies as well as systemic diseases with cardiac involvement. Pathologies on the cellular level, such as ion channel dysfunctions, also correlate with fragmented QRS. Besides the diagnostic relevance, fragmented QRS is known to have prognostic properties, for example in identifying high risk patients with coronary artery disease, cardiomyopathy, Brugada syndrome and acquired long QT syndrome; however, fragmented QRS may also be detected in ECGs of healthy individuals.

Cardiomyocyte Remodeling in Atrial Fibrillation and Hibernating Myocardium: Shared Pathophysiologic Traits Identify Novel Treatment Strategies?

Atrial fibrillation (AF) is the most common arrhythmia and is associated with a high risk of morbidity and mortality. However, there are limited treatment strategies for prevention of disease onset and progression. Development of novel therapies for primary and secondary prevention of AF is critical and requires improved understanding of the cellular and molecular mechanisms underlying the AF disease process. Translational and clinical studies conducted over the past twenty years have revealed that atrial remodeling in AF shares several important pathophysiologic traits with the remodeling processes exhibited by hibernating myocardium that develop in response to chronic ischemia. These shared features, which include an array of structural, metabolic, and electrophysiologic changes, appear to represent a conserved adaptive myocyte response to chronic stress that involves dedifferentiation towards a fetal phenotype to promote survival. In this review, we discuss the pathophysiology of AF, summarize studies supporting a common remodeling program in AF and hibernating myocardium, and propose future therapeutic implications of this emerging paradigm. Ultimately, better understanding of the molecular mechanisms of atrial myocyte remodeling during the onset of AF and the transition from paroxysmal to persistent stages of the disease may facilitate discovery of new therapeutic targets.

Valoración del daño miocárdico mediante la medición de la heart-fatty acid-binding protein en cirugía de revascularización coronaria sin circulación extracorpórea. Estudio preliminar / Evaluation of postoperative myocardial injury by heart-type fatty acid-binding protein in off-pump coronary artery bypass grafting surgery

Introducción y objetivos del estudio. El infarto de miocardio posoperatorio es una complicación grave y frecuente de la cirugía cardiaca. El diagnóstico en este contexto es, en ocasiones, difícil. El objetivo de este estudio es evaluar la cinética y la precisión diagnóstica de un nuevo marcador, la heart-type fatty acid-binding protein (h-FABP), en la detección precoz de daño miocárdico en pacientes sometidos a cirugía de revascularización coronaria sin circulación extracorpórea en comparación con los biomarcadores clásicos. Materiales y métodos. Se estudiaron prospectivamente 17 pacientes consecutivos sometidos a cirugía cardiaca de revascularización sin circulación extracorpórea. Se analizaron biomarcadores de lesión de isquemia miocárdica (h-FABP, troponina, creatincinasa [CK] y CK-MB) al inicio de la cirugía (T1), inmediatamente después de la revascularización (T2), al ingreso en la UCC (T3) y después de 4 (T4), 8 (T5), 24 (T6) y 48 h (T7). Se registraron las complicaciones isquémicas perioperatorias, definidas de acuerdo con criterios electrocardiográficos, ecocardiográficos y hemodinámicos. Resultados. Los valores plasmáticos pico de la troponina se alcanzaron en T4 (2,9 ± 5,2 ng/ml) y en T5 con h-FABP (37,9 ± 55,5 ng/ml). Los valores máximos de CK y CK-MB fueron más tardíos, en T6 (741 ± 779 y 37 ± 51 U/L, respectivamente). El punto de corte obtenido para h-FABP para la detección de eventos isquémicos fue de 19 ng/ml, proporcionando una sensibilidad y especificidad del 77 y 75%, respectivamente, para el diagnóstico de la lesión isquémica perioperatoria, con un área bajo la curva ROC para h-FABP de 0,83 (IC 95% 0,6-1,0) vs. 0,63 (IC 95% 0,33-0,83) para troponina. Se alcanza este valor de corte para la h-FABP en promedio en T2 (18,9 ± 21,5 ng/ml). Conclusión. Este es el primer estudio que evalúa la cinética del biomarcador h-FABP en el perioperatorio de la cirugía de revascularización sin circulación extracorpórea, y el valor de corte establecido podría ayudar a la detección temprana de la isquemia miocárdica en este contexto (AU)

Background and goal of study. Postoperative myocardial infarction is a serious and frequent complication of cardiac surgery. Nonetheless, diagnosis in this context it is occasionally challenging. We sought to evaluate the kinetics and diagnostic accuracy of the new biomarker «heart-type fatty acid-binding protein» (h-FABP) in the early detection of myocardial injury in patients undergoing off-pump coronary artery bypass grafting, compared with classical biomarkers. Materials and methods. A prospective study was conducted on 17 consecutive patients who underwent off-pump coronary artery bypass grafting during a 2 month period. Blood samples were drawn for measurement of myocardial ischemic injury biomarkers (h-FABP, troponin, creatine kinase [CK] and CK-MB), at baseline (T1), immediate post-coronary artery bypass grafting (T2), on ICU admission (T3), and after 4 (T4), 8 (T5), 24 (T6) and 48 h (T7). Perioperative ischemic complications, defined according to electrocardiographic, echocardiographic and hemodynamic criteria, were recorded. Results. Earlier biomarkers peak plasma values occurred at T4 with troponin (2.9 ± 5.2 ng/mL), and at T5 with h-FABP (37.9 ± 55.5 ng/mL). Maximum values of CK and CK-MB occurred later, both in T6 (741 ± 779 and 37 ± 51 U/L, respectively). The optimized cut-off obtained for h-FABP was 19 ng/mL, providing a sensitivity and specificity of 77 and 75%, respectively, for diagnosis of perioperative ischemic injury, with an area under the ROC curve for h-FABP of 0.83 (95% CI 0.6-1.0) vs. 0.63 (95% CI 0.33-0.83) for troponin. This cut-off value for h-FABP is reached on average at T2 (mean value of h-FABP at T2: 18.9 ± 21.5 ng/mL). Conclusion. This is the first study evaluating the kinetics of h-FABP biomarker in perioperative off-pump coronary artery bypass grafting, and the cut-off value established could help to extend earlier detection of myocardial ischemia in this context (AU)

Regional mapping of myocardial hibernation phenotype in idiopathic end-stage dilated cardiomyopathy.

Myocardial hibernation (MH) is a well-known feature of human ischaemic cardiomyopathy (ICM), whereas its presence in human idiopathic dilated cardiomyopathy (DCM) is still controversial. We investigated the histological and molecular features of MH in left ventricle (LV) regions of failing DCM or ICM hearts. We examined failing hearts from DCM (n = 11; 41.9 ± 5.45 years; left ventricle-ejection fraction (LV-EF), 18 ± 3.16%) and ICM patients (n = 12; 58.08 ± 1.7 years; LVEF, 21.5 ± 6.08%) undergoing cardiac transplantation, and normal donor hearts (N, n = 8). LV inter-ventricular septum (IVS) and antero-lateral free wall (FW) were transmurally (i.e. sub-epicardial, mesocardial and sub-endocardial layers) analysed. LV glycogen content was shown to be increased in both DCM and ICM as compared with N hearts (P < 0.001), with a U-shaped transmural distribution (lower values in mesocardium). Capillary density was homogenously reduced in both DCM and ICM as compared with N (P < 0.05 versus N), with a lower decrease independent of the extent of fibrosis in sub-endocardial and sub-epicardial layers of DCM as compared with ICM. HIF1-α and nestin, recognized ischaemic molecular hallmarks, were similarly expressed in DCM-LV and ICM-LV myocardium. The proteomic profile was overlapping by ~50% in DCM and ICM groups. Morphological and molecular features of MH were detected in end-stage ICM as well as in end-stage DCM LV, despite epicardial coronary artery patency and lower fibrosis in DCM hearts. Unravelling the presence of MH in the absence of coronary stenosis may be helpful to design a novel approach in the clinical management of DCM.