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.

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.

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.

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.

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.

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.

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.

Reversible T-wave inversions and neurogenic myocardial stunning in a patient with recurrent stress-induced cardiomyopathy.

A 72-year-old female was diagnosed as a stress-induced cardiomyopathy from apical ballooning pattern of left ventricular dysfunction without coronary artery stenosis after the mental stress. ECG showed the transient T-wave inversions after the ST-segment elevations. By the mental stress after 1 year, she showed a transient dysfunction with similar ECG changes again. T-wave inversions recovered earlier, and cardiac sympathetic dysfunction showed a lighter response corresponding to the less severe dysfunction than those after the first onset. Wellens' ECG pattern was associated with the degree of neurogenic myocardial stunning with sympathetic hyperinnervation caused by mental stress.

Infective rhomboencephalitis and inverted Takotsubo: neurogenic-stunned myocardium or myocarditis?

Here we originally describe the clinical scenario of a young immune-competent patient affected by acute rhomboencephalitis with severe parenchymal edema and acute hydrocephalus who developed sudden life-threatening cardiac derangement. Hemodynamic and perfusion parameters revealed cardiogenic shock, so intensive circulatory support with epinephrine infusion and intra-aortic balloon pump was needed to restore organ perfusion. Transesophageal echocardiographic examination showed severe left ventricular dysfunction (ejection fraction as low as 20%) with wall motion abnormalities resembling a pattern of Takotsubo-inverted cardiomyopathy. Cultural investigations revealed infection by Listeria monocytogenes. Nevertheless, her conditions rapidly improved, and she had full cardiac recovery within few days. Acute cerebral damage, pattern of echocardiographic wall motion abnormalities, and clinical course may suggest neurogenic stunned as pathological mechanism responsible for cardiac dysfunction, but differential diagnosis with acute myocarditis is to be considered too. Acute cardiogenic shock during the course of rhomboencephalitis by L monocytogenes has not been yet reported; prompt clinical suspicion and intensive care are needed to manage this life-threatening condition.

Hibernating myocardium results in partial sympathetic denervation and nerve sprouting.

Hibernating myocardium due to chronic repetitive ischemia is associated with regional sympathetic nerve dysfunction and spontaneous arrhythmic death in the absence of infarction. Although inhomogeneity in regional sympathetic innervation is an acknowledged substrate for sudden death, the mechanism(s) responsible for these abnormalities in viable, dysfunctional myocardium (i.e., neural stunning vs. sympathetic denervation) and their association with nerve sprouting are unknown. Accordingly, markers of sympathetic nerve function and nerve sprouting were assessed in subendocardial tissue collected from chronically instrumented pigs with hibernating myocardium (n = 18) as well as sham-instrumented controls (n = 7). Hibernating myocardium exhibited evidence of partial sympathetic denervation compared with the normally perfused region and sham controls, with corresponding regional reductions in tyrosine hydroxylase protein (-32%, P < 0.001), norepinephrine uptake transport protein (-25%, P = 0.01), and tissue norepinephrine content (-45%, P < 0.001). Partial denervation induced nerve sprouting with regional increases in nerve growth factor precursor protein (31%, P = 0.01) and growth associated protein-43 (38%, P < 0.05). All of the changes in sympathetic nerve markers were similar in animals that developed sudden death (n = 9) compared with electively terminated pigs with hibernating myocardium (n = 9). In conclusion, sympathetic nerve dysfunction in hibernating myocardium is most consistent with partial sympathetic denervation and is associated with regional nerve sprouting. The extent of sympathetic remodeling is similar in animals that develop sudden death compared with survivors; this suggests that sympathetic remodeling in hibernating myocardium is not an independent trigger for sudden death. Nevertheless, sympathetic remodeling likely contributes to electrical instability in combination with other factors.

Transplant of stunned donor hearts rescued by pharmacological stress echocardiography: a "proof of concept" report.

BACKGROUND: Due to the shortage of donor hearts, the criteria for acceptance have been considerably expanded. Hearts with regional or global left ventricular dysfunction are excluded from donation, but stress echo might be useful to identify patients with reversible wall motion abnormalities, potentially eligible for donation. METHODS: Six marginal candidate donors (mean age, 40 ± 13 years; three men) were enrolled. Resting echocardiography showed in all subjects a LV ejection fraction ≥ 45% (mean 51 ± 5%), but multiple risk factors were present. All donors had either global or discrete wall motion abnormalities: Wall Motion Score Index (WMSI) rest = 1.33 ± 0.25. Stress echocardiography was performed with the dipyridamole high dose of 0.84 mg/kg given over 6 min. RESULTS: The stress echo results were abnormal in three donors (WMSI rest = 1.51 ± 0.19 vs peak = 1.41 ± 0.30). These hearts were excluded from donation and cardiac pathology verification was available in two cases of confirmed LV myocardial fibrosis and/or severe coronary stenosis. The remaining three hearts improved during stress (WMSI rest = 1.15 ± 0.13 vs peak = 1.04 ± 0.06) and were transplanted uneventfully. Recipients (three males, mean age 53 ± 4 years) underwent post-TX coronary angiography, IVUS and endomyocardial biopsies. No recipient had primary graft failure, and all showed normal coronary angiography and normal LV function (EF = 57 ± 6%; WMSI = 1 ± 0) at 1-month post-TX. The recipients were alive at 12-month median follow-up. CONCLUSIONS: Dipyridamole stress echo performed in brain-dead potential donors with LV resting global or discrete wall motion abnormalities identifies hearts with severe morphologic abnormalities excluded from donation (with fixed response during stress echo) from hearts eligible for donation, showing improvement in regional wall motion during stress (viability response) and normal function and coronary anatomy following transplantation.

Stress cardiomyopathy: a syndrome of catecholamine-mediated myocardial stunning?

During the past few years, a novel syndrome of heart failure and transient left ventricular systolic dysfunction precipitated by acute emotional or physical stress has been described. While patients with "stress cardiomyopathy"(SCM) typically present with signs and symptoms that resemble an acute coronary syndrome, it has become clear that this syndrome has unique clinical features that can readily be distinguished from acute infarction.In particular, in contrast to the irreversible myocardial injury seen with infarction, the myocardial dysfunction of SCM is completely reversible and occurs in the absence of plaque rupture and coronary thrombosis. There is increasing evidence that exaggerated sympathetic stimulation may play a pathogenic role in the development of SCM. Plasma catecholamine levels have been found to be markedly elevated in some patients with SCM, and the syndrome has been observed in other clinical states of catecholamine excess such as central neurologic injury and pheochromocytoma.Further, intravenous catecholamines can precipitate SCM in humans and can reproduce the syndrome in animal models. The precise mechanism in which excessive sympathetic stimulation may result in transient left ventricular dysfunction remains controversial. Abnormal myocardial blood flow due to sympathetically mediated microvascular dysfunction has been suggested and is supported by decreased coronary flow reserve during the acute phase of this syndrome. An alternative explanation is the direct effect of catecholamines on cardiac myocytes, possibly through cyclic AMP-mediated calcium overload. This manuscript will review the clinical and diagnostic features of SCM and will summarize the evidence supporting a sympathetically mediated pathogenesis. Clinical risk factors that appear to increase susceptibility to SCM, possibly by modulating myocyte and microvascular sensitivity to catecholamines, will also be highlighted.

Mitral annular velocity in patients with postoperative atrial fibrillation.

BACKGROUND: Subclinical atrial stunning (AS) (left atrial dysfunction) may increase vulnerability to oxidative and inflammatory stressors, thus increasing the likelihood of postoperative supraventricular arrhythmias, especially atrial fibrillation (AF). Evaluation of mitral annular velocities by tissue Doppler imaging (TDI) may be useful in seeking subclinical AS. This prospective study aimed to evaluate the relationship between atrial fibrillation after bypass surgery and presurgical determination of subclinical AS by assessing mitral annular velocities by TDI. METHODS: We enrolled patients who underwent coronary artery bypass graft (CABG) surgery into this prospective study. Inclusion criteria were sinus rhythm and a negative history of atrial tachycardia during the previous 3 mo. An experienced cardiologist performed transthoracic echocardiography in all patients. We recorded standard two-dimensional, mitral inflow conventional Doppler interrogation and TDI pulsed wave data from the lateral and septal annulus. All patients underwent CABG surgery at our Cardiovascular Surgery Unit. Patients were divided into two groups based on their postoperative AF status: group 1 patients had postoperative AF and group 2 patients did not. RESULTS: This study included 44 patients. Age and the presence of chronic obstructive pulmonary disease were the only two significantly different parameters among clinical characteristics between groups. Echocardiographic findings that were statistically significantly different between groups were as follows: lateral A diastolic mitral annular velocity, group 1: 0.11 ± 0.19 ms(-1)versus group 2: 0.08 ± 0.19 ms(-1) (P = 0.001); lateral E diastolic mitral annular velocity, group 1: 0.69 ± 0.24 ms(-1)versus group 2: 0.62 ± 0.31 ms(-1) (P = 0.016); Septal E diastolic mitral annular velocity, group 1: 0.05 ± 0.01 ms(-1)versus group 2: 0.04 ± 0.01 ms(-1) (P = 0.033); septal A diastolic mitral annular velocity, group 1: 0.08 ± 0.02 ms(-1)versus group 2: 0.05 ± 0.02 ms(-1) (P = 0.005). CONCLUSIONS: There is no relationship between AF after CABG surgery and preexisting subclinical AS determined with mitral annular velocities by TDI. Preoperative appropriate prophylactic treatment should be administered to all patients.

Improvement of myocardial performance (Tei) index closely reflects intrinsic improvement of cardiac function: assessment in revascularized hibernating myocardium.

BACKGROUND: Myocardial performance index (MPI), or Tei index, is an indicator of systolic and diastolic myocardial function. MPI increases in case of cardiac dysfunction; however, whether reversal of left ventricular dysfunction is also reflected by concomitant improvement (i.e., decrease) of MPI is unknown. METHODS: Fifty-two patients with chronic ischemic cardiomyopathy and viable myocardium by dobutamine stress echocardiography were studied by echocardiography before and more than 4 months after cardiac revascularization. Patients were in optimal medical therapy, which remained unchanged following revascularization. RESULTS: At baseline, ejection fraction (EF: 32 ± 6%) and wall motion score index (WMSI: 2.37 ± 0.32) were impaired, and MPI averaged 0.71 ± 0.19. Revascularization markedly improved EF (44 ± 10%, P < 0.0001) and WMSI (1.77 ± 0.44, P < 0.0001). MPI also improved (0.59 ± 0.26, P < 0.0001), and its decrease was significantly correlated with the improvement in EF (r =-0.68, P < 0.0001) and to the extent of viable myocardium (r =-0.45, P = 0.0007). Responders to revascularization (≥5% increase in EF at follow-up, n = 40% and 77%) achieved a significant improvement in MPI at follow-up in contrast with nonresponders (-23 ± 25% vs. 0.02 ± 0.18%, P = 0.001). Improvement in MPI was largely driven by a significant reduction in isovolumic contraction time (P < 0.001) with consequent prolongation of the ejection phase. CONCLUSION: In patients with chronic ischemic cardiomyopathy, MPI improves along with recovery of function, reflecting the intrinsic improvement of viable segments induced by revascularization.

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.

Takotsubo cardiomyopathy followed by neurogenic stunned myocardium in the same patient: gradations of the same disease?

Takotsubo cardiomyopathy is a phenomenon of transient acute left ventricular dysfunction without obstructive coronary disease seen predominantly in postmenopausal women in the setting of acute emotional or physical stress. Neurocardiogenic injury from acute neurologic events such as intracranial bleeding can precipitate transient left ventricular dysfunction (termed 'neurogenic stunned myocardium') that may be indistinguishable from takotsubo cardiomyopathy. There is controversy about the diagnosis of takotsubo cardiomyopathy in the setting of acute neurologic disorders. We describe a case of a 67-year-old female who initially presented with takotsubo cardiomyopathy due to an acute gastrointestinal illness and 4 years later developed a recurrence in the setting of an ischemic cerebrovascular accident that was associated with more prominent EKG changes and much higher cardiac biomarker release but similar degree of left ventricular dysfunction. This case suggests that susceptibility to this disorder is likely due to patient-specific factors rather than etiology, and acute neurologic disorders should be included as precipitants of takotsubo cardiomyopathy. We also theorize that there may be patients with milder forms of stress-related cardiac injury who do not develop left ventricular dysfunction, being similar to the wide range of cardiac manifestations in patients with acute neurologic disorders. We review published literature on neurologic precipitants of takotsubo cardiomyopathy.

[Ball thrombus induced by hibernating myocardium in the left ventricle; report of a case].

An 80-year-old man was admitted to our hospital for examination of a ball thrombus incidentally found in the left ventricle (LV). Coronary angiogram revealed severe triple vessel disease and LV dysfunction. Although LV wall motion in the septum and the apex was akinetic, there were no signs of myocardial infarction. It was diagnosed as an acute LV ball thrombus with hibernating myocardium due to ischemia of the left anterior descending coronary artery. Emergency coronary artery bypass grafting (CABG) and excision of the thrombus were performed. Two weeks after surgery, LV function improved and the patient was discharged from the hospital without any complication. A LV ball thrombus without myocardial infarction is rare, and thought to be caused by hibernating myocardium.

11C-meta-hydroxyephedrine defects persist despite functional improvement in hibernating myocardium.

BACKGROUND: Regional cardiac sympathetic nerve dysfunction develops in hibernating myocardium and may play a role in its association with sudden cardiac death. Interventions to improve cardiac function (i.e., revascularization) improve survival, but the potential reversibility of sympathetic nerve dysfunction remains unclear. METHODS AND RESULTS: Pigs (n = 11) were chronically instrumented with a proximal left anterior descending coronary artery (LAD) stenosis to produce hibernating myocardium. Prior to therapeutic interventions, there was LAD occlusion with collateral-dependent myocardium, reduced regional function (echocardiographic LAD wall-thickening 23% +/- 4% vs 83% +/- 6% in Remote, P < .001), and large defects in (11)C-meta-hydroxyephedrine (HED) PET (48% +/- 4% of LV area, 26% +/- 2% integrated reduction). Successful PCI or pravastatin therapy improved regional (LAD wall-thickening 23% +/- 4% to 42% +/- 6%, P < .05) and global LV function (fractional shortening 24% +/- 2% to 31% +/- 2%, P < .01), but did not alter regional HED uptake, retention, defect size, or defect severity. CONCLUSIONS: Despite significant functional improvement of hibernating myocardium as a result of PCI or pravastatin therapy, there were no changes in HED defect size or severity. Thus, inhomogeneity in myocardial sympathetic innervation persisted, and the lack of plasticity suggests that even in the absence of significant infarction, structural rather than functional defects are responsible for reduced myocardial norepinephrine uptake in chronic ischemic heart disease.

Ablation of post-myocardial infarction focal ventricular tachycardia.

In the chronic phase of myocardial infarction, the presence of scar areas allows the development of macro-reentries which become the most frequent mechanism underlying ventricular tachycardia (VT). A focal mechanism has been already described in the presence of scar in animal models or in humans but only during surgery. We report a case of focal automatic VT arising from postinfarction scar fibrosis, successfully mapped and ablated during an electro-physiological procedure.