Recovery Of Left Ventricular Function Research Articles

Predictors of recovery of left ventricular dysfunction after ablation of frequent ventricular premature depolarizations

Frequent ventricular premature depolarizations (VPDs) can cause reversible left ventricular (LV) dysfunction. However, not all patients normalize their LV function after VPD elimination. To evaluate predictors of recovery of LV function following the elimination of frequent VPDs. We identified patients with ≥10% VPDs/24 h and an LV ejection fraction of <50% who underwent successful ablation between 2007 and 2011. Subjects were classified as having reversible (≥10% increase to a final LV ejection fraction of ≥50%) or irreversible (≤10% increase or final LV ejection fraction <50%) LV dysfunction on the basis of echocardiographic follow-up. A reference group with ≥10% VPDs but normal LV function was identified. One hundred fourteen patients with ≥10% VPDs were identified; 66 had preserved and 48 had impaired LV function. Over a median follow-up of 10.6 months, 24 of 48 were classified as reversible and 13 of 48 as irreversible and 11 of 44 were excluded. There was a gradient of VPD QRS duration between the control, reversible, and irreversible groups (mean VPD QRS 135, 158, and 173 ms, respectively; P < .001). This gradient persisted even for the same site of origin. In multivariate analysis, the only independent predictor of irreversible LV function was VPD QRS duration (odds ratio 5.07 [95% confidence interval 1.22-21.01] per 10-ms increase). In patients with LV dysfunction and frequent VPDs, we identified VPD QRS duration as the only independent predictor for the recovery of LV function after ablation. This suggests that VPD QRS duration may be a marker for the severity of underlying substrate abnormality.

Temporal evolution of left ventricular dyssynchrony after myocardial infarction: relation with changes in left ventricular systolic function

The relationship between temporal changes in left ventricular (LV) dyssynchrony and LV functional recovery after acute myocardial infarction (MI) remains unclear. Accordingly, the aim of the present study was to evaluate the temporal evolution of LV synchronicity after acute MI, and to explore the relationship between changes in LV systolic function and LV synchronicity. In 193 patients with a first acute MI, LV dyssynchrony (SDI) and global systolic function were evaluated with real-time three-dimensional echocardiography 48 h after percutaneous coronary intervention and at 6 months follow-up. Changes in LV systolic function and synchronicity were evaluated at the follow-up and the relationship between these changes was explored. A total of 59 (40%) patients had an anterior acute MI. Median peak value of troponin T was 2.97 µg/L (1.41-6.06 µg/L). Mean LVEF was 47 ± 8% and mean SDI was 5.01 ± 2.10%, respectively. At 6 months follow-up, a significant improvement in LVEF (50 ± 9 vs. 47 ± 8%; P < 0.001) and SDI (4.52 ± 1.97 vs. 5.01 ± 2.10%; P = 0.003) was noted. A strong correlation was found between LVEF change and SDI change (β = -0.63; P < 0.001). At multivariate analysis, SDI change was an independent factor associated with changes in LVEF. Importantly, an addition of SDI change to the multivariate model significantly increased the R(2) from 0.41 to 0.57 (F change 49.0, P < 0.001). A temporal evolution of LV synchronicity was observed after a first, mechanically reperfused, acute MI. The reduction in LV dyssynchrony independently influenced LV functional recovery in these patients.

Recovery of left ventricular function after percutaneous revascularization of a left main chronic total occlusion

Surgical revascularization of left main and/or three-vessel coronary artery disease (CAD) is associated with improved survival in patients with left ventricular dysfunction when compared to medical therapy and can result in improved left ventricular ejection fraction (LVEF) [1]. Multivessel percutaneous coronary intervention (PCI) is equivalent to surgery regarding short and intermediate term mortality, and left main PCI has emerged as a safe and effective alternate to surgical revascularization [2]. However, outcomes of unprotected left main PCI in patients with severely depressed LVEF have not been examined. We report a patient with left main chronic total occlusion, multivessel CAD, and dilated cardiomyopathy, in whom complete revascularization via PCI resulted in decreased left ventricular size and improved LVEF.

Unexpected and rapid recovery of left ventricular function in patients with peripartum cardiomyopathy: impact of cardiac resynchronization therapy

Aim Peripartum cardiomyopathy (PPCM) is a rare cause of dilated cardiomyopathy responsible for heart failure toward the end of pregnancy, which can lead to chronic heart failure in 50% of cases. In this short report, we assessed the benefit of cardiac resynchronization in patients with PPCM and chronic systolic dysfunction despite optimal medical treatment. For the last 10 years, we managed eight patients diagnosed with PPCM. Two of them presented severe systolic dysfunction, and medical treatment resulted in limited improvement from 10% to 25% and from 25% to 28% despite optimal treatment for 9 and 6 years, respectively. These two patients were porposed to receive an implantatable cardioverter defibrillator (ICD) and cardiac resynchronization therapy (CRT). Six months after ICD-CRT treatment, we observed a significant improvement in systolic function from 25% to 45% and 28% to 50%, respectively, and positive remodelling with reduction of left ventricular end-diastolic volume from 216 to 144 mL and from 354 to 105 mL, which represent a 34% and a 70% reduction, respectively. Physicians in charge of patients with PPCM should offer the opportunity of CRT for patients whose cardiac function has not significantly improved under standard medical treatment.

Rest left ventricular function and contractile reserve by dobutamine stress echocardiography in peripartum cardiomyopathy

AimsTo assess whether contractile reserve during dobutamine stress echocardiography (DSE) can predict left ventricular functional recovery in patients with peripartum cardiomyopathy and to assess myocardial fibrosis by magnetic resonance imaging (MRI) in these patients. MethodsNine patients with peripartum cardiomyopathy were enrolled. All patients underwent DSE and were followed for six months, when a rest Doppler echocardiogram was repeated. MRI was also performed at the beginning of follow-up to identify myocardial fibrosis. ResultsMean age was 29±7.9 years and mean left ventricular ejection fraction at baseline was 39.4±8.6% (range 24–49%). Eight of the nine patients showed left ventricular functional recovery with mean ejection fraction at follow-up of 57.1±13.8%. The ejection fraction response to DSE did not predict recovery at follow-up. On the other hand, left ventricular ejection fraction at baseline correlated with ejection fraction at follow-up. Mild fibrosis was detected in only one patient. ConclusionLeft ventricular ejection fraction at baseline was a predictor of left ventricular functional recovery in patients with peripartum cardiomyopathy. Dobutamine stress echocardiography at presentation of the disease did not predict recovery at follow-up. Myocardial fibrosis appeared to be uncommon in this cardiomyopathy.

A change of heart: case series: peripartum cardiomyopathy

IntroductionCardiac disease is the leading cause of maternal death in the United Kingdom. Peripartum cardiomyopathy (PPCM) accounts for about 17% of these deaths.We present a series of five women who...

Adenosine-mediated inhibition of 5′-AMP-activated protein kinase and p38 mitogen-activated protein kinase during reperfusion enhances recovery of left ventricular mechanical function

Attenuation of excessive rates of myocardial glycolysis limits proton production and Ca(2+) overload during reperfusion and improves recovery of post-ischemic left ventricular (LV) function. In order to elucidate mechanisms underlying glycolytic inhibition by adenosine (ADO), this study tested the hypothesis that the beneficial effects of ADO are due to Ser/Thr protein phosphatase (PP)-mediated inhibition of 5'-AMP-activated protein kinase (AMPK) and phosphofructokinase-2 (PFK-2). In isolated perfused working rat hearts subjected to global ischemia (GI) and reperfusion, ADO (500μmol/l), added 5min prior to the onset of GI and present throughout reperfusion, inhibits glycolysis and proton production during reperfusion and improves post-ischemic LV work. These metabolic effects of ADO are also evident during aerobic perfusion. Assays of glycolytic intermediates show that ADO-induced glycolytic inhibition occurs at the step catalyzed by PFK-1, an effect mediated by reduced activation of PFK-2 by AMPK. The PP1 and PP2A inhibitors, cantharidin (5μmol/l) or okadaic acid (0.1μmol/l), added 10min prior to ADO prevent ADO-induced inhibition of glycolysis and AMPK, as well as ADO-induced cardioprotection. ADO also inhibits p38 MAPK phosphorylation during reperfusion in a cantharidin-sensitive manner, and pharmacological inhibition of p38 MAPK (by SB202190, 10μmol/l) during reperfusion also reduces glycolysis and is cardioprotective. These results indicate that attenuation of glycolysis during reperfusion and cardioprotection can be achieved by inhibition of the stress kinases, AMPK and p38 MAPK.

Central Extracorporeal Life Support in Pheochromocytoma Crisis

Pheochromocytoma is a catecholamine-secreting tumor associated with clinical presentations ranging from paroxysmal hypertension to intractable cardiogenic shock. We report the use of central extracorporeal life support (ECLS) in a young woman admitted to the intensive care unit with cardiogenic shock. Her medical history included neurofibromatosis type I and pheochromocytoma. ECLS was needed because of severe left ventricular failure and inotropic therapy unresponsiveness. ECLS permitted full recovery of left ventricular function. Right adrenelectomy was performed 4 months later. In this case, central ECLS was used to treat pheochromocytoma-induced cardiogenic shock complicated by pulmonary edema.

Rest left ventricular function and contractile reserve by dobutamine stress echocardiography in peripartum cardiomyopathy

AimsTo assess whether contractile reserve during dobutamine stress echocardiography (DSE) can predict left ventricular functional recovery in patients with peripartum cardiomyopathy and to assess myocardial fibrosis by magnetic resonance imaging (MRI) in these patients. MethodsNine patients with peripartum cardiomyopathy were enrolled. All patients underwent DSE and were followed for six months, when a rest Doppler echocardiogram was repeated. MRI was also performed at the beginning of follow-up to identify myocardial fibrosis. ResultsMean age was 29±7.9 years and mean left ventricular ejection fraction at baseline was 39.4±8.6% (range 24–49%). Eight of the nine patients showed left ventricular functional recovery with mean ejection fraction at follow-up of 57.1±13.8%. The ejection fraction response to DSE did not predict recovery at follow-up. On the other hand, left ventricular ejection fraction at baseline correlated with ejection fraction at follow-up. Mild fibrosis was detected in only one patient. ConclusionLeft ventricular ejection fraction at baseline was a predictor of left ventricular functional recovery in patients with peripartum cardiomyopathy. Dobutamine stress echocardiography at presentation of the disease did not predict recovery at follow-up. Myocardial fibrosis appeared to be uncommon in this cardiomyopathy.

Mitral valve surgery in low ejection fraction, severe ischemic mitral regurgitation patients

The optimal surgical treatment of chronic ischemic mitral regurgitation still is the subject of much debate in the surgical and cardiological communities. Although combined restrictive mitral annuloplasty and revascularization has demonstrated good results with regard to improvement of clinical status, low rates of recurrent mitral regurgitation and sustained left ventricular reverse remodeling, a survival benefit still has not been demonstrated. In addition, not all patients improve. Remaining issues in this field relate to identification of patients who will benefit from treatment, and to further improve and individualize treatment modalities. More data support the use of restrictive mitral annuloplasty and revascularization. New surgical techniques to improve mitral competence (posterior leaflet augmentation) and to promote left ventricular reverse remodeling in severely dilated hearts (addressing the subvalvular apparatus) are promising. Disease-specific annuloplasty rings have not (yet) proven additional value. New imaging modalities are available to assess the many components that constitute the complex pathophysiology of remodeling. The remaining challenge for cardiologists and surgeons is how to integrate data from different imaging techniques that assess mitral valve geometry and left ventricular size, geometry, function and potential functional recovery in order to individualize and optimize the surgical approach to patients with chronic ischemic mitral regurgitation.

T2-Imaging of the ischemic area-at-risk predicts recovery of cardiac function after acute ST-elevation myocardial infarction

Background T2-weighted edema imaging identifies the ischemic area at risk during acute myocardial infarction. Myocardial salvage occurs in the area at risk without late gadolinium enhancement (LGE). The degree of myocardial salvage is prognostically important, but its effect on recovery of left ventricular (LV) function is not known. The purpose of this study was to determine if the degree of myocardial salvage predicts recovery of function after an acute ST-elevation myocardial infarction (STEMI). Methods We assessed patients with no known prior CAD postSTEMI. Imaging was performed within 72 hours of the acute event and was then repeated 6-12 weeks postinfarction. The degree of myocardial salvage was obtained by subtracting the percentage LGE from the T2 area at risk. The degree of salvage was compared to the percentage improvement in LVEF by nonparametric Spearman rank correlation coefficient analysis. Results Twenty-three patients were recruited for the study. One patient refused a second study, 2 had technical difficulties, and 5 had a baseline LV ejection fraction (EF) of ≥50%, leaving a final study population of 15 subjects. The mean age of the sample was 59.3 ± 11.7 years; 86.7% were male and 93.3% were Caucasian. Hypertension, hyperlipidemia, and tobacco use was present in 40.0%, 73.3%, and 46.7%, respectively. The mean BMI was 30.8 ± 4.1, and 9/15 (60%) had a BMI ≥30. The mean LDL was 118.7 ± 33.0, and the mean HgA1c was 6.7 ± 1.8. The baseline mean LVEF was 42.1 ± 6.6%, and increased to 45.1 ± 9.8%, a mean increase of 3.0%. The mean percentage T2 enhancement was 41.2 ± 17.4%, and the mean burden of LGE was 23.5 ± 14.0%, giving a percentage myocardial salvage of 17.7%. The degree of myocardial salvage correlated moderately with an improvement of LVEF from the acute to recovery CMR, with a Spearman correlation coefficient of 0.59 (p= 0.020). Conclusions

Reversal of oxidant-mediated biochemical injury and prompt functional recovery after prolonged single-dose crystalloid cardioplegic arrest in the infantile piglet heart by terminal warm-blood cardioplegia supplemented with phosphodiesterase III inhibitor

The benefit of terminal blood cardioplegia (TWBCP) is insufficient after prolonged ischemia associated with inevitable oxidant-mediated injury by this modality alone. We tested the effects of TWBCP supplemented with high-dose olprinone, which is a phosphodiesterase III inhibitor, a clinically available compound with the potential to reduce oxidant stress and calcium overload. We evaluated the effects with respect to avoiding oxidant-mediated myocardial reperfusion injury and prompt functional recovery after prolonged single-dose crystalloid cardioplegic arrest in a infantile piglet cardiopulmonary bypass (CPB) model. Fifteen piglets were subjected to 90 min of cardioplegic arrest on CPB, followed by 30 min of reperfusion. In group I, uncontrolled reperfusion was applied without receiving TWBCP; in group II, TWBCP was given; in group III, TWBCP was supplemented with olprinone (3 μg/ml). Myocardial performance was evaluated before and after CPB by a left ventricular (LV) function curve and pressure-volume loop analyses. Biochemical injury was determined by measurements of troponin-T and lipid peroxide (LPO) in coronary sinus blood. Group III showed significant LV performance recovery (group I, 26.5% ± 5.1%; group II, 42.9% ± 10.8%; group III, 81.9% ± 24.5%, P < 0.01 vs. groups I and II), associated with significant reduction of troponin-T and LPO at the reperfusion phase. No piglets in group III needed electrical cardioversion. We concluded that TWBCP with olprinone reduces myocardial reperfusion injury by reducing oxidant-mediated lipid peroxidation, and it accelerates prompt and persistent LV functional recovery with suppression of reperfusion arrhythmia.

In This Issue

HomeCirculation ResearchVol. 110, No. 1In This Issue Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIn This Issue Originally published6 Jan 2012https://doi.org/10.1161/RES.0b013e3182471126Circulation Research. 2012;110:2Fetal Cell Differentiation in Maternal Hearts (p 82)Placentas could be a source of heart-repairing cells, sayKara et al.Download figureDownload PowerPointPregnant women with cardiomyopathy are known to have a higher recovery rate than other individuals with the disease. It is also known that during pregnancy, fetal cells can pass to the mother and incorporate into her tissues, sometimes remaining there for years. Kara et al suspected that fetal cells might be contributing to the repair process in mothers with cardiomyopathy. To test this, they induced myocardial infarction in pregnant mice and studied what the fetal cells were doing. They discovered that these cells homed to the injured heart, and once there, they differentiated into cardiomyocytes, smooth muscle cells, and endothelial cells. In fact, the fetal cells could form entirely new blood vessels. Approximately 40% of the fetal cells in the mothers' hearts expressed a transcription factor, called Cdx2, which is a marker of trophoblast stem cells—the cells that give rise to the placenta during embryogenesis. Until now, trophoblast stem cells had been thought only to contribute to the formation of the placenta. Thus, the new work suggests that placentas, which are routinely discarded in hospital maternity wards, could be a valuable source of multipotent stem cells.Circadian Infarct Size in STEMI (p 105)Time of day affects both severity of and recovery from heart attacks in humans, reportReiter et al.Download figureDownload PowerPointBoth blood pressure and baseline heart rate follow circadian rhythms. Even the heart cells themselves display a daily rhythm in their expression levels of clock proteins. Hence, it is not surprising that heart attacks tend to occur during a particular part of the day: the early hours of the morning. But, that the severity of heart attacks and the recovery from them were also worse in these early hours was an unexpected discovery made in mice last year and reported in Circulation Research. Now Reiter et al have found that the same time-of-day effect on severity and recovery also applies to human patients. A retrospective study of 1031 heart attack patients admitted to the Minneapolis Heart Institute between 2006 and 2010 revealed that infarct size was largest in patients that suffered heart attacks at 1 am. The subsequent recovery of left ventricular function was also more impaired in these patients. These results have implications not only for patient prognosis, but also for evaluations of potential ischemia/reperfusion therapies. Previous Back to top Next FiguresReferencesRelatedDetails January 6, 2012Vol 110, Issue 1 Advertisement Article InformationMetrics © 2012 American Heart Association, Inc.https://doi.org/10.1161/RES.0b013e3182471126 Originally publishedJanuary 6, 2012 PDF download Advertisement

Coronary artery fistula with myocardial infarction due to steal syndrome

Sirs: Coronary artery fistulas are anomalous connections between a coronary artery and a cardiac chamber or great vessel [1]. They are rare abnormalities with a reported incidence of 0.13–0.18% of patients undergoing coronary angiography [2, 3]. The majority of coronary artery fistulas are congenital in origin, but they have been reported as acquired complications of chest trauma and surgery also. Most of them are diagnosed incidentally in asymptomatic patients, but depending on shunt volume, congestive heart failure can develop [1]. Furthermore, myocardial ischemia due to a ‘steal’ from the adjacent myocardium has been reported [4–12], but true existence of this phenomenon is a controversial issue [13]. We present the case of a young female with a large coronary artery fistula originating from the proximal left anterior descending artery (LAD), and evidence of a coronary steal syndrome is provided by fractional flow reserve (FFR). A so far healthy 36-year-old female without cardiovascular risk factors presented in our emergency department with sudden onset chest pain following a long exhausting motorbike trip. Physical examination was unremarkable, and no cardiac murmur was audible. Baseline electrocardiogram showed T inversions in the anterior leads, and the cardiac biomarkers were elevated with a peak high sensitive Troponin T of 0.55 lg/l and a peak creatine kinase of 623 U/l. Subsequent left heart catheterization ruled out coronary artery disease, but a large coronary artery fistula originating from the proximal LAD draining into to the pulmonary trunk was found (Fig. 1). Ventriculography showed a hypokinesis of the anterior segments distal to the origin of the fistula, and magnetic resonance tomography revealed a late enhancement pattern of subendocardial myocardial infarction (Fig. 2). Hypothesizing a coronary steal syndrome due to the fistula, a second procedure with left and right heart catheterization was performed. Hemodynamic and oximetric measurements revealed a systemic blood flow (QS) of 6.0 l/min and a pulmonary blood flow (QP) of 6.7 l/min, leading to a relatively small calculated left-to-right shunt of 0.68 l/min (QP/QS = 1.12), and pulmonary artery pressure was in normal range. FFR in the distal LAD was 0.78 under maximal hyperemia, raising to 0.95 while temporary experimental occlusion of the fistula using a 3.0/15 mm standard balloon catheter. In consideration of this evidence of steal syndrome, coil embolization of the fistula was performed in the same procedure, using 2 Detach embolization coils (Cook Medical, Bloomington, IN, USA) [2–2 and 2–4 (diameter in mm–length in cm)] in each of the two main branches and another two coils (3–4 and 3–6) in the bifurcation of the fistula (Fig. 1). Finally, a FFR of 1.0 was measured in the distal LAD. The patient was discharged free of symptoms the following day. At 3-month follow-up, the patient was free of symptoms, and echocardiography revealed complete recovery of left ventricular function. A coronary artery fistula is a rare but not an exceptional finding on a routine coronary angiogram. Small fistulas need no specific treatment, but if they are hemodynamically important, elective closure is recommended. Coil embolization of coronary artery fistulas is considered as a safe and effective treatment [14–16], and the aim of the procedure is to achieve complete occlusion at as distal a location as possible in the fistulous vessel [1]. Based on case reports, coronary artery fistulas are considered as a rare cause of myocardial infarctions that T. Harle (&) K. Kronberg A. Elsasser Department of Cardiology, Heart Center, Klinikum Oldenburg gGmbH, Rahel-Straus-Str. 10, 26133 Oldenburg, Germany e-mail: t.haerle@gmx.de

Endothelin-B Receptors and Left Ventricular Dysfunction after Regional versus Global Ischaemia-Reperfusion in Rat Hearts

Background. Endothelin-1 (ET-1) is implicated in left ventricular dysfunction after ischaemia-reperfusion. ETA and ETB receptors mediate diverse actions, but it is unknown whether these actions depend on ischaemia type and duration. We investigated the role of ETB receptors after four ischaemia-reperfusion protocols in isolated rat hearts. Methods. Left ventricular haemodynamic variables were measured in the Langendorff-perfused model after 40- and 20-minute regional or global ischaemia, followed by 30-minute reperfusion. Wild-type (n = 39) and ETB-deficient (n = 41) rats were compared. Infarct size was measured using fluorescent microspheres after regional ischaemia-reperfusion. Results. Left ventricular dysfunction was more prominent in ETB-deficient rats, particularly after regional ischaemia. Infarct size was smaller (P = 0.006) in wild-type (31.5 ± 4.4%) than ETB-deficient (45.0 ± 7.3%) rats after 40 minutes of regional ischaemia-reperfusion. Although the recovery of left ventricular function was poorer after 40-minute ischaemia-reperfusion, end-diastolic pressure in ETB-deficient rats was higher after 20 than after 40 minutes of regional ischaemia-reperfusion. Conclusion. ETB receptors exert cytoprotective effects in the rat heart, mainly after regional ischaemia-reperfusion. Longer periods of ischaemia suppress the recovery of left ventricular function after reperfusion, but the role of ETB receptors may be more important during the early phases.

A Simple Electrocardiographic Predictor of Early Recovery of Left Ventricular Function in Stress Cardiomyopathy

Objective: To identify electrocardiographic parameters that predict extent of early improvement in ejection fraction (EF) in patients with stress cardiomyopathy. Methods: We collected baseline clinical, ECG and imaging data and follow up echocardiography data on 30 consecutive patients with stress cardiomyopathy. The relationship between baseline ECG parameters and Delta EF was evaluated by univariate and multivariable analysis. Results: Median EF improved from 35% to 55% (p Conclusion: The number of leads with T wave inversion is negatively correlated with and is an independent predictor of the extent of early improvement of EF in patients with stress cardiomyopathy. Hence the ECG at initial presentation can be used as a simple tool to predict LV function recovery.

Enhancement of Chronic Intermittent Hypobaric Hypoxia Adaptation on Cardiac Protection of Anandamide in Rats

Anandamide (AEA) has cardiac protective effect and chronic intermittent hypobaric hypoxia (CIHH) adaptation can change the reactivity of the body to some chemicals. We hypothesized that CIHH adaptation could enhance the cardiac protective effect of AEA against ischemia/reperfusion injury. Sprague-Dawley rats were randomly divided into five groups: CIHH for 14 days (CIHH14), CIHH for 28 days (CIHH28), anandamide (AEA), CIHH plus AEA (CIHH+AEA) and control groups. The rats in the CIHH groups were exposed to CIHH for 14 or 28 days, 6 h per day, respectively. The isolated hearts in the AEA rats were treated with 1 nM AEA. The rats in the CIHH+AEA were treated with both CIHH and AEA. Under normal condition, there was no significant in cardiac function among the groups significantly (P ＞ 0.05). In the CIHH+AEA rats, like the CIHH28 rats, the recovery of left ventricular function after ischemia/ reperfusion (30 min global no-flow ischemia followed by 60 min of reperfusion, I/R) was much better than that in the CIHH14 and control rats. Also, LDH in coronary artery effluent was decreased in the CIHH+AEA rats. Compared with the CIHH14, the AEA and control rats, superoxide dismutase (SOD) and malondialdehyde (MDA) in myocardium of the CIHH+AEA rats were increased and decreased after I/R, respectively. The cardiac protective effect in the CIHH+AEA rats was offset by AM630, a CB2 receptor antagonist, but not by AM251, a CB1 receptor antagonist. These data suggest that CIHH adaptation enhances the cardiac protection of AEA through activation of CB2 receptor and increase of anti-oxidation in the myocardium of rats.

Peripartum Cardiomyopathy Presenting with Predominant Left Ventricular Diastolic Dysfunction: Efficacy of Bromocriptine

Management of patients with peripartum cardiomyopathy (PPCM) is still a major clinical problem, as only half of them or slightly more show complete recovery of left ventricular (LV) function despite conventional evidence-based treatment for heart failure. Recent observations suggested that bromocriptine might favor recovery of LV systolic function in patients with PPCM. However, no evidence exists regarding its effect on LV diastolic dysfunction, which is commonly observed in these patients. Tissue Doppler (TD) is an echocardiographic technique that provides unique information on LV diastolic performance. We report the case of a 37-year-old white woman with heart failure (NYHA class II), moderate LV systolic dysfunction (ejection fraction 35%), and severe LV diastolic dysfunction secondary to PPCM, who showed no improvement after 2 weeks of treatment with ramipril, bisoprolol, and furosemide. At 6-week followup after addition of bromocriptine, despite persistence of LV systolic dysfunction, normalization of LV diastolic function was shown by TD, together with improvement in functional status (NYHA I). At 18-month followup, the improvement in LV diastolic function was maintained, and normalization of systolic function was observed. This paper might support the clinical utility of bromocriptine in patients with PPCM by suggesting a potential benefit on LV diastolic dysfunction.

Hypocalcemia as a reversible cause of heart failure

Calcium plays a key role in heart muscle contraction and relaxation. Hypocalcemic heart failure is a rare and potentially reversible disturbance, which reflects this intrinsic relationship.The authors present the case of a 35-year-old woman who developed acute heart failure during the early postoperative period following total thyroidectomy. The echocardiogram showed severe global left ventricular dysfunction. Laboratory tests showed severe hypocalcemia and new-onset hypoparathyroidism. Cardiac catheterization showed angiographically normal coronary arteries. After clinical, hemodynamic and metabolic stabilization, a repeat echocardiogram revealed recovery of left ventricular function. Subsequently, cardiac magnetic resonance imaging was performed, which also showed no alterations. The patient was discharged asymptomatic, medicated with calcium carbonate, calcitriol and levothyroxine.This case highlights the importance of considering hypocalcemia as a cause of reversible myocardial dysfunction.

Abstract P285: Impaired Recovery of Left Ventricular Function After Acute Myocardial Reperfusion Injury Is Rescued by the Anti-inflammatory Peptide Annexin-A1 ex Vivo

The glucocorticoid-regulated protein annexin-A1 (ANX-A1) is a key effector molecule of anti-inflammatory glucocorticoid actions. We have shown that the N-terminal derived peptide ANX-A1(2–26) preserves cardiomyocyte viability after metabolic inhibition in vitro. Our hypothesis was that ANX-A1 preserves the myocardium post-ischemic injury. ANX-A1(2–26)(0.3μM) prevented adult rat cardiomyocyte injury, whether present for hypoxia-reoxygenation (LDH release reduced from 4.1±0.7- to 1.1±0.2-fold n=11 P&lt;0.001) or only on reoxygenation (LDH release reduced to 1.4±0.4-fold n=11, P&lt;0.001). Similar protection at both time points was also evident on cardiomyocyte viability (trypan blue exclusion). The recovery of post-ischemic left ventricular (LV) function in intact rodent hearts was also protected. After 20mins reperfusion, the recovery of LV developed pressure (LVDP) remained significantly impaired in untreated rat hearts (47±5% baseline, n=11) whereas addition of ANX-A1(2–26)(0.3μM) on reperfusion improved LVDP recovery (to 66±7% baseline, n=13, p&lt;0.05). Phosphorylation of both Akt (1.9±0.2-fold, P&lt;0.05) and phospholamban (3.4±0.4-fold, P&lt;0.05) was also enhanced by ANX-A1(2–26). Similar ANX-A1(2–26)-induced rescue of LV function was observed in mouse hearts after acute myocardial reperfusion injury (57±7% of baseline, n=11 untreated hearts vs 78±8% baseline, n=6 ANX-A1(2–26)-treated hearts, p&lt;0.05). ANX-A1(2–26) cardioprotection was associated with attenuated cardiac enzyme release (LDH, CK) and Akt phosphorylation (3.1±0.8-fold, P&lt;0.005). In contrast, deficiency of endogenous ANX-A1 further exacerbated recovery of post-ischemic LV function, across LVDP (to 29±4% baseline, P&lt;0.001), LV end-diastolic pressure (to 5.5±1.0-fold baseline, P&lt;0.001), LV+dP/dt (to 33±4% baseline, P&lt;0.001), LV-dP/dt (to 36±4% baseline, P&lt;0.001) and rate-pressure product (to 24±4% baseline, P&lt;0.001). This is the first evidence that ANX-A1 or its mimetic ANX-A1(2-26) preserve post-ischemic recovery of LV function. ANX-A1 is thus an endogenous regulator of LV function. Furthermore, ANX-A1-based therapies may thus represent a novel clinical approach for the prevention and treatment of reperfusion injury.