Investigation of Myocardial Stunning after Cardiopulmonary Resuscitation in Pigs

Objective To investigate cardiac function and myocardial perfusion during 48 h after cardiopulmonary resuscitation （CPR）, further to test myocardial stunning and seek indicators for long‐term survival after CPR. Methods After 4 min of untreated ventricular fibrillation, fifteen anesthetized pigs were studied at baseline and 2 h, 4 h, 24 h, and 48 h after restoration of spontaneous circulation （ROSC）. Hemodynamic data, echocardiography and gated‐single photon emission computed tomography myocardial perfusion images were carried out. Results Mean arterial pressure （MAP）, coronary perfusion pressure （CPP） and cardiac troponin I （CTNI） showed significant differences between eventual survival animals and non‐survival animals at 4 h after ROSC （109.2±10.7 mmHg vs. 94.8±12.3 mmHg, P=0.048; 100.8±6.9 mmHg vs. 84.4±12.6 mmHg, P=0.011; 1.60±0.13 ug/L vs. 1.75±0.10 ug/L, P=0.046）. Mitral valve early‐to‐late diastolic peak velocity ratio, mitral valve deceleration time recovered 24 h; ejection faction and the summed rest score recovered 48 h after ROSC. Conclusion Cardiac systolic and early active relaxation dysfunctions were reversible within survival animals; cardiac stunning might be potentially adaptive and protective after CPR. The recovery of MAP, CPP, and CTNI could be the indicators for long‐term survival after CPR.

Mechanisms of Myocardial Stunning in Stress-Induced Cardiomyopathy

Stress-induced cardiomyopathy,in contrast to acute myocardial infarction,is a type of acute heart failure characterized by reversible left ventricular dysfunction.Cardiac imaging primarily reveals left ventricle myocardial stunning,81.7%of which is apical type.Emotional or psychological stress usually precedes the onset of stress-induced cardiomyopathy,which is increasingly being recognized as a unique neurogenic myocardial stunning disease.To distinguish between acute myocardial infarction and acute viral or auto-immune myocarditis,this review summarizes specific mechanisms of myocardial stunning in stress-induced cardiomyopathy,such as calcium disorders,metabolic alterations,anatomical and histological variations in different parts of the left ventricle,and microvascular dysfunction.

Effects of sevoflurane preconditioning and postconditioning on rat myocardial stunning in ischemic reperfusion injury

Ischemic preconditioning and postconditioning distinctly attenuate ventricular arrhythmia after ischemia without affecting the severity of myocardial stunning. Therefore, we report the effects of sevofiurane preconditioning and postconditioning on stunned myocardium in isolated rat hearts. Isolated rat hearts were underwent 20 min of global ischemia and 40 min of reperfusion. After an equilibration period （20 min）, the hearts in the preconditioning group were exposed to sevoflurane for 5 min and next washout for 5 min before ischemia. Hearts in the sevoflurane postconditioning group underwent equilibration and ischemia, followed immediately by sevoflurane exposure for the first 5 min of reperfusion. The control group received no treatment before and after ischemia. Left ventricular pressure, heart rate, coronary flow, electrocardiogram, and tissue histology were measured as variables of ventricular function and cellular injury, respectively. There was no significant difference in the duration of reperfusion ventricular arrhythmias between control and sevoflurane preconditioning group （P=0.195）. The duration of reperfusion ventricular arrhythmias in the sevoflurane postconditioning group was significantly shorter than that in the other two groups （P〈0.05）. ＋（dPIdt）max in the sevoflurane preconditioning group at 5, 10, 15, 20, and 30 min after reperfusion was significantly higher than that in the control group （P〈0.05）, and there were no significant differences at 40 min after reperfusion among the three groups （P〉0.05）. As expected, for a 20-min general ischemia, infarct size in heart slices determined by 2,3,5-triphenyltetrazolium chloride staining among the groups was not obvious. Sevofiurane postconditioning reduces reperfusion arrhythmias without affecting the severity of myocardial stunning. In contrast, sevoflurane preconditioning has no beneficial effects on reperfusion arrhythmias, but it is in favor of improving ventricular function and recovering myocardial stunning. Sevoflurane preconditioning and postconditioning may be useful for correcting the stunned myocardium.

Autonomic neurocardiogenic syndrome is stonewalled by the universal definition of myocardial infarction

Myocardial infarction(MI)is defined as myocardial cell death due to prolonged myocardial ischemia.Clinically,troponin rise and/or fall have become the“defining feature of MI”according to the universal definition of MI(UD-MI).Takotsubo syndrome(TS)and TS-related disease conditions also cause troponin elevation with typical rise and/or fall pattern but through a mechanism other than coronary ischemia.By strict application of the clinical diagnostic criteria for type-1 MI,type-2 MI,type-3 MI,and MI with non-obstructive coronary arteries according to the UD-MI including the fourth one published recently,TS and most of the 26 other causes of troponin elevation mentioned in the fourth UD-MI may erroneously be classified as MI.The existing evidence argues for the case that TS by itself is not a MI.Hyper-activation of the autonomic-sympathetic nervous system including local cardiac sympathetic hyper-activation and disruption with nor-epinephrine churn and spillover is the most probable cause of TS.This autonomic neuro-cardiogenic(ANCA)mechanism results in myocardial“cramp”(stunning),the severity and duration of which depend on the degree of the sympathetic-hyperactivation and nor-epinephrine spillover.The myocardial cramp may squeeze the cytosolic free troponin pools causing mild to moderate troponin elevation in TS and TS-related disease conditions.This ANCA syndrome,which has hitherto been enveloped by the UD-MI over more than one decade,may occur in acute,recurrent,and chronic forms.In this critical review,the controversies of UD-MI,evidence for ANCA syndrome,and a hypothetical mechanism for the troponin elevation in ANCA syndrome are provided.

Effects of Berberineon Cardiac Function and ATPase Activity of Postischemic Myocardial Stunned Rat Hearts

This is a report of a study on the protective effect of berberine(Ber) on postischemic myocardial stunning and the role it plays in ATPase activity. Isolated working rat hearts were used with global ischemia for 30 min followed by reperfusing for 40 min. Both systolic and diastolic functions of stunned myocardium were significantly decreased. The recovery of LVSP×HR and CO was 52%±8% and 40%±8% respectively; LVEDP and T were elevated; while both Na +, K +ATPase activity and Ca 2+ , Mg 2+ ATPase activity of myocardial membrane and mitochondria were depressed. Berberine(25 mg·kg -1 ·d -1 , ip, 3 d, and 10 μmol L -1 for isolated heart perfusion) was able to enhance the percent recovery of LVSP×HR and CO to 85%±12% and 75%±11%, respectively, and reduce LVEDP from 298%±64% to 166%±44%, with an improvement in myocardial membrane Na +, K +ATPase activity and mitochondria Ca 2+ , Mg 2+ ATPase activity. This study suggested that berberine can protect cardiac function from ischemia reperfusion stunning injury by preserving ATPase activity in ischemic myocardium.

Takotsubo syndrome:Advances in the understanding and management of an enigmatic stress cardiomyopathy

Takotsubo cardiomyopathy is a syndrome mimicking an acute myocardial infarction in absence of obstructive epicardial coronary artery disease to explain the degree of the wall motion abnormalities. Typically more common in the elderly women, this condition is usually triggered by unexpected emotional or physical stress situations, and is associated with electrocardiogram abnormalities and slight elevation of cardiac biomarkers. The pathophysiological mechanism is not clear yet, but it is believed that a high circulating concentration of catecholamines causes an acute dysfunction of the coronary microcirculation and metabolism of cardiomyocytes, leading to a transient myocardial stunning. Typically, it presents with acute left ventricular systolic dysfunction that in most cases is completely resolved at short term. Recurrences are rare and it is thought that the long-term prognosis is good. We present here a review of the clinical features, pathophysiology and management of this enigmatic condition.

Predictors of left atrial appendage stunning after electrical cardioversion of non-valvular atrial fibrillation

Objective To identify predictors of left atrial appendage stunning after the use of electrical cardioversion to restore sinus rhythm in patients with non-valvular atrial fibrillation. Methods A total of 68 consecutive patients (45 men,23 women,60.5±8.7 years of age) with non-valvular atrial fibrillation undergoing electrical cardioversion were enlisted in this study. Clinical and echocardiographic variables were analyzed by univariate regression and multivariate logistic regression to investigate the relationship between occurrences of left atrial appendage stunning and these factors. Results Univariate analysis revealed that,in comparing patients without and with left atrial appendage stunning,there were significant differences in the duration of atrial fibrillation > 8 weeks (32.3% vs 75.5%,P <0.001),left atrial diameter > 50 mm (29.0% vs 54.1%,P <0.05),left atrial emptying fraction (31.5%±7.8% vs 27.1%±8.5%,P <0.05),left ventricular ejection fraction < 50% (38.7% vs 67.6%,P <0.05),maximum electrical energy (96.8 J±65.8 J vs 156.8 J±100.8 J,P <0.01),cumulative electrical energy 146.8 J±142.6 J vs 290.5 J±242.1 J, P <0.01) and number of electrical cardioversion shocks (1.7±0.9 vs 2.43±1.20,P <0.05). However,backward stepwise multivariate logistic regression analysis identified as significant and independent predictors of left atrial appendage stunning only duration of atrial fibrillation > 8 weeks (OR=7.249,95%CI=1.998-26.304, P <0.01),left atrial diameter > 50 mm (OR=3.896,95%CI=1.105-13.734,P <0.05),left ventricular ejection fraction < 50% (OR=4.465,95%CI=1.51713.140, P <0.01) and cumulative energy of electrical cardioversion (OR=1.004,95%CI=1.000-1.008, P <0.05). Conclusions Duration of atrial fibrillation >8 weeks,left atrial diameter >50 mm,left ventricular ejection fraction <50%,and cumulative energy of electrical cardioversion are independent predictors of left atrial appendage stunning. Anticoagulation treatment should be individualized for patients undergoing electrical cardioversion to reduce the risk of both cardioversion-related thromboembolic events and hemorrhagic complications caused by warfarin treatment.