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.

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.

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.

Viabilidade miocárdica: visão do clínico / Myocardial viability: a clinician perspective

A pesquisa de viabilidade miocárdica permite identificar segmentos disfuncionantes causados por obstruções arteriais que têm a capacidade de recobrar parcial ou totalmente a capacidade contrátil. Estima-se que 20% a mais de 50% dos pac ientes com disfunção crônica do ventriculo esquerdo t6êm significativa quantidade de miocárdio viável e, portanto, com potencial recuperação de contratilidade miocárdica após revascularização. Várias dfiferentes técnicas podem ser utilizadas para a identificação de miocárdio viável. Estudos demonstraram melhora acima de 5% da FEVE após revascularização em torno de 60% dos pacientes. Uma metanálise demonstrou associação significativa entre revascularização e melhora nas taxas de sobrevida em pacientes com evidência de viabilidade miocárdica, independente da técnica de imagem utilizada. Uma série de limitações dos estudos prévios de viabilidade deve ser considerada. Estes esteudis envolvem amostras com pequeno número de pacientes, são retrospectivos, ocorre uma inequívoca seleção seleção de pacientes e um bias de referência pós-teste. Foi recentemente publicado o Estudo STICH viability, estudo randomizado entre tratamento clínico e cirúrgico. Pacientes portadores de viabilidade miocárdica aprsentaram menores taxas de mortalidade, assim como menores taxas de do evento combinado de óbito e hospitalização por causas cardovasculares. Entretanto, após ajuste para outras variáveis de risco de um modelo multivariado, apresença de viabilidade não foi significativamente associada com a taxa de óbito, e sim a FEVE, volumes diastólicos e sistólicos finais. A viabilidade não deve, portanto, ser considerada obrigatória para a indicação cirúrgica, mas é p elevado e anatomia mais complexa.(AU)articularmente importante naqueles pacientes com risco.

Ressonância magnética: a palavra final? / Magnetic resonance: the final word?

A viabilidade miocárdica pode ser avaliada por testes de imagem não invasivos. Recentemente, a técnica de realce tardio miocárdico por ressonância magnética cardíaca se juntou a esta família de testes e é considerada, hoje, como a técnica padrão-ouro pela diretrizes nacionais e internacionais e pelo consenso de especialistas. Em medicina, não há palavra final; porém, no momento e baseado na literatura atual, a ressonância magnética cardíaca pode ser considerada pelo clínico como o mais próximo da palavra final em termos de viabilidade miocárdica para a decisão de revascularização miocárdica. As evidências atuais demonstram que a ressonância é um método capaz de definir áreas de miocárdio viável e não viável até nível quase microscópico. A correlação da viabilidade celular com a viabilidade contrátil, isto é, a probabilidade de melhora ou recuperação contrátil após revascularização miocárdica pode se predita com alta acurácia pela técnica de realce tardio miocárdio por ressonância magnética. Nos casos complexos, pode-se, ainda, aumentar a especificidade, associando-se a técnica de cinerressonância com dobutamina. Uma vasta gama de informações adicionais, como a detecção da obstrução microvascular ou no-reflow, entre muitas outras, conferem uma impressionante capacidade diagnóstica e prognóstica à ressonância magnética cardíaca na doença arterial coronária aguda e crônica. Os dados controversos do recente subestudo de viabilidade do estido STICH não responderam de forma definitiva às questões clínicas essenciais, que permanecem em aberto e, em especial, levantaram a hipótese de que a viabilidade deva ser investigada de rotina com métodos mais acurados, como a ressonância magnética cardíaca.

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.

[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.

Anesthetic management of a patient with deteriorated cardiac function following cardiopulmonary resuscitation.

A 73-year-old woman suffering from an abdominal aortic aneurysm (AAA), unstable angina, and low cardiac function (32% of ejection fraction) was scheduled for abdominal aortic replacement and coronary artery bypass grafting. However, before the scheduled operation the patient fell into cardiopulmonary arrest with ventricular fibrillation due to rupture of the AAA. Immediate cardiopulmonary resuscitation (CPR) using epinephrine and electrical defibrillation restored the spontaneous circulation. Following CPR, a continuous high-dose dopamine infusion (15 µg/kg/min) was initiated and emergent abdominal aortic replacement was performed. On arrival at the operating room, the patient showed serious hypotension, atrial fibrillation with multifocal ventricular premature contractions, and metabolic acidosis. Transesophageal echocardiography (TEE) suggested that the circulatory collapse might have resulted from diastolic dysfunction and deteriorated compliance of the left ventricular (LV) wall, possibly due to myocardial stunning induced by myocardial ischemia, and tachycardia induced by hypovolemia, both of which are influenced by high doses of catecholamine. We accordingly transfused adequate amounts of blood products and gradually decreased the infusion rate of dopamine to 4 µg/kg/min, while carefully monitoring blood pressure, central venous pressure, and TEE. By the end of surgery hemodynamic parameters had recovered to near normal levels. In post-resuscitated and hypovolemic patients, caution should be taken when administering high levels of exogenous catecholamines, which can induce myocardial stunning and circulatory collapse.

Acute myelitis with neurogenic stunned myocardium in a boy.

Neurogenic stunned myocardium is characterized by reversible left ventricular dysfunction, which occurs after severe central nervous system injury in patients without coronary artery disease. It has been described in association with subarachnoid hemorrhage, Guillain-Barré syndrome, and metastatic brain tumors in adults, but has been rarely reported in association with acute myelitis. Described here is a novel case of acute myelitis in a child associated with neurogenic stunned myocardium. This case demonstrates that patients with acute myelitis may harbor a risk of sympathetic dysregulation, leading to neurogenic myocardial dysfunction.

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.

[Influence of coronary revascularization on chronic ischemic stunning of the conduction system of the heart]. / Influência da revascularização coronária sobre o atordoamento isquémico crónico do sistema de condução cardíaco.

UNLABELLED: About one fourth of patients (pts) with coronary artery disease (CAD) referred for coronary bypass surgery (CABG) exhibits some kind of intraventricular conduction defect (IVCD). OBJECTIVE: To assess CABG influence on the behavior of intraventricular conduction in pts submitted to CABG. MATERIAL AND METHODS: Prospective study of 504 pts with severe CAD (3-vessel and/or left main trunk disease), divided in 2 groups (Gr) - GrA, composed of 252 pts with on-pump CABG, and GrB, with 252 pts submitted to off-pump CABG - whose pts were matched for age, gender, angiographic data, additive Euroscore, prior myocardial infarction, diabetes and hypertension. Other data (GrA vs GrB): nr of bypasses/pt 2.9 vs 2.4 (p<0.01); bypass to LAD 100% vs 100%; complete revascularization 60% vs 60%; left ventricular dysfunction 39% vs 34% (NS). Electrocardiographic study: pre-operative 12-lead ECG (within 72 hrs prior to CABG); post-operative (post-op) continuous ECG monitoring by telemetry (1 lead), including recording of data, until the discharge; post-op 12-lead ECG (up to 24 hrs after CABG), eventually repeated accordingly to the telemetric ECG evolution; ECG recordings were always performed by the same technician, with the same ECG recorder (25 mm/sec; 1 mV=10 mm). Results (GrA vs GrB): 1) Pre-operative IVCD 27% vs 24% (NS). 2) Post-op regression/abolition of IVCD (due to reversion of chronic stunning of the conduction system) 24%vs 28% (NS), occurring shortly (up to 24 hrs) after CABG termination in 95% of cases. IVCD aggravation/new IVCD 9.9% vs 0.8% (p<0.001). 3) Post-op IVCD: global figure 28% (+4.5%) vs 21% (-13%), p>0,05; stable IVCD + aggravated IV conduction 30% vs 18% (p<0.01). Post-op permanent pacing: 2 pts vs 0 pts. CONCLUSIONS: 1) A significant number (at least 24%) of pts with severe CAD and stable IVCD shows chronic ischemic stunning of the IV conduction system, which reverts after CABG. 2) Off-pump CABG (in opposition to on-pump CABG), by assuring a better intra-operative protection of the ventricular septum, promotes an improvement of intraventricular conduction in pts submitted to CABG.

Functional outcome and quality of life after coronary artery bypass surgery in patients with severe heart failure and hibernated myocardium.

BACKGROUND: Myocardial viability is an important parameter, predictive of improvement in left ventricular function after coronary artery bypass surgery (CABG). We wanted to define the relationship between the extent of hibernated myocardium and improvement in ejection fraction function and quality of life after CABG. METHODS: Sixty-five consecutive patients with ischaemic cardiomyopathy (mean LVEF <40%) undergoing surgical revascularization were studied with (99m)Tc-sestamibi myocardial perfusion Gated SPECT imaging (MPI) to assess preoperative myocardial viability. Patients were divided into two groups, based on the extent of viable myocardium before CABG: group 1, 39 patients with more than four viable segments; and group 2, 26 patients with fewer than four viable segments. Regional and global ejection fraction function, heart failure symptoms and quality of life were measured before and 14+/-4 months after revascularization. We used bull's eye quantitative analysis of MPI scans and a 17-segment model of ejection fraction function and perfusion evaluation. RESULTS: The number of viable segments per patient was directly related to the improvement in LVEF after revascularization (r=0.79, P<0.01). Patients with more than four viable segments representing 24% of the left ventricle yielded the sensitivity of 83% and specificity of 79%, respectively, for predicting improvement in LVEF. Furthermore, the presence of four or more viable segments predicted improvement in heart failure symptoms and quality of life after revascularization. CONCLUSION: The presence of more than four viable segments (24% of the left ventricle) on MPI in patients with ischaemic heart failure before CABG surgery is significantly correlated with the improvement in LVEF, heart failure symptoms and quality of life post-operatively.

Pharmacologic treatment of heart failure due to ventricular dysfunction by myocardial stunning: potential role of levosimendan.

The treatment of heart failure continues to pose a real challenge for clinicians. This condition is sometimes reversible and therapy should therefore pursue this outcome. In the context of coronary ischemic syndromes, myocardial stunning can cause heart failure and even cardiogenic shock, with important prognostic repercussions. Myocardial stunning is mainly due to calcium overload in the cytosol of myocardial cells, the loss of myofilaments and their reduced sensitivity to calcium. Enhanced immune activation with inflammatory phenomena also plays an important role in the pathophysiology of cardiac dysfunction. Increasing evidence has shown that the myocardial ATP-dependent potassium channel (K(ATP)) plays an important role in many myocardial cell functions and that it is involved in ischemia-reperfusion injury and myocardial stunning. K(ATP) is thus considered a therapeutic target in this setting. Currently used inotropic drugs improve contractility by increasing intracellular concentrations of free calcium, but they increase myocardial consumption of energy and even produce arrhythmia; therefore, in this clinical context, they do not seem to be 'pathophysiologically correct' drugs. Levosimendan, a new calcium-sensitizing agent, increases contractility by enhancing the sensitivity of myofilaments to calcium by binding to the C cardiac troponin in cardiac muscle in a calcium-dependent way. Levosimendan also exerts a coronary and systemic vasodilatory effect through its K(ATP) channel-opening properties and may exert other cardioprotective actions through this mechanism. Levosimendan produces positive hemodynamic effects without increasing myocardial oxygen demand or causing arrhythmias. Intravenous levosimendan is generally well tolerated and has been approved by several European countries, and recently recommended in European Society of Cardiology guidelines, as inotropic therapy for the short-term treatment of acute severe decompensated heart failure in adults. Randomized, double-blind trials have shown that levosimendan is not only more clinically and hemodynamically effective but also that it significantly reduces morbidity and mortality when compared with dobutamine or placebo. Clinical trials addressing the use and efficacy of intravenous levosimendan in acute heart failure in patients with systolic dysfunction or cardiogenic shock due to myocardial stunning are scarce. Beneficial effects on myocardial contractility in patients with myocardial stunning have only been shown in small clinical trials. A positive experience with levosimendan in a small series of patients with cardiogenic shock complicating ST-elevation myocardial infarction suggests that the use of this drug in cardiogenic shock should be further evaluated.

Diastolic dysfunction in stunned myocardium: a state of abnormal excitation-contraction coupling that is limited by Na+-H+ exchange inhibition.

OBJECTIVE: The systolic and diastolic effects of myocardial stunning were studied to evaluate the contributions of the endocardial and epicardial segments of the ventricular myocardial band, and determine if preconditioning by Na+-H+ exchange (NHE) inhibition effected post-stunning dysfunction. METHODS: Thirteen Yorkshire-Duroc pigs (27.3-38.2 kg) underwent 15 min of mid-LAD clamping. Seven had no protective measures and six were pretreated with IV Cariporide 5 mg/kg 15 min before ischemia. Sonomicrometer crystals evaluated systolic dysfunction (impaired regional shortening) and diastolic dysfunction (contraction extending into early diastole). RESULTS: Before ischemia, contraction started first on the endocardial side followed 82+/-23 ms later by the subepicardium. Endocardial shortening stopped first, coinciding with negative dP/dt onset, while epicardial shortening phase persisted for 92+/-33 ms more during occurrence of rapid LVP descent and development of peak negative dP/dt. Ischemia produced paradoxical bulging of both segments. Sixty minutes after ischemia systolic segment shortening recovered 36+/-24% of baseline values without pretreatment, compared to 75.8+/-15% with Cariporide (p<0.05). Global ejection force (maximum dP/dt) fell 32+/-20% in the unprotected group, but was maintained by Cariporide pretreatment. Diastolic dysfunction always showed continued endocardial contraction into early diastole (occupying 38+/-16% of diastole in untreated hearts), whereas Cariporide treatment reduced this dysfunction to 5+/-10% (p<0.05). Persistent diastolic dysfunction raised left ventricle end diastolic pressure (LVEDP) 4 mmHg in untreated hearts, whereas Cariporide returned LVEDP to normal. Less elevation of creatine kinase MB (CK-MB) and conjugated dienes followed Cariporide pretreatment. CONCLUSIONS: Temporary LAD ischemia alters the normal sequential pattern of contraction responsible for ejection and suction by (a) reducing systolic contractile force, and (b) prolonging endocardial contraction into early diastole to disrupt the normal endocardial-epicardial sequence responsible for ventricular suction. NHE inhibition before ischemia limits postischemic systolic and diastolic dysfunction by re-establishing the expected shortening sequences within the ventricular myocardial band model.