Myocardial Stunning Research Articles

P185 META–ANALYSIS OF PLACEBO–CONTROLLED TRIALS OF LEVOSIMENDAN IN ACUTE MYOCARDIAL INFARCTION

Abstract Introduction Despite the potential beneficial effects in the acute phase of myocardial infarction, the use of Levosimendan in recent guidelines is currently limited to patients with heart failure and a severe reduction in cardiac output not responding to standard therapy. In spite of everything, the haemodynamic effects of the drug that reduces afterload, the beneficial pleiotropic effects on myocardial stunning and the improvement of microcirculatory indices make Levosimendan still an interesting therapeutic prospect in AMI. Purpose of the Study The study aimed to analyse the available data of the use of Levosimendan in the acute setting of myocardial infarction Materials and Methods This review was registered in the International Prospective Register of Systematic Reviews (PROSPERO) and was conducted and presented according to best practice recommendations, including the Preferred Reporting Items for Systematic Reviews and Meta–Analyses (PRISMA) reporting guidelines. Seven selected studies were included in the meta–analysis. Meta–Analysis Levosimendan treatment was associated with a reduction in one year mortality and adverse event rates, without inconsistency. A trend of the increase of cardiac index and reduction of wedge pressure was evident, with an inconsistent effect on blood pressure and heart rate. No evidence of small study effects was found upon the inspection of funnel plots or regression tests. Finally, possibly given the limited number of included studies, metaregression analysis did not identify any major effect modifier. Discussion A clearly significant mortality reduction in the acute phase and long–term mortality induced by Levosimendan in AMI is evident. In the acute ischemic field, the haemodynamic properties of Levosimendan may explain part of the benefits. Levosimendan, over an inotropic effect, has a positive effect on ventriculo–arterial coupling, peripheral vasodilation consequently increasing tissue perfusion, anti–stunning effects and anti–inflammatory effects. Conclusions Our data support the idea that Levosimendan may already have a role in the treatment of acute ischemic heart disease. Further studies, specifically designed to investigate the early role in the treatment of ischemic heart failure are needed.

P141 CORRELATION BETWEEN TAKO–TSUBO SYNDROME AND OCCULT CANCER

Abstract Introduction Tako–Tsubo Syndrome (“TTS”) is a cardiomyopathy characterized by an acute reversible left ventricular dysfunction, mainly triggered by emotional or physical stress. Several variants have been reported, including reverse TTS, characterized by hypokinesia of basal segments and hyperkinesis of the apical ones. TTS has a clinical presentation similar to acute coronary syndrome but without evidence of obstructive coronary artery disease. A surprising association between TTS and cancer arose out of recent studies. Case Presentation 74–year–old patient got to the emergency room of our hospital for the appearance, apparently in the health, in the absence of physical or emotional stress of oppressive chest pain. On the ECG, there was evidence of ST–segment elevation in inferior leads, for which urgent coronary angiography was performed. It did not show significant stenotic lesions nor evidence of elevated troponin values. The Echocardiogram showed hypokinesia of the basal segments and hyperkinesis of the mid–apical ones, with EF 40%. In the following days, the patient performed MRI–heart with detection of LGE of the intramyocardial type (non–ischemic pattern) in correspondence with the inferior wall in the medioventricular area. During hospitalization on routine chest x–ray, hypodiaphanous image was found in the left apex for which an HR CT scan of the chest was performed which a lesion in the left apical lung area with spiculated margins of a heteroplastic nature, associated with multiple bilateral lesions suggestive of secondaryism. Therefore, the patient was taken over by the Oncology service. Conclusions Such case confirms the association between TTS and occult cancer. In the absence of obvious physical or emotional stress that may explain the onset of TTS, it is important to research for any silent neoplastic pathology. The literature shows that the prevalence of malignant diseases is high in patients with TTS. Recent studies have pinpointed the activation of the sympathetic nervous system promotes cardiac inflammation by upregulating ICAM–1 and the expression of p53. Furthermore, inflammation can lead to the activation of p38 MAP Kinase, thus contributing to myocardial stunning. The specific role of inflammation as a cofactor of adrenaline–induced stunning deserves further investigation in the specific context of malignant tumors, which are frequently associated with an enhanced inflammatory state.

Shocked into Shock: Cardioversion-Induced Shock with Multi-Organ Injury

Direct current cardioversion (DCCV) is an increasingly prevalent procedure to disrupt abnormal rhythms and restore normal sinus rhythm. While considered a relatively safe procedure, complications can be severe. We add to the emerging research surrounding delayed presentations of cardiogenic shock post-DCCV. Together with a review of the current literature, we extrapolate that a combination of post-conversion cardiac shifts, myocardial stunning, and a unique cardioversion stress-induced cardiomyopathy contributed to this occurrence. To our knowledge, this represents one of only a few examples of delayed, non-arrhythmic, cardioversion-induced cardiogenic shock and the first to cause the combination of non-ST elevation myocardial infarction, acute liver injury, and acute kidney injury. Our case adds to the growing body of research highlighting this rare, but serious consequence of direct current cardioversion.

Takotsubo Syndrome from Coronavirus Disease 2019

Takotsubo syndrome (TTS) or stress-induced cardiomyopathy is a rare form of acute, reversible left ventricular dysfunction. Catecholaminergic surge, myocardial inflammation, impaired microvascular perfusion, and electrophysiologic derangements may all contribute to its clinical manifestations of myocardial stunning and apical ballooning.1

Ventriculography for the study of TAKO-TSUBO Syndrome

Tako-Tsubo Cardiomyopathy (TTC) is an acute syndrome, identified in the early 1990s by Japanese researchers, which mimics an acute myocardial infarction. Cardiomyopathy is transient and begins with a clinical picture similar to that of an acute myocardial infarction. This pathology seems to be related to intense psychological and physical stress with a prevalence in the female sex (95%) in post-menopause. The term Tako-Tsubo means ‘octopus trap’ in Japanese: the left ventricle takes on a peculiar appearance in systole, similar to a narrow-necked amphora, morphologically identical to the vessel (tsubo) that Japanese fishermen use to catch octopuses (tako). The appearance of the left ventricle (tako-tsubo shape) is due to a ‘complete’ depletion of cardiac muscle activity (myocardial stunning), a kind of ‘stunning’ or paralysis of the middle and apical portions of the heart. Coronarography and ventriculography are an essential step in the diagnosis of TTC. The mere demonstration of a coronary tree free of angiographically significant stenosis is not sufficient for the diagnosis of TTC. The other key diagnostic element is, in fact, the demonstration of left ventricular hypokinesia or akinesia. Since left ventricular wall motility disorders change rapidly, ventriculography performed immediately after coronary examination is the gold standard examination to allow the characteristic appearance of the syndrome to be verified and, consequently, to distinguish it from an acute coronary syndrome with uninjured coronary arteries, thus avoiding a diagnostic error.

Ventriculography for the study of TAKO-TSUBO Syndrome

Tako-Tsubo Cardiomyopathy (TTC) is an acute syndrome, identified in the early 1990s by Japanese researchers, which mimics an acute myocardial infarction. Cardiomyopathy is transient and begins with a clinical picture similar to that of an acute myocardial infarction. This pathology seems to be related to intense psychological and physical stress with a prevalence in the female sex (95%) in post-menopause. The term Tako-Tsubo means 'octopus trap' in Japanese: the left ventricle takes on a peculiar appearance in systole, similar to a narrow-necked amphora, morphologically identical to the vessel (tsubo) that Japanese fishermen use to catch octopuses (tako). The appearance of the left ventricle (tako-tsubo shape) is due to a 'complete' depletion of cardiac muscle activity (myocardial stunning), a kind of 'stunning' or paralysis of the middle and apical portions of the heart. Coronarography and ventriculography are an essential step in the diagnosis of TTC. The mere demonstration of a coronary tree free of angiographically significant stenosis is not sufficient for the diagnosis of TTC. The other key diagnostic element is, in fact, the demonstration of left ventricular hypokinesia or akinesia. Since left ventricular wall motility disorders change rapidly, ventriculography performed immediately after coronary examination is the gold standard examination to allow the characteristic appearance of the syndrome to be verified and, consequently, to distinguish it from an acute coronary syndrome with uninjured coronary arteries, thus avoiding a diagnostic error.

Neurogenic stunned myocardium resulting from surgical brainstem handling during resection of paediatric recurrent medulloblastoma—a possible brain heart interaction

Neurogenic stunned myocardium (NSM) is characterised by an acute onset cardiac dysfunction following an acute neurological insult which mimics acute coronary syndrome. A 12-year-old male child was admitted to the neuro-intensive care unit (NICU) following midline suboccipital craniotomy and resection of recurrent medulloblastoma. Postoperatively, in NICU, he developed tachycardia and hypotension, which was unresponsive to fluid challenge requiring norepinephrine infusion. Intraoperatively, during tumour resection from the dorsal medulla, episodes of hypertension and bradycardia were observed. Intraoperative blood loss was adequately managed with a stable hemodynamic profile without postoperative anaemia. An electrocardiogram showed sinus tachycardia with T wave inversion, and blood investigation revealed elevated cardiac troponin T levels. Point of care ultrasound (POCUS) of heart and lung showed features of NSM. Infusion dobutamine was added to achieve a target mean arterial pressure of 65mm Hg with concomitant furosemide infusion and fluid restriction. Daily POCUS assessment of cardiac contractility and volume status was done. The patient was weaned from vasoactive drugs and ventilator following improvement of cardiac function and was discharged from NICU after 17days. NSM results from the excessive release of catecholamines following stimulation of trigger zones in the brain. To date, a handful of cases of pediatric NSM following primary brain tumour are reported where hydrocephalus resulted in trigger zone activation. In this presented case, direct brain stem stimulation during tumour resection might have triggered NSM. Irrespective of the cause, timely diagnosis and execution of supportive management in our patient resulted in a positive outcome.

P045 Octopus Toes?

Abstract Background/Aims Takotsubo cardiomyopathy is a relatively rare condition. Its name derives from the distinctive apical ballooning seen on cardiac angiography, which resembles the shape of takotsubo, a Japanese octopus trap. The clinical presentation is similar to acute coronary syndrome (ACS). Ischaemic ECG changes and elevated serum cardiac biomarkers are seen despite normal coronary artery angiography. Methods: History A 72-year-old female presented with a five-day history of constant bilateral foot pain and toe discolouration, associated with reduced sensation. She had a past history of hypertension and Raynaud’s phenomenon. She had recently been admitted with an alcohol withdrawal seizure and had recent severe stressful life events. She denied chest pain or dyspnoea and was a non-smoker. Her medications were ramipril and thiamine. Examination: Both feet were warm to touch proximal to the toes, with tenderness and diminished sensation in the distal feet. The toes were dusky but pedal pulses were palpable with good biphasic Doppler signal. Blood pressure was 117/105 mmHg on admission, with normal nail folds and heart sound, and no splinter haemorrhages were seen. Results: Investigations Blood parameters were CRP 60 mg/L, eGFR 47 mL/min, troponin >25,000 ng/L, and negative RF, ANA, ANCA, MPO, PR3, C3, C4. ECG showed lateral ST-segment elevation but normal coronary vessels were seen on coronary angiography. Echocardiogram revealed hypokinetic apical region and mid-anterior wall, reduced ejection fraction 35-40 % with apical ballooning, consistent with Takotsubo cardiomyopathy. Urine catecholamines, normetadrenaline, metadrenaline and 3-methoxytyramine levels were normal when measured eight days after the initial presentation. Management Daily Iloprost was given for five days with aspirin, furosemide, spironolactone and ivabradine, but no significant improvement was observed in the ischaemic feet. Her foot pain gradually subsided but the toes remained necrotic. Over the next six months, her toes mummified and auto-amputated. She has had no further ischaemic events. Conclusion Takotsubo cardiomyopathy accounts for 1-2% of troponin positive suspected ACS. It is most common in older females. The cause is not clear, but the predominant hypothesis is that a catecholamine surge leads to microvascular spasm and myocardial stunning. Raised catecholamine levels at presentation have been documented in patients with takotsubo cardiomyopathy, and the syndrome has been described in patients exposed to exogenous catecholamines. Digital ischaemia has been described in phaeochromocytoma. We postulate that our patient’s background of Raynaud’s phenomenon predisposed her to digital ischaemia during a period of catecholamine excess, which led to takotsubo cardiomyopathy. To our knowledge, this phenomenon has not previously been described. Given the profound effect of the presumed catecholamine surge on cardiac function in takotsubo cardiomyopathy and the high prevalence of Raynaud's phenomenon in the general population, it is perhaps surprising that ischaemia in digits and other organs is not more commonly observed. Disclosure K. Yeap: None. C. Badu-Boateng: None. M. Lloyd: None.

Myocardial stunning in patients with coronary artery disease before and after treatment by method of coronary artery bypass grafting (own studies)

Aim of the study: Determination of quantitative radiological indicators of myocardial revascularization effectiveness in patients with coronary artery disease in the early postoperative period.
 Materials and methods of research: For the implementation of the clinical objectives, 62 patients with coronary artery disease, heart failure, with preserved systolic function and systolic dysfunction were examined in the early postoperative period (up to 7 days). The patients' age ranged from 40 to 79 years, the average age of the examined was 59.6 ± 8.2 years. 35 (56%) patients had HF with LV systolic dysfunction with EF of 49% or less. 27 (44%) patients had preserved systolic function - ejection fraction greater than or equal to 50%.
 Results: In the group before treatment, the average value ​​of MV was 69.4% CI 95% [65.3%; 73.5%], and after treatment the value of MV was 75.0% CI 95% (70.8%; 79.3%], p = 0.0000. Percentage of RFP inclusion in the anterior wall was 69.5% CI [66.2%; 72.8%] before treatment and significantly improved to 72.3% CI [69.1%; 75.4%] after treatment (p = 0.023). Lateral wall had a parameter value of 73.9% CI [70.7%; 77.1%] before treatment and improved perfusion up to 77.2% CI [74.3%; 80.2%] (p = 0.018). Parameter values for the intraventricular septum were 64.5% CI [60.7%; 68.3%] before treatment and 69% CI [65.2%; 72.8%] after treatment (p = 0.000034) and for the inferior wall those were 54.0% CI (49.7%; 58.3%] and 61.7% CI (57.9%); 65.6%] before and after treatment respectively (p = 0.000032).
 Conclusion: The determination of quantitative radiological parameters proposed as a result of this study is extremely important for the early postoperative period (7-10 days) for determination of stunned myocardial reserve and late stage of patients` management (1-1.5 years) for determination of hibernation reserve and final assessment of CABG effectiveness.

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.

Peritoneal Dialysis for Refractory Heart Failure from a Congenitally Corrected Transposition of the Great Arteries who has not Undergone Definitive Surgery: A Case Report

Heart failure (HF) is a major cause of significant morbidity, mortality, and hospitalization worldwide including the Philippines. Congenitally corrected transposition of the great arteries (C-TGA) occurs when the right atrium enters the morphological left ventricle which gives rise to the pulmonary artery and the left atrium communicates with the right ventricle which gives rise to the aorta. Heart failure can occur in C-TGA especially if associated with other heart defects. Ideal management is anatomic correction via surgery to prevent or address heart failure. Peritoneal dialysis has been used as a therapeutic intervention for patients with refractory heart failure and kidney injury with or without kidney failure due to its gentler fluid removal compared to conventional ultrafiltration resulting in less myocardial stunning and neurohormonal activation. We present the case of a patient with heart failure who started on peritoneal dialysis (PD) as an adjunct therapy for fluid management after failing to satisfactorily achieve volume control with diuretics. The patient is a 56-year-old man with C-TGA admitted for decompensated heart failure. He was initially treated with intravenous diuretics on the first admission but was readmitted after 3 months for decompensation this time with borderline low blood pressure making diuresis difficult. The patient was given loop diuretics, tolvaptan, and angiotensin receptor neprilysin inhibitor (ARNI) but still with decreasing trends in urine output and inadequate symptom control. PD was initiated before discharge with subsequent improvement in heart failure symptoms. The patient was on regular follow-up for PD maintenance and titration of heart failure medication. In this case report, we have shown how PD can be an effective adjunct to guideline-directed medical therapy in patients with severely symptomatic heart failure who have an unstable hemodynamic status and for which volume management cannot be satisfactorily achieved with diuretics.

Pivotal role of the sympathetic nerves of the human heart in mental stress responses and triggered cardiovascular catastrophes.

Mental stress can trigger cardiac catastrophes, explicitly evident during national disasters such as earthquakes. Activation of the cardiac sympathetic outflow and inhibition of the cardiac vagus are important mediating mechanisms. This manuscript describes efforts by the Human Neurotransmitters Research Laboratory of the Baker Institute in Melbourne to develop investigative methods to study the sympathetic nerves of the human heart, and to apply these in mental stress research. With laboratory mental stress, activation of the adrenal medulla was found to occur, accompanied by a regionalized sympathetic nervous response directed to the heart, but sparing the sympathetic outflow to the skeletal muscle vasculature. Patients with panic disorder are at increased cardiovascular risk. They exhibit high-level sympathetic activation during a panic attack, sometimes accompanied by coronary artery spasm. Patients with sudden ventricular arrhythmias causing collapse in the community were found to have as the predisposing substrate high baseline cardiac sympathetic activity, from previously unrecognized mild heart failure; it was surprising at the time that we did not find critical coronary artery stenosis as the substrate. In some the arrhythmia event had a behavioural trigger. In Takotsubo cardiomyopathy ("Broken Heart Syndrome") the myocardial stunning appears to represent a catecholamine cardiomyopathy, from astronomically high plasma adrenaline concentrations, rather than be caused by activation of the cardiac sympathetic nerves. Some diseases (essential hypertension, heart failure, panic disorder) have forms of sympathetic neural enhancement which contribute to cardiovascular risk: reuptake of noradrenaline by sympathetic nerves after release is faulty and single sympathetic fibres fire in multiple salvos within a single cardiac cycle. Paradoxically, obesity-hypertension does not share in this sympathetic neural augmentation, which is present only in normal-weight hypertensive patients, providing the possible basis for an observed "Obesity Paradox" (longer survival in obesity-hypertension than in normal weight hypertension). Community-wide specific prevention of cardiovascular triggering is not currently possible, due to there being no available simple screening tests which could be applied to the community at-large for the commonest substrates, silent coronary artery disease and mild heart failure. Standard medical preventive measures for coronary atherosclerosis will of course be helpful. Targeted prevention of triggering can be done in those with a detected predisposing substrate, such as genetic Long QT Syndrome, and in survivors of a serious triggered event, who need detailed, appropriate testing.

Takotsubo Syndrome: A Review of Presentation, Diagnosis and Management.

Takotsubo Syndrome (TTS) is a condition of transient left ventricular dysfunction that is typically triggered by emotional or physical stress. Since first described in Japan in 1990, it has increasingly been recognised in clinical practice, accounting for up to 2% of Acute Coronary Syndrome (ACS) presentations. In fact, the clinical presentation can be indistinguishable from a myocardial infarction. Although current evidence suggests a catecholamine induced myocardial stunning, the pathophysiological mechanisms remain unknown. Interestingly, it is more common in woman, particularly those who are post-menopausal. This review aims to summarise the current research and provide an overview of the diagnostic strategies and treatment options.

Оглушенный миокард при острых формах ишемической болезни сердца

This article summarizes modern views on the pathogenesis, clinical presentation and treatment of myocardialstunning. The methods of visualization and their comparative characteristics in the diagnosis of stunningare described in detail. The clinical significance of determining myocardial viability before myocardialrevascularization was also analyzed, as well as the results of multicenter studies of STICH, PARR2, etc.Considering the multifaceted clinical and prognostic positive values of determining myocardial stunning aftermyocardial infarction, conducting clinical studies in this direction is considered justified and relevant.

61-Year-Old Man With Nausea and Vomiting

61-Year-Old Man With Nausea and Vomiting

Pharmacological inhibition of translocon is sufficient to alleviate endoplasmic reticulum stress and improve Ca2+ handling and contractile recovery of stunned myocardium

IntroductionThe function of endoplasmic reticulum (ER), a Ca2+ storage compartment and site of protein folding, is altered by disruption of intracellular homeostasis. Misfolded proteins accumulated in the ER lead to ER stress (ERS), unfolded protein response (UPR) activation and ER Ca2+ loss. Myocardial stunning is a temporary contractile dysfunction, which occurs after brief ischemic periods with minimal or no cell death, being oxidative stress and Ca2+ overload potential underlying mechanisms. Myocardial stunning induces ERS response with negatively impact on the post-ischemic mechanical performance through an unknown mechanism. AimsIn this study, we explored whether ER Ca2+ efflux through the translocon, a major Ca2+ leak channel, contributes to Ca2+ mishandling and the consequent contractile abnormalities of the stunned myocardium. MethodsMechanical performance, cytosolic Ca2+, UPR markers and oxidative state were evaluated in perfused rat/mouse hearts subjected to a brief ischemia followed by reperfusion (I/R) in absence or presence of the translocon inhibitor, emetine (1 μM), comparing its effects with those of the chaperones TUDCA (30 μM) and 4-PBA (3 mM). ResultsEmetine treatment precluded the I/R-induced increase in UPR signaling markers and improved the contractile recovery together with a remarkable attenuation in myocardial stiffness when compared to I/R hearts with no drug. This alleviation of I/R-induced mechanical abnormalities was more effective than that obtained with the chemical chaperones, TUDCA and 4-PBA. Moreover, emetine treatment produced a striking improvement in diastolic Ca2+ handling with a partial recovery of the I/R-induced oxidative stress. ConclusionBlocking ER Ca2+ store depletion via translocon suppressed ER stress and improved mechanical performance and diastolic Ca2+ handling of stunned myocardium. Modulation of translocon permeability emerges as a therapeutic approach to face dysfunctional consequences of the I/R injury.

Abstract 10536: Adenosine Triphosphate - Sensitive Potassium Channel Opener Diazoxide Reduces Myocardial Stunning in a Porcine Lad Occlusion Model

Introduction: Adenosine triphosphate - sensitive potassium (K ATP ) channels provide endogenous myocardial protection by coupling cell membrane potential to metabolism, as they are inhibited by ATP and open during times of metabolic stress. Pharmacologic opening of K ATP channels mimics ischemic preconditioning, and diazoxide (DZX) preserves myocardial function following prolonged global ischemia. Hypothesis: We hypothesized that DZX would reduce myocardial stunning after left anterior descending coronary artery (LAD) occlusion followed by global ischemia, similar to a clinical situation of acute myocardial infarction followed by coronary revascularization. Methods: Twelve swine underwent LAD occlusion (30 min), followed by 120 min global ischemia protected with hyperkalemic cardioplegia (CPG) +/- DZX (N=6 each), followed by intermittent CPG (q 20 min), then 60 min reperfusion (RF). Cardiac output (CO), mean time to wean from cardiopulmonary bypass (CPB), left ventricular ejection fraction (LVEF), left ventricular developed pressure (LVDP), caspase - 3 (apoptosis), and infarct size were compared. Results: All 6 animals in the DZX group separated from CPB by 30 min RF whereas only 1 and 4 animals in the CPG group had separated at 15 and 30 min, respectively (Figure). DZX was associated with shorter average time to wean from CPB (17.5 vs 27.0 min, p=0.13) and higher CO at all time points during reperfusion (2.9 vs 1.5 L/min at 30 min RF, p=0.05), however, these were not significantly different. DZX was associated with higher LVEF after 30 minutes of reperfusion (42.5 vs 15.8%, p=0.009; Figure). There were no differences between groups in vasopressor use, infarct size, caspase - 3, or LVDP. Conclusions: DZX reduces myocardial stunning and facilitates separation from CPB following LAD occlusion and subsequent global ischemia in a porcine model. The addition of DZX to hyperkalemic cardioplegia has the potential to reduce myocardial stunning in the clinical setting.

Hawk´s Beak Form in Midventricular Takotsubo Syndrome: Two Case Reports from Latin America

Takotsubo syndrome is a type of acute reversible heart failure that can involve a form of acute catecholaminergic myocardial stunning. This clinical entity shows a pattern of temporary left ventricular dysfunction in the absence of occlusion of any coronary artery. A midventricular type is a form of Takotsubo syndrome where the atypical morphological variant is Hawk’s beak. The prevalence of this type is estimated to be 10-15% in several series in Asian and Western countries (predominantly Caucasian patients). In Latin America, there are no studies reporting this type of presentation. Two cases are reported in women initially diagnosed with acute myocardial infarction with the finding of the atypical hawk's beak morphology of Takotsubo syndrome, confirmed by left ventriculography. One of them was followed up early, observing recovery in her ventricular function without structural compromise at the level of contractility and with a good response to the outpatient treatment proposed. As there is a low prevalence and few published reports, these 2 cases are presented to promote long-term studies and increase the information regarding the evolution and morbidity/mortality of this type of presentation compared with the classical form of the syndrome.

High D-dimer levels in patients with Takotsubo syndrome: 2.5 years follow-up

Abstract Background Takotsubo syndrome (TTS) was initially described as an acute reversible left ventricular (LV) dysfunction associated with emotional trigger and good prognosis. However, several clinical conditions and physical stresses have recently been reported to favor episodes of TTS. Besides myocardial stunning and endothelial dysfunction, a pro-inflammatory status represents a critical point in TTS patients. D-dimer, a specific metabolite of cross-linked fibrin, has recently been proposed as a prognostic tool in critical patients for its connection to proinflammatory and coagulation state. Purpose The aim of our study was to evaluate whether high D-dimer levels at admission were related to disease severity and worse outcomes at mid-term follow-up in TTS patients. Methods We retrospectively analysed clinical, laboratory, echocardiographic (left ventriucular ejection fraction, LVEF) and angiographic characteristics of 40 consecutive cases of TTS admitted to our department from January 2016. Elevated circulating D-dimer levels (defined as >550 μg/l) were correlated with characteristics of patients, in-hospital major adverse cardiac events (MACE, defined as the composite of acute pulmonary oedema, cardiogenic shock, sustained ventricular tachycardia, ventricular fibrillation, cardiac arrest or death) and mortality at 2.5 year follow-up. Results Of 40 patients with Takotsubo syndrome, 38 completed 2.5 years follow-up. All patients were women, with a mean age of 69.5±13.9 years. High D-dimer levels were detected in 21 patients (55.3%). Similar age, cardiovascular risk factors and angiographic findings were found between two groups. Patients with high D-dimer levels were more frequently associated with reduced LVEF (<40%) at discharge (23.8% vs 0%, p=0.041) and in-hospital MACE (33.3% vs 5.9%, p=0.045). Furthermore, high D-dimer levels significantly correlated with admission C-reactive protein and high-sensitive troponin T values (rS 0.570, p<0.001 and rS 0.433, p=0,007, respectively) and first LVEF% (rS −0.358 p=0.028). At mean of 2.5-year follow-up, 6 patients died. Patients who died were significantly older (81.3±5.3 vs 67.2±14.1, p=0.010) and with higher admission GRACE score (131.4±9.4 vs 101.5±25.6, p=0.003) than patients who survived. Moreover, higher admission D-dimer levels (28.6% vs 0%, p=0.020), physical trigger (66.7% vs 21.9%, p=0047) and discharge LVEF<40% (66.7% vs 15.6%, p=0.020) were significantly more frequently among patients who died. Conclusions Elevated circulating D-dimer levels at admission for TTS were associated with higher mortality rate at 2.5 years follow-up, along with physical trigger and depressed LVEF at discharge. Moreover, high D-dimer levels were associated with in-hospital higher incidence of MACE and depressed LVEF. These results support the hypothesis that different pathophysiological mechanisms may be implicated in LV dysfunction in TTS, leading to different prognosis. Funding Acknowledgement Type of funding sources: None.

Миокардиальный станнинг в медицине неотложных и критических состояний, ассоциированных с системной гипоксией

Актуальность. Миокардиальный станнинг — феномен, заключающийся в продолжительном снижении сократительной способности миокарда после краткого периода ишемии/реперфузии, при котором не происходит омертвения ткани сердечной мышцы. Если изначально феномен станнинга ассоциировали исключительно с проявлениями ишемической болезни сердца, то в настоящее время имеется все больше свидетельств о том, что миокардиальный станнинг может осложнять совсем другую патологию. Цель: изучение результатов работ оте-чественных и зарубежных ученых, посвященных наблюдению феномена станнинга в медицине неотложных состояний, и систематизация накопленного клинического материала. Материалы и методы. Детальное изучение результатов современных клинических исследований, посвященных диагностике снижения сократительной способности миокарда у пациентов, находящихся в критических состояниях, которые развились не вследствие манифестации острого коронарного синдрома, обсуждению механизмов патогенеза миокардиальной дисфункции при этих состояниях и принципам оказания таким больным экстренной и специализированной медицинской помощи. Результаты. Для феномена миокардиального станнинга характерны следующие отличительные признаки: 1. Коронарный кровоток после перенесенного эпизода ишемии практически полностью восстанавливается. После ишемии очень часто регистрируется кратковременный период гиперперфузии. 2. Несмотря на восстановление коронарного кровотока, имеет место продолжительное снижение сократимости миокарда. 3. Необратимого повреждения кардиомиоцитов в период ишемии не происходит. 4. Снижение сократительной способности сердца, наблюдающееся после ишемии и последующей реперфузии, является полностью обратимым. Основными механизмами развития миокардиального станнинга являются: усиленная генерация активных форм кислорода в период реперфузии; перегрузка кардиомиоцитов кальцием; снижение сопряженности между процессами электрического возбуждения миокарда и его сократимостью. Продукция простациклина, активность ангиотензина I, II и ангиотензинпревращающего фермента, продукция брадикинина моделируют тяжесть мио-кардиальной дисфункции при станнинге. Причиной станнинга может быть индуцированная катехоламинами кардиотоксичность. Миокардиальный станнинг можно наблюдать у пациентов с геморрагическим, септическим шоком, субарахноидальными кровоизлияниями, на фоне проведения гемодиализа, после криза при феохромоцитоме, после реанимационной акции. Выводы. Миокардиальный станнинг требует своевременной диагностики, поскольку проведение гемодинамической коррекции не с помощью инотропной поддержки, а по другим направлениям, а именно за счет увеличения скорости объемной нагрузки (агрессивная инфузионная терапия) или применения вазопрессоров, может резко ухудшить состояние пациента вследствие увеличения нагрузки на ослабленное сердце.