Acute Stress Cardiomyopathy Research Articles

The Science Behind Stress: From Theory to Clinic, Is Basal Septal Hypertrophy the Missing Link between Hypertension and Takotsubo Cardiomyopathy?

The modern theory of stress, initially proposed by Hans Selye in 1956, signifies an important development in our understanding of this phenomenon. Selye’s The Stress of Life serves as a foundational book for subsequent scientific questions. In this article, we focus on a comprehensive look at stress and use a literature review to explain its theoretical foundations as well as its clinical equivalent. Our research focuses on the complex mechanisms of stress, with a particular emphasis on the consequences of cardiac remodeling and adaptation processes. Myocardial remodeling might be seen as a response to increased stress in acute or chronic situations. Stressed heart morphology (SHM) is a very interesting description representing basal septal hypertrophy (BSH), which is detectable in both acute emotional stress and chronic stress due to increased afterload in hypertension. Acute stress cardiomyopathy (ASC) and hypertension in the same individuals could be clinically linked. Also, in this report, we mention the geometric and functional similarity of the left ventricle (LV) septal base in both acute and chronic clinical situations. Therefore, cardiac imaging methods are crucial to assessing LV segmental aspects in ASC patients. We propose a new paradigm that ASC may develop in hypertensive patients with SHM. We document the segmental progression of microscopic LV remodeling using a third-generation microscopic ultrasound and note that BSH takes a longer time to occur morphologically than an acutely developed syndrome. However, the majority of ASC events have a predominant base, and the absence of segmental remodeling details, including BSH and cardiac decompensation with apical ballooning, on echocardiographic reports may mask the possible underlying hypertensive disease. In fact, beyond ASC cases, previously undiagnosed hypertension is very common, even in developed countries, and is associated with masked target organ damage.

Stress and Heart in Remodeling Process: Multiple Stressors at the Same Time Kill.

Myocardial remodeling is developed by increased stress in acute or chronic pathophysiologies. Stressed heart morphology (SHM) is a new description representing basal septal hypertrophy (BSH) caused by emotional stress and chronic stress due to increased afterload in hypertension. Acute stress cardiomyopathy (ASC) and hypertension could be together in clinical practice. Therefore, there are some geometric and functional aspects regarding this specific location, septal base under acute and chronic stress stimuli. The findings by our and the other research groups support that hypertension-mediated myocardial involvement could be pre-existed in ASC cases. Beyond a frequently seen predominant base, hyperkinetic tissue response is detected in both hypertension and ASC. Furthermore, hypertension is the responsible factor in recurrent ASC. The most supportive prospective finding is BSH in which a hypercontractile base takes a longer time to exist morphologically than an acutely developed syndrome under both physiologic exercise and pressure overload by transaortic binding in small animals using microimaging. However, cardiac decompensation with apical ballooning could mask the possible underlying hypertensive disease. In fact, enough time for the assessment of previous hypertension history or segmental analysis could not be provided in an emergency unit, since ASC is accepted as an acute coronary syndrome during an acute episode. Additional supportive findings for SHM are increased stress scores in hypertensive BSH and the existence of similar tissue aspects in excessive sympathetic overdrive like pheochromocytoma which could result in both hypertensive disease and ASC. Exercise hypertension as the typical form of blood pressure variability is the sum of physiologic exercise and pathologic increased blood pressure and results in increased mortality. Hypertension is not rare in patients with a high stress score and leads to repetitive attacks in ASC supporting the important role of an emotional component as well as the potential danger due to multiple stressors at the same time. In the current review, the impact of multiple stressors on segmental or global myocardial remodeling and the hazardous potential of multiple stressors at the same time are discussed. As a result, incidentally determined segmental remodeling could be recalled in patients with multiple stressors and contribute to the early and combined management of both hypertension and chronic stress in the prevention of global remodeling and heart failure.

Broken Heart Syndrome: A Rare Case of Recurrent Reverse Takotsubo Cardiomyopathy Associated with Acute Respiratory Failure.

Takotsubo cardiomyopathy accounts for one percent of acute coronary syndrome presentations and has been increasingly recognized [1]. Reverse Takotsubo cardiomyopathy, a variant form of Takotsubo cardiomyopathy presenting with the hyperdynamic function of the apical segments and hypokinesis of the basal or mid-ventricular segments is the rarest type of acute stress cardiomyopathy, with mid-ventricular akinesia and preservation of apical and basal contractility [2]. We report a rare case of an elderly woman admitted to the Intensive Care Unit at Case Western Reserve University Hospital in Cleveland, USA. The patient experienced acute respiratory failure as a result of exacerbated chronic obstructive lung disease and heart failure. Echocardiography revealed reverse Takotsubo cardiomyopathy. Cardiac catheterization showed nonobstructive coronary artery disease. The wall motion abnormalities resolved within two weeks. The case is unique in that she had an identical presentation one year earlier after she had entered the same dusty room! Our case report is unique and describes the rarest form of recurrent reverse Takotsubo cardiomyopathy. Our case demonstrates that reverse Takotsubo cardiomyopathy with identical wall motion abnormalities can recur in a patient upon re-exposure to a similar stressful situation. Early recognition and appropriate treatment can prevent catastrophic outcomes.

STRESSED HEART MORPHOLOGY: A SPECIFIC LOCATION FOR VARIETY OF STRESS STIMULI

Objective: Myocardial on-specifi is a response to increased stress in acute or chronic situations. Stressed heart morphology (SHM) is a very interesting description representing basal septal hypertrophy (The early Imaging Biomarker in Hypertension, J Aplied Physiol 2019) caused by both acute emotional stress, functional due to increased afterload in hypertension and mechanic in aortic stenosis. Design and method: Echocardiography and coronary angiography were used to evaluate underlying mechanism of the symptoms of the particular patient who applied for health care. Results: In this case, we detected ampulla shape geometry with chronic stress and hypertension. 72 years old lady with 25 years of hypertension history was examined for exercise intolerance and dyspnea Echocardiography showed a left ventricular dysfunction with 40 % ejection fraction and basal septal hypertrophy. Coronary anjiography was planned and no coronary stenosis detected. The patient gave a typical history for chronic emotional disturbance and was on longstanding antidepressive medication. Conclusions: While SHM is associated with acute stress cardiomyopathy, hypertension and aortic stenosis (Blood Press Monitor 2020, Am J Cardiovasc Dis 2021, ATCS 2021), it also could be seen in those with chronic hypertension and emotional disturbance. This support the notion that SHM could be a specific location for variety of on-specific stress stimuli.

Stress Cardiomyopathy Triggered by Respiratory Illness – A Retrospective Australian Cohort

Physical and emotional stressors can both precipitate acute stress cardiomyopathy. International data suggest respiratory disease triggers a minority of cases and is associated with worse prognosis. The aim of this study was to describe the association between acute and chronic respiratory disease and stress cardiomyopathy in an Australian cohort.

C26. Case report: COVID-19 associated Takotsubo cardiomyopathy

BackgroundCOVID-19 infection can lead to several cardiovascular sequelae, including Takotsubo cardiomyopathy (TCM), which may portend worse clinical outcomes.Case DescriptionA 56-years-old woman with history of hypertension presented to the emergency room for dyspnea and gradual decrease of consciousness for seven days. She was positive for COVID-19 and transferred to intensive care unit to receive mechanical ventilation due to respiratory failure. Electrocardiogram showed pathological Q wave and ST elevation in inferior and anterior. Troponin I was mildly elevated (5.52 ng/ml). Inflammatory marker CRP and procalcitonin were increased (3.6 mg/dl and 0.235 ng/ml, respectively). Serum cortisol level was 525.8 ng/ml. Echocardiography showed reduced left ventricular ejection fraction (LVEF 41%), with severe hypokinetic of the apical segments and preserved basal myocardial function consistent with visual signs of apical ballooning in TCM. Her follow-up echocardiography showed normal contractility of the apical myocardial segments, with normalization of the left ventricular systolic function, further supporting the reversibility of acute stress cardiomyopathy.DiscussionMechanisms of TCM in viral infections include catecholamine-induced myocardial toxicity and inflammation related to sepsis. A presumptive diagnosis of TCM was made based on the characteristic echocardiogram findings of apical ballooning, normalization of left ventricular systolic function, unremarkable past cardiac history and spontaneous improvement in serum troponin-I levels in the setting of a severe systemic illness.ConclusionClinicians should be aware of the diversity of cardiovascular complications of COVID-19, including Takotsubo cardiomyopathy and should strategize appropriately for diagnosing and managing them.

C26. Case report: COVID-19 associated Takotsubo cardiomyopathy

BackgroundCOVID-19 infection can lead to several cardiovascular sequelae, including Takotsubo cardiomyopathy (TCM), which may portend worse clinical outcomes.Case DescriptionA 56-years-old woman with history of hypertension presented to the emergency room for dyspnea and gradual decrease of consciousness for seven days. She was positive for COVID-19 and transferred to intensive care unit to receive mechanical ventilation due to respiratory failure. Electrocardiogram showed pathological Q wave and ST elevation in inferior and anterior. Troponin I was mildly elevated (5.52 ng/ml). Inflammatory marker CRP and procalcitonin were increased (3.6 mg/dl and 0.235 ng/ml, respectively). Serum cortisol level was 525.8 ng/ml. Echocardiography showed reduced left ventricular ejection fraction (LVEF 41%), with severe hypokinetic of the apical segments and preserved basal myocardial function consistent with visual signs of apical ballooning in TCM. Her follow-up echocardiography showed normal contractility of the apical myocardial segments, with normalization of the left ventricular systolic function, further supporting the reversibility of acute stress cardiomyopathy.DiscussionMechanisms of TCM in viral infections include catecholamine-induced myocardial toxicity and inflammation related to sepsis. A presumptive diagnosis of TCM was made based on the characteristic echocardiogram findings of apical ballooning, normalization of left ventricular systolic function, unremarkable past cardiac history and spontaneous improvement in serum troponin-I levels in the setting of a severe systemic illness.ConclusionClinicians should be aware of the diversity of cardiovascular complications of COVID-19, including Takotsubo cardiomyopathy and should strategize appropriately for diagnosing and managing them.

Skewed Cytokine Responses Rather Than the Magnitude of the Cytokine Storm May Drive Cardiac Dysfunction in Multisystem Inflammatory Syndrome in Children.

BackgroundCardiac dysfunction is a prominent feature of multisystem inflammatory syndrome in children (MIS‐C), yet the etiology is poorly understood. We determined whether dysfunction is global or regional, and whether it is associated with the cytokine milieu, microangiopathy, or severity of shock.Methods and ResultsWe analyzed echocardiographic parameters of myocardial deformation and compared global and segmental left ventricular strain between 43 cases with MIS‐C ≤18 years old and 40 controls. Primary outcomes included left ventricular global longitudinal strain, right ventricular free wall strain), and left atrial strain. We evaluated relationships between strain and profiles of 10 proinflammatory cytokines, microangiopathic features (soluble C5b9), and vasoactive‐inotropic requirements. Compared with controls, cases with MIS‐C had significant impairments in all parameters of systolic and diastolic function. 65% of cases with MIS‐C had abnormal left ventricular function (|global longitudinal strain|<17%), although elevations of cytokines were modest. All left ventricular segments were involved, without apical or basal dominance to suggest acute stress cardiomyopathy. Worse global longitudinal strain correlated with higher ratios of interleukin‐6 (ρ −0.43) and interleukin‐8 (ρ −0.43) to total hypercytokinemia, but not absolute levels of interleukin‐6 or interleukin‐8, or total hypercytokinemia. Similarly, worse right ventricular free wall strain correlated with higher relative interleukin‐8 expression (ρ −0.59). There were no significant associations between function and microangiopathy or vasoactive‐inotropic requirements.ConclusionsMyocardial function is globally decreased in MIS‐C and not explained by acute stress cardiomyopathy. Cardiac dysfunction may be driven by the relative skew of the immune response toward interleukin‐6 and interleukin‐8 pathways, more so than degree of hyperinflammation, refining the current paradigm of myocardial involvement in MIS‐C.

BITTEN FINGERS AND BROKEN HEARTS

Acute stress cardiomyopathy (ASC), also known as broken heart syndrome, has become increasingly recognized among patients presenting with suspected acute coronary syndrome since it was first described in Japan in 1990. The classic presentation is most common in older females following emotional or

Management of an acute catecholamine-induced cardiomyopathy and circulatory collapse: a multidisciplinary approach.

A phaeochromocytoma (PC) is a rare, catecholamine-secreting neuroendocrine tumour arising from the adrenal medulla. Presenting symptoms of this rare tumour are highly variable but life-threatening multiorgan dysfunction can occur secondary to catecholamine-induced hypertension or hypotension and subsequent cardiovascular collapse. High levels of circulating catecholamines can induce an acute stress cardiomyopathy, also known as Takotsubo cardiomyopathy. Recent studies have focused on early diagnosis and estimation of the prevalence of acute stress cardiomyopathy in patients with PC, but very little is reported about management of these complex cases. Here, we report the case of a 38-year-old lady who presented with an acute Takotsubo or stress cardiomyopathy and catecholamine crisis, caused by an occult left-sided 5 cm PC. The initial presenting crisis manifested with symptoms of severe headache and abdominal pain, triggered by a respiratory tract infection. On admission to hospital, the patient rapidly deteriorated, developing respiratory failure, cardiogenic shock and subsequent cardiovascular collapse due to further exacerbation of the catecholamine crisis caused by a combination of opiates and intravenous corticosteroid. An echocardiogram revealed left ventricular apical hypokinesia and ballooning, with an estimated left ventricular ejection fraction of 10–15%. Herein, we outline the early stabilisation period, preoperative optimisation and intraoperative management, providing anecdotal guidance for the management of this rare life-threatening complication of PC.Learning points:A diagnosis of phaeochromocytoma should be considered in patients presenting with acute cardiomyopathy or cardiogenic shock without a clear ischaemic or valvular aetiology.Catecholamine crisis is a life-threatening medical emergency that requires cross-disciplinary expertise and management to ensure the best clinical outcome.After initial resuscitation, treatment of acute catecholamine-induced stress cardiomyopathy requires careful introduction of alpha-blockade followed by beta-blockade if necessary to manage β-receptor-mediated tachycardia.Prolonged α-adrenergic receptor stimulation by high levels of circulating catecholamines precipitates arterial vasoconstriction and intravascular volume contraction, which can further exacerbate hypotension. Invasive pressure monitoring can aid management of intravascular volume in these complex patients.

Activation of Inflammatory and Pro-Thrombotic Pathways in Acute Stress Cardiomyopathy.

Stress cardiomyopathy (SCM) is a unique cardiac disorder that more often occurs in women. SCM presents in a similar fashion as acute myocardial infarction (AMI), with chest pain, ECG changes, and congestive heart failure. The primary distinguishing feature is the absence of thrombotic coronary occlusion in SCM. How this reduction in cardiac function occurs in the absence of coronary occlusion remains unknown. Therefore, we tested the hypothesis that a targeted proteomic comparison of patients with acute SCM and AMI might identify relevant mechanistic differences. Blood was drawn in normal controls (n = 6), women with AMI (n = 12), or women with acute SCM (n = 15). Two-week follow-up samples were available in AMI (n = 4) and SCM patients (n = 11). Relative concentrations of 1,310 serum proteins were measured in each of the 48 samples using the SOMAscan assay. Women with AMI had greater myocyte necrosis, as reflected by a higher peak troponin I concentration (AMI 32.03 ± 29.46 vs. SCM 2.68 ± 2.6 ng/ml, p < 0.05). AMI and SCM patients had equivalent reductions in left ventricular ejection fraction [LVEF (%) 39 ± 12 vs. 37 ± 12, p = 0.479]. In follow-up, women with SCM had a greater improvement in cardiac function [LVEF (%) 60 ± 7 vs. 45 ± 13, p < 0.001]. No differentially expressed proteins were detected (absolute log2-fold change >1; q < 0.05) between AMI and SCM in the acute or recovery phase. However, when we compared normal controls to patients with AMI, there was differential expression of 35 proteins. When we compared normal controls to patients with SCM, 45 proteins were differentially expressed. In comparison to normal controls, biological processes such as complement, coagulation, and inflammation were activated in both AMI and SCM. There were four proteins that showed a non-significant trend to be increased in acute SCM vs. AMI (netrin-1, follistatin-like 3, kallikrein 7, kynureninase). Despite a lesser degree of myocardial necrosis than AMI, SCM is characterized by a similar activation of inflammatory, complement, and coagulation pathways. These findings may explain reported thromboembolic complications in the short term and elevated risk of mortality in the long term of SCM.

Complete reverse remodeling in acute stress cardiomyopathy. Is preserved tissue contractility under stress related to reverse remodeling

Acute stress cardiomyopathy is the unique disease which represents exaggerated and dysfunctional regions of the same cardiac tissue at the same episode. The impressive clinical course which involves the specific region is the stress-mediated exaggerated function of LV base under acutely developed stress induction. After abolishment of stress induction, dysfunctional part of LV which is the midapical myocardium undergoes a complete tissue functional recovery. The evolution of reverse remodeling in acute stress cardiomyopathy has been described using 2 and 3-dimensional echocardiography in the literature. This is the second report regarding reverse LV remodeling in acute stress cardiomyopathy in which we rather evaluate the underlying mechanisms leading complete reverse LV remodeling of dysfunctional myocardium. Therefore, we focus on the existence of preserved and exaggerated regional tissue under stress which possibly represents the predicted myocardial tissue recovery in this acute clinical entity. We also discuss the potential contribution of short-term disease course and lack of prior disease episodes to complete reverse remodeling differently from the heavy burden of chronic diseases leading to permanent tissue jeopardy.

Clinical Course, Management and Outcomes of Patients with Acute Stress Cardiomyopathy (ASC)

Clinical Course, Management and Outcomes of Patients with Acute Stress Cardiomyopathy (ASC)

Clinical Characteristics, Sex Hormones, and Long‐Term Follow‐Up in Swiss Postmenopausal Women Presenting With Takotsubo Cardiomyopathy

The overwhelming majority of patients with stress cardiomyopathy (SC) are postmenopausal women, suggesting an important pathophysiologic role of the female sex hormones. Preliminary data suggest that myocardial stunning might be provoked by estrogen deficiency. We hypothesized that, compared with age- and gender-matched patients with myocardial infarction (MI) or patients with normal coronary arteries, patients with SC would exhibit altered levels of sex hormones. Furthermore, we aimed to describe the clinical course and the pattern of sex hormones of the SC patients during long-term follow-up. Blood samples obtained on hospital admission were analyzed for estradiol (E2), progesterone (P), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in women with SC (n = 17), age-matched women with acute MI (n = 16), and women with normal coronary arteries (n = 15). Six years after the initial event, SC patients underwent a clinical and echocardiographic follow-up and reassessment of sex hormones. Estrogen concentrations at hospital admission were significantly higher in the SC group compared with the MI and the control groups, with no difference in P, FSH, and LH concentrations. Follow-up E2 after 6 years in SC patients was lower than during the acute SC episode. Follow-up P in these patients was lower than P in the MI and control groups during the acute event, with a similar trend for E2. After a median follow-up of 6.4 years, 1 sudden cardiac death occurred and 2 patients suffered from SC recurrence. During the acute event, E2 concentrations are elevated in postmenopausal SC patients compared with women with acute MI or with normal coronary arteries. The higher E2 concentrations might have exerted atheroprotective effects and thus diverted the stress response to SC rather than MI. Recurrence and/or sudden cardiac death remains a potential risk of SC.

Can quantitative regional myocardial dynamics contribute to the differential diagnosis of acute stress cardiomyopathy?

Acute stress-induced cardiomyopathy has excessive sympathetic stimulation, microvascular dysfunction similar to hypertension. Regional prominence of left ventricular (LV) septal base and stress-induced LV hypercontractility are the particular features of both acute and chronic stress-related conditions. Novel imaging methods have shown that stress-induced cavity dilation and myocardial wall abnormalities can be a reflection of underlying previous exaggerated hypertensive episodes due to sympathetic overdrive, which results in microvascular dysfunction. Hypertension-mediated chronic stress due to increased after load episodes is possibly the main reason for blunted LV myocardial wall motion capability in patients with stress-related exaggerated hypertension. In this short report, we discussed the interrelation of myocardial dynamics and stress-induced exaggerated hypertension episodes. In addition, quantitative echocardiographic methods which previously were used for description of particular features including LV regional dynamics in hypertensive heart disease can be an option in differential diagnosis of potential cases of acute stress-induced cardiomyopathy.

315: Catecholamines in Simulated Arrest Scenarios

The mechanisms of death in many arrest-related deaths are unclear. Law enforcement devices or tactics are often scrutinized in these unexplained cases. Unexplained arrest-related deaths have occurred after the use of electronic control devices. The primary concern has been direct cardiac arrhythmias induced by the delivered charge. Some authors have opined that the temporal relationship between electronic control device use and arrest-related deaths may be related to an acute stress cardiomyopathy induced by high circulating catecholamines, rather than an immediate electrically induced arrhythmia. In this study, we compared the stress response during several simulated use of force encounters.

Acute Stress Cardiomyopathy Following Treatment of Status Asthmaticus

Broken heart syndrome, otherwise known as takotsubo syndrome, is stress-induced cardiomyopathy. Clinical presentation mimics acute ST segment elevation myocardial infarction, but with characteristic left ventricular apical ballooning. The mechanism is linked to overstimulation of the sympathetic system from high circulating catecholamine levels. We report a 46-year-old Caucasian female whose treatment of status asthmaticus with ketamine and epinephrine precipitated this syndrome. She required hemodynamic support with an intra-aortic balloon pump and dobutamine infusion. Myocardial function improved dramatically with supportive treatment. Iatrogenically induced takotsubo syndrome with vasoactive agents should be suspected in acute left ventricular dysfunction without coronary artery disease.

The Heart-Brain Connection Begets Cardiovascular Psychiatry and Neurology

In many Asian languages, the same ancient letter/symbol is used for heart and mind. For the last couple of millennia, physicians and scientists across different civilizations have posited close links between the brain and heart, even arguing that the site of intelligence and emotions is in one of these two organs. Through an integrative empirical approach in modern biology/physiology and behavioral sciences, much has since been learned to confirm the anatomical and functional links between the brain and the heart. Arguably, the ultimate applicability of this knowledge will advance our health and improve disease treatment. Modern medicine is characterized by a high degree of specialization, and the heart-brain connection is typically considered from the point of view of a particular medical specialty. Hence, focusing on the brain, for example, in neurology, cardiovascular involvement is critical in certain pathologies such as stroke and vascular dementia. In cardiology, on the other hand, the influence of the brain becomes clearly apparent in “the broken heart syndrome” (also known as acute stress cardiomyopathy). However, recent epidemiological studies point to new associations that typically present as co-occurring pathologies of both the brain and the heart. A case in point is the association between depression and coronary heart disease. Such co-occurrences have stimulated research into possible novel mechanisms that could be targeted to treat these complex cardiovascular/brain disorders. At least three scenarios could be at play in these illnesses: (i) the primary pathological mechanism in the nervous system triggers a cardiovascular pathology by disrupting physiological links between the two systems (hence, the term “psychogenic”cardiovascular disease), (ii) the primary pathological mechanism in the cardiovascular system triggers a nervous system dysfunction (e.g., atherosclerosis leading to ischemic conditions causes subsequent cognitive impairment), and (iii) the primary pathology is in a biological mechanism that is normally operative in both the nervous and the cardiovascular systems, thus causing the co-occurrence of pathologies (i.e., the co-occurring pathologies share a pathobiological mechanism but do not necessarily cause each other). To be successful, research in co-occurring cardiovascular and brain disorders needs contributions from multiple medical specialties, including psychiatry, neurology, medicine, and cardiology. It should encompass clinical and basic research as well as the development of therapeutic approaches. The purpose of Cardiovascular Psychiatry and Neurology is to provide a platform for the latest research and for timely and expert reviews and comments in the emerging field of cardiovascular psychiatry and neurology. Although the term cardiovascular psychiatry and neurology is introduced here for the first time, retrieving publications from PubMed using either cardiovascular psychiatry or cardiovascular neurology generates relevant information (oftentimes because the terms psychiatry or neurology appear in the tile of a journal publishing the work). A quick survey of PubMed for the publication period from 1940 to 2008 (Table 1) revealed, not surprisingly, that the number of items per search term has increased dramatically over the years. Whereas the term cardiovascular showed a sharp increase in the early sixties, both neurology and psychiatry “exploded” in the early nineties. Even though the term cardiovascular psychiatry appeared earlier than cardiovascular neurology, the later term has become more prevalent since the early sixties (Table 1). Normalizing the data, that is, by expressing cardiovascular psychiatry as a percentage of corresponding psychiatry and cardiovascular neurology as a percentage of the corresponding neurology (Figure 1), showed that cardiovascular neurology rose sharply in the early sixties and has remained at about 5% of all neurology-related items. On the other hand, cardiovascular psychiatry had been below 1% of all psychiatry-related items until the early eighties, but has gradually increased. Possibly, the ischemia-related brain disorders have contributed to the relatively high presence of cardiovascular neurology and the relatively recent revelation of an unsuspected association of cardiovascular disorders with mood disorders might have contributed to the increase in cardiovascular psychiatry. The journal Cardiovascular Psychiatry and Neurology was created to provide for the first time a unified forum to consider the physiological and pathological interactions between the nervous and the cardiovascular systems. The journal aims to stimulate the development of relevant interdisciplinary and collaborative biomedical research and to foster multidisciplinary efforts in advancing medical practices. Figure 1 The proportions of retrieved PubMed terms Cardiovascular Psychiatry versus Psychiatry and Cardiovascular Neurology versus Neurology. The PubMed search was performed as described in Table 1. The percentages of items found for Cardiovascular Psychiatry ... Table 1 A number of PubMed items retrieved on January 13, 2009. The terms indicated in the table were searched (http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed) for the indicated publication dates (years). No systematic checking was performed for the actual ... Hari Manev

Acute stress cardiomyopathy

A unique syndrome of heart failure and transient left ventricular systolic dysfunction precipitated by acute emotional or physical stress has recently emerged in the medical literature. The syndrome is referred to by several names, including stress cardiomyopathy, takotsubo cardiomyopathy, left ventricular apical ballooning syndrome, and broken heart syndrome. Because most patients with stress cardiomyopathy present with chest pain, electrocardiographic abnormalities, elevated cardiac enzymes, and focal left ventricular wall motion abnormalities, it is not surprising that for years this syndrome went relatively unrecognized because physicians mistook it for acute myocardial infarction. As reports of this condition have increased worldwide during the past 5 years, it has become clear that stress cardiomyopathy has unique clinical features that can be readily distinguished from those of an acute myocardial infarction. This article reviews the clinical features of stress cardiomyopathy and discusses potential pathophysiologic mechanisms of this disorder.

Mending broken hearts: Acute stress cardiomyopathy

It has long since been suggested that people can suffer a ‘broken heart’ as a result of severe emotional upset. However, the phenomenon of ‘broken heart’ has only recently been subjected to rigorous scientific enquiry where it now formally recognized as acute stress cardiomyopathy. Acute stress cardiomyopathy, a distinct form of acute dilated cardiomyopathy, results in abrupt left ventricular dysfunction which can be acutely damaging and potentially fatal. However, the old adage ‘time mends a broken heart’ rings true with this condition as prognosis is very favorable with a period of time and appropriate nursing and medical care.