Left Ventricular Apical Ballooning Research Articles

Takotsubo Cardiomyopathy and Autoimmune Disorders: A Systematic Scoping Review of Published Cases.

Takotsubo cardiomyopathy (TCM) features transient left ventricular apical dysfunction or ballooning. The underlying mechanism remains elusive; however, evidence suggests the role of different physical and psychological stressors. We systematically reviewed patients presenting with TCM and autoimmunity to explore the link between the two conditions. We applied the Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) to report this review. Using keywords related to autoimmune/immune-mediated diseases and TCM, we searched PubMed, Scopus, and WOS in March 2022. The final results were added to a data extraction sheet. Data were analyzed by SPSS version 26.0. Our search yielded 121 studies, including 155 patients. Females were considerably predominant. Most patients had a history of autoimmune disease, and almost a third had a history of cardiovascular disease. Dyspnea and chest pain were the most common chief complaints. More than 70% of patients had experienced physical stress. Myasthenia gravis, systemic lupus erythematosus, and multiple sclerosis were the most frequently reported autoimmune diseases. There were similarities in age and sex compared to classic TCM. TCM should be considered as a differential diagnosis for ACS, especially in patients with a positive background of autoimmunity. A precise reporting system is required for further studies.

Myocardial strain changes over a 1-month follow-up in Takotsubo syndrome: a case report

Among various diagnostic methods, echocardiography (EchoCG) is most often used to identify Takotsubo syndrome. Left ventricular apical ballooning and the absence of permanent local contractility disturbances makes it possible to confirm the diagnosis. Currently, the available literature provides insufficient data on longitudinal strain (LS) of various cardiac chambers in this condition. The current case report demonstrates complete restoration of left heart LS within 1 month with its initial significant decrease.

Takotsubo cardiomyopathy following blunt trauma: Early recognition and diagnosis

Takotsubo Cardiomyopathy (TTC) is characterized by reversible left ventricular apical ballooning in the absence of angiographically significant coronary artery disease. While TTC is usually preceded by an emotionally stressful event, physical trauma has been documented as a precipitating incident as well.An 82-year-old female with no past medical history, presented to the emergency department following a motor vehicle collision. Trauma workup was significant for an ulnar fracture, elevated cardiac enzymes, and ST-segment changes. Bedside echocardiogram revealed apical ballooning. She underwent cardiac catheterization, which failed to demonstrate significant coronary artery disease. The patient developed cardiogenic shock and required temporary vasopressor support after failing a trial of intra-aortic balloon pump.Takotsubo Cardiomyopathy is a rare complication of trauma, which presents with signs and symptoms similar to acute coronary syndrome (ACS) but without evidence of obstructive coronary artery disease. Following trauma, signs of ACS in elderly women should raise provider's suspicion for TTC and prompting bedside echocardiography, which can assist with early diagnosis.

Changes in CMR findings over time following acute Takotsubo cardiomyopathy

Takotsubo cardiomyopathy (TTS) is characterized by acute reversible left ventricular dysfunction showing typical left ventricular apical ballooning in the absence of obstructive coronary artery disease. Cardiac magnetic resonance (CMR) provides functional and inflammatory findings in contrast with the absence of late gadolinium enhancement (LGE). TTS generally heals within the first two weeks after the onset of symptoms, with the ECG and echocardiogram normalizing. However, data on CMR dynamics are scarce. In the present study, we aimed to describe how CMR findings change over time in acute TTS. Between December 2008 and May 2021, we retrospectively included all the patients hospitalized in the tertiary University Hospital of Angers, France who underwent CMR and received a diagnosis of acute TTS. Sixty-two patients fulfilled the diagnostic criteria from the 2018 ESC international expert consensus and underwent CMR. Patients were classified into three groups based on the delay between their first day of hospitalization and their assessment using CMR: less than five days (n = 31, 50%), between 5 and 15 days (n = 16, 25.8%), and more than 15 days [median 27 days (IQR: 20–36)] (n = 15, 24.2%). Compared to the 0–5 d group, the patients in the > 15 d group showed resolution of the LVEF alterations (55.9 ± 10.7 vs. 44.8 ± 13.3, P = 0.07), less apical akinesia (40% vs. 83%, P = 0.01) and normalized apical T2 values (44.5 ± 3.5 vs. 57 ± 2, P = 0.049). T1 and T2 quantitative measurements showed a base-to-apex gradient in 88.2% and 85.7% of patients, irrespective of the delay (P = 0.12 and P = 0.88). When CMR cannot be performed early after the onset of a suspected TTS, wall motion abnormalities disappear, and LVEF alteration resolve. However, a parametric assessment searching for a base-to-apex gradient in T1 and T2 values with higher apical values may be helpful to confirm the diagnosis. Main CMR findings at different time points (Fig. 1).

Takotsubo Syndrome in Orthotopic Liver Transplant: A Systematic Review and Pooled Analysis of Published Studies and Case Reports

Takotsubo syndrome (TTS) has been reported in solid-organ transplant recipients. However, the pooled data regarding TTS after liver transplant remain limited. A systematic review was performed through February 2022 using PubMed, Embase, Scopus, and Google Scholar to review case reports/series and original studies on liver transplant-associated TTS. Descriptive analysis was performed for case reports and pooled analysis for the prevalence using random effects models. A total of 56 case reports were included from 30 articles (51.8 % male; mean age, 53 years; India 56%, US 27%, and Europe 8.93%) and 10 original studies (US 88.65%, India 10.92%) revealing liver transplant-associated TTS. The pooled prevalence of TTS was 1.1% (95% Cl, 0.6%-1.7%) of all liver transplants with comparable rates in studies from India and the US (P = .92). Indications for liver transplant included end-stage liver disease due to alcohol-related cirrhosis (25%), hepatitis C virus infection (17.9%), hepatocellular carcinoma (10.7%), and non-alcohol-related steatohepatitis (8.9%); the average Model for End-Stage Liver Disease score was 24.75. TTS commonly presented as hypotension (30%), dyspnea (14%), and oliguria, occurring mostly post-transplant (82%), whereas 14% were intraoperative. Common electrocardiogram findings were ST changes, ventricular tachycardia, and atrial fibrillation. Common echocardiogram findings showed left ventricular apical ballooning in 46.5% of cases and reduced ejection fraction < 20% in 41.9% of cases. Common complications were cardiogenic shock (32.1 %), acute kidney injury (12.5%), arrhythmia, stroke, cardiac arrest, and hepatic artery thrombosis. Mechanical circulatory support was required in 30.3%. Recurrence was reported in 15, and mortality in 30.4% of patients. Takotsubo syndrome prevalence after liver transplant is significantly higher than TTS prevalence in general US hospitalizations with potentially worse outcomes. Prospective registries reporting TTS in liver transplant recipients are warranted.

Reverse Takotsubo Stress Cardiomyopathy During Liver Transplantation

Reverse Takotsubo Stress Cardiomyopathy During Liver Transplantation

Abstract 13293: Albuterol and Hyperthyroidism as Potential Causes of Stress Cardiomyopathy

Introduction Takotsubo cardiomyopathy (TCM) is a recognized reversible process associated with emotional or physical stressors characterized by left ventricular apical ballooning in the absence of obstructive coronary artery disease. We present a unique case of TCM after albuterol use in the setting of hyperthyroidism. Results A 74-year-old woman with history of hyperthyroidism and asthma presented with acute substernal chest pain and progressive dyspnea. She was diagnosed with an asthma exacerbation, started oral prednisone 3 days before presentation, and reported using 16 puffs of her albuterol inhaler the day before. Examination revealed blood pressure 157/100 mmHg, heart rate 135 beats per minute, respiratory rate of 35 breaths per minute, and SpO2 94% on a 5-liter nasal cannula. Lung exam revealed bilateral end-expiratory wheezes, and she appeared in respiratory distress. The remainder of the exam was unremarkable, including cardiac exam. ECG revealed atrial tachycardia with ST elevations in the anterolateral leads concerning for injury. High sensitivity troponin was 1484 ng/L (ref &lt;19), free T4 level 3.63 ng/dL (ref 0.56-1.64 ng/dL), TSH &lt;0.02 μU/mL (ref 0.35-3.30 μU/mL ) with TSH-receptor Ab 8.62 IU/L (ref &lt;1.75 IU/L) consistent with worsening hyperthyroidism when compared to one month prior (free T4: 1.19 ng/dL; TSH: 0.84 μU/mL/mL). Emergent cardiac catheterization showed non-obstructive coronary artery disease and reduced ejection fraction (EF) of 30% with akinesia of the anterolateral, apical, and diaphragmatic segments consistent with TCM. She had a full recovery of systolic function noted on repeat echocardiogram 10 weeks after treatment with guideline-directed therapy. Conclusion TCM is primarily driven by a high catecholamine state that, paradoxically, increases β-2 adrenergic receptor inhibitory signaling, thus, causing preferential depression of apical myocardial function possibly due to topographic receptor distribution. Hyperthyroidism mimics a state of adrenergic excess partially mediated by the upregulation of β-adrenergic receptors by thyroid hormones, and the use of β-2 agonists potentiated the development of TCM.

Abstract 10420: Spontaneous Coronary Artery Dissection in a Young Man Taking Sumatriptan

Introduction: Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome. There is an approximate 9:1 female predominance, and commonly cited risk factors include fibromuscular dysplasia, pregnancy, and cocaine use. We present a case of SCAD in a young man with migraines and triptan use, initially misdiagnosed as panic disorder. Case: A 25-year-old man with a history of migraines treated with sumatriptan presented with several months of intermittent chest pain and syncopal episodes. He had been evaluated in an emergency department at the onset of symptoms and diagnosed with panic disorder. His EKG now showed Q waves in leads V1-V2 and T wave inversions in leads I and AVL. Serial troponins were stable at 0.04 ng/mL. An echocardiogram showed left ventricular apical ballooning and large thrombus. Left heart catheterization revealed significant stenosis of the proximal LAD and 50% stenosis of the mid LAD (Fig. 1A). A follow-up CT angiogram showed intimal thickening and perivascular fat stranding in the proximal and mid LAD, confirming a diagnosis of SCAD (Fig. 1B). A full-body CTA showed no additional aneurysm or dissection. Inflammatory markers and autoimmune serologies were negative. Urine toxicology was negative for cocaine or amphetamines. Given an otherwise unrevealing workup, migraines and triptan use were identified as the significant risk factors for SCAD. He was discharged with clopidogrel, warfarin, and metoprolol and counseled against further use of triptans Discussion: Multiple studies have reported increased prevalence of SCAD in patients with migraines, particularly those using triptans. This phenomenon likely relates to stimulation of 5-HT1B and 5-HT1D receptors in the coronary vasculature. Greater recognition of SCAD and its risk factors is essential for timely diagnosis and treatment, particularly in young patients whose chest pain may be falsely attributed to non-cardiac causes.

Upregulation of neuropeptide Y in cardiac sympathetic nerves induces stress (Takotsubo) cardiomyopathy.

Substantial emotional or physical stress may lead to an imbalance in the brain, resulting in stress cardiomyopathy (SC) and transient left ventricular (LV) apical ballooning. Even though these conditions are severe, their precise underlying mechanisms remain unclear. Appropriate animal models are needed to elucidate the precise mechanisms. In this study, we established a new animal model of epilepsy-induced SC. The SC model showed an increased expression of the acute phase reaction protein, c-Fos, in the paraventricular hypothalamic nucleus (PVN), which is the sympathetic nerve center of the brain. Furthermore, we observed a significant upregulation of neuropeptide Y (NPY) expression in the left stellate ganglion (SG) and cardiac sympathetic nerves. NPY showed neither positive nor negative inotropic and chronotropic effects. On the contrary, NPY could interrupt β-adrenergic signaling in cardiomyocytes when exposure to NPY precedes exposure to noradrenaline. Moreover, its elimination in the left SG via siRNA treatment tended to reduce the incidence of SC. Thus, our results indicated that upstream sympathetic activation induced significant upregulation of NPY in the left SG and cardiac sympathetic nerves, resulting in cardiac dysfunctions like SC.

The Impact of Mental Stress on Cardiovascular Health-Part II.

Endothelial dysfunction is one of the earliest manifestations of atherosclerosis, contributing to its development and progression. Mental stress induces endothelial dysfunction through increased activity of the sympathetic nervous system, release of corticotropin-releasing hormone from the hypothalamus, inhibition of nitric oxide (NO) synthesis by cortisol, and increased levels of pro-inflammatory cytokines. Mental-stress-induced increased output of the sympathetic nervous system and concomitant withdrawal of the parasympathetic inflammatory reflex results in systemic inflammation and activation of a neural–hematopoietic–arterial axis. This includes the brainstem and subcortical regions network, bone marrow activation, release of leukocytes into the circulation and their migration to the arterial wall and atherosclerotic plaques. Low-grade, sterile inflammation is involved in all steps of atherogenesis, from coronary plaque formation to destabilisation and rupture. Increased sympathetic tone may cause arterial smooth-muscle-cell proliferation, resulting in vascular hypertrophy, thus contributing to the development of hypertension. Emotional events also cause instability of cardiac repolarisation due to brain lateralised imbalance of cardiac autonomic nervous stimulation, which may lead to asymmetric repolarisation and arrhythmia. Acute emotional stress can also provoke severe catecholamine release, leading to direct myocyte injury due to calcium overload, known as myocytolysis, coronary microvascular vasoconstriction, and an increase in left ventricular afterload. These changes can trigger a heart failure syndrome mimicking acute myocardial infarction, characterised by transient left ventricular dysfunction and apical ballooning, known as stress (Takotsubo) cardiomyopathy. Women are more prone than men to develop mental-stress-induced myocardial ischemia (MSIMI), probably reflecting gender differences in brain activation patterns during mental stress. Although guidelines on CV prevention recognise psychosocial factors as risk modifiers to improve risk prediction and decision making, the evidence that their assessment and treatment will prevent CAD needs further evaluation.

Takotsubo cardiomyopathy in a bedridden patient with dementia and communication difficulties due to Alzheimer's disease.

Takotsubo cardiomyopathy is a transient wall motion abnormality of the left ventricular apex, accompanied by emotional or physical stress. Although Takotsubo cardiomyopathy is generally considered a benign disease, severe clinical complications may occur, and early detection of the disease is important. In this report, we present the case of an 86-year-old bedridden woman with a history of bronchial asthma who was transferred to our hospital because of wheezing. She was diagnosed with Alzheimer’s disease and had communication difficulties. After an asthma attack and improvement, Takotsubo cardiomyopathy was identified via electrocardiography. She was unable to complain of any symptoms but showed serial electrocardiographic changes, elevated myocardial markers, and transient left ventricular apical ballooning. The prevalence of dementia increases dramatically with age. This case indicates that Takotsubo cardiomyopathy may occur even in patients with severe dementia, who are bedridden and show communication difficulties in a clinical setting.

A rare manifestation of Takotsubo Cardiomyopathy associated with non-tuberculous mycobacterium

BackgroundTakotsubo Cardiomyopathy or broken heart syndrome is a rare cause of non-ischemic cardiomyopathy that produce left ventricular dysfunction with characteristic left ventricular apical ballooning. It rarely caused by infection. We present an atypical manifestation of non-tuberculous mycobacterial (NTM) infection with myocardial involvement and its diagnostic challenge. Case illustrationA 57-year-old female presented with prolonged fever, fatigue and weight loss for one and half months. General examination was unremarkable with elevated C-Reactive Protein and normal troponin. Electrocardiogram (ECG) showed diffuse T wave inversion with prolonged QTc. Echocardiography showed hypokinetic apical with normal ejection fraction. Angiography showed patent coronary arteries. Ventriculography showed apical ballooning. Workup with ethambutol scan revealed active mycobacterial infection in both lung and mesentery. Sputum polymerase chain reaction (PCR) was positive for non-tuberculous mycobacterium. Follow up ECG and echocardiography showed improvement in QTc interval and left ventricular wall motion abnormalities. ResultsTakotsubo Cardiomyopathy may manifest as asymptomatic ventricular dysfunction following non-tuberculous mycobacterial infection. A thorough investigation will help identify the systemic disease with cardiac involvement which potentially could be fatal. ConclusionTakotsubo cardiomyopathy may be triggered by infection. Identification of causal is crucial as a management strategy to restore cardiac function.

Plasma brain natriuretic peptide level on admission predicts long-term outcome in patients with non-traumatic subarachnoid hemorrhage

IntroductionNon-traumatic subarachnoid hemorrhage (SAH) is a type of stroke that still has a high mortality rate. Some patients with SAH have electrocardiography (ECG) abnormalities or asymptomatic left ventricular apical ballooning, and requires intervention by cardiologists. However, the impact of cardiac abnormalities after SAH onset remains unclear. We investigated whether ECG abnormalities, myocardial damage, sympathetic nervous activity or echocardiographic left ventricular wall motion abnormalities (WMA) could provide additional risk stratification in patients with SAH. MethodsWe studied 118 SAH patients (78 women, age 63 ± 15) without a history of heart disease. Neurological grade (Hunt and Kosnik Grade) and clinical factors were evaluated. A standard 12-lead ECG, echocardiography and blood samples were obtained within 48 h after SAH onset. ECG abnormalities were defined as abnormal Q wave, ST elevation, giant T-wave inversion or QT prolongation. ResultsTwenty of 118 patients (17%) died during the follow-up (35 ± 31 months). Death was significantly associated with higher age (p < 0.0001), neurological grade (p < 0.0001), elevated BNP level (p < 0.0001), increased plasma norepinephrine levels (p < 0.0001) and WMA (p = 0.0070), while ECG abnormalities were not significantly associated. Neurological grade (p < 0.0001), age (p = 0.0047) and BNP (p = 0.0014, hazard ratio 1.0255 for each 1 pg/mL increase in BNP, 95%CI 1.0088 to 1.0499) were independently associated with death. Patients with BNP ≥ 96.6 had a higher risk of death (log- rank p < 0.0001). ConclusionPlasma BNP might provide an additional risk stratification in patients with non-traumatic SAH that requires intervention by cardiologists for both its prevention management after onset.

A Novel Disease Entity in Search of Its Own Identity - Takotsubo Syndrome. Is It Really "Cardiomyopathy"?

Background: The term “takotsubo cardiomyopathy” is commonly used in clinical practice. However, there is conceptual problem with the term “cardiomyopathy” in this context because “cardiomyopathy” implies a primary and chronic myocardial disease of unknown etiology. In this study we reviewed the literature related to takotsubo cardiomyopathy to investigate whether it is appropriate to use the term “cardiomyopathy” for this condition.Methods and Results: A literature review revealed that this condition was originally described in 1990 in Japan as postischemic myocardial stunning with unique left ventricular apical ballooning and that it gradually gained global attention thereafter. Subsequently, the term “takotsubo cardiomyopathy” was introduced to describe this heart failure phenotype. However, this term has been called into question because several recent studies investigating the mechanism underlying this condition have provided evidence of myocardial ischemia possibly due to microvascular dysfunction. The term “takotsubo syndrome” was suggested to describe this microvascular acute coronary syndrome, which is in agreement with the original description of the condition as myocardial stunning following acute myocardial ischemia.Conclusions: Based on the accumulating evidence of acute myocardial ischemia due to microvascular dysfunction as the mechanism underlying this condition, in addition to the fact that the term “cardiomyopathy” literally implies a primary and chronic myocardial disease, it is advisable that the term “takotsubo syndrome” is used until the etiology and underlying mechanism of this condition are fully clarified.

Takotsubo cardiomyopathy and pituitary apoplexy: a case report

BackgroundTakotsubo cardiomyopathy (TTC) has been widely recognized in recent decades and is triggered by either physical or psychological stressors.Case presentationA 70-year-old woman presented to the Emergency Department due to confusion, hypotension, fever, chills, and cough. She had a one-year history of diabetes insipidus. Pituitary function examination at admission revealed decreased thyroid, sex and adrenal hormones. Pituitary MRI displayed findings suggestive of nonhemorrhagic pituitary apoplexy. Electrocardiogram (ECG) revealed T-wave inversion and extended QT interval. Transthoracic echocardiogram (TTE) showed left ventricular apical dysplasia and ballooning, accompanied by reduced left ventricular ejection fraction. Coronary angiography (CAG) revealed no obvious coronary arterial stenosis. The left ventriculogram demonstrated an octopus clathrate appearance. Most ECG and TTE changes recovered 10 days later.ConclusionsTo the best of our knowledge, this is the first report of newly diagnosed TTC associated with pituitary apoplexy.

Silent left ventricular apical ballooning and Takotsubo cardiomyopathy in an Australian intensive care unit.

AimsRecent reports have shown a high incidence of silent left ventricular apical ballooning (LVAB) in the intensive care unit (ICU) setting with potential implications for safe use of inotropes and vasopressors. We examined the incidence, predictors, and associated outcomes of LVAB in patients in a contemporary tertiary Australian ICU.Methods and resultsIn a prospective cohort study, patients were screened within 24 h of admission to the ICU and enrolled if they were deemed critically unwell based on mechanical ventilation, administration of >5 mg/min of noradrenaline, or need for renal replacement therapy. Exclusion criteria were a primary diagnosis of Takotsubo cardiomyopathy, admission to ICU after cardiac surgery, or with acute myocardial infarction or heart failure. Echocardiography was performed, and the presence/absence of LVAB was documented. A total of 116 patients were enrolled of whom four had LVAB (3.5%, 95% confidence interval 0.9–8.6%). Female sex was the only baseline demographic or clinical characteristic associated with incident LVAB. Medical history, ICU admission indication, and choice of inotropes were not associated with increased risk. Patients with LVAB had no deaths and had similar lengths of ICU and hospital stay compared with patients with no LVAB.ConclusionsThe incidence of silent LVAB suggestive of TC was substantially lower in this study than recently reported in other international ICU settings. We did not observe a suggestion of worse outcomes. A larger, multi‐centre study, prospectively screening for LVAB may help understand any variation between centres and regions, with important implications for ICU management.

Takotsubo cardiomyopathy in aneurysmal subarachnoid hemorrhage: A case report

Introduction. Subarachnoid haemorrhage (SAH) can be followed by cardiac abnormalities. We describe a patient with Takotsubo cardiomyopathy and neurogenic pulmonary edema (NPE) after aneurysmal SAH. Case report. A previously healthy, postmenopausal woman, suffered from aneurysmal SAH with consequent hydrocephalus. After external ventricular drainage, craniotomy and clipping of the posterior inferior cerebellar artery aneurysm, the patient developed acute heart failure and NPE. Transthoracic echocardiogram showed the left ventricular apical ballooning and hypercontractile basal segments. On chest radiography, bilateral pulmonary infiltrates were seen. Seventeen days after the SAH attack, the patient was discharged from hospital. Postponed coronary angiography revealed no signs of coronary artery disease. Conclusion. This case and review of the relevant literature suggest that Takotsubo cardiomyopathy and neurogenic pulmonary edema are not uncommon after aneurysmal SAH.

Hypertrophic cardiomyopathy with dynamic obstruction and high left ventricular outflow gradients associated with paradoxical apical ballooning.

Acute left ventricular (LV) apical ballooning with normal coronary angiography occurs rarely in obstructive hypertrophic cardiomyopathy (OHCM); it may be associated with severe hemodynamic instability. We searched for acute LV ballooning with apical hypokinesia/akinesia in databases of two HCM treatment programs. Diagnosis of OHCM was made by conventional criteria of LV hypertrophy in the absence of a clinical cause for hypertrophy and mitral-septal contact. Among 1519 patients, we observed acute LV ballooning in 13 (0.9%), associated with dynamic left ventricular outflow tract (LVOT) obstruction and high gradients, 92±37mmHg, 10 female (77%), age 64±7years, LVEF 31.6±10%. Septal hypertrophy was mild compared to that of the rest of our HCM cohort, 15 vs 20mm (P<0.00001). An elongated anterior mitral leaflet or anteriorly displaced papillary muscles occurred in 77%. Course was complicated by cardiogenic shock and heart failure in 5, and refractory heart failure in 1. High-dose beta-blockade was the mainstay of therapy. Three patients required urgent surgical relief of LVOT obstruction, 2 for refractory cardiogenic shock, and one for refractory heart failure. In the three patients, surgery immediately normalized refractory severe LV dysfunction, and immediately reversed cardiogenic shock and heart failure. All have normal LV systolic function at 45-month follow-up, and all have survived. Acute LV apical ballooning, associated with high dynamic LVOT gradients, may punctuate the course of obstructive HCM. The syndrome is important to recognize on echocardiography because it may be associated with profound reversible LV decompensation.

Zumba-induced Takotsubo cardiomyopathy: a case report

BackgroundTakotsubo cardiomyopathy or stress cardiomyopathy is characterized by transient left ventricular apical ballooning in the absence of coronary occlusion. The underlying pathophysiological mechanism is still unclear but possible causes have been proposed mainly catecholamine cardiotoxicity, followed by metabolic disturbance, coronary microvascular impairment, and multivessel epicardial coronary artery vasospasm. Takotsubo cardiomyopathy accounts for 1–2% of patients presenting with acute coronary syndrome with the majority of patients diagnosed with Takotsubo cardiomyopathy being women > 55 years of age. Here, we discuss the case of a 38-year-old woman presenting with typical chest pain, electrocardiography changes and cardiac markers consistent with acute coronary syndrome, who was subsequently diagnosed with Takotsubo cardiomyopathy.Case presentationA 38-year-old healthy American woman with negative past medical history presented to our Emergency Department with chest pain developing while participating in intense outdoor physical activities (Zumba) at a fundraising event. Our patient had typical substernal chest pain induced with exercise and was relieved by sublingual nitroglycerin in the Emergency Department. The pain started after 2 h of intensive Zumba workout. On review of her history, our patient was noted to be taking spironolactone 125 mg once daily for hirsutism for the past year. Our patient denied any family history of cardiac disease or heart failure. She admitted to being a former occasional smoker and to drinking alcohol socially. She denied any illicit drug use. She works as a social worker, and reported that she does not experience much stress in her life and denied any “one big life-changing event” or any major stressful news. While in the Emergency Department, our patient was hemodynamically stable and an electrocardiography was performed and showed sinus rhythm with no ST elevation/depression but noted T-wave inversion in leads I and aVL, and T wave flattening in leads V1 and V2. Her troponin levels were 0.294 and 0.231 consecutively. An echocardiogram was done and showed hypokinetic apical and mid-distal walls and hyperdynamic basal walls of the left ventricle with an ejection fraction of 35–40%, consistent with apical ballooning syndrome. Cardiac catheterization was subsequently done and showed depressed left ventricle systolic function, ejection fraction of 30–35% with anteroapical dyskinesia and no evidence of coronary artery disease.Our patient was diagnosed with Takotsubo cardiomyopathy after fulfilling all four of the Mayo Clinic’s diagnostic criteria and was subsequently treated with a beta blocker, and angiotensin-converting enzyme inhibitor.ConclusionsOur patient did not have one clear trigger for her overt Takotsubo cardiomyopathy other than the Zumba activity. Zumba is considered an activity with excessive sympathetic stimulation leading to catecholamine-induced microvascular spasm or through to direct myocardial toxicity, which is postulated to be behind the pathophysiology of Takotsubo cardiomyopathy. Another interesting finding in our patient was her use of spironolactone, as treatment for hirsutism, which is an aldosterone antagonist. Aldosterone actually potentiates the effects of catecholamine and thus activates the sympathetic system. Spironolactone can thus be considered as cardioprotective against the effects of catecholamine on the heart and that is why it is considered to be beneficial and subsequently improves mortality in chronic heart failure as described in several studies.

A 68-year-old with cranial nerve neuropathies and a troponin rise

In this case study, we summarise the inpatient investigations and management of a 68-year-old woman with Takotsubo cardiomyopathy secondary to a Varicella zoster encephalitis and the difficulties inherent with making this diagnosis. She presented with evolving cranial nerve neuropathies, which started with a vagal nerve mononeuritis and eventually included left-sided sensorineural hearing loss and a facial nerve palsy. These symptoms were concomitant with a variety of cardiac abnormalities, including fast atrial fibrillation and electrocardiographic changes. We summarise some of the current understanding of Takotsubo cardiomyopathy and the criteria for its diagnosis. Although left ventricular apical ballooning has been described in association with severe infections and states of high stress, we have not seen it reported in association with a Varicella zoster encephalitis.