Triggers Of Takotsubo Cardiomyopathy Research Articles

Takotsubo cardiomyopathy complicating acute pancreatitis: a case report

BackgroundAcute pancreatitis as a trigger of Takotsubo cardiomyopathy has been infrequently described in the literature. Misdiagnosis of this phenomenon can often occur due to overlap in symptomology, particularly in those outside of the usual patient demographic.Case presentationA 27-year-old man with a history of alcohol abuse presented with epigastric and chest pain. Electrocardiography showed ischemic changes, and laboratory workup revealed elevated lipase and troponin. He was diagnosed with acute pancreatitis and managed presumptively as acute coronary syndrome. Subsequent coronary angiography was negative for obstructive coronary artery disease, and left ventriculography demonstrated basal hyperkinesis and apical akinesis, characteristic of Takotsubo cardiomyopathy.ConclusionsTakotsubo cardiomyopathy is a rare complication of acute pancreatitis. Increased awareness of this phenomenon is required to prevent delays in diagnosis and avoid unnecessary interventions and complications.

Abstract 14875: Chronic Obstructive Pulmonary Disease Negatively Affects In-hospital Outcomes in Patients With Takotsubo Cardiomyopathy

Introduction: Chronic obstructive pulmonary disease (COPD) is a known comorbidity of takotsubo cardiomyopathy (TCM), and COPD exacerbation is a potential trigger of TCM. The association between COPD and in-hospital outcomes and complications in TCM patients is not well established. Aim: We aimed to assess the effect of COPD on hospitalized patients with a primary diagnosis of TCM. Methods: Using the latest National Inpatient Sample from 2016-2017, we conducted a retrospective cohort study in patients with a primary diagnosis of TCM with or without COPD. The diagnosis was identified by the ICD-10-CM coding system. We identified 3,139 patients admitted with a primary diagnosis of TCM; 684 of those patients also had a diagnosis of COPD. We performed propensity score matching in a 1:2 ratio (n=678 patients, matched COPD group; n=1,070, matched non-COPD group) and compared in-hospital outcomes and complications between TCM patients with and without a COPD diagnosis. Results: Before matching, the COPD group had worse outcomes compared with the non-COPD group in inpatient death (2.9% vs. 1.3%, p=0.006), length of stay (LOS) (4.02±2.99 days vs. 3.27±3.39 days, p<0.001), hospitalization costs ($55,242.68±47,637.40 vs. $48,316.97±47,939.84, p=0.001), and acute respiratory failure (ARF) (22.5% vs. 7.7%, p<0.001), respectively. After propensity score matching, the matched COPD group, compared with the matched non-COPD group, had a higher inpatient mortality rate (2.9% vs.1.0%, p=0.005), longer LOS (4.02±3.00 days vs. 3.40±3.54 days, p<0.001), higher hospitalization costs ($55,409.23±47,809.13 vs. $44,6469.60±42,209.10, p<0.001), and a higher incidence of ARF (22.6% vs. 8.2%, p<0.001) and cardiogenic shock (5.6% vs. 3.3%, p=0.024), respectively. Conclusions: Patients who are hospitalized for TCM and have COPD have higher rates of inpatient mortality, ARF, and cardiogenic shock, as well as a longer LOS and a higher cost of stay than TCM patients without COPD. Prospective studies are warranted to examine the effect of early intervention or treatment of COPD on short and long-term outcomes of TCM.

Drugs as Possible Triggers of Takotsubo Cardiomyopathy: A Comprehensive Literature Search - Update 2015.

In 2011 a list of 20 drugs linked to drug-induced Tako-Tsubo cardiomyopathy (TCM) was published. Thus, the objectives were both to identify cases of drug-induced TCM, and update the 2011 list of drugs as possible triggers of this cardiomyopathy. As the 2011 report of drug-induced TCM, case reports of drug-induced TCM were identified by a comprehensive search in Medline/PubMed database. From December 2010 to March 2015 search terms were Takotsubo cardiomyopathy, Takotsubo cardiomyopathy, stress cardiomyopathy, transient-left-ventricular ballooning syndrome, ampulla cardiomyopathy, apical ballooning syndrome, OR broken heart syndrome; together with "iatrogenic", "drug-induced", OR "induced by". Publications limited to English, Spanish, and French, in humans, and with full texts were retrieved. Articles that recognized any drug as a possible trigger of TCM were selected. Overall, 405 different references were retrieved and 67 were selected (62 case reports and 5 case series) involving 78 patient cases with TCM possibly associated to drugs were reviewed. At total of 44 drugs were recognized as possible drug-induced TCM, mainly with sympathetic effect, and 37 (84.1%) were different to those 20 identified in the 2011 review; therefore, a list of 57 drugs associated to TCM was obtained. There are new case reports that linked drug-use with the development of TCM. The list of 57 drugs obtained is principally integrated by drugs that generate sympathetic overstimulation. Consequently, the recommendation "drug-induced TCM would be considered in patients with TCM, particularly those in which no clear emotional or stress trigger could be identified" is endorsed.

Early treatment with isoflurane improves cardiac function and increases survival in a rat model of TAKO-TSUBO cardiomyopathy

Tako-tsubo cardiomyopathy (TCM) is an acute cardiac syndrome with severe hypokinesia of the left ventricle (LV), often affecting the apex causing apical ballooning and heart failure. Sympathetic stress is a trigger of TCM and is probably underdiagnosed and not uncommon in ICU patients [1]. We have developed an experimental rat model of TCM, in which LV apical akinesia develops after intraperitoneal (i.p.) injection of isoprenaline with many similarities to clinical TCM [2]. We recently demonstrated that pre-treatment with isoflurane could prevent the development of LV apical akinesia in this TCM animal model [3].

“Ballooning” patterns in takotsubo cardiomyopathy reflect different clinical backgrounds and outcomes: a BOREAS-TCM study

Whether different patterns of ventricular ballooning in takotsubo cardiomyopathy (TCM) reflect differences in trigger mechanisms or clinical outcomes is unclear. Here we examined differences in the clinical characteristics of typical and atypical forms of TCM. TCM patients (n = 251) in the BOREAS Registry were enrolled for comparison of TCM with apical ballooning (type A, n = 217) and TCM with non-apical ballooning (type non-A, n = 34). The percentage of females was significantly lower in the type non-A group (58.8 vs. 75.6 %), while other demographic parameters and triggers of TCM were similar in the two groups. Rate of mid-ventricular obstruction (MVO) was lower (2.9 vs. 14.3 %) in the type non-A group than in the type A group, though left ventricular ejection fractions in the two groups were comparable. During a follow-up period of 2.6 ± 2.8 years, TCM recurred in 2.9 % of the patients and cardiac death occurred in 4.0 %. Cox proportional hazard analysis indicated that body mass index (hazard ratio [HR]: 0.75, 95 % confidence interval [CI] 0.54-0.99) and MVO (HR: 14.71, CI 1.87-304.66) were determinants of TCM recurrence and that advanced age (HR: 1.09, CI 1.02-1.17) and cardiogenic shock (HR: 4.27, CI 1.07-18.93) were significantly associated with cardiac death. In conclusion, approximately 20 % of TCM patients show non-apical left ventricular ballooning, and female sex and MVO are less frequent in this type than in apical ballooning type TCM. Low body mass index and MVO are risk factors of recurrence, and advanced age and cardiogenic shock are risk factors of cardiac death in TCM.

PP-260 MELPHALAN INDUCED TAKOTSUBO CARDIOMYOPATHY

Case: A 53 year old women presented to the outpatient clinic with dyspnea and chest pain. She also complained about burning sensation in both arms. Her medical history included a cardiac surgery for secundum type atrial septal defect 25 years ago and a recent lower respiratory tract infection. She had also neurological diseases such as migreine and restless leg syndrome. Her ECG showed negative T waves in all leads with a mild QT prolongation (QTc =460ms). Laboratory examination showed increased troponin I levels (0.6 ng/ml). Coronary angiography showed normal coronary arteries, but ventriculography was demonstrative for an apical ballooning (Figure 1). Transthoracic echocardiography approved the mid-apical akinesia with basal hyperkinesia (Figure 2). Hence the possible diagnosis was takotsubo cardiomyopathy (TC), the patient was went on serial echocardiographic evaluation. On the 10th day of admission echocardiography showed nearly complete normalization of left ventricular dysfunction (Figure 3). When the patient was further questioned for possible triggers of TC, although there was no emotional or physical stres, a recent history of polymedication including antimigreine drugs and antibiotics was evident. The patient received clarithromycin 1000mg/day for the last 14 days which was prescribed for lower respiratory tract infection. She also received ergotamine tartarate 1.5mg /day for the last 5 days owing to her increased migreine headache. She was already on therapy for restless leg syndrome including pramipexole 0.25mg/day and fluoxetine 20mg/day. When the drugs she used were analyzed, ergotamine toxicity was seen as a possible etiology. Ergotamine, because of its a-adrenergic effects and extensive first pass metabolism via cytochrome p450–3A4 isoenzyme, could possibly cause such a condition in presence of concomitant use of clarithromycin and fluoxetine which were powerful inhibitors of CYP450. The proposed mechanisms of TC; coronary microvasculature vasospasm and catecholamine excess could readily be a consequence of ergotamine toxicity. Ergotamine tartrate and clarithromycin were stopped during the hospital stay. Clinical follow up was uneventful for the next 6 months with totally normal left ventricular functions. TC is a syndrome of transient cardiac dysfunction precipitated by intense emotional or physical stress. Published case reports of TC associated with drug usage consist of sympathomimetic drugs, inotropic agents, thyroid hormone, cocaine and 5 fluorouracil [1]. To the best of our knowledge the peresent case is the first defining an association between ergotamin toxicity and TC.

PP-259 ERGOTAMINE INDUCED TAKOTSUBO CARDIOMYOPATHY

Case: A 53 year old women presented to the outpatient clinic with dyspnea and chest pain. She also complained about burning sensation in both arms. Her medical history included a cardiac surgery for secundum type atrial septal defect 25 years ago and a recent lower respiratory tract infection. She had also neurological diseases such as migreine and restless leg syndrome. Her ECG showed negative T waves in all leads with a mild QT prolongation (QTc =460ms). Laboratory examination showed increased troponin I levels (0.6 ng/ml). Coronary angiography showed normal coronary arteries, but ventriculography was demonstrative for an apical ballooning (Figure 1). Transthoracic echocardiography approved the mid-apical akinesia with basal hyperkinesia (Figure 2). Hence the possible diagnosis was takotsubo cardiomyopathy (TC), the patient was went on serial echocardiographic evaluation. On the 10th day of admission echocardiography showed nearly complete normalization of left ventricular dysfunction (Figure 3). When the patient was further questioned for possible triggers of TC, although there was no emotional or physical stres, a recent history of polymedication including antimigreine drugs and antibiotics was evident. The patient received clarithromycin 1000mg/day for the last 14 days which was prescribed for lower respiratory tract infection. She also received ergotamine tartarate 1.5mg /day for the last 5 days owing to her increased migreine headache. She was already on therapy for restless leg syndrome including pramipexole 0.25mg/day and fluoxetine 20mg/day. When the drugs she used were analyzed, ergotamine toxicity was seen as a possible etiology. Ergotamine, because of its a-adrenergic effects and extensive first pass metabolism via cytochrome p450–3A4 isoenzyme, could possibly cause such a condition in presence of concomitant use of clarithromycin and fluoxetine which were powerful inhibitors of CYP450. The proposed mechanisms of TC; coronary microvasculature vasospasm and catecholamine excess could readily be a consequence of ergotamine toxicity. Ergotamine tartrate and clarithromycin were stopped during the hospital stay. Clinical follow up was uneventful for the next 6 months with totally normal left ventricular functions. TC is a syndrome of transient cardiac dysfunction precipitated by intense emotional or physical stress. Published case reports of TC associated with drug usage consist of sympathomimetic drugs, inotropic agents, thyroid hormone, cocaine and 5 fluorouracil [1]. To the best of our knowledge the peresent case is the first defining an association between ergotamin toxicity and TC.

Tako-tsubo cardiomyopathy precipitated by alcohol withdrawal

A 57 year-old woman with no history of cardiac disease presented to the emergency department with confusion and seizures secondary to alcohol withdrawal. Elevated troponin levels and an electrocardiogram demonstrating global T-wave inversions prompted coronary angiography, which revealed coronary vessels free of significant disease. An echocardiogram showed both hypokinesis of the left-ventricular mid-segments with apical involvement and a hyperkinetic base consistent with tako-tsubo cardiomyopathy (TCM). Several clinical conditions have been reported as triggers of TCM. We report a case of TCM in a post-menopausal woman that was precipitated by alcohol withdrawal.

Seizure-associated Takotsubo cardiomyopathy

Takotsubo cardiomyopathy is characterized by chest pain, dyspnea, electrocardiographic changes resembling an acute coronary syndrome, and transient wall-motion abnormalities without identifiable coronary culprit lesion explaining the wall-motion abnormality. Takotsubo cardiomyopathy occurs frequently after emotional or physical stress. Seizures have been reported as triggers of takotsubo cardiomyopathy. It is unknown if seizure-associated takotsubo cardiomyopathy differs from takotsubo cardiomyopathy associated with other triggers. Seizure-associated takotsubo cardiomyopathy cases from the literature were compared with takotsubo cardiomyopathy series comprising 30 or more patients. Thirty-six seizure-associated takotsubo cardiomyopathy cases (6 male, mean-age 61.5 years) were found. Seizure-type were tonic-clonic (n = 13), generalized (n = 5), status epilepticus (n = 6), grand mal (n = 2), or not reported (n = 13). Twelve patients had a history of epilepsy, in 15 patients takotsubo cardiomyopathy-associated seizure was the first or the information was not given (n = 9). In 17 patients takotsubo cardiomyopathy occurred immediately after the seizure, in 9 patients 1-72 h postictally, and in 10 patients, the interval was not reported. In 20 patients neurologic disorders were reported and in 14 psychiatric disorders were reported. There were medical comorbidities in 17 patients, arterial hypertension (n = 11), hyponatremia (n = 2), and cancer (n = 2). Compared with 974 patients reported in takotsubo cardiomyopathy -series, patients with seizure-associated takotsubo cardiomyopathy were younger (61.5 vs. 68.5 years, p < 0.0001), more frequently males (17 vs. 9%, p = 0.004), had less frequent chest pain (6 vs.76%, p < 0.005), more frequent cardiogenic shock (25 vs. 8%, p = 0.003), and more frequent recurrency (14 vs. 3%, p = 0.004). Seizure-associated takotsubo cardiomyopathy manifests frequently as sudden hemodynamic deterioration, which could result in death in the absence of adequate help. Probably some cases of sudden unexpected death in epilepsy are attributable to takotsubo cardiomyopathy.

A Comprehensive Literature Search: Drugs as Possible Triggers of Takotsubo Cardiomyopathy

Takotsubo cardiomyopathy (TCM) is a syndrome of transient cardiac dysfunction precipitated by intense emotional or physical stress. Excessive sympathetic stimulation is believed to be central to the pathogenesis of this condition, thus drugs with sympathetic effect could precipitate TCM. The aim of this study was to conduct a comprehensive literature search to identify drugs that could precipitate TCM. Published case reports of TCM associated with drug-used were identified by a comprehensive literature search using the Medline/PubMed database, from January 1990 to November 2010. Search terms included Takotsubo cardiomyopathy, Tako-tsubo cardiomyopathy, stress cardiomyopathy, transient-left-ventricular ballooning syndrome, ampulla cardiomyopathy, apical ballooning syndrome, OR broken heart syndrome; together with "iatrogenic", "drug-induced", OR "induced by". Only publications in English or Spanish, in Humans, and with links to full text were retrieved. Then, articles that recognized any drug as a possible drug-induced TCM were selected. Additionally, citation lists from identified articles were subsequently reviewed to identify additional relevant articles. Overall, 401 different references were retrieved and 42 selected. Additionally, 5 articles were identified from citation list of selected articles. Thus, 47 articles with one report of more drugs as a possible trigger of 58 cases of SCM were reviewed, in which 20 different drugs were recognized as possible drug-induced TCM. There are some reports that linked the drug-used, mainly associated to sympathetic overstimulation, with the development of TCM. Consequently, drug-induced TCM would be considered in patients with TCM, particularly those in which no clear emotional or stress trigger could be identified.

Near-drowning syndrome: a possible trigger of tako-tsubo cardiomyopathy

We report a case of transient tako-tsubo cardiomyopathy characterized by an unusual trigger in a woman victim of near-drowning syndrome. After 24 h, electrocardiogram changes and a typical echocardiographic pattern of apical ballooning with a mild increase of serum troponin level induced the suspicion of tako-tsubo cardiomyopathy despite the absence of chest pain. Left ventriculography confirmed the apical ballooning, and coronary angiography revealed normal coronary arteries. Electrocardiogram changes and apical contraction abnormalities were reversed within 1 month. In conclusion, we hypothesize that hypoxemia related to near-drowning syndrome could have induced transient myocardial dysfunction mediated by a sympathetic nerve activation.