Diagnosis Of Apical Ballooning Syndrome Research Articles

Apical ballooning (takotsubo) syndrome with concurrent ST-segment elevation myocardial infarction

We present the case of a 61-year-old woman admitted with chest pain and an ECG demonstrating ST-segment elevation in the lateral leads. Emergency coronary angiography demonstrated an occluded obtuse marginal...

A Case of Persistent Apical Ballooning in a Patient with SLE

Apical ballooning syndrome (ABS), also referred to as stress cardiomyopathy, is characterized by acute left ventricular dysfunction following a stressful situation. Diagnosis of ABS is made in the following scenarios: transient hypokinesia or dyskinesia of the left ventricular segment, absence of obstructive coronary disease, new electrocardiogram abnormalities, absence of recent significant head trauma, pheochromocytoma, myocarditis, and hypertrophic cardiomyopathy. Prognosis is usually favorable since the wall motion abnormality returns to normal within days, and certainly within the first month. We encountered a case of SLE with apical ballooning on echocardiography in a 44-year-old woman. She was suffering from severe left ventricular dysfunction that has persisted on 5 year follow-up echocardiography. We report this case along with a review of the relevant literature.

Transient left ventricular and stomach apical ballooning syndromes: when the trigger is also a clinical emergency

A 59-year-old woman was referred to our emergency department because of epigastric pain and incoercible vomit. Electrocardiogram showed ST-segment elevation in anterior-lateral leads, but coronary angiogram revealed normal coronary tree and left ventricular angiography showed apical and midventricular akinesis with preserved basal systolic function: a diagnosis of apical ballooning syndrome was made. During the following days, the patient complained about persistent abdominal pain, and a nasogastric tube drained more than 1000 cc of dark fecaloid material. Urgent abdominal computed tomography scan showed a mural thrombus in the apex of the left ventricle and a huge diaphragmatic hernia through which more than one-half of the stomach was herniated and presented a sort of “apical stomach ballooning.” Gastropexy was done; surgical diagnosis was a type IV giant diaphragmatic hernia complicated by recent gastric volvulus caused by rotation along the longitudinal cardiopyloric axis. Type IV giant diaphragmatic hernia is relatively rare, representing only about 5% to 7% of all hernias. Gastric volvulus is a severe complication, with acute mortality reported to be as high as 30% to 50%. In our case, a severe life-threatening condition as gastric volvulus triggered an apical ballooning syndrome, a transient cardiomyopathy, usually induced by emotional stressors with a long-term good prognosis. Apical ballooning syndrome must be considered an epiphenomenon of other organic diseases that may have an important role in the prognosis of the patient not only in acute but also in chronic setting. Only early determination of the true cause of apical ballooning syndrome ensures a proper treatment.

Apical Ballooning Syndrome Associated With Isolated Severe Hyponatremia: Case Report and Suggested Pathophysiology

An 82-year-old woman who presented to her primary care physician for preoperative evaluation was incidentally found to have severe hyponatremia (sodium = 118 mmol/L). The patient was then admitted for workup and treatment of hyponatremia. On day 2 of the admission, the patient was found to have new T-wave inversions on a telemetry monitor. Further workup, including an electrocardiogram, cardiac markers, echocardiogram, and a cardiac catheterization were consistent with the diagnosis of apical ballooning syndrome (ABS). Mechanisms of how severe hyponatremia may lead to ABS are discussed as well as a possible approach to the management of severe hyponatremia in postmenopausal women.

Apical ballooning syndrome following perioperative anaphylaxis is likely related to high doses of epinephrine

Apical ballooning syndrome, a reversible left ventricle dysfunction, has been reported following anaphylaxis and, during this clinical circumstance, is seemingly linked to the use of either low or high doses of epinephrine. We report a severe succinylcholine-induced IgE-mediated anaphylaxis in a 65-year-old woman, in whom the diagnosis of apical ballooning syndrome following anaphylaxis was established. As a thorough description of the clinical features and resuscitative measures could be obtained, we discuss the reasons for apical ballooning syndrome occurrence and highlight the fact that optimal care management of anaphylaxis should include a progressive titration of epinephrine.

A Case of Takotsubo Cardiomyopathy - Apical Ballooning Syndrome Mimicking Myocardial Infarction after Colonoscopy

Purpose: Takotsubo cardiomyopathy is a well known cardiac phenomenon also known as a transient apical ballooning syndrome (ABS) which mimics acute coronary syndrome (ACS) in 1 to 2% cases leading to angiography. These events result in EKG changes, moderate elevations of cardiac enzymes, and left ventricular (LV) wall motion abnormalities. Preceding emotional and physical stressors often trigger ABS in up to two-thirds cases. One theory describes a toxic stunning of myocardium by a catecholamine surge during stress. Nearly 90% cases occur in postmenopausal women for unclear reasons. Here we make a first time case report of ABS after an elective surveillance colonoscopy. Case: A 56 y/o female with Crohn's disease in remission with no cardiac history, underwent her 5th surveillance colonoscopy under anesthesia with propofol as usual for prior difficulty tolerating sedation. The colonoscopy was uneventful and biopsies were taken to rule out dysplasia. In the recovery room, she complained of chest pressure, shortness of breath, and lightheadedness. She remained stable and was initiated on routine ACS treatment protocol. EKG showed nonspecific changes. Troponin was elevated to 0.70. Echocardiogram showed a hypokinetic septum consistent with LAD distribution wall motion abnormalities, and a mildly reduced LVEF 45%. Cardiac catheterization finds angiographically normal coronary arteries despite hypokinetic anterolateral and inferior wall motion. She was diagnosed with Takotsubo variant cardiomyopathy-ABS. After observation overnight, she was discharged home to follow up with her PCP. She denied any recent viral illness and did not report any recent psychosocial stressors. Discussion: Diagnosis of ABS is often made after the exclusion of ACS and myocarditis. These transient phenomenon are usually triggered by common emotional and physical stressors, including: a recent death in the family, personal conflict, a new diagnosis of illness, or after having non-cardiac surgery and procedures. One review reports the exacerbation of IBD as inducing a case of ABS. In our case, recovery from anesthesia was likely the stressor. There are no reliable predictable factors for the initial occurrence of ABS and these events are not preventable. Recurrence can occur in 3 to 11% cases reported. In patients with chronic disease who will need routine scheduled procedures, e.g., surveillance colonoscopies, it raises the question of whether they will have recurrent ABS. Overall prognosis is good with relatively quick recovery, similar to an age and gender matched population. Future studies should investigate and address the recurrence rate of ABS after repeat scheduled procedures.

Apical Ballooning Syndrome

HomeCirculationVol. 115, No. 5Apical Ballooning Syndrome Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplementary MaterialsFree AccessReview ArticlePDF/EPUBApical Ballooning SyndromeAn Important Differential Diagnosis of Acute Myocardial Infarction Abhiram Prasad, MD, FRCP, FESC Abhiram PrasadAbhiram Prasad From the Division of Cardiovascular Diseases and Department of Internal Medicine, and Mayo Clinic and Mayo Foundation, Rochester, Minn. Search for more papers by this author Originally published6 Feb 2007https://doi.org/10.1161/CIRCULATIONAHA.106.669341Circulation. 2007;115:e56–e59Case presentation: A 60-year-old woman presented to the emergency department 2 hours after the onset of severe retrosternal chest pain that started soon after she was told that her son had died in a car accident. A 12-lead ECG demonstrated ST-elevation in the precordial leads (Figure 1), and the plasma troponin T level was elevated at 0.07 ng/mL. A diagnosis of acute ST-elevation myocardial infarction was made, and the patient was admitted for emergency coronary angiography, which revealed normal coronary arteries. The left ventriculogram showed severe systolic dysfunction involving the mid and apical segments (Data Supplement Movie I). Download figureDownload PowerPointFigure 1. Twelve-lead ECG demonstrating ST-segment elevation in precordial leads.Recognition of Clinical SyndromePhysicians have long been aware of the possible association between stress and cardiovascular events. Awareness has increased of a distinct cardiac syndrome that was originally described in the Japanese population and was called Takotsubo cardiomyopathy, named after the octopus-trapping pot with a round bottom and narrow neck that resembles the left ventriculogram during systole in these patients.1,2 Other names used to describe the condition include apical ballooning syndrome (ABS), broken heart syndrome, and stress or ampulla cardiomyopathy. The precise incidence of ABS is unknown, but it may account for 1% to 2% of patients who present with an acute myocardial infarction.3Clinical FeaturesThe majority of patients have a clinical presentation that is indistinguishable from an acute coronary syndrome. Most present with chest pain at rest, although some patients have dyspnea alone as their initial presenting symptom. Rarely, patients present with syncope or an out-of-hospital cardiac arrest.4 ABS appears to occur almost exclusively in postmenopausal women; however, a few cases have been reported in younger women and males.4 The patients are usually hemodynamically stable, but clinical findings of mild-to-moderate congestive heart failure commonly coexist. In a minority of patients, hypotension may occur from reduced stroke volume and occasionally from dynamic left ventricular outflow tract obstruction. Cardiogenic shock may be a rare complication. A unique feature of ABS is the occurrence of a preceding emotionally or physically stressful event in approximately two thirds of patients. Importantly, such a trigger is not observed in all individuals, and its absence does not exclude the diagnosis.DiagnosisThe most frequent finding on the admission ECG is mild ST-segment elevation, which occurs in approximately 50% to 60% of patients. It is typically present in the precordial leads, but the ECG can be normal or can show nonspecific T-wave abnormality or major ST elevation across the precordial and limb leads. In general, the 12-lead ECG alone is not helpful in differentiating ABS from an ST-elevation myocardial infarction.5 Characteristic evolutionary changes that occur over 2 to 3 days include resolution of the ST-segment elevation and subsequent development of diffuse and often deep T-wave inversion that involves most leads (Figure 2). New pathological Q waves may be seen occasionally, and there is frequent prolongation of the corrected QT interval. Most, if not all, patients have a small early increase in cardiac biomarkers, especially when cardiac troponins are measured. Transthoracic echocardiography can detect the regional wall-motion abnormality, but the diagnosis is frequently made in the cardiac catheterization laboratory because the patients are initially suspected of suffering from an acute coronary syndrome and are referred for urgent or emergency coronary angiography. Patients with ABS typically do not have obstructive coronary artery disease. The left ventriculogram shows characteristic regional wall-motion abnormalities involving the mid and usually the apical segments. There is sparing of the basal systolic function, and the wall-motion abnormality extends beyond the distribution of any 1 single coronary artery (Data Supplement Movie I). Apical sparing variants have also been described (Data Supplement Movie II).6 Cardiac magnetic resonance imaging may be helpful in excluding myocardial infarction, because delayed gadolinium hyperenhancement is not a feature of ABS.7Download figureDownload PowerPointFigure 2. Twelve-lead ECG demonstrating resolution of ST-segment elevation and development of diffuse T-wave inversion.On the basis of our experience, we have previously proposed criteria for making a clinical diagnosis of ABS, and all 4 criteria must be present. The Table illustrates a modified version of the criteria that incorporates contemporary knowledge about the syndrome.4 The diagnosis of ABS is most likely to be made at institutions where primary percutaneous coronary intervention and an early invasive strategy are practiced for the management of acute coronary syndromes. The absence of obstructive coronary artery disease and the characteristic regional wall-motion abnormality are likely to lead to the diagnosis. Diagnosis of ABS in patients who present at hospitals without cardiac catheterization laboratories requires a high index of suspicion. The diagnosis should be considered in a postmenopausal woman who presents with cardiac symptoms that are temporally related to an emotional or physical stressor, with positive cardiac biomarkers or an abnormal ECG. Establishing the diagnosis is particularly important if fibrinolytic therapy is being considered for a presumed diagnosis of ST-elevation myocardial infarction. Inappropriate administration of fibrinolytics to a patient with ABS may lead to harm, and it would be appropriate to transfer a patient suspected of having ABS for emergency coronary angiography. Proposed Mayo Clinic Criteria for the Clinical Diagnosis of ABS*There are rare exceptions to these criteria, such as those patients in whom the regional wall-motion abnormality is limited to a single coronary territory.†It is possible that a patient with obstructive coronary atherosclerosis may also develop ABS. However, this is very rare in our experience and in the published literature, perhaps because such cases are misdiagnosed as an acute coronary syndrome.In both of the above circumstances, the diagnosis of ABS should be made with caution, and a clear stressful precipitating trigger must be sought.1. Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid segments with or without apical involvement. The regional wall-motion abnormalities extend beyond a single epicardial vascular distribution.*2. Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.†3. New ECG abnormalities (either ST-segment elevation and/or T-wave inversion) or elevated cardiac troponin.4. Absence of: recent significant head trauma intracranial bleeding pheochromocytoma myocarditis hypertrophic cardiomyopathyManagementThe optimal management of ABS has not been established, but supportive therapy invariably leads to spontaneous recovery. Because the presentation in these patients is indistinguishable from an acute coronary syndrome, initial management should be directed toward the treatment of myocardial ischemia, with continuous ECG monitoring and administration of aspirin, intravenous heparin, and β-blockers. Once the diagnosis of ABS has been made, aspirin can be discontinued unless there is coexisting coronary atherosclerosis. β-Blocker therapy may be continued, if tolerated, especially because an excess of catecholamines may play a role in precipitating the conditions. Diuretics are effective for the treatment of congestive heart failure. The right ventricle is also involved in approximately one third of cases, and these patients are sicker and more likely to develop congestive heart failure (Data Supplement Movie III).8 On rare occasions, when there is significant hypotension, it is important to exclude dynamic left ventricular outflow tract obstruction with echocardiography. If present, a cautious trial of β-blockers may help by reducing the hypercontractility of the base of the left ventricle. Alternatively, an infusion of phenylephrine may be effective by increasing the afterload and left ventricular cavity size. Inotropes would be contraindicated in this situation. In contrast, cardiogenic shock owing to pump failure is treated with standard therapies that include inotropes and intra-aortic balloon counterpulsation. Anticoagulation should be considered in cases of severe left ventricular systolic dysfunction to prevent thromboembolism until there has been recovery.PrognosisPatients with ABS generally have a good prognosis in the absence of significant underlying comorbid conditions. The systolic dysfunction and the regional wall-motion abnormalities are transient and resolve completely within a matter of days to a few weeks. This is such a uniform finding that an alternative diagnosis should be considered in patients in whom the cardiomyopathy does not resolve. Typically, assessment of the ejection fraction should be performed at approximately 4 to 6 weeks after discharge from the hospital to document recovery of function. At this time, the ECG usually shows complete resolution, although T-wave inversion may persist for a longer period of time. In-hospital mortality from ABS is very low and unlikely to be greater than 1% to 2%. The recurrence rate of ABS is no more than 10%.9 In our practice, in the absence of contraindications, we recommend chronic β-blocker therapy, with the aim of reducing the likelihood of a recurrent episode. Annual clinical follow-up is advisable because the natural history of ABS remains unknown.PathophysiologyThe pathophysiology of ABS is poorly understood. Several mechanisms for the reversible cardiomyopathy have been proposed, including multivessel epicardial spasm, coronary microvascular spasm, catecholamine-induced myocardial stunning, and myocarditis. Multivessel epicardial coronary artery spasm has not been observed in any of the patients at our institution, but it is possible that the routine administration of nitrates for ischemic chest pain may obscure its presence. Microvascular dysfunction is present in at least two thirds of patients at the time of presentation, and its severity correlates with the magnitude of troponin elevation and ECG abnormalities.10 It remains to be established whether impairment in microvascular function is the primary mechanism for the injury or is an epiphenomenon. Catecholamines may play a role in triggering the syndrome.11Case ConclusionThe left ventricular end-diastolic pressure was 30 mm Hg, and the patient was markedly hypotensive. An intra-aortic balloon was inserted. Her symptoms and hypotension resolved over 48 hours. She was discharged on the fourth day with a prescription for an ACE inhibitor and β-blocker. An echocardiogram 4 weeks later revealed normal left ventricular function. The ACE inhibitor was discontinued, and she remains well 1 year after her admission.The online-only Data Supplement, consisting of movies, is available with this article at http://circ.ahajournals.org/cgi/content/full/115/5/e56/DC1.DisclosuresNone.FootnotesReprint requests to Abhiram Prasad, MD, Cardiac Catheterization Laboratory, Mayo Clinic, 200 First St SW, Rochester, MN 55905. E-mail [email protected] References 1 Sato H, Tateishi H, Uchida T, Dote K, Ishihara M, Sasaki K. Tako-tsubo-like left ventricular dysfunction due to multivessel coronary spasm. In: Kodama K, Haze K, Hori M, eds. Clinical Aspect of Myocardial Injury: From Ischemia to Heart Failure [in Japanese]. Tokyo, Japan: Kagakuhyoronsha Publishing Co; 1990: 56–64.Google Scholar2 Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N, Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze K, Ogawa H, Honda T, Hase M, Kai R, Morii I. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction: Angina Pectoris-Myocardial Infarction Investigations in Japan. J Am Coll Cardiol. 2001; 38: 11–18.CrossrefMedlineGoogle Scholar3 Bybee KA, Prasad A, Barsness G, Wright RS, Rihal CS. Clinical characteristics, outcomes, and impaired myocardial microcirculation in patients with transient left ventricular apical ballooning syndrome: a case-series from a U.S. medial center. Am J Cardiol. 2004; 94: 343–346.CrossrefMedlineGoogle Scholar4 Bybee KA, Kara T, Prasad A Lerman A, Barsness GW, Wright RS, Rihal CS. Transient left ventricular apical ballooning syndrome: a mimic of ST-segment elevation myocardial infarction. Ann Intern Med. 2004; 141: 858–865.CrossrefMedlineGoogle Scholar5 Bybee K, Motiei A, Syed I, Kara T, Prasad A, Lennon RJ, Murphy JG, Hammill SC, Rihal CS, Wright RS. Electrocardiography cannot reliably differentiate transient left ventricular apical ballooning syndrome from anterior ST-segment elevation myocardial infarction. J Electrocardiol. 2007; 40: 38.e1–e6.Google Scholar6 Hurst RT, Askew JW, Reuss CS, Lee RW, Sweeney JP, Fortuin FD, Oh JK, Tajik AJ. Transient midventricular ballooning syndrome: a new variant. J Am Coll Cardiol. 2006; 48: 579–583.CrossrefMedlineGoogle Scholar7 Sharkey SW, Lesser JR, Zenovich AG, Maron MS, Lindberg J, Longe TF, Maron BJ. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation. 2005; 111: 472–479.LinkGoogle Scholar8 Elesber A, Prasad A, Bybee KA, Valeti U, Motiei A, Lerman A, Chandrasekaran K, Rihal CS. Transient cardiac apical ballooning syndrome: prevalence and clinical implications of right ventricular involvement. J Am Coll Cardiol. 2006; 47: 1082–1083.CrossrefMedlineGoogle Scholar9 Elesber AA, Prasad A, Wright S, Lerman A, Rihal C. Recurrence rate and long term prognosis of the apical ballooning syndrome. Circulation. 2006; 114 (suppl II): II-625. Abstract.Google Scholar10 Elesber A, Lerman A, Bybee KA, Murphy JG, Barsness G, Singh M, Rihal CS, Prasad A. Myocardial perfusion in apical ballooning syndrome: correlate of myocardial injury. Am Heart J. 2006; 152: 469.e9–e13.CrossrefGoogle Scholar11 Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G, Wu KC, Rade JJ, Bivalacqua TJ, Champion HC. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med. 2005; 352: 539–548.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Xu Y, Liu M, Li J and Rong J (2022) Takotsubo cardiomyopathy as an overlooked cause of cardiac arrest in a patient undergoing ureteral stenting: a case report and literature review, Journal of International Medical Research, 10.1177/03000605221099255, 50:5, (030006052210992), Online publication date: 1-May-2022. 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Myocardial perfusion in apical ballooning syndrome: Correlate of myocardial injury

The pathophysiology of the apical ballooning syndrome (ABS) is poorly understood. This study evaluated myocardial perfusion abnormalities at the time of presentation in patients with ABS and examined whether abnormal microvascular blood flow predicts the extent of myocardial injury. We evaluated 42 consecutive patients, all women, with a diagnosis of ABS and technically adequate angiograms for the assessment of the TIMI myocardial perfusion grade (TMPG), an index of myocardial perfusion. Abnormal myocardial perfusion was present in 29 (69%) patients. There were no differences in age, frequency of conventional coronary atherosclerosis risk factors, left ventricular ejection fraction at either presentation or follow-up, congestive heart failure at presentation, or length of hospital stay between patients with normal versus those with abnormal TMPG. Patients with abnormal TMPG had higher peak troponin level compared with patients with normal TMPG (0.84 +/- 0.68 vs 0.42 +/- 0.33 ng/mL, P = .047). Similarly, ST elevation or deep T-wave inversion on the electrocardiogram was more common in patients with abnormal perfusion (86% vs 46%, P = .006). Impaired myocardial perfusion due to abnormal microvascular blood flow is frequently present in patients with ABS and correlates with the extent of myocardial injury. Microvascular dysfunction likely play a pivotal role in the pathogenesis of myocardial stunning in ABS.

Early Diagnosis of Stress-Induced Apical Ballooning Syndrome Based on Classic Echocardiographic Findings and Correlation with Cardiac Catheterization

Stress-induced apical ballooning has been described as a reversible condition involving the apical left ventricular wall, sparing the base, and causing a ballooning appearance of the left ventricle during systole despite normal coronaries. We are presenting 4 cases of apical ballooning seen at our institution with echocardiographic correlation. Echocardiography showed similar anatomical apical ballooning of the left ventricular apex. The diagnosis of apical ballooning syndrome was suspected based on echocardiography in conjunction with clinical data before cardiac catheterization was performed. In one case, in addition to classic left ventricular apical ballooning, marked right ventricular apical akinesia was present on the initial echocardiographic examination. This makes diagnosis of apical ballooning syndrome most likely in this patient before cardiac catheterization. Therefore, we suggest using echocardiography more often for the early diagnosis of this disease, based on careful anatomic evaluation in conjunction with clinical data. Wall motion analysis should reveal an apical ballooning appearance involving many coronary territories. Furthermore, the additional presence of right ventricular apical akinesia during echocardiographic examination makes the diagnosis of this syndrome more likely.