Cancer therapy-associated Takotsubo cardiomyopathy: A narrative review of mechanisms, drug associations, and clinical implications.

Background

Takotsubo cardiomyopathy (TTC), or stress-induced cardiomyopathy, is a transient left ventricular systolic dysfunction that mimics acute coronary syndrome but occurs without obstructive coronary disease [1] . It accounts for roughly 1–2% of suspected acute coronary syndrome cases and predominantly affects postmenopausal women [2] . While most data on TTC come from the general population, cancer patients appear to have a disproportionately higher risk due to emotional stress, critical illness, and exposure to cardiotoxic cancer therapeutic agents [3] , [4] . Yet despite this growing recognition, evidence describing TTC in oncology patients remains limited and fragmented. This narrative review aims to synthesize the available evidence on the association between cancer therapeutic agents and TTC, summarize clinical features, discuss proposed mechanisms, and highlight management considerations in cancer therapy-induced TTC.

To compile the tables, a literature search was conducted using PubMed, Embase, Google Scholar, and Web of Science to identify English-language articles published between January 2010 and May 2025. Search terms included “Takotsubo Syndrome,” “Stress Cardiomyopathy,” “Apical Ballooning,” and individual drug names. Approximately 30 articles describing a confirmed or strongly suspected TTC diagnosis with a temporal association to a cancer therapeutic agent were included and summarized. Reports with insufficient clinical detail or alternative likely causes were not emphasized. Agent-level associations and proposed mechanisms are summarized in Table 1 , while individual reported case characteristics, including clinical presentation, diagnostic findings, and outcomes, are summarized in Table 2 .

a. Definition, triggers, and epidemiology

The term “takotsubo” originates in Japan and refers to the distinctive ballooning shape of the left ventricle, which resembles an octopus trap [5] . This form of cardiomyopathy features a narrow neck and rounded apex, seen in the majority of cases. Data from the International Takotsubo Registry, which analyzed 1750 patients across the United States and Europe, further emphasizes that the condition, as previously mentioned, predominantly affects women (89.8%) with a mean age of 66.8 years. While emotional triggers accounted for 27.7% of cases, 29% had no identifiable trigger at all, and physical stressors were identified in 36% of patients [1] . Although rare, TTC has also been reported following COVID-19 vaccination, suggesting a temporal link potentially mediated by sympathetic activation and catecholamine surge [6] . Acute emotional stressors have been shown to induce brain activation, increasing the bioavailability of cortisol, epinephrine, and norepinephrine [7] , [8] .

b. Clinical features

Clinically, TTC patients typically present with sudden chest pain, dyspnea, or syncope, closely resembling acute coronary syndrome [1] . TTC accounts for approximately 2% of patients hospitalized with suspected acute coronary syndrome, underscoring its clinical relevance and diagnostic challenge. The higher incidence in postmenopausal women (5.2 per 100,000) compared to men (0.6 per 100,000) highlights potential hormonal influences in its pathogenesis. Although the prognosis is generally favorable with a low mortality rate (1–3%), a subset of patients may experience recurrent episodes or high-risk features associated with poorer outcomes [8] , [9] .

A comprehensive review reported that the most common symptoms of TTC are acute chest pain (in >75% of cases), followed by shortness of breath (∼50%), dizziness (>25%), and syncope (5–10%) [4] . On physical examination, patients may also present with signs of hemodynamic compromise such as respiratory distress, hypotension, narrow pulse pressure, and an S3 gallop. Additional findings may include jugular venous distention, pulmonary crackles, a systolic ejection murmur due to left ventricular outflow tract obstruction (LVOTO) or mitral regurgitation, and, in some cases, lower extremity edema [10] , [11] .

The most common anatomical variant of TTC is apical ballooning, seen in 75–80% of cases, characterized by apical akinesis and basal hyperkinesis. Medina de Chazal et al. describe less common variants, including midventricular (10–20%), basal/inverted (<5%), and rare forms such as biventricular, right ventricular, and focal types. These variants differ in severity and hemodynamic impact, though the reasons for this variability remain unclear [8] , [10] . A multinational analysis from the International Takotsubo Registry ( n = 3957) spanning 2004 to 2021 revealed shifting trends in TTC presentations across Europe and the U.S. First, the proportion of male patients increased from 10% to 15% over the study period, indicating a growing recognition of TTC in men. Second, physical triggers became more prevalent, rising from 39% to 58% ( p < 0.001). Emotional triggers became relatively less common [12] . Lastly, the incidence of midventricular TTC increased from 18% to 28% ( p = 0.018), suggesting an improvement in the detection of non-apical variants. However, apical ballooning remains the most common variant [13] .

Several diagnostic criteria exist for TTC, including those of the Heart Failure Association of the European Society of Cardiology [2] , InterTAK [14] , Diagnostic Criteria and Revised Mayo Clinic Criteria [15] ,—all of which emphasize transient left ventricular dysfunction, absence of obstructive coronary disease, new electrocardiogram (ECG) or biomarker changes, and exclusion of alternate diagnoses such as myocarditis or pheochromocytoma [2] , [14] , [15] .

c. Pathophysiology

While the exact pathophysiology remains unclear, a leading hypothesis suggests that stress-induced catecholamine surges result in myocardial stunning and microvascular dysfunction [16] , [17] . Other proposed mechanisms include coronary microvascular dysfunction, which may reduce myocardial perfusion without obstructive coronary artery disease, and estrogen deficiency, which could explain the higher prevalence of TTC in postmenopausal women [18] .

Medina de Chazal et al. highlight the central autonomic nervous system (CANS) as a key regulator of stress-induced myocardial dysfunction in their systematic review [10] . Their findings, supported by neuroimaging studies, demonstrate increased cerebral blood flow in the hippocampus, brainstem, and basal ganglia during acute TTC episodes, suggesting the role of stress-induced neural activation. This phenomenon is similar to “neurogenic stunned myocardium,” previously observed in patients with acute stroke, seizures, or electroconvulsive therapy. In response to extreme emotional or physical stress, activation of brainstem and hypothalamic centers triggers a surge in sympathetic nervous system output, leading to the spillover of norepinephrine and neuropeptide Y (NPY) from sympathetic nerve terminals into the myocardium. This excessive release can induce direct cardiotoxicity and promote epicardial and microvascular dysfunction, ultimately contributing to the transient ventricular impairment seen in TTC [10] .

Relationship between cancer therapy and TTC

Cancer therapy-induced cardiotoxicity (CIC), including TTC, has been increasingly recognized as a significant concern in cancer patients. The cardiotoxic effects of cancer therapy can manifest acutely or in a delayed fashion, with some patients developing heart failure or arrhythmias months or years after treatment. The relationship between cancer therapy and cardiovascular complications is complex, involving both direct myocardial toxicity and indirect mechanisms such as vascular injury or inflammation, [20] and has garnered increasing attention, particularly concerning cancer therapy-induced TTC. There is emerging evidence linking a range of cancer therapeutic agents implicated in TTC, such as cardiotoxic cancer therapy agents, immune checkpoint inhibitors (ICIs), hormonal therapy, targeted therapy, and radiation therapy. Specific cancer therapeutic agents, such as the anti-metabolite 5-fluorouracil, have been implicated in triggering TTC, possibly due to coronary vasospasm or direct myocardial toxicity [2] , [21] , [22] . Notably, ICIs, including agents targeting the CTLA-4 and PD-1/PD-L1 pathways, have revolutionized cancer treatment but are associated with immune-related adverse events that affect various organ systems, including the cardiovascular system [23] , [24] , [25] . Given the increasing use of ICIs and other agents in oncology, understanding cancer therapy-induced TTC is crucial for early recognition and management [20] , [26] .

Pathophysiology & proposed mechanisms of cancer therapy-associated TTC

Cancer therapy and TTC

Cancer therapy-associated TTC has been described across multiple drug classes, though nearly all available evidence comes from isolated case reports rather than controlled studies. Cytotoxic agents—including 5-fluorouracil (5-FU), anthracyclines, antimetabolites, platinum compounds, and combination regimens such as carboplatin and paclitaxel have been temporally linked to TTC in the literature [23] , [24] , [25] , [26] , [27] , [28] , [29] , [30] , [31] , [32] , [33] , [34] , [35] , [36] , [37] , [38] , [39] . Proposed mechanisms reflect established TTC physiology and include coronary vasospasm, microvascular dysfunction, autonomic dysregulation, oxidative stress, and myocardial stunning. Among these agents, 5-FU has the most frequently reported association, with TTC episodes hypothesized to arise from vasospasm, microvascular injury, and energy depletion within cardiomyocytes [21] , [38] , [39] , [40] , [41] , [42] , [43] , [44] , [45] , [46] , [47] .

Anthracyclines such as doxorubicin may predispose patients to TTC by generating reactive oxygen species, causing mitochondrial injury and myofibrillar disruption, while platinum agents like oxaliplatin may influence TTC risk through autonomic imbalance, peripheral neurotoxicity that affects cardiac regulation, or ion-channel alterations [28] , [29] , [30] , [31] , [32] . Because TTC can also be triggered by cancer-related physiological stressors—including systemic inflammation, anemia, pain, metabolic derangements, or psychological distress—causality cannot be assigned to any individual drug.

Other targeted cancer therapeutics and TTC

Targeted therapies, which are cancer drugs that block specific molecular pathways involved in tumor growth, and immunotherapies have also been linked to TTC through small, published reports. VEGF pathway inhibitors (bevacizumab, axitinib, sunitinib) and EGFR inhibitors (afatinib, osimertinib) may promote TTC via microvascular injury, endothelial dysfunction, or autonomic imbalance, mechanisms that align closely with TTC's established pathophysiologic triggers [22] , [48] , [49] , [50] , [51] , [52] , [53] , [54] , [55] , [56] .

Endocrine therapies such as tamoxifen, a selective estrogen receptor modulator, have also been linked to rare TTC cases, with reports suggesting that estrogen suppression may heighten catecholamine sensitivity and microvascular vulnerability in predisposed post-menopausal women [57] . TTC has also been described with HER2-directed therapies such as trastuzumab and pertuzumab, with proposed pathways involving impaired myocardial resilience to catecholamine surges when HER2-related signaling is disrupted [51] , [52] , [53] , [54] .

Immune checkpoint inhibitors (ipilimumab, nivolumab) may rarely precipitate TTC through T-cell–driven cytokine-mediated inflammation, creating a state of heightened physiologic stress that is conducive to TTC [56] , [58] , [59] . Given the absence of prospective studies and the reliance on anecdotal case reports, these associations should be interpreted cautiously. Table 1 summarizes cancer therapeutic agents reported to be associated with TTC, along with hypothesized TTC-specific mechanisms described in the literature.

Multifactorial etiology and diagnostic challenges in TTC in patients with cancer

While certain anti-neoplastic drugs have known associated cardiotoxicity, no study to date has clearly linked TTC to any particular drug [60] . A history of cancer itself carries a higher risk of TTC [9] , [61] . The increased incidence of TTC in cancer patients and multifactorial etiology suggest that multiple factors make the cancer patient uniquely vulnerable to this phenomenon. Before attributing TTC to the anti-neoplastic regimen, the clinician must consider other potential triggers.

Diagnosis

Precise diagnosis of TTC can be challenging. The clinical presentation overlaps substantially with acute coronary syndrome as well as other cardiomyopathies, and up to one-third of cases lack an identifiable trigger [8] . A patient's cancer history broadens the differential diagnosis, given the various cardiotoxicities associated with anti-neoplastic agents. Cancer-related physiological stress, such as systemic inflammation, elevated catecholamines, metabolic derangements, anemia, pain, and psychological distress, has been recognized as a trigger in large TTC registries, including the International Takotsubo Registry. These factors, combined with comorbid conditions common in oncology patients (infection, renal dysfunction, electrolyte abnormalities), may lower the threshold for TTC even in the absence of cardiotoxic therapies [1] , [2] , [5] . Cancer history should simultaneously raise the index of suspicion for TTC, given predisposing factors unique to cancer patients. Beyond diagnostic challenges, the appropriate management of anti-neoplastic therapy in patients who develop TTC is uncertain, with no specific guidelines to date.

Whenever TTC is suspected, it is imperative to rule out acute coronary syndrome given the time-sensitive nature of revascularization. Both syndromes commonly present with chest pain and/or dyspnea. An initial ECG may show ST elevations. In contrast to ST-elevation myocardial infarction (STEMI), the ECG in TTC often lacks reciprocal ST depressions, although it may exhibit diffuse T-wave inversions. The echocardiogram in TTC classically shows basal to mid-ventricular hyperkinesis with apical ballooning [8] . While focal phenotypes have been described, wall motion abnormalities in TTC generally span beyond a single coronary perfusion territory [8] . Other clues that point toward TTC rather than acute coronary syndrome include right ventricular involvement, higher B-type natriuretic peptide elevation, and mild troponin elevation, which is disproportionate to the degree of left ventricular dysfunction [62] . However, these markers can also be abnormal/elevated among patients experiencing cancer therapy-associated cardiac dysfunction [60] . While coronary disease and TTC are not mutually exclusive, elucidation of coronary disease on angiogram that does not explain the acute onset of cardiomyopathy strengthens the diagnosis of TTC [8] .

Triggers

Medical stress in various forms can precede TTC. Sepsis is a well-documented trigger. Lozahic et al. propose a two-hit model in cancer patients, in which the immunocompromised state, combined with a systemic inflammatory response (e.g., from COVID-19), leads to cardiac complications. They attributed these complications to the virus's ACE2 downregulation, IL-6, other cytokines, endothelial dysfunction, and thromboembolic phenomena [63] .

Anemia-induced myocardial hypoxia may be another factor that increases vulnerability in the cancer patient. Numerous cytotoxic agents cause anemia due to bone marrow suppression and worsening renal function [64] . Baik et al. propose that anemia in the setting of high-cardiac-output states, such as sepsis, tumor lysis syndrome, or cytokine release syndrome, can exacerbate hypoxia in cancer patients [64] .

Systemic cancer therapy or radiotherapy to the thoracic region may cause coronary endothelial dysfunction [7] . Other medical stressors to consider in the cancer patient are anesthesia, surgery, cancer pain, or even the stress of the cancer diagnosis. In the general population, patients with TTC have more cardiovascular risk factors at baseline [1] . Thus, it is plausible that cardiac co-morbidities mediate the risk of TTC or other cardiotoxicities in the cancer patient.

Management & prognosis

Overall consideration for the management of TTC in the cancer patient

The management of cancer therapy-associated TTC is guided almost entirely by case reports and small observational studies [1] , [62] . Treatment principles, therefore, mirror those used in the general TTC population, with modifications based on oncologic status, treatment-related toxicities, and comorbidities.

The cancer patient is overall quite vulnerable to developing TTC given various medical and psychosocial stressors that create a high catecholamine state, treatment-mediated mechanisms, and baseline cardiac co-morbidities. When TTC follows anti-neoplastic treatment, the patient and clinician are left with a management dilemma due to the inability to pinpoint the trigger with certainty. In a small retrospective cohort study of cancer patients at MD Anderson Cancer Center who developed TTC, a majority of patients were able to safely resume anti-neoplastic therapy after recovery of the left ventricular ejection fraction without relapse of TTC. In contrast, the literature on 5-FU generally does not encourage reinstatement of 5-FU therapy after restoration of cardiac function, given high rates of further cardiac complications in patients already affected by cardiotoxicity [60] . Since there are no large-scale studies or guidelines to support decision-making in this scenario, the decision whether to adjust anti-neoplastic therapy after TTC may be made on a case-by-case basis, conveying the honest uncertainty of the exact etiology to the patient and using shared decision-making.

Acute settings

Acute management typically includes supportive care and guideline-directed heart failure therapy when hemodynamically tolerated. Beta-blockers and ACE inhibitors are often used to reduce sympathetic drive and afterload, though evidence for benefit in cancer therapy-induced TTC is limited to case reports and registry data [65] , [66] , [67] , [68] . Careful dosing is required because cancer patients frequently have hypotension, renal dysfunction, and treatment-related cytopenias [1] .

In severe presentations, including cardiogenic shock, management must be individualized. Up to 10% of TTC cases may develop shock, and LVOT obstruction must be recognized early because inotropes can worsen obstruction [1] , [69] . Case reports support a cautious approach to beta-blockers in LVOTO and the use of temporary mechanical circulatory support when needed [70] , [71] .

Thromboembolic risk

Thromboembolic risk is higher in TTC patients with malignancy due to both apical ballooning and cancer-associated hypercoagulability. This includes the documented incidence of left ventricular thrombus in TTC (1.3% in the International Takotsubo Registry and up to 2.5% in GEIST) [1] , [70] , [72] . Anticoagulation is considered when a left ventricular thrombus is present or strongly suspected [73] , but bleeding risk is significant in patients receiving myelosuppressive cancer therapy; therefore, therapy must be individualized [34] , [74] , [75] .

Long-term considerations

Long-term considerations emphasize close follow-up during the first 4–12 weeks, when LV function typically normalizes [76] , [77] . Cancer treatment may be cautiously resumed once cardiac function stabilizes, and recurrence of TTC due to cancer therapy appears uncommon [25] . An interdisciplinary cardio-oncology evaluation is recommended for risk stratification and decisions around treatment re-initiation [5] , [78] , [79] , [80] .

Overall, management of TTC in cancer patients remains poorly defined, with limited data guiding treatment decisions [81] . Most recommendations are extrapolated from non-cancer TTC populations, highlighting the need for prospective studies in this high-risk group.

Future directions & research gaps/limitations

Despite growing awareness of cancer therapy-induced TTC, important gaps remain. Most current data are limited to case reports and retrospective series, showing the need for prospective studies to clarify incidence, risk factors, and outcomes specifically in the cancer population [1] . The role of biomarkers, such as B-type natriuretic peptide, troponins, and inflammatory markers, in the early detection or prediction of TTC warrants further exploration. Similarly, preventive strategies, including the potential use of beta-blockers, statins, or antioxidants, have not been rigorously tested in this population. Genetic susceptibility also remains poorly understood; identifying patient-specific risk factors could help refine screening and prevention efforts. Finally, the absence of standardized diagnostic and management guidelines contributes to variability in clinical practice, underscoring the need for consensus-driven, evidence-based protocols.

Conclusion

TTC represents a unique intersection of cardiology and oncology, where physiological vulnerability, pharmacologic insult, and psychological stress converge. While traditionally associated with emotional or physical stress, emerging evidence now implicates a wide range of cancer therapies, including cytotoxic agents, endocrine therapies, targeted treatments, and immune checkpoint inhibitors, as potential triggers. These agents may induce TTC through distinct yet overlapping mechanisms such as sympathetic overactivation, coronary vasospasm, endothelial dysfunction, and direct myocardial toxicity. Cancer patients are particularly at risk due to their baseline cardiovascular burden, cumulative treatment-related insults, and the systemic stressors imposed by their disease.

The diagnosis of cancer therapy-associated TTC remains challenging, as TTC often mimics acute coronary syndromes and lacks pathognomonic features. Standardized diagnostic criteria help guide evaluation; however, clinical judgment remains essential, especially in oncology settings where confounding cardiac pathologies are common. Management strategies should be individualized, focusing on hemodynamic support, prevention of thromboembolic complications, and careful consideration of whether to continue or modify cancer therapy.

Despite the growing recognition of cancer therapy-associated TTC, high-quality data to guide prevention, long-term monitoring, and treatment decision-making are limited. A multidisciplinary approach, involving both cardiology and oncology teams, is essential to balance oncologic efficacy with cardiovascular safety. Continued research is needed to better elucidate and understand this phenomenon among patients with cancer, and to develop evidence-based guidelines for risk stratification, recurrence prevention, and the safe reinitiation of therapy in affected patients.

CRediT authorship contribution statement

Michael Simeon: Conceptualization, Writing – original draft, Writing – review & editing. Elizabeth Evans: Writing – original draft. Sally Arif: Writing – original draft. Thomas Granado: Writing – original draft. Tochukwu M. Okwuosa: Writing – original draft, Writing – review & editing. Annabelle Santos Volgman: Writing – review & editing. Salaheldin Abusin: Writing – review & editing.

Ethical statement

This manuscript is a narrative review of previously published literature and did not involve human participants or animal subjects. Ethical approval was therefore not required.

Declaration of Generative AI and AI-assisted technologies in the writing process

ChatGPT-5 (OpenAI, San Francisco, CA, USA) was used to assist with language editing and table formatting. All AI-generated suggestions were reviewed and verified by the authors, who take full responsibility for the content.

Declaration of competing interest

None.

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