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Takotsubo (stress) cardiomyopathy (TTC) is an uncommon acute heart failure syndrome characterized by transient hypocontractility that usually affects a circumferential segment of the myocardium along the heart’s apicobasal axis and spans multiple coronary artery territories. Classically, TTC occurs after an intense physical or emotional insult and is thought to be caused by catecholamine toxicity. The most frequent anatomic variant presents with apical hypokinesis and basal hyperkinesis, but the hypocontractility may also localize to the mid-ventricle or base, also known as “reverse TTC.” Here, we describe a middle-aged woman who developed profound acute hypoxemic respiratory failure and mixed cardiogenic-distributive shock after an adverse reaction to alteplase treated with high-dose epinephrine. The patient was found to have a severely depressed left ventricular ejection fraction (10–15%) with apex-sparing hypokinesis and no evidence of obstructive coronary artery disease, consistent with reverse TTC. The patient’s ejection fraction recovered to the normal range within days with supportive measures. This case highlights the distinctive echocardiographic features of this rare, potentially life-threatening form of TTC.
Alteplase can be associated with severe drug reactions that induce hypotension.
High doses of intravenous epinephrine administered to treat intraoperative hypotension may cause takotsubo cardiomyopathy (TTC), particularly the non-apical variants thereof.
Non-apical TTC generally affects younger patients and is thought to be milder than the more common apical TTC, but it may cause a severely reduced left ventricular ejection fraction.
The β2-adrenoreceptor gradient along the left ventricle does not fully account for the localization of hypocontractility in TTC.
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Introduction
Initially described in Japan in the early 1990s [1], takotsubo (stress) cardiomyopathy (TTC) has quickly gained recognition as an important cause of reversible acute heart failure. TTC presents with regional wall motion abnormalities that affect multiple coronary artery territories [2]. In its typical anatomic form (82% of cases), TTC produces circumferential apical hypokinesis and basal hyperkinesis, leading to the apical end-systolic ballooning that causes the left ventricle to resemble a traditional Japanese octopus trap, or takotsubo [3]. TTC typically occurs in post-menopausal women after an intense physical or emotional trigger and may present with chest pain and shortness of breath, mimicking an acute myocardial infarction [2]. In fact, it has been estimated that 5–6% of women presenting with a suspected acute coronary syndrome instead have TTC [4]. The temporary wall motion abnormalities are believed to be related to catecholamine-induced myocardial stunning [5].
TTC may also occur with hypokinesis and ballooning affecting the mid-ventricle (15% of cases); the base (2%), in what is known as “reverse TTC”; or a focal region of the myocardium (2%) [3, 6]. These non-apical anatomic patterns have been suggested to portend a more favorable prognosis. For instance, a prospective cohort study in Germany found that patients with non-apical TTC were younger, had a higher left ventricular ejection fraction (LVEF), and had 10.8-fold lower 6-month mortality than those with apical TTC [7]. A retrospective analysis of data from the International Takotsubo Registry similarly demonstrated that patients with non-apical TTC were younger and had less severe reductions in their LVEF [8]. However, after controlling for confounders, the mortality difference between apical and non-apical TTC was no longer present [8]. Here, we report a particularly severe case of reverse TTC that occurred intraoperatively after an adverse reaction to alteplase treated with high-dose epinephrine.
Case Presentation
A 54-year-old woman with May–Thurner syndrome complicated by multiple deep venous thromboses and chronic venous insufficiency, hypothyroidism, obesity, and generalized anxiety disorder presented for elective venous revascularization of the left lower extremity. For general anesthesia with elective intubation, the patient received midazolam, fentanyl, propofol, rocuronium, and sevoflurane, with cefazolin and bivalirudin administered for surgical prophylaxis and procedural anticoagulation, respectively. A low-dose phenylephrine infusion (10–30 mcg/min) was started to counteract vasodilation induced by the anesthetic agents. Immediately after pharmaco-mechanical thrombolysis with alteplase, the patient became acutely hypoxemic and then hypotensive to 56/30 mmHg. Peak inspiratory pressures increased from 21 to 28 cmH2O. The patient received a total of 1 mg epinephrine intravenously in three doses over 3 min (0.2 mg initially, 0.2 mg 2 min after the first dose, and 0.6 mg 1 min after the second dose), transiently increasing her blood pressure to 246/133 mmHg. She subsequently became hypotensive to 85/50 mmHg and was started on an epinephrine infusion and inhaled epoprostenol. The rate of the phenylephrine infusion was increased. An invasive pulmonary digital subtraction angiogram showed no pulmonary embolism to the level of the segmental pulmonary arteries. Pulmonary artery pressures were directly measured at ~65/45 mmHg via pulmonary artery catheterization. The electrocardiogram was remarkable for diffuse T-wave inversions and down-sloping ST-segment depressions, most marked in the anterior precordial leads (Fig. 1). Intraoperative transesophageal echocardiogram (TEE) showed an LVEF of 10–15%, global left ventricular hypokinesis with apical sparing, mild mitral regurgitation, and normal right ventricular systolic function (Fig. 2, Videos 1 and 2). The planned procedure was aborted.
Fig. 1
12-lead electrocardiogram obtained 35 min after the initial epinephrine bolus. The electrocardiogram shows normal sinus rhythm at 75 beats per minute with a normal axis and normal intervals. Diffuse T-wave inversions and flattening are observed. Significant down-sloping ST-segment depressions (≥ 0.5 mm) are present diffusely but are most pronounced (≥ 1 mm) in leads V1–V5
Transesophageal echocardiogram obtained 25 min after the initial epinephrine bolus. Representative images from the mid-esophageal four-chamber view (transducer angle 0°) are shown at A end-diastole and B end-systole. Representative images from the mid-esophageal long-axis view (transducer angle 116°) are shown at C end-diastole and D end-systole. Significant contractility is observed only in the apical third of the left ventricle. The basal and mid-segments of the left ventricle appear nearly akinetic. The mid- and basal segments of the interventricular septum bow into the right ventricle. E Doppler imaging of the mitral valve showing a small, central regurgitant jet
Video 1: Mid-esophageal four-chamber view from the transesophageal echocardiogram obtained 25 min after the initial epinephrine bolus. Still images from this view are reproduced in Fig. 2A and 2B (MP4 28088 KB)
Video 2: Mid-esophageal long-axis view from the transesophageal echocardiogram obtained 25 min after the initial epinephrine bolus. Still images from this view are reproduced in Fig. 2C and 2D (MP4 29517 KB)
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The patient was transferred immediately to the intensive care unit with worsening acute hypoxemic respiratory failure, ultimately requiring pressure-control mechanical ventilation at pressure control 10 cmH2O, respiratory rate 20/min, positive end-expiratory pressure 18 cmH2O, and FiO2 1.00 on inhaled epoprostenol at 0.05 mcg/kg/min. Initial laboratory evaluation was remarkable for a creatinine of 1.30 mg/dL (up from a baseline of ~0.90 mg/dL), lactic acid of 4.1 mmol/L, and leukocyte count of 22,700/µL. No differential was performed. Initial high-sensitivity troponin T was not reported due to hemolysis. High-sensitivity troponin T drawn 5 h after the initial epinephrine bolus was 516 ng/L, with a hemolysis index of 112 (indicating that this result may have been decreased by up to 20% due to hemolysis). Urinalysis showed no nitrites or leukocyte esterase. Chest X-ray showed pulmonary vascular congestion and hypo-inflated lungs. Blood cultures were drawn.
A transthoracic echocardiogram (TTE) obtained 4.5 h after the intraoperative TEE showed persistent global hypokinesis with left ventricular apical sparing but improvement in the LVEF to 30–35% (Fig. 3, Videos 3 and 4). Right heart catheterization revealed severely elevated right- and left-sided filling pressures with a preserved cardiac index (Table 1) on 5 mcg/min epinephrine, 120 mcg/min phenylephrine, and 0.05 mcg/kg/min epoprostenol. Invasive coronary angiography demonstrated no obstructive coronary artery disease or spontaneous coronary vasospasm. Provocative testing for coronary vasospasm was not performed. The patient underwent diuresis with an intravenous furosemide infusion. Given concern for a distributive component to the patient’s shock (Table 1) and worsening lactic acidosis to 7.4 mmol/L, the patient was started on stress-dose hydrocortisone, vancomycin, cefepime, and metronidazole. The vasopressors were cross-titrated from epinephrine and phenylephrine to norepinephrine.
Fig. 3
Transthoracic echocardiogram obtained 4.5 h after the initial epinephrine bolus. Representative images from the apical four-chamber view are shown at A end-diastole and B end-systole. Representative images from the apical two-chamber view are shown at C end-diastole and D end-systole. Relative to Fig. 2, increased contractility is visualized in the mid- and basal segments of the left ventricle. E Polar plot of the longitudinal strain mapping derived from this echocardiogram, illustrating basal-predominant hypokinesis with relative apical sparing
Measurements were obtained on 5 mcg/min epinephrine, 120 mcg/min phenylephrine, and 0.05 mcg/kg/min epoprostenol. The cardiac output and cardiac index were calculated via Fick’s formula
Video 3: Apical four-chamber view from the transthoracic echocardiogram obtained 4.5 hours after the initial epinephrine bolus. Still images from this view are reproduced in Fig. 3A and 3B (MP4 23773 KB)
Video 4: Apical two-chamber view from the transthoracic echocardiogram obtained 4.5 hours after the initial epinephrine bolus. Still images from this view are reproduced in Fig. 3C and 3D (MP4 26501 KB)
With these measures, the mixed shock and acute hypoxemic respiratory failure resolved over the next 20 h. All cultures showed no growth. TTE performed on the sixth day of admission showed recovery of the LVEF to 58%, with residual hypokinesis of the basal inferior and mid-inferolateral walls (Fig. 4, Videos 5 and 6). After discharge, the patient had positive allergy skin testing to alteplase but negative testing to rocuronium, midazolam, and fentanyl. TTE obtained 16 weeks after discharge revealed an LVEF of 63%, with no regional wall motion abnormalities. Cardiac magnetic resonance imaging (MRI) performed 33 weeks after discharge showed a mildly dilated left ventricle (left ventricular end-diastolic volume index of 83 mL/m2), normal left ventricular systolic function (LVEF of 58%) without regional wall motion abnormalities, normal native T1 values, no myocardial edema by T2-weighted imaging, and no resting first-pass myocardial perfusion defect. Nonspecific mid-wall late gadolinium enhancement was visualized at the inferior right ventricular insertion site. The patient presented in this case report granted permission for publication of her clinical course. We thank her for her participation.
Fig. 4
Transthoracic echocardiogram obtained 5 days after the aborted procedure. Representative images from the apical four-chamber view are shown at A end-diastole and B end-systole. Representative images from the apical two-chamber view are shown at C end-diastole and D end-systole. The contractile function of the basal two-thirds of the left ventricle appears grossly recovered. The septal bowing observed in Figs. 2 and 3 is no longer evident
Video 5: Apical four-chamber view from the transthoracic echocardiogram obtained 5 days after the aborted procedure. Still images from this view are reproduced in Fig. 4A and 4B (MP4 35512 KB)
Video 6: Apical two-chamber view from the transthoracic echocardiogram obtained 5 days after the aborted procedure. Still images from this view are reproduced in Fig. 4C and 4D (MP4 30052 KB)
Discussion and Clinical Implications
In summary, we describe the case of a middle-aged woman who had a serious adverse reaction to alteplase, was treated with epinephrine, and then developed severe acute hypoxemic respiratory failure and mixed cardiogenic-distributive shock. Echocardiographic evidence of transient, apex-sparing left ventricular hypokinesis with an LVEF of 10–15% and no obstructive coronary artery disease most strongly supports a diagnosis of reverse TTC. Other diagnostic considerations include hypersensitivity myocarditis and Kounis syndrome (coronary vasospasm provoked by inflammatory mediators released during an allergic reaction) [9, 10]. Hypersensitivity myocarditis is difficult to exclude without an endomyocardial biopsy or a contemporaneous cardiac MRI, but myocardial dysfunction would not be expected to develop within minutes of exposure to the offending drug or to resolve quickly, as it did here [11].
It is difficult to definitively establish whether the adverse reaction to alteplase or the epinephrine used to treat it triggered reverse TTC in our patient. Serious allergic reactions, including anaphylaxis, have been reported in association with alteplase [12]. Severe apical TTC occurred in a young woman who developed anaphylaxis after ingesting Chinese food and was treated with corticosteroids, but not epinephrine or antihistamines [13], arguing that severe allergic reactions alone may suffice to trigger TTC. On the other hand, numerous cases of apical, mid-ventricular, and reverse TTC have been reported in association with epinephrine administration for various indications, including anaphylaxis [14‐17]. Provocation of TTC may be more likely when high doses (at least 1 mg) of intravenous epinephrine are used (as in cardiac arrest) [18‐21] but has also been observed with standard intramuscular 0.3-mg epinephrine autoinjectors [22] and with doses as low as 0.1 mg subcutaneously administered epinephrine [23]. It is unclear whether 1 mg epinephrine in divided doses over 3 min—as was administered in this case—differs significantly from a single 1-mg bolus in terms of its ability to provoke TTC. Current guidelines for intraoperative anaphylaxis advise intravenous epinephrine in small boluses (0.05 mg) plus large-volume isotonic fluid boluses [24] to reduce the risk of TTC.
Given that high levels of catecholamines are thought to underlie myocardial stunning in TTC [5], it may be unsurprising that exogenous epinephrine can cause TTC. Compared to patients with Killip class III myocardial infarction, patients with TTC had significantly higher serum concentrations of dopamine, norepinephrine, and epinephrine during their first two hospital days [25]. Intravenous injection of high-dose epinephrine (equivalent to ~5 mg in an adult human), but not norepinephrine, into anesthetized rats was shown to recapitulate the apical hypokinesis and basal hyperkinesis observed in human patients with apical TTC [26]. Interestingly, however, 33% of patients with epinephrine-induced TTC present with basal hypokinesis [14], compared to only 2% of all patients with TTC [3]. The reverse variant also occurs in a disproportionate 30% of patients with pheochromocytoma-associated TTC [27].
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The overrepresentation of the reverse anatomic variant in patients with epinephrine-induced TTC challenges the β2-adrenoreceptor hypothesis, which has been advanced as an explanation for TTC’s predilection for causing apical hypokinesis. In mammalian left ventricles, sympathetic nerve terminals are densest at the base, whereas β-adrenoreceptors, especially the β2 subtype, are most concentrated at the apex [26, 28]. Presumably, under normal circumstances, these opposing apicobasal gradients ensure that the pro-contractile effects of direct sympathetic innervation and circulating catecholamines are spread evenly along the left ventricle [5]. At high epinephrine concentrations, the β2-adrenoreceptor begins to couple with the inhibitory Gi rather than stimulatory Gs, inducing negative inotropy [29, 30]. Pretreatment with pertussis toxin, which inhibits Gi, blocks epinephrine-stimulated apical hypokinesis in rats [26].
Overall, these data support a model in which high-catecholamine states preferentially stun the apical myocardium due to hyperstimulation of apex-enriched β2-adrenoreceptors, resulting in coupling to Gi rather than Gs. This pathway may have evolved to protect cardiomyocytes from apoptosis in hyperadrenergic states [31]. This mechanism could conceivably also account for the non-apical variants of TTC, provided that the distribution of β2-adrenoreceptors along the left ventricle varies among humans. Hypokinesis would then occur at the regions of highest β2-adrenoreceptor density.
Regardless of the inciting event and anatomic subtype, the diagnostic workup for TTC largely involves excluding other causes of acute heart failure, especially myocardial infarction. Cardiac biomarkers are increased in TTC, though cardiac troponin is lower than in myocardial infarction, whereas B-type natriuretic peptide is usually higher [32, 33]. The electrocardiogram typically demonstrates ST-segment elevation (especially in leads V3–V6), ST-segment depression, and/or T-wave inversions in the acute phase, followed by QT interval prolongation that may precipitate torsades de pointes [34, 35]. In reverse TTC, ST-segment depressions, as seen in our patient in leads V1–V5, are more common [8]. Prompt echocardiography enables visualization of the archetypal circumferential wall motion abnormalities and assessment for mechanical complications, such as apical thrombosis, mitral regurgitation, and left ventricular outflow tract obstruction (LVOTO) [36]. Because TTC mimics myocardial infarction, coronary angiography is often pursued. While significant obstructive coronary artery disease may be identified in patients with TTC [37], it should not fully account for the observed wall motion abnormalities [36].
After other causes of heart failure have been exonerated and inciting triggers have been removed, management of TTC is largely supportive. Pulmonary congestion without cardiogenic shock should be managed with loop diuretics with or without venodilators [2]. Patients who develop cardiogenic shock may require inotropes, vasopressors, or mechanical circulatory support [2]. Cardiogenic shock is particularly perilous with significant LVOTO in TTC, as inotropic support may exacerbate the basal hyperkinesis underlying the obstruction [2]. As many as 20% of patients may develop recurrent TTC within 10 years [2]. Although no medications have been definitively shown to prevent recurrence [38], experts often advise prophylactic β-blockers [35].
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Conclusion
The case presented here provides a striking example of reverse TTC with a severely reduced LVEF after an adverse reaction to alteplase caused profound hypotension that was managed with epinephrine. We chronicle the echocardiographic evolution of this rare anatomic variant of TTC, which captured an initial recovery in the LVEF within hours of onset. This patient’s cardiomyopathy may have been provoked by high-dose epinephrine, which, when it causes TTC, often presents with non-apical variants [14]. We suggest that all forms of TTC, but particularly the atypical anatomic variants, be considered in the differential diagnosis for patients who develop acute heart failure after adverse drug reactions treated with epinephrine.
Declarations
Conflict of Interest
Dr. Robert P. Giugliano discloses research grant support to the Brigham and Women’s Hospital from Amgen to conduct clinical trials; honoraria for lectures and continuing medical education (CME) programs from Amgen, Medical Education Resources, Merck, and Pfizer; and honoraria for consulting from Amgen, Bayer, Janssen, Novartis, and Pfizer. Dr. Robert P. Giugliano is a former Editor-in-Chief of Cardiology and Therapy. Dr. Charles G. Kinzig, Dr. Matthew R. Carey, and Dr. Lauren P. Waldman have nothing to disclose.
Ethical Approval
The patient presented in this case report granted permission for publication of her clinical course. We thank her for her participation.
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