Hypothermia-triggered biventricular Takotsubo cardiomyopathy: the octopus that survived the polar vortex

Abstract

Takotsubo cardiomyopathy (TTC) is most commonly characterised by transient apical ballooning in response to physical or emotional stress without significant coronary artery disease (CAD). Various physical and emotional factors can trigger TTC. We report a case of hypothermia-induced biventricular TTC in an 84-year-old man admitted with a core body temperature of 29.8°C, followed by quick recovery of systolic function and resolution of wall motion abnormality after discharge. TTC should be suspected in hypothermic patients presenting with evidence of new onset heart failure and be added to the expanding list of factors triggering TTC. Similar to TTC induced by various other factors, hypothermia-induced TTC also carries a favourable prognosis with relatively quick recovery of wall motion abnormalities.

Background

Takotsubo cardiomyopathy (TTC) is most commonly characterised by transient apical ballooning in response to physical or emotional stress without significant coronary artery disease (CAD). It affects 0.02% of all hospitalisations in the USA, mainly elderly women with history of smoking, hyperlipidaemia and alcohol use.¹ It generally carries a good prognosis; however, significant mortality and morbidity rates have been reported, especially during the acute phase. The typical form of this condition involves apical and pericapical akinesia along with preservation of the base of the left ventricle (LV). Other variants include the mid-ventricular, basal and focal subtypes.² Although right ventricular (RV) involvement in TTC is rare, there are increasing reports of concomitant RV and LV involvement.^{3 4}

Hypothermia (core body temperature below 35°C/95°F) is precipitated by cold exposure, hypothyroidism, alcohol use and adrenal insufficiency.⁵ It has significant effects on the cardiovascular system, including decreased cardiac output, systemic vascular constriction and bradycardia.⁶

Hypothermia-induced TTC has been reported in two previous case reports.^{5 7} Here we report another case of hypothermia-induced TTC and the first one demonstrating biventricular involvement to our knowledge.

Case presentation

An 84-year-old man with medical history of hypertension and hyperlipidaemia was found unconscious inside his apartment. Family reported that when they found him, the apartment was cold due to a dysfunctional thermostat. Initial examination revealed temperature of 29.8°C (85.64°F), blood pressure of 124/66 mm Hg, heart rate of 40 beats/min and oxygen saturation of 97%. His cardiopulmonary examination revealed normal S1 and S2 with no rubs, gallop or murmurs along with clear lung fields on both sides. His peripheral pulses were 2+ and symmetrical. Further examination showed a 2×3 cm sized haematoma on the right knee.

Investigations

Blood work revealed troponin level of 0.40 ng/mL (normal <0.04 ng/mL), lactic acid level of 2.9 mmol/L (normal 0.4–2 mmol/L), creatine kinase level of 6684 U/L (normal 30–223 U/L) and creatinine level of 1.25 mg/dL (normal 0.7–1.3 mg/dL). ECG showed sinus bradycardia, diffuse T wave inversion and prolonged corrected QT interval (598 ms) (figure 1).

Figure 1.

ECG on admission showing diffuse T wave inversion and prolonged QT.

CT scan of the head did not show any abnormalities. Echocardiogram revealed reduced LV systolic function with estimated ejection fraction (LVEF %) of 30%, apical akinesis, mid-segment hypokinesis along with hyperkinetic basal segments. It also revealed RV apical hypokinesis concerning for biventricular TTC (figures 2 and 3, video 1).

Figure 2.

Echocardiographic image of apical four-chamber view showing: (A) end diastolic frame of the left ventricle (LV) and (B) end systolic frame of the LV. Green arrows indicate thickening and preservation of the mid-segments and basal segments of the LV as opposed to the non-thickened hypokinetic apical segment (red arrows).

Figure 3.

Echocardiographic image with contrast enhancement showing apical four-chamber view. (A) End diastolic frame of the right ventricle (RV). (B) End systolic frame of the RV. Blue arrows indicate RV apical hypokinesia.

Video 1.

Download video file ^{(912.3KB, mp4)}

DOI: 10.1136/bcr-2019-229761.video01

Apical four-chamber view showing the biventricular apical hypokinesis and the preserved contractility of mid-segments and basal segments.

Coronary angiogram was performed showing 40% diffuse stenosis involving the left anterior descending artery; however, no other significant obstructive CAD was noted.

Differential diagnosis

The patient’s presentation along with the ECG findings, elevated troponin level and echocardiographic findings of apical hypokinesia involving both LV and RV was concerning for acute coronary syndrome versus biventricular TTC. However, in the absence of significant obstructive coronary artery disease on coronary angiogram that can explain his echocardiographic findings, a diagnosis of biventricular TTC likely induced by physical stress (hypothermia) was pursued.

Another differential diagnosis includes infectious myocarditis. Although it cannot be ruled definitively, the presence of a possible triggering factor (hypothermia), the biventricular distribution of the wall motion abnormality and absence of suggestive clinical history of myocarditis favoured the decision to repeat echocardiogram and proceed with cardiac MRI if no improvement was noted. However, since the ejection fraction and wall motion of both ventricles were normalised on the repeat echocardiogram, the MRI was deemed unnecessary and TTC became the more plausible diagnosis.

Treatment

In light of the elevated lactic acid level and impaired LV systolic function, cautious repletion with intravenous fluids was used for resuscitation and internal re-warming. Sinus bradycardia quickly resolved after re-warming prior to the coronary angiogram.

The patient was then started on ACE inhibitor prior to discharge to a rehabilitation facility.

Outcome and follow-up

Three weeks following discharge, the patient’s follow-up echocardiography revealed complete recovery of LV and RV systolic function with resolution of previously observed wall motion abnormality (figure 4, video 2).

Figure 4.

Echocardiographic image of apical four-chamber view showing: (A) end diastolic frame of the left ventricle (LV), (B) end systolic frame of the LV and (C) end systolic frame of the right ventricle (RV). Red arrows demonstrate recovery of the contractile function of the apical segments of the LV and RV.

Video 2.

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DOI: 10.1136/bcr-2019-229761.video02

Apical four-chamber view showing the normal contractility of both ventricles following recovery. The left ventricular (LV) dimensions as seen on the echocardiogram have not shown evidence of dilation, with normal LV end diastolic diameter of 5.2 cm (normal 4.2–5.9 cm) and normal LV end systolic diameter of 3.5 cm (normal <4 cm).

Discussion

Our case met the requisite diagnostic criteria for TTC, including transient wall motion abnormality extending beyond a single vascular territory, presence of a triggering stressful physical condition (hypothermia), presence of new ECG findings and elevated troponin levels in the absence of obstructive CAD.⁸

Various physical and emotional factors resulting in catecholamine surge have been reported to trigger TTC. Hypothermia-induced TTC was previously described in two case reports.^{5 7} Davin et al⁷ described an 81-year-old woman, presenting with hypothermia (30°C, 86°F), found to have typical form of TTC with isolated LV involvement. The second case reported by Katayama et al,⁵ a 59-year-old woman with hypothermia (30.9° C, 87.62°F), also found to have Isolated LV TTC. Complete recovery of LV function and resolution of wall motion abnormalities were documented in both reported cases without any complications during hospitalisation or on follow-up.

In our case, no haemodynamic complications were encountered besides elevated lactic acid level concerning for dehydration and hypoperfusion. Patients with significant hypothermia can be volume depleted and need resuscitation with warmed intravenous fluids (40–42°C). However, in the setting of depressed LV systolic function, such as in our patient, clinicians need to be cautious with the total volume administered as well as the rate of fluid replenishment. Low dose pressors in euvolemic patients can be helpful when blood pressure is persistently low despite appropriate fluid resuscitation.⁹

RV involvement in TTC is gaining increasing attention in recent years. Haghi et al⁴ investigated 32 patients with TTC, 26% of whom had evidence of RV involvement. Furthermore, Elesber et al¹⁰ investigated 25 cases of TTC with 32% noted to have RV involvement. Similar to isolated LV TTC, the transient wall motion abnormality affects the apical portion of the RV. Baseline characteristics including age, clinical presentation, ECG changes, troponin levels and coronary angiogram findings were similar among isolated LV TTC versus biventricular TTC groups; however, patients with biventricular TTC had lower LVEF%, longer hospital stay and higher complication rates.

Overall prognosis of TTC is favourable, with quick recovery of regional wall motion abnormalities soon after the inciting event. Long-term mortality from any cause following development of TTC is 5.6% per patient-year and the rate of major adverse cardiac and cerebrovascular events is 9.9% per patient-year.² The use of ACE inhibitors and angiotensin receptor blockers after discharge was shown to improve survival rates at 1 year follow-up in patients with TTC.

Patient’s perspective.

I never had any issues with my heart but when I went to the hospital they told me that my heart is not working well and they needed to take a closer look into the arteries of my heart. I was very happy when they told me I had no blockages and that my heart condition is not permanent and it will improve soon and when I had the ultrasound of my heart in the cardiology clinic after I left the hospital, it did show that it did go back to normal state.

Learning points.

• Takotsubo cardiomyopathy (TTC) should be suspected in hypothermic patients presenting with evidence of new onset heart failure and characteristic echocardiographic wall motion abnormality.

• Hypothermia should be added to the list of triggering factors inciting TTC, including biventricular TTC.

• Fluid resuscitation in hypothermic patients should be done cautiously, especially in patients with depressed left ventricular function.

• Similar to TTC cases induced by various other factors, hypothermia-induced TTC also carries excellent prognosis with relatively quick recovery of wall motion abnormalities soon after the inciting event.