Background: Stress cardiomyopathy (SCM) or broken heart syndrome or apical ballooning syndrome is a rare cardiac disorder characterized by transient, reversible left ventricular dysfunction. We report a case of stress cardiomyopathy and shock ina 37-year-oldfemale with alleged history of suicidal attempt with hanging. She presented with hypotension, tachycardia, and hypoxia. Requiring one session of prone ventilation and inotropes for hemodynamic instability. Two-dimensional echocardiography (2D Echo) showed hypokinesia of distal interventricular septum and the apex of the left ventricle with reduced ejection fraction. CT coronary angiogram revealed normal coronary arteries. Clinically she improved, shock resolved, and repeat 2D Echo showed improved left ventricular function. She got extubated and shifted out of ICU in a stable condition.
Stress cardiomyopathy is a relatively uncommon cardiac complication after hanging. Symptoms usually mimic coronary artery disease with normal coronary vasculature. It is associated with extreme physical and emotional stress (1). Attempting suicide reflects extreme emotional stress. Here we report a case of SCM in a 37-year-old female with alleged attempt of suicide by hanging. Point of Care Ultrasound (POCUS)is a non-invasive diagnostic tool for rapid identification and management of SCM (2). But in case of tachycardia the characteristic 2D Echo findings can be missed leading to delayed or missed diagnosis.
Case
37-year-old female with no known co-morbidities was shifted to our multidisciplinary intensive care unit (MICU) with alleged history of hanging. She was found hanging by her relatives approximately 90 minutes after last seen in the normal state. Immediately she was taken to the local hospital. On arrival at the emergency department, she was deeply unconscious and hypotensive. She was intubated there for airway protection. CT brain was done which was normal. Dual inotropes were started for hypotension, and she was shifted to our hospital for further care.
On arrival to our emergency, her GCS was E1VTM1, she was hypotensive with SBP of 80mmHg and tachycardic with HR of 150/min and hypoxic with SPO2 of 60% with FiO2 of 100%. The ABG at admission was showingpH of 7.04, PCO2- 71.8mmHg, PO2 of 35 mmHg, lactates of 6.4, HCO3- 18.9, BE of -11. Pupils were bilaterally equal 3.5mm and sluggishly reacting to light. 12 lead ECG was showing sinus tachycardia. A ligature mark of 10X0.2 cm was noted.Around 300ml of aspirate came after ET suctioning.CT angiography of brain and neck vessels did not show any dissection or thrombosis or stenosis in common or internal carotid and vertebral arteries.CT C-spine and neck was done which showed cricoid ring fracture but intact cervical spine. She was continued on dual inotropes and was shifted to ICU for further management.
In the ICU, invasive lines were secured, and lung protective ventilation was initiated with optimal PEEP, sedation and paralysis. Screening bedside lung ultrasound revealed bilateral shreds with diffuse B lines suggestive of aspiration/consolidation.The initial 2D-Echo screening performed by our ICU registrar might have appeared normal, likely due to a misinterpretation caused by tachycardia, which made it challenging to accurately assess the findings through visual inspection.She continued to be hypoxemic. After taking clearance from ENT (in view of cricoid fracture), it was decided to prone the patient given refractory hypoxemia even after optimisation of ventilatory strategy. Just before proning, a repeat 2D Echocardiography was indicative of severe LV dysfunction with apical ballooning which was immediately reconfirmed with the cardiology team which showed an ejection fraction of 25%, grade 2 diastolic dysfunction, mild mitral regurgitation, tricuspid regurgitation grade 1 with moderate pulmonary artery hypertensionwith apical segment akinesia and basal segment hypercontractility with apical ballooning suggestive of SCM. [Figure 1(A and B).]
An EEG was done in view of suspected seizures which showed left temporal interictal epileptiform discharges. Anti-epileptic drugs were added. Toxicology screening and thorough medical history ruled out drug-induced cardiomyopathy. She responded well to prone ventilation and oxygenation improved after a single proning session. A 128-slice MDCT (WithSnapshot Freeze software to reduce cardiac motion artifact) coronary angiogram done in the coming days ruled out any coronary occlusion. [Figure.2] Her shock resolved gradually. Repeat echocardiogram showed improved cardiac function with EF of 55%. She was weaned off the ventilator and extubated. She was monitored for another one day and shifted to the ward.\
Figure 1(A and B). 2D Echocardiogram Showing Apical Ballooning
Figure 2. A 128 slice MDCT Coronary Angiogram Showing Normal Coronary Vessels
Stress cardiomyopathy is a rare cardiovascular disorder characterised by temporary and reversible left ventricular dysfunction without coronary blockage. It is seen in extreme emotional and physical stress. Symptoms mimic
acute coronary syndrome. Cases have been reported after severe positive or negative emotional stress like the death of a loved one, divorce, breakup, etc. and after extreme physical stress like severe pain, running marathon, asthma attack, stroke surgery, etc. (1) Attempting suicide reflects a challenging and overwhelming mental health crisis (3). Suicide by hanging is associated with high mortality (4). Our best literature search showed less than 12 cases of SCM after hanging. (9,10,11)
The exact cause of SCM is unknown, but it is presumed to be caused by high levels of catecholamine released during acute stress. High catecholamine levels lead to micro-vascular endothelial dysfunction and myocardial stunning. Sympathetic overdrive and catecholamine excess lead to coronary spasm. The apical myocardium, which has a higher concentration of beta-2 adrenergic receptors, may be more prone to damage compared to the basal myocardium, potentially resulting in apical stunning. Regional vulnerability to blood flow alterations, and changes in the mechanics of heart contraction all lead to apical ballooning. (1,5)Stress cardiomyopathy can get complicated with acute pulmonary edema, heart failure, cardiogenic shock, LV outlet obstruction, arrhythmias, systemic thromboembolism, and intramyocardial hemorrhage and rupture. (16)
The cause for SCM after suicidal hanging could hence be due to the psychological or physiologic stress before, during, and after the event. Catecholamine excess, micro vascular dysfunction, inflammation, oestrogen deficiency, spasm of epicardial coronary vessels, aborted myocardial infarction can lead to takotsubo cardiomyopathy. Acute respiratory failure after hanging can also be a potential cause. Ghadri et al. (6) reported a case of transient severe LV dysfunction secondary to acute respiratory distress in a patient undergoing bilateral lung transplantation.
Other cardiovascular complications include acute negative pressure or neurogenic pulmonary edema, hypotension or shock, carotid artery dissection and /or occlusion, acute myocardial infarction, heart blocks, ventricular tachycardia or fibrillation (7). Hypotension or shock may or may not be present at admission. Cardiac arrest is the most important determinant of a favourable neurologic outcome after an attempted hanging, which significantly impacts neurologic recovery (8).
Takotsubo cardiomyopathy is a relatively uncommon complication after hanging. To the best of our knowledge less than 12 cases have been reported so far in the available literature. J Chacko et al. (9) reported a case of 45-year-old female with takotsubo cardiomyopathy after attempted suicidal hanging. Mini cohort of case reports by R Manfredini et al. (10) included six cases of hanging which triggered Takotsubo syndrome. Sengupta S. et al. (11) also reported two cases of inverted takotsubo cardiomyopathy. We believe there is a high potential to underreport the condition due to lack of awareness by treating physicians, which results in not ordering an Echocardiogram, especially in the absence of hypotension or shock.
There is also a risk for over administration of fluids when the physicians are unaware of the subtle cardiac issue. A normal ECG is possible, especially in early stages, as happened in our case where sinus tachycardia was the only finding. The ECGs may also show ST elevations & depressions, T inversions, left bundle branch block and prolonged QT interval (12).
Our patient presented with unwitnessed partial hanging with shock, tachycardia, and hypoxemia with altered level of consciousness. She was continued on mechanical ventilation and inotropes. She was refractorily hypoxemic requiring prone ventilation. The mechanism of hypoxemia following hanging is likely to be multifactorial. Aspiration pneumonitis, breathing efforts against closed compressed airway leading to negative pressure pulmonary edema, stress cardiomyopathy, neurogenic pulmonary edema and release of inflammatory mediators from reperfusion injury in partial hanging may all lead to ARDS (4). Hypotension or shock following partial hanging may be attributed to severe left ventricular dysfunction caused by SCM or to a systemic inflammatory response resulting from reperfusion injury.The initial presentation of florid shock and hypoxemia led us to suspect vasodilatory shock secondary to aspiration pneumonia and ARDS. However, the echocardiogram revealed poor left ventricular function, prompting us to reconsider and evaluate for cardiogenic shock and pulmonary edema. With this in mind, we restricted fluid intake and initiated gentle diuresis despite the patient being on inotropes, resulting in a significant improvement in oxygenation.
In our case, ECG at admission had shown sinus tachycardia and Troponin and NT pro BNP were elevated. Initial ECG can be normal with modest increase in troponin levels according to revised Mayo Clinic diagnostic criteria (15). However, Echo showed significant left ventricular dysfunction and apical stunning. A 128 slice MDCT (With Snapshot Freeze software to reduce cardiac motion artifact) coronary angiogram ruled out any coronary occlusion. Repeat Echo after 2 days showed significant improvement in left ventricular function with ejection fraction of 55%. As reported by Juho et al., POCUS is an effective screening tool for takotsubo cardiomyopathy (13).
Suicide by hanging has high mortality. Survival as well as neurologic prognosis after hanging depends on several factors. Reported prognostic factors include duration of hanging, depth of initial coma, glycaemic level, arterial lactates and cardiorespiratory arrest. As per authors' experience,patients who present without cardiac arrest have a favourable outcome. Six cases reported by R. Manfredini et al. (3) all had a favourable outcome. In a retrospective study done by Salvetti M et al. (14) showed only 79 (18%) patients out of 450 were discharged alive after hanging induced cardiac arrest.
There are no guidelines for management of SCM. In a hemodynamically stable patient, Beta blockers, ACE inhibitors, anti-platelets and lipid lowering agents have been used. In a patient who presents with cardiogenic shock without left ventricular outflow tract obstruction, inotropes and even mechanical circulatory devices have been tried.
Stress cardiomyopathy is a rarely reported complication of suicidal hanging. A huge potential for under reporting is possible due to a lack of adequate awareness among treating physicians. Prompt recognition and treatment along with management of associated complications leads to favourable outcomes.
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