Over the Exceptions: Psychiatric Disorder, Medical Stress, and Takotsubo Cardiomyopathy.

Exact natural history and physiopathology of takotsubo cardiomyopathy (TC) are incompletely understood. In the last years, a lot of special cases of TC appeared in the literature. This case report is a typical case of TC, which meets all Mayo Clinic diagnosis criteria, over the exceptions; its main feature is that it has both physical (medical) and emotional (psychiatric) triggers. The protagonist is a woman affected by anxious-depressive syndrome, hospitalized for a cardiogenic syncope. After pacemaker (PMK) implantation, she first has convulsive hysteric crisis, and the following day, she has a transient left ventricular apical ballooning without coronary artery stenosis: takotsubo syndrome. This case underlines the depth and strong relationship between takotsubo syndrome and psychiatric illness, which is both clinical substrate and triggering acute event, with the significant role of PMK implantation which might have had a role both as flare of psychiatric disease and as a trigger for the syndrome itself.

Introduction

The annual incidence of takotsubo cardiomyopathy (TC) is 1%–2% of all troponin positive acute coronary syndromes. In the International Takotsubo Registry, emotional triggers were in 27.7% of patients, physical triggers were in 36%, 7.8% of patients had both triggers; 55.6% of patients had an acute or a past neurological or psychiatry disorder.[1]

Even if the knowledge about TC is increasing in the last decades, the physiopathology of this clinical entity remains mysterious and the exact mechanism leading to TC is still unknown.

Our case report, characterized by the presence of both physical and psychiatric triggers, is a typical case of TC and it underlines the strong relationship between TC, psychiatry, and medical stress.

Case Report

A 70-year-old woman, affected by anxious-depressive syndrome in antidepressant and antipsychotic therapy, was referred to our hospital ward for a syncope occurring during vomiting and diarrhea. In the emergency room, the electrocardiogram (ECG) showed a junctional rhythm, and the echocardiography was normal. During the cardiology stay, ECG monitoring recorded a sinus bradycardia with significant pauses, 6 s long [Figure 1].

Figure 1

Electrocardiogram monitoring records sinus bradycardia with a significant pause 6 s long.

Next day, a bicameral pacemaker (PMK) was implanted. The patient came back to the cardiology ward after PMK implantation, and ECG showed activity PMK-induced [Figure 2].

Figure 2

Electrocardiogram after pacemaker implantation shows activity pacemaker-induced.

A few minutes later, the woman had an acute episode of detachment from reality and generalized muscle spasms, considered first as a comital crisis, and treated with intravenous midazolam. We immediately required a psychiatry advice; an accurate psychiatry evaluation made diagnosis of convulsive hysteric crisis.

Next day, ECG showed activity PMK-induced with significant persistent anterior (V2–V6) ST-segment elevation [Figure 3]. Troponin levels were elevated (2.74 ng/ml, the cutoff is 0.04 ng/ml). Echocardiography showed left ventricular apical and midventricular segments - akinesis, basal segments - hyperkinesis, and reduced left ventricular ejection fraction [Figure 4].

Figure 3

Electrocardiogram after pseudoseizures shows activity pacemaker-induced with significant persistent anterior (V2–V6) ST-segment elevation (doubled electrocardiogram amplitude).

Figure 4

Transthoracic echocardiography (apical 2-chamber view) shows apical and midventricular hypokinesis and hypercontractile basal sections.

We decided for an urgent coronary angiography to exclude an acute coronary syndrome; it showed the absence of obstructive coronary disease. Ventriculography confirmed our ECG suspicion demonstrating left ventricular apical ballooning, a typical feature of TC [Figure 5].

Figure 5

Ventriculography shows ballooning of apical and midventricular sections and hypercontractile basal sections.

In the following days, ECG [Figure 6] and troponin levels came back normal; serial ECG assessments revealed progressive recovery of systolic left ventricular function, first midventricular segments recovered a normal contractility and then apical segments too.

Figure 6

Electrocardiogram in the following days highlights the evolution of ST-segment.

Diagnosis of TC was sure, meeting every criterion proposed by Mayo Clinic.[2]

The patient kept continuous disorientation, narrowing of the state of consciousness; she never reported chest pain or dyspnea; a lot of other pseudoseizures occurred.

Treatment was mainly guided by psychiatric disease using sedatives, antidepressant, and antipsychotic drugs; cardiologic therapy was occasionally administered, with difficulty.

Discussion

TC is a syndrome described in Japan in 1990 for the first time by Sato et al.[3]

Since its first description, the knowledge about its issues is enormously increased.

We have a definition

A disease characterized by transient systolic and diastolic regional left ventricular dysfunction with a variety of wall motion abnormalities, usually related with psychophysical stress, typically reversible.[4]

We know that the wall motion abnormalities generally involve the apex of left ventricle that takes the typical aspect of apical ballooning which gives the syndrome its name (takotsubo is a traditional Japanese octopus pot) but it is not always true; there are several cases of TC which have not apical akinesia but involve other segments of the left ventricle.[5]

We have criteria for clinical diagnosis of TC proposed by Mayo Clinic:

Transient akinesis or dyskinesis of the left ventricular apical and midventricular segments with regional wall motion abnormalities extending beyond a single epicardial vascular distribution;

absence of obstructive coronary disease or angiographic evidence of acute plaque rupture;

new ECG abnormalities (either ST-segment elevation or T-wave inversion);

absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial coronary artery disease, myocarditis, hypertrophic cardiomyopathy.[2]

We know the epidemiology

Analyzing the International Takotsubo Registry, a consortium of 26 centers in Europe and the United States, we can investigate the features of the patients with diagnosis of TC.

Of 1750 patients, 89.8% were women, mean age was 66.8 years; emotional triggers were in 27.7% of patients, physical triggers were in 36%, 7.8% of patients had both triggers, TC occurred without any evident trigger in 28.5% of patients; 55.6% of patients had an acute or a past neurological or psychiatry disorder, of which 9.1% had acute neurologic disorder, 21.7% had past or chronic neurologic disorder, 1.3% had acute psychiatric disorder, and 36.6% had past or chronic psychiatric disorder.

We can say that the syndrome predominantly affects elderly women and is often preceded by emotional or physical trigger and the 55.6% of patients have a history or an acute episode of a neurologic or psychiatric disorder.[67]

However, although the better understanding of this disease, our knowledge remains limited.

We do not know the exact pathogenesis of the syndrome

The role of the brain–heart axis in the pathogenesis of the disease has been described, but several etiological hypotheses were identified. It has been suggested that coronary vascular dysfunction, abnormal coronary microcirculation, excessive sympathetic stimulation, neurogenic stunning, and left ventricular outflow obstruction might be involved in the pathogenesis.[89] However, the exact mechanism leading to TC is still unknown.

We do not know the exact prognosis

Patient is at risk for recurrence even years after the first event, but data on in-hospital and long-term outcomes are limited.[1011]

We do not know the better therapeutic strategy

We administer supportive and symptomatic therapy, but we do not have a specific therapy for this syndrome, and we do not know if antiischemic therapy with aspirin, beta-blockers, angiotensin converting enzyme inhibitors or nitrates is really useful in the long-term treatment.

Exact natural history and physiopathology of TC are incompletely understood.

In the last years, a lot of special cases of TC appeared in the medical literature: conditions with no evident triggers or with only mild physical trigger; conditions with involvement of midventricular segments or basal segments or other focal segments, sparing apex, typically involved; conditions with evidence of coexisting coronary artery disease on angiography.

Our case report is a typical case of TC, which respects every diagnosis criterion proposed by Mayo Clinic, over the exceptions. It is a case with the presence of both physical (medical) and emotional (psychiatric) triggers, in a patient with both chronic and acute psychiatric disorder.

Furthermore, it stresses the depth and strong relationship between takotsubo syndrome and psychiatric illness, which is both clinical substrate (the patient had anxious-depressive syndrome) and triggering acute event (TC occurred the day after first pseudoseizure), with the significant role of medical stress (PMK implantation) which might have had a role both as flare of psychiatric disease and as a trigger for the syndrome itself.

Conclusions

In a scenery characterized by special case of TC, our case report is a typical case of TC, which respects every diagnosis criterion, over the exceptions, with the presence of both physical (medical) and emotional (psychiatric) triggers.

In scenery characterized by uncompleted knowledge of this clinical entity, our case report highlights the strong relationship between takotsubo syndrome, medical stress, and psychiatric illness.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.