Clinical management in the takotsubo syndrome

The Use of Beta Blockers in Takotsubo Syndrome as Compared to Acute Coronary Syndrome

“…Besides the missing effects on long-term mortality in our study Santoro et al stated in their meta-analysis that neither beta-blockers nor angiotensin-converting-enzyme inhibitors were able to reduce recurrence of TTS (Santoro et al, 2014). As TTS is considered to be often self-limiting and unnecessary treatment should be avoided (Jha et al, 2019) it can be considered to take distance of this therapy regime by the treating physicians.…”

Takotsubo Cardiomyopathy: Current Treatment

“…When patients with TTS are asymptomatic with normal blood pressure (BP) and heart rate (HR), and their chest pain, dyspnea, or other symptoms or signs of disease, which brought them to seek medical attention have abated, supportive care suffices, along the lines of the Hippocratic “primum non nocere” (“first do no harm”) principle [ 20 , 21 , 22 ]. Indeed, one should be cognizant of the possibility that pharmacological interventions in mild cases of TTS may contribute to complications, otherwise not expected had the natural course was left to evolve without any iatrogenic interference [ 21 ]. Certain drugs taken for previously present comorbidities should not be held.…”

“…Certain drugs taken for previously present comorbidities should not be held. A short course of limited anticoagulation therapy may be needed to prevent stroke, systemic embolism, or pulmonary embolism [ 20 , 21 , 22 , 23 ], particularly if there is sizeable apical/midventricular akinesis/dyskinesis with apical ballooning, which predisposes to thrombus formation when coupled with the sympathetic overdrive, which induces hypercoagulability [ 24 , 25 ], even in asymptomatic patients and in the absence of heart failure (HF), while the patient is self-healing. In reference to prophylactic administration of anticoagulation, restraint should be exercised until one has excluded the presence of ACS or AMI via coronary angiography [ 21 ]; in the same vein, one should avoid using anticoagulants if it is suspected or shown that the underlying trigger for the TTS episode was intracerebral bleeding [ 21 , 26 , 27 , 28 ].…”

“…A short course of limited anticoagulation therapy may be needed to prevent stroke, systemic embolism, or pulmonary embolism [ 20 , 21 , 22 , 23 ], particularly if there is sizeable apical/midventricular akinesis/dyskinesis with apical ballooning, which predisposes to thrombus formation when coupled with the sympathetic overdrive, which induces hypercoagulability [ 24 , 25 ], even in asymptomatic patients and in the absence of heart failure (HF), while the patient is self-healing. In reference to prophylactic administration of anticoagulation, restraint should be exercised until one has excluded the presence of ACS or AMI via coronary angiography [ 21 ]; in the same vein, one should avoid using anticoagulants if it is suspected or shown that the underlying trigger for the TTS episode was intracerebral bleeding [ 21 , 26 , 27 , 28 ]. Continuous electrocardiographic (ECG) monitoring for emergence of arrhythmias and for QTc prolongation [ 29 ], associated with ventricular arrhythmias (VA), should be instituted and maintained throughout hospitalization, and even beyond, if left ventricular (LV) wall motion abnormalities (LVWMA), or LV thrombus, detected during hospitalization, persist at follow-up [ 20 , 30 , 31 , 32 , 33 ].…”

“…Although some physicians continue or start angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEi/ARB), β-blockers, diuretics and aspirin (in patients with a history of atherosclerosis or CAD), one should not forget that any therapy not proven in patients with TTS, particularly when they are asymptomatic, should be considered “quasi-experimental”, tentative, and subject to close monitoring ( which applies to ALL pharmacological or other therapies administered ), continuation, or termination, depending on the response of the patients. Any treatment recommendations discussed herein emanate from general clinical reasoning consensus among experts, observational studies, and case series of patients with TTS (level of evidence C) [ 21 , 22 ]. Intuitively, inclusion of β-blockers may be justified, considering the nosogenic role of catecholamines in TTS; however, patients have recovered without the use of such therapy, and there is no evidence that the catecholamine-based injurious effect continues to be exerted hours or days after the inception of disease, when patients come under our care, and thus therapy with β-blockers is essential.…”