On animal pathophysiology-seeking models of takotsubo syndrome.

The aim of this viewpoint/commentary on a recent contribution by the Gothenburg takotsubo syndrome (TTS) laboratory, in which the authors provide a comprehensive review/state of the art report on the animal models, currently employed in the elucidation of the pathophysiology of TTS, is to intensify the debate as to what constitutes a suitable TTS animal model with as promising as possible translational potential to the human TTS.

Left ventricular outflow tract obstruction/hypertrophic cardiomyopathy/takotsubo syndrome: A new hypothesis of takotsubo syndrome pathophysiology.

The pathophysiology of TTS is still elusive. This viewpoint proposes that TTS is an acute coronary syndrome, engendered by an ASNS/catecholamine-induced LVOTO, which results in an enhanced wall stress and afterload-based supply/demand mismatch, culminating in a segmental myocardial ischemic injury state, in susceptible individuals. Such individuals are felt to be particularly women with chronic hypertension, known or latent HCM, or non-HCM segmental myocardial hypertrophy, and certain structural abnormalities involving the LV and the MV apparatus. Recommendations are provided to explore further this hypothesis, while maintaining our focus on all other advanced TTS pathophysiology hypotheses for all patients, or those who do not experience LVOTO, men, the young, and patients with reverse, mid-ventricular, or right ventricular TTS, in whom more prolonged hyperadrenergic stimulation and/or larger amounts of blood-ridden catecholamines, segmental particularities of cardiac innervation and/or density of α-, and ß-adrenergic receptors, pheochromocytoma, neurological chronic or acute comorbidities/catastrophies, coronary epicardial/microvascular vasospasm, and CMD.

Serial Home Blood Pressure and Heart Rate Measurements for Optimized Management.

BACKGROUND: Serial blood pressure and heart rate measurements, particularly obtained by the patients at home, are currently recommended for the management of patients. METHODS: Home blood pressure and heart rate measurements were obtained by an 81-year old husband and his 74-year old wife in the morning and evening, over the course of an entire month. RESULTS: Morning and evening systolic blood pressure (129.9 ± 5.5, 125.9 ± 10.2, respectively), and diastolic blood pressure (69.2 ± 4.0, 70.1 ± 5.3) were not different (P > .05), heart rate (61.2 ± 2.9, 69.0 ± 5.5) was higher in the evening (P = .00001) in the husband, while systolic blood pressure (134.7 ± 9.6, 119.0 ± 12.0) and diastolic blood pressure (78.6 ± 5.6, 72.1 ± 7.3) were higher in the morning (P = .00001, P = .00031), and heart rate (62.7 ± 4.7, 68.2 ± 4.6) was higher in the evening (P = .00017) in the wife. CONCLUSIONS: Patient-generated serial home blood pressure and heart rate logs provide essential data for the patients' management and could potentially be useful in research; circadian variation of blood pressure and heart rate calls for implementation of chronotherapeutic principles for the time of drug administration.

Frequent POCUS and auscultation for an earlier diagnosis of takotsubo syndrome and unraveling of its pathophysiology: The possible crucial role of LVOTO.

There is ample literature associating LVOTO with hypertension, AMI, LV hypertrophy, sigmoid septum, HCM, and TTS, particularly in midde aged/elderly/postmenopausal women, suggestive of a causal role for LVOTO in the pathophysiology of TTS. Although there is significant evidence that TTS is triggered by a sudden autonomic sympathetic nervous system surge and/or elevated blood-ridden catecholamines, the exact pathophysiologic trajectory leading to the clinical expression of the disease is still being debated. This review expounds on the possibility that LVOTO is a causal early component of this trajectory, and proposes that TTS is a malady within the broad spectrum of the myocardial ischemic injury/stunned myocardium states. The postulated underlying mechanism by which LVOTO causes TTS is a sudden abterload rise, with resultant oxygen/energy supply/demand mismatch, leading to a transient myocardial ischemia/injury myocardial stunning state. This needs to be explored painstakingly, and this review includes some suggestions for such undertaking. Ellucidation of the pathophysiology of TTS, and possible proof about a mechanistic role of LVOTO, may ensure that our current pharmacological and device panoply is adequate for the management of TTS.

Comments on "QT interval prolongation in Takotsubo syndrome: a frightening feature with no major prognostic impact".

Dear Editor, Pinho et al. reported on the acquired corrected QT-interval (QTc) prolongation in a retrospective analysis of 113 patients (aged 67.6±11.7, 94.7% female)...

The recurrence rate of takotsubo syndrome may be higher than currently reported.

Various rates of the short- and long-term recurrence of takotsubo syndrome (TTS) (RTTS) have been reported, but the absence, or the short length of the follow-up implemented is such, that the true rate of RTTS continues to be unknown. Experience has shown that a sizeable proportion of patients with an index TTS suffer a RTTS episode beyond 5 years, and even 20 years later. In a cohort of 215 patients with RTTS from the world literature, a mean of 30.2 and 37.2 months separated the index TTS from the 1st and last RTTS episodes, respectively, with 21.9 % of patients suffering more than 1 RTTS episode, over a course of maximum of 20 years. Also, 39.5 % and 19.5 % of patients had their only or last RTTS episode(s), at or beyond the 3rd and 5th year of follow-up, respectively. The true rate of RTTS is unknown, probably is higher that currently reported, and it is hoped that existing registries may provide the answer, if they implement an open-ending long-term follow-up of their registered patients.

Serial electrocardiograms at follow-up for early detection of transplanted heart rejection: A viewpoint.

This viewpoint proposed that serial electrocardiograms (ECG) could be used to monitor for heart transplantation (HT) rejection, based on the expected attenuation of the amplitude of ECG QRS complexes (attQRS) engendered by the rejection-induced decrease in electrical resistance due to the underlying myocardial edema (ME). Previous work in humans has shown attQRS in the setting of a diverse array of edematous states, affecting the myocardium (i.e, ME) and the body volume conductor "enveloping" the heart. Also, animal and human experience has revealed low electrical resistance during mild/moderate HT rejection. Studies with serial correlations of endomyocardial biopsy (EMB), echocardiography, cardiac magnetic resonance imaging, and ECG are recommended, which will merely require recording of an ECG, when EMB and imaging studies are carried out for monitoring of post-HT rejection.