The syndrome of inferior non-infarctional Q-waves due to segmental basal left ventricular hypertrophy.

Non-infarctional Q-waves in general are often recorded in the ECG, and are attributed to anatomical and electrical ECG axis shifts, presence of accessory pathways, pregnancy, HCM, and other HCM-like segmental LV myocardial hypertrophic states, that are currently not fully characterized, as to their nosological nature. The present focused review concerns in particular inferior Q-waves and their association with segmental basal anterior and/or septal LV hypertophies due to HCM, and other not yet fully characterized basal segmental LV hypertophies. Insights from the currently available literature on the topic are reviewed, and varying opinions about the nature of such hypertophic states are discussed, with some suggestions, for what is needed to be done, for their further pathlogenetic characterization.

Blood Pressure/Heart Rate-Derived Ratios as Indices of Health and Cardiovascular Pathology.

This communication, based on a review of the relevant literature on ratios deriving from blood pressure and heart rate measurements, and their conformance/nonconformance to the mathematical golden rule (ie, 1.681), proposes that such ratios, particularly emanating from large numbers of home blood pressure and heart rate measurements obtained by the patients themselves or their caretakers, may constitute new risk markers, useful in the assessment of health and cardiovascular pathologies, prognosis of morbidity and mortality, and implementation to clinical practice and research.

Takotsubo Syndrome in Patients With COVID-19: A Systematic Review.

Background: Respiratory conditions are major physical triggers of takotsubo syndrome (TTS) and portend worse outcomes. However, data on TTS in patients with coronavirus disease-2019 infection (COVID-19) are limited. Methods: We searched PubMed, Embase, and Cochrane Library databases for case reports for the period 2019-2022 describing TTS in patients with COVID-19 pneumonia (TTS-COVID). We summarized the clinical data and outcomes and compared them to those in patients with TTS with an acute respiratory disease other than COVID-19 as a trigger (TTS-acute respiratory disease) and those with TTS with no respiratory disease (TTS-no respiratory disease). Results: The mortality rate was higher in those with TTS-COVID (26.0%) than those with TTS-acute respiratory disease (5.7%) or TTS-no respiratory disease (4.2%; P < 0.001 for both). The proportion of men was higher in TTS-COVID (33.3%) than it was in TTS-no respiratory disease (9.1%; P < 0.001). The manifestations of TTS in COVID patients were atypical (dyspnea [70.3%] and cough [40.6%]); few had chest pain (23.4%). Cardiovascular risk factors were common in the TTS-COVID cohort, but fewer patients were on cardioprotective medications in this group than in the other 2 groups. Level of catecholamine use was higher in the TTS-COVID group (37.7%) than it was in the TTS-no respiratory disease (10.9%; P < 0.001) group. Apical ballooning (72.6%) was the most common TTS subtype, and basal segment type was seen in 11.0% of TTS-COVID patients. Conclusions: COVID-19 patients who developed TTS had high mortality rates and unique features, compared with those in the TTS-acute respiratory disease group or the TTS-no respiratory disease group. Understanding the pathophysiology of TTS in COVID-19 may help prevent TTS and direct therapy in this setting.

Contexte: Les troubles respiratoires sont des déclencheurs physiques importants du syndrome de Takotsubo (STT) et présagent une issue funeste. Les données sur le STT chez les personnes ayant contracté la maladie à coronavirus de 2019 (COVID-19) sont néanmoins limitées. Méthodologie: Nous avons fait une recherche dans les bases de données PubMed, Embase et Cochrane Library pour trouver des rapports de cas signalés entre 2019 et 2022 faisant état du STT chez des patients ayant contracté une pneumonie associée à la COVID-19 (STT-COVID). Nous avons synthétisé les données cliniques et les résultats pour les comparer à ceux de patients atteints du STT déclenché par une autre maladie respiratoire aiguë que la COVID-19 (STT-maladie respiratoire aiguë) et de patients atteints du STT sans maladie respiratoire (STT-sans maladie respiratoire). Résultats: Le taux de mortalité a été plus élevé chez les patients atteints du STT-COVID (26,0 %) que chez ceux atteints du STT-maladie respiratoire aiguë (5,7 %) ou du STT-sans maladie respiratoire (4,2 %; p < 0,001 dans les deux cas). La proportion d'hommes était plus élevée dans le groupe STT-COVID (33,3 %) que dans le groupe STT-sans maladie respiratoire (9,1 %; p < 0,001). Les manifestations du STT chez les patients atteints de la COVID étaient atypiques (dyspnée [70,3 %] et toux [40,6 %]); quelques patients présentaient une douleur thoracique (23,4 %). Les facteurs de risque cardiovasculaires étaient courants dans la cohorte STT-COVID, mais les patients qui prenaient des médicaments cardioprotecteurs étaient moins nombreux dans ce groupe que dans les deux autres groupes. Le taux d'utilisation de la catécholamine était plus élevé dans le groupe STT-COVID (37,7 %) que dans le groupe STT-sans maladie respiratoire (10,9 %; p < 0,001). La ballonisation de l'apex (72,6 %) était le sous-type de STT le plus courant, et le type caractérisé par un trouble du segment basal a été observé chez 11,0 % des patients atteints du STT-COVID. Conclusions: Les patients atteints de la COVID-19 ayant développé un STT présentaient des taux de mortalité élevés et des manifestations singulières, comparativement à ceux du groupe STT-maladie respiratoire aiguë ou du groupe STT-sans maladie respiratoire. Comprendre la physiopathologie du STT chez les patients atteints de la COVID-19 pourrait contribuer à prévenir le STT et à orienter le traitement dans ce contexte.

Electrocardiogram repolarization markers and ventricular arrhythmias in patients with takotsubo syndrome.

The predictive value of various ECG repolarization markers for the emergence of VA in patients with TTS was reviewed. The literature reports on QT, more recently on Tpe, and rarely on some more QT-derived metrics, revealing a contribution of these variables for the prediction of VA, complicating the acute, subacute, and follow-up clinical trajectory of patients with TTS. More recent literature reveals that Tpe and some other QT-based metrics, have outperformed the traditionally employed QT marker, although certainty about this awaits confirmation by future carefully designed and implemented studies.

Association of spontaneous coronary artery dissection and takotsubo syndrome: What has been suspected has been found.

There is ample literature revealing an association of SCAD with TTS, while it is not clear whether these 2 pathological entities are mechanistically linked in the sense that the one triggers the other. Considering that physical/emotional stress triggers TTS, it is plausible that stress related to SCAD, could result in the emergence of TTS. Conversely, it has been speculated that the junction between hypercontractile and akinetic/dyskinetic myocardium regions in TTS could lead to a "hinge pivoting point", imparting vascular disruption in coronary arteries, crossing these abutting myocardial planes, in susceptible individuals, causing SCAD.

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.

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)...

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.

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.