Hyponatremia and takotsubo syndrome: a review of pathogenetic and clinical implications.

Hyponatremia is a common electrolyte abnormality with important prognostic and therapeutic implications. It might exert detrimental effects on various organ systems including the central nervous system (CNS), bone, and heart along with its potential association with poor quality of life. These adverse effects might be largely mediated through a variety of mechanisms including osmotic stress, dysfunctional transmembrane exchangers, and enhanced oxidative stress.Interestingly, hyponatremia might also have an important association with takotsubo syndrome (TTS) that has been universally considered as a reversible form of cardiomyopathy usually emerging in response to various stressors. In this context, severe hyponatremia was previously reported to serve as a direct trigger of TTS evolution largely through its potential impact on CNS and heart. However, pathogenetic and clinical implications of hyponatremia still need to be thoroughly evaluated in patients with TTS. This paper aims to analyze the clinical features of published cases with TTS primarily triggered by hyponatremia and also aims to discuss the association between hyponatremia and TTS from a broader perspective.

Cardiac myxoma as a potential trigger of takotsubo cardiomyopathy: A brief review on mechanistic and clinical perspectives.

In clinical practice, cardiac myxomas constitute the majority of benign cardiac neoplasms, and might potentially present with a variety of embolic, obstructive as well as constitutional symptoms. On the other hand, these neoplasms might be potentially associated with the evolution of takotsubo cardiomyopathy (TTC) that is universally considered as a transient form of acute myocardial dysfunction. Accordingly, the present paper primarily aims to focus on potential mechanisms and associated clinical implications of TTC evolution in the setting of cardiac myxomas.

Systemic inflammation in patients with Takotsubo syndrome: a review of mechanistic and clinical implications.

Over recent decades, systemic inflammation  as  quantified  with  inflammation  markers  or  indices has been extensively  investigated  in the setting of  various  cardiovascular  conditions  including heart failure (HF),  acute coronary syndromes (ACS). In contrast, systemic inflammation  in patients with  takotsubo syndrome (TTS) has been an underrated  phenomenon in clinical practice. On the other hand, experimental and clinical data  have been  rapidly  accumulating  in the recent years  regarding   pathogenetic, prognostic as well as therapeutic implications of  systemic inflammation in TTS.  Accordingly, the present article  aims to provide a general perspective  on mechanistic and  clinical aspects of  systemic  inflammation in the setting of  TTS.

Takotsubo syndrome in association with pheochromocytoma: clinical and practical considerations.

In clinical practice, pathophysiology of Takotsubo syndrome (TTS) has been attributed to adrenergic discharge mostly associated with a variety of stressors. Occasionally, organic sources of adrenergic discharge (including pheochromocytoma) might also account for this phenomenon and are not considered as exclusion criteria for the diagnosis of TTS (as opposed to previous suggestions). We read with great interest the recently published article by Maffè et al. that describes a case of fatal TTS due to a ruptured pheochromocytoma in a middle-aged male. In this context, we would like to comment on this interesting case and potential implications of TTS associated with pheochromocytoma....

Cardiac Biomarkers in the Setting of Asthma Exacerbations: a Review of Clinical Implications and Practical Considerations.

PURPOSE OF REVIEW: The present paper aims to highlight clinical implications of elevated cardiac biomarkers and associated myocardial dysfunction in a variety of cardiac and non-cardiac scenarios in patients with an asthma exacerbation, and to propose a basic algorithm for cardiovascular evaluation and triage (and hence, for further management) of these patients primarily based on evaluation of cardiac biomarkers along with basic diagnostic modalities and specific cardiac symptoms in the hospital setting. RECENT FINDINGS: Elevation of cardiac biomarkers in the setting of an asthma exacerbation mostly signifies a new-onset subclinical myocardial dysfunction/injury generally associated with certain asthma-related factors including acute hypoxemia and bronchodilator therapy, and usually has a limited prognostic value in these patients. On the other hand, elevation of these biomarkers in patients with an asthma exacerbation might also denote a variety of certain life-threatening cardiac or non-cardiac conditions associated with significant myocardial dysfunction (acute coronary syndromes (ACSs), sepsis, etc.) that might be masked by the rampant course of the asthma exacerbation, and hence, might possibly go undetected potentially aggravating the prognosis in a portion of these patients. In patients with an asthma exacerbation, it seems imperative to timely diagnose and manage emerging diverse clinical conditions particularly through the guidance of cardiac biomarkers and associated myocardial dysfunction patterns in an effort to improve overall prognosis in these patients.

Takotsubo cardiomyopathy in the setting of multiple sclerosis: a multifaceted phenomenon with important implications.

Dear Editor, Takotsubo cardiomyopathy (TTC) has been universally regarded as a unique form of reversible myocardial dysfunction associated with a variety of emotional and physical stressors. In their recently published elegant article, Dell'Aquila et al. have reported an interesting case of TTC triggered by an exacerbation of relapsing-remitting multiple sclerosis (MS). However, we would like to comment on this interesting case and its particular implications...

Ignored Role of Paroxysmal Atrial Fibrillation in the Pathophysiology of Cryptogenic Stroke in Patients with Patent Foramen Ovale and Atrial Septal Aneurysm.

The association between cryptogenic stroke (CS) and patent foramen ovale (PFO) with or without atrial septal aneurysm (ASA) has been a debate for decades in terms of pathophysiologic processes and clinical courses. This issue has become more interesting and complex, because of the concerns associating the CS with so-called normal variant pathologies of interatrial septum, namely ASA and PFO. While there is an anatomical pathology in the interatrial septum, namely PFO and ASA, the embolic source of stroke is not clearly defined. Moreover, in patients with PFO and CS, the risk of recurrent stroke has also been associated with other PFOunrelated factors, such as hyperlipidemia, body mass index, diabetes mellitus, and hypertension, leading to the difficulty in understanding the pathophysiologic mechanism of CS in patients with PFO and/or ASA. Theoretically, the embolic source of cryptogenic stroke in which PFO and/or ASA has been involved can be categorized into three different anatomical locations, namely PFO tissue and/or ASA tissue itself, right or left atrial chambers, and venous vascular territory distal to the right atrium, i.e., inferior vena cava and lower extremity venous system. However, the possible role of paroxysmal atrial fibrillation associated with PFO and/or ASA as a source of cryptogenic stroke has never been mentioned clearly in the literature. This review aims to explain the association of cryptogenic stroke with PFO and/or ASA in a comprehensive manner, including anatomical, clinical, and mechanistic aspects. The potential role of paroxysmal atrial fibrillation and its contribution to clinical course have been also discussed in a hypothetical manner to elucidate the pathophysiology of CS and support further treatment modalities.

Looking at the Golden Ratio from the Blood Pressure Perspective: Assessing the Hypertensive Patients and Normotensive Subjects.

BACKGROUND: The representatives of mathematical concepts and indices allied to the Golden Ratio (GR) have been shown in the human body in superimposed human hands, phalangeal lengths of the digits, human ears, and the cardiovascular system. Recently, it has been demonstrated that the systolic blood pressure (SBP) to diastolic blood pressure (DBP) ratio measured by ambulatory blood pressure monitoring (ABPM) is close to GR. Accordingly, we aimed to evaluate the ratios between the SBP, DBP, and PP in normotensive and hypertensive patients who were on medical treatment or not, to assess the existence of golden proportions in 24-hour ambulatory blood pressure monitoring results. MATERIAL AND METHOD: Five hundred and twenty-nine patients who underwent ABPM were retrospectively enrolled in the study population. The ABPM was programmed to measure blood pressure every 30 min during the daytime and 60 min night time. Based on the ABPM results, patients were classified as hypertensive (SBP/DBP≥130/80 mmHg) and normotensive (SBP/DBP<130/80 mmHg), depending on ESC/ESH 2018 guidelines. They were also divided into two subgroups: medicated and nonmedicated. Systolic to diastolic blood pressure ratio (SBP/DBP) and diastolic blood pressure to pulse pressure (DBP/PP) were calculated in the usual fashion in all study populations and subgroups. RESULTS: After the exclusion of 133 patients who did not fulfill the inclusion criteria, 396 patients were included in the statistical analysis. Mean SBP/DBP ratios were 1.66±0.15 in all the study population, 1.63±0.11 in normotensive without medication, 1.66±0.13 in normotensive with medications, 1.62±0.15 in hypertensive without medication, and 1.76±0.20 with medications. CONCLUSION: We have documented that SBP to DBP ratios of untreated patients, irrespective of having normal or high blood pressure, run close around the GR. However, SBP to DBP ratios of patients having antihypertensive treatment are far from the GR.

Serum Copeptin in Cardiooncology Practice: Review of Pathophysiological and Clinical Implications.

In cardiooncology practice, "early cardiotoxicity" refers to an emerging subclinical myocardial dysfunction/injury in response to certain chemotherapeutic regimens. This condition can progress to overt cardiotoxicity in time and hence warrants proper and timely diagnostic and preventive strategies. Current diagnostic strategies for "early cardiotoxicity" are largely based on conventional biomarkers and certain echocardiographic indices. However, a significant gap still exists in this setting, warranting further strategies to improve diagnosis and overall prognosis in cancer survivors. Copeptin (surrogate marker of the arginine vasopressine axis) might serve as a promising adjunctive guide for the timely detection, risk stratification, and management of early cardiotoxicity on top of conventional strategies largely due to its multifaceted pathophysiological implications in the clinical setting. This work aims to focus on serum copeptin as a marker of "early cardiotoxicity" and its general clinical implications in patients with cancer.

The Correlation between Elevated HDL-Cholesterol, Body Mass Index, and Presence of Thyroid Nodules: A Retrospective Analysis.

BACKGROUND: Elevated high-density lipoprotein-cholesterol (HDL-cholesterol) levels have been linked to unfavorable outcomes in various clinical settings, but the association with thyroid nodules remains unclear. We aimed to analyze the correlation between elevated HDL-cholesterol and the presence of thyroid nodules along with certain demographic and clinical findings. METHODS: In this retrospective study, the patients were divided into three groups based on their body mass index (BMI): <25, 25-29, and >30 and evaluated. Data of 677 patients aged between 15 and 95 years (52.6 ± 15.6) were evaluated. The entire study population comprised 516 females (76.2%). RESULTS: Thyroid nodules (67.1%) and left ventricle diastolic dysfunction (LVDD) (58.1%) were the two most frequent findings in the overall cohort. In the multivariate regression model, BMI, heart rate, and HDL-cholesterol values were significant and independent predictors (p = 0.000 for all) of the presence of thyroid nodules. The presence of thyroid nodules is higher in females, particularly within the higher BMI groups [odds ratio (OR) = 1.048 (CI = 1.02-1.08) for BMI < 25, p = 0.003; OR = 1.094 (CI = 1.05-1.14) for BMI 25-29, p = 0.000; OR = 1.115 (CI = 1.05-1.19) for BMI ≥ 30]. This higher incidence is not observed in males. CONCLUSION: While the precise mechanisms underlying this association are yet to be fully elucidated, elevated HDL-cholesterol may serve as an indicator of thyroid nodules rather than a marker of cardiovascular protection.

Cancer Therapy-Related Pulmonary Hypertension: A Review of Mechanisms and Implications for Clinical Practice.

Cancer therapy-related pulmonary hypertension is a rare yet potentially fatal cardiotoxicity. However, it is a reversible cause of pulmonary hypertension if detected in its early stages. Cancer therapy-related pulmonary hypertension has been encountered in patients using tyrosine kinase inhibitors, particularly dasatinib. However, it is also well known that many agents used in cancer treatment such as alkylating agents, proteasome inhibitors, thoracic radiation exposure, and immune checkpoint inhibitors are particularly associated with pulmonary hypertension evolution. In case that history, symptoms, and clinical findings suggest a potential cancer therapy-related pulmonary hypertension, echocardiography is considered as the initial tool to detect pulmonary hypertension. If the possibility of pulmonary hypertension is high based on echocardiographic data, cancer treatment, as the initial step, should be discontinued due to its potential risks and other causes for pulmonary hypertension should be investigated thoroughly. Right heart catheterization should be the next step to establish the final diagnosis, and medical management, where appropriate, should be started without delay in these patients according to their pulmonary hypertension subgroup. There exists limited information regarding the diagnostic and management strategies of cancer therapy-related pulmonary hypertension in the current guidelines. In this review article, we aim to present current literature data on the mechanisms and management of cancer therapy-related pulmonary hypertension along with its follow-up algorithm in the setting of cardio-oncology practice.

Balloon Shaft Fracture: A Nightmare Scenario in the Setting of Percutaneous Coronary Intervention.

These images illustrate an attempt to pull back the balloon of an implanted proximal stent swiftly (before it was completely deflated) just following unplanned disengagement of the guiding catheter from the right coronary ostium. This maneuver resulted in abrupt balloon shaft fracture (outside the guiding catheter), leading to a freely swinging shaft appearance in the descending aorta. Unfortunately, several attempts to retrieve the swinging fragment of the shaft failed. Moreover, intracoronary snare technique in an effort to grasp the distal portion of the shaft also failed. Finally, the shaft fragment was surgically removed along with a bypass graft operation for the severely stenotic circumflex artery.

A Stent Misplaced in the Septal Perforating Artery: Right Ventricular Fistula, Interventricular Septal Hematoma, and Right Ventricular Outflow Tract Obstruction. / Um Stent Mal Colocado na Artéria Septal Perfurante: Fístula Ventricular Direita, Hematoma do Septo Interventricular e Obstrução da Via de Saída do Ventrículo Direito.

Coronary-cameral fistulas, though mostly regarded as congenital entities, have also been encountered as complications of major traumas and percutaneous coronary interventions (PCIs).1 On the other hand, interventricular septal (IVS) hematoma might potentially arise mostly during retrograde chronic total occlusion (CTO) interventions and has a benign course in this context.2 Herein, we describe a challenging PCI complication (and its management strategy) presenting with IVS hematoma, right ventricular fistula, and right ventricular outflow tract (RVOT) obstruction due to a misimplanted coronary stent in the septal perforating artery (SPA).

As fístulas coronário-camerais, embora consideradas em sua maioria como entidades congênitas, também têm sido encontradas como complicações de grandes traumas e intervenções coronárias percutâneas (ICPs).1 Por outro lado, o hematoma do septo interventricular (SIV) pode potencialmente surgir principalmente durante intervenções de oclusão total crônica retrógrada (OTC) e tem um curso benigno nesse contexto.2 Aqui, descrevemos uma complicação desafiadora da ICP (e sua estratégia de manejo) apresentando hematoma do SIV, fístula ventricular direita e obstrução da via de saída do ventrículo direito (VSVD) devido a um stent coronário mal implantado na artéria septal perfurante (ASP).

Impact of chronic total occlusion in a non-infarct-related coronary artery on contrast-associated nephropathy in acute ST-elevation myocardial infarction.

OBJECTIVES: Co-existing chronic total occlusion (CTO) in a non-infarct-related artery (IRA) might serve as an important trigger of adverse outcomes in ST-segment elevation myocardial infarction (STEMI). Therefore, we planned to analyse the potential impact of non-IRA CTO on the evolution of contrast-associated nephropathy (CAN) in STEMI patients managed with primary percutaneous coronary intervention (P-PCI). METHODS: A total of 537 subjects with STEMI undergoing P-PCI during the first 12 h after the onset of their symptoms were enrolled in this retrospective study. The subjects were categorised based on the angiographic presence of non-IRA CTO. Moreover, the subjects were also divided into 2 groups based on their CAN status following P-PCI (CAN (+) and CAN (-)). RESULTS: Co-existing non-IRA CTO was demonstrated in 86 subjects (16%). During the hospitalisation period, we identified 81 (15.1%) subjects with CAN. Subjects with non-IRA CTO had a significantly higher incidence of CAN compared with those without (56 [12.4%] vs 25 [29.1%], respectively, p < 0.001). In a logistic regression analysis, an existing non-IRA CTO (odds ratio: 2.840, 95%CI: 1.451-5.558, p = 0.002), as well as age, haemoglobin, diabetes mellitus, creatinine, and white blood cell count, were independent of predictors of CAN. CONCLUSION: In STEMI patients managed with P-PCI, a co-existing non-IRA CTO had an independent association with the evolution of CAN.