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Patients with heart failure and preserved ejection fraction may experience increased systemic vascular resistance, left ventricular afterload, and decreased left ventricular ejection fraction if their hemoglobin levels are elevated.3 Heart failure can arise from any structural or functional heart issue,4 potentially explaining the inverse relationship between hemoglobin levels and left ventricular ejection fraction observed in some studies.1 Atrial fibrillation is one of the most common clinically significant arrhythmias5 and is linked to higher ventricular rates and stress, increasing the risk of developing heart failure, known as tachyarrhythmia-induced cardiomyopathy. Left ventricular overload, transferred to the atria through the mitral valve,6 causes atrial stretch and fibrosis, resulting in atrial fibrillation in advanced stages of heart failure. [...]NT-proBNP is a better biomarker for atrial fibrillation than for heart failure in stable outpatients with cardiovascular risk factors. Authorship Contributions: Concept- N.G.K., V.M., A.C.; Design- N.G.K., V.M., A.C.; Data Collection or Processing- N.G.K., V.M., A.C.; Analysis or Interpretation- N.G.K., V.M., A.C.; Literature Search- N.G.K., V.M., A.C.; Writing- N.G.K., V.M., A.C. Conflict of Interest: No conflict of interest was declared by the authors.

The adrenaline, takotsubo, anaphylaxis, and Kounis (ATAK) complex constitutes a challenging contemporary clinicopharmacological combination of syndrome ATAK.1 “Αttacking” is needed to elucidate its etiology and pathophysiology and implement preventive and therapeutic measures. [...]coronary spasms through direct myocardial stunning can lead to Takotsubo syndrome (TS).2 During anaphylaxis, the released mediators can also initiate coronary spasms and again TS.3 Adrenaline administration as hemodynamic support during anaphylactic shock could also increase the plasma catecholamine levels and perpetuate this vicious cycle. Both α- (α1- and α2-) and β1-adrenergic receptors are present in the coronary arteries but with different distributions. [...]adrenaline may cause coronary vasoconstriction, reduce coronary blood flow, increase myocardial oxygen demand, worsen myocardial ischemia, and induce Kounis syndrome.9 Takotsubo (蛸 壺 in Japanese) Syndrome TS is referred to the medical literature with various names such as TS, stress-induced cardiomyopathy, takotsubo cardiomyopathy, apical ballooning syndrome, transient left ventricular apical ballooning, atypical apical ballooning, ampulla cardiomyopathy, broken heart syndrome, or transient left ventricular dysfunction syndrome. [...]stress from various causes can precipitate via an adrenaline surge, TS, and cardiac disease through a release of inflammatory mediators, and Kounis syndrome. [...]ATAK constitutes a challenging, contemporary, and novel syndrome. The measurement of some specific anaphylactic inflammatory mediators such as histamine, tryptase, chymase, leukotrienes, thromboxane, and platelet activating factor may help in diagnosing and treating the ATAK complex. [...]the use of corticosteroids or mast cell stabilizers for prevention and treatment may elucidate the etiology and pathophysiology of this complex.

Percutaneous Coronary Intervention (PCI) has advanced significantly with the incorporation of imaging and physiology assessment techniques. Fractional Flow Reserve (FFR) and Non-Hyperemic Pressure indices (NHPIs) provide information regarding the functional significance of coronary lesions, while Intravascular Ultrasound (IVUS) and Optical Coherence Tomography (OCT) enhance anatomical characterization and guide stent implantation. This review explores the implementation of physiology- and imaging-guided strategies in clinical practice, comparing their efficacy and limitations. Novel technologies now allow for physiology estimation without hyperemic agents, and hybrid techniques, such as OCT-derived FFR, are increasingly integrated into clinical practice. These approaches offer the combined advantages of functional assessment and detailed anatomical imaging.

Coronary angiography and percutaneous coronary intervention (PCI) procedural details in swine are similar to those performed to humans, since their heart and coronary anatomy closely resembles. However, only a few detailed descriptions of the procedure are available, containing notable differences. We present a feasible and reproducible protocol for percutaneous coronary interventions in porcine experimental models, utilizing ultrasound-guided femoral approach. Nine female pigs were studied to explore the feasibility of superficial femoral arterial (SFA) access for coronary angiography and provisional PCI, as well as the most suitable guiding coronary catheters and angiographic projections for the above interventions. Experiments were performed under general anesthesia, using ultrasound-guided puncture of the SFA to gain arterial access. The Amplatzer AR1 ® catheter, and the Right Coronary Bypass ® catheter were used for the selective engagement of the right and the left coronary artery, respectively. Successful arterial access and subsequent cardiac catheterization were performed in all pigs. Only one animal required a second puncture for femoral artery access. None of the 9 animals presented any significant tachycardia or hypotensive episode. One animal developed an access site-related complication following the first catheterization procedure. During follow-up, 100% success of SFA catheterization was achieved using the same ultrasound-guided technique. The ultrasound-guided superficial femoral artery access for coronary angiography and provisional interventions in porcine models is a quick and safe alternative to the carotid artery approach. The RCB and AR1 catheters may be the best choice for the quick and easy selective coronary engagement of the right and left ostia, respectively.

Mast cell degranulation and other interacting and linked cells, including T-lymphocytes, macrophages, eosinophils, and platelets, as well as a range of inflammatory mediators produced during an anaphylactic or allergic reaction, constitute the main causes of Kounis syndrome. Acute ischemia episodes, coronary spasm, atheromatous plaque erosion/rupture, and platelet activation can all be caused by histamine, tryptase, arachidonic acid derivatives, and chymase in the Kounis syndrome cascade. Kounis syndrome can be triggered by a variety of factors, including medications, hymenopteran stings, metals, foods, environmental exposures, illnesses, and immunizations. In addition, some unusual, rare, intriguing, and significant causes of Kounis syndrome have been discovered recently, namely the “kiss of death”, where human kissing and pet kissing can induce fatal Kounis syndrome. Moreover, the clinical conundrum is that several of the main drugs and substances used to treat myocardial infarction and Kounis syndrome, such as adrenaline (epinephrine), aspirin, atropine, clopidogrel, corticosteroids, heparins, protamine sulfate, and hirudotherapy can also initiate it. Therefore, physicians should be aware of this clinical discrepancy to prevent catastrophic consequences.

This narrative review explains the history of anaphylactic or hypersensitivity reactions, their connection to the cardiovascular system, and Kounis syndrome, which is linked to hypersensitivity. Additional subjects discussed include immunoglobulin E and serum tryptase, common pathways of allergic and nonallergic cardiovascular events, current perspectives on Kounis syndrome, allergic myocardial infarction, allergic angina, and the impact of COVID-19 and its vaccination on Kounis syndrome. Kounis syndrome is a distinct kind of acute vascular disease that affects the coronary, cerebral, mesenteric, peripheral, and venous systems. Kounis syndrome is currently used to describe coronary symptoms linked to disorders involving mast cell activation and inflammatory cell interactions, such as those involving T-lymphocytes and macrophages, which further induce allergic, hypersensitive, anaphylactic, or anaphylactic insults. Platelet activating factor, histamine, neutral proteases like tryptase and chymase, arachidonic acid products, and a range of cytokines and chemokines released during the activation process are among the inflammatory mediators that cause it. Proinflammatory cytokines are primarily produced by mast cells in COVID-19 infections. Mast cell-derived proteases and eosinophil-associated mediators are also more prevalent in the lung tissues and sera of COVID-19 patients. As a modern global threat to civilization, COVID-19 is linked to chemical patterns that can activate mast cells; therefore, allergic stimuli are usually the reason. Virus-associated molecular patterns can activate mast cells, but allergic triggers are typically the cause. By activating SARS-CoV-2 and other toll-like receptors, a variety of proinflammatory mediators, including IL-6 and IL-1β, are released, potentially contributing to the pathology of COVID-19.

Heart failure (HF) and atrial fibrillation (AF) are two cardiovascular (CV) entities that affect millions of individuals worldwide and their prevalence is translated into a significant impact on health care systems. The common pathophysiological pathways that these two share have created an important clinical interrelation, as the coexistence of HF and AF is associated with worse prognosis and treatment challenges. Renin-angiotensin-aldosterone system (RAAS), a critical mechanism in blood pressure (BP) control, was proved to be involved in the pathogenesis of both conditions contributing to their further coexistence. Successful control of BP is of great importance to the management of HF, crucial for the prevention of arrhythmiogenic substrates, while RAAS antagonists may possibly affect the development of new-onset AF as well. There are numerous studies that evaluated the effectiveness of RAAS blockade in AF/HF population and despite comparable or modest results, there is a well-established suggestion that RAAS blockers may contribute to a reduction of HF, CV events and recurrence of AF, along with their potential effective role in the new-onset AF prophylaxis. Angiotensin receptor blockers, according to the evidence, are more effective in that direction, followed by angiotensin converting enzyme inhibitors, whereas the data on aldosterone antagonists are not encouraging, yet do have the potential of significant CV disease modificators regardless of their effects on BP.