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IntroductionHeart failure (HF) with reduced ejection fraction (HFrEF) remains a challenging problem due to its high mortality rate. The PARADIGM HF trial and a new class of drugs – angiotensin receptor–neprilysin inhibitors (ARNIs) – managed to change the current perception of HF treatment by reducing cardiovascular mortality and morbidity as well as HF hospitalizations compared with enalapril and have emerged as an evidence-based therapy for HFrEF. Another novelty in HF therapy is dapagliflozin, a sodium-glucose transporter-2 inhibitor (SGLT2i) which decreased the rates of cardiac death and worsening of HF in the DAPA-HF trial, when added in other guideline recommended therapy. A recent study evaluated the potency of dapagliflozin in terms of mortality and deterioration of HF, in patients taking sacubitril/valsartan and in patients who were naive.Material and methodsA prospective cohort study of 30 symptomatic HF patients with EF < 35% (aged 65 ±10 years) was conducted. Diabetic (2TDM) patients of NYHA status II–III, previously treated with ARNI, -blocker, and mineralocorticoid receptor antagonists (MRA) were included. Dapagliflozin was added to their therapy.ResultsEchocardiographic evaluation revealed improvement of both conventional tissue Doppler and diastolic strain parameters by dapagliflozin addition on HF therapy.ConclusionsDapagliflozin impact on diastolic function may explain the symptom amelioration and the improvement of quality of life. And more specifically, the ratio of early diastolic transmitral flow velocity to global strain rate at the early filling phase of diastole (E/SRE)may be considered a reliable index of HF therapy responders.

The assumption that light cigarette smoking, meaning smoking one to five cigarettes per day, is not so harmful has been dissipated by several studies. Regardless of the quantity of tobacco cigarettes, smoking remains a leading risk factor for the development and progression of cardiovascular diseases. Smoke is a mixture of several toxic chemicals, such as nicotine, carbon monoxide, and oxidants, implicated in the pathogenesis of cardiovascular and pulmonary diseases. Despite anti-smoking campaigns, a misconception concerning “safe smoking” still exists. The purpose of this literature review is to highlight the deleterious effect of light cigarette smoking and claim the consensus that there is no safe smoking.

The Hellenic Heart Failure Association has undertaken the initiative to develop a national network of heart failure clinics (HFCs) and cardio‐oncology clinics (COCs). We conducted two questionnaire surveys among these clinics within 17 months and another during the coronavirus disease 2019 outbreak to assess adjustments of the developing network to the pandemic. Out of 68 HFCs comprising the network, 52 participated in the first survey and 55 in the second survey. The median number of patients assessed per week is 10. Changes in engaged personnel were encountered between the two surveys, along with increasing use of advanced echocardiographic techniques (23.1% in 2018 vs. 34.5% in 2020). Drawbacks were encountered, concerning magnetic resonance imaging and ergospirometry use (being available in 14.6% and 29% of HFCs, respectively), exercise rehabilitation programmes (applied only in 5.5%), and telemedicine applications (used in 16.4%). There are 13 COCs in the country with nine of them in the capital region; the median number of patients being assessed per week is 10. Platforms for virtual consultations and video calls are used in 38.5%. Coronavirus disease 2019 outbreak affected provision of HFC services dramatically as only 18.5% continued to function regularly, imposing hurdles that need to be addressed, at least temporarily, possibly by alternative methods of follow‐up such as remote consultation. The function of COCs, in contrast, seemed to be much less affected during the pandemic (77% of them continued to follow up their patients). This staged, survey‐based procedure may serve as a blueprint to help building national HFC/COC networks and provides the means to address changes during healthcare crises.

The blood–brain barrier (BBB) constitutes the complex anatomic and physiologic interface between the intravascular compartment and the central nervous system, and its integrity is paramount for the maintenance of the very sensitive homeostasis of the central nervous system. Arterial hypertension is a leading cause of morbidity and mortality. The BBB has been shown to be disrupted in essential hypertension. BBB integrity is important for central autonomic control and this may be implicated in the pathophysiology of hypertension. On the other hand, evidence from experimental studies indicates that BBB disruption can be present in both hypertensive disease and dementia syndromes, suggesting a possibly key position of loss of BBB integrity in the pathophysiological pathways linking arterial hypertension with cognitive decline. Although much still remains to be elucidated with respect to the exact underlying mechanisms, the discovery of novel pathological pathways has changed our understanding of adult dementia and central nervous system disease overall, pointing out—in parallel—new potential therapeutic targets. The aim of this review is to summarize current scientific knowledge relevant to the pathophysiologic pathways that are involved in the disruption of the BBB function and potentially mediate hypertension-induced cognitive impairment. In parallel, we underline the differential cognition-preserving effect of several antihypertensive agents of similar blood pressure-lowering capacity, highlighting the presence of previously under-recognized BBB-protective actions of these drugs.

Abstract: Diabetes mellitus type 1 (T1DM) is an autoimmune disease characterized by a markedly elevated cardiovascular (CV) risk due to premature atherosclerosis. Previous studies have shown that intense glycemic control reduces the incidence of CV disease. Antiplatelet therapy is considered to be a very important therapy for secondary prevention of recurrent atherothrombotic events in patients with DM, while it may be considered for primary prevention in individuals with T1DM with additional CV risk factors. The aim of the present review is to summarize existing literature data regarding the thrombotic risk in T1DM patients and discuss current treatment strategies.

In recent years, the Angiotensin-(1-7)/Mas receptor [Ang-(1-7)/Mas] sub-branch of the Renin-Angiotensin System (RAS) in the brain, and Angiotensin Type 2 Receptors (AT2R), have attracted scientific interest, as there is evidence that they constitute an essential pathway in cardiovascular regulation, in health and in disease. By acting centrally, the Ang-(1-7)/Mas axis - that has been termed ‘the axis of good’- can exert blood pressure-lowering effects, while also favourably altering baroreflex sensitivity and noradrenergic neurotransmission. Thus, research has focused on the possible neuro- and cardioprotective effects of this pathway in the setting of cardiovascular disease, ultimately aiming to evaluate the potential for development of novel therapeutic strategies based on its modulation. : We summarize the available evidence from experimental studies in this context, aiming to assess current limits of scientific knowledge relevant to this newly-described ‘player’ in haemodynamic regulation, that may become a potential therapeutic target.

Heart failure (HF) is rapidly growing, conferring considerable mortality, morbidity, and costs. Dedicated HF clinics improve patient outcomes, and the development of a national HF clinics network aims at addressing this need at national level. Such a network should respect the existing health care infrastructures, and according to the capacities of hosting facilities, it can be organized into three levels. Establishing the continuous communication and interaction among the components of the network is crucial, while supportive actions that can enhance its efficiency include involvement of multidisciplinary health care professionals, use of structured HF‐specific documents, such as discharge notes, patient information leaflets, and patient booklets, and implementation of an HF‐specific electronic health care record and database platform.

Introduction Acute cholecystitis and biliary colic may have signs and symptoms similar to those of Acute Coronary Syndrome(ACS) along with ischemic ECG changes. Cholecystitis and/or biliary colic have been both reported as trigger factors for bradyarrhythmia in the literature. Case Report A 78-year-old male patient was admitted to our Emergency Department (ED) due to acute abdominal pain. The ECG on admission showed sinus bradycardia with a rate of 40 beats per minute (bpm) without signs of acute ischemia and a brief period (7 s) of complete atrioventricular (AV) block. He was initially treated with analgesics. After the remission of the pain, a subsequent ECG was performed which showed sinus bradycardia of 55 bpm. The AV block terminated one hour after the patient's admission. The patient remained hemodynamically stable during the episode. He underwent an ultrasound of the abdomen in the ED which revealed sludge and one stone in the gallbladder without signs of inflammation. Laboratory test results for D-dimer and troponin were negative, while the coronary angiography showed coronary vessels without significant lesions. Conclusion Biliary colic can cause severe reversible reflex bradycardia (Cope's Sign), even complete heart block. Pain relief is very important in the management of such cases.

The blood-brain barrier (BBB) constitutes the complex anatomic and physiologic interface between the intravascular compartment and the central nervous system, and its integrity is paramount for the maintenance of the very sensitive homeostasis of the central nervous system. Arterial hypertension is a leading cause of morbidity and mortality. The BBB has been shown to be disrupted in essential hypertension. BBB integrity is important for central autonomic control and this may be implicated in the pathophysiology of hypertension. On the other hand, evidence from experimental studies indicates that BBB disruption can be present in both hypertensive disease and dementia syndromes, suggesting a possibly key position of loss of BBB integrity in the pathophysiological pathways linking arterial hypertension with cognitive decline. Although much still remains to be elucidated with respect to the exact underlying mechanisms, the discovery of novel pathological pathways has changed our understanding of adult dementia and central nervous system disease overall, pointing out-in parallel-new potential therapeutic targets. The aim of this review is to summarize current scientific knowledge relevant to the pathophysiologic pathways that are involved in the disruption of the BBB function and potentially mediate hypertension-induced cognitive impairment. In parallel, we underline the differential cognition-preserving effect of several antihypertensive agents of similar blood pressure-lowering capacity, highlighting the presence of previously under-recognized BBB-protective actions of these drugs.

Current national and international guidelines, including those of the European Society of Cardiology, recognize that the assessment of prognosis should be a part of the standard management for patients with chronic heart failure (CHF). However, these same guidelines recognize the inherent difficulty of this process. A variety of factors contribute to this difficulty, including the varying etiology, frequent co-morbidity and, perhaps most importantly, huge inter-individual variability in the disease progression and outcome. Although CHF is chronic, it is also a condition in which significant proportions of patients experience apparently ‘sudden’ death, which almost certainly contributes to our difficulty in assessing individual patient prognosis. A useful tool for the risk stratification of heart failure patients is dobutamine stress echocardiography (DSE), which determines the myocardial viability in ischemic cardiomyopathy and myocardial contractile reserve in idiopathic cardiomyopathy.

We describe the case of a 45-year-old female patient with coronary fistulas arising from both the left and right coronary artery system and emptying in the left ventricle. Only sporadically do coronary artery fistulas drain into the left ventricle. In our patient, the most likely explanation of the fistulous communications was a congenital cause. We review the literature on coronary cameral fistulas and discuss the etiology of the diagnostic findings. Small coronary artery fistulas are generally well-tolerated and should impose no significant restriction on daily routine and activities. Nevertheless, small fistulas may under certain conditions produce a "steal" phenomenon and shunt blood flow away from the myocardial capillary network, causing ischemia.

Acute coronary syndromes secondary to allergy-induced coronary vasospasm are known as “Kounis syndrome.” The main pathophysiological mechanism of coronary spasm in Kounis syndrome is the release of inflammatory mediators during a hypersensitivity reaction triggered by food, insect bites, or drugs. Here, we report a case of an acute coronary syndrome secondary to allergic reaction following levofloxacin administration in a 68-year-old female without a prior history of coronary artery disease. Our patient's coronary angiography revealed moderate lesions in the coronary vasculature and she was diagnosed as having a type II variant Kounis syndrome. Type II variant includes patients in whom the acute release of inflammatory mediators due to mast cell degranulation such as histamine, serotonin, and leukotrienes can induce either coronary artery spasm with normal cardiac enzymes and troponins or plaque erosion or rupture manifesting as acute myocardial infarction. According to our knowledge, this is the first case report of Kounis syndrome attributed to levofloxacin administration.