Ischemic hepatitis is an important

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Background: Transcatheter aortic valve implantation (TAVI) has become an established and increasingly used approach for management of severe symptomatic aortic stenosis, showing similar or even superior outcomes compared with standard surgical aortic valve replacement (SAVR). Stroke after TAVI is a relatively rare, but serious complication, associated with potential prolonged disability and increased mortality. Areas of Uncertainty: The overall incidence of 30-day stroke in TAVI patients is 3%–4%, but varies between different trials. Initial data suggested a higher risk of stroke after TAVI when compared with SAVR. The association between subclinical leaflet thrombosis and cerebral embolism, presented as stroke, transient ischemic accident, or silent cerebral ischemia is not entirely elucidated yet. Moreover, TAVI for severe bicuspid aortic stenosis is a relatively new issue, bicuspid anatomy being initially excluded from the pivotal clinical trials investigating TAVI procedure. Efficient stroke prevention strategies are under investigation. Data Sources: In the present manuscript, we used the available published data from the most relevant clinical trials, registries, and meta-analysis of patients from different risk categories who underwent TAVI or SAVR. Therapeutic Advances: Predictors of acute stroke are mainly procedure related. Technological development, improvements in bioprosthesis valve delivery catheters, and implantation technique may explain the decrease of stroke over the years since the beginning of TAVI procedures. Conclusions: The overall evidences confirm similar or lower rate of stroke in TAVI versus SAVR. Risk predictors for acute stroke after TAVI are generally related to procedural factors, whereas late stroke is mainly associated with patient characteristics, with a variable impact on cognitive function. The optimal choice for the antithrombotic treatment in TAVI for stroke prevention is yet to be determined. Current data do not support routine use of cerebral embolic protection devices during TAVI.

Advanced heart failure (AHF) is the stage of heart failure (HF) refractory to maximal medical treatment, cardiac devices (CRT - cardiac resynchronization, ICD - implantable defibrillator) and surgical treatment. AHF has become of interest through the experience and favorable results of treatment by mechanical circulatory support (MCS) and cardiac transplant (CT). The article reviews the criteria for defining the AHF (2018 ESC statement), natural history and prognosis outside the advanced treatment forms. Evaluation of risk and prognostic factors is required before the decision of advanced therapy: clinical factors (HF severity and reduction of cardiorespiratory functional capacity), RV function, biological markers and elements of organ dysfunction, as well as reduction of tolerance to conventional medication.Finally, the principles of treatment and the results of mechanical circulatory support and cardiac transplant are presented.

Cardiac amyloidosis (amyloid cardiomyopathy, CA) is an increasingly diagnosed condition which is most frequently seen in older patients with heart failure and preserved ejection fraction as well as in those with biventricular hypertrophies and tight aortic stenosis (AS). Almost 15% of patients with tight AS can also have CA ATTR, an element with diagnostic, prognostic and therapeutic significance.The CA diagnostic, associated with AS or not, is laborious and it should be made on the basis of determining the severity of the associated AS, depending on the case. The presence of both ventricular hypertrophy (≥15 mm) and red flags indicates a high suspicion of CA. Extra tests, bone scintigraphy and an absence of light free chains in blood or urine have a high specificity and sensitivity for diagnostic. Genetic investigations identify the senile or hereditary ATTR type.Pharmacologic treatment of CA with heart failure has some peculiarities, including stopping or careful usage of beta-blockers, non-dihydropyridine calcium blockers, and angiotensin system inhibitors. Diuretic treatment, which is almost always necessary, must preserve euvolemia.Replacing the aortic valves through transcatheter aortic valve replacement (TAVR) or surgical aortic valve replacement (SAVR) is recommended in tight AS associated with CA. The comparative results between the two methods of AVR favor TAVR, although perioperative complications are more frequent when the latter is used. Ongoing comparative studies of TAVR versus SAVR could define the options.Lately, pharmacological agents targeting CA ATTR can significantly change the management of ATTR amyloidosis.

Acute stroke (the first hours after its onset) is accompanied in over 70% of cases by rapid and significant increases in blood pressure, above normal values. The acute or reactive hypertensive response occurs both in patients with a history of hypertension and in normotensive patients. The greatly increased BP values, not controlled therapeutically, can be followed by the increase in the volume of the cerebral infarct and hemorrhagic transformation or the expansion of the hematoma and the increase in intracerebral pressure, respectively in ischemic or hemorrhagic stroke. This paper especially refers to the therapeutic control of hypertension in various situations (conditions): 1. Laboratory emergencies; 2. Hospital treatment with out thrombolytics or thrombolysis; 3. Endovascular treatment in acute stroke; 4. BP control in hemorrhagic stroke; 5. Continuation or discontinuation of antihypertensive treatment. The updated recommendations for the treatment of HTN in acute stroke result from clinical studies and recommendations of the recent ESO and AHA/ASA Guidelines.

The Stroke-Heart Syndrome is a major chapter in neurocardiology. Both brain-heart and stroke-heart correlations are based on neurophysiological studies that define and describe the relation between the central autonomic system and cardiac function and it will be presented in this narrative review. The Stroke-Heart syndrome groups the entire spectrum of cardiac changes - clinical, ECG, echocardiographic, biological, morphological – that occur in the first 30 days from the onset of stroke, especially in the first days. Their presence significantly marks the evolution and prognosis of stroke. The damage resulted from hypothalamus-pituitary-adrenal axis activation and high catecholamine release (adrenergic storm) targets mainly the myocyte and the microcirculation.The Takotsubo Syndrome and Stunned myocardium are distinct forms of neurogenic myocardial ischemia - with changes in ECG, parietal motility, and biological markers - usually reversible although evolution towards cardiac dysfunction is also possible. The concept of Stroke-Heart syndrome and the brain-heart correlation brought new scientific information regarding stress cardiomyopathy or neurogenic myocardial injury.

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