Risk of Stroke After Transcatheter Aortic Valve Implantation: Epidemiology, Mechanism, and Management.

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.

New Advanced Imaging Parameters and Biomarkers-A Step Forward in the Diagnosis and Prognosis of TTR Cardiomyopathy.

Transthyretin amyloid cardiomyopathy (ATTR-CM) is an infiltrative disorder characterized by extracellular myocardial deposits of amyloid fibrils, with poor outcome, leading to heart failure and death, with significant treatment expenditure. In the era of a novel therapeutic arsenal of disease-modifying agents that target a myriad of pathophysiological mechanisms, timely and accurate diagnosis of ATTR-CM is crucial. Recent advances in therapeutic strategies shown to be most beneficial in the early stages of the disease have determined a paradigm shift in the screening, diagnostic algorithm, and risk classification of patients with ATTR-CM. The aim of this review is to explore the utility of novel specific non-invasive imaging parameters and biomarkers from screening to diagnosis, prognosis, risk stratification, and monitoring of the response to therapy. We will summarize the knowledge of the most recent advances in diagnostic, prognostic, and treatment tailoring parameters for early recognition, prediction of outcome, and better selection of therapeutic candidates in ATTR-CM. Moreover, we will provide input from different potential pathways involved in the pathophysiology of ATTR-CM, on top of the amyloid deposition, such as inflammation, endothelial dysfunction, reduced nitric oxide bioavailability, oxidative stress, and myocardial fibrosis, and their diagnostic, prognostic, and therapeutic implications.

Cumulative impact of cardiovascular risk factors on regional left ventricular function and reserve: progressive long-axis dysfunction with compensatory radial changes.

BACKGROUND: The risk factors that contribute to atherosclerosis also predict clinical heart failure, but it is unclear how they affect myocardial function. Aims were to assess if major cardiovascular risk factors cause subclinical myocardial dysfunction in asymptomatic subjects. METHODS: We measured regional left ventricular (LV) function at rest and during dobutamine stress echocardiography in 246 subjects (54 ± 12 years, 54% men) analyzed in five groups according to the presence of six risk factors (diabetes, hypertension, obesity, dyslipidemia, smoking, and family history; age was similar in the five groups). LV longitudinal function was assessed from the mean velocities of four basal segments, and radial function from the velocities of the basal posterior wall. RESULTS: Risk factors did not affect LV ejection fraction, but longitudinal systolic velocity decreased progressively with the number of risk factors, at rest (6.8 ± 1.3 vs. 6.2 ± 1.6 vs. 5.8 ± 1.5 vs. 5.4 ± 1.3 vs. 5.3 ± 1.3 cm/sec, for the five groups, respectively) and at peak stress (14.3 ± 3.3 vs. 12.9 ± 3.2 vs. 11.8 ± 3.4 vs. 11.3 ± 2.6 vs. 11.1 ± 2.3 cm/sec) (both P < 0.0001). Radial systolic velocity increased according to the number of risk factors (P < 0.01). By multivariate regression, determinants of reduced longitudinal systolic velocity at rest were body mass index, diastolic blood pressure, age, and fasting plasma glucose (r = 0.57, r(2) = 0.32, P < 0.0001). CONCLUSION: Asymptomatic subjects have impaired LV long-axis function at rest and during stress, according to their number of major cardiovascular risk factors. Global LV systolic function is maintained by compensatory increases in radial function. These changes provide new targets for preclinical diagnosis and for monitoring responses to preventive strategies.

Ischemic Hepatitis - Intercorrelated Pathology.

Ischemic hepatitis is an important, yet underdiagnosed pathological condition seen in either cardiology or hepatology clinics or intensive care units. The main causes are severe heart failure, circulatory and septic shock. Close monitoring of biological tests (AST, ALT, LDH) together with hemodynamic parameters (blood pressure, cardiac output and central venous pressure) allow for rapid and accurate diagnosis. Correction of hemodynamic parameters, hypoxemia, hepatic and/or renal dysfunction leads to a more favorable outcome of these patients.

New Echocardiographic Protocol for the Assessment of Experimental Myocardial Infarction in Rats.

BACKGROUND: The rat infarct model was used extensively to study the pathophysiology of myocardial infarction and to evaluate different therapies. Transthoracic echocardiography is used in rats in order to assess cardiac anatomy and function, being a safe and reliable non-invasive technique. However, studies combining conventional with new echo techniques, such as tissue Doppler imaging (TDI) and speckletracking echocardiography (STE), are lacking. OBJECTIVES: To validate a protocol using the available conventional and new echocardiographic techniques (TDI and STE) for a comprehensive assessment of cardiac remodelling and function, after myocardial infarction in rats. METHODS: Ten Wistar (W) and five Sprague Dawley (SD) male rats (aged 21±2 weeks, mean weight 355±43 g) were evaluated by echocardiography, before and 24 hours post-ligation of the left coronary artery, with previous anaesthesia. Left ventricular (LV) structure was assessed by end-diastolic and endsystolic anterior wall thickness and LV diameters (from the SAX view), while LV function by fractional shortening (FS) and ejection fraction (EF) (by area-length formula), septal mitral annular plane systolic excursion (MAPSE), cardiac output (CO), myocardial performance index (MPI), septal mitral annular systolic velocity (S', by TDI), and global circumferential and radial systolic strain (GCS, GRS) and strain rate (GCSr, GRSr) by STE, from the SAX view at the level of papillary muscles. RESULTS: Feasibility of measuring the above mentioned parameters was 100%. Twenty-four hours after myocardial infarction, rats had lower heart rate (373±44 vs. 351±32 bpm, p<0.05) and thinner LV anterior wall, while LV diameters and volumes were significantly higher. FS (54±7 vs. 33±9%), EF (72±9vs. 47±10%), septal MAPSE (2.02±0.17 vs. 1.44±0.22 mm), CO (76±15 vs. 48±12 ml/min), MPI (0.33±0.11 vs. 0.50±0.14), S' (5.58±1.20 vs. 3.84±1.06 cm/s), and LV strain and strain rate (GCS: -23.52±2.44 vs. -13.33±1.51% and GRS: 50.45±13.11 vs. 17.27±5.2%, GCSr: -8.42±0.85 vs. -4.68±0.53; and GRSr: 11.93±2.39 vs. 4.89±1.18 1/s) were significantly lower, all p<0.01. CONCLUSIONS: Our echocardiographic protocol of experimental myocardial infarction in rats is feasible. The impact of myocardial infarction in rats could be more extensively assessed using a comprehensive echocardiographic protocol of conventional and specific myocardial parameters, measured by TDI and STE, in order to quantify better the LV structure and function. Therefore, we suggest that this protocol may be used in order to assess the effect of different regenerative therapies in experimental myocardial infarction in rats.