Evidence of Myocardial Edema in Obstructive Tako-tsubo Cardiomyopathy Complicated by Cardiogenic Shock

the contemporary presence of left ventricular (LV) outflow tract obstruction, systolic anterior motion of the anterior mitral leaflet, and acute mitral regurgitation may occur in t ako-tsubo cardiomyopathy. Although myocardial edema has been reported in patients with tako-tsubo cardiomyopathy, to the best of our knowledge it has never been described in the setting of LV outflow obstruction and the presence of cardiogenic shock. We report the case of a 65-year-old woman who developed t ako-tsubo cardiomyopathy followed by acute cardiogenic shock. the echo-Doppler assessment revealed LV apical ballooning, moderate-to-severe mitral regurgitation, and an estimated peak systolic pressure gradient at LV outflow tract of 64 mmHg. the LV outflow obstruction and mitral regurgitation resolved shortly after the intravenous administration of atenolol (1.25 mg). the cardiogenic shock was completely resolved following the infusion of low-dose dobutamine: 2 γ/kg/min. In the following days, an echo-Doppler examination revealed a marked reduction in the thickness of the LV proximal hypertrophied septum (from 20 mm to 14 mm), while a cardiac magnetic resonance imaging study showed signs of mild edema of the mid-ventricular and apical septum

Researches regarding the analysis of the factors that influence the embryogenesis in microspore cultures of Brassica napus

In order to develop an efficient technique of microspore culture for oilseed rape, we studied the influence of the developmental stage of floral buds on the embryogenesis potential of in vitro culture of microspores. We observed that the floral buds size may be a good indicator of the microspores developmental stage. For this purpose we determined the mean number of nucleus per microspore in five genotypes of Brassica napus at different developmental stages of floral buds. This index was correlated with the microspores embryogenesis capacity cultivated on MS medium supplemented with 1 mg/l 2.4D and 1 mg/l BAP

The role of natriuretic peptides and echocardiography in the management and follow up of patients with chronic heart failure

Background. The concept of echo and natriuretic peptide (NP) guided therapy is appealing since currently there is no objective guide to optimal dosing of therapy and loop diuretics in particular in patients with chronic heart failure (CHF). Aim. To assess whether echo and NP guided therapy may be useful for the management of patients with CHF due to left ventricular systolic dysfunction. Materials and methods. We retrospectively analyzed the multicentric individual data of 414 patients with CHF with reduced ejection fraction; during ambulatory follow-up, the therapy (including loop diuretics) was titrated according to the presence of echocardiographic signs of elevated left ventricular filling pressures and NP serum levels. Mortality rate, changes in renal function, NP levels, cardiac function and medication doses were analyzed. Results. The median follow-up duration was 1030 days. The mortality rate was 3,7% per year. During the observation period, the dose of loop diuretics increased by 20%. An increase of ≥ 0.3 mg/dL in serum creatinine was reported in 15% of the patients. Newly diagnosed renal dysfunction (eGFR <60 ml/min/1.73m2) occurred in 10% of patients. There was a significant decrease in NP levels and an improvement in LV filling pressures and systolic function. Regarding other therapies, significantly more patients were using beta blockers at follow up and the doses were increased. Non significant changes in the percentage of patients treated and in the medication dose was noted for Angiotensin Converting Enzyme Inhibitors/ Angiotensin Type 1 Receptor Blockers (ACEi/ARB) and for Mineralocorticoid Receptor Antagonists (MRA). Conclusion. Our study suggests that the outcome of patients with CHF might be improved by the integrative use of clinical examination, biochemical and echocardiographic parameters. These effects are likely to be mediated by an appropriate use of loop diuretics and kidney function preservation

Evidence of Myocardial Edema in Obstructive Tako-tsubo Cardiomyopathy Complicated by Cardiogenic Shock

The contemporary presence of left ventricular (LV) outflow tract obstruction, systolic anterior motion of the anterior mitral leaflet, and acute mitral regurgitation may occur in Tako-tsubo cardiomyopathy. Although myocardial edema has been reported in patients with Tako-tsubo cardiomyopathy, to the best of our knowledge it has never been described in the setting of LV outflow obstruction and the presence of cardiogenic shock. We report the case of a 65-year-old woman who developed Tako-tsubo cardiomyopathy followed by acute cardiogenic shock. The echo-Doppler assessment revealed LV apical ballooning, moderate-to-severe mitral regurgitation, and an estimated peak systolic pressure gradient at LV outflow tract of 64 mmHg. The LV outflow obstruction and mitral regurgitation resolved shortly after the intravenous administration of atenolol (1.25 mg). The cardiogenic shock was completely resolved following the infusion of low-dose dobutamine: 2 γ/kg/min. In the following days, an echo-Doppler examination revealed a marked reduction in the thickness of the LV proximal hypertrophied septum (from 20 mm to 14 mm), while a cardiac magnetic resonance imaging study showed signs of mild edema of the mid-ventricular and apical septum

Evidence of Myocardial Edema in Obstructive Tako-tsubo Cardiomyopathy Complicated by Cardiogenic Shock

the contemporary presence of left ventricular (LV) outflow tract obstruction, systolic anterior motion of the anterior mitral leaflet, and acute mitral regurgitation may occur in t ako-tsubo cardiomyopathy. Although myocardial edema has been reported in patients with tako-tsubo cardiomyopathy, to the best of our knowledge it has never been described in the setting of LV outflow obstruction and the presence of cardiogenic shock. We report the case of a 65-year-old woman who developed t ako-tsubo cardiomyopathy followed by acute cardiogenic shock. the echo-Doppler assessment revealed LV apical ballooning, moderate-to-severe mitral regurgitation, and an estimated peak systolic pressure gradient at LV outflow tract of 64 mmHg. the LV outflow obstruction and mitral regurgitation resolved shortly after the intravenous administration of atenolol (1.25 mg). the cardiogenic shock was completely resolved following the infusion of low-dose dobutamine: 2 γ/kg/min. In the following days, an echo-Doppler examination revealed a marked reduction in the thickness of the LV proximal hypertrophied septum (from 20 mm to 14 mm), while a cardiac magnetic resonance imaging study showed signs of mild edema of the mid-ventricular and apical septum

The potential value of integrated natriuretic peptide and echo-guided heart failure management

There is increasing interest in guiding Heart Failure (HF) therapy with Brain Natriuretic Peptide (BNP) or N-terminal prohormone of Brain Natriuretic Peptide (NT-proBNP), with the goal of lowering concentrations of these markers (and maintaining their suppression) as part of the therapeutic approach in HF. However, recent European Society of Cardiology (ESC) and American Heart Association/American College of Cardiology (AHA/ACC) guidelines did not recommend biomarker-guided therapy in the management of HF patients. This has likely to do with the conceptual, methodological, and practical limitations of the Natriuretic Peptides (NP)-based approach, including biological variability, slow time-course, poor specificity, cost and venipuncture, as well as to the lack of conclusive scientific evidence after 15 years of intensive scientific work and industry investment in the field. An increase in NP can be associated with accumulation of extra-vascular lung water, which is a sign of impending acute heart failure. If this is the case, an higher dose of loop diuretics will improve symptoms. However, if no lung congestion is present, diuretics will show no benefit and even harm. It is only a combined clinical, bio-humoral (for instance with evaluation of renal function) and echocardiographic assessment which may unmask the pathophysiological (and possibly therapeutic) heterogeneity underlying the same clinical and NP picture. Increase in B-lines will trigger increase of loop diuretics (or dialysis); the marked increase in mitral insufficiency (at baseline or during exercise) will lead to increase in vasodilators and to consider mitral valve repair; the presence of substantial inotropic reserve during stress will give a substantially higher chance of benefit to beta-blocker or Cardiac Resynchronization Therapy (CRT). To each patient its own therapy, not with a "blind date" with symptoms and NP and carpet bombing with drugs, but with an open-eye targeted approach on the mechanism predominant in that individual patient. A monocular, specialistic, unidimensional approach to HF can miss its pathogenetic and clinical complexity, which only can be overcome with an integrated, versatile and tailored approach

Asymmetrical myocardial expression of natriuretic peptides in pacing-induced heart failure.

High-frequency pacing of the left ventricle (LV) free wall causes a dyssynchronous pattern of contraction that leads to progressive heart failure (HF) with pronounced differences in regional contractility. Aim of this study was to evaluate possible changes in brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) mRNA expression in the anterior/anterior lateral region (pacing site, PS) as compared to the infero-septal region (opposite site, OS) and to explore possible association between the contractiling pattern and biomarker expression. Cardiac tissue was collected from minipigs with pacing-induced HF (n=8) and without (control, n=6). The samples were selectively harvested from the anterior left ventricular (LV) wall, PS, and from an area remote to the pacing-site, OS. BNP and CNP mRNA expression was evaluated by semi-quantitative polymerase chain reaction (PCR). A significant difference in BNP expression was found in the PS between HF animals and controls (BNP/GAPDH: 0.65+/-0.11 vs. 0.35+/-0.04, p=0.02), but not in the OS (BNP/GAPDH: 0.36+/-0.05, ns vs. controls). CNP expression was not different compared to controls, although higher levels were observed in the PS and in the OS with respect to the controls (CNP/GAPDH: controls 0.089+/-0.036, PS 0.289+/-0.23, OS 0.54+/-0.16). This finding was in tune with an increase of CNP tissue concentration (controls: 0.69+/-0.13; PS=1.56+/-0.19; OS=1.70+/-0.42 pg/mg protein; p=0.039 controls vs. OS). Higher BNP mRNA expression in the PS is consistent with a reduction in contractile function in this region, while higher CNP mRNA expression in the OS suggests the presence of concomitant endothelial dysfunction in the remote region