Prophylaxis for infective endocarditis - an endless story with a colorful past, an uncertain presence and unclear future.

Opinions on the prevention of infective endocarditis (IE) have significantly changed in recent years. A gradual departure from antibiotic prophylaxis can be observed, both in terms of the spectrum of procedures and the profile of individuals in whom it is indicated. The extreme case is the rejection of all antibiotic prophylaxis in all patients and for all procedures in some countries. Concise conclusions are primarily provided by European recommendations. Patients at the highest risk are currently recommended for prophylaxis; this in particular concerns valvular prostheses, some complex congenital heart defects, sewn palliative shunts, conduits or prostheses, and conditions after IE. Prophylaxis should be administered before dental procedures involving manipulation of the gums and before implantation of pacemakers and similar devices (Implantable Cardioverter Defibrillator - ICD). Prophylaxis is administered with 2 grams of amoxicillin or ampicillin given within 30-60 min before the procedure, in case of penicillin allergy clindamycin is recommended, before implantation of pacemakers or ICD are given first-generation cephalosporins or vancomycin. Proper oral hygiene and regular dental checkups should be the basic rule for at-risk patients as well as strictly sterile performance of all risk involving interventions.

[Thoughts about valvular abnormalities yesterday and today]. / Zamyslení nad chlopenními vadami vcera a dnes.

The article deals with the problems of acquired valvular disorders. It mainly focuses on the new findings regarding ethiopathogenesis, diagnostics, evaluation and treatment, especially catheterization. In advanced countries, post-rheumatic abnormalities have almost disappeared, their current etiology has substantially changed (mitral stenosis). The earlier relatively rare degenerative changes now predominate, mainly affecting older patients (aortic stenosis). Also the treatment methods for acquired abnormalities have substantially changed - currently catheterization approaches are used more frequently in their correction.Key words: aortic regurgitation - aortic stenosis - echocardiography for valvular abnormalities - magnetic resonance abnormalities - mitral regurgitation - mitral stenosis - valve replacement.

Variants in miRNA regulating cardiac growth are not a common cause of hypertrophic cardiomyopathy.

OBJECTIVES: A substantial proportion of patients with hypertrophic cardiomyopathy (HCM) do not have causative mutations in the genes for heart sarcomere. The purpose of this study was to evaluate the association between microRNA (miRNA) sequence variants and HCM. METHODS: We performed genetic testing on 56 HCM patients who had previously been found to be negative for mutations in the 4 major genes for sarcomeric proteins. The coding and adjacent regions (120-220 nt) of selected miRNAs were analyzed for the presence of sequence variants. The testing was based on PCR amplification of DNA-encoding miRNAs and subsequent denaturing capillary electrophoresis. RESULTS: A total of 3 different variants were detected in the 11 selected miRNAs. These included polymorphisms rs45489294 in miRNA 208b, rs13136737 in miRNA 367 and rs9989532 in miRNA 1-2. In the patient group, the most frequent polymorphism was in miRNA 208b (10 times) followed by miRNA 367 (7 times). Both polymorphisms were found to occur with similar frequencies in the group of healthy controls. The remaining detected variant was not present in the control group, but was not connected with the HCM phenotype in the children of the probands. CONCLUSION: Sequence variants in miRNAs of patients with HCM are not frequent and the contribution of these variants to the development of this disease was not demonstrated.

[Mitral stenosis]. / Mitrální stenóza.

This paper deals with mitral stenosis in the light of current knowledge. Currently, defect is in developed countries very rare (about 10% of defects). Its etiology has changed over the period of time mainly due to decline in rheumatic fever. Review discusses clinical, echocardiographic and catheterization findings, as well as treatment and prognosis.

Comparison of long-term effect of dual-chamber pacing and alcohol septal ablation in patients with hypertrophic obstructive cardiomyopathy.

INTRODUCTION: Nonpharmacological treatment of patients with hypertrophic obstructive cardiomyopathy (HOCM) comprises surgical myectomy (SME), alcohol septal ablation (ASA), and dual-chamber (DDD) pacing. The aim of the study was to compare the long-term effect of DDD pacing and ASA in symptomatic HOCM patients. PATIENTS AND METHODS: We evaluated retrospective data from three cardiocenters; there were 24 patients treated with DDD pacing included and 52 treated with ASA followed for 101 ± 49 and 87 ± 23 months, respectively. RESULTS: In the group treated with DDD pacing, the left ventricle outflow tract gradient (LVOTG) decreased from 82 ± 44 mmHg to 21 ± 21 mmHg, and NYHA class improved from 2.7 ± 0.5 to 2.1 ± 0.6 (both P < 0.001). In the ASA-treated group, a decline in LVOTG from 73 ± 38 mmHg to 24 ± 26 mmHg and reduction in NYHA class from 2.8 ± 0.5 to 1.7 ± 0.8 were observed (both P < 0.001). The LVOTG change was similar in both groups (P = 0.264), and symptoms were more affected by ASA (P = 0.001). CONCLUSION: ASA and DDD pacing were similarly effective in reducing LVOTG. The symptoms improvement was more expressed in patients treated with ASA.

Spectrum and clinical manifestations of mutations in genes responsible for hypertrophic cardiomyopathy.

INTRODUCTION: Hypertrophic cardiomyopathy (HCM) is a cardiovascular disease with autosomal dominant inheritance. It is caused by mutations in the genes coding for structural and/or regulatory proteins found in the sarcomere of cardiomyocytes. A group of genes, including the heavy chain of beta-myosin (MYH7), myosin binding protein C (MYBPC3), cardiac troponin I (TNNI3) and cardiac troponin T (TNNT2) are frequently affected by causal mutations. While exact mutation frequency data has been obtained for various populations, no screening has been reported for Central European populations. PATIENTS AND METHODS: We performed a complete sequencing of MYH7, MYBPC3, TNNI3 and TNNT2 genes in 100 HCM patients. RESULTS: We discovered mutations in a total of 40 patients (40%), including 4 patients with double mutations. A total of 35 different mutation types were detected, of which 17 were novel. The contributions from individual genes were: 24 mutations in MYBPC3 (54.5%), 14 in MYH7 (31.8%), 4 in TNNI3 (9%) and 2 mutations in TNNT2 (4.5%). We have observed a wide variability in disease manifestation across the different genes/mutation types. In addition, we have discovered differences in both frequency and distribution of mutations of the two most common genes (MYBPC3 and MYH7) compared to other populations. CONCLUSION: The most common gene responsible for HCM in our study population was MYBPC3, followed by MYH7, TNNI3 and TNNT2. Phenotypic heterogeneity, as well as the dissimilarity to other populations, prevents effective use of a pre-screening test, which would be directed at the most common mutation hotspots, in our population.

The effects of candesartan on left ventricular hypertrophy and function in nonobstructive hypertrophic cardiomyopathy: a pilot, randomized study.

Hypertrophic cardiomyopathy is caused by mutations in the genes that encode sarcomeric proteins and is primarily characterized by unexplained left ventricular hypertrophy, impaired cardiac function, reduced exercise tolerance, and a relatively high incidence of sudden cardiac death, especially in the young. The extent of left ventricular hypertrophy is one of the major determinants of disease prognosis. Angiotensin II has trophic effects on the heart and plays an important role in the development of myocardial hypertrophy. Here in a double-blind, placebo-controlled, randomized study, we show that the long-term administration of the angiotensin II type 1 receptor antagonist candesartan in patients with hypertrophic cardiomyopathy was associated with the significant regression of left ventricular hypertrophy, improvement of left ventricular function, and exercise tolerance. The magnitude of the treatment effect was dependent on specific sarcomeric protein gene mutations that had the greatest responses on the carriers of ss-myosin heavy chain and cardiac myosin binding protein C gene mutations. These data indicate that modulating the role of angiotensin II in the development of hypertrophy is specific with respect to both the affected sarcomeric protein gene and the affected codon within that gene. Thus, angiotensin II type 1 receptor blockade has the potential to attenuate myocardial hypertrophy and may, therefore, provide a new treatment option to prevent sudden cardiac death in patients with hypertrophic cardiomyopathy.

Anti-calreticulin antibodies and calreticulin in sera of patients diagnosed with dilated or hypertrophic cardiomyopathy.

Distinct cellular level of the Ca2+-binding chaperone calreticulin (CRT) is essential for correct embryonal cardiac development and postnatal function. However, CRT is also a potential autoantigen eliciting formation of antibodies (Ab), whose role is not yet clarified. Immunization with CRT leads to cardiac injury, while overexpression of CRT in cardiomyocytes induces dilated cardiomyopathy (DCM) in animals. Hence, we analysed levels of anti-CRT Ab and calreticulin in the sera of patients with idiopatic DCM and hypertrophic cardiomyopathy (HCM). ELISA and immunoblot using human recombinant CRT and Pepscan with synthetic, overlapping decapeptides of CRT were used to detect anti-CRT Ab. Serum CRT concentration was tested by ELISA. Significantly increased levels of anti-CRT Ab of isotypes IgA (p < 0.001) and IgG (p < 0.05) were found in patients with both DCM (12/34 seropositive for IgA, 7/34 for IgG) and HCM (13/38 seropositive for IgA, 11/38 for IgG) against healthy controls (2/79 for IgA, 1/79 for IgG). Titration analysis in seropositive DCM and HCM patients documented anti-CRT Ab detected at 1/1600 dilution for IgG and 1/800 for IgA (and IgA1) and at least at 1/200 dilution for IgA2, IgG1, IgG2 and IgG3. Pepscan identified immunogenic CRT epitopes recognized by IgA and IgG Ab of these patients. Significantly increased levels of CRT relative to healthy controls were found in sera of patients with HCM (p < 0.01, 5/19). These data extend the knowledge of seroprevalence of anti-CRT Ab and CRT, and suggest possible involvement of autoimmune mechanisms directed to CRT in some forms of cardiomyopathies, which are clinically heterogeneous.

Pericardial Effusion as a Consequence of Acute Myocardial Infarction.

Pericarditis is a common complication of acute myocardial infarction (MI). Its incidence during the first few days after acute MI is 24%-43% when echocardiographic criteria are used, whereas the frequency of clinical pericarditis is much less (from 5% for all acute MIs to 21% for anterior Q wave MIs). Clinical, electrocardiographic findings are discussed. Effusions are mostly small, and the resolution is frequently slow, lasting 1-18 months. Tamponade is extremely rare in the absence of cardiac rupture. Q wave MIs (especially anterior) are more frequently accompanied by pericardial effusion. The prognostic significance of echocardiographically proved pericarditis is questionable.

Myocardial viability and cardiac dyssynchrony as strong predictors of perioperative mortality in high-risk patients with ischemic cardiomyopathy having coronary artery bypass surgery.

OBJECTIVE: Myocardial viability and left ventricular dyssynchrony are important predictors of long-term outcomes in patients with ischemic left ventricular dysfunction. The objective of this study was to test the hypothesis that assessment of myocardial viability and left ventricular dyssynchrony will predict perioperative mortality in high-risk patients with ischemic left ventricular dysfunction having coronary artery bypass surgery. METHODS: The study consisted of 79 consecutive patients with ischemic cardiomyopathy (age 65 +/- 9 years; 81% men; ejection fraction 30% +/- 6%) and logistic European system for cardiac operative risk evaluation > 10% having coronary artery bypass surgery. Myocardial viability was assessed by delayed contrast-enhanced magnetic resonance imaging. Left ventricular dyssynchrony was calculated using tissue Doppler from measurements of regional electromechanical coupling times in left ventricular basal segments before coronary artery bypass surgery. RESULTS: Twenty (25.3%) patients died within 30 days following coronary artery bypass surgery. Survivors (n = 59) showed a larger extent of viable myocardium (6.9 +/- 3.6 viable segments vs 3.4 +/- 3.3 viable segments, P < .001) and smaller left ventricular dyssynchrony (75 +/- 5 ms vs 179 +/- 83 ms, P < .001) than nonsurvivors. The presence of significant dyssynchrony (>or=105 ms) and absence of myocardial viability (<5 viable segments) independently predicted 30-day mortality with hazard ratio 3.26, 95% confidence interval 1.61 to 8.33 (P < .01) and hazard ratio 1.72, 95% confidence interval 1.59 to 1.89 (P < .01), respectively. All but 2 patients (94.1%) with viable myocardium and without left ventricular dyssynchrony survived coronary artery bypass surgery as compared with only 12 (52.2%) patients with nonviable myocardium and severe dyssynchrony (P < .001). CONCLUSIONS: In high-risk patients with ischemic left ventricular dysfunction having coronary artery bypass surgery, both myocardial viability and left ventricular dyssynchrony are important predictors of perioperative outcome. Assessment of myocardial viability and left ventricular dyssynchrony should be a routine part of the preoperative evaluation of these patients.

Low prevalence and variable clinical presentation of troponin I and troponin T gene mutations in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder caused by mutations in cardiac sarcomeric proteins. Troponin I (TNNI3) and troponin T (TNNT2) are important parts of the sarcomere in heart muscle, and mutations in their genes are responsible for development of HCM. The prevalence of mutations in these two genes is low; hence, the data on clinical outcome are scarce. Yet, some of these mutations were shown to be malignant with a high incidence of sudden death. Here, we describe the disease course in three families affected with TNNI3 and one family with TNNT2 gene mutations. In TNNI3-HCM, the phenotypic manifestation ranged from clinically silent to sudden cardiac death with the worst prognosis observed in carriers of Ala157Val mutation in exon 7. In contrast, TNNT2-HCM was associated with favorable prognosis. Thus, the findings of the present study add evidence on the phenotypic presentation of this genetic disease.

Identification of hibernating myocardium with myocardial contrast echocardiography: comparison with late gadolinium-enhanced magnetic resonance.

Very little is known about the accuracy of intravenous myocardial contrast echocadiography (MCE) in the detection of myocardial hibernation. There are also currently no data on the comparison of MCE to late gadolinium-enhanced magnetic resonance (LGE-MR) in this clinical setting. The aim of this pilot study was to predict recovery of regional function in patients with ischemic LV dysfunction undergoing bypass surgery and to compare the accuracy of MCE with LGE-MR in this clinical setting. The sensitivity of preserved myocardial perfusion during MCE for segmental function recovery (hibernating myocardium) of akinetic segments was 78% and was similar to LGE-MR (87%, p--NS). Specificity of MCE was higher than for LGE-CMR (72%, and 52%, respectively; p<0.01). This pilot study has showed good diagnostic accuracy of MCE for prediction of function recovery after bypass surgery, which is comparable to "gold standard" in assessing myocardial viability--LGE-MR.

Inter-hospital transport for primary angioplasty does not compromise left ventricular function: six-month echocardiographic follow-up of the PRAGUE 1 Study.

The main aim of the present study was to investigate whether long distance interhospital transport for primary angioplasty (delayed mechanical reperfusion) influences the resulting left ventricular function after myocardial infarction as compared with thrombolysis at the nearest hospital (immediate pharmacological reperfusion). Primary coronary angioplasty is more effective than thrombolysis in restoring coronary flow in patients with acute myocardial infarction. It is not known whether a delay in reperfusion due to transport to an angioplasty centre compromises left ventricular function, and whether combination therapy (ie, thrombolysis during transport to an angioplasty centre) would help preserve ejection fraction. The "PRAGUE-1" Study randomised 300 patients with myocardial infarction admitted to community hospitals without a cath-lab into 3 groups: group A (thrombolysis, no transport, n = 99), group B (thrombolysis during transport to an angioplasty centre, n = 100), and group C (transport for primary angioplasty, n = 101). Transport distances were below 75 kilometres, and mean transport time was 38 minutes. This paper presents for the first time the echocardiographic data from the early (discharge, day 30) and mid-term (6 months) follow-up. Only patients who survived until discharge (A: 85, B: 88, C: 94) could be analysed. Ejection fraction improved between discharge and 6 months (P < 0.01) in all three groups: from 47% to 51% in group A, from 47% to 52% in group B, and from 48% to 52% in group C. The differences between the groups were not significant. The same differences were found for the wall motion score index. Left ventricular end-diastolic diameter did not differ between the groups/examinations. Greater improvement was documented in the period between hospital discharge and day 30, compared to the period between day 30 and 6 months. The time delay associated with an inter-hospital transport strategy for primary angioplasty did not compromise left ventricular function. The strategy of thrombolysis during transport did not further improve left ventricular function compared to transport for primary angioplasty alone.

Cardioprotective effects of adenosine transport inhibition during reversible ischaemia in patients with coronary artery disease.

BACKGROUND: Adenosine plays a major role in protecting ischaemic myocardium and may potentiate ischaemic preconditioning. Nucleosine transport inhibition may enhance these favourable effects. DESIGN: Randomized, double blind, placebo controlled study, to investigate the haemodynamic and cardioprotective effects of nucleoside transport inhibition during ischaemia in patients with coronary artery disease. PATIENTS AND METHODS: Elective left anterior descending (LAD) coronary angioplasty was used to produce reversible ischaemia in 24 patients with stable angina and a single LAD lesion. They were randomized to receive either the nucleoside transport inhibitor draflazine or placebo. The study medication was infused between the 2nd and 3rd balloon inflation. The primary endpoint was ischaemia-induced wall motion abnormalities as measured by left septal echo amplitude, which was plotted against time to produce an area under the curve. RESULTS: No differences were observed in the systemic haemodynamics or the myocardial collateral circulation of the two groups. The ischaemia-induced regional wall motion abnormalities improved significantly after draflazine, while no difference was observed in the placebo group. This improvement was even more pronounced in patients with low caffeine levels compared with those with high caffeine levels. CONCLUSIONS: Draflazine, in the dose and route used, is associated with a significant improvement in regional myocardial function of the ischaemic area, without affecting systemic or collateral circulation, when compared with placebo. This implies that draflazine has a cardio-protective effect in ischaemic myocardium. High caffeine blood levels reduce these effects.