Background Management of venous thromboembolism (VTE), encompassing both deep vein thrombosis (DVT) and pulmonary embolism (PE), varies worldwide. Methods The Global Anticoagulant Registry in the FIELD - Venous Thromboembolism (GARFIELD-VTE) is a prospective, observational study of 10,685 patients with objectively diagnosed VTE recruited from May 2014 to January 2017 at 417 sites in 28 countries. All patients are followed for at least 3 years. We describe the baseline characteristics of the study population and their management within 30 days of diagnosis. Results The median age was 60.2 years; 50.4% were male; 61.7% had DVT and 38.3% had PE +/- DVT; and 32.3% were obese (body mass index >= 30 kg/m(2)). The most common risk factors were surgery (12.5%), hospitalization (12.0%) and trauma to the lower limbs (7.8%). At the time of VTE diagnosis, 10.1% had active cancer and 5.7% were chronically immobilized. Treatment for VTE was anticoagulant (AC) therapy alone in 90.9% of patients; 5.1% received thrombolytic and/or surgical/mechanical therapy +/- AC and 4.0% received no therapy. Pre-diagnosis, 12.8% received AC therapy alone and 0.2% received thrombolytic and/or surgical/mechanical therapy +/- AC. After diagnosis, parenteral AC therapy alone was administered in 17.6% of patients, and it was followed by a direct oral AC (DOAC) in 16.4% or a vitamin K antagonist (VKA) in 26.8%. DOACs alone were prescribed to 32.3% of patients, while 5.9% received VKA alone. Conclusion The initial findings from this global registry highlight the heterogeneity in characteristics and management of VTE patients. Prospective follow-up will reveal the impact of this heterogeneity on outcomes.

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 die 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 H 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 die carriers of beta-myosin heavy chain and cardiac myosin binding protein C gene mutations. These data indicate that modulating the role of angiotensin H in die development of hypertrophy is specific with respect to both die affected sarcomeric protein gene and the affected codon within that gene. Thus, angiotensin H 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. (J Mol Diagn 2009, 11:35-41; DOI: 10.2353/jmoldx.09.080082)

The identification of viable myocardium after myocardial infarction (MI) carries major prognostic impact. Due to myocardial stunning early after successful mechanical reperfusion of acute myocardial infarction, analysis of myocardial perfusion but not of contractile function can be used to differentiate between necrotic and viable myocardium. Although being widely regarded as an indicator of infarct transmurality, the relation between post-infarct Q-wave formation and the amount of viable myocardium has not been studied. We hypothesized that there was a correlation between the extent of Q-wave formation and the extent of perfusion abnormalities on myocardial contrast echocardiography early after successful mechanical reperfusion of first acute myocardial infarction and that the extent of post-infarct Q-wave formation might therefore be used as a simple estimate of the amount of viable myocardium. Methods and results 47 patients with first MI and treated by direct PCI were enrolled. Patients were divided into 3 groups according the presence and number of abnormal Q waves (group A—no abnormal Q wave; group B—≤2 abnormal Q waves, group C—≥3 abnormal Q waves). Left ventricular pumpfunction was defined by ejection fraction (EF) on ventriculography and wall motion score index (WMSI) on echocardiography. Myocardial perfusion was defined by perfusion score index (PSI) on myocardial contrast echocardiography. Patients in group A had significantly better LV function than patients in other groups [EF 57±5 vs. 48±11% (group B) and 47±10% (group C); p<0.05], also WMSI was the best in this group [1.34±0.22 vs. 1.67±0.39 (group B) and 1.68±0.31 (group C); p<0.01]. Myocardial perfusion assessed by PSI was best in group A (1.2±0.3, p<0.05). With respect to PSI, there was a significant difference between group B and C (1.41±0.21 vs. 1.56±0.29; p<0.05), even though EF and WMSI did not differ in these groups. The amount of perfused segments with severe wall motion abnormality was higher in group B compared to group C (47% vs. 25%; p<0.05). Conclusion In patients after successful mechanical reperfusion of first MI, the extent of Q-wave formation on ECG may be regarded as a corollary of the amount of myocardial microvascular damage and may, therefore, be used to estimate the amount of viable myocardium post-infarct.

OBJECTIVE:The objective of this study is to assess the feasibility and safety of interhospital transfer (within up to 60 minutes) for primary/rescue coronary angioplasty of patients with myocardial infarction (AMI) complicated by an early onset of acute heart failure (AHF) admitted to a community hospital without PCI facilities.DESIGN AND PATIENTS:From the multicenter randomized PRAGUE-1 study, a subgroup of 66 patients with AMI complicated by AHF on the first presentation to the community hospital were retrospectively analyzed. Group A patients (n = 21) were treated on site in community hospitals using thrombolysis (streptokinase), group B patients (n = 20) were transported with thrombolytic infusion to a PCI center for coronary angioplasty, and group C patients (n = 25) were immediately transported to a PCI center for primary angioplasty without thrombolysis.RESULTS:No patient died during transportation. One group B patient developed ventricular fibrillation during transfer. The time delay from the onset of chest pain to reperfusion was > 142 minutes, and 253 and 251 minutes in groups A, B, and C, respectively. Hospital stay (16 vs 11 vs 10 days, P = NS) was shorter in the angioplasty groups. Transported patients (groups B, C) displayed a significant decrease in heart failure progression within the first 24 hours after treatment (48% vs 15% vs 8%, P < 0.05). The combined end point, i.e., mortality + nonfatal reinfarction (43% vs 25% vs 8%, P < 0.05), was significantly less frequent in the coronary angioplasty group.CONCLUSIONS:Interhospital transfer for coronary angioplasty of patients with AMI complicated by an early onset of AHF is feasible and safe. Transport for angioplasty may even reduce the risk of heart failure progression and improve clinical outcome compared to immediate thrombolysis in the nearest community hospital.

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.

Uvod a cile prace:Syndrom omraceneho myokardu byl opakovaně popsan po revaskularizacnich zakrocich u akutniho transmuralniho infarktu myokardu leceneho trombolytickou terapii ci PTCA. Zcela neznamý je vsak jeho výskyt v populaci nemocných s non-Q-infarktem myokardu a nestabilni anginou pectoris, neni znam ani casový průběh poruchy kinetiky u těchto stavů. Tyto otazky byly předmětem nasi prace. Soubor nemocných a metodika:Od roku 1997 bylo podrobně vysetřeno celkem 266 pacientů (40 mužů a 126 žen) s non--Q-infarktem myokardu a nestabilni anginou pectoris, kteři byli zachyceni do 6 hodin od vzniku bolesti. U 36 z nich byla prokazana regionalni porucha kinetiky, 9 bylo vyřazeno pro nutnost provedeni akutniho koronarniho bypassu nebo PTCA. Zbylých 27 nemocných splňovalo přislusna EKG, a laboratorni kriteria, u 24 z nich byla provedena koronarografie. Tito nemocni byli sledovani echokardiograficky po 6 hodinach do uplne normalizace kinetiky myokardu. Výsledky a zavěr:Median poruchy kinetiky byl u nich 12 hodin (rozsah 6-72 hodin). Slo vždy o akinezi nebo hypokinezi, nikdy ne o dyskinezi. Omracený myokard bylo možno nalezt přibližně u jedne desetiny nemocných s non-Q-infarktem myokardu a nestabilni anginou pectoris.