[Anticoagulation strategies in patients with deep vein thrombosis and pulmonary artery embolisms]. / Strategien zur Antikoagulation bei Patienten mit tiefer Beinvenenthrombose und Lungenarterienembolie.

Deep vein thrombosis and pulmonary artery embolisms share pathophysiological features and are therefore collectively referred to as venous thromboembolisms (VTE). While the incidence of VTE has been increasing for years as a result of demographic changes and improved diagnostics, the morbidity and mortality are decreasing. This is particularly due to more sensitive diagnostics, improvements in risk stratification and more effective anticoagulation strategies. The aim of effective anticoagulation therapy is the avoidance of early events up to death and prevention of recurrent events. Anticoagulation treatment should be started with either heparins (unfractionated or low molecular weight), the pentasaccharide fondaparinux or direct oral anticoagulants. Patients with recurrent events qualify for indefinite anticoagulation treatment. For a first episode of VTE anticoagulation treatment for at least 3 months is recommended (maintenance therapy). Subsequently, prolonged maintenance therapy for secondary prevention can be meaningful, depending on the individual patient risk (provoked event, risk for recurrence or bleeding). The non-vitamin K antagonist oral anticoagulants (NOACs) have now also been approved for this indication. As a result of a probably permanently high risk for recurrent events of up to 10% per year after cessation of anticoagulation, insufficient scores for estimation of the risk of bleeding and recent data documenting the safety and efficacy of NOACs for secondary prevention, a shift towards prolonged anticoagulation of 3-6 months or even indefinite (>1 year) treatment can be anticipated for patients after thromboembolic diseases.

[The thickened left ventricle: etiology, differential diagnosis and implications for cardiovascular radiology]. / Der dicke linke Ventrikel: Ursachen und Differenzialdiagnose der linksventrikulären Hypertrophie und Implikationen für die kardiovaskuläre Radiologie.

Hypertrophy of the left ventricular myocardium is a common finding and can be reliably detected by echocardiography, CT and MRI. Common causes include diseases associated with increased cardiac afterload as well as primary and secondary cardiomyopathy. With the opportunity to determine functional parameters and myocardial mass precisely as well as to detect structural changes of the cardiac muscle simultaneously, cardiac MRI is the most precise imaging method for quantifying left ventricular hypertrophy as well as determining the cause and the exact characterization of the myocardial changes. It is mandatory, however, to create a flexible, individually adapted examination protocol. This review presents useful diagnostic algorithms in relation to different underlying pathologies in patients with left ventricular hypertrophy.

Comparative assessment of drug-eluting balloons in an advanced porcine model of coronary restenosis.

The advent of drug-eluting balloon (DEB) therapy has represented an important development in interventional cardiology. Nevertheless, preclinical data with this technology remain scant, and comparative studies have not previously been published. Bare metal stents were implanted in the coronary arteries of 15 pigs followed by balloon angioplasty. Animals were allocated to treatment with a 60-second inflation of one of four different balloon catheters: a conventional untreated plain angioplasty balloon (PBA, Biotronik AG), the Pantera Lux DEB (3.0 µg/mm2 paclitaxel; BTHC excipient, Biotronik AG), the Elutax DEB (2.0 µg/mm2 paclitaxel; no excipient; Aachen Resonance), or the SeQuent Please DEB (3.0 µg/mm2 paclitaxel; iopromide excipient: B. Braun). Twenty-eight days following balloon deployment, animals underwent repeat angiography for quantitative coronary angiography analysis and euthanasia for histopathologic assessment. By histology, the mean neointimal thickness was 0.44 ± 0.19 mm with PBA, 0.35 ± 0.13 mm with Pantera Lux , 0.61 ± 0.20 mm with Elutax , and 0.47 ± 0.21 mm with SeQuent Please DEB (p=0.02). In comparison with PBA, deployment of the Pantera Lux or the SeQuent Please DEB resulted in delayed healing characterised by significant increases in fibrin, neointimal cell vacuity and delayed re-endothelialisation. In conclusion, investigation of comparative DEB performance in a porcine model of advanced coronary restenosis reveals significant heterogeneity of neointimal suppression between the devices tested with numerically lowest values seen in the Pantera Lux group. On the other hand, evidence of delayed healing was observed in the most effective DEB groups.

[Patient care in the acute phase of stress induced cardiomyopathy (Tako-Tsubo cardiomyopathy)--and thereafter?]. / Patientenversorgung in der akuten Phase der stressinduzierten Kardiomyopathie (Tako-Tsubo-Kardiomyopathie)--und danach?

The prognosis of patients presenting with Tako-Tsubo cardiomyopathy (TTC) is generally considered to be favorable. However, in the acute phase of the disorder complications are not infrequent and, therefore, continuous monitoring and consistent therapy in an intensive care unit is essential. Typical complications in patients with TTC are cardiogenic shock, obstruction of the left ventricular outflow tract (LVOT), occasionally accompanied by acute mitral regurgitation, arrhythmias, predominantly torsade de pointes tachycardias due to QT prolongation, left ventricular (LV) thrombus formation with or without consecutive thromboembolic events, and LV rupture. After confirmation of TTC by coronary angiography, repeat echocardiography should be performed. A standardized therapy for patients with TTC has so far not been established. Recommendations for the acute phase include the administration of anxiolytic agents for patients who present with preceding emotional stress, consistent therapy of physical stressors (such as pain or asthma) and avoidance of catecholamine therapy. Shock due to LVOT obstruction is treated by administration of volume and ß-blockers. With respect to the occurrence of torsade de pointes tachycardias, drugs which might cause QT prolongation should not be given. The notable incidence of LV thrombus formation justifies therapeutic anticoagulation. Systematic studies and treatment recommendations for the prophylaxis of recurrent TTC do not exist. The recently reported association between TTC and malignant disorders should prompt tumor screening and subsequent preventive medical checkups in patients affected by TTC.

Superiority of sirolimus eluting stent compared with intracoronary beta radiation for treatment of in-stent restenosis: a matched comparison.

OBJECTIVE: To compare acute and follow up clinical and angiographic results after treatment of in-stent restenosis (ISR) by sirolimus eluting stents (SES) with results obtained after intracoronary radiation therapy (IRT). DESIGN: Matched pair analysis. METHODS: 62 consecutive ISR lesions (< 30 mm lesion length, reference diameter < 3.5 mm) in 62 patients were treated with SES. From a database of 174 lesions (n = 141 patients) treated for ISR by intracoronary beta radiation, 62 lesions (62 patients) were pair matched with the SES group for diabetes mellitus, lesion length, vessel size, and pattern of ISR. Six month angiographic and 12 month clinical follow up results were obtained. RESULTS: Baseline clinical and angiographic characteristics were similar between the groups (not significant). SES implantation resulted in significantly lower postprocedural in-lesion diameter stenosis than did IRT (mean (SD) 14.2 (9.5)% v 21.1 (10.6)%, p = 0.001), significantly higher minimum lumen diameter at follow up (1.91 (0.58) v 1.55 (0.72) mm, p = 0.005), and a higher net gain (1.16 (0.55) v 0.77 (0.70) mm, p = 0.002). Angiographic binary in-lesion restenosis rate at six months was 11% in the SES group and 29% in the IRT group (p = 0.046). In 16 ISR lesions SES were used after failed IRT and in 46 lesions for first time ISR. In-lesion late loss was higher after use of SES for failed IRT than after use of SES for first time ISR (0.61 (0.67) mm v 0.24 (0.41) mm, p = 0.018). In a multivariate analysis prior failed IRT was the only independent predictor for recurrent restenosis after SES for ISR (p = 0.052, odds ratio 5.8). Six patients (10%) in the SES group and 17 patients (27%) in the IRT group underwent target lesion revascularisation during the 12 months of follow up (p = 0.022). CONCLUSIONS: In this non-randomised matched cohort SES achieved acute and follow up results superior to IRT for treatment of ISR even if cases of failed IRT are included. Failed IRT is a predictor of impaired SES effectiveness.

Effects of intramyocardial pVEGF165 delivery on regional myocardial blood flow: evidence for a spatial 'delivery-efficacy' mismatch.

The aim of this study was to determine the effects of direct intramyocardial pVEGF165 gene transfer on regional myocardial blood flow in a porcine model of chronic myocardial ischaemia. Pigs underwent placement of an ameroid constrictor around the left circumflex coronary artery. After 3 weeks, animals received direct intramyocardial injections of pVEGF165 (20 x 50 microl at 1 microg/microl, n=11) or a plasmid vector encoding chloramphenicol acetyltransferase (20 x 50 microl at 1 microg/microl, n=11) into a specified target area (TA) of the left lateral wall. At 3 weeks after gene transfer, animals underwent final evaluation including a systematic assessment of regional myocardial blood flow (MBF) under resting and stress conditions. In all, 20 animals (10 per group) reached final studies. There was no change in mean arterial blood pressure or Rentrop collateral score from gene delivery to final studies in either group, nor were there differences between study groups. MBF was significantly higher in the areas adjacent to the TA in the VEGF group under resting (P<0.001) and stress conditions (P<0.05). In addition, pVEGF165 gene transfer abolished flow differences between the adjacent areas and the septum. MBF was not different between study groups in the TA, the anterior wall, or the septum. In conclusion, direct intramyocardial pVEGF165 gene transfer significantly improves myocardial blood flow. However, this effect is limited to the myocardial segments adjacent to the area of gene delivery. These data, therefore, demonstrate a spatial 'delivery-efficacy' mismatch with implications for myocardial gene delivery sites and detection of treatment effects in vivo.

Outcome after treatment of coronary in-stent restenosis; results from a systematic review using meta-analysis techniques.

AIMS: To evaluate the clinical outcome after treatment of coronary in-stent restenosis. METHODS AND RESULTS: For identification of the relevant literature a specific search strategy was conducted and explicit inclusion criteria were defined to avoid selection bias. Based on the selected literature, a systematic review using descriptive statistics and meta-analysis methods regarding the outcome after treatment of coronary in-stent restenosis was performed. The proportion of patients experiencing a major adverse cardiac event (MACE) as defined by death, myocardial infarction, and target lesion revascularization was the main outcome measure. A total of 1304 citations were identified. Among these, 28 studies (six different treatment modalities) including a total of 3012 patients met the inclusion criteria and were incorporated into this analysis. The estimated average probability of experiencing a major cardiac adverse event after treatment for in-stent restenosis with a follow-up period of 9+/-4 months was 30.0% (25.0-34.9%, 95% confidence interval) with strong evidence for heterogeneity between study specific results (P=0.0001). The clinical outcome was not significantly different between treatment modalities. After adjustment for confounding factors (i.e. lesion length), however, patients undergoing intracoronary radiation showed an estimated advantage of 16.9% (-37.7+/-4.0%, 95% confidence interval) in MACE free survival, as compared to balloon angioplasty. The post-interventional diameter stenosis was the only independent predictor for the long-term outcome after treatment of in-stent restenosis. CONCLUSIONS: Treatment of in-stent restenosis is associated with an overall 30% rate of major adverse cardiac events. Currently, repeat angioplasty is the treatment option of choice, especially when a sufficient acute procedural result can be achieved. Intracoronary radiation should be considered in cases with therapy refractory forms of diffuse in-stent restenosis.

Rotational atherectomy for the treatment of in-stent restenosis.

Restenosis after coronary stent implantation remains the major limitation of this treatment modality. At present, re-dilatation is considered the therapeutic option of choice for focal lesions, however, long restenotic lesions (>10 mm) do not respond favourably. Despite the emerging concept of intracoronary radiation, encouraging acute procedural results are also reported for different debulking techniques (Excimer laser angioplasty, directional coronary atherectomy, and rotational atherectomy, or rotablation). Rotablation has been studied most extensively with acute and long- term results published in a total of more than 850 patients. Experimental and first clinical data indicate favourable results for the rotablator as compared to balloon angioplasty alone for the treatment of in-stent restenosis. Data from the first 2 randomized clinical trials (ROSTER-, and ARTIST-trial) have now been published with conflicting results: The european multicenter ARTIST-trial including 300 patients could not prove a benefit for the rotablator as compared to re-dilatation in patients with diffuse stent restenosis. On the contrary, the monocenter ROSTER-trial, which has been presented as an abstract until today, suggests a clinical benefit of patients treated by the rotablator if they were studied with intracoronary ultrasound prior to randomization. Currently, rotablation for the treatment of restenosis cannot be considered as the first line treatment modality in patients with in-stent restenosis. As a result of unsatisfying angiographic and clinical long-term results by the use of a variety of treatment modalities in diffuse stent restenosis, prevention of this iatrogenic entity has become mandatory.

Comparison of oesophageal and gastric air tonometry in patients with circulatory failure.

BACKGROUND: Gastric PCO2 measured by balloon tonometry can estimate the adequacy of splanchnic perfusion. However, enteral feeding and gastric content can interfere with gastric PCO2 assessment. Tonometry in other sites of the body could avoid these problems. We therefore tested the hypothesis that oesophageal air tonometry would give results similar to gastric tonometry. METHODS: We studied 20 consecutive patients (mean age 68 (SD 9) [range 49-81] yr, 18 males, SAPS II score 55 (SD 18), ICU mortality 55%) with circulatory disorders during mechanical ventilation in the intensive care unit. Tonometer probes were placed via the nose, one into the stomach and the other in the oesophagus. PCO2 was measured with two automated gas analysers, at admission and 30 min, 1, 2, 3, 32, 40, and 48 h thereafter. RESULTS: One hundred and forty-eight paired measurements were obtained. Gastric PCO2 was greater than oesophageal PCO2 on admission (7.19 (1.43) vs 5.89 (0.73) kPa, P < 0.01) and subsequently. Differences between the measures correlated (r = 0.67) with the mean absolute value, indicating that overestimation increased as gastric PCO2 increased. CONCLUSIONS: Oesophageal PCO2 is less than gastric PCO2, and the difference is greater when gastric PCO2 levels are greater. Air tonometry may not measure regional PCO2 levels in the oesophagus satisfactorily. Other methods and sites for carbon dioxide tonometry should be examined.

Three-year follow-up after rotational atherectomy for the treatment of diffuse in-stent restenosis: predictors of major adverse cardiac events.

Restenosis remains the major limitation of coronary stent implantation, especially in diffuse forms of in-stent restenosis. In this study, rotablation (RA) with adjunct angioplasty of in-stent restenosis was performed in 84 patients. Clinical follow-up and control angiography were obtained 6-month postprocedure. The rate of recurrent restenosis after rotablation for in-stent restenosis at 6-month angiographic follow-up was 45%, resulting in a rate of major adverse cardiac events of 35%. At 3-year follow-up, the cumulative event-free survival rate was 57% for the entire population. The only predictor of MACE at 3-year clinical follow-up by multivariate logistic regression analysis was in-stent lesion length. RA for the treatment of diffuse in-stent restenosis is thereby characterized by high procedural success rates and recurrent angiographic restenosis in 45% of patients with diffuse lesions. Major adverse cardiac events occur most likely within the first 6 months postprocedure. Three years after rotablation of in-stent restenosis, 43% of patients had experienced at least one major adverse cardiac event. Cathet Cardiovasc Intervent 2001;53:334-340.