Increased CHD risk is associated with an impaired endothelium-dependent vasodilatation and capillary recruitment in skin, suggesting that microvascular function in skin is a valid model to study the relationships between cardiovascular risk factors and microvascular function.
AimsThe purpose of this study was to evaluate the GenousTM endothelial progenitor cell capturing stent vs. the Taxus Liberté paclitaxel-eluting stent in patients with de novo coronary lesions with a high-risk of coronary restenosis.Methods and resultsWe randomly assigned 193 patients with lesions carrying a high risk of restenosis to have the Genous stent or the Taxus stent implanted. Lesions were considered high risk of restenosis if one of the following applied: chronic total occlusion, lesion length >23 mm, vessel diameter <2.8 mm, or any lesion in a diabetic patient. At 1-year, the rate of the primary end point, target vessel failure (TVF), was 17.3% in the Genous stent group when compared with 10.5% in the Taxus stent group [risk difference (RD) 6.8%, 95% CI −3.1 to 16.7%], a difference predominantly due to a higher incidence of repeat revascularization in patients treated with the Genous stent. In contrast, no stent thrombosis was observed in the Genous stent group compared to 4 stent thromboses in the Taxus stent group (RD −4.2%; 95% CI −10.3 to 0.3%). Repeat angiography between 6 and 12 months in a subgroup of patients showed a significantly higher late loss in the Genous stent compared with the Taxus stent (1.14 ± 0.64 and 0.55 ± 0.61 mm).ConclusionIn patients with lesions carrying a high risk of restenosis, the Genous stent resulted in a non-significant higher rate of TVF compared with the Taxus stent mainly due to more repeat revascularizations in the Genous stent group. There were four stent thromboses with Taxus stent, none with the Genous stent.
Our data suggest that addition of a multimarker to a model including established risk factors improves the prediction of mortality in STEMI patients undergoing primary percutaneous coronary intervention. Furthermore, the use of a simple risk score based on these biomarkers identifies a high-risk subgroup.
Aims: Mortality in cardiogenic shock patients remains high. Short-term mechanical circulatory support with Impella can be used to support the circulation in these patients, but data from randomised controlled studies and ‘real-world’ data are sparse. The aim is to describe real-life data on outcomes and complications of our 12 years of clinical experience with Impella in patients with cardiogenic shock after acute myocardial infarction and to identify predictors of 6-month mortality. Methods: We describe a single-centre registry from October 2004 to December 2016 including all patients treated with Impella for cardiogenic shock after acute myocardial infarction. We report outcomes and complications and identify predictors of 6-month mortality. Results: Our overall clinical experience consists of 250 patients treated with Impella 2.5, Impella CP or Impella 5.0. A total of 172 patients received Impella therapy for cardiogenic shock, of which 112 patients had cardiogenic shock after acute myocardial infarction. The mean age was 60.1±10.6 years, mean arterial pressure was 67 (56–77) mmHg, lactate was 6.2 (3.6–9.7) mmol/L, 87.5% were mechanically ventilated and 59.6% had a cardiac arrest before Impella placement. Overall 30-day mortality was 56.2% and 6-month mortality was 60.7%. Complications consisted of device-related vascular complications (17.0%), non-device-related bleeding (12.5%), haemolysis (7.1%) and stroke (3.6%). In a multivariate analysis, pH before Impella placement is a predictor of 6-month mortality. Conclusions: Our registry shows that Impella treatment in cardiogenic shock after acute myocardial infarction is feasible, although mortality rates remain high and complications occur.
In patients with ISR, treatment with DEB was noninferior compared with DES in terms of 6-month MLD. There were no differences in clinical endpoints, including target vessel revascularization up to 12 months. Therefore, use of a DEB is an attractive treatment option for in-stent restenosis, withholding the need for additional stent implantation.
Vasospastic angina (VSA) is considered a broad diagnostic category including documented spontaneous episodes of angina pectoris produced by coronary epicardial vasospasm as well as those induced during provocative coronary vasospasm testing and coronary microvascular dysfunction due to microvascular spasm. The hallmark feature of VSA is rest angina, which promptly responds to short-acting nitrates; however, VSA can present with a great variety of symptoms, ranging from stable angina to acute coronary syndrome and even ventricular arrhythmia. VSA is more prevalent in females, who can present with symptoms different from those among male patients. This may lead to an underestimation of cardiac causes of chest-related symptoms in female patients, in particular if the coronary angiogram (CAG) is normal. Evaluation for the diagnosis of VSA includes standard 12-lead ECG during the attack, Holter monitoring, exercise testing, and echocardiography. Patients suspected of having VSA with a normal CAG without a clear myocardial or non-cardiac cause are candidates for provocative coronary vasospasm testing. The gold standard method for provocative coronary vasospasm testing involves the administration of a provocative drug during CAG while monitoring patient symptoms, ECG and documentation of the coronary artery. Treatment of VSA consists of lifestyle adaptations and pharmacotherapy with calcium channel blockers and nitrates.
Background-This article reports the 2-year clinical, angiographic, and intravascular ultrasound outcomes of the everolimus-eluting stent (EES) compared with the paclitaxel-eluting stent (PES) in the randomized SPIRIT II trial. Methods and Results-This was a prospective, single-blind clinical trial in which a total of 300 patients with de novo native coronary artery lesions were randomized to either EES or PES in a 3:1 fashion. Clinical follow-up was planned at 2 years in all patients. A subset of 152 patients underwent serial angiographic and intravascular ultrasound analyses at 6 months and 2 years. After 2 years, target lesion failure (cardiac death, myocardial infarction, and ischemia-driven target lesion revascularization) rates were 6.6% and 11% in EES and PES, respectively (Pϭ0.31). At 6 months, a significant reduction in angiographic in-stent late loss and percentage volume obstruction measured by intravascular ultrasound was observed in the EES group. However, at 2-year follow-up, a late increased intimal hyperplasia growth after implantation of an EES was observed. There were no significant differences between EES and PES for in-stent late loss (EES, 0.33Ϯ0.37 mm versus PES, 0.34Ϯ0.34 mm; Pϭ0.84) and percentage volume obstruction (EES, 5.18Ϯ6.22% versus PES, 5.80Ϯ6.31%; Pϭ0.65) at 2 years. The incidence of stent thrombosis was low and comparable in both groups (EES, 0.9%; PES, 1.4%). Conclusions-Although the previously reported angiographic and clinical superiority of the EES has vanished over time, this report confirms and extends the previously demonstrated noninferiority in terms of in-stent late loss of the EES when compared with the PES up to 2-year follow-up. There were no significant differences between EES and PES in clinical, angiographic and intravascular ultrasound outcomes at 2 years. (Circ Cardiovasc Intervent. 2009;2:339-347.)
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