Ziele: Korrelation von CT-Angiographie Obstruktionsscores mit dem Vorliegen einer Rechtsherzbelastung und dem klinischen Verlauf bei Patienten mit akuter Lungenembolie (LE). Methode: CTA Obstruktionsscores (Quanadli/Mastora) von 32 Patienten (66±12,9 Jahre) mit akuter LE wurden im Konsensus von 2 Radiologen ermittelt. Alle Patienten erhielten innerhalb von 24 Stunden zur CT eine Echokardiographie zur Bewertung der Rechtsherzbelastung. Zusätzlich wurde die Rechtsherzbelastung (RHB) in der CT durch Berechnung des Verhältnisses des rechtsventrikulären (RV)/linksventrikulären (RV/LV) Diameters in transversalen Schichten (RV/LVtrans) und rekonstruierten 4-Kammer MPR (RV/LV4ch) sowie durch Berechnung des Verhältnisses beider Ventrikelvolumina quantifiziert (RV/LVvol). CTA Obstruktionsscores wurden mit der RHB und dem Vorliegen eines komplizierten klinischen Verlauf (definiert durch Tod, Intensivpflichtigkeit oder NYHAGrad III) korreliert. Ergebnis: Der mittlere Quanadli und Mastora-Score betrug 14,3±11,5 bzw. 28,3±19,9. Die Echokardiographie zeigte eine moderate oder schwere RHB in 4 bzw. 7 Patienten (12,5%/21,9%). Der Mastora-Score war signifikant höher bei Patienten mit echokardiographisch bestätigter schwerer bzw. moderater RHB als bei Patienten ohne RHB (44,3/50 vs. 18,9). Der Quanadli-Score unterschied sich dagegen nur zwischen Patienten mit schwerer und fehlender RHB (22,6 vs. 10,4). Eine relevante Korrelation (R0,6) zwischen den CTA Obstruktionsscores und CT Parametern der RHB lag nur für den Mastora-Score vor (RV/LV4ch: R=0,64, RV/LVvol: R=0,69). 14 Patienten (43,8%) zeigten einen komplizierten klinischen Verlauf. Beide Obstruktionsscores zeigten keinen relevanten Unterschied zwischen Patienten mit oder ohne kompliziertem klinischen Verlauf. Schlussfolgerung: Der Mastora-Score zeigt eine deutlichere Korrelation mit der RHB als der Quanadli-Score. Beide Obstruktionsscores korrelieren nicht mit einem komplizierten klinischen Verlauf.
Background: In the REPAIR-AMI trial, intracoronary administration of autologous bone marrow-derived mononuclear cells (BM-MNC) was associated with a significantly greater recovery of contractile fu...
We aimed to test, for the first time, the feasibility of intracoronary delivery of an innovative, injectable bioabsorbable scaffold (IK-5001), to prevent or reverse adverse left ventricular remodeling and dysfunction in patients after ST-segment-elevation myocardial infarction.Patients (n=27) with moderate-to-large ST-segment-elevation myocardial infarctions, after successful revascularization, were enrolled. Two milliliters of IK-5001, a solution of 1% sodium alginate plus 0.3% calcium gluconate, was administered by selective injection through the infarct-related coronary artery within 7 days after myocardial infarction. IK-5001 is assumed to permeate the infarcted tissue, cross-linking into a hydrogel and forming a bioabsorbable cardiac scaffold. Coronary angiography, 3 minutes after injection, confirmed that the injection did not impair coronary flow and myocardial perfusion. Furthermore, IK-5001 deployment was not associated with additional myocardial injury or re-elevation of cardiac biomarkers. Clinical assessments, echocardiographic studies, 12-lead electrocardiograms, 24-hour Holter monitoring, blood tests, and completion of Minnesota Living with Heart Failure Questionnaires were repeated during follow-up visits at 30, 90, and 180 days after treatment. During a 6-month follow-up, these tests confirmed favorable tolerability of the procedure, without device-related adverse events, serious arrhythmias, blood test abnormalities, or death. Serial echocardiographic studies showed preservation of left ventricular indices and left ventricular ejection fraction.This first-in-man pilot study shows that intracoronary deployment of an IK-5001 scaffold is feasible and well tolerated. Our results have promoted the initiation of a multicenter, randomized controlled trial to confirm the safety and efficacy of this new approach in high-risk patients after ST-segment-elevation myocardial infarction.http://www.clinicaltrials.gov. Unique identifier: NCT01226563.
A 41-year-old woman with a history of severe cigarette smoking complained of recurrent angina pectoris and palpitations that began in 1997.In the course of an uncomplicated STelevation inferior myocardial infarction 6 years ago, coronary angiography showed no stenosis of the epicardial vessels but revealed a catheter-induced vasospasm of the right coronary artery (RCA).At that time the echocardiogram and biplane ventriculography documented normal systolic left ventricular
We present the case of a 91-year-old male whose percutaneous aortic valve replacement was complicated by perforation of the left ventricular (LV) apex caused by an extra-stiff guidewire. Although two-dimensional echocardiography was able to demonstrate a small hole at the LV apex and the presence of an LV pseudo-aneurysm, the exact size and shape of the hole could not be readily appreciated. Thus, three-dimensional (3D) echocardiography was performed and an oval-shaped hole of roughly 0.8 cm 2 could be clearly visualized. This case illustrates the unique value of 3D echocardiography in visualizing geometry and flow across LV rupture sites.
Epicardial adipose tissue (EAT) is an active metabolic and endocrine organ. Previous studies focusing mainly on patients with preserved left ventricular function (LVF) could show a correlation between increased amounts of EAT and the extent and activity of coronary artery disease (CAD). However, to date, there are no data available about the relationship between EAT and the severity of CAD with respect to the whole spectrum of LVF impairment. Therefore, we evaluated this relationship in patients with CAD.250 patients with CAD and 50 healthy controls underwent CMR examination to assess EAT. The severity of CAD was defined using the angiographic Gensini score (GSS).The GSS ranged from 2-364. Linear regression analysis revealed a significant correlation between EAT and GSS (r = 0.177, p = 0.01). Patients with mild (GSS≤10) and moderate CAD (GSS>10-≤40) showed comparable EAT to healthy controls. However, in patients with severe CAD (GSS>40) EAT was significantly reduced (p<0.0001) compared to healthy controls. Interestingly, patients with the same GSS revealed different EAT depending on the left ventricular function (LVF). Patients with preserved LVF (LVF≥50%) showed more EAT mass compared to those with reduced LVF (LVF<50%) regardless of the GSS. In patients with preserved LVF and mild CAD, EAT was comparable to healthy controls (61.8±19.4 g vs. 62.9±14.4 g, p = 0.8). In patients with moderate CAD, EAT rose significantly to 83.1±24.9 g (p = 0.01) and started to decline to 66.4±23.6 g in patients with severe CAD (p = 0.03). Contrary, in CAD patients with reduced LVF, EAT was already significantly reduced in patients with mild CAD as compared to healthy controls (p = 0.001) and showed a stepwise decline with increasing CAD severity.The relationship between EAT and the severity of CAD depends on LVF. These findings emphasize the multifactorial interaction between EAT and the severity of CAD.
