Bioresorbable everolimus-eluting vascular scaffold for the treatment of chronic total occlusions: CTO-ABSORB pilot study.

AIMS: We sought to assess the safety and performance of the Absorb everolimus-eluting bioresorbable vascular scaffold (BVS) in percutaneous chronic total occlusion (CTO) revascularisation guided by intracoronary imaging. The feasibility of using the BVS in CTO lesions is unknown. METHODS AND RESULTS: Thirty-five consecutive true CTO lesions (EuroCTO Club definition) were included in this prospective registry. After mandatory predilatation and IVUS analysis, all target lesions were treated with BVS and no other stents were deployed. Optical coherence tomography (OCT) was performed after BVS implantation. Multislice computed tomography (MSCT) was performed at baseline and at six to eight months. The mean age was 60.7±9.7 years; 80% were male; 20% were diabetic; 37% had a previous PCI. The most frequently treated vessel was the RCA (46%). According to the Japanese-CTO (J-CTO) complexity score, most lesions were classified as intermediate (49%) or difficult-very difficult (26%); 34% were moderate-severely calcified. Most cases (86%) were treated with an anterograde strategy, 60% by radial or biradial approach. In 71% a cutting balloon was used. The total scaffold length implanted per lesion was 52.5±22.9 mm. All scaffolds were successfully delivered and deployed. Post-dilatation was undertaken in 63%. By OCT, final minimum scaffold area and lumen stenosis were 7.1±1.5 mm2 and 11.7±6.6%, without areas of significant strut malapposition. At complete six-month follow-up, no major adverse events were observed. MSCT identified two cases of scaffold reocclusion. CONCLUSIONS: BVS for CTO recanalisation demonstrates excellent feasibility and safety as well as midterm efficacy. Appropriate lesion preparation is key to aiding adequate expansion of these scaffolds in this setting.

Dobutamine stress echocardiography and exercise electrocardiography for risk stratification in medically treated unstable angina.

UNLABELLED: Previous reports have demonstrated the superiority of exercise echocardiography over exercise electro-cardiography (ex-ECG) for risk stratification in patients with medically stabilized unstable angina (UA). We sought to analyze the prognostic value of dobutamine stress echocardiography (DSE) compared with ex-ECG for risk stratification in patients with UA. METHODS: Ninety-two patients with medically treated UA were studied (mean age 65 +/- 11 years, 24 women, 42% of patients had electrocardiographic abnormalities on admission). Dobutamine stress echocardiography and treadmill ex-ECG were performed on the third day after hospital admission. End points were recurrent UA, myocardial infarction (MI), or cardiac death. RESULTS: Mean follow-up was 24 +/- 7 months. During follow-up, 22 patients had cardiac events (18 recurrent UA, 2 MI, 2 cardiac deaths). The event-free survival rate was 80% for patients with negative DSE results for ischemia and 52% for those with positive DSE results (log rank 9.57; P =.002), compared with an event-free survival rate of 79% for patients with negative ex-ECG results and 66% for those with positive ex-ECG results (log rank 2.06; P = not significant). Left ventricular dysfunction (P =.01) and a positive dobutamine stress echocardiogram (P =.03), but not a positive exercise electrocardiogram, were independent predictors of cardiac events during follow-up. CONCLUSIONS: Dobutamine stress echocardiography performed early in medically treated patients with UA predicts cardiac events during follow-up more accurately and with more specificity than ex-ECG does in this population.

Feasibility and prognostic value of dobutamine-atropine stress echocardiography early in unstable angina.

BACKGROUND AND AIM: Because unstable angina has always been considered a contraindication for dobutamine-atropine stress echocardiography (DSE), the role of dobutamine-atropine stress echocardiography in unstable angina is unknown. Our aim was to assess the safety and prognostic value of dobutamine-atropine stress echocardiography in unstable angina. METHODS: One hundred and thirty-two patients were studied (mean age 64+/-12 years, 29 women). Dobutamine-atropine stress echocardiography was performed on the third day after hospital admission. End-points were unstable angina, myocardial infarction or cardiac death at 1 year follow-up. RESULTS: No major complications occurred during dobutamine-atropine stress echocardiography. Ninety-six (78%) patients were on beta-blocker therapy during the test; mean maximum heart rate achieved was 106+/-23 beats x min(-1). Nine of the 21 patients (43%) with a positive dobutamine-atropine stress echocardiography presented cardiac events during follow-up: two patients died, one had a myocardial infarction and six had recurrent class III-IV angina. Among 80 patients with negative dobutamine-atropine stress echocardiography, one (1%) had myocardial infarction and six patients (7.5%) had recurrent angina. Event-free survival after 1 year for patients with a negative dobutamine-atropine stress echocardiography for ischaemia was 91% compared to 57% for those with a positive dobutamine-atropine stress echocardiography (P<0. 0001). Left ventricular dysfunction (P=0.01), prior myocardial infarction (P=0.03) and a positive dobutamine-atropine stress echocardiography (P=0.004) were independent predictors of cardiac events during follow-up. CONCLUSIONS: Dobutamine-atropine stress echocardiography is safe in unstable angina if it is performed when patients remain asymptomatic for at least 48 h. A negative dobutamine-atropine stress echocardiogram for ischaemia predicts a good prognosis in medically treated patients with unstable angina and may allow their early discharge from hospital. Good prognostic information was obtained despite the use of beta-blockers and low heart rates during dobutamine-atropine stress echocardiography.

[In-hospital evolution and current prognosis of unstable angina]. / Evolución hospitalaria y pronóstico actual de la angina inestable.

INTRODUCTION AND PROGNOSIS: The prognosis of patients with unstable angina has improved in recent years resulting in a progressive reduction in hospital stay and treatment. The aim of this study was to know the current prognosis of patients with unstable angina in a non-selected population followed for up to 3 months. PATIENTS AND METHODS: 478 consecutive patients with unstable angina were studied. They were treated following a strict protocol and a management policy guided by symptoms and the results of an exercise test or a pharmacological stress test performed before hospital discharge. RESULTS: The mean age was 66 +/- 11 years with 30% being females. Thirty-five percent had a prior history of myocardial infarction, 61% presented ischemic changes on the admission ECG, and 16% had elevation of the CK-MB plasma levels. An echocardiogram was performed in 80% of the patients, a stress test in 62%, coronary angiography in 51%, and a revascularization procedure in 27% of the patients. During hospitalization, the incidence of mortality or myocardial infarction, refractory angina or ischemic complications was of 3.6%, 11% and 13%, respectively. After hospital discharge and during a 3-month follow-up, the incidence of these complications was of 3.3%, 9% and 10% (NS compared to the in-hospital period). Overall, from the time of hospital admission to the 3-month follow-up, 4.2% of the patients died, 7% died or had an infarction, 20% had refractory angina, and 26% had some ischemic complication. CONCLUSION: The in-hospital prognosis of unstable angina is currently good. However, patients discharged from hospital after stabilization, present an important number of ischemic complications during the following 3 months, similar to that presented by all patients during the acute phase.

[The role of inflammation in the pathogenesis and prognosis of unstable angina]. / Papel de la inflamación en la patogenia y el pronóstico de la angina inestable.

Unstable angina is a clinical syndrome which results from the unstabilization of the coronary atherosclerothic plaque, leading to its ulceration or rupture and to the formation of superimposed thrombus. The mechanism underlying plaque unstabilization is a subject of intense basic research. In the last few years, new knowledge has emerged that relates inflammation in the atherosclerothic lesion with its gradual growth and development, as well as with its sudden transformation into a complicated plaque causing unstable angina or myocardial infarction. In this article we will review the evidence that links inflammation with the pathogenesis of unstable angina and its prognosis.

Blockade of pressure natriuresis induced by inhibition of renal synthesis of nitric oxide in dogs.

To evaluate the participation of nitric oxide (NO) on pressure-induced natriuresis in pentobarbital-anesthetized dogs, renal perfusion pressure (RPP) was increased twice from 100 to 150 mmHg before and during the intrarenal administration of an NO-synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), while determining changes in glomerular filtration rate (GFR), renal blood flow (RBF), and urine sodium and water excretion. Before the inhibition of NO, the increase in RPP induced diuresis (5-fold) and natriuresis (4.2-fold) with no change in RBF or GFR. However, the intrarenal infusion of L-NAME (1 microgram.kg-1.min-1) blunted the diuretic and natriuretic responses without altering RBF or GFR. The infusion of the NO synthesis precursor L-arginine prevented the inhibitory effect that L-NAME exerted on the diuretic and natriuretic responses to the increase in RPP. These results indicate that the increase in RPP stimulates NO synthesis and suggest that NO might play an important role in the control of sodium and water excretion during acute changes in RPP.

Effects of NG-nitro-L-arginine methyl ester on renal function and blood pressure.

The dose-dependent effects of intravenous infusions of nitric oxide (NO) synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 0.1, 1, 10, and 50 micrograms.kg-1.min-1), were studied in anesthetized rats to determine whether the inhibitory actions of L-NAME are manifested primarily in alterations of renal function or whether they are the consequences of the increase in systemic blood pressure. Mean arterial pressure (MAP) was not altered by the intravenous L-NAME infusions of 0.1 and 1.0 microgram.kg-1.min-1. However, 0.1 microgram.kg-1.min-1 L-NAME induced a 30% decrease in urine flow rate (UV). The administration of 1.0 microgram.kg-1.min-1 L-NAME, in addition to decreasing UV, also decreased urinary sodium excretion (UNaV) and renal plasma flow (RPF). The intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 produced significant increases in MAP that reversed the initial fall in UV and UNaV, despite decreasing RPF and glomerular filtration rate (GFR). The administration of L-arginine alone (10 micrograms.kg-1.min-1) did not modify any of the parameters measured, but it effectively prevented all the hemodynamic and renal changes induced by the infusion of 50 micrograms.kg-1.min-1 L-NAME. These results suggest that the decrease in nitric oxide production induced by the intravenous infusion of L-NAME affects renal excretion of sodium and water in the absence of any significant change in blood pressure. At larger doses, L-NAME also produces hypertension that overrides the initial antinatriuretic effect.