Background— The evaluation of new therapeutic modalities to induce collateral growth in coronary artery disease require improved methods of angiographic characterization of collaterals, which should be validated by quantitative assessment of collateral function. Methods and Results— In 100 patients with total chronic occlusion of a major coronary artery (duration >2 weeks) collaterals were assessed angiographically by the Rentrop grading, by their anatomic location, and by a new grading of collateral connections (CC grade 0: no continuous connection, CC1: threadlike continuous connection, CC2: side branch–like connection). The interobserver variability was 10%. Collateral function was assessed by Doppler flow (average peak velocity) and pressure recordings distal to the occlusion before recanalization. A collateral resistance index (R _Coll ) was calculated. Recruitable collateral flow was measured during a final balloon inflation >30 minutes after the baseline measurement. The comparison of the anatomic location, the Rentrop, and the collateral connection grade showed only for the latter an independent and significant relation with R _Coll . CC2 collaterals preserved regional left ventricular function better than did CC1 collaterals and provided a higher collateral flow reserve during adenosine infusion. CC0 collaterals were predominantly observed in recent occlusions of 2 to 4 weeks’ duration, with the highest R _Coll . During balloon reocclusion, recruitable collateral function was best preserved with CC2 and least with CC0. Conclusions— The angiographic grading of collateral connections in total chronic occlusions could differentiate collaterals according to their functional capacity to preserve regional left ventricular function and was closely associated with invasively determined parameters of collateral hemodynamics.

Background—: Acute cardiogenic shock after myocardial infarction is associated with high in-hospital mortality attributable to persisting low-cardiac output. The Impella–EUROSHOCK-registry evaluates the safety and efficacy of the Impella-2.5–percutaneous left-ventricular assist device in patients with cardiogenic shock after acute myocardial infarction. Methods and Results—: This multicenter registry retrospectively included 120 patients (63.6±12.2 years; 81.7% male) with cardiogenic shock from acute myocardial infarction receiving temporary circulatory support with the Impella-2.5–percutaneous left-ventricular assist device. The primary end point evaluated mortality at 30 days. The secondary end point analyzed the change of plasma lactate after the institution of hemodynamic support, and the rate of early major adverse cardiac and cerebrovascular events as well as long-term survival. Thirty-day mortality was 64.2% in the study population. After Impella-2.5–percutaneous left-ventricular assist device implantation, lactate levels decreased from 5.8±5.0 mmol/L to 4.7±5.4 mmol/L ( P =0.28) and 2.5±2.6 mmol/L ( P =0.023) at 24 and 48 hours, respectively. Early major adverse cardiac and cerebrovascular events were reported in 18 (15%) patients. Major bleeding at the vascular access site, hemolysis, and pericardial tamponade occurred in 34 (28.6%), 9 (7.5%), and 2 (1.7%) patients, respectively. The parameters of age >65 and lactate level >3.8 mmol/L at admission were identified as predictors of 30-day mortality. After 317±526 days of follow-up, survival was 28.3%. Conclusions—: In patients with acute cardiogenic shock from acute myocardial infarction, Impella 2.5–treatment is feasible and results in a reduction of lactate levels, suggesting improved organ perfusion. However, 30-day mortality remains high in these patients. This likely reflects the last-resort character of Impella-2.5–application in selected patients with a poor hemodynamic profile and a greater imminent risk of death. Carefully conducted randomized controlled trials are necessary to evaluate the efficacy of Impella-2.5–support in this high-risk patient group.

Aims Chronic total coronary occlusions (CTOs) with angiographically well-developed collaterals may be considered to provide sufficient blood supply to the occluded segment, and the indication for revascularization may be questioned. Therefore, the collateral function and functional reserve in patients with a CTO without a prior Q-wave myocardial infarction (MI) were assessed. Methods and results Invasive assessment of collateral function was done during successful percutaneous coronary intervention in 107 patients with a CTO and no prior Q-wave MI. Intracoronary Doppler flow velocity and pressure recordings were obtained distal to the occlusion before the first balloon inflation and collateral function indexes calculated. In 62 patients, additional pharmacological stress testing was done by intravenous adenosine (140 µg/kg/min) to assess the collateral flow reserve. Patients with normal and impaired regional dysfunction were compared. Collateral function was similar in patients with and without regional left ventricular (LV) dysfunction. In both groups, 78% collaterals provided a collateral pressure index at baseline >0.3, sufficient to prevent ischaemia during a balloon occlusion, with a minimum of 0.2 in those with preserved LV function. A Doppler-derived function index showed a wider variation due to the high prevalence of microvascular dysfunction in CTOs. Only 7% of patients had an increase in collateral flow reserve >2.0 during pharmacological stress, whereas coronary steal occurred in one-third independent of regional LV function. Conclusion A limited increase in collateral flow and the high prevalence of coronary steal during stress underscore the functional limitation of collaterals in CTOs without prior Q-wave MI. Even presumably ‘well-collateralized’ CTOs may benefit from a revascularization.

Transcatheter treatment of heart valve disease is well established today. However, for the treatment of tricuspid regurgitation (TR), no effective catheter-based approach is available. Herein, we report the first human case description of transcatheter treatment of severe TR in a 79-year-old patient with venous congestion and associated non-cardiac diseases. In this patient, surgical treatment had been declined and pharmacological therapy had been ineffective. After ex vivo and animal studies, the treatment of TR was performed by percutaneous caval valve implantation. In a transcatheter approach through the right femoral vein, a custom-made self-expanding heart valve was implanted into the inferior vena cava (IVC). The device was anchored in the IVC at the cavoatrial junction with the level of the valve aligned immediately above the hepatic inflow and protruding into the right atrium. After deployment, excellent valve function was observed resulting in a marked reduction in caval pressure and an abolition of the ventricular wave in the IVC. Sequential echocardiographic exams over a follow-up period of 8 weeks confirmed continuous device function without paravalvular leakage or remaining venous regurgitation. The patient experienced improved physical capacity and was able to resume off-bed activities. There was no recurrence of right heart failure during follow-up and a partial reduction of ascites. The patient was discharged from hospital into a rehabilitation programme. Transcatheter treatment of severe TR by caval valve implantation is feasible resulting in an immediate abolition of IVC regurgitation and mid-term clinical improvement. Thus, in selected non-surgical patients, caval valve implantation may become a therapeutic option to treat venous regurgitation and improve associated non-cardiac diseases. Further confirmatory experience with longer follow-up is required to evaluate the long-term clinical benefit of the procedure as well as potential deleterious effects.

Background— Intracoronary Doppler guidewires can be used for real-time detection and quantification of microembolism during percutaneous coronary interventions (PCIs). We investigated whether the frequency of Doppler-detected microembolism is related to the incidence of myonecrosis during elective PCI. Methods and Results— The study population included 52 consecutive patients (aged 64±10 years; 36 men, 16 women) with coronary artery disease who underwent elective PCI of a single-vessel stenosis. Using intracoronary Doppler ultrasound, we compared the frequency of microembolism during PCI in 22 patients with periprocedural non–ST-segment elevation myocardial infarctions (pNSTEMI) and 30 patients without pNSTEMI. The 2 groups were comparable with regard to their clinical and procedural characteristics. In the group with pNSTEMI, the total number of coronary microemboli after PCI (27±10 versus 16±8, P <0.001) was higher than in the group without pNSTEMI. Although high-sensitivity C-reactive protein plasma levels were similar before PCI (2.9±2.2 versus 3.4±1.7 mg/L, P =NS), they were higher in the group with pNSTEMI after PCI (12.6±10.4 versus 6.1±5.1 mg/L, P <0.05). Microembolic count independently correlated to postprocedural cardiac troponin I elevation ( r =0.565, P <0.001), coronary flow velocity reserve ( r =−0.506, P <0.001), and baseline average peak velocity ( r =0.499, P <0.001). Conclusions— Patients with pNSTEMI had a significantly higher frequency of coronary microembolization during PCI, and their systemic inflammatory response and microvascular impairment after PCI were more pronounced. Intracoronary Doppler ultrasound provides evidence that pNSTEMI in patients undergoing elective PCI is caused by microembolization during the procedure.