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Background: Recent guidelines recommend a risk-adjusted non-invasive workup in patients presenting with chest discomfort to support or exclude the diagnosis of stable coronary artery disease (CAD). However, a risk-adjusted diagnostic approach remains challenging in clinical practice. An acoustic detection device for analyzing micro-bruits induced by stenosis-generated turbulence in the coronary circulation has now been developed and has shown potential for ruling out CAD in patients with low to intermediate likelihood.Objective: To examine the diagnostic value of an acoustic detection device in a high-prevalence cohort.Methods: Between 1/2016 and 2/2017, a total of 226 patients without prior invasive coronary angiography (ICA) were prospectively enrolled at two centers and were examined using a portable acoustic detection system. In a double-blinded fashion, the acoustic analysis was performed both prior to ICA with quantitative coronary analysis and following percutaneous coronary intervention (PCI).Results: A CAD score was obtained in 213 of 226 patients (94%). The mean CAD score prior to ICA was 41.2±11.9 in patients with obstructive CAD compared with 33.8±13.4in patients without obstructive CAD (p

ACCF : American College of Cardiology Foundation ACS : acute coronary syndrome AHA : American Heart Association CAD : coronary artery disease CABG : coronary artery bypass grafting CKMB : creatine kinase MB isoform cTn : cardiac troponin CT : computed tomography CV : coefficient of variation ECG : electrocardiogram ESC : European Society of Cardiology FDG : fluorodeoxyglucose h : hour(s) HF : heart failure LBBB : left bundle branch block LV : left ventricle LVH : left ventricular hypertrophy MI : myocardial infarction mIBG : meta-iodo-benzylguanidine min : minute(s) MONICA : Multinational MONItoring of trends and determinants in CArdiovascular disease) MPS : myocardial perfusion scintigraphy MRI : magnetic resonance imaging mV : millivolt(s) ng/L : nanogram(s) per litre Non-Q MI : non-Q wave myocardial infarction NSTEMI : non-ST-elevation myocardial infarction PCI : percutaneous coronary intervention PET : positron emission tomography pg/mL : pictogram(s) per millilitre Q wave MI : Q wave myocardial infarction RBBB : right bundle branch block sec : second(s) SPECT : single photon emission computed tomography STEMI : ST elevation myocardial infarction ST–T : ST-segment –T wave URL : upper reference limit WHF : World Heart Federation WHO : World Health Organization Myocardial infarction (MI) can be recognised by clinical features, including electrocardiographic (ECG) findings, elevated values of biochemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that …

BACKGROUND: Cangrelor is an intravenous P2Y 12 inhibitor approved to reduce periprocedural ischemic events in patients undergoing percutaneous coronary intervention not pretreated with a P2Y 12 inhibitor. METHODS: A total of 11 145 patients were randomized to cangrelor or clopidogrel in the CHAMPION PHOENIX trial (Cangrelor versus Standard Therapy to Achieve Optimal Management of Platelet Inhibition). We explored the effects of cangrelor on myocardial infarction (MI) using different definitions and performed sensitivity analyses on the primary end point of the trial. RESULTS: A total of 462 patients (4.2%) undergoing percutaneous coronary intervention had an MI as defined by the second universal definition. The majority of these MIs (n=433, 93.7%) were type 4a. Treatment with cangrelor reduced the incidence of MI at 48 hours (3.8% versus 4.7%; odds ratio [OR], 0.80; 95% confidence interval [CI], 0.67–0.97; P =0.02). When the Society of Coronary Angiography and Intervention definition of periprocedural MI was applied to potential ischemic events, there were fewer total MIs (n=134); however, the effects of cangrelor on MI remained significant (OR, 0.65; 95% CI, 0.46–0.92; P =0.01). Similar effects were seen in the evaluation of the effects of cangrelor on MIs with peak creatinine kinase-MB ≥10 times the upper limit of normal (OR, 0.64; 95% CI, 0.45–0.91) and those with peak creatinine kinase-MB ≥10 times the upper limit of normal, ischemic symptoms, or ECG changes (OR, 0.63; 95% CI, 0.48–0.84). MIs defined by any of these definitions were associated with increased risk of death at 30 days. Treatment with cangrelor reduced the composite end point of death, MI (Society of Coronary Angiography and Intervention definition), ischemia-driven revascularization, or Academic Research Consortium definite stent thrombosis (1.4% versus 2.1%; OR, 0.69; 95% CI, 0.51–0.92). CONCLUSIONS: MI in patients undergoing percutaneous coronary intervention, regardless of definition, remains associated with increased risk of death in the current era. Cangrelor compared with clopidogrel significantly reduces MI regardless of the definition. CLINICAL TRIAL REGISTRATION: URL: http://clinicaltrials.gov . Unique identifier: NCT01156571.

OBJECTIVES The aim of this landmark exploratory analysis, ATLANTIC-H-24, was to evaluate the effects of pre-hospital ticagrelor during the first 24 h after primary percutaneous coronary intervention (PCI) in the ATLANTIC (Administration of Ticagrelor in the cath Lab or in the Ambulance for New ST elevation myocardial infarction to open the Coronary artery) study. BACKGROUND The ATLANTIC trial in patients with ongoing ST-segment elevation myocardial infarction showed that pre-hospital ticagrelor was safe but did not improve pre-PCI coronary reperfusion compared with in-hospital ticagrelor. We hypothesized that the effect of pre-hospital ticagrelor may not have manifested until after PCI due to the rapid transfer time (31 min). METHODS The ATLANTIC-H-24 analysis included 1,629 patients who underwent PCI, evaluating platelet reactivity, Thrombolysis In Myocardial Infarction flow grade 3, >= 70% ST-segment elevation resolution, and clinical endpoints over the first 24 h. RESULTS Following PCI, largest between-group differences in platelet reactivity occurred at 1 to 6 h; coronary reperfusion rates numerically favored pre-hospital ticagrelor, and the degree of ST-segment elevation resolution was significantly greater in the pre-hospital group (median, 75.0% vs. 71.4%; p = 0.049). At 24 h, the composite ischemic endpoint was lower with pre-hospital ticagrelor (10.4% vs. 13.7%; p = 0.039), as were individual endpoints of definite stent thrombosis (p = 0.0078) and myocardial infarction (p = 0.031). All endpoints except death (1.1% vs. 0.2%; p = 0.048) favored pre-hospital ticagrelor, with no differences in bleeding events. CONCLUSIONS The effects of pre-hospital ticagrelor became apparent after PCI, with numerical differences in platelet reactivity and immediate post-PCI reperfusion, associated with reductions in ischemic endpoints, over the first 24 h, whereas there was a small excess of mortality. (Administration of Ticagrelor in the cath Lab or in the Ambulance for New ST elevation myocardial infarction to open the Coronary artery [ATLANTIC, NCT01347580]) (C) 2016 by the American College of Cardiology Foundation.

Coronary venous blood flow measured by continuous thermodilution, myocardial oxygen consumption and lactate extraction rate were estimated at rest and during graded heart rate exercise in 21 patients with compensated aortic valve stenosis and in 10 patients without heart disease. Significant differences between the groups were found only in coronary sinus flow, however not in coronary perfusion related to 100 g of left ventricular muscle mass. As regards indication for operation patients with aortic valve stenosis were differentiated according to transvalvular pressure differences. Pressure gradients of more than 90 mm Hg (n = 5) were associated with significant lowering of weight-related myocardial perfusion and oxygen consumption and high lactate production during stimulation. This evidence of myocardial ischaemia was also seen in 3 out of 11 patients with a pressure gradient between 51 and 90 mm Hg. The rest of the patients showed no significantly different measurements in comparison with the control group. Thus insufficient myocardial perfusion during exercise is likely in patients with transvalvular pressure differences of more than 90 mm/Hg and possible when the difference is more than 50 mm Hg.

Intracoronary thrombi were found in 20 of 52 patients (38%) who had coronary angiography because of treatment-resistant unstable angina. Unrelated to the angiographic finding, eight patients (15%) sustained a myocardial infarction, and two died during their hospital stay. Only one patient (5%) with and six patients (19%) without intracoronary thrombi were stabilized and discharged from hospital. The remaining patients either had an aortocoronary bypass (n = 31) or transluminal balloon angioplasty (n = 13). These findings underline the importance of intracoronary thrombus formation in the pathogenesis of treatment-resistant unstable angina.

In a prospective study, platelet aggregation in platelet-rich plasma after ADP stimulation (0.5, 1.0 and 10 mumol/l) and collagen (1 and 5 micrograms/ml) was measured in 36 patients with coronary heart disease, 18 with angina at rest during the eight hours preceding the time of blood sampling, and 18 patients with stable, exercise-dependent angina, matched for age and sex. In addition, c-AMP was determined, before and (as a measure of platelet adenylate cyclase activity) after stimulation of this enzyme by prostaglandin E1 (10 mumol/l for 30 sec). There were no differences between all the tested ADP and collagen concentrations with regard to platelet aggregation. c-AMP levels were also similar. Thus, in patients with unstable angina there was no evidence for generalized hyperaggregation of platelets in comparison with control subjects who had stable exercise-dependent angina.

Elf Patienten mit einer chronischen Herzinsuffizienz im NYHA-Stadium III oder IV wurden nach Vorbehandlung mit Digitalis, Diuretika und Vasodilatatoren uber 7 Tage mit Dobutamin in einer mittleren Dosis von 6,2 ± 2,2 µg/kg · min behandelt. Vor Infusionsbeginn, 30 Minuten und 7 Tage danach sowie 24 Stunden nach Beendigung der Infusionen wurden die hamodynamischen Parameter gemessen, auserdem wurde vor und nach siebentagiger Behandlung ein zweidimensionales Echokardiogramm angefertigt. Bei vier Patienten muste das Protokoll aus technischen oder medizinischen Grunden vorzeitig beendet werden. Ergebnisse: Arterieller Blutdruck, Korpergewicht, Verkurzungsfraktion und enddiastolischer Durchmesser des linken Ventrikels anderten sich nicht signifikant. Der Herzindex stieg akut an und fiel nach 7 Tagen wieder auf den Ausgangspunkt ab. Der initial signifikant erniedrigte periphere Gesamtwiderstand nahm nach siebentagiger Infusion wieder zu. Eine anhaltende Verminderung des Pulmonalkapillardrucks auch einen Tag nach Beendigung der Behandlung konnte bei drei Patienten mit einer enddiastolischen Wanddicke des linken Ventrikels > 7 mm beobachtet werden. Bei geringerer Wanddicke zeigte sich dagegen ein Anstieg des Pulmonalkapillardrucks bei gleichzeitigem Ruckgang des Herzindexes noch unter die Ausgangswerte. Eleven patients with chronic heart failure (NYHA stage III or IV) were given dobutamine infusions over 7 days, mean dose 6.2 ± 2.2 µg/kg · min. The patients were pretreated with digitalis, diuretics, and vasodilators. Haemodynamic parameters were measured prior to infusion, 30 minutes and 7 days thereafter as well as 24 hours after the end of therapy. Before and after the 7-day therapy a two-dimensional echocardiogram was taken. In four patients, the protocol had to be discontinued prematurely for technical or medical reasons. Results: Arterial blood pressure, body weight, fractional shortening and end-diastolic diameter of the left ventricle were not changed significantly. Cardiac index rose acutely and returned to initial values after 7 days. Total peripheral resistance, which was initially significantly reduced, again rose after infusion over 7 days. Permanent reduction in pulmonary artery wedge pressure, even one day after the end of therapy, was observed in three patients showing a left-ventricular end-diastolic wall thickness > 7 mm. However, in patients whose wall thickness was

OBJECTIVESWe evaluated C-reactive protein (CRP) and troponin T (TnT) for predicting six-month cardiac risk in patients with unstable angina.BACKGROUNDTroponin T is predictive of cardiac risk in patients with unstable angina. The clinical implications of elevated CRP in such patients remains controversial.METHODSBaseline TnT and CRP values were determined in 447 patients with unstable angina enrolled in the placebo group of the Chimeric c7E3 AntiPlatelet Therapy in Unstable angina REfractory to standard treatment trial (CAPTURE) trial. All patients underwent a coronary intervention and were followed for a six month period in which 13 deaths and 47 myocardial infarctions were documented (MIs).RESULTSTroponin T was >0.1 μg/liter in 30% and CRP was >10 mg/L in 41% of the patients. For the initial 72-h period (including coronary intervention), TnT (17.4% vs. 4.2%; p < 0.001) but not CRP (10.3% vs. 8%; p = 0.41) was predictive of mortality and MI. The TnT-positive patients displayed more frequent recurrent instability before the planned intervention (44.8% vs. 16.9%; p < 0.001), but in the CRP-positive patients, no such increase was observed (25.9% vs. 24.8%; p = 0.92). In contrast, for the six month follow-up period, CRP was predictive of cardiac risk (mortality, MI) (18.9% vs. 9.5%; p = 0.003). Using multivariate analysis, both CRP and TnT emerged as independent predictors of mortality and MI at six- month follow-up. Furthermore, the incidence of coronary restenosis during six-month follow-up was not related to TnT status (3% vs. 4.5%; p = 0.49); however, it was significantly related to CRP status (7% vs. 2.3%; p = 0.03).CONCLUSIONSTroponin T, but not CRP, was predictive of cardiac risk during the initial 72-h period, whereas CRP was an independent predictor of both cardiac risk and repeated coronary revascularization (coronary artery bypass graft surgery and percutaneous transluminal coronary angioplasty) during six month follow-up.

OBJECTIVES This study evaluated safety and efficacy of excimer laser angioplasty for treatment of restenosed or occluded coronary stents. BACKGROUND Balloon angioplasty of in-stent restenosis is limited by a high recurrence rate. Debulking by laser angioplasty is a novel concept to treat in-stent restenosis. METHODS A total of 440 patients with restenoses or occlusions in 527 stents were enrolled for treatment with concentric or eccentric laser catheters and adjunctive balloon angioplasty. RESULTS Laser angioplasty success (≤50% diameter stenosis after laser treatment or successful passage with a 2.0-mm or 1.7-mm eccentric laser catheter) was achieved in 92% of patients. Adjunctive balloon angioplasty was performed in 99%. Procedural success (laser angioplasty success followed by ≤30% stenosis with or without balloon angioplasty) was 91%. There was neither a significant difference in success with respect to lesion length, nor were there differences between small and large vessels or native vessels and vein grafts. Success was higher and residual stenosis lower using large or eccentric catheters. Serious adverse events included death (1.6%, not directly laser catheter related), Q-wave myocardial infarction (0.5%), non–Q-wave infarction (2.7%), cardiac tamponade (0.5%) and stent damage (0.5%). Perforations after laser treatment occurred in 0.9% of patients and after balloon angioplasty in 0.2%. Dissections were visible in 4.8% of patients after laser treatment and in 9.3% after balloon angioplasty. Reinterventions during hospitalization were necessary in 0.9% of patients; bypass surgery was performed in 0.2%. CONCLUSIONS Excimer laser angioplasty with adjunctive balloon angioplasty is a safe and efficient technology to treat in-stent restenoses. These data justify a randomized comparison with balloon angioplasty.

ACE : angiotensin-converting enzyme ACS : acute coronary syndrome ADP : adenosine diphosphate AF : atrial fibrillation AMI : acute myocardial infarction AV : atrioventricular AIDA-4 : Abciximab Intracoronary vs. intravenously Drug Application APACHE II : Acute Physiology Aand Chronic

Eur Heart J