[Elevated troponin I levels in patients with acute coronary syndrome without ST elevation are associated with increased complexity of the culprit lesion]. / Las elevaciones importantes de troponina I en el síndrome coronario aguso sin elecación del segmento ST se asocian a estenosis coronarias más complejas.

INTRODUCTION: The prognosis in patients with acute coronary syndrome without persistent ST segment elevation (NSTEACS) differs depending on cardiac troponin levels. Clinical practice guidelines published by the Spanish Society of Cardiology and the ACC/AHA consider patients with NSTEACS and markedly elevated troponin levels as high risk patients. The aim of this study was to identify factors related to markedly elevated troponin I levels in NSTEACS. PATIENTS AND METHOD: We measured troponin I levels in 219 consecutive patients with NSTEACS and normal CK-MB values, and identified 2 groups: patients with markedly elevated troponin levels (more than 10-fold the normal upper limit), and patients with normal or slightly elevated troponin levels (less than a 10-fold increase above the normal limit). We also analyzed clinical and angiographic variables. Logistic regression was used to calculate age- and sex-adjusted associations for the main variables. RESULTS: Forty-one patients (19%) had markedly elevated troponin levels, and 178 (81%) showed normal or slightly elevated troponin I levels. Patients with markedly elevated levels had more frequently prolonged angina, class IIb angina, more severe ECG changes, a higher number of diseased vessels on coronary angiography, and greater severity of the culprit lesion. The culprit stenosis in these patients was more often characterized as ulcerated, showing visible thrombus, and excentric, bifurcated and irregular. Class IIIb angina (odds ratio [OR] = 3.1; CI 95%, 1.1-8.6), bifurcation (OR=6.04; CI 95%, 2.5-14.3), ulceration (OR=3.2; CI 95%, 1.07-9.7) and visible thrombus (OR=2.7; CI 95%, 1.1-6.3) in the culprit lesion were predictive factors associated with markedly elevated levels of troponin I independently of age or sex. CONCLUSIONS: Markedly elevated troponin I levels in patients with NSTEACS are associated with a more severe clinical presentation and increased complexity of the culprit lesion on coronary angiography.

The potential of photoacoustic microscopy as a tool to characterize the in vivo degradation of surgical sutures.

The ex vivo and in vivo imaging, and quantitative characterization of the degradation of surgical sutures (∼500 µm diameter) up to ∼1cm depth is demonstrated using a custom dark-field photo-acoustic microscope (PAM). A practical algorithm is developed to accurately measure the suture diameter during the degradation process. The results from tissue simulating phantoms and mice are compared to ex vivo measurements with an optical microscope demonstrating that PAM has a great deal of potential to characterize the degradation process of surgical sutures. The implications of this work for industrial applications are discussed.

Lumen enlargement of the coronary segments located distal to chronic total occlusions successfully treated with drug-eluting stents at follow-up.

AIMS: Chronic total occlusions (CTO) are the final stage of atherosclerosis. Occluded coronary arteries have large plaque burden and negative remodelling. The aim of this study was to assess lumen and vessel changes of segments located distal to successfully recanalised CTO. METHODS AND RESULTS: Ninety-one CTO treated with drug-eluting stents underwent quantitative coronary angiography (QCA) at baseline and at 12-18 months; 31 underwent serial intravascular ultrasound (IVUS) imaging. Angiographic changes were assessed with QCA as differences in minimal, mean and maximal lumen diameter (MinLD, MeanLD and MaxLD, respectively). Vessel changes were assessed with IVUS as changes in plaque and vessel volume. At follow-up, angiographic MinLD increased 23.9% (from 0.88±0.32 to 1.09±0.35 mm; p<0.01), MeanLD 16.4% (from 1.59±0.44 to 1.85±0.45 mm; p<0.01) and MaxLD 11.7% (from 2.39±0.67 to 2.67±0.70 mm; p<0.01). Lumen enlargement was greater in non-restenotic lesions, small lumen area at the end of the index procedure and low LDL-cholesterol levels during the study. By IVUS, lumen volume increased 26.9% (from 108.1±89.2 to 137.3±115.3 mm3; p<0.01), vessel volume increased 12.1% (from 207.1±170.2 to 232.2±196.0 mm3; p<0.01) and plaque volume tended to decrease 3.9% (from 98.9±88.7 to 94.9±89.3 mm3; p=0.07). Small lumen at baseline was related to greater lumen enlargement. CONCLUSIONS: Segments distal to recanalised CTO showed a notable lumen and vessel enlargement with a trend toward mild plaque regression. Low LDL-cholesterol levels increase lumen enlargement.

Use of Impella Recover LP 2.5 in elective high risk percutaneous coronary intervention.

We describe a single-center experience in using the Impella Recover LP 2.5 in the setting of high-risk elective percutaneous coronary interventions. This device is placed percutaneously to support cardiac output and has a better profile than other left ventricular assist devices. Our study shows that the use of the Impella Recover LP 2.5 device is feasible, has an overall favorable safety profile, and may help prevent periprocedural and short-term complications derived from high-risk procedures.

Minor myocardial damage during percutaneous coronary intervention does not affect long-term prognosis.

INTRODUCTION AND OBJECTIVES: To determine whether long-term prognosis is affected by myocardial damage taking place during percutaneous coronary intervention (PCI). METHODS: The study included consecutive patients undergoing PCI. Those with elevated baseline cardiac marker levels were excluded. Cardiac markers were evaluated and an ECG was recorded before and 12 and 24 hours after PCI. Patients were divided into three groups after PCI according to their cardiac marker levels: no myocardial damage (i.e. normal troponin and creatine kinase MB fraction [CK-MB]), minor damage (elevated troponin with normal CK-MB), and myonecrosis (elevated troponin and CK-MB). The occurrence of death, myocardial infarction or repeat revascularization during follow-up was recorded. RESULTS: Minor myocardial damage associated with PCI was observed in 127 (16.8%) of the 757 patients included in the study and myonecrosis, in 46 (6.1%). During a follow-up of 45+/-14 months, cardiac events occurred in 151 (19.1%) patients. Mortality during follow-up was significantly higher in patients with myonecrosis (13%) than in the other two groups (4.8% and 3.9%; log rank, 6.83; P=.032). No difference was observed in the rate of myocardial infarction or repeat revascularization during follow-up. CONCLUSIONS: Minor myocardial damage during PCI had no effect on long-term prognosis. In contrast, myonecrosis was associated with increased mortality. Consequently, the CK-MB level should be measured after all PCIs because of its prognostic implications, and strategies for reducing the risk of myonecrosis developing should be implemented.

Endothelial-dependent vasoconstriction in the infarct-related artery early after myocardial infarction is smaller following primary angioplasty than thrombolytic therapy.

INTRODUCTION AND OBJECTIVES: In patients with ST-elevation acute myocardial infarction treated by thrombolysis, both early endothelial dysfunction and long-term improvement in the infarct-related artery have been reported. Our aims were to assess the degree of endothelial dysfunction present after primary angioplasty and to compare it with that after thrombolysis. METHODS: Endothelial function was assessed 9 days after infarction by infusing acetylcholine, at an increasing concentration, and subsequently nitroglycerine into the infarct-related artery in 16 patients who had undergone primary angioplasty and bare-metal stent implantation. In addition, endothelial function was compared with that in a group of 16 patients treated by thrombolysis in a different time period. The mean change in the diameters of segments distal to the culprit lesion or the treated lesion were evaluated by quantitative coronary angiography. RESULTS: Baseline characteristics were similar in the two groups, except that patients in the primary angioplasty group were treated with clopidogrel and there were differences in residual stenosis in the infarct-related artery (3% in the primary angioplasty group compared with 62% in the thrombolysis group). At the maximum acetylcholine concentration, the degree of vasoconstriction was less in the primary angioplasty group than in the thrombolysis group (-4+/-5% vs. -20+/-21%; P=.018). CONCLUSIONS: Early endothelium-dependent vasoconstriction in the infarct-related artery was lower in acute myocardial infarction patients treated by primary angioplasty and bare-metal stent implantation than in those treated by thrombolysis.