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(1/321) Reciprocal changes in 12-lead electrocardiography can predict left main coronary artery lesion in patients with acute myocardial infarction.

Acute left main coronary artery (LMCA) occlusion may result in acute myocardial infarction (AMI) or sudden death. ST elevation in the aVR and V1 leads is reported to be valuable in recognizing LMCA occlusion. Early recognition of electrocardiogram (ECG) changes, such as reciprocal ST depression in other leads, is helpful in averting this disaster. This study aimed to determine the reciprocal ST segment depression of 12-lead ECGs associated with acute LMCA occlusion. From January 2000 to December 2004, 61 patients who underwent emergency percutaneous coronary intervention in 3 hospitals due to AMI associated with LMCA (n = 18) and a left anterior descending coronary artery (LADCA) (n = 43) proximal lesion were selected. Reciprocal ST segment depression occurred in leads aVF, V(2), V(3), V(4), V(5), and V(6) with significantly higher incidence in the LMCA group than in the LADCA group. Stepwise linear multivariate discriminant analysis indicated that ST segment depression in leads aVF, V(2), and V(4) could distinguish the LMCA group from the LADCA group. We concluded that reciprocal ST segment depression in leads V(2), V(4), and aVF of a 12-lead ECG is an important predictor of acute LMCA occlusion.  (+info)

(2/321) Embolised stent into the circumflex coronary artery during percutaneous coronary intervention.

Dislodgement and embolisation of the new generation of coronary stents before deployment are rare. If it is impossible to withdraw the embolised stent from the coronary artery, the stent may be crushed into the side wall of the coronary artery with a balloon over a wire passed alongside the embolised stent.  (+info)

(3/321) Microcirculatory dysfunction in ST-elevation myocardial infarction: cause, consequence, or both?

AIMS: Despite advancements over the past years, normal reperfusion at the myocardial level is not achieved in approximately every other patient with ST-elevation myocardial infarction. In the current work, we aimed at reviewing the role of the coronary microcirculation in the development and outcome of this acute coronary syndrome entity. METHODS AND RESULTS: A PubMed/Medline search was performed with the key words acute coronary syndrome, acute myocardial infarction, coronary artery disease, endothelial dysfunction, microcirculation, and reperfusion. The synthesis of the information points to myocardial microcirculatory dysfunction as a consequence of a primary epicardial event, based on the vulnerable plaque concept. As an alternative theory, microcirculatory dysfunction may contribute to the clinical course of the acute coronary event, based on the vulnerable patient concept. The pros and cons of these two viewpoints are to be discussed and their influence on patient management is to be considered. CONCLUSION: Microcirculatory dysfunction in ST-elevation myocardial infarction can be cause, consequence or both according to non-traditional and traditional concepts.  (+info)

(4/321) Troponin-I concentration 72 h after myocardial infarction correlates with infarct size and presence of microvascular obstruction.

OBJECTIVES: The aim of this study was to use late gadolinium hyper-enhancement cardiac magnetic resonance (LGE-CMR) imaging to determine if a 72-h troponin-I measurement would provide a more accurate estimation of infarct size and microvascular obstruction (MVO) than serial creatine kinase (CK) or early troponin-I values. METHODS: LGE-CMR was performed 3.7+/-1.4 days after medical treatment for acute ST elevation or non-ST elevation myocardial infarction. Infarct size and MVO were measured and correlated with serum troponin-I concentrations, which were sampled 12 h and 72 h after admission, in addition to serial CK levels. RESULTS: Ninety-three patients, of whom 71 had received thrombolysis for ST elevation myocardial infarction, completed the CMR study. Peak CK, 12-h troponin-I, and 72-h troponin-I were related to infarct size by LGE-CMR (r = 0.75, p<0.0001; r = 0.56, p = 0.0003; r = 0.62, p<0.0001 respectively). Serum biomarkers demonstrated higher values in the group with MVO compared with those without MVO (Peak CK 3085+/-1531 vs 1471+/-1135, p<0.001; 12-h troponin-I 58.3+/-46.9 vs 33.4+/-40.0, p = 0.13; 72-h troponin-I 11.5+/-9.9 vs 5.5+/-4.6, p<0.005). The correlation between the extent of MVO and 12-h troponin-I was not significant (r = 0.16), in contrast to the other serum biomarkers (peak CK r = 0.44, p<0.0001; 72-h troponin-I r = 0.46, p = 0.0002). CONCLUSION: A single measurement of 72-h troponin-I is similar to serial CK measurements in the estimation of both myocardial infarct size and extent of MVO, and is superior to 12-h troponin-I measurements.  (+info)

(5/321) Type A aortic dissection with partial ostial occlusion of left main coronary artery.

A 48-year-old hypertensive male presented with acute retrosternal pain and aortic regurgitation. The electrocardiogram showed ST-segment depression with T-wave inversion in anterolateral leads. Transesophageal echocardiography in long axis view of aorta revealed a spiral intimal flap in ascending aorta extending to the arch, diagnostic of Type A aortic dissection. The short axis view of the aorta showed partial obstruction of the left main coronary artery (LMCA) by the intimal flap with turbulent flow at its ostium. An emergency repair of aortic dissection with reconstruction of aortic wall was done. Postoperative period and ECG were normal. At 12-months of follow up, patient was doing well.  (+info)

(6/321) Detection and characterization of coronary bifurcation lesions with 64-slice computed tomography coronary angiography.

AIMS: To compare the performance of 64-slice computed tomography coronary angiography (CTCA) and invasive coronary angiography (ICA) in the detection and classification (according to the Medina system) of bifurcation lesions (BLs). METHODS AND RESULTS: We studied 323 consecutive patients undergoing 64-slice CTCA prior to ICA. All coronary segments >or=2 mm in diameter were evaluated for the presence of a significant (>or=50% diameter reduction on quantitative coronary angiography) BL. Evaluation of BL by CTCA included the assessment of significant lumen obstruction in both main and side branch vessels. Forty-one out of 43 patients (46/48 lesions) with significant BL were identified by CTCA. Excluding coronary segments with non-diagnostic image quality (5%), the sensitivity, specificity, and positive and negative predictive values of CTCA for detecting significant BL were 96, 99, and 85 and 99%, respectively. In 39 of these 41 patients, CTCA assessment was concordant with the Medina lesion classification on ICA. CONCLUSION: Sixty-four-slice CTCA allows accurate assessment of complex BL.  (+info)

(7/321) Mechanistic investigation into the arrhythmogenic role of transmural heterogeneities in regional ischaemia phase 1A.

AIMS: Studies of arrhythmogenesis during ischemia have focused primarily on reentrant mechanisms manifested on the epicardial surface. The goal of this study was to use a physiologically-accurate model of acute regional ischemia phase 1A to determine the contribution of ischaemia-induced transmural electrophysiological heterogeneities to arrhythmogenesis following left anterior descending artery occlusion. METHODS AND RESULTS: A slice through a geometrical model of the rabbit ventricles was extracted and a model of regional ischaemia developed. The model included a central ischaemic zone incorporating transmural gradients of I(K(ATP)) activation and [K+]o, surrounded by ischaemic border zones (BZs), with the degree of ischaemic effects varied to represent progression of ischaemia 2-10 min post-occlusion. Premature stimulation was applied over a range of coupling intervals to induce re-entry. The presence of ischaemic BZs and a transmural gradient in I(K(ATP)) activation provided the substrate for re-entrant arrhythmias. Increased dispersion of refractoriness and conduction velocity in the BZs with time post-occlusion led to a progressive increase in arrhythmogenesis. In the absence of a transmural gradient of I(K(ATP)) activation, re-entry was rarely sustained. CONCLUSION: Knowledge of the mechanism by which specific electrophysiological heterogeneities underlie arrhythmogenesis during acute ischaemia could be useful in developing preventative treatments for patients at risk of coronary vascular disease.  (+info)

(8/321) The mechanistic basis for the disparate effects of angiotensin II on coronary collateral growth.

OBJECTIVE: We hypothesize that controversial effects of angiotensin II (Ang II) are attributable to its regulation of reactive oxygen species (ROS) and ROS-dependent signaling. METHODS AND RESULTS: Coronary collateral growth (CCG) was stimulated in normal (WKY) and syndrome X (JCR) rats by transient/repetitive ischemia (RI). Blood flow was measured in the normal (NZ) and the collateral-dependent (CZ) zone. In WKY, RI increased CZ flow (0.84 mL/min/g), but RI+subpressor Ang II increased it more (1.24 mL/min/g). This was associated with transient p38 and sustained Akt activation. A hypertensive dose of Ang II decreased CZ flow (0.69 mL/min/g), which was associated with sustained p38 and transient Akt activation. AT1R blockade by candesartan abrogated CZ flow in WKY (0.58 mL/min/g), reduced myocardial superoxide, and blocked p38 and Akt activation. RI-induced CZ flow in JCR was significantly decreased compared with WKY (0.12 mL/min/g), associated with a large increase in superoxide and lack of p38 and Akt activation. CZ flow in JCR was partially restored by candesartan (0.45 mL/min/g), accompanied by reduction in superoxide and partial restoration of p38 and Akt activation. CONCLUSIONS: Ang II/AT1R blockade, at least in part, regulates CCG via generating optimal ROS amounts and activating redox-sensitive signaling.  (+info)