Grade 3 ischemia on the admission electrocardiogram is associated with severe microvascular injury on cardiac magnetic resonance imaging after ST elevation myocardial infarction.

BACKGROUND: Grade 3 ischemia during ST elevation myocardial infarction (STEMI) is defined as ST elevation with distortion of the terminal portion of the QRS on electrocardiogram (ECG). The aim of this study was to evaluate the effect of ischemic grade on cardiac magnetic resonance (CMR) imaging infarct characteristics such as infarct size, microvascular obstruction (MVO), intramyocardial hemorrhage (IMH), and myocardial salvage. METHODS: Patients with STEMI treated with primary percutaneous coronary intervention had a 12-lead ECG on presentation for analysis of ischemic grade. Gadolinium-enhanced CMR imaging was performed within 7 days to assess infarct size, MVO, IMH, and myocardial salvage. RESULTS: Of the 37 patients enrolled in the study, grade 3 ischemia was present in 32%. Those with grade 3 ischemia had higher peak troponin I levels (P = .013), more MVO (P < .001), more IMH (P < .001), larger infarct size (P = .025), and less myocardial salvage (P = .012). Regression analysis found that grade 3 ischemia, infarct size, and peak troponin I level were significantly associated with MVO and IMH. CONCLUSION: Grade 3 ischemia on the admission ECG during STEMI is closely associated with the development of severe microvascular damage on CMR imaging.

Dynamic Changes in ST Segment Resolution After Myocardial Infarction and the Association with Microvascular Injury on Cardiac Magnetic Resonance Imaging.

BACKGROUND: persistent ST elevation after reperfused ST elevation myocardial infarction (STEMI) is believed to be related to poor microvascular perfusion. Cardiac magnetic resonance imaging (CMR) can evaluate microvascular obstruction (MVO) and intramyocardial haemorrhage (IMH) both of which represent severe microvascular damage, have independent prognostic value and are dynamic and evolving over the first 48hours after reperfusion. The aim of this study was to assess whether the development of MVO or IMH has an impact upon ST segment resolution. METHODS: patients undergoing primary percutaneous coronary intervention (PCI) for STEMI had serial 12 lead electrocardiograms (ECG) from one hour after PCI until discharge. Persistent single lead maximal residual ST elevation (maxSTE) at each time point was calculated. ST segment deterioration (re-elevation) was calculated on each ECG until discharge compared with one hour post PCI ECG. CMR was performed within seven days post infarct utilising T2 weighted imaging to evaluate culprit artery area at risk (AAR) and IMH. Gadolinium delayed enhancement CMR quantified infarct size and MVO. RESULTS: in the 41 patients studied 58% had MVO and 41% had IMH. ST segment deterioration was more common in those with MVO or IMH (p=0.03 and p=0.008 respectively). MaxSTE was higher at each time point after PCI in those with MVO but only became statistically significant after 24hours. The measurement of maxSTE at 48 or 72hours after revascularisation provided the best correlation with the combination of infarct size, AAR, MVO and intramyocardial haemorrhage. CONCLUSION: microvascular injury as defined on CMR is associated with dynamic changes and persistence of ST segment elevation in the first 72hours after reperfusion.

Serum thromboxane B2 compared to five other platelet function tests for the evaluation of aspirin effect in stable cardiovascular disease.

BACKGROUND: To assess the role of serum thromboxane B(2) (TXB(2)) measurements and the correlation between platelet function studies, in patients with stable cardiovascular disease on aspirin or clopidogrel. METHODS: 76 patients (47 on aspirin, 16 clopidogrel, 13 both) underwent assessment of TXB(2), whole blood aggregometry (WBA) after stimulation with (i) arachidonic acid (0.5mM), (ii) ADP (5 microM), (iii) collagen (1 and 5 microg/ml), PFA-100, and Cone and Plate Analyzer. Clopidogrel patients were additionally assessed by the VerifyNow System. RESULTS: TXB(2) values ranged between 0.2 and 56.2 ng/ml, with significant separation between those taking aspirin, clopidogrel and controls (0.45 ng/ml vs 6.85 ng/ml vs 12.97 ng/ml, p<0.001). There was moderate correlation between WBA-AA and TXB(2) (r=0.487, p<0.001), PFA-100((R)) (r=0.599, p<0.001), WBA-Col1 (r=0.424, p<0.001), WBA-Col1:5 (r=0.417, p<0.001), and between TXB(2) and PFA-100((R)) (r=0.509, p<0.001). The prevalence of aspirin non-responders for WBA-AA, TXB(2), PFA-100((R)), CPA and Coll1:5 was 13.1%, 8.2%, 14.8%, 9.7% and 16.4% respectively. Individual patients were not consistently classified as aspirin non-responders in all tests. Those with inadequate aspirin response on > or =3 tests had higher TXB(2) levels (mean 1.57+/-1.66, range 0.553-4.45 vs mean 0.45+/-0.18, range 0.23-1.50) (p=0.001). Clopidogrel suppressed TXB(2) (p=0.02), WBA-AA (p<0.001), WBA-Col1 (p=0.012) and WBA-ADP (p<0.001) compared to controls. TXB(2) in patients ingesting fish oil tablets was lower compared to those without (0.4 ng/ml vs 0.52 ng/ml, p=0.004). Obesity was associated with higher TXB(2) values (0.61 vs 0.41, p=0.01). CONCLUSION: Serum TXB(2) measurements are a direct measure of the pharmacological effect of aspirin, are easily performed and correlate with other measures of platelet function. Serum TXB(2) measurements could be a useful sole measure of aspirin non-response, and may be even more predictive when performed in tandem with a global measure of platelet function. Aspirin and clopidogrel both suppressed several platelet pathways.

Radiation exposure during elective coronary angioplasty: the effect of flat-panel detection.

BACKGROUND: Coronary angiography and angioplasty have to date been performed using digital angiography and fluoroscopic systems which incorporate an image intensifier (II). More recently flat-panel (FP) detectors have been introduced which are thought to improve spatial resolution. However, there is limited data on the effect of flat-panel detection on radiation exposure. We sought to determine the impact of flat-panel on cumulative radiation exposure in patients undergoing elective coronary angioplasty at our institution. METHODS: Patients who underwent elective coronary angioplasty in the six months prior to and following upgrade of our Toshiba catheterisation laboratory from image intensifier to flat-panel were included. Demographic and radiation data were collected prospectively and the same five operators performed interventions during the 12-month period. Radiation data was obtained from the dose-area product meter intrinsic to the fluoroscopy system. RESULTS: One hundred and thirty seven patients underwent elective angioplasty over the 12-month period (68 II, 69 FP). Cumulative radiation exposure was increased in flat-panel cases (99, 129 Gy cm(2) versus 71, 77 Gy cm(2), p=0.001). This increase was independent of patient weight (78+/-15 kg versus 78+/-17 kg, p=NS), screening time (19+/-12 min versus 18+/-13 min, p=NS) and total number of digital acquisitions (1475, 820 versus 1668, 1365, p=NS). The total amount of contrast dye did not differ between flat-panel and image intensifier cases (195+/-76 ml versus 194+/-79 ml, p=NS). CONCLUSIONS: Adoption of flat-panel detector technology increases radiation exposure. This may have important safety implications for catheterisation laboratory staff and patients undergoing multiple interventional procedures.

Selective anti-scatter grid removal during coronary angiography and PCI: a simple and safe technique for radiation reduction.

Objectives The aim of this study was to quantify the radiation dose reduction during coronary angiography and percutaneous coronary intervention (PCI) through removal of the anti-scatter grid (ASG), and to assess its impact on image quality in adult patients with a low body mass index (BMI). Methods A phantom with different thicknesses of acrylic was used with a Westmead Test Object to simulate patient sizes and assess image quality. 129 low BMI patients underwent coronary angiography or PCI with or without the ASG in situ. Radiation dose was compared between both patient groups. Results With the same imaging system and a comparable patient population, ASG removal was associated with a 47% reduction in total dose-area product (DAP) (p < 0.001). Peak skin dose was reduced by 54% (p < 0.001). Operator scatter was reduced to a similar degree and was significantly reduced through removal of the ASG. Using an image quality phantom it was demonstrated that image quality remained satisfactory. Conclusions Removal of the ASG is a simple and effective method to significantly reduce radiation dose in coronary angiography and PCI. This was achieved while maintaining adequate diagnostic image quality. Selective removal of the ASG is likely to improve the radiation safety of cardiac angiography and interventions.

Real-time colour pictorial radiation monitoring during coronary angiography: effect on patient peak skin and total dose during coronary angiography.

AIMS: The aim of this study was to evaluate whether a real-time (RT) colour pictorial radiation dose monitoring system reduces patient skin and total radiation dose during coronary angiography and intervention. METHODS AND RESULTS: Patient demographics, procedural variables and radiation parameters were recorded before and after institution of the RT skin dose recording system. Peak skin dose as well as traditionally available measures of procedural radiation dose were compared. A total of 1,077 consecutive patients underwent coronary angiography, of whom 460 also had PCI. Institution of the RT skin dose recording system resulted in a 22% reduction in peak skin dose after accounting for confounding variables. Radiation dose reduction was most pronounced in those having PCI but was also seen over a range of subgroups including those with prior coronary artery bypass surgery, high BMI, and with radial arterial access. This was associated with a significant reduction in the number of patients placed at risk of skin damage. Similar reductions in parameters reflective of total radiation dose were also demonstrated after institution of RT radiation monitoring. CONCLUSIONS: Institution of an RT skin dose recording reduced patient peak skin and total radiation dose during coronary angiography and intervention. Consideration should be given to widespread adoption of this technology.

Multivessel coronary-ventricular fistulae and ischaemia on cardiac MRI.

Multivessel coronary ventricular fistulae is a rare coronary anomaly whose origin is believed to be from an arterioluminal or arteriosinusoidal connection with the ventricle. The clinical and haemodynamic significance of these fistulae have been a source of controversy despite varying methods of evaluation. A 69 year old female with exertional dyspnoea, atypical chest pain and multivessel coronary to left ventricular fistulae underwent cardiac MRI with adenosine stress. Subendocardial ischaemia was present in multiple coronary territories therefore confirming a coronary steal phenomenon.

Myocardial release of nitric oxide during ischaemia and reperfusion: effects of L-arginine and hypercholesterolaemia.

AIMS: Nitric oxide (NO) may modulate myocardial ischaemia/reperfusion (I/R) injury, but effects of hypercholesterolaemia on myocardial NO release during I/R are unknown. METHODS: A NO-specific carbon fibre electrode continuously measured coronary sinus [NO] during 60 min low-flow ischaemia (1 ml/min) and 60 min free reperfusion (I/R) in isolated rabbit hearts. Experimental groups (n=7 per group) were control, L-arginine supplement (200 microM), N-nitro-L-arginine methyl ester (L-NAME) treatment (8 microM) and hypercholesterolaemic. RESULTS: During early I, NO release decreased markedly in control (-1356+/-286 pmol/min/g) and L-arginine (-1972+/-172) groups, but less in L-NAME (-441+/-89) and hypercholesterolaemic (-602+/-164) groups (both p<0.01 vs. controls). No increase in NO release during I was seen in any group. After R, NO release increased above baseline in control (+2333+/-591 pmol/min/g) and L-arginine (+1048+/-278) groups and hypercholesterolaemic (+1100+/-478) (p<0.05 vs. pre-ischaemia each group). There was little increase in NO release in the L-NAME group (+436+/-247 pmol/min/g, p<0.05 vs. controls). In each group, myocardial NO release declined towards pre-ischaemic levels during 60 min R. Hearts treated with L-arginine had similar NO release but better functional recovery than controls (p<0.01). Treatment with L-NAME was also associated with better functional recovery than in controls or hypercholesterolaemic hearts. CONCLUSION: Myocardial NO release declines rapidly during ischaemia, but increases above baseline during early reperfusion. Improved function after L-arginine treatment appears to be independent of effects upon NO release. Hypercholesterolaemia is associated with reduced myocardial NO release, under both baseline conditions and during ischaemia and reperfusion.

Final myocardial blush grade predicts troponin I elevation in unstable angina patients undergoing percutaneous intervention.

BACKGROUND: Improved myocardial blush grade is associated with better MACE outcomes in acute myocardial infarction patients but there are no data on myocardial blush grade (MBG) assessment in unstable angina (UA) patients treated with coronary intervention. We sought to evaluate the use of angiographic MBG assessment in a cohort of UA patients treated with angioplasty. METHODS: Three hundred and seventy-two consecutive UA patients (mean age 68+/-1 years) treated with PCI were included. No patients had a pre-procedural troponin I (TnI) elevation. Final MBG was recorded for the territory subserving the PCI treated culprit lesion in each patient and graded 0 (no blush), 1 (minimal blush), 2 (moderate blush) and 3 (normal blush). TnI (normal range <0.1 microg/L) was measured 24h post-procedure. Patients who did not have a TnI elevation (i.e. <0.1 microg/L) were ascribed a value of 0.1 microg/L. Patients were followed up (mean 962+/-83 days) by postal questionnaire. RESULTS: Baseline risk factors were comparable between final MBG groups. There was no significant difference in mortality rate between groups. Post-procedural troponin I elevations were 0.34+/-0.12, 0.68+/-0.26, 0.14+/-0.01 and 0.11+/-0.01 for MBG groups 0, 1, 2 and 3 (p<0.001). Patients with minimal MBG underwent proportionately more target vessel revascularisation (p<0.05). CONCLUSIONS: Improved blush grade in UA patients undergoing PCI is associated with lower post-procedural TnI elevation. Identification of UA patients with poor final MBG may allow a window of opportunity for the administration of adjuvant therapies to improve microvascular perfusion in the future.

Serial angiography in patients with acute coronary syndromes: effect of antithrombotic therapy on angiographic lesion severity.

BACKGROUND: Patients presenting with acute coronary syndromes (ACS) commonly have a responsible culprit coronary lesion. There is limited data on the natural history of this culprit lesion in the short term and whether there is a change in morphology of this lesion in the days following presentation. Furthermore, the effect of antithrombotic therapy on this process is unknown. METHODS: Sixty-eight patients presenting with ACS had their diagnostic study performed at our institution and had coronary angioplasty performed a few days later at a different hospital. Culprit lesion characteristics including minimum luminal diameter (MLD) and percentage diameter stenosis were determined on each occasion. RESULTS: Acute myocardial infarction patients (n=14) had improved culprit lesion characteristics at angioplasty compared to baseline (diameter stenosis 78.9% versus 62.4%, p<0.01). Similarly, patients presenting with unstable angina (UA) or non-ST elevation myocardial infarction (non-STEMI) (n=54) had improved diameter stenosis (78.0% versus 72.7%, p<0.001). The change in MLD was greater in MI patients than UAP/non-STEMI patients (0.6mm versus 0.16mm, p<0.01). CONCLUSION: Treatment of ACS patients with aspirin with anticoagulant therapy followed by delayed intervention results in angiographic improvement in lesion severity which may provide a more favourable environment in which to undertake percutaneous coronary intervention.

Angioplasty facilitated permanent pacing in de novo superior vena cava obstruction.

The finding of complete occlusion of the superior venal cava during the performance of cardiac pacing is rare. We report a case where performance of angioplasty aided the successful completion of permanent pacemaker implantation.

Proteomics of ischemia/reperfusion injury in rabbit myocardium reveals alterations to proteins of essential functional systems.

Brief periods of myocardial ischemia prior to timely reperfusion result in prolonged, yet reversible, contractile dysfunction of the myocardium, or "myocardial stunning". It has been hypothesized that the delayed recovery of contractile function in stunned myocardium reflects damage to one or a few key sarcomeric proteins. However, damage to such proteins does not explain observed physiological alterations to myocardial oxygen consumption and ATP requirements observed following myocardial stunning, and therefore the impact of alterations to additional functional groups is unresolved. We utilized two-dimensional gel electrophoresis and mass spectrometry to identify changes to the protein profiles in whole cell, cytosolic- and myofilament-enriched subcellular fractions from isolated, perfused rabbit hearts following 15 min or 60 min low-flow (1 mL/min) ischemia. Comparative gel analysis revealed 53 protein spot differences (> 1.5-fold difference in visible abundance) in reperfused myocardium. The majority of changes were observed to proteins from four functional groups: (i) the sarcomere and cytoskeleton, notably myosin light chain-2 and troponin C; (ii) redox regulation, in particular several components of the NADH ubiquinone oxidoreductase complex; (iii) energy metabolism, encompassing creatine kinase; and (iv) the stress response. Protein differences appeared to be the result of isoelectric point shifts most probably resulting from chemical modifications, and molecular mass shifts resulting from proteolytic or physical fragmentation. This is consistent with our hypothesis that the time course for the onset of injury associated with myocardial stunning is too brief to be mediated by large changes to gene/protein expression, but rather that more subtle, rapid and potentially transient changes are occurring to the proteome. The physical manifestation of stunned myocardium is therefore the likely result of the summed functional impairment resulting from these multiple changes, rather than a result of damage to a single key protein.

Disassembly of a rotablator: getting out of a trap.

The rotablator burr rarely becomes trapped within calcified lesions. Manual traction can be ineffective and dangerous. We report a case that illustrates a novel technique involving use of a percutaneous snare in conjunction with partial disassembly of the rotablator device to remove a trapped burr without need for open surgical intervention.

New bifurcation stenting technique: shunt stenting.

The optimal treatment of bifurcation lesions remains controversial. We describe a new technique we term shunt stenting. This technique incorporates both the new technology of drug-eluting stents and a novel procedure for optimizing the ostial side branch stent positioning. To date, early angiographic and clinical follow-up have been encouraging.

Effect of treatment on ventricular function and troponin I proteolysis in reperfused myocardium.

Effects of ischemia time and treatment interventions upon troponin I (TnI) proteolysis and function of reperfused myocardium were examined in isolated, perfused rabbit hearts. Hearts were randomized to 90 min aerobic perfusion, 15 min low-flow (1 ml/min) ischemia (I) and 60 min reperfusion (R) or 60 min low-flow I and 60 min R. Hearts subject to 60 min I and 60 min R received either no treatment, l -arginine treatment, or treatment with oxygen free radical (OFR) scavengers (mercapto-proponyl-glycine, catalase and superoxide dismutase). Hearts from cholesterol-fed rabbits were also studied after 60 min I and R. Isovolumic LV pressure and heart rate were recorded throughout and Western analysis of ventricular myocardium, using 3 specific antibodies, detected intact TnI (29 kDa) and TnI fragment (25 kDa). Hearts subject to 15 min I had minimal irreversible injury (TTC negative region=0.6+/-0.4% LV) but hearts subject to 60 min I had more extensive injury (TTC negative=40.7+/-5.8% LV). Recovery of rate-pressure product after 15 min I and 60 min R (56+/-9% of baseline) was better than after 60 min I and 60 min R (23+/-9%, P<0.01). Both l -arginine and OFR scavengers were associated with better recovery of function after 60 min I, (66+/-7% and 72+/-3% of baseline respectively, P<0.01 v no treatment) but cholesterol hearts had poor recovery after 60 min I (37+/-8%). The 25 kDa TnI (% total TnI immunoreactivity) was 8.7+/-0.9% in controls, 10.0+/-1.6% after 15 min I and 60 min R, and 17.4+/-2.4% after 60 min I and 60 min R (P<0.01 v controls and 15 min I). The proportion of 25 kDa TnI was increased in all hearts after 60 min I and did not change with treatment (l -arginine 16.8+/-1.8%, OFR scavengers 16.0+/-3.2%, cholesterol 14.0+/-1.9%). There was no relation between proportion of 25 kDa TnI and recovery of function. Samples from freshly excised rabbit hearts and human right atria also had 25 kDa TnI (relative intensities 8.5+/-2.3% and 5.1+/-2.6% respectively). Although TnI fragmentation increases after prolonged ischemia and reperfusion, the functional recovery of stunned myocardium is independent of degree of TnI fragmentation.

Duration of ischaemia determines matrix metalloproteinase-2 activation in the reperfused rabbit heart.

It has been hypothesised that activation of matrix metalloproteinase-2 (MMP-2) contributes to reversible myocardial dysfunction (stunning) following short-term ischaemia and reperfusion. Gelatin zymography was used to measure release of both pro-MMP-2 (72 kDa) and MMP-2 (62 kDa), into the coronary effluent from isolated, perfused rabbit hearts during 90 min aerobic perfusion (control), or low-flow ischaemia (15 or 60 min at 1 mL/min), followed by 60 min reperfusion. In controls, pro-MMP-2 was detected in the coronary effluent throughout the first 30 min of aerobic perfusion, but MMP-2 was not detected. In contrast, MMP-2 was detected in the coronary effluent during reperfusion after both 15 and 60 min ischaemia. However, while left ventricular systolic function was impaired after both 15 min and 60 min ischaemia, a significant increase in the release of MMP-2 was only detected in hearts following 60 min ischaemia. The dissociation between mechanical function and MMP-2 levels suggest that MMP-2 does not contribute to myocardial stunning in this model, but may contribute to myocardial dysfunction following prolonged ischaemia.