A prospective intravascular ultrasound investigation of the necessity for and efficacy of postdilation beyond nominal diameter of 3 current generation DES platforms for the percutaneous treatment of the left main coronary artery.

OBJECTIVES: To define the size of the left mainstem coronary artery (LMS) in the Northern Irish population and investigate the clinical feasibility, safety, and efficacy of post dilation beyond nominal diameter of current generation Drug eluting stent (DES) when treating the LMS. BACKGROUND: There is no prospective data examining the need, feasibility, and safety of over-expansion of current generation DES beyond nominal diameter. METHODS: Patients with flow-limiting coronary atheroma requiring IVUS assessment of the LMS were recruited. Standardized measurements of the distal LMS were made. Subsequently, patients requiring post dilation of current generation DES within the LMS were entered into a PCI registry. RESULTS: Overall, 125 patients were recruited into the initial study. Mean cross-sectional area (CSA) of the distal LMS was 22.6 mm(2) (SD ± 5.4 mm(2) ). Mean maximal vessel diameter was 5.7 mm (SD ± 0.7 mm). Increasing plaque burden was associated with reduced CSA (P < 0.001). In 31 consecutive patients undergoing IVUS guided PCI of the LMS with 5.5 and 6.0 mm balloon catheters, mean maximal stent diameters were >5.0 mm with the Biomatrix Flex 9 crown and Promus Element Large vessel platforms. No intraprocedural complications occurred. Mean follow up was 13.4 months. Clinical restenosis rate was 3.2%, with 2 deaths unrelated to index procedure. CONCLUSIONS: The majority of patients with angiographic coronary atheroma have a mean LMS diameter of >4 mm indicating the requirement for post dilation beyond nominal diameter all of current generation DES in almost all patients when treating the LMS. This is achievable with current DES platforms with no intraprocedural complication. Clinical follow up indicates excellent short-term efficacy.

An audit of outcomes after same-day discharge post-PCI in acute coronary syndrome and elective patients.

OBJECTIVES: To investigate the outcomes of a cohort of acute and elective percutaneous coronary intervention (PCI) patients who were discharged home 6 hours postprocedure. BACKGROUND: Contemporary PCI is safe with a low rate of acute complications. It is well established as a day procedure in elective cases; however, data are lacking in acute cases. METHODS: We describe a prospective observational audit of routine clinical practice in the 3 PCI centers in Northern Ireland. Patients were selected for same-day discharge after 6 hours of post-PCI observation. Both elective and acute coronary syndrome (ACS) cases were included. Criteria for same-day discharge were based on the technical result of the procedure rather than lesion complexity or clinical presentation. Radial access was preferred but not mandatory. Patients were contacted directly to assess for 30-day major adverse cardiovascular events (MACE). Reported events were corroborated with the general practitioner or hospital notes. RESULTS: A total of 1,059 patients were selected for same-day discharge with 30-day follow-up available for all cases. Of these, 766 (72.3%) were elective and 293 (27.7%) were ACS patients. Radial access was almost universal (98%). A total of 1,224 lesions were stented, of which 432 (40.8%) were high risk (highest risk lesion in each case by AHA/ACC classification). MACE rate at 30 days was 0.85% with a sub-acute stent thrombosis rate of 0.4%. There were no MACE events from discharge to 24 hours. CONCLUSIONS: Selected acute and elective patients with a range of lesion complexity and risk can be discharged safely home early after PCI.

In-hospital percutaneous coronary intervention improves in-hospital survival in patients with acute inferior myocardial infarction particularly with right ventricular involvement.

OBJECTIVE: Assess the interaction between fibrinolysis and in-hospital percutaneous coronary intervention (PCI) in patients with inferior myocardial infarction (MI), particularly those with electrocardiographic evidence of right ventricular infarction (RVI). DESIGN: Retrospective observational study. PATIENTS: Consecutive patients with inferior MI identified from an MI registry between January 1998 and January 2004. INTERVENTIONS: Propensity analyses and multiple regression analysis were used to determine the mortality benefit of PCI. MAIN OUTCOME MEASURES: In-hospital morbidity and mortality. RESULTS: In total, 465 patients with inferior MI received fibrinolytic therapy (median pain-to-needle time of 167 minutes; IQR 100-311 minutes). The main predictors of PCI were recurrent chest pain, peak creatine kinase, age, reinfarction, presence of heart failure and male gender. Significant independent predictors of in-hospital mortality were age > or = 75 years, RVI, initial systolic blood pressure < or = 80 mmHg, female gender and no in-hospital PCI. In-hospital PCI was performed in 184/465 (40%) patients; 55 (30%) had rescue PCI performed < or = 6 hours post fibrinolysis, 45 (24%) within 6-24 hours and 84 (46%) > or = 24 hours. In-hospital PCI was associated with reduced in-hospital mortality (PCI: 9 [5%] vs. no PCI: 40 [14%]; p < 0.001) mainly in those with RVI (PCI: 8 [8%] vs. no PCI 33 [23%]; p = 0.002) compared with no RVI (PCI: 1 [1%] vs. no PCI 7 [5%]; p = 0.1). CONCLUSION: A strategy of timely fibrinolysis combined with in-hospital PCI including rescue PCI may result in a significant reduction in in-hospital mortality and morbidity in patients with inferior MI, particularly those with RVI.

Comparison of value of leads from body surface maps to 12-lead electrocardiogram for diagnosis of acute myocardial infarction.

We aimed to develop 12-lead electrocardiographic (ECG) models testing ST-elevation criteria with QRST variables and compare their performance with the 80-lead body surface map (BSM) in detection of acute myocardial infarction (AMI). Because the prevalence of non-ST-elevation AMI is increasing worldwide, advances in early ECG detection of AMI are urgently needed. The study population was 755 consecutive patients presenting with ischemic chest pain from January 2002 to June 2004. All patients had electrocardiography and body surface mapping performed at initial presentation. AMI occurred in 519 patients (69%, cardiac troponin T or I level > or =0.1 ng/ml). Of these 519 patients, 303 (58%) had no ST-elevation on the initial 12-lead electrocardiogram. Ten patients were classified as having an "aborted AMI" and were included in the AMI analysis. The American College of Cardiology/European Society of Cardiology criteria for ST-elevation on 12-lead electrocardiogram identified 236 patients with AMI (sensitivity 45%, specificity 92%). Additional QRST features improved sensitivity (51% to 68%) but with decreased specificity (71% to 89%), with the optimal multivariate ECG model having a c-statistic of 0.75. The optimal BSM model identified 402 patients as having AMI (sensitivity 76%, specificity 92%, c-statistic 0.84). This improvement in sensitivity over the 12-lead electrocardiogram was due mainly to detection of ST-elevation in the high right anterior, posterior, and right ventricular territories and AMI in the presence of left bundle branch block. In conclusion, QRST variables added to criteria for ST-elevation result in improvement in sensitivity of the 12-lead electrocardiogram, although with decreased specificity. The BSM is superior in detecting AMI and demonstrates the importance of electroanatomic evaluation of patients with acute coronary syndromes.

Activation patterns during selective pacing of the left ventricle can be characterized using noninvasive electrocardiographic imaging.

BACKGROUND: Noncontact endocardial mapping allows accurate beat-to-beat reconstruction of the reentrant pathway of ventricular tachycardia and improves outcomes after ablation. Several studies support electrocardiographic imaging (ECGI) as a means of noninvasively outlining epicardial activation despite constraints of internal geometry. However, few have explored its clinical application. This study aims to evaluate ECGI during selective left ventricular (LV) pacing, relative to an invasive approach. METHODS: Multisite pacing was performed within the left ventricles of 3 patients undergoing invasive procedures. Simultaneous recording of endocardial potentials using a noncontact multielectrode array and body surface potentials (BSP) using an 80-electrode torso vest was performed. A total of 16 recordings were made. The inverse solution was applied to BSP to reconstruct epicardial activation. Single-paced beats from real and virtual electrograms were used to construct 3-dimensional isochronal and isopotential maps. Endocardial and epicardial data were then superimposed onto a single geometry to allow quantitative comparison of activation foci. RESULTS: Good correlation was observed between endocardial activation patterns and those reconstructed from BSP using ECGI. This was repeatedly demonstrated in all LV regions except for the septum (3 recordings). Epicardial isochronal maps were able to locate early and late activation to mean distances of 13.8 +/- 4.7 and 12.5 +/- 3.7 mm from endocardial data. Isopotential maps localized pacing sites with comparable accuracy (14 +/- 5.3 mm). CONCLUSIONS: Body surface potentials and reconstructed epicardial activation patterns during LV pacing correlate well with endocardial data acquired invasively. The exception was during pacing of the septum. Although early results are encouraging, further quantitative data are required to fully validate and apply this noninvasive tool in the clinical arena.

Usefulness of body surface maps to demonstrate ventricular activation patterns during left ventricular pacing and reentrant activation during ventricular tachycardia in men with coronary heart disease and left ventricular dysfunction.

Epicardial electrical events were reconstructed using an inverse model for left ventricular (LV) pacing and during ventricular tachycardia (VT) induced during implantation of a biventricular pacemaker and/or internal defibrillator. The electrocardiographic position of the pacing lead, determined from the region of most negative potential 30 ms after the pacing spike, was compared with the radiographic position. Activation characterized by isochronal maps was correlated with the echocardiographic/myocardial scintigraphic data. Reconstructed epicardial isopotential/isochronal maps during VT were used to determine the presence of reentry. In 7 patients during LV pacing, epicardial isopotential maps located the maximum negative potentials anterolaterally (n = 3), posterolaterally (n = 2), and posteriorly (n = 2). Isochronal maps demonstrated activation patterns including regions of delayed activation that, in 5 patients, correlated with areas of akinesia/hypokinesia or fixed defects on echocardiography/myocardial scintigraphy. The mean difference between the radiographically measured right ventricular to LV pacing lead distance and calculated electrocardiographic right ventricular to LV pacing site distance was 1.7 cm. During VT, induced in 5 patients, single-loop reentry was observed in 3 and figure-of-8 reentry in 2. Exit site and regions of fast/slow conduction and conduction block that correlated with anatomic areas of infarction defined by echocardiography/myocardial scintigraphy were demonstrated. In conclusion, epicardial maps reconstructed from the body surface map can identify LV pacing sites and demonstrate reentry during VT. The body surface map could thus identify optimal pacing sites for LV pacing and targets for VT ablation.

Clopidogrel in the treatment of ischaemic heart disease.

Clopidogrel is an effective antiplatelet agent that has undergone rigorous assessment in the setting of ischaemic heart disease over the last decade. There is extensive evidence for the use of this drug in patients undergoing percutaneous coronary intervention, in those with stable ischaemic heart disease and also in those with acute coronary syndromes. This article examines the use of clopidogrel in patients with ischaemic heart disease.

Improved detection of acute myocardial infarction using a diagnostic algorithm based on calculated epicardial potentials.

BACKGROUND: New methods for detecting myocardial infarction in patients with suspected acute coronary syndromes are needed particularly in an era where the majority of patients with myocardial infarction present with non-diagnostic 12-lead electrocardiograms (ECG). We compared a novel epicardial diagnostic algorithm using epicardial potentials from the 80-lead body surface map with other electrocardiographic techniques in detection of myocardial infarction. METHODS: Between February 1999 and February 2001, consecutive patients (n=427) with ischemic type chest pain had an initial 12-lead ECG and body surface map recorded. Detecting myocardial infarction using an epicardial algorithm was first performed in a training set (n=213) and tested in a validation set of patients (n=214). The results from this epicardial algorithm in myocardial infarction detection were compared with the physician's interpretation of the 12-lead ECG, the body surface map algorithm (PRIME) and physician's interpretation of the body surface map. RESULTS: Myocardial infarction occurred in 205 patients (creatine kinase >or=2x upper limit of normal with creatine kinase-MB >or=7% CK). The physician's interpretation of the 12-lead ECG identified 122 with myocardial infarction (sensitivity 60%, specificity 99%), the body surface map algorithm 137 (sensitivity 67%, specificity 89%), the physician's interpretation of the body surface map 153 (sensitivity 75%, specificity 91%) and the epicardial algorithm 158 (sensitivity 77% specificity 99%). Combining the physician's interpretation of the 12-lead ECG with the epicardial algorithm increased significantly the detection of myocardial infarction (sensitivity 85%, specificity 98%, p<0.001) compared with the 12-lead ECG. CONCLUSIONS: An epicardial algorithm based on epicardial potentials increases significantly the detection of myocardial infarction particularly among those with non-diagnostic 12-lead ECG's.

Impedance compensated biphasic waveforms for transthoracic cardioversion of atrial fibrillation: a multi-centre comparison of antero-apical and antero-posterior pad positions.

AIMS: To compare the success rate for transthoracic direct current cardioversion (DCC) of atrial fibrillation (AF) with antero-posterior (AP) and antero-apical (AA) electrode positions using an impedance compensated biphasic (ICB) waveform. METHODS AND RESULTS: Three-hundred and seven patients [mean age 66 (SD+/-13), 195 male] with AF were recruited in three centres. Patients were randomized to an AA (n=150) or AP (n=144) pad position. Thirteen patients with implanted pacemakers were defaulted to the AP pad position. Cardioversion was performed using an ICB waveform with a 70, 100, 150, and 200 J energy selection protocol. If the fourth shock was unsuccessful, the pads were crossed over to the alternative position for a final 200 J shock. Shock 1 was successful in 54/150 (36%) AA and 45/144 (31%) AP patients, whereas success was achieved by shock 2 in 99/150 (66%) AA and 74/144 (51%) AP, by shock 3 in 123/150 (82%) AA and 109/144 (76%) AP, and by shock 4 in 143/150 (95%) AA and 127/144 (88%) AP and after cross-over in 144/150 (96%) AA and 135/144 (94%) AP. Overall success rate was higher than expected at 95%. Pad position was not associated significantly with success. There was a trend towards an improved outcome with the AA configuration (P=0.05). CONCLUSION: The influence of pad position for DCC of AF may be less pertinent with ICB waveforms than with monophasic waveforms.

Percutaneous coronary intervention and 1 year survival in patients treated with fibrinolytic therapy for acute ST-elevation myocardial infarction.

AIMS: To assess the predictors of 1 year mortality in patients treated with fibrinolytic therapy for ST-segment elevation myocardial infarction (STEMI) and to determine whether a strategy of early percutaneous coronary intervention (PCI) improves outcome. METHODS AND RESULTS: Consecutive patients (n = 474) admitted to our unit (1998-2001) with STEMI were treated with fibrinolytic therapy. For each patient, age, gender, admission via mobile coronary care unit (MCCU), infarct location, initial systolic blood pressure and Killip class, prior history of ischaemic heart disease, hypertension, diabetes mellitus, smoking status, family history, hyperlipidaemia, and in-hospital PCI (n = 154) were recorded. Mortality at 1 year was obtained from medical records (n = 473). Binary logistic regression analysis was performed to determine independent predictors of 1 year mortality. Mortality in the non-PCI group was 21 vs. 7% in the PCI group. Independent predictors of 1 year mortality were age (risk ratio 1.12, 95% CI 1.08-1.15, P < 0.0001), initial SBP < or = 80 mmHg (risk ratio 4.34, 95% CI 1.68-11.2, P = 0.002), initial Killip class > or = 3 (risk ratio 2.97, 95% CI 1.42-6.2, P = 0.004), and lack of in-hospital PCI (risk ratio 0.39, 95% CI 0.19-0.81, P = 0.012). Although the PCI group were younger (P = 0.007), more likely to be admitted via the MCCU (P = 0.008), with a shorter pain to needle time (P = 0.04), multivariable analysis adjusted for these differences. CONCLUSION: In-hospital PCI in patients treated with fibrinolytic therapy for STEMI is associated with a substantial reduction in 1 year mortality.

Prehospital 80-LAD mapping: does it add significantly to the diagnosis of acute coronary syndromes?

UNLABELLED: Early detection of acute myocardial infarction (MI) is vital in the management of acute coronary syndromes (ACS). Hence we compared the diagnostic capability of the standard 12-lead electrocardiogram (ECG) with the 80-lead ECG body surface map (BSM) prehospital. METHODS: Consecutive patients (n = 294) presenting prehospital with ischemic type chest pain were included. All had an ECG and BSM pretreatment and a baseline and 12-hour cardiac troponin-T or I (cTnT or cTnI). Acute MI was defined as cTnT > 0.09 or cTnI > 0.1 ng/mL. Acute MI on the BSM was defined as ST elevation measured at the J-point, > or = 1 mm inferior/right ventricular/high right anterior/lateral regions, > or = 2 mm anterior region, > or = 0.5 mm posterior region. RESULTS: Acute MI occurred in 182/294 (62%) based on cTnT or I. ST elevation on the standard ECG predicted acute MI in 103 (sensitivity 57%, specificity 94%; c-statistic 0.73). The optimal model for the standard ECG included ST elevation, summed ST depression and past history of MI (c-statistic 0.82; Chi-square (Wald) 120.7, 3df). The BSM predicted acute MI in 146 (sensitivity 80%, specificity 92%; c-statistic 0.86). The optimal model for the BSM included BSM criteria for acute MI and past history of MI (c-statistic 0.91; Chi-square (Wald) 180.3, 2df). CONCLUSION: The 80-lead BSM is superior to the standard 12-lead ECG in predicting acute MI prehospital.

Efficacy of distinct energy delivery protocols comparing two biphasic defibrillators for cardiac arrest.

Limited data have been published on the use of external defibrillators that deliver impedance compensated biphasic (ICB) waveforms in patients. We compared 2 ICB defibrillators, the Heartstream XL (150-150-150 J protocol) and Heartsine Samaritan (100-150-200 J protocol) in 78 consecutive patients in cardiac arrest. The performance of the 2 devices over the first 2 shocks was statistically equivalent. By the third shock, the Heartsine Samaritan had significantly better performance in removing ventricular fibrillation (p = 0.029). Energy selection for ICB waveforms requires further validation.

Comparison of the 80-lead body surface map to physician and to 12-lead electrocardiogram in detection of acute myocardial infarction.

Diagnosis of non-ST-elevation acute myocardial infarction (AMI) by a 12-lead electrocardiogram has poor sensitivity and specificity and, therefore, relies on biochemical markers of myocardial necrosis, which can only be reliably detected within 14 to 16 hours from symptom onset. The body surface map (BSM) improves AMI detection but is limited by its interpretation by inexperienced medical staff. To facilitate interpretation, an automated BSM algorithm was developed and is evaluated in this study. One hundred three patients with ischemic-type chest pain were recruited for this study from December 2001 to April 2002. A 12-lead electrocardiogram (Marquette Mac 5K) and BSM (PRIME-ECG) were recorded at initial presentation, and cardiac troponin I and/or creatine kinase-MB levels measured at 12 hours after symptom onset. The admitting physician's 12-lead electrocardiographic (ECG) interpretation, 12-lead ECG algorithm (Marquette 12 SL V233) diagnosis, and BSM algorithm diagnosis were documented for each patient. AMI, defined by elevation of troponin I to >1 microg/L and/or creatine kinase-MB to >25U/L, occurred in 53 patients. The admitting physician diagnosed 24 patients with AMI (sensitivity 45%, specificity 94%), the 12-lead ECG algorithm diagnosed 17 patients with AMI (sensitivity 32%, specificity 98%), and the BSM algorithm diagnosed 34 patients with AMI (sensitivity 64%, specificity 94%). The BSM algorithm improved the diagnostic sensitivity by 2.0 (p <0.001) and 1.4 (p = 0.002) compared with the 12-lead ECG algorithm or the admitting physician, respectively. There was no significant difference in specificity. Thus, the BSM algorithm improves detection of AMI compared with the 12-lead ECG algorithm or physician's 12-lead ECG interpretation.

The use of calculated epicardial potentials improves significantly the sensitivity of a diagnostic algorithm in the detection of acute myocardial infarction.

Inverse electrocardiography can calculate epicardial potentials (EP) from body surface potentials (BSP) taking into account a thoracic volume conductor model (TVCM). Previous studies have shown that a tailored TVCM is superior to a general TVCM in calculating EP. However, construction of a tailored TVCM for a patient in an acute clinical setting is impractical. In this study we used a general TVCM in our EP calculations to determine whether this improves detection of acute myocardial infarction (AMI) using a diagnostic algorithm. BSP were derived from the 80-lead body surface map (BSM). Consecutive patients (n=379) with ischemic type chest pain were recruited. The BSM and a 12-lead electrocardiogram (ECG) were recorded at initial presentation and creatine kinase (CK) and/or CK-MB were measured initially, 12 and 24 hours postsymptom onset. A physician interpreted the 12-lead electrocardiogram and documented ST elevation if present. AMI was defined by the World Health Organization (WHO) criteria. The diagnostic algorithm result for each patient using BSP and calculated EP were documented. AMI occurred in 171 patients. The diagnostic algorithm using BSP identified 106 of these as ST elevation AMI (STEMI) (sensitivity 62%, specificity 80%). The same algorithm using EP identified 133 as STEMI (sensitivity 78%, specificity 80%). Calculated EP improved the algorithm's diagnostic sensitivity by a factor of 1.25 (P<.001) with no significant difference in specificity. Calculated EP using a general TVCM significantly improves the sensitivity of a diagnostic algorithm based on BSP in detection of AMI with no significant loss in specificity.