Electrocardiographic prediction of lateral involvement in acute non-anterior wall myocardial infarction

AbstractPurposeRecent research has established that a tall R-wave in V1 indicates lateral wall involvement in non-anterior wall myocardial infarction (MI). The objective of this study was to assess the value of the admission electrocardiogram (ECG) to predict R-waves and consequently lateral wall damage in the late phase of non-anterior MI.MethodsECGs of 69 patients were analyzed. ST-segment changes in representative leads for lateral wall infarction such as V1, V2, V6 and I were correlated with the extent of QRS-wave changes in V1 and V6.ResultsST-segment elevation in V6 showed correlations with R/S ratio in V1 (r=0.802, B=0.440, P=<0.001) and with the depth of Q-waves in V6 (r=0.671, B=0.441, P=0.007). This correlation was higher in a small subgroup where the left circumflex branch (Cx) was the culprit vessel (r=0.888, B=1.469 and P=0.018). ST-segment depression in lead I correlated with the height of R and the surface of R in V1 (height times width of R) (r=0.542, B=−0.150, P=0.005 and r=0.538, B=−0.153, P=0.005 respectively), especially in the subgroup without proximal occlusions of RCA (r=0.711 and r=0.699). ST-segment depression in lead I also predicted Q-waves in V6 (r=0.538, B=0.114, P=0.006). ST-segment changes in V2 showed no significant correlation with either R- or Q-wave measurements.ConclusionsST-segment elevation in V6 in the acute phase of non-anterior MI predicts lateral involvement as expressed by the R/S ratio in V1 in the post reperfusion phase. A subgroup with Cx occlusion showed especially strong correlations, although the size of the group was small. In lead I ST-segment depression is correlated to height and surface of R in V1 and Q-waves in V6

Reperfusion cardiac arrhythmias and their relation to reperfusion induced cell death

The aim of this dissertation was to analyse why cardiac arrhythmias occur after opening of the coronary arteries when a patient suffers an acute myocardial infarction. During this event, the heart muscle sustains damage due to a lack of oxygen. It was hypothesised that these arrhythmias indicate extra damage due to the reperfusion of oxygen-deprived heart muscle tissue. This is called a reperfusion injury. Cardiac arrhythmias could be the first marker of reperfusion injury. This marker could be used to indicate and develop treatment options for this type of injury

Editor's Choice- Reperfusion cardiac arrhythmias and their relation to reperfusion-induced cell death

Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death which is called lethal reperfusion injury. The time of reperfusion is often accompanied by ventricular arrhythmias, i.e. reperfusion arrhythmias. While both conditions are seen as separate processes, recent research has shown that reperfusion arrhythmias are related to larger infarct size. The pathophysiology of fatal reperfusion injury revolves around intracellular calcium overload and reactive oxidative species inducing apoptosis by opening of the mitochondrial protein transition pore. The pathophysiological basis for reperfusion arrhythmias is the same intracellular calcium overload as that causing fatal reperfusion injury. Therefore both conditions should not be seen as separate entities but as one and the same process resulting in two different visible effects. Reperfusion arrhythmias could therefore be seen as a potential marker for fatal reperfusion injury

Evaluation of the electrocardiogram in identifying and quantifying lateral involvement in nonanterior wall infarction using cardiovascular magnetic resonance imaging

AbstractPurposeThe objective of this study was to assess the involvement and extent of lateral wall myocardial infarction (MI) in patients with a first nonanterior wall MI, as reflected by changes in precordial leads. Delayed enhancement cardiac magnetic resonance imaging was used as a gold standard to localize and quantify myocardial scar tissue.MethodsElectrocardiogram and cardiac magnetic resonance were studied in 56 patients. Areas involved were related to QRS changes in precordial leads.ResultsSignificant correlations were found between lateral wall involvement and R waves in V1 and V6 (P = 0.009-0.022). For patients with circumflex branch occlusions, the MI size of the apical and lateral segments correlated strongly with the characteristics of R waves in V1 and V2 (P = 0.001-0.034).ConclusionsTall and broad R waves in V1 reflect lateral wall MI, especially in circumflex occlusions

The predictive value of an ECG-estimated Acute Ischemia Index for prognosis of myocardial salvage and infarct healing 3months following inferior ST-elevated myocardial infarction

Identification of prognostic markers can be used to stratify patients in the acute phase of ST-elevated myocardial infarction (STEMI) according to their potential to retain viable myocardium after reperfusion. The percentage of the myocardial area at risk (MaR) that is ischemic at admission, defined as the Acute Ischemia Index, is potentially salvageable. The percentage of the MaR viable at 3months post-reperfusion, by salvage and healing, was defined as the Chronic Salvage Index. A positive relationship between the Acute Ischemia Index and the Chronic Salvage Index was hypothesized. Both indices were assessed by using the ECG indices Aldrich ST and Selvester QRS scores estimating the ischemic and infarcted myocardium. The study population comprised inferior STEMI patients. (N=59). A correlation of 0.253 (P=0.053) was found. These results are relevant and suggest evidence of a trend in the association between these indice

Reperfusion ventricular arrhythmia bursts identify larger infarct size in spite of optimal epicardial and microvascular reperfusion using cardiac magnetic resonance imaging

Ventricular arrhythmia (VA) bursts following recanalisation in acute ST-elevation myocardial infarction (STEMI) are related to larger infarct size (IS). Inadequate microvascular reperfusion, as determined by microvascular obstruction (MVO) using cardiac magnetic resonance imaging (CMR), is also known to be associated with larger IS. This study aimed to test the hypothesis that VA bursts identify larger infarct size in spite of optimal microvascular reperfusion. All 65 STEMI patients from the Maastricht ST elevation (MAST) study with brisk epicardial flow (TIMI 3), complete ST recovery post-percutaneous coronary intervention and early CMR were included. Using 24-hour Holter registrations from the time of admission, VA bursts were identified against subject-specific Holter background VA rates using a statistical outlier method. MVO and final IS were determined using delayed enhancement CMR. MVO was present in 37/65 (57%) of patients. IS was significantly smaller in the group without MVO (median 9.4% vs. 20.5%; p < 0.001). IS in the group with MVO did not differ depending on VA burst ( n = 28/37; median 20.8% vs. 19.7%; p = 0.64). However, in the group without MVO, VA burst was associated with significantly larger IS ( n = 17/28; median 10.5% vs. 4.1%; p = 0.037). In multivariable analyses, VA burst as well as anterior infarct location remained independent predictors of larger infarct size. In the presence of suboptimal reperfusion with MVO by CMR, VA burst does not further define MI size. However, with optimal TIMI 3 reperfusion and optimal microvascular perfusion (i.e. no MVO), VA burst is associated with larger IS, indicating that VA burst is a marker of additional cell deat