Kirian Van Der Weg - Academia.edu (2024)

Netherlands Heart Journal, 2019

European Heart Journal, 2013

European Heart Journal, 2013

Journal of Electrocardiology, 2011

The aim of this study was to assess the relationship between initial ST-segment deviation and fin... more The aim of this study was to assess the relationship between initial ST-segment deviation and final QRS complex changes related to the posterolateral left ventricular wall in patients with acute inferior myocardial infarction receiving reperfusion therapy. The secondary aim was to determine if this relationship is stronger for patients who present early in the ischemia/infarction process in comparison with patients who present late. The ST-segment depression in the leads V(1), V2, and -V6 were measured in the electrocardiograph (ECG) just before initiation of myocardial reperfusion. These leads were chosen because they represent the posterolateral wall in the Selvester score. In addition, the Anderson-Wilkins acuteness score was calculated in the admission ECG. Selvester criteria related to the posterolateral wall were identified in the ECG performed before hospital discharge to assess final infarct size. Fifty-six patients were included in this study. No significant relationship was found between the sum of initial ST-segment depression in the leads V(1), V(2), and -V(6), and final infarct size in the posterolateral left ventricular wall for the total study population (r = 0.19, P = .16). Patients were subgrouped by Anderson-Wilkins acuteness score of less than 3 vs 3 or more. In those with a low acuteness score, the amount of ST-segment depression had no relationship with final infarct size (r = -0.16, P = .41). However, the correlation was statistically significant for those with a high acuteness score (r = 0.42, P = .04). The initial ST-segment depression in leads V(1), V(2), and -V(6) can predict ECG-estimated amount of infarction in the posterolateral left ventricular wall in patients with acute inferior myocardial infarction receiving reperfusion therapy, but only in those who present early in the ischemia/infarction process.

European Heart Journal: Acute Cardiovascular Care, 2017

Aims: Ventricular arrhythmia (VA) bursts following recanalisation in acute ST-elevation myocardia... more Aims: 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. Methods: 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. Results: MVO was present in 37/65 (57%) of patients. IS was significantly smalle...

International journal of cardiology, Jan 20, 2015

Early reperfusion of ischemic myocytes is essential for optimal salvage in acute myocardial infar... more Early reperfusion of ischemic myocytes is essential for optimal salvage in acute myocardial infarction. VA (ventricular arrhythmia) bursts after recanalization of the culprit vessel have been found to be related to larger infarct size (IS), using SPECT. The hypothesis was tested that this finding could be confirmed in an independent cohort using a more accurate technique, i.e. delayed-enhancement cardiovascular magnetic resonance imaging (DE-CMR). All 196 patients from the PREPARE and MAST studies who had 24-hour, continuous, 12-lead Holter, started before primary percutaneous coronary intervention resulting in brisk TIMI (thrombolysis in myocardial infarction) 3 flow and stable ST-recovery were included. VA bursts were identified against subject-specific background VA rates using a previously published statistical outlier method. IS was assessed using DE-CMR. Angiography, Holter and DE-CMR results were assessed in core laboratories, blinded to all other data. VA bursts were present...

Journal of Electrocardiology, 2010

Journal of electrocardiology, Jan 8, 2016

We hypothesized that ventricular arrhythmia (VA) bursts during reperfusion phase are a marker of ... more We hypothesized that ventricular arrhythmia (VA) bursts during reperfusion phase are a marker of larger infarct size despite optimal epicardial and microvascular perfusion. 126 STEMI patients were studied with 24h continuous, 12-lead Holter monitoring. Myocardial blush grade (MBG) was determined and VA bursts were identified against subject-specific background VA rates in core laboratories. Delayed-enhancement cardiovascular magnetic resonance imaging was used to determine infarct size. In the group with MBG 3 no significant differences were found for baseline characteristics between burst versus no burst (102 vs. 24). In those with optimal epicardial and microvascular reperfusion (TIMI 3, stable ST-recovery, and MBG 3), VA burst was associated with larger infarct size (N=102/126; median 11.0 vs. 5.1%; p=0.004). In the event of MBG 3, VA bursts were associated with significantly larger infarct size even if optimal epicardial and microvascular reperfusion was present.

International journal of cardiology, Jan 30, 2018

The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger ... more The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger infarct size (IS). However it is unclear whether the initial area at risk (AAR), also a determining factor for IS, is responsible for this correlation. We hypothesized that IS would be significantly larger in the presence of VA, while AAR would not differ. 68 STEMI patients from the MAST study with 24-hour, continuous, 12‑lead Holter monitoring initiated prior to primary percutaneous coronary intervention (PCI) resulting in TIMI 3 flow post PCI were included. VA bursts were identified against subject-specific background VA rates using a previously validated statistical outlier method. IS, and infarct endocardial surface area (ESA) were obtained using CMR at mean 4.9 days after admission. Holter and CMR results were determined in core laboratories blinded to all other data. VA bursts were present in 69% (45/65) of patients. No significant differences were found for demographic characteris...

International Journal of Cardiology

The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger ... more The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger infarct size (IS). However it is unclear whether the initial area at risk (AAR), also a determining factor for IS, is responsible for this correlation. We hypothesized that IS would be significantly larger in the presence of VA, while AAR would not differ. 68 STEMI patients from the MAST study with 24-hour, continuous, 12‑lead Holter monitoring initiated prior to primary percutaneous coronary intervention (PCI) resulting in TIMI 3 flow post PCI were included. VA bursts were identified against subject-specific background VA rates using a previously validated statistical outlier method. IS, and infarct endocardial surface area (ESA) were obtained using CMR at mean 4.9 days after admission. Holter and CMR results were determined in core laboratories blinded to all other data. VA bursts were present in 69% (45/65) of patients. No significant differences were found for demographic characteristics, comorbidities, infarct location, number of diseased coronary vessels, or duration of ischemia between groups with and without VA burst. IS was significantly smaller in the group without VA bursts (median 9.3% vs 17.0%; p = 0.025). Infarct ESA did not significantly differ between the population with and without VA burst; median 24.3% vs 20.0%; p = 0.15. VA bursts are a marker for larger IS independent of AAR, assessed by surrogate markers. These findings support the hypothesis that VA bursts are a marker of reperfusion damage occurring downstream at myocellular level.

European Heart Journal: Acute Cardiovascular Care

Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death w... more 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.

Journal of the American College of Cardiology, 2013

Journal of Electrocardiology, 2015

Recent research has established that a tall R-wave in V1 indicates lateral wall involvement in no... more Recent 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. ECGs 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. ST-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. ST-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.

Journal of Electrocardiology, 2012

Journal of Electrocardiology, 2013

Identification of prognostic markers can be used to stratify patients in the acute phase of ST-el... more 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 indices.

International Journal of Cardiology, 2015

ABSTRACT Studies comparing Q waves of necrosis in antero-lateral leads with the site and extent o... more ABSTRACT Studies comparing Q waves of necrosis in antero-lateral leads with the site and extent of myocardial infarction (MI) at contrast-enhanced cardiac magnetic resonance show that patients can be clustered into four different locations of MI. 1) Septal MI. In these patients Q waves are present in leads V1-V2 and an MI scar is located in the interventricular septum. Sensitivity 100%; specificity 97%. Due to the great variability in coronary artery distribution and because the diagnosis depends on the presence of Q wave in lead V3, the sensitivity and specificity may change unless a strict methodology of positioning of precordial electrodes is followed. 2) Apical-anterior MI. In such a case Q waves are present from leads V1-V2 to V3-V6 and MI scars are located in the anterior wall and apex. Sensitivity 85%; specificity 98%. If the inferior involvement is large, Q waves in leads II, III and aVF are frequently associated. Even in the absence of inferior Q waves, 13% of the "anterior" infarction scar is extended to the inferior and/or inferoseptal apical segments, and 6% is extended to the lateral apical segment. 3) Mid-anterior MI: In these patients Q waves, QS or qr complexes are present in lead aVL and/or I, and sometimes in leads V2-V3. In the past this pattern was considered to correspond to a high lateral MI, involving the portion of the LV lateral wall perfused by the left circumflex artery or the obtuse marginal branch. More recently, this pattern has been found to correspond to a mid-anterior MI, involving the portion of lateral wall perfused by the first diagonal branch. Sensitivity 67%; specificity 100%. 4) Extensive anterior MI: In this case Q waves appear both from leads V1-V2 to V4-V6, and in leads I and aVL. This pattern suggests that the infarction scar is more extensive than the apical zone, also involving the anterior, septal and mid-low lateral walls. Sensitivity 83%; specificity 100%. Finally, the greater the number of anterior Q-waves, the larger the MI size and its transmural extent. This classification is limited by the variability in coronary artery distribution, in the anatomical and electrical orientation of the heart inside the thorax, and finally, by a possible misplacement of precordial electrodes.

Netherlands Heart Journal, 2019

European Heart Journal, 2013

European Heart Journal, 2013

Journal of Electrocardiology, 2011

The aim of this study was to assess the relationship between initial ST-segment deviation and fin... more The aim of this study was to assess the relationship between initial ST-segment deviation and final QRS complex changes related to the posterolateral left ventricular wall in patients with acute inferior myocardial infarction receiving reperfusion therapy. The secondary aim was to determine if this relationship is stronger for patients who present early in the ischemia/infarction process in comparison with patients who present late. The ST-segment depression in the leads V(1), V2, and -V6 were measured in the electrocardiograph (ECG) just before initiation of myocardial reperfusion. These leads were chosen because they represent the posterolateral wall in the Selvester score. In addition, the Anderson-Wilkins acuteness score was calculated in the admission ECG. Selvester criteria related to the posterolateral wall were identified in the ECG performed before hospital discharge to assess final infarct size. Fifty-six patients were included in this study. No significant relationship was found between the sum of initial ST-segment depression in the leads V(1), V(2), and -V(6), and final infarct size in the posterolateral left ventricular wall for the total study population (r = 0.19, P = .16). Patients were subgrouped by Anderson-Wilkins acuteness score of less than 3 vs 3 or more. In those with a low acuteness score, the amount of ST-segment depression had no relationship with final infarct size (r = -0.16, P = .41). However, the correlation was statistically significant for those with a high acuteness score (r = 0.42, P = .04). The initial ST-segment depression in leads V(1), V(2), and -V(6) can predict ECG-estimated amount of infarction in the posterolateral left ventricular wall in patients with acute inferior myocardial infarction receiving reperfusion therapy, but only in those who present early in the ischemia/infarction process.

European Heart Journal: Acute Cardiovascular Care, 2017

Aims: Ventricular arrhythmia (VA) bursts following recanalisation in acute ST-elevation myocardia... more Aims: 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. Methods: 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. Results: MVO was present in 37/65 (57%) of patients. IS was significantly smalle...

International journal of cardiology, Jan 20, 2015

Early reperfusion of ischemic myocytes is essential for optimal salvage in acute myocardial infar... more Early reperfusion of ischemic myocytes is essential for optimal salvage in acute myocardial infarction. VA (ventricular arrhythmia) bursts after recanalization of the culprit vessel have been found to be related to larger infarct size (IS), using SPECT. The hypothesis was tested that this finding could be confirmed in an independent cohort using a more accurate technique, i.e. delayed-enhancement cardiovascular magnetic resonance imaging (DE-CMR). All 196 patients from the PREPARE and MAST studies who had 24-hour, continuous, 12-lead Holter, started before primary percutaneous coronary intervention resulting in brisk TIMI (thrombolysis in myocardial infarction) 3 flow and stable ST-recovery were included. VA bursts were identified against subject-specific background VA rates using a previously published statistical outlier method. IS was assessed using DE-CMR. Angiography, Holter and DE-CMR results were assessed in core laboratories, blinded to all other data. VA bursts were present...

Journal of Electrocardiology, 2010

Journal of electrocardiology, Jan 8, 2016

We hypothesized that ventricular arrhythmia (VA) bursts during reperfusion phase are a marker of ... more We hypothesized that ventricular arrhythmia (VA) bursts during reperfusion phase are a marker of larger infarct size despite optimal epicardial and microvascular perfusion. 126 STEMI patients were studied with 24h continuous, 12-lead Holter monitoring. Myocardial blush grade (MBG) was determined and VA bursts were identified against subject-specific background VA rates in core laboratories. Delayed-enhancement cardiovascular magnetic resonance imaging was used to determine infarct size. In the group with MBG 3 no significant differences were found for baseline characteristics between burst versus no burst (102 vs. 24). In those with optimal epicardial and microvascular reperfusion (TIMI 3, stable ST-recovery, and MBG 3), VA burst was associated with larger infarct size (N=102/126; median 11.0 vs. 5.1%; p=0.004). In the event of MBG 3, VA bursts were associated with significantly larger infarct size even if optimal epicardial and microvascular reperfusion was present.

International journal of cardiology, Jan 30, 2018

The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger ... more The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger infarct size (IS). However it is unclear whether the initial area at risk (AAR), also a determining factor for IS, is responsible for this correlation. We hypothesized that IS would be significantly larger in the presence of VA, while AAR would not differ. 68 STEMI patients from the MAST study with 24-hour, continuous, 12‑lead Holter monitoring initiated prior to primary percutaneous coronary intervention (PCI) resulting in TIMI 3 flow post PCI were included. VA bursts were identified against subject-specific background VA rates using a previously validated statistical outlier method. IS, and infarct endocardial surface area (ESA) were obtained using CMR at mean 4.9 days after admission. Holter and CMR results were determined in core laboratories blinded to all other data. VA bursts were present in 69% (45/65) of patients. No significant differences were found for demographic characteris...

International Journal of Cardiology

The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger ... more The presence of reperfusion ventricular arrhythmias (VA) has been shown to correlate with larger infarct size (IS). However it is unclear whether the initial area at risk (AAR), also a determining factor for IS, is responsible for this correlation. We hypothesized that IS would be significantly larger in the presence of VA, while AAR would not differ. 68 STEMI patients from the MAST study with 24-hour, continuous, 12‑lead Holter monitoring initiated prior to primary percutaneous coronary intervention (PCI) resulting in TIMI 3 flow post PCI were included. VA bursts were identified against subject-specific background VA rates using a previously validated statistical outlier method. IS, and infarct endocardial surface area (ESA) were obtained using CMR at mean 4.9 days after admission. Holter and CMR results were determined in core laboratories blinded to all other data. VA bursts were present in 69% (45/65) of patients. No significant differences were found for demographic characteristics, comorbidities, infarct location, number of diseased coronary vessels, or duration of ischemia between groups with and without VA burst. IS was significantly smaller in the group without VA bursts (median 9.3% vs 17.0%; p = 0.025). Infarct ESA did not significantly differ between the population with and without VA burst; median 24.3% vs 20.0%; p = 0.15. VA bursts are a marker for larger IS independent of AAR, assessed by surrogate markers. These findings support the hypothesis that VA bursts are a marker of reperfusion damage occurring downstream at myocellular level.

European Heart Journal: Acute Cardiovascular Care

Reperfusion does not only salvage ischaemic myocardium but can also cause additional cell death w... more 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.

Journal of the American College of Cardiology, 2013

Journal of Electrocardiology, 2015

Recent research has established that a tall R-wave in V1 indicates lateral wall involvement in no... more Recent 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. ECGs 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. ST-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. ST-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.

Journal of Electrocardiology, 2012

Journal of Electrocardiology, 2013

Identification of prognostic markers can be used to stratify patients in the acute phase of ST-el... more 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 indices.

International Journal of Cardiology, 2015

ABSTRACT Studies comparing Q waves of necrosis in antero-lateral leads with the site and extent o... more ABSTRACT Studies comparing Q waves of necrosis in antero-lateral leads with the site and extent of myocardial infarction (MI) at contrast-enhanced cardiac magnetic resonance show that patients can be clustered into four different locations of MI. 1) Septal MI. In these patients Q waves are present in leads V1-V2 and an MI scar is located in the interventricular septum. Sensitivity 100%; specificity 97%. Due to the great variability in coronary artery distribution and because the diagnosis depends on the presence of Q wave in lead V3, the sensitivity and specificity may change unless a strict methodology of positioning of precordial electrodes is followed. 2) Apical-anterior MI. In such a case Q waves are present from leads V1-V2 to V3-V6 and MI scars are located in the anterior wall and apex. Sensitivity 85%; specificity 98%. If the inferior involvement is large, Q waves in leads II, III and aVF are frequently associated. Even in the absence of inferior Q waves, 13% of the "anterior" infarction scar is extended to the inferior and/or inferoseptal apical segments, and 6% is extended to the lateral apical segment. 3) Mid-anterior MI: In these patients Q waves, QS or qr complexes are present in lead aVL and/or I, and sometimes in leads V2-V3. In the past this pattern was considered to correspond to a high lateral MI, involving the portion of the LV lateral wall perfused by the left circumflex artery or the obtuse marginal branch. More recently, this pattern has been found to correspond to a mid-anterior MI, involving the portion of lateral wall perfused by the first diagonal branch. Sensitivity 67%; specificity 100%. 4) Extensive anterior MI: In this case Q waves appear both from leads V1-V2 to V4-V6, and in leads I and aVL. This pattern suggests that the infarction scar is more extensive than the apical zone, also involving the anterior, septal and mid-low lateral walls. Sensitivity 83%; specificity 100%. Finally, the greater the number of anterior Q-waves, the larger the MI size and its transmural extent. This classification is limited by the variability in coronary artery distribution, in the anatomical and electrical orientation of the heart inside the thorax, and finally, by a possible misplacement of precordial electrodes.