Clinical significance of R-wave amplitude in lead V1 and inferobasal myocardial infarction in patients with inferior wall myocardial infarction.

OBJECTIVE: To assess electrocardiogram (ECG) for risk stratification in inferior ST-elevation myocardial infarction (STEMI) patients within 24 h. METHODS: Three hundred thirty-four patients were divided into four ECG-based groups: Group A: R V1 <0.3 mV with ST-segment elevation (ST↑) V7-V9, Group B: R V1 <0.3 mV without ST↑ V7-V9, Group C: R V1 ≥0.3 mV with ST↑ V7-V9, and Group D: R V1 ≥0.3 mV without ST↑ V7-V9. RESULTS: Group A demonstrated the longest QRS duration, followed by Groups B, C, and D. ECG signs for right ventricle (RV) infarction were more common in Groups A and B (p < .01). ST elevation in V6, indicative of left ventricle (LV) lateral injury, was more higher in Group C than in Group A, while the ∑ST↑ V3R + V4R + V5R, representing RV infarction, showed the opposite trend (p < .05). The estimated LV infarct size from ECG was similar between Groups A and C, yet Group A had higher creatine kinase MB isoform (CK-MB; p < .05). Cardiac troponin I (cTNI) was higher in Groups A and C than in B and D (p < .05 and p = .16, respectively). NT-proBNP decreased across groups (p = .20), with the highest left ventricular ejection fraction (LVEF) observed in Group D (p < .05). Group A notably demonstrated more cardiac dysfunction within 4 h post-onset. CONCLUSIONS: For inferior STEMI patients, concurrent R V1 <0.3 mV with ST↑ V7-V9 suggests prolonged ventricular activation and notable myocardial damage. RV infarction's dominance over LV lateral injury might explain these observations.

[Characteristics of Inferior Myocardial Infarction With a Special Electrocardiographic Pattern (Aslanger) in Metabolic Syndrome].

AIM: To evaluate the features of ST-segment elevation myocardial infarction with the Aslanger pattern in comparison with traditional forms of inferior myocardial infarction in metabolic syndrome. MATERIAL AND METHODS: This study included 30 patients with inferior myocardial infarction in the presence of metabolic syndrome: 9 patients with the Aslanger electrocardiographic pattern (group 1, age 59.7 [58.4; 63.1] years) and the rest with one of the traditional forms (control group, 59.9 [57.2; 63.8] years, matched by all criteria of metabolic syndrome). All patients underwent primary percutaneous intervention with assessment of the angiographic picture. The magnitude of ST-segment elevation was measured in lead III at the J point and following 0.06 seconds, and the optimal threshold value of this indicator was determined for a new picture of myocardial infarction. RESULTS: The infarct-related artery in the Aslanger pattern was more often the circumflex artery (p=0.0099), and coronary thrombosis was characterized by a lower TIMI thrombus grade (p=0.014). SYNTAX values for the Aslanger pattern and for the traditional picture of inferior infarction with ST elevation in lead II≥III were higher than for a similar picture with ST elevation in lead III>II. The level of cTnI at admission (p=0.013) and after 24 hours (p=0.0017), the platelet count (p=0.0011) and mean volume (p=0.0047) in group 1 had smaller values than with traditional inferior infarction. The ST elevation at J point and at J+0.06 s point for lead III with the Aslanger pattern was significantly lower than values of such shift in lead III>II and lead II≥III with traditional inferior infarction (p<0.001). An elevation value ≤1.5 mm at J point +0.06 s was a predictor of infarction with the Aslanger pattern. Constructing the ROC curve made it possible to determine that with the Aslanger pattern, the best cutoff value for this index is 2 mm. CONCLUSION: Myocardial infarction with the Aslanger pattern as compared with traditional lower infarction in metabolic syndrome is characterized by specific individual angiographic signs, lower ST segment elevation, cTnI level, and thrombotic disorders.

Diagnostic value of electrocardiographic indices in discriminating the culprit vessel based on the coronary dominancy in inferior acute myocardial infarction.

BACKGROUND: Identifying the culprit during inferior myocardial infarction (MI) is still challenging. We determined the diagnostic effect of electrocardiographic (ECG) indices in identifying the culprit vessel of acute MI and the impact of coronary artery dominance on it. METHODS: This cross-sectional study included patients with acute inferior MI who presented to Imam Khomeini Hospital and Tehran Heart Center and underwent primary PCI within 12 h of the onset of symptoms. A standard 12­lead ECG was recorded and interpreted by two cardiologists. Based on the coronary angiography, the patients were divided into two groups of LCX or RCA involvement and were compared for general variables and ECG indices. The diagnostic values of the ECG indices for predicting the culprit vessel were then calculated. RESULTS: We evaluated 411 patients with inferior STEMI (321 [77.5%] male, age 58.1 ± 11.1 years). RCA was the culprit vessel in 286 patients (69.1%) and LCX in 128 patients (30.9%). 321 patients (77.5%) were right dominant, 40 (9.7%) patients were left dominant, and 53 patients (12.8%), were codominant. Coronary dominance had minimal impact on the ECG indices regarding culprit identification even after adjustment for confounders. STE in lead III > lead II had the highest sensitivity for detecting RCA as the culprit (sensitivity: 89.2% and specificity: 57.8%). STE ≥0.1 mV in V5 or V6 leads had the highest sensitivity for detecting LCX as the culprit (sensitivity: 51.6, specificity: 93.7%). CONCLUSION: In inferior STEMI, ECG indices can predict the culprit vessel with acceptable sensitivity and specificity independent of coronary artery dominance.

A rare case of concurrent left ventricular aneurysm and ventricular septal rupture complicating an inferior myocardial infarction: a case report.

Complications following acute myocardial infarction (MI) such as ventricular septal rupture (VSR) and left ventricular (LV) aneurysm are rare and can be dreadful. Their simultaneous presence in the same patient is extremely rare. We aimed to present a rare case of concomitant association of ventricular aneurysm and VSR complicating an inferior myocardial infarction. We report the unusual case of Mr. A. D, a 63-year-old, active smoker, with a history of diabetes mellitus and hypertension, admitted for the management of inferior MI within 6 days. The MI was complicated by an LV aneurysm in the inferoposterior and the inferoseptal walls associated with a VSR in the inferoseptal wall. The patient had only signs of right heart failure on admission. This observation illustrates on the one hand the rarity of the association of VSR and LV aneurysm after an inferior myocardial infarction, and on the other hand the possibility of founding them at an early stage of MI without any signs of cardiogenic shock.

Enhancing Diagnosis of Anterior and Inferior Myocardial Infarctions Using UWB Radar and AI-Driven Feature Fusion Approach.

Despite significant improvement in prognosis, myocardial infarction (MI) remains a major cause of morbidity and mortality around the globe. MI is a life-threatening cardiovascular condition that requires prompt diagnosis and appropriate treatment. The primary objective of this research is to identify instances of anterior and inferior myocardial infarction by utilizing data obtained from Ultra-wideband radar technology in a hospital for patients of anterior and inferior MI. The collected data is preprocessed to extract spectral features. A novel feature engineering approach is designed to fuse temporal features and class prediction probability features derived from the spectral feature dataset. Several well-known machine learning models are implemented and fine-tuned to obtain optimal performance in the detection of anterior and inferior MI. The results demonstrate that integration of the fused feature set with machine learning models results in a notable improvement in both the accuracy and precision of MI detection. Notably, random forest (RF) and k-nearest neighbor showed superb performance with an accuracy of 98.8%. For demonstrating the capacity of models to generalize, K-fold cross-validation is carried out, wherein RF exhibits a mean accuracy of 99.1%. Furthermore, the examination of computational complexity indicates a low computational complexity, thereby indicating computational efficiency.

Acute inferior myocardial infarction combined with papillary muscle rupture: A case report. / 急性下壁心肌梗死合并乳头肌断裂1例.

The incidence of acute myocardial infarction (AMI) is increasing. Acute papillary muscle rupture is one of the serious and rare mechanical complications of AMI, which occurs mostly in inferior and posterior myocardial infarction. A patient with acute inferior myocardial infarction developed pulmonary edema and refractory shock, followed by cardiac arrest. After cardiopulmonary resuscitation (CPR), revascularization of criminal vessels was carried out by emergency percutaneous transluminal coronary angioplasty (PTCA) under the support of intra-aortic balloon pump (IABP) and extra corporeal membrane oxygenation (ECMO). Although the patient was given a chance for surgery, his family gave up treatment due to unsuccessful brain resuscitation. It reminds that mechanical complications such as acute papillary muscle rupture, valvular dysfunction and rupture of the heart should be highly suspected when cardiogenic pulmonary edema and cardiogenic shock are difficult to correct in acute inferior myocardial infarction. Echocardiogram and surgery should be put forward when revascularization of criminal vessels is available.

Two Giant Right Coronary Artery Aneurysms Presenting as Late ST-Segment Elevation Inferior Wall Myocardial Infarction.

Coronary artery ectasia is reported 1.2% up to 7.4% of patients. Giant coronary artery aneurysms are seen in 0.02% of patients. The best therapeutic approach is not yet defined. To our knowledge, this case report is the first to show 2 giant, partially thrombosed aneurysms of such enormous dimensions presenting as late ST-segment elevation infarction.

Autoimmune limbic encephalitis mimicking inferior myocardial infarction on ECG.

A man in his 60s with prior history of coronary artery bypass graft was found collapsed, unresponsive on the floor by family. ECG demonstrated an inferior ST elevation myocardial infarction. However, coronary angiography was negative for a culprit lesion. A faciobrachial dystonic seizure was witnessed during his hospitalisation, ultimately leading to a diagnosis of leucine-rich glioma-inactivated 1 (LGI-1) autoimmune encephalitis. It is likely that neurogenic stunned myocardium led to this presentation.

Prediction of massive coronary thrombosis of the infarct-related artery in ST-elevation myocardial infarction.

Aim    To identify clinical, laboratory and angiographic predictors for development of massive coronary thrombosis in patients with ST-segment elevation myocardial infarction (STEMI).Material and methods    This prospective, single-site study included 137 patients with STEMI (mean age, 66.5±13.2 years). Among these patients, 59 were in the group of massive coronary thrombosis and 78 patients were in the group of minor thrombosis. To identify predictors for the development of massive coronary thrombosis, medical history data, blood count and biochemistry, coagulogram, and angiography data were analyzed. A predictive model was constructed using the method of binary logistic regression followed by a search for the optimum value of the prognostic function with a ROC analysis. Results    The study showed statistically significant roles of total bilirubin, platelets, prothrombin ratio (PTR), activated partial thromboplastin time (APTT), and presence of inferior myocardial infarction in prediction of massive coronary thrombosis in STEMI. The model sensitivity was 71.2 %, specificity 75.6 %, and overall diagnostic efficacy 73.7 %.Conclusion    The predictive model for the development of massive coronary thrombosis in STEMI based on laboratory and instrumental data potentially allows assessing the thrombus load in the infarction-involved coronary artery and determining the optimum tactics of percutaneous coronary intervention in patients with STEMI. This reduces the probability of distal embolization with fragments of the disintegrated thrombus and improves the prognosis of STEMI patients both during the stay in the hospital and in the long-term. According to results of this study, the prognostic model for massive coronary thrombosis in STEMI based on such indexes as the platelet count, PTR, APTT, total bilirubin, and presence of inferior myocardial infarction provides accurate predictions in 73.7 % of cases. Independent predictors of massive coronary thrombosis were inferior myocardial infarction and total bilirubin.

Acute Pancreatitis and Myocardial Infarction: A Narrative Review.

BACKGROUND: Acute pancreatitis can rarely present with electrocardiographic changes that imitate myocardial ischemia. Even rarer is for acute pancreatitis to present with ST segment elevation in contiguous leads, suggestive of an acute coronary syndrome. In this comprehensive review article, we highlight diagnostic challenges and examine possible pathophysiological causes as seen through 34 total cases in which acute pancreatitis has been found to mimic an acute myocardial infarction. SUMMARY: It has been shown that regardless of the severity of acute pancreatitis, it can be associated with myocardial injury of varying presentation. Thus far, there have been 34 total cases where acute pancreatitis presented with electrocardiographic changes consistent with acute myocardial infarction without true coronary artery thrombosis. An inferior wall ST-elevation myocardial infarction pattern was the most frequently demonstrated. Many hypotheses have been proposed as to the mechanism of injury including decreased coronary perfusion, direct myocyte damage by pancreatic proteolytic enzymes, indirect parasympathetic injury, electrolyte derangements, and coronary vasospasms. Given the complexity of the clinical presentation, thorough subjective and objective evaluation can be vital in guiding to diagnosis and possibly more invasive testing. KEY MESSAGES: It is imperative that clinicians are aware that acute pancreatitis can mimic an acute myocardial infarction. Although we have started to better understand the pathological mechanisms for this phenomenon, further research focused on specific molecular target areas is needed.

Successful percutaneous coronary intervention with extracorporeal membrane oxygenation in a patient with acute inferior wall myocardial infarction complicated by electrical storm, cardiogenic shock, and cardiac arrest: a case report.

BACKGROUND: High-risk patients with coronary heart disease who develop acute myocardial infarction (AMI) have severe coronary lesions. If severe complications occur, such as malignant ventricular arrhythmia, cardiogenic shock, and cardiac arrest, implementation of emergency percutaneous coronary intervention (PCI) may be hindered, leading to a higher perioperative mortality rate. Extracorporeal membrane oxygenation (ECMO) can pave the way for rapid myocardial reperfusion therapy. When cardiac arrest occurs, hemodynamic support with ECMO can facilitate revascularization with PCI, which can increase the time available for further salvage and treatment and reduce intraoperative risk during PCI. CASE PRESENTATION: Herein, we report a case of a 61-year-old man with AMI who suffered electrical storm of sustained malignant ventricular fibrillation, cardiogenic shock, and cardiac arrest and was successfully treated with PCI with ECMO support. During PCI, repeated aspiration and removal of the right coronary artery thrombus were performed, and blood flow was restored after right coronary artery balloon dilation. One episode of defibrillation was delivered to restore sinus rhythm. Then, stents were implanted in the distal and proximal right coronary artery lesions to achieve revascularization. After PCI with ECMO support, irreversible malignant arrhythmia returned to sinus rhythm through coronary perfusion, which prevented death following unsuccessful cardiopulmonary resuscitation. After applying active treatments, including anti-shock, mechanical ventilation, anti-inflammation, and organ support, the patient was discharged after his condition and vital signs stabilized. The patient was followed up once a week after hospital discharge, and his cardiopulmonary function recovered well. CONCLUSIONS: With ECMO support, PCI should be performed immediately in patients with inferior wall AMI complicated by electrical storm of sustained ventricular fibrillation, cardiogenic shock, and cardiac arrest to facilitate stent placement, achieve complete revascularization, restore coronary perfusion, and avoid death.

Identifying the culprit artery via 12-lead electrocardiogram in inferior wall ST-segment elevation myocardial infarction: A meta-analysis.

BACKGROUND: Inferior wall ST-segment elevation myocardial infarction (STEMI) is mostly caused by acute occlusion of right coronary artery (RCA) and left circumflex artery (LCX). Several methods and algorithms using 12-lead ECG were developed to localize the lesion in inferior wall STEMI. However, the diagnostic properties of these methods remain under-recognized. AIMS: The aim of this meta-analysis is to compare the diagnostic properties among the methods of identifying culprit artery in inferior wall STEMI using 12-lead ECG. METHODS: We performed a meta-analysis to calculate the pooled sensitive, specificity, area under the curve (AUC) and diagnostic odds ratio (DOR) of each method. RESULTS: Thirty-three studies with 4414 participants were included in the analysis. Methods using double leads had better diagnostic properties, especially ST-segment elevation (STE) in III > II [with pooled sensitivity 0.89 (0.84-0.93), specificity 0.68 (0.57-0.79), DOR 17 (9-32), AUC 0.88 (0.85-0.91)], ST-segment depression (STD) in aVL > I [with pooled sensitivity 0.82 (0.72-0.90), specificity 0.69 (0.48-0.86), DOR 11 (4-29), AUC 0.85 (0.81-0.88)], and STD V3/STE III ≤1.2 [with pooled sensitivity 0.88 (0.78-0.95), specificity 0.59 (0.42-0.75), DOR 12 (5-27), AUC 0.82 (0.78-0.85)]. Diagnostic algorithms, including Jim score[pooled sensitivity 0.70 (0.55-0.85), specificity 0.88 (0.75-0.96)], Fiol's algorithm [pooled sensitivity 0.54 (0.44-0.62), specificity 0.92 (0.88-0.96)] and Tierala's algorithm [pooled sensitivity 0.60 (0.49-0.71), specificity 0.91 (0.86-0.96)], were not superior to these simple methods. CONCLUSIONS: Our meta-analysis indicated that diagnostic methods using double leads had better properties. STE in III > II together with STD in aVL > I may be the most ideal method, for its accuracy and convenience.

Early right ventricular dysfunction after primary percutaneous coronary intervention in anterior versus isolated inferior myocardial infarction assessed by tissue Doppler imaging and speckle tracking echocardiography.

This study hypothesized that imaging provides information indicating the right ventricular (RV) involvement after anterior or inferior ST-elevation myocardial infarction (STEMI), beyond standard electrocardiogram (ECG) due to the increasing interest in RV function and assessment techniques. This study aimed to compare RV function between anterior and inferior MI without RV involvement using different echocardiographic modalities. This study included 100 patients with anterior (50 patients) and inferior (50 patients) STEMI, who underwent primary percutaneous coronary intervention (PPCI) and two-dimensional echocardiographic imaging within 24 h after PPCI with RV function analysis by left ventricular (LV) infarct size, LV filling pressure, and RV strain rate. Our primary endpoint was the subclinical RV dysfunction in anterior or inferior MI using tissue Doppler and speckle tracking (STE). The study population included 80 (80%) males and 20 (20%) females. Patients with the anterior STEMI had higher mean creatine kinase-MB (CKMB) and troponin than those with inferior STEMI. This study revealed worse RV dysfunction in patients with anterior than those with inferior STEMI, as reflected by significantly lower RV systolic function, tricuspid annular plane systolic excursion (p ≤ 0.0001), tissue Doppler-derived velocity (p ≤ 0.0001), and STE-derived strain magnitude and rate (p ≤ 0.0001). RV dysfunction occurs in patients without ECG evidence of RV STEMI. RV dysfunction is worse in anterior than inferior MI. Moreover, RV systolic functions were affected by declined LV ejection fraction irrespective of the infarction site, which clinically implies prognostic, treatment, survival rate, and outcome improvement between both conditions. (Trial registration ZU-IRB#:4142/26-12-2017 Registered 26 December 2017, email: IRB_123@medicine.zu.edu.eg).

Acute inferior myocardial infarction combined with papillary muscle rupture: A case report / 中南大学学报(医学版)

The incidence of acute myocardial infarction (AMI) is increasing. Acute papillary muscle rupture is one of the serious and rare mechanical complications of AMI, which occurs mostly in inferior and posterior myocardial infarction. A patient with acute inferior myocardial infarction developed pulmonary edema and refractory shock, followed by cardiac arrest. After cardiopulmonary resuscitation (CPR), revascularization of criminal vessels was carried out by emergency percutaneous transluminal coronary angioplasty (PTCA) under the support of intra-aortic balloon pump (IABP) and extra corporeal membrane oxygenation (ECMO). Although the patient was given a chance for surgery, his family gave up treatment due to unsuccessful brain resuscitation. It reminds that mechanical complications such as acute papillary muscle rupture, valvular dysfunction and rupture of the heart should be highly suspected when cardiogenic pulmonary edema and cardiogenic shock are difficult to correct in acute inferior myocardial infarction. Echocardiogram and surgery should be put forward when revascularization of criminal vessels is available.

Characteristics and mechanism of reciprocal ST-segment depression in acute ST segment elevation myocardial infarction: Reciprocal ST-segment depression and ST segment elevation myocardial infarction.

At present, the mechanism of reciprocal ST-segment depression (RSTD) is unclear. ST-segment changes may be caused by the potential difference between the positive and negative electrodes, although this requires further investigation. The characteristics of RSTD and their relationship with ST-segment elevation in acute ST segment elevation myocardial infarction (STEMI) patients were analyzed. We replaced the negative electrode of the precordial leads of an inferior wall myocardial infarction patient and observed the changes in the ST-segment of the precordial leads. A total of 85 patients were included, of which 75 were patients with RSTD. All 45 patients with inferior myocardial infarction had limb lead RSTD, and 37 had anterior lead ST-segment depression. All ST-segment changes in STEMI can be explained by the proposed mechanism, and the value of ST segment depression in limb leads can be calculated by the value of ST segment elevation. In summary, the mechanism of RSTD in acute myocardial infarction may be that the action potential (AP) of the negative electrode of the lead weakens or disappears and the AP of the positive electrode may not be completely offset, resulting in ST-segment depression. Animal experimental studies are needed for further confirmation. When the negative electrode of the precordial lead is changed in acute inferior wall myocardial infarction patient, the ST-segment of the precordial lead changes accordingly. All the changes are consistent with our analysis.

Subepicardial burn injuries in bullfrog heart induce electrocardiogram changes mimicking inferior wall myocardial infarction.

Using bullfrog hearts, we previously reproduced a ST segment elevation in electrocardiogram (ECG), mimicking human ischemic heart disease. In the present study, by inducing subepicardial burn injuries on the inferior part of the frog heart ventricle, we could reproduce typical ECG changes observed in human inferior wall myocardial infarction, such as the marked elevation of the ST segments in inferior limb leads (II, III, aVF) and their reciprocal depression in the opposite limb leads (I, aVL). Due to the decrease in Na+/K+-ATPase protein expression, the resting membrane potential of injured cardiomyocytes shifted toward depolarization. Such induced electrical difference between the injured and intact cardiomyocytes was thought to be responsible for the creation of "currents of injury" and the subsequent ST segment changes.