Olson method for locating and calculating the extent of transmural ischemic areas at risk of infarction.

OBJECTIVES: The purpose of this study is to present a new and improved method for translating the electrocardiographic changes of acute myocardial ischemia into a display which reflects the location and extent of the ischemic area and the associated culprit coronary artery. This method could be automated to present a graphic image of the ischemic area in a manner understandable by all levels of caregivers; from emergency transport personnel to the consulting cardiologist. BACKGROUND: Current methods for the ECG diagnosis of ST elevated myocardial infarction (STEMI) are criteria driven, and complex, and beyond the interpretive capability of many caregivers. New methods are needed to accurately diagnose the presence of acute transmural myocardial ischemia in order to accelerate a patient's clinical "door to balloon time." The proposed new method could potentially provide the information needed to accomplish this objective. METHODS: The new method improves the precision of diagnosis and quantification of ischemia by normalizing the ST segment inputs from the standard 12 lead ECG, transforming these into a three dimensional vector representation of the ischemia at the electrical center of the heart. The myocardial areas likely to be involved in this ischemia are separately analyzed to assess the probability that they contributed to this event. The source of the ischemia is revealed as a specific region of the heart, and the likely location of the associated culprit coronary artery. Seventy 12 lead ECGs from subjects with known single artery occlusion in one of the three main coronary arteries were selected to test this new method. Graphic plots of the distribution of ischemia as indicated by the method are consistent with the known occlusion. The analysis of the distribution of ischemic areas in the myocardium reveals that the relationships between leads with either ST elevation or ST depression, provide critical information improving the current method.

Maximal increase in sensitivity with minimal loss of specificity for diagnosis of acute coronary occlusion achieved by sequentially adding leads from the 24-lead electrocardiogram to the orderly sequenced 12-lead electrocardiogram.

OBJECTIVES: This study investigates whether sequential addition of inverted (negative) leads from the 24-lead electrocardiogram (ECG) to the orderly sequenced 12-lead ECG would identify a number of leads with which the sensitivity for diagnosis of acute transmural ischemia is significantly increased with minimal loss of specificity. BACKGROUND: Acute transmural ischemia due to thrombotic coronary occlusion typically progresses to infarction. Its recognition is based on currently accepted ST-elevation myocardial infarction (STEMI) criteria with suboptimal sensitivity, which could be potentially increased by consideration of the principle that each of the 12 ECG leads can be inverted to provide an additional lead with the opposite (180 degrees ) orientation, generating a 24-lead ECG. METHODS: The study population included 162 patients who underwent prolonged coronary occlusion during elective percutaneous transluminal coronary angioplasty. Balloon occlusion was performed in the left anterior descending coronary artery (51 patients), in the right coronary artery (67 patients), or in the left circumflex coronary artery (44 patients). To be classified as indicative of the epicardial injury current of acute ischemia, the ECGs had to fulfill either the criteria of a consensus document from the American College of Cardiology or the European Society of Cardiology or thresholds for the inverted leads based on a population study from Scotland. RESULTS: The addition of -V1, -V2, -V3, -aVL, -I, aVR, and -III increased sensitivity from 61% to 78% (P

Consideration of pitfalls in and omissions from the current ECG standards for diagnosis of myocardial ischemia/infarction in patients who have acute coronary syndromes.

The ECG is the key clinical test available for the emergency determination of which patients who presenting with acute coronary syndromes indeed have acute myocardial ischemia/infarction. Because typically the etiology is thrombosis, the correct clinical decision regarding reperfusion therapy is crucial. This review follows the efforts of an AHA working group to develop new standards for clinical application of electrocardiology. The pitfalls in the current diagnostic standards regarding ischemia/infarction that have been identified by sufficiently documented studies are corrected in their report. This article focuses on the pitfalls for which new standards will emerge in future years.

Cytomegalovirus stimulated mRNA accumulation and cell surface expression of the oxidized LDL scavenger receptor, CD36.

OBJECTIVE: Cytomegalovirus (CMV) has been epidemiologically associated with multiple disease processes including coronary, carotid and cardiac graft atherosclerosis. An early initiating event in atherogenesis is the uptake by macrophages of oxidized low-density lipoproteins (OxLDL) via the scavenger receptor, CD36. Because CMV can activate host-cell gene transcription, we hypothesized that CMV may upregulate CD36 expression. METHODS AND RESULTS: THP-1 monocyte/macrophage cells were treated with Davis strain CMV and cell surface CD36 expression measured by flow cytometry. Virus challenge increased the percentage of cells expressing CD36 from 21.8 +/- 1.7 to 48.2 +/- 4.0% (mean +/- S.D. for three experiments, P=0.0005); CD36 mRNA accumulation was increased by CMV treatment as determined by reverse transcription-polymerase chain reaction. Viral challenge also upregulated the mitogen-activated protein kinase p38; further, the specific p38 inhibitor, SB203580, reversed the CMV-induced CD36 cell surface expression from 57.2% of cells to baseline levels (29.0 and 30.1% for SB203580 treated and control cells, respectively; P=0.001). Treatment with virus also stimulated uptake of OxLDL: microscopically, virus-treated cells had a mean of 32 +/- 4.0 lipid vacuoles compared with 20 +/- 1.3 for control cells (P=0.01). CONCLUSIONS: These findings suggest that CMV-induced CD36 expression is one mechanism through which CMV may promote atherosclerosis. Other CMV-associated atherogenic mechanisms may exist; additional investigation is necessary.

Cardiorespiratory fitness and C-reactive protein among a tri-ethnic sample of women.

BACKGROUND: Elevated C-reactive protein (CRP) is associated with increased coronary heart disease (CHD) risk. Cardiorespiratory fitness ("fitness") is related with lower CHD risk; however, its relationship with CRP is relatively unknown. METHODS AND RESULTS: Cross-sectional associations between fitness and plasma CRP were examined among 135 African American (AA), Native American (NA), and Caucasian (CA) women (55+/-11 year; 28+/-6 kg/m2). Fitness was assessed with a maximal treadmill exercise test. Plasma CRP concentrations were determined with the Dade Behring high-sensitivity immunoassay. Geometric mean CRP levels were 0.43, 0.25, and 0.23 mg/dL, and average maximal MET levels of fitness were 7.2, 9.1, and 10 METs for AA, NA, and CA, respectively. CRP decreased across tertiles of fitness (P=0.002), increased across tertiles of BMI (P=0.0007), and varied by race (P=0.002). After adjustment for covariates, lower CRP (P<0.05) was observed across tertiles of fitness among NA and CA, but not AA. Among all women, after adjusting for race and covariates, the odds of high-risk CRP (>0.19 mg/dL) were 0.67 (95% CI=0.19 to 2.4) among fit (>6.5 METs) versus unfit women. CONCLUSIONS: The health benefits from enhanced fitness may have an antiinflammatory mechanism.