Background-The ability to distinguish dysfunctional but viable myocardium from nonviable tissue has important prognostic implications after myocardial infarction. The purpose of this study was to validate the accuracy of contrast-enhanced multidetector computed tomography (MDCT) for quantifying myocardial necrosis, microvascular obstruction, and chronic scar after occlusion/reperfusion myocardial infarction. Methods and Results-Ten dogs and 7 pigs underwent balloon occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. Contrast-enhanced (Visipaque, 150 mL, 325 mg/mL) MDCT (0.5 mm ϫ 32 slice) was performed before occlusion and 90 minutes (canine) or 8 weeks (porcine) after reperfusion. MDCT images were analyzed to define infarct size/extent and microvascular obstruction and compared with postmortem myocardial staining (triphenyltetrazolium chloride) and microsphere blood flow measurements. Acute and chronic infarcts by MDCT were characterized by hyperenhancement, whereas regions of microvascular obstruction were characterized by hypoenhancement. MDCT infarct volume compared well with triphenyltetrazolium chloride staining (acute infarcts 21.1Ϯ7.2% versus 20.4Ϯ7.4%, mean difference 0.7%; chronic infarcts 4.15Ϯ1.93% versus 4.92Ϯ2.06%, mean difference Ϫ0.76%) and accurately reflected morphology and the transmural extent of injury in all animals. Peak hyperenhancement of infarcted regions occurred Ϸ5 minutes after contrast injection. MDCT-derived regions of microvascular obstruction were also identified accurately in acute studies and correlated with reduced flow regions as measured by microsphere blood flow. Conclusions-The

Adenosine-augmented MDCT myocardial perfusion imaging provides semiquantitative measurements of myocardial perfusion during first-pass MDCT imaging in a canine model of LAD stenosis.

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Multidetector row computed tomography angiography (MDCTA) is seen as a potential alternative to current imaging methods for the assessment of vessel anatomy and atherosclerotic plaque composition/morphology in a great variety of arterial beds. Recent advances represented by the increase in gantry speed to <500 ms per rotation and in the number of detector rows from 4 to 64, in addition to the decrease in slice thickness to submillimetric levels, brought significant improvement in diagnostic accuracy by coronary MDCTA. In general, it has a good correlation with both intravascular ultrasound (IVUS) and histopathology for discrimination between soft, intermediate, and calcified plaques. Plaque area and volume tend to be underestimated by 12-detector row MDCTA and overestimated by 16-detector row MDCTA, but the number of patients studied so far is relatively small. However, it seems that 64-detector row MDCTA can measure plaque area and volume with greater accuracy. Plaque remodeling is overestimated in small vessels by 12-detector row MDCTA, whereas 16- and 64-detector row MDCTA show a good correlation with IVUS. Although still under development, the potential of MDCTA to characterize atherosclerotic plaque composition as well as to precisely determine plaque area, volume, and remodeling in the future is quite promising.

This modified automated 3D approach is equivalent to and significantly less time consuming than the traditional manual 2D method for evaluation of >or=50%-stenoses by 16 x 0.5-MDCTA in native coronary arteries of patients with high calcium scores.

Coronary 32 x 0.5-MDCTA accurately excludes > or = 50% stenoses in patients with advanced CAD and high calcium scores with an overall diagnostic accuracy of 91%.

The purpose of this study is to evaluate the relationship between LV structure and function with regional myocardial function in participants of the Multi-Ethnic Study of Atherosclerosis, which is a prospective study including 4 ethnic groups free from clinical cardiovascular disease. Peak systolic strain (Ecc) and regional strain rates (SRS and SRE) were calculated by harmonic phase from tagged CMR of 1100 participants. The relationships of ejection fraction (EF), end-systolic volume (ESV) and end-diastolic volume (EDV) with Ecc and strain rate were studied before and after adjustment for cardiovascular risk factors. Direct linear relationships between EF and regional systolic and diastolic functions (Ecc, SRS and SRE) were present in almost all of the regions (p < 0.05, i.e., greater EF, greater Ecc, SRS and SRE). LVESV demonstrated a negative relationship with Ecc and SRS (i.e., greater ESV, lower systolic function, indexed by Ecc and SRS) in all regions (p < or = 0.05). LVEDV was inversely related to systolic function, indexed by SR(S) (p < 0.05) in all regions. In conclusion, LVEF is directly related to systolic myocardial function, indexed as the absolute magnitude of systolic strain and strain rate. In addition, left ventricular size, indexed as end-diastolic and end-systolic volumes are inversely related to absolute systolic myocardial strain rate (SRS). These results are crucial to the interpretation of strain alterations induced by left ventricular remodeling in early heart failure.

The stress response is adaptive and aims to guarantee survival. However, the persistence of a stressor can culminate in pathology. Catecholamines released as part of the stress response over activate beta adrenoceptors (β-AR) in the heart. Whether and how stress affects the expression of components of the intracellular environment in the heart is still, however, unknown. This paper used microarray to analyze the gene expression in the left ventricle wall of rats submitted to foot shock stress, treated or not treated with the selective β2-AR antagonist ICI118,551 (ICI), compared to those of non-stressed rats also treated or not with ICI, respectively. The main findings were that stress induces changes in gene expression in the heart and that β2-AR plays a role in this process. The vast majority of genes disregulated by stress were exclusive for only one of the comparisons, indicating that, in the same stressful situation, the profile of gene expression in the heart is substantially different when the β2-AR is active or when it is blocked. Stress induced alterations in the expression of such a large number of genes seems to be part of stress-induced adaptive mechanism.