Myocardial mass

Left ventricle myocardial mass at end systole is calculated as ... 

Hoffmann U, Globits S, Stefenelli T et al. (2001) The effects of ACE inhibitor therapy on left ventricular myocardial mass and diastolic filling in previously untreated hypertensive patients a cine MRI study. J Magn Reson Imaging 14 16-22... 

Figure 1.2 Echocardiography see example of volumes, wall thickening and myocardium mass in a normal case and in a patient with post-MI. Above (A) End-diastolic and (B) end-systolic apical long-axis views of a normal left ventricle. The endocardial and epicardial contours are traced and the built-in computer software of the ultrasound system allows calculation of volumes, wall thickening and myocardial mass. Below Segmental wall...

Generally, they are not large infarctions, especially when the ECG is normal or near normal (Figure 10.2). However, in presence of normal ECG recording in some cases, the myocardial mass involved may be relatively important, because a great part of the lateral wall depolarises after 40 milliseconds and, therefore, does not generate... 

Abnormalities in filling are also associated with changes in chamber stiffness that occur in HCM. This stiffness may be the result of myocardial fibrosis, cellular disorganization, or increased myocardial mass. The decreased distensibility leads to an abnormally steep slope of the diastolic pressure-volume curve such that an increase in LV volume results in a disproportionate increase in diastolic pressure. 

McCann GP, Van Dockum WG, Beek AM, et al. Extent of MRI delayed enhancement of myocardial mass is related to right ventricular dysfunction in pulmonary artery hypertension. Am J Roentgenol 2007 188 349-55. 

Accurate quantitation of the shape and dimensions of all cardiac chambers and myocardium is possible with the Dynamic Spatial Reconstructor (DSR). Generally a single bolus injection of approximately 2ml/kg roentgen contrast agent in the right atrium will provide information of the chamber volumes and myocardial mass within 5% of the actual value. The detailed shape of the chambers and myocardium facilitates evaluation of heart deformed by complex congenital heart disease or myocardial infarction (aneurysm). 

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

Causes of systolic dysfunction (decreased contractility) are reduction in muscle mass (e.g., myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hypertrophy. Ventricular hypertrophy can be caused by pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation, shunts, high-output states). 

B Thiede, A Otto, U Zimny-Arndt, E-C Muller, P Jungblut. Identification of human myocardial proteins separated by two-dimensional electrophoresis with matrix-assisted laser desorption/ionization mass spectrometry. Electrophoresis 17 588-599, 1996. 

Gerhardt W, Nording G, Ljungdahl L. Can troponin T replace CK-MB mass as "goldstandard for acute myocardial infarction ( AMI ) Scand J Clin Lab Invest 1999 59(suppl 230) 83-89. 

Kennedy, L. M., Dickstein, K., Anker, S. D., Kristianson, K., and Willenheimer, R. 2005. The prognostic importance of body mass index after complicated myocardial infarction. J. Am. Coll. Cardiol. 45 156-158. 

It is conceivable that the PBN-lipid alkoxyl and PBN/ OH adducts have similar ESR parameters in various solvents [128], The PBN-lipid alkoxyl adduct, because it is more lipophilic, should be associated with the myocardial tissue and is unlikely to be released into the perfusate. The present study shows that PBN/ OH adduct is also fairly nonpolar. It is clear that other strategies to differentiate between the PBN/ OH and PBN-lipid alkoxyl adduct should be undertaken, such as isotopic substitution and mass spectrometry. 

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