Myocardial disease

HBD is a biochemical rather than electrophoretic assessment of the LD isoenzyme which is associated with heart. All five isoenzymes of LD exhibit some activity toward cx-hydroxy-butyrate as substrate, but heart LD shows the greatest activity. Serum HBD measurement is not as valuable as the electrophoretic determination of heart LD isoenzyme. High HBD activity has also been found in diseases of the liver. Rises associated with the hepatic effects of congestive heart failure can be disconcerting in the differential diagnosis of myocardial infarction. Wilkinson has used the serum HBD/LD ratio for the differentiation of myocardial disease from other disorders in which HBD activity is elevated, whereas Rosalki has not found the ratio to be helpful (39). 

Infiltrative myocardial diseases (e.g., amyloidosis, sarcoidosis, endomyocardial fibrosis)... 

VF is electrical anarchy of the ventricle resulting in no cardiac output and cardiovascular collapse. Sudden cardiac death occurs most commonly in patients with ischemic heart disease and primary myocardial disease associated with LV dysfunction. VF associated with acute MI may be classified as either (1) primary (an uncomplicated MI not associated with heart failure [HF]) or (2) secondary or complicated (an MI complicated by HF). 

Causes of diastolic dysfunction (restriction in ventricular filling) are increased ventricular stiffness, ventricular hypertrophy, infiltrative myocardial diseases, myocardial ischemia and infarction, mitral or tricuspid valve stenosis, and pericardial disease (e.g., pericarditis, pericardial tamponade). 

Cardiomyopathy A general diagnostic term designating primary myocardial disease, often of obscure or unknown etiology. [EU]... 

Transaminases are also found in other tissues, from which they leak from the cells into the blood when injury occurs. Measurement of serum enzyme activity (serum enzyme diagnosis see also p. 98) is an important method of recognizing and monitoring the course of such injuries. Transaminase activity in the blood is for instance important for diagnosing liver disease (e.g., hepatitis) and myocardial disease (cardiac infarction). 

Magnesium chloride Renal impairment marked myocardial disease coma. 

Oral Oral dosage forms are preferable for less urgent arrhythmias as well as for long-term maintenance after initial parenteral therapy. Individualize dosage based on clinical assessment of the degree of underlying myocardial disease, the patient s age and renal function. ... 

Speciai risk Use with caution in patients with impaired pulmonary function, particularly those with obstructive pulmonary disease severely impaired cardiac function caused by myocardial disease history of previous liver disease or... 

Severe myocardial disease or coronary occlusion psychoses hypersensitivity to disulfiram or to other thiuram derivatives used in pesticides and rubber vulcanization patients receiving or who have recently received metronidazole, paraldehyde, alcohol, or alcohol-containing preparations. 

Theophylline should be used with caution in patients with myocardial disease, liver disease, and acute myocardial infarction. The half-life of theophylline is prolonged in patients with congestive heart failure. Because of its narrow margin of safety, extreme caution is warranted when coadministering drugs, such as cime-tidine or zUeuton, that may interfere with the metabolism of theophylline. Indeed, coadministration of zileu-ton with theophylline is contraindicated. It is also prudent to be careful when using theophylline in patients with a history of seizures. 

Chagas disease, the South American variety of trypanosomiasis, is caused by Trypanosoma cruzi. It is quite different from African trypanosomiasis in its clinical and pathological presentation and in its failure to respond to many agents effective in that disease. It has both an acute and chronic phase. The latter frequently results in gastrointestinal and myocardial disease that ends in death. 

L. E. Hudsmith and S. Neubauer, Magnetic resonance spectroscopy in myocardial disease. /. Am. Coll. Cardiol. Imaging, 2009, 2, 87-96. 

R. Beadle and M. Erermeaux, Magnetic resonance spectroscopy in myocardial disease. Expert Rev. Cardiovasc. Ther., 2010, 8, 269-277. 

Wasaki, S., Sakaida, I., Uchida, K., Kimura, T., Kayano, K., and Okita, K., 1997, Preventive effect of cyclosporin A on experimentally induced acute liver injury in rats, Liver 17, pp. 107-114 Weiss, J.N., Korge, P., Honda, H. M., and Ping, P., 2003, Role of the mitochondrial permeability transition in myocardial disease, Circ. Res 93, pp. 292-301 Wingrove, D.E. and Gunter, T. E., 1986a, Kinetics of mitochondrial calcium transport. I. Characteristics of the sodium-independent calcium efflux mechanism of liver mitochondria, J. Biol. Chem. 261, pp.15159-15165... 

Zhao et al. (36) found that some citric acid metabolites are decreased in acute ischemia and acute myocardial disease. The citric acid plays an important role in oxidative phosphorylation and ATP production in the cardiomyo-cytes in which levels of citric acid cycle intermediates are supplied by glycolysis and (1-oxidation of fatty acids. 

Role of AMPK in Myocardial Disease Ally or Adversary Myocardial ischemia... 

The labeling of fatty acids aims at a noninvasive diagnosis of myocardial diseases. The labeled fatty acids should follow the fatty acid metabolism which is distinct in the heart. Radioiodinated iodo-phenyl fatty acid [47] is the golden standard which features have to be exceeded by a corresponding 99mTc complex. Since all attempts... 

The negative inotropic effects of class I antidysrhythmic agents, such as disopyramide, procainamide, quinidine, and tocainide can be accentuated by beta-blockers this is most pronounced in patients with pre-existing myocardial disease and can result in left ventricular failure or even asystole (413). Digoxin can obviate the negative inotropic effect of beta-blockers in patients with poor left ventricular function. 

The authors assumed that she had developed neurogenic pulmonary edema, probably worsened by the co-existing myocardial disease. 

Elevations in cTnl and cTnT are highly specific for myocardial injury. However, in individuals without myocardial disease, their levels are very low to undetectable. This is in contrast to the low but measurable concentrations of CK-2 and myoglobin detected in serum from skeletal muscle turnover in patients with noncardiac-related diseases and in normal individuals. Therefore release of cTnl or cTnT from myocardium into the blood following AMI and after the washout that accompanies successful reperfusion generates an excellent signal compared with no detectable baseline levels before myocardial damage. The initial rapid release of cardiac troponin subunits I and T following successful reperfusion is most hkely derived from the soluble cytosolic myocardial fraction (6% cTnT 3% cTnl). 

It should be concretely appreciated that the findings emerging from laboratory animals, within their overwhelming majority - normal hearts, cannot be reasonably extrapolated to the human with coronary or myocardial disease. The various plights afflicting the myocardium in these conditions should be addressed. 

S. C. Winter, Metabolic aspects of myocardial disease and a role for L-camitine in the treatment of childhood cardiomyopathy, Pediatrics 105, 1260-1270 (2000). 

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