Cardiac masses

CT scanning is used rarely as a primary diagnostic procedure in the evaluation of CVD and function because it provides similar information as other diagnostic procedures (e.g., ECHO) and is significantly more expensive. Enhanced definition and spatial resolution of structures are possible with CT scanning, which is useful in some specific indications such as to evaluate aortic and pericardial disease and assess paracardiac and cardiac masses. More accurate determination of chamber volume and size and mass calculations of myocardial wall thickness can be obtained from CT scanning than with other methods... 

In the evaluation of cardiac masses, CT scanning shows the mass as a distinct space-occupying entity. Tissue density differentiation as seen on a CT scan allows characterization of density, aiding in determination of the nature of masses. Masses as small as 0.5 to 1 cm can be identified on CT scans. 

Imaging of cardiac mass in daily routine in mainly dedicated to the assessment of cardiac thrombi rather than primary cardiac neoplasms. Although not being superior to cardiac MR in terms of reliability and accuracy, cardiac CT allows for a substantially faster clot imaging and therefore eases the workflow in noninvasive clot assessment. 

Assessment of real cardiac masses, no matter whether primary or secondary, may necessitate imaging techniques more sophisticated in order to narrow the final diagnosis and to be able to assess the true extent of a primary cardiac mass or the cardiac involvement of a primary extracardiac lesion (e.g., bronchiogenic carcinoma). 

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). 

The Cardiac Cycle. The heart (Eig. lb) performs its function as a pump as a result of a rhythmical spread of a wave of excitation (depolarization) that excites the atrial and ventricular muscle masses to contract sequentially. Maximum pump efficiency occurs when the atrial or ventricular muscle masses contract synchronously (see Eig. 1). The wave of excitation begins with the generation of electrical impulses within the SA node and spreads through the atria. The SA node is referred to as the pacemaker of the heart and exhibits automaticity, ie, it depolarizes and repolarizes spontaneously. The wave then excites sequentially the AV node the bundle of His, ie, the penetrating portion of the AV node the bundle branches, ie, the branching portions of the AV node the terminal Purkinje fibers and finally the ventricular myocardium. After the wave of excitation depolarizes these various stmetures of the heart, repolarization occurs so that each of the stmetures is ready for the next wave of excitation. Until repolarization occurs the stmetures are said to be refractory to excitation. During repolarization of the atria and ventricles, the muscles relax, allowing the chambers of the heart to fill with blood that is to be expelled with the next wave of excitation and resultant contraction. This process repeats itself 60—100 times or beats per minute... 

The heart, a four-chambered muscular pump has as its primary purpose the propelling of blood throughout the cardiovascular system. The left ventricle is the principal pumping chamber and is therefore the largest of the four chambers in terms of muscle mass. The efficiency of the heart as a pump can be assessed by measuring cardiac output, left ventricular pressure, and the amount of work requHed to accomplish any requHed amount of pumping. 

The progenitor cells of the kidney produce 90% of the hormone erythropoietin (EPO), which stimulates red blood cell (RBC) production. Reduction in nephron mass decreases renal production of EPO, which is the primary cause of anemia in patients with CKD. The development of anemia of CKD results in decreased oxygen delivery and utilization, leading to increased cardiac output and left ventricular hypertrophy (LVH), which increase the cardiovascular risk and mortality in patients with CKD. 

Reduced lean body mass Reduced muscle strength Reduced exercise performance Thin, dry skin cool peripheries poor venous access Depressed affect, labile emotions Impaired cardiac function... 

Cardiac cachexia Physical wasting with loss of weight and muscle mass caused by cardiac disease a wasting syndrome that causes weakness and a loss of weight, fat, and muscle. 

The size of the body is another factor that determines cardiac output. Healthy young men have a cardiac output of about 5.5 to 6.0 1/min the cardiac output in women averages 4.5 to 5.0 1/min. This difference does not involve gender per se, but rather the mass of body tissue that must be perfused with blood. Cardiac index normalizes cardiac output for body size and is calculated by the cardiac output per square meter of body surface... 

Wang, F. Li, W. Emmett, M.R. Marshall, A.G. Corson, D. Sykes, B.D. Fourier transform ion cyclotron resonance mass spectrometric detection of small Ca +-induced conformational changes in the regulatory domain of human cardiac troponin C. J. Am. Soc. Mass Spectrom. 1999, 10, 703—710. 

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