Cardiac tumor

Corticotropin has been reported to cause enlargement of cardiac tumors in tuberous sclerosis (1). 

Other uses of TEE include identification of cardiac thrombus, especially thrombi in the left atrium, and assessment of atrial dilation. After transient ischemic attacks or cerebrovascular accidents, TEE may enable identification of the site of cardiac emboli by providing excellent images of likely sources of such, namely, ventricular or atrial thrombus, valvular vegetation, cardiac shunts, cardiac tumors, or atrial and ventricular septal defects. In a study of almost 1500 patients with cerebral ischemia or nonvalvular atrial fibrillation, atrial thrombi were seen in 183 patients when evaluated by TEE versus only 2 patients using TTE. TEE can be used for intraoperative cardiac imaging to ascertain development of ischemia. 

Atrial myxoma is a rare atrial tumor that causes multiple emboli of either thrombus or myxomatous tissue. When myxomatous material is embolized from the left atrium into the brain arteries, they may cause the formation of multiple distal cerebral aneurysms with risk of hemorrhage [46]. Papillary fibroelastomas are rare benign cardiac tumors usually involving a heart valve. They are small vascular growths with marked papillary projections. They usually grow on the aortic or mitral valves. The tumor consists of fibrous tissue surrounded by an elastic membrane, which in turn is covered by endothelium. One of the most conunon clinical presentations is of transient ischemic attack or stroke [47,48]. 

Although ischemic disease makes up a large proportion of the overall patient population, there is a stunning variety of other cardiac diseases that also need to be addressed in noninvasive diagnostic procedures. This variety include diseases such as the entire range of CHD, the widespread range of cardiomyopathies and inflammatory diseases, and cardiac tumors. 

Inflammatory cytokines have been implicated in the pathophysiology of HF.9 Several proinflammatory (e.g., tumor necrosis factor-a [TNF-a], interleukin-1, interleukin-6, and interferon-y) and anti-inflammatory cytokines (e.g., interleukin-10) are overexpressed in the failing heart. The most is known about TNF-a, a pleiotrophic cytokine that acts as a negative inotrope, stimulates cardiac cell apoptosis, uncouples 3-adrenergic receptors from adenylyl cyclase, and is related to cardiac cachexia. The exact role of cytokines and inflammation in HF pathophysiology continues to be studied. 

Electrolyte disturbances that develop in patients with tumor lysis syndrome should be managed aggressively to avoid renal failure from hyperphosphatemia and hypocalcemia and cardiac signs from hyperkalemia. One exception pertains to the use of intravenous calcium for hypocalcemia. Adding calcium may cause further calcium phosphate precipitation in the presence of hyperphosphatemia and should be used cautiously. 

Burton PBJ, Raff MC, Kerr P, Yacoub MH, Barton PJR 1999 An intrinsic timer that controls cell-cycle withdrawal in cultured cardiac myocytes. Dev Biol 216 659—670 Chen X, Ko LJ, Jayaraman L, Prives C 1996 p53 levels, functional domains, and DNA damage determine the extent of the apoptotic response of tumor cells. Genes Dev 10 2438—2451 Duesbery NS, Choi T, Brown KD et al 1997 CENP-E is an essential kinetochore motor in maturing oocytes and is masked during mos-dependent cell cycle arrest at metaphase II. Proc Natl Acad Sci USA 94 9165-9170... 

The neurohormonal model of HF recognizes that an initiating event (e.g., acute MI) leads to decreased cardiac output but that the HF state then becomes a systemic disease whose progression is mediated largely by neurohormones and autocrine/paracrine factors. These substances include angiotensin II, norepinephrine, aldosterone, natriuretic peptides, arginine vasopressin, proinflammatory cytokines (e.g., tumor necrosis factor a, interleukin-6 and interleukin-1 ft), and endothelin-1. 

Long-term complications of radiotherapy, chemotherapy, and chemora-diotherapy include gonadal dysfunction, secondary malignancies, and cardiac disease. Patients treated for HL are at increased risk of developing leukemia, GI tumors, lung cancer, and breast cancer. 

Y., Kawamura, N. Feldman, A. M., Tsutsui, H., Shimokawa, H., Takeshita, A., Involvement of inducible nitric oxide synthase in cardiac dysfunction with tumor necrosis factor-alpha, Am. J. Physiol. Heart Circ. Physiol. 282 (2002),... 

In vitro Disaggregated cells Repolarizing currents (e.g., IKs, IK1, Ito), depolarizing currents (e.g., INa) currents, ICa (whole cell patch-clamp) Disaggregated cells ventricular myocytes mouse atrial tumor cells (AT-1) immortalized cardiac muscle cells (HL-1) Jost et al.,-65 Liu and Antzelevitch 66 Jurkiewicz and Sanguinetti 67 Li et al. 68 Yang and Roden 69 Banyasz et al. 70 Xia et al.71... 

Hypertension infrequently results from another disease, such as a catecholamine-secreting tumor (pheochro-mocytoma) in most cases the cause carmot be determined essential (primary) hypertension. Antihypertensive drugs are indicated when blood pressure cannot be sufficiently controlled by means of weight reduction or a low-salt diet. In principle, lowering of either cardiac output or peripheral resistance may decrease blood pressure (cf p. 306,... 

IR concentrated oral solution and tablets/suppositories - Respiratory insufficiency or depression severe CNS depression attack of bronchial asthma heart failure secondary to chronic lung disease cardiac arrhythmias increased intracranial or CSF pressure head injuries brain tumor acute alcoholism delirium tremens convulsive disorders after biliary tract surgery suspected surgical abdomen surgical anastomosis concomitantly with MAOIs or within 14 days of such treatment paralytic ileus. 

Type II tumor True carcinoma of the cardia arising from the cardiac epithelium or short segments with intestinal metaplasia at the esophagogastric junction. 

Dopamine (Intropin) [Vasopressor/Adrenergic] Uses Short-tOTn use in cardiac decompensation secondary to X contractility when no hypovolemia is present T organ p fusion (at low dose) Action Renal dose 2-5 mcg/kg/min Inotropic dose 5-10 mcg/kg/min Pressor dose >10 mcg/kg/min Dose Adults Feds. 5-20 mcg/kg/min by cont inf, start at 5 and t by 5 mcg/kg/min to 20 mcg/kg/min max to effect (mix 400 mg in 250 mL DjW to make 1600 mcg/mL) (see Table 1-3) Caution [C, ] Contra Pheochromocytoma (adrenal gland tumor), VF, sulfite sensitivity Disp Inj 40, 80, 160 mg/mL, premixed 0.8, 1.6, 3.2 mg/mL SE Tach, vasoconstriction, 4- BP, HA, N/V, dyspnea Notes >10 mcg/kg/min X renal p fiision Interactions t Effects W/ a-blockers, diuretics, ergot alkaloids, MAOIs, BBs, anesthetics, phenytoin X effects W/ guanethidine EMS Correct hypovolemia before use use microdrip set or inf pump check soln- discolored... 

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