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Ventricular performance

Radionuclide angiocardiography is used to measure ejection fraction (EF), regional ventricular performance, cardiac output, ventricular volumes, valvular regurgitation, asynchrony or wall motion abnormalities, and intracardiac shunts. [Pg.146]

Cardiovascular anatomy and physiology Ventricular performance Electrophysiology Coronary artery distribution Human skin... [Pg.607]

Finally, there is variability of the treatment given and the underlying disease process for any individual patient. For example, a patient may have substantial ventricular mechanical dyssynchrony and have a successfully placed CRT device with appropriate lead locations. If very careful measures of ventricular performance are made, the patient s heart functions better with CRT on than off. However, if the patient suffers from a subsequent myocardial infarction or progressive ischemia, he may not improve clinically. Accordingly, at the end of a trial period, such a patient is termed a nonresponder even though he may be doing better with the device... [Pg.60]

Manolis AG, Katsivas AG, Lazaris EE, Vassilopoulos CV, Louvros NE. Ventricular performance and quality of life in patients who underwent radiofrequency AV junction ablation and permanent pacemaker implantation due to medically refractory atrial tachyarrhythmias. J. Interv. Card. Electrophysiol. 1998 2 71-6. [Pg.64]

Sogaard P, Kim WY, Jensen HK, et al. Impact of acute biventricular pacing on left ventricular performance and volumes in patients with severe heart failure. A tissue doppler and three-dimensional echocardio-graphic study. Cardiology 2001 95 173-82. [Pg.66]

Nikolaidis LA, Elahi D, Hentosz T, et al. Recombinant glucagon-like peptide-1 increases myocardial glucose uptake and improves left ventricular performance in conscious dogs with pacing-induced dilated cardiomyopathy. Circulation. Aug 24 2004 110(8) 955-961. [Pg.141]

No data exist regarding the efficacy of antiarrhythmic therapy in mitral valve prolapse patients with hemodynamically significant mitral regurgitation. At present, /3-blockers seem preferable when ventricular performance permits. Class I agents should be used with careful follow-up by ambulatory monitoring and/or exercise testing to avoid any proar-rhythmic effects. [Pg.605]

Sodium nitroprusside is used in the management of hypertensive crisis. Although it is effective in every form of hypertension because of its relatively favorable effect on cardiac performance, sodium nitroprusside has special importance in the treatment of severe hypertension with acute myocardial infarction or left ventricular failure. Because the drug reduces preload (by venodila-tion) and after load (by arteriolar dilation), it improves ventricular performance and in fact is sometimes used in patients with refractory heart failure, even in the absence of hypertension. [Pg.231]

Endogenous norepinephrine stimulates cardiac beta receptors. Receptor-linked cAMP-dependent protein kinases phosphorylate calcium channels to increase intracellular calcium. Elevated intracellular calcium increases conduction velocity (phase 0) and decreases the threshold potential in normal SA and AV node cells (see Figure 12.13). Beta blockers slow spontaneous conduction velocity in the SA node by approximately 10-20 percent. In addition, beta blockers can slow conduction velocity while increasing the refractory period of the AV node. These effects control the ventricular rate in atrial fibrillation or flutter and terminate paroxysmal supraventricular tachycardias. They are also safer, although somewhat less effective, than other drugs for suppression of premature ventricular complexes (PVCs). Drugs in this class approved by the FDA for treatment of various arrhythmias include propranolol, acebutolol, and esmolol. Problems with the beta blockers include drowsiness, fatigue, impotence, and depressed ventricular performance. [Pg.260]

Romson JL, Haack DW, Lucchesi BR (1980b) Electrical induction of coronary artery thrombosis in the ambulatory canine a model for in vivo evaluation of anti-thrombotic agents. Thromb Res 17 841-853 Ruebsamen K, Kirchengast M (1998) Thrombin inhibition and intracoronary thrombus formation effect of polyethylene glycol-coupled hirudin in the stenosed, locally injured canine coronary artery. Coron Artery Dis 9 35-42 Sullivan J, Hansen P, Rahko PS, Folts JD (1992) Continous measurement of left ventricular performance during and after maximal isometric deadlift exercise. Circulation 85 1406-1413... [Pg.282]

By one estimate, since the first report in 1982, over 250 cases of myocardial infarction due to cocaine have been reported, mostly in the USA The first report from the UK was published in 1999 (63). Acutely, cocaine suppresses myocardial contractility, reduces coronary caliber and coronary blood flow, induces electrical abnormalities in the heart, and increases heart rate and blood pressure. These effects can lead to myocardial ischemia (36,37). However, intranasal cocaine in doses used medicinally or recreation-ally does not have a deleterious effect on intracardiac pressures or left ventricular performance (38). [Pg.490]

Tumor Necrosis Factor Alpha Tumor necrosis factor alpha (TNFa) is an inflammatory cytokine and interleukin that is involved in the genesis of sepsis, arthritis, and a variety of other inflammatory states (see Chapter 22). It also has hemodynamic effects and reduces ventricular performance. It is also a common signaling molecule. Assays for it or its receptor have been developed, but the failure of recent therapeutic trials has led to concern about how to properly interpret the high levels seen in patients with CHF and coronary heart disease. At present, there are no standardized assays and no reference interval studies or consistent assay validations. [Pg.1634]

K. W. Mahaffey, T.E. Raya, G.D. Pennock, E. Morkin and S. Goldman, Left ventricular performance and remodeling in rabbits after myocardial infarction effects of a thyroid hormone analogue, Circulation 91(3), 794-801 (1995). [Pg.97]

It was reported35 that morphine does not act as a S3rm-patholytic on the isolated heart nor does it alter catecholamine levels or the response of the heart to sympathomimetic amines. On the other hand, iu vivo experiments in the dog3° reveal that morphine increased contractile force. This careful study revealed that the improved ventricular performance induced by morphine is indirect and probably the result of sympathoadrenal discharge. [Pg.37]

Cardiac catheterization and angiography are used to assess coronary anatomy and ventricular performance. [Pg.149]

Tracers used for assessment of myocardial metabolism are selected based on the type of metabolism of interest EDO traces glucose metabolism, ["Cjpalmitate traces mitochondrial fatty acid metabolism, and ["Cjacetate is an indirect marker for myocardial oxygen consumption, allowing assessment of ventricular performance. [ CjPalmitate is a useful marker for normal myocardial oxygen consumption because baseline energy needs of the myocardium... [Pg.163]

Martin C, Viviand X, Arnaud S, et al. Effects of norepinephrine plus dobutamine or norepinephrine alone on left ventricular performance of septic shock patients. Crit Care Med 1999 27 1708-1713. [Pg.477]

Serious untoward effects are unusual if dosing is appropriate and the patient is carefully monitored during initial treatment. Levothyroxine replacement in athyrotic hypothyroid patients restores systolic and diastolic left ventricular performance within 2 weeks, and the use of levothyroxine may increase the frequency of atrial premature beats, but not necessarily ventricular premature beats. Excessive doses of... [Pg.1385]

DITPA treatment improved left ventricular performance in rat and rabbit post-M I models of heart failure. In a double-blind, placebo controlled, pilot phase II clinical study in 19 patients with NYHA class II or III CHF in 2003, DITPA demonstrated a significant increase in cardiac index, as well as improvements in diastolic function, systemic vascular resistance, and cholesterol and triglyceride levels. In this study, DITPA was well tolerated, with no significant increase in heart rate or significant adverse events. Subsequently, a larger trial was initiated which, however, was discontinued in October 2006, based on a business decision by Titan. [Pg.417]

In patients with pulmonary hypertension, calcium channel blocking drugs have been found to produce pulmonary artery dilation and therefore improvement in cardiac output and relief of hypoxia [233, 234]. Most of the studies have used short-term administration to carefully selected patients. Thus, the beneficial effects need to be confirmed in longer studies using more patients with advanced pulmonary hypertension. Detrimental deterioration in right ventricular performance has been found in some patients with severe right ventricular dysfunction following the administration of verapamil or nifedipine [233]. [Pg.286]

Benjamin PP (1969) A rapid and efficient method of preparing " Tc-human serum albumin its clinical applications. Int J Appl Radiat Isot 20 187-194 Benjamin PP, Rejali A, Friedell H (1970) Electrolytic complexation of " Tc at constant current its application in nuclear medicine. J Nucl Med 11 147-154 Berger HJ, Matthay RA, Pytlik L, Gottschalk A, Zaret BL (1979) First-pass radionuclide assessment of right and left ventricular performance in patients with cardiac and pulmonary disease. Semin Nucl Med 9 275-295... [Pg.185]

Flecainide produces few subjective complaints in most patients dose-related blurred vision is the most common noncardiac adverse effect. It can exacerbate CHF in patients with depressed left-ventricular performance. The most serious adverse effects are provocation or exacerbation of potentially lethal arrhythmias. These include acceleration of ventricular rate in patients with atrial flutter, increased frequency of episodes of reentrant ventricular tachycardia, and increased mortality in patients convalescing from myocardial infarction. [Pg.273]

Bepridil has been demonstrated to reduce blood pressure and heart rate in patients with stable exertional angina. It also produces an increase in left-ventricular performance in patients with angina, but its side-effect profile limits its use to truly refractory patients. [Pg.494]

In patients with impaired function of the left ventricle, NO has a potential to further impair left ventricular performance by dilating the pulmonary circulation and increasing the blood flow to the left ventricle, thereby increasing left atrial pressure and promoting pulmonary edema formation. Careful monitoring of cardiac output, left atrial pressure, or pulmonary capillary wedge pressure is important in this situation. [Pg.260]

Burkhoff, D., Schnellbacher, M., Stennett, R.A. et al. Explaining load-dependent ventricular performance and energetics based on a model of E-C coupling, in Cardiac Energetics from Emax... [Pg.953]

Preliminary studies explored preparation of " Ta-labeled myocardial perfusion agents (Holman et al. 1979 Layne et al. 1991) and also applications for lung and liver imaging (Neirinckx et al. 1979). High resolution and statistical quality FPRNA studies of ventricular performance were demonstrated in a group of 38 patients in comparison with the traditional Tc methods (Lacy et al. 1991). Verani et al. (1992a) demonstrated the usefulness of this... [Pg.1957]

Beyar R, Sideman S (1984b) A computer study of the left ventricular performance based on the fiber structure, sarcomere dynamics and transmural electrical propagation velocity. Circ Res 55 358-375... [Pg.17]


See other pages where Ventricular performance is mentioned: [Pg.305]    [Pg.292]    [Pg.447]    [Pg.147]    [Pg.207]    [Pg.90]    [Pg.222]    [Pg.327]    [Pg.104]    [Pg.69]    [Pg.91]    [Pg.536]    [Pg.77]    [Pg.140]    [Pg.478]    [Pg.1958]    [Pg.1958]   
See also in sourсe #XX -- [ Pg.163 , Pg.202 ]




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