Left ventricular function, effects

Arnold RJ, Kaniecki DJ, Frishman WH. Cost-effectiveness of antihypertensive agents in patients with reduced left ventricular function. Pharmacotherapy 1994 14 178-84. 

Hirsch, A., Gervine, E., Nakso, S., Come, P., Silverman, K. and Grossman, W., The effect of caffeine on exercise tolerance and left ventricular function in patinets with coronary heart disease. Annals of Internal Medicine 110, 593-598, 1989. 

Edema Edema, mild to moderate, typically associated with arterial vasodilation and not due to left ventricular dysfunction, occurs in 10% to 30% of patients receiving nifedipine. It occurs primarily in the lower extremities and usually responds to diuretics. In patients with CHF, differentiate this peripheral edema from the effects of decreasing left ventricular function. 

With regard to left ventricular function, cardiac stem cell therapy is well tolerated overall. No proar-rhythmic effects have been observed to date with ABMMNC therapy, although other deleterious effects are possible. Early concerns about abnormal transdifferentiation and tumorigenesis have subsided, but the potential for accelerated atherogen-esis remains, given the limited clinical experience... 

Chen SL, Fang WW, Ye F, Liu YH, Qian J, Shan SJ, Zhang JJ, Chunhua RZ, Liao LM, LinS, Sun JP. Effect on left ventricular function of intracoronary transplantation of autologous bone marrow mesenchymal stem cell in patients with acute myocardial infarction. Am J Cardiol 2004 94 92-95. 

Torp-Pedersen C, Kober L. Effect of ACE inhibitor tran-dolapril on life expectancy of patients with reduced left-ventricular function after acute myocardial infarction. TRACE Study Group. TrandolaprU Cardiac Evaluation. Lancet 1999 354(9172) 9-12. 

The cornerstone of therapy for ventricular fibrillation is electrical deflbrillation. In the acute setting, defibrination is first-line therapy. Intravenous bretylium can occasionally contribute to conversion, but this is infrequent. In the management of out-of-hospital cardiac arrest, high-dose epinephrine (5 mg intravenously) improves the rate of successful resuscitation in patients with asystole, but not in those with ventricular fibrillation, when compared with the standard dose of 1 mg. Vasopressin (40 U intravenously) may more effective than 1 mg intravenous epinephrine in out-of-hospital patients with ventricular fibrillation that is resistant to electrical defibrillation. The OPTIC smdy (see Connolly et al., 2006) showed that amiodarone plus jS-blocker is superior than sotalol or jS-blocker alone for reducing ICD shocks in patients with reduced left ventricular function and history of sustained VT, VF, or cardiac arrest. 

As with other antiarrhythmic drugs, moricizine has proarrhythmic activity, which may manifest as new ventricular ectopic beats or a worsening of preexisting ventricular arrhythmias. These effects are most common in patients with depressed left ventricular function and a history of congestive heart failure. Cardiovascular ef-... 

Flecainide produces modest negative inotropic effects that may become significant in the subset of patients with compromised left ventricular function. 

Mechanism of Action A cardiac agent that slows impulse formation in the SA node and conduction time through the AV node. Adenosine also acts as a diagnostic aid in myocardial perfusion imaging or stress echocardiography. Therapeutic Effect Depresses left ventricular function and restores normal sinus rhythm. 

Life-threatening recurrent ventricular fibrillation or hemodgnamkally unstable ventricular tachycardia PO Initially, 800-1600 mg/dayin 2-4 divided doses for 1-3 wk. After arrhythmia is controlled or side effects occur, reduce to 600-800 mg/day for about 4 wk. Maintenance 200-600 mg/day. IVInfusion Initially, 1050 mg over 24 hr 150 mg over 10 min, then 360 mg over 6 hr then 540 mg over 18hr. May continue at 0.5 mg/min for up to 2-3 wk regardless of age or renal or left ventricular function. 

Thus, the patient with a toxic TCA concentration (see the case at the start of the Metabolism section) developed excessively high amitriptyline plasma levels due to the additive effects of diminished left ventricular function leading to decreased hepatic arterial blood flow alcohol and age-related decline in liver function and, finally. 

TCAs may adversely affect left ventricular function (LVF). This phenomenon was addressed using the systolic time interval (STI), a measurement partly dependent on the QRS duration. However, TCAs prolong QRS, and hence the STI method can overestimate the effect of TCAs on LVF because of their prolongation of the QRS interval. 

Giardina EGV, Johnson LL, Vita J, Bigger JT Jr, etal. Effect of imipramine and nortriptyline on left ventricular function and blood pressure in patients treated for arrhythmias. Am Heart J 1985 109 992-998. 

Toxic concentrations of disopyramide can precipitate all of the electrophysiologic disturbances described under quinidine. As a result of its negative inotropic effect, disopyramide may precipitate heart failure de novo or in patients with preexisting depression of left ventricular function. Because of this effect, disopyramide is not used as a first-line antiarrhythmic agent in the USA. It should not be used in patients with heart failure. 

Sotalol is well absorbed orally with bioavailability of approximately 100%. It is not metabolized in the liver and is not bound to plasma proteins. Excretion is predominantly by the kidneys in the unchanged form with a half-life of approximately 12 hours. Because of its relatively simple pharmacokinetics, solatol exhibits few direct drug interactions. Its most significant cardiac adverse effect is an extension of its pharmacologic action a dose-related incidence of torsade de pointes that approaches 6% at the highest recommended daily dose. Patients with overt heart failure may experience further depression of left ventricular function during treatment with sotalol. 

Cardiac function may be evaluated by the determination of left (or right) ventricular ejection fraction (VEF). In this procedure, regions of interest are defined at the end diastolic and end systolic phases of heart beat. The ejection fraction is defined as the ratio of tracer (blood) in the heart in the contracted (systolic) versus the relaxed (diastolic) phases of the heart cycle with appropriate corrections for decay and gamma camera dead time. The value obtained provides a measure of the ability of the heart to pump blood through the lungs (RVEF) or the body (LVEF). A criticism of Ir-191m for this application has been that the half-life (4.96s) is too short to allow effective visualization and quantitation of left ventricular function in adults, particularly those with delayed transit times. A recent... 

I I Chung CM, Nakamura S, Tanaka K, et al. Effect of recanalization of chronic total occlusions on global and regional left ventricular function in patients with or without previous myocardial infarctions. Catheter Cardiovasc Interv2003 60 368-374. 

Actions This Class IA drug shows actions similar to those of quinidine. Disopyramide [dye so PEER a mide] produces a negative inotropic effect that is greater than the weak effect exerted by quinidine and procainamide, and unlike the latter drugs, disopyramide causes peripheral vasoconstriction. The drug may produce a clinically important decrease in myocardial contractility in patients with preexisting impairment of left ventricular function. Disopyramide is used for treatment of ventricular arrhythmias as an alternative to procainamide or quinidine. 

Adverse effects Lidocaine has a fairly wide toxic-to-therapeutic ratio it shows little impairment of left ventricular function, and has no negative inotropic effect. The CNS effects include drowsiness, slurred speech, paresthesia, agitation, confusion, and convulsions cardiac arrhythmias may also occur. 

Bames GE, Horwith LD, Bishop VS (1979) Reliability of the maximum derivatives of left ventricular pressure and internal diameter as indices of the inotropic state of the depressed myocardium. Cardiovasc Res 13 652-662 Bishop VS, Horwitz LD (1971) Effects of altered autonomic control on left ventricular function in conscious dogs. Am J Physiol 221 1278-1282... 

As many as 20% of patients taking adequate doses of a tricyclic antidepressant experience marked postural hypotension. This effect is not consistently correlated with plasma concentrations and tolerance does not develop during treatment (35-37). The mechanism for this effect is uncertain it has been attributed to a peripheral antiadrenergic action, to a myocardial depressant effect, and to an action mediated by alpha-adrenoceptors in the central nervous system (38). Studies of left ventricular function in man are conflicting. One study of systolic time intervals showed a decrement in left ventricular function with therapeutic doses (39), while two in which cardiac function was observed directly during cardiac catheterization after overdosage showed no evidence of impaired myocardial efficiency, whereas the hypotension persisted after left ventricular filling pressures and cardiac output had returned to normal (40,41). 

The effects of amlodipine and isosorbide-5-mono-nitrate for 3 weeks on exercise-induced myocardial stunning have been compared in a randomized, double-blind, crossover study in 24 patients with chronic stable angina and normal left ventricular function (4). Amlodipine attenuated stunning, evaluated by echocardiography, significantly more than isosorbide, without difference in anti-ischemic action or hemodynamics. Amlodipine was better tolerated than isosorbide, mainly because of a lower incidence of headache (4). 

Udelson JE, DeAbate CA, Berk M, Neuberg G, Packer M, Vijay NK, Gorwitt J, Smith WB, Kukin ML, LeJemtel T, Levine TB, Konstam MA. Effects of amlodipine on exercise tolerance, quality of life, and left ventricular function in patients with heart failure from left ventricular systolic dysfunction. Am Heart J 2000 139(3) 503-10. 

The results of SPICE (The Study of Patients Intolerant of Converting Enzyme Inhibitors) and of the previously published RESOLVD led to the design of the current CHARM trial, which is investigating the effect of candesartan in 6600 patients with heart failure in three different ways versus an ACE inhibitor in patients with preserved left ventricular function versus placebo in patients intolerant of ACE inhibitors and in addition to ACE inhibitors in all other patients. While waiting for the results of this trial it is advisable to continue to use ACE inhibitors as the initial therapy for heart failure. In patients with documented intolerance of ACE inhibitors (which may represent 10-20% of patients with heart failure) angiotensin receptor antagonists may be useful as a substitute to block the renin-angiotensin-aldosterone system. 

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. 

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