Left ventricular ejection fraction LVEF

If adenosine therapy is unsuccessful for termination of PSVT, subsequent choices of therapy depend on whether the patient has HF and/or a depressed left ventricular ejection fraction (LVEF). 

The echocardiogram is the single most useful evaluation procedure because it can identify abnormalities of the pericardium, myocardium, or heart values and quantify the left ventricular ejection fraction (LVEF) to determine if systolic or diastolic dysfunction is present. 

Evaluation of left ventricular ejection fraction (LVEF) is recommended prior to administration of the initial dose of mitoxantrone. Subsequent LVEF evaluations are recommended if signs or symptoms of CFIF develop, and prior to all doses administered to patients who have received a cumulative dose of 100 mg/m or more. Do not administer mitoxantrone to MS patients who have received a cumulative lifetime dose of 140 mg/m or more, or those with either LVEF of less than 50% or a clinically significant reduction in LVEF. 

Figure 2.6 illustrates stunned myocardium with normal resting perfusion but a severe stress induced perfusion defect that indicates severe ischemia in the distribution of the RCA and the LAD proximal to the first septal perforator. Metabolic imaging with FDG is not necessary, since resting perfusion is normal without scar with a left ventricular ejection fraction (LVEF) of 30% thereby indicating stunned myocardium that normalized after bypass surgery. This patient with severe stress induced ischemia and reduced LV function characteristic of stunned myocardium contrasts with the patient of Fig. 2.2 with severe ischemia but normal LV function and no stunning. 

Conduction system abnormalities are common in chronic heart failure, occurring in 15-30% of the population with low left ventricular ejection fraction (LVEF) [1-3]. The prevalence in ischemic heart disease is roughly similar to that seen in other forms of dilated cardiomyopathy. Conduction system disease can occur both at the time of an acute myocardial infarction as well as slowly progressing in chronic ischemic heart disease. Intraventricular conduction delays are associated with a poor prognosis in heart failure, with up to a 70% increase in the risk of death, and are also more prevalent in patients with advanced symptoms [2,4]. In ischemic heart disease, all components of the conduction system are at risk of ischemic injury, from the sinoatrial node to the His-Pukinje system. These conduction system abnormalities have the potential to impair cardiac function by a number of mechanisms. Since conduction abnormalities impair cardiac function, it is logical that pacing therapies to correct or improve these conduction abnormalities may improve cardiac function. 

Most of the clinical experience gained with stem cells has involved therapy for AMI, particularly intracoronary infusion of bone marrow cells since skeletal myoblasts are too large for this purpose [133]. Table 7.2 summarizes the experience to date. In all of these trials, revascularization was performed promptly after the index myocardial infarction, and left ventricular systolic compromise was minor (in the BOOST trial, the baseline left ventricular ejection fraction [LVEF] was 50%). 

Congestive heart failure (CHF), other high-risk patients Angiotensin-converting enzyme (ACE) inhibition Enalapril Captopril Ramipril Reduction in cardiovascular, all-cause mortality reduced hospitalizations and recurrent CHF in patients post-MI, with CHF and with decreased left ventricular ejection fraction (LVEF) CONSENSUS SAVE SOLVD AIRE HOPE >23,000 14... 

The importance of other factors additional to amount ofnecrosis has also been studied. In patients with first acute MI treated with PCI, LAD-related MI show for a similar amount of myocardial necrosis as determined by enzymatic infarct size, lower left-ventricular ejection fraction (LVEF) when compared to non-LAD-related MI. LVEF-measured 6-month post-MI showed a decrease, for every 1000 cumulative lactate dehydrogenase release, of 4.8% for LAD and 2.4% for non-LAD-related infarcts (p < 0.0001), and these results remain in the multivariate analysis (Elsman et al., 2006). 

A number of potential methods for risk stratification exist, including use of clinical parameters such as left ventricular ejection fraction (LVEF), electrophysiologic markers, imaging assessments, biochemical and genetic markers, and functional assessments (Table 1.1). A number of these methods will be discussed below. Some of the initial lessons were learned from ICD trials involving secondary prevention of SCD that is, trials in patients... 

Figure 110.4 Relationships between T3 and left ventricular ejection fraction in patients with left ventricular dysfunction. Scatterplots showing the relationship between total T3 (TT3) and left ventricular ejection fraction (LVEF) in patients without (panel a) and with overt heart failure (panel b). Data from Pingitore etal., (2006) (left side) and from Pingitore etal., (2005) (right side).

Trastuzumab (Herceptin) is a humanized monoclonal antibody against the extracellular domain of the human epidermal growth factor receptor 2 (HER2). Treatment of cancer patients with trastuzumab has been associated with an increased incidence of cardiac toxicity including left ventricular cardiac dysfunction, arrhythmias, hypertension, disabling cardiac failure, cardiomyopathy, and cardiac death. Trastuzumab can also cause asymptomatic decline in left ventricular ejection fraction (LVEF) (Herceptin PI 2010). 

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