What blood chemistry components are useful for evaluating heart failure?

Haboratory tests are useless for diagnosing heart failure. However, they are important in making a differential diag-i nosis, identifying the precipitating factors of destabilization, assessing the severity of heart failure, and monitoring the side effects of therapy. Some tests also serve as prognostic indicators.

Complete blood count

A complete blood count can identify anemia, and hence a reduced oxygen transport capacity, as a trigger of destabilization. A hematocrit <25% can cause the signs and symptoms of heart failure in patients free of heart disease. Anemia with a low hematocrit can also be due to dilution; on the other hand, a high hematocrit indicates hemoconcentration, but may also suggest a pulmonary cause of dyspnea. Anemia is also an independent negative prognostic indicator. The Studies Of Left Ventricular Dysfunction (SOLVD) found that a basal white cell count >7000 was associated with higher mortality (RR 1.22, P=0.001); a recent reanalysis in 1274 heart failure patients showed that a low lymphocyte count (<20%) was also an independent prognostic indicator (RR 1.73, P=0.002). These findings underline the importance of neurohumoral and inflammatory factors in heart failure outcome. The complete blood count should therefore be performed routinely and repeated 6-monthly unless more frequent testing is warranted. In moderate-to-severe heart failure, reduced fibrinogen synthesis may lower the erythrocyte sedimentation rate (ESR). The ESR correlates with tumor necrosis factor (TNF)-oc, TNF soluble receptors, and interleukin (IL)-6. An ESR >15 mm in the first hour suggests a poorer prognosis with a relative risk of 2.62 independent of age, New York Heart Association (NYHA) class, ejection fraction, and oxygen peak. Although these data require confirmation, the ESR should be monitored at the same intervals as the complete blood count.

Sodium and creatinine

Sodium and creatinine levels help in differentiating between heart failure and renal disease. Volume overload in renal disease readily mimics and/or aggravates heart failure. Both parameters are also useful in monitoring secondary renal failure and treatment side effects;

* Diuretics may slightly increase sodium levels, with normal or slightly increased creatinine. In prerenal failure, sodium levels are disproportionately higher than those of creatinine. Aggressive diuretic therapy may markedly decrease glomerular filtration velocity and induce hypokalemia.

Angiotensin-converting enzyme (ACE) inhibitors may increase creatinine levels with sodium levels remaining normal.

Renal dysfunction is a simple prognostic indicator. In the SOLVD Prevention Trial, multivariate analysis showed that modest renal failure (clearance <60 mL/min) was associated with significantly higher mortality (RR 1.41; P=0.007). The SOLVD Treatment Trial obtained similar results: the risk of death (RR 1.41; P=0.001), and the risk of death from heart failure (RR 1.49; P=0.007), increased significantly in moderate renal failure. These data suggest that renal function is not only a marker of heart failure severity, but a disease determinant in its own right. Thus, improving renal function may slow the progression of heart failure. Renal function should therefore be evaluated: Every 6 months in stable patients on stable therapy. During and after dose titration with an ACE inhibitor, angiotensin receptor blocker, or spironolactone. Whenever a sudden increase is needed in the dose of diuretic (edema). Whenever combination diuretic therapy is needed. Serum electrolytes Hypokalemia (and hypomagnesemia) are the most serious side effects of potassium-losing diuretics. The risk can be avoided by using an ACE inhibitor, angiotensin receptor blocker, or spironolactone combined with a potassium-sparing diuretic. Hypokalemia carries a high risk of major fatal arrhythmia. Potassium levels must therefore be closely monitored whenever the dose of diuretic is increased and regularly monitored when the patient is stable. Potassium levels should be held between 4.0 and 5.0 mEq/L. Hyperkalemia may be due to renal failure or excessive potassium intake, or it may be a side effect of spironolactone, other potassium-sparing diuretics, ACE inhibitors, or angiotensin receptor blockers. The SOLVD trials showed higher mortality due to arrhythmia with non-potassium-sparing vs potassium-sparing diuretics (RR 1.37,P=0.009). Hyponatremia may be due to hemodilution (fluid overload) or excessive diuretic use (increased natriuresis); it may also indicate marked renin-angiotensin system activation or renal failure. Hyponatremia is also useful in grading heart failure severity and, if <134 mEq/L, serves as a prognostic indicator as it is correlated with excessive plasma renin activity. The serum electrolytes should be monitored whenever testing renal function and also: Daily until stabilizing the dose of diuretic, ACE inhibitor, angiotensin receptor blocker, or spironolactone Every 2 to 3 months in stable patients. Uric acid Hyperuricemia may be due to renal dysfunction, and is a side effect of diuretic therapy (increased tubular resorption and decreased excretion of uric acid). However, this is not the whole story. Throughout the cardiovascular system, endothelial cells are the main site of uric acid and xanthine oxidase production. Serum uric acid levels reflect the degree of xanthine oxidase activation; high levels of these enzymes generate free radicals and may thus cause peripheral vasculature dysfunction. High uric acid levels may be due to anabolic/catabolic imbalance with resulting protein degradation, muscle atrophy, and cachexia. They are seen in cardiac cachexia in conjunction with a marked endothelial vasodilator response. Interaction between glycolytic and xanthine oxidase metabolic pathways may also occur, particularly as due to the high frequency of insulin resistance in advanced heart failure, an increased shift of glycolytic intermediates toward purine and uric acid synthesis is thought to alter glycolytic metabolism. Uric acid levels should be monitored: Every 6 months in stable patients. Every 3 months in patients on high diuretic doses. Whenever making a sustained increase in the diuretic dose. Liver function tests Elevated y-GT values are a sensitive but nonspecific indicator of heart failure. Hyperbilirubinemia and increased alkaline phosphatase and transaminase levels are due to congestion. Hypoalbuminemia is due to malnutrition, but may also be due to renal or hepatic failure. A multivariate analysis of 552 patients followed for 13 years showed that aspartate transaminase and bilirubin were the liver function parameters significantly correlated with mortality. Liver function should be monitored: Every 6 to 12 months in stable patients. During heart failure episodes. In pathologic weight loss. Urinalysis Proteinuria suggests renal dysfunction; glycosuria indicates decompensated diabetes; and hematuria or cells suggest glomerulonephritis. The 24-hour urinary electrolytes may also be of assistance in differential diagnosis. Thyroid hormones T4 and thyroid stimulating hormone (TSH) levels must be measured in de novo or paroxysmal atrial fibrillation, suspected thyroid disease, amiodarone therapy, and in patients over 65 years of age. T4 and TSH abnormalities suggest hyperthyroidism or hypothyroidism. The prognostic significance of low T3 syndrome (common in more severely compromised patients) is debated; it is unlikely to be an independent marker. Blood glucose High diuretic doses may increase glucose levels. Glycosylated hemoglobin levels should be monitored in diabetics to assess metabolic control over the preceding 3 months. Lipid function High levels of low-density lipoprotein (LDL) are a risk factor for progression of atherosclerotic disease. An LDL >100 mg/dL in a patient with ischemic heart disease and >130 mg/dL in a patient without ischemic heart disease is an indication for dietary therapy followed, in the absence of a satisfactory response, by medical therapy. The effects (and side effects) of medical therapy should be monitored every 3 to 6 months (high transaminase and creatine phosphokinase levels suggest hepatic dysfunction or myopathy). Lipid levels total cholesterol, HDL, LDL, and triglycerides should also be measured in unwanted weight loss (incipient cachexia). Recent data indicate that mortality in heart failure patients may be significantly reduced if cholesterol levels exceed 220 mg/dL. A possible explanation is that the reduced mesenteric blood flow in heart failure encourages the growth of gut flora that produce toxins such as lipopolysaccharides (LPS). Cholesterol then binds to LPS, for which it has a high affinity, thereby indirectly reducing the production of cytotoxic cytokines. Further studies are necessary to elucidate this effect.

Therapeutic drug monitoring; digoxin

Digoxin levels should be monitored:

Every 3 to 6 months in the elderly.

Every 3 months in renal dysfunction.

Every 3 to 6 months during amiodarone therapy.

Every 3 months during concomitant therapy interfering with digoxin levels (quinidine, amiloride, triamterene, spironolactone, antibiotics depressing the gut flora).

When making changes in the treatment regimen that may affect electrolyte levels and/or renal function.

If the patient is suspected of noncompliance.

In overdose (suggested by nausea, bradycardia, visual disturbances).

Coagulation tests

The international normalized ratio (INR) must be monitored during anticoagulant therapy, in major or minor bleeding, anemia, hepatic dysfunction, and treatment with drugs that interfere with coagulation.

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