Diagnostic and Therapeutic Challenges in Patients With Coexistent Chronic Obstructive Pulmonary Disease and Chronic Heart Failure
Thierry H. Le Jemtel, MD*,*,
Margherita Padeletti, MD and
Sanja Jelic, MD
* Division of Cardiology, Tulane University, New Orleans, Louisiana
Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, New York
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Figure 1 Evaluation of Heart Failure During COPD Exacerbation
Brain natriuretic peptide (BNP) serum levels and detection of chronic heart failure (CHF) in patients with exacerbation of chronic obstructive pulmonary disease (COPD). CHF is unlikely when BNP levels are <100 pg/ml. A BNP level of >500 pg/ml indicates overt left-sided (L) CHF and the need for treatment. BNP levels ranging from 100 to 500 pg/ml indicate right-sided (R) heart failure, moderate left-sided heart failure, or both and the need for treatment. Once patients have returned to baseline status, cardiac imaging needs to be performed and therapy adjusted. 2D = 2-dimensional; ACE = angiotensin-converting enzyme; RNV = radionuclide ventriculography.
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Figure 2 Evaluation of Heart Failure in Stable COPD Patients
Two-dimensional (2D) Doppler echocardiography is indicated in patients with stable chronic obstructive pulmonary disease (COPD). A normal (Nl) echocardiogram (echo) excludes chronic heart failure (CHF). No further therapy ( ) is needed. When left ventricular (LV) ejection fraction (EF) is  40%, full CHF therapy, including beta-blockade, is recommended. When LVEF is >40%, LV mass is increased, and left atrium is enlarged, the diagnosis of diastolic heart failure needs to be entertained and therapy with angiotensin-converting enzyme (ACE) inhibitors and diuretics considered. When the echocardiogram is technically (Tech.) inadequate, radionuclide ventriculography (RNV) is indicated and therapy needs to be adjusted to the findings. Imp. = impaired.
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Figure 3 Progression of CHF and COPD
Time course of loss of cardiac or pulmonary function (A), loss of skeletal muscle mass (B), and functional incapacity (C) during the progression of chronic heart failure (CHF) or chronic obstructive pulmonary disease (COPD). Curves A and C in CHF patients are based on data collected during studies of left ventricular dysfunction (101). Curve B in CHF patients and curves A, B, and C in COPD patients are based on clinical experience in the absence of quantitative data.
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Figure 4 Mechanisms of Skeletal Muscle Atrophy in Patients With CHF or COPD
Disuse, low-level systemic inflammation (Inflam.), and increased oxidative (oxidat.) stress decrease protein synthesis while increasing protein degradation. CHF = chronic heart failure; COPD = chronic obstructive pulmonary disease.
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Figure 5 Signaling Pathways of Disuse and Inflammation
Reduced insulin growth factor-1 (IGF-1) tissue level and insulin resistance combine to decrease phosphorylation of phospatidyinositol-2-OH kinase (PI3K), which in turn reduces activation of Akt (protein kinase B), thereby reducing protein synthesis via reduced phosphorylation of mammalian target of rapamycin (mTOR) and glucogen synthase kinase (GSK). Reduced Akt activation increases activity of forkhead box O (FOXO) transcription factors, thereby activating the ubiquitin-proteasome pathway and promoting protein degradation. Reduced IGF-1 levels and insulin resistance activate caspase-3, resulting in protein breakdown and degradation. Whether activated caspase-3 results in muscle apoptosis is controversial.
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