Diagnostic and Therapeutic Challenges in Patients With Coexistent Chronic Obstructive Pulmonary Disease and Chronic Heart Failure

Chronic obstructive pulmonary disease (COPD) and heart failure (CHF) are common conditions. The prevalence of COPD ranges from 20% to 30% in patients with CHF. The diagnosis of CHF can remain unsuspected in patients with COPD, because shortness of breath is attributed to COPD. Measurement of plasma B-type natriuretic peptide (BNP) levels helps to uncover unsuspected CHF in patients with COPD and clinical deterioration. Noninvasive assessment of cardiac function may be preferable to BNP to uncover unsuspected left ventricular (LV) systolic dysfunction in patients with stable COPD. Patients with COPD or CHF develop skeletal muscle alterations that are strikingly similar. Functional intolerance correlates with severity of skeletal muscle alterations but not with severity of pulmonary or cardiac impairment in COPD and CHF, respectively. Improvement of pulmonary or cardiac function does not translate into relief of functional intolerance in patients with COPD or CHF unless skeletal muscle alterations concomitantly regress. The mechanisms responsible for skeletal muscle alterations are incompletely understood in COPD and in CHF. Disuse and low-level systemic inflammation leading to protein synthesis/degradation imbalance are likely to contribute. The presence of COPD impacts on the treatment of CHF, as COPD is still viewed as a contraindication to beta-blockade. Therefore, COPD often deprives patients with CHF due to LV systolic dysfunction of the most beneficial pharmacologic intervention. A large body of data indicates that patients with COPD tolerate well selective beta-blockade that should not be denied to CHF patients with concomitant COPD

Effects of cardiac resynchronization therapy on systemic inflammation and neurohormonal pathways in heart failure

Background: The effect of cardiac resynchronization therapy (CRT) on systemic inflammation and neurohormonal alterations associated with heart failure is not well characterized. Accordingly, we aimed to assess the long term effects of CRT on systemic inflammation and neurohormonal factors in heart failure patients. Methods and results: In 47 HF patients (NYHA III–IV) we evaluated, at baseline and after one year of CRT: TNF-α, TNF soluble receptors (sTNFR1 and sTNFR2), insulin-like growth factor-1α (IGF-1α), adiponectin, norepinephrine, pro-atrial natriuretic peptide (pro-ANP), N-terminal-pro-brain natriuretic peptide (NT-proBNP) and angiotensin II, NYHA functional class, quality of life (the Minnesota Living with Heart Failure questionnaire), a 6-minute walk test and an echocardiogram. Long-term CRT decreased activation of renin–angiotensin system (RAS) only in patients with reverse remodelling. It failed to prevent a decline in adiponectin levels, regardless of reverse remodelling. NT-proBNP remained unchanged in patients with reverse remodelling, whereas its levels increased in those without reverse remodelling. IGF-1α increased with CRT, whereas CRT had no effect on pro-ANP and inflammatory markers. Conclusions: Long-term CRT is associated with decreased RAS activation and stabilization of NT-proBNP in heart failure patients with reverse remodelling. Long-term CRT, with or without reverse remodelling, does not affect systemic inflammation and fails to prevent a decline in adiponectin

Massive mitral regurgitation secondary to acute ischemic papillary muscle rupture: The role of echocardiography

Papillary muscle rupture is an infrequent but often fatal mechanical complication of acute myocardial infarction (AMI). We report the case of an AMI complicated by the development of an abrupt cardiogenic shock due to the rupture of the head of the postero-medial papillary muscle with echocardiographic demonstration of severe mitral regurgitation due to flail posterior mitral valve leaflet. After initial stabilization with medical therapy and diagnostic coronary angiography, the patient was referred for urgent cardiac surgery and successfully underwent mitral valve replacement with implantation of a bioprosthesis. This case confirms the importance of transthoracic echocardiography in diagnosing mechanical acute complications during an AMI and in the decision making of patients with sudden onset of hemodynamic compromise. Transthoracic echogardiography should be immediately carried out in all patients in whom a mechanical complication during an AMI is suspected. (Cardiol J 2010; 17, 4: 397-400