Predictors of low exercise cardiac output in patients with severe pulmonic regurgitation

Background and objectivesChronic pulmonic regurgitation (PR) following repair of congenital heart disease (CHD) impairs right ventricular function that impacts peak exercise cardiac index (pCI). We aimed to estimate in a non-invasive way pCI and peak oxygen consumption (pVO2) and to evaluate predictors of low pCI in patients with significant residual pulmonic regurgitation after CHD repair.MethodWe included 82 patients (median age 19 years (range 10–54 years)) with residual pulmonic regurgitation fraction >40%. All underwent cardiac MRI and cardiopulmonary testing with measurement of pCI by thoracic impedancemetry. Low pCI was defined <7 L/min/m2.ResultsLow pCI was found in 18/82 patients. Peak indexed stroke volume (pSVi) tended to compensate chronotropic insufficiency only in patients with normal pCI (r=−0.31, p=0.01). Below 20 years of age, only 5/45 patients had low pCI but near-normal (≥6.5 L/min/m2). pVO2 (mL/kg/min) was correlated with pCI (r=0.58, p=0.0002) only in patients aged >20 years. Left ventricular stroke volume in MRI correlated with pSVi only in the group of patients with low pCI (r=0.54, p=0.02). No MRI measurements predicted low pCI. In multivariable analysis, only age predicted a low pCI (OR=1.082, 95% CI 1.035 to 1.131, p=0.001) with continuous increase of risk with age.ConclusionsIn patients with severe PR, pVO2 is a partial reflection of pCI. Risk of low pCI increases with age. No resting MRI measurement predicts low haemodynamic response to exercise. Probably more suitable to detect ventricular dysfunction, pCI measurement could be an additional parameter to take into account when considering pulmonic valve replacement.

Carcinoid Heart Disease: Pathophysiology, Pathology, Clinical Manifestations, and Management

Carcinoid heart disease (CHD) is a rare and potentially lethal manifestation of an advanced carcinoid (neuroendocrine) tumor. The pathophysiology of CHD is related to vasoactive substances secreted by the tumor, of which serotonin is most prominent in the pathophysiology of CHD. Serotonin stimulates fibroblast growth and fibrogenesis, which can lead to cardiac valvular fibrosis. CHD primarily affects right heart valves, causing tricuspid and pulmonic regurgitation and less frequently stenosis of these valves. Left heart valves are usually spared because vasoactive substances such as serotonin are enzymatically inactivated in the lung vasculature. The pathology of CHD is characterized by plaque-like deposition of fibrous tissue on valvular cusps, leaflets, papillary muscles, chordae, and ventricular walls. Symptomatic CHD usually presents between 50 and 70 years of age, initially as dyspnea and fatigue. Echocardiography is the mainstay of imaging and demonstrates thickened right heart valves with limited mobility and regurgitation. Treatment focuses on control of the underlying carcinoid syndrome, targeting subsequent valvular heart disease and managing consequent heart failure. Surgical valve replacement and catheter-directed valve procedures may be effective for selected patients with CHD.

Bacterial Endocarditis of the Pulmonic Valve in a Dog

ABSTRACT An 11 yr old female spayed golden retriever weighing 30.3 kg presented for evaluation of progressive lethargy, anorexia, tachypnea, stiff gait, and nonlocalized pain. On physical exam, the patient was febrile and tachycardic, and an arrhythmia with pulse deficits was noted. Clinicopathological abnormalities included thrombocytopenia, leukocytosis, nonregenerative anemia, and mild hypoalbuminemia. The patient progressed overnight to develop a productive cough, and an echocardiogram performed the next morning revealed irregular proliferative lesions of the pulmonic valve with moderate pulmonic regurgitation. Subsequent blood cultures grew two organisms: alpha-hemolytic streptococci spp. and Empedobacter brevis. The dog was treated with appropriate intravenous antibiotics for 2 wk and then switched to oral therapy. The clinicopathologic abnormalities, fever, and clinical signs resolved with oral antibiotic treatment. To the authors' knowledge, this case report represents the first detailed published case of bacterial endocarditis with E brevis bacteremia involving the pulmonic valve. The clinical presentation, diagnosis, treatment, and follow-up are discussed.

Retrospective Investigation on the Prevalence of Pulmonary Hypertension in Dogs with Bronchial and Upper Respiratory Diseases

Bronchial and upper respiratory diseases have been associated with hypoxia and subsequent development of pulmonary arterial hypertension (PAH). However, there are no known studies assessing the prevalence of PAH in dogs with these conditions. The aim of this study was to assess the frequency of PAH in dogs with bronchial and upper respiratory diseases. Medical records of dogs with confirmed diagnosis (by endoscopic examination) of bronchial and/or upper respiratory diseases referred for cardiovascular investigation (January 2009 - May 2013) were retrospectively reviewed. Diagnosis of PAH was made by echocardiography (tricuspid regurgitation > 2.8 m/s and/or pulmonic regurgitation > 2.2 m/s); possible PAH was diagnosed when two or more specific echocardiographic findings were present. 52 dogs (30 with upper respiratory diseases, 17 with bronchial disease and 5 with both) were included. Diagnosis of PAH was performed in 3 dogs (5.7%). Two dogs were considered as probably affected by PAH; a total of 5 dogs (9.4%) resulted in being affected or probably affected by PAH. Our study shows that the prevalence of PAH in dogs with bronchial and/or upper respiratory diseases is low; PAH seems to occur mostly in older dogs and/or with very advanced disease: echocardiography may therefore be a useful tool in this category of patients.