Utility of vertebral left atrial size and vertebral heart size to aid detection of congestive heart failure in dogs with respiratory signs.

BACKGROUND: Differentiating cardiogenic vs noncardiogenic causes of respiratory signs can be challenging when echocardiography is unavailable. Radiographic vertebral left atrial size (VLAS) and vertebral heart size (VHS) have been shown to predict echocardiographic left heart size, with VLAS specifically estimating left atrial size. HYPOTHESIS/OBJECTIVES: Compare the diagnostic accuracy of VLAS and VHS to predict left-sided congestive heart failure (CHF) in dogs presenting with respiratory signs. ANIMALS: One-hundred fourteen dogs with respiratory signs and radiographic pulmonary abnormalities. METHODS: Retrospective cross-sectional study. Dogs had to have an echocardiogram and thoracic radiographs obtained within 24 hours. Diagnosis of CHF was confirmed based on the presence of respiratory signs, cardiac disease, LA enlargement, and cardiogenic pulmonary edema. RESULTS: Fifty-seven dogs had CHF and 57 did not have CHF. Compared to VHS (area under the curve [AUC] 0.85; 95% confidence interval [CI], 0.77-0.91), VLAS was a significantly (P = .03) more accurate predictor of CHF (AUC, 0.92; 95% CI, 0.85-0.96). Optimal cutoff for VLAS was >2.3 vertebrae (sensitivity, 93.0%; specificity, 82.5%). Murmur grade (P = .02) and VLAS (P < .0001) were independently associated with CHF and VHS was not. Increased VHS (54%) was significantly (P = .01) more common than increased VLAS (24%) in dogs without CHF. Results were similar in a subsample of older and smaller dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: When echocardiography is unavailable, VLAS and murmur grade have clinically utility to aid in differentiating cardiogenic from noncardiogenic respiratory signs. These findings might be especially useful to help rule out CHF in dogs with increased VHS that present with respiratory signs.

Optical mapping of sarcoplasmic reticulum Ca2+ in the intact heart: ryanodine receptor refractoriness during alternans and fibrillation.

RATIONALE: Sarcoplasmic reticulum (SR) Ca(2+) cycling is key to normal excitation-contraction coupling but may also contribute to pathological cardiac alternans and arrhythmia. OBJECTIVE: To measure intra-SR free [Ca(2+)] ([Ca(2+)]SR) changes in intact hearts during alternans and ventricular fibrillation (VF). METHODS AND RESULTS: Simultaneous optical mapping of Vm (with RH237) and [Ca(2+)]SR (with Fluo-5N AM) was performed in Langendorff-perfused rabbit hearts. Alternans and VF were induced by rapid pacing. SR Ca(2+) and action potential duration (APD) alternans occurred in-phase, but SR Ca(2+) alternans emerged first as cycle length was progressively reduced (217±10 versus 190±13 ms; P<0.05). Ryanodine receptor (RyR) refractoriness played a key role in the onset of SR Ca(2+) alternans, with SR Ca(2+) release alternans routinely occurring without changes in diastolic [Ca(2+)]SR. Sensitizing RyR with caffeine (200 µmol/L) significantly reduced the pacing threshold for both SR Ca(2+) and APD alternans (188±15 and 173±12 ms; P<0.05 versus baseline). Caffeine also reduced the magnitude of spatially discordant SR Ca(2+) alternans, but not APD alternans, the pacing threshold for discordance, or threshold for VF. During VF, [Ca(2+)]SR was high, but RyR remained nearly continuously refractory, resulting in minimal SR Ca(2+) release throughout VF. CONCLUSIONS: In intact hearts, RyR refractoriness initiates SR Ca(2+) release alternans that can be amplified by diastolic [Ca(2+)]SR alternans and lead to APD alternans. Sensitizing RyR suppresses spatially concordant but not discordant SR Ca(2+) and APD alternans. Despite increased [Ca(2+)]SR during VF, SR Ca(2+) release was nearly continuously refractory. This novel method provides insight into SR Ca(2+) handling during cardiac alternans and arrhythmia.