Artificial pacing (AP) is a treatment for symptomatic bradyarrhythmias unresponsive to medical therapy. This retrospective study was designed to define the practices and outcome of AP in dogs at 7 referral institutions participating in the Companion Animal Pacemaker Registry and Repository (CANPACERS). The indications, implantation techniques, complications, long-term outcome, and owner satisfaction were examined. One hundred fifty-four dogs were identified as undergoing AP from January 1, 1991, to January 1, 1996. Third-degree atrioventricular (AV) block (n = 91; 59%) and sinus node dysfunction (n = 45; 29%) were the most common indications for AP Transvenous endocardial AP systems were implanted in 136 dogs (88%), and epicardial systems were implanted in 18 (12%). Complications associated with AP were reported in 84 dogs (55%). Major complications occurred in 51 dogs (33%), including dislodgement of the pacing lead (n = 15; 10%), generator failure (n = 10; 6%), cardiac arrest during implantation (n = 9; 6%), and infection (n = 7; 5%). Minor complications occurred in 47 dogs (31%), including seroma formation (n = 18; 12%), muscle twitch (n = 17; 11%), and inconsequential arrhythmias (n = 15; 10%). Fourteen dogs (9%) experienced both major and minor complications. Survival analysis revealed 1-, 2-, and 3-year survival rates of 70, 57, and 45%, respectively. Age and presence of preexisting congestive heart failure (CHF) had a negative effect on survival (P = .001). Sixty percent of dogs with preexisting CHF died within 1 year of implantation, whereas 25% of dogs without heart failure died during the same period. Owners rated their satisfaction with the procedure as high in 80% of the dogs.

Cardiac troponin-I (cTnI) is a highly sensitive and specific marker of myocardial injury and can be detected in plasma by immunoassay techniques. The purpose of this study was to establish a reference range for plasma cTnI in a population of healthy dogs using a human immunoassay system and to determine whether plasma cTnI concentrations were high in dogs with acquired or congenital heart disease, specifically cardiomyopathy (CM), degenerative mitral valve disease (MVD), and subvalvular aortic stenosis (SAS). In total, 269 dogs were examined by physical examination, electrocardiography, echocardiography, and plasma cTnI assay. In 176 healthy dogs, median cTnI was 0.03 ng/mL (upper 95th percentile = 0.11 ng/mL). Compared with the healthy population, median plasma cTnI was increased in dogs with CM (0.14 ng/mL; range, 0.03-1.88 ng/mL; P < .001; n = 26), in dogs with MVD (0.11 ng/mL; range, 0.01-9.53 ng/mL; P < .001; n = 37), and in dogs with SAS (0.08 ng/mL; range, 0.01-0.94 ng/mL; P < .001; n = 30). In dogs with CM and MVD, plasma cTnI was correlated with left ventricular and left atrial size. In dogs with SAS, cTnI demonstrated a modest correlation with ventricular wall thickness. In dogs with CM, the median survival time of those with cTnI >0.20 ng/mL was significantly shorter than median survival time of those with cTnI <0.20 ng/mL (112 days versus 357 days; P = .006). Plasma cTnI is high in dogs with cardiac disease, correlates with heart size and survival, and can be used as a blood-based biomarker of cardiac disease.

Blood pressure (BP) measurements obtained using 3 indirect BP measuring instruments, a Doppler ultrasonic flowmeter, an oscillometric device, and a photoplethysmograph, were compared with direct arterial pressure measurements in 11 anesthetized cats. The standard deviation of the differences (SDD) between direct and indirect pressure measurements were not significantly different from each other (P < .01), and ranged from 10.82 to 24.32 mm Hg. The high SDD values indicate that indirect BP estimates obtained with all these devices must be interpreted cautiously in individual patients. The mean errors (calculated as the sum of the differences between direct and indirect pressure measurements divided by the number of observations) of the 3 indirect devices were significantly different for systolic (SAP), diastolic (DAP), and mean (MAP) arterial pressures (P < .05). The Doppler and photoplethysmographic devices had the highest overall accuracy, as indicated by mean error values of less than 10 mm Hg. Correlation coefficients varied from .88 to .96 for the Doppler flowmeter, and from .85 to .94 for the photoplethysmograph; for both devices, the regression line slopes were close to unity. The Doppler flowmeter detected a pulse under all experimental conditions. The photoplethysmograph was also efficient in obtaining BP measurements, obtaining over 90% of SAP, DAP, and MAP readings attempted. The oscillometric device was the least accurate, with mean error values varying from 10 to 22 mm Hg. Correlation coefficients were high (.90 to .94) for this device, but the slopes of the regression lines were 0.7 to 0.8, indicating a trend for increased error at higher BP. The oscillometric device tended to underestimate BP by increasing amounts as the BP increased. The oscillometric device was the least efficient device for obtaining BP measurements (P < .01).

Cardiac troponin-I (cTnI) is a highly sensitive and specific marker of myocardial injury and can be detected in plasma by immunoassay techniques. The purpose of this study was to establish a reference range for plasma cTnI in a population of healthy dogs using a human immunoassay system and to determine whether plasma cTnI concentrations were high in dogs with acquired or congenital heart disease, specifically cardiomyopathy (CM), degenerative mitral valve disease (MVD), and subvalvular aortic stenosis (SAS). In total, 269 dogs were examined by physical examination, electrocardiography, echocardiography, and plasma cTnI assay. In 176 healthy dogs, median cTnI was 0.03 ng/mL (upper 95th percentile = 0.11 ng/mL). Compared with the healthy population, median plasma cTnI was increased in dogs with CM (0.14 ng/mL; range, 0.03-1.88 ng/mL; P < .001; n = 26), in dogs with MVD (0.11 ng/mL; range, 0.01-9.53 ng/mL; P < .001; n = 37), and in dogs with SAS (0.08 ng/mL; range, 0.01-0.94 ng/mL; P < .001; n = 30). In dogs with CM and MVD, plasma cTnI was correlated with left ventricular and left atrial size. In dogs with SAS, cTnI demonstrated a modest correlation with ventricular wall thickness. In dogs with CM, the median survival time of those with cTnI >0.20 ng/mL was significantly shorter than median survival time of those with cTnI <0.20 ng/mL (112 days versus 357 days; P = .006). Plasma cTnI is high in dogs with cardiac disease, correlates with heart size and survival, and can be used as a blood-based biomarker of cardiac disease.

Permanent transvenous cardiac pacemakers were implanted in 40 dogs. Electrocardiographic diagnoses included persistent atrial standstill (3 dogs), sick sinus syndrome (8 dogs), and high-grade second-degree or third-degree atrioventricular (AV) block (29 dogs). Thirteen dogs were alive and well 4 to 42 months after pacemaker implantation (mean, 16.9 months). The mean and median survival times of the 26 dogs that died or were euthanatized during the study were 17.9 months and 13 months, respectively. Most of these dogs succumbed to problems unrelated to the arrhythmia and pacemaker implant. One dog was lost to follow-up. Complications associated with permanent transvenous pacemaker implantation included lead dislodgement, infection, hematoma formation, skeletal muscle stimulation, ventricular arrhythmia, migration of the pulse generator, and skin erosion. Lead dislodgement was the most common complication, occurring in 7 of 9 dogs paced using untined electrode leads and in 6 of 30 dogs paced using tined leads. Lead dislodgement did not occur in the only dog paced using an actively fixed endocardial lead. It was concluded that permanent transvenous cardiac pacing is a feasible, less traumatic alternative to epimyocardial pacing in dogs, but that successful use of this technique requires careful implantation technique and anticipation of the potential complications. (Journal of Veterinary Internal Medicine 1991; 5:322-331) THE FIRST totally implantable artificial cardiac pacemakers were developed more than 30 years ago.' Since then, the equipment and techniques available to accomplish artificial cardiac pacing have changed dramatially.^-^ One of the most important technologic advances in artificial pacemaker design has been the development of durable pacing and sensing endocardial electrodes (leads) that can be introduced into the heart from a peripheral vein6-* Before the development of permanent transvenous leads, reliable artificial cardiac pacing could only be accomplished by surgical implantation of an epimyocardial electrode. Currently, transvenous