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- Author or Editor: Steven Rosenthal x
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Objective—To determine reference values for M-mode echocardiographic parameters in nonsedated healthy adult Maine Coon cats and compare those values with data reported for nonsedated healthy adult domestic cats.
Animals—105 healthy adult Maine Coon cats.
Procedure—Over a 3-year period, M-mode echocardiographic examinations (involving a standard right parasternal transthoracic technique) were performed on Maine Coon cats as part of prebreeding evaluations;values of M-mode parameters in healthy individuals were collected, and mean values were calculated for comparison with those reported for healthy adult domestic cats.
Results—The mean ± SD weight of Maine Coon cats was significantly greater than that of domestic cats. Mean values of left ventricular internal dimension at end diastole and end systole (LVIDd and LVIDs, respectively), interventricular septal thickness at end systole (IVSs), left ventricular posterior wall thickness at end systole (LVPWs), left atrial dimension at end systole (LADs), and aortic root dimension (Ao) in Maine Coon cats differed significantly from values in healthy domestic cats. The greatest differences detected between the 2 groups involved values of LVIDd, LADs, and Ao. Linear regression analysis revealed a weak but significant correlation between weight and each of LVIDd, LVPWs, IVSs, Ao, LADs, and left ventricular posterior wall thickness at end diastole.
Conclusions and Clinical Relevance—Values of several M-mode echocardiographic parameters in Maine Coon cats differ from those reported for domestic cats; these differences should be considered during interpretation of echocardiographic findings to distinguish between cardiac health and disease in this breed. (J Am Vet Med Assoc 2005;226:734–737)
OBJECTIVE To evaluate a group of related Rhodesian Ridgebacks with a family history of sudden death for the presence of arrhythmia and to identify possible patterns of disease inheritance among these dogs.
DESIGN Prospective case series and pedigree investigation.
ANIMALS 25 Rhodesian Ridgebacks with shared bloodlines.
PROCEDURES Pedigrees of 4 young dogs (1 female and 3 males; age, 7 to 12 months) that died suddenly were evaluated, and owners of closely related dogs were asked to participate in the study. Dogs were evaluated by 24-hour Holter monitoring, standard ECG, echocardiography, or some combination of these to assess cardiac status. Necropsy reports, if available, were reviewed.
RESULTS 31 close relatives of the 4 deceased dogs were identified. Of 21 dogs available for examination, 8 (2 males and 6 females) had ventricular tachyarrhythmias (90 to 8,700 ventricular premature complexes [VPCs]/24 h). No dogs had clinical signs of cardiac disease reported. Echocardiographic or necropsy evaluation for 7 of 12 dogs deemed affected (ie, with frequent or complex VPCs or sudden death) did not identify structural lesions. Five of 6 screened parents of affected dogs had 0 to 5 VPCs/24 h (all singlets), consistent with a normal reading. Pedigree evaluation suggested an autosomal recessive pattern of inheritance, but autosomal dominant inheritance with incomplete penetrance could not be ruled out.
CONCLUSIONS AND CLINICAL RELEVANCE Holter monitoring of Rhodesian Ridgebacks with a family history of an arrhythmia or sudden death is recommended for early diagnosis of disease. An autosomal recessive pattern of inheritance in the studied dogs was likely, and inbreeding should be strongly discouraged.
Objective—To determine the effect of long-term administration of enalapril on renal function in dogs with severe, compensated mitral regurgitation.
Design—Randomized controlled trial.
Animals—139 dogs with mitral regurgitation but without overt signs of heart failure.
Procedure—Dogs were randomly assigned to be treated with enalapril (0.5 mg/kg [0.23 mg/lb], PO, q 24 h) or placebo, and serum creatinine and urea nitrogen concentrations were measured at regular intervals for up to 26 months.
Results—Adequate information on renal function was obtained from 132 dogs; follow-up time ranged from 0.5 to 26 months (median, 12 months). Mean serum creatinine and urea nitrogen concentrations were not significantly different between dogs receiving enalapril and dogs receiving the placebo at any time, nor were concentrations significantly different from baseline concentrations. Proportions of dogs that developed azotemia or that had a ≥ 35% increase in serum creatinine or urea nitrogen concentration were also not significantly different between groups.
Conclusions and Clinical Relevance—Results suggest that administration of enalapril for up to 2 years did not have any demonstrable adverse effects on renal function in dogs with severe, compensated mitral regurgitation. (J Am Vet Med Assoc 2002;221: 654–658)
Objective—To determine the efficacy of long-term enalapril administration in delaying the onset of congestive heart failure (CHF).
Design—Placebo-controlled, double-blind, multicenter, randomized trial.
Animals—124 dogs with compensated mitral valve regurgitation (MR).
Procedures—Dogs randomly assigned to receive enalapril or placebo were monitored for the primary endpoint of onset of CHF for ≤ 58 months. Secondary endpoints included time from study entry to the combined endpoint of CHF-all-cause death; number of dogs free of CHF at 500, 1,000, and 1,500 days; and mean number of CHF-free days.
Results—Kaplan-Meier estimates of the effect of enalapril on the primary endpoint did not reveal a significant treatment benefit. Chronic enalapril administration did have a significant benefit on the combined endpoint of CHF-all-cause death (benefit was 317 days [10.6 months]). Dogs receiving enalapril remained free of CHF for a significantly longer time than those receiving placebo and were significantly more likely to be free of CHF at day 500 and at study end.
Conclusions and Clinical Relevance—Chronic enalapril treatment of dogs with naturally occurring, moderate to severe MR significantly delayed onset of CHF, compared with placebo, on the basis of number of CHF-free days, number of dogs free of CHF at days 500 and study end, and increased time to a combined secondary endpoint of CHF-all-cause death. Improvement in the primary endpoint, CHF-free survival, was not significant. Results suggest that enalapril modestly delays the onset of CHF in dogs with moderate to severe MR.