Alterations in body composition and nutritional status are common in humans with heart failure and are related, in part, to increases in cytokine concentrations. Cytokines have not been studied previously in dogs with naturally occurring cardiac disease nor has fish oil administration been used in this population to decrease cytokine production. The purposes of this study were to characterize nutritional and cytokine alterations in dogs with heart failure and to test the ability of fish oil to reduce cytokines and improve clinical outcome. Body composition, insulinlike growth factor-1, fatty acids, and cytokines were measured in 28 dogs with heart failure and in 5 healthy controls. Dogs with heart failure then were randomized to receive either fish oil or placebo for 8 weeks. All parameters were measured again at the end of the study period. At baseline, 54% of dogs with heart failure were cachectic and the severity of cachexia correlated with circulating tumor necrosis factor-alpha concentrations (P = .05). Cytokine concentrations at baseline, however, were not significantly increased in dogs with heart failure compared to controls. Baseline plasma arachidonic acid (P = .02), eicosapentaenoic acid (P = .03), and docosahexaenoic acid (P = .004) concentrations were lower in dogs with heart failure than in controls. Fish oil supplementation decreased interleukin-1 beta (IL-1) concentrations (P = .02) and improved cachexia (P = .01) compared to the placebo group. The mean caloric intake of the heart failure dogs as a group was below the maintenance energy requirement (P < .001), but no difference was found in food intake between the fish oil and placebo groups. Insulinlike growth factor-1 concentrations (P = .01) and reductions in circulating IL-1 concentrations over the study period (P = .02) correlated with survival. These data demonstrate that canine heart failure is associated with cachexia, alterations in fatty acids, and reduced caloric intake. Fish oil supplementation decreased IL-1 concentrations and improved cachexia. In addition, reductions in IL-1 predicted survival, suggesting that anticytokine strategies may benefit patients with heart failure.
We examined in conscious dogs the effects of reductions in myocardial blood flow (MBF) in three different layers across the wall on regional myocardial contractile function in the ischemic zone, measured as systolic wall thickening (%WT). In 16 dogs, %WT was measured with sonomicrometry and MBF was determined with microspheres (10- to 12-microns diam) during coronary stenosis of the left circumflex coronary artery. The stenoses were categorized into six groups by the effect on %WT (each group representing progressive 20% decrements in %WT from control), and individual and pooled regression analyses were performed on data from six of the dogs having multiple data points to evaluate the shape (linear or curvilinear) of the relationships between MBF and changes in %WT. Transmural contractile function was highly sensitive to acute reductions in MBF, especially reductions in the subendocardium. The shape of the normalized subendocardial MBF-%WT relation was mildly curvilinear by regression analysis (quadratic equation, gamma = -0.75x2 + 2.15x -0.39, r2 = 0.92). Likewise, mean transmural and midmyocardial MBF correlated well and closely with changes in %WT. Subepicardial MBF, however, correlated poorly with changes in %WT, there being no change in subepicardial MBF until %WT had been reduced more than 50%.
A novel method for quantitative echocardiographic interpretations is introduced based on the calculation of ratio indices in which each raw M-mode measurement is divided by the aortic root dimension (Ao). ''Aorta-based'' indices were calculated with the animal's measured aortic root dimension (Ao m ) as the length standard. Conversely, ''weight-based'' indices employed an idealized estimate of aortic dimension (Ao w ) with a weighted least squares linear regression against the cube root of body weight (Ao w ϭ kW 1/3 ). Use of these indices circumvented undesirable statistical characteristics inherent in linear regression of echocardiographic dimensions against body weight and, to a lesser extent, body surface area. Compared with the regressions, ratio indices resulted in substantial refinement of the predictive range for each M-mode measurement in dogs, particularly with decreasing body size. Weight-based indices outperformed aorta-based indices in this regard. To refine the predictive range, neither type of index was clearly advantageous in cats compared with the simple average method typically employed for that species. Several of the raw Mmode measurements, however, were correlated with body weight in cats and horses, indicating the need for an appropriate correction for body size in these species. The ratio index method was suitable for this purpose. Summary statistics derived from normal dogs (n ϭ 53), cats (n ϭ 32), and horses (n ϭ 17) are presented for each index, including novel clinical indices calculated from area ratios. The latter were designed to represent body size-adjusted left ventricular stroke area (ie, volume overload) and myocardial wall area (ie, hypertrophy).Key words: Cardiac; Echocardiography; Heart. E chocardiographic studies have become routine for the diagnosis and evaluation of heart disease in veterinary medicine. Two-dimensional echocardiography (2DE) is used to visualize complex anatomic relationships, and Mmode echocardiography is used predominantly for quantification of cardiac dimensions. Increasingly, 2DE also is used for quantification. [1][2][3][4][5] Numerous quantitative evaluations of M-mode echocardiographic and 2DE recordings have been published. Echocardiographic interpretations by cardiologists, however, often are accomplished by visual inspection of the 2DE in real time and not necessarily by reference to published normal dimensions. This implies that these interpretations are the result of comparisons between structures visible on the 2DE in conjunction with extensive experience and knowledge of cardiac pathophysiology. An experienced echocardiographer is distinguished by a practiced eye and intimate familiarity with these relationships.Quantitative echocardiographic measurements still are required to establish whether cardiac dimensions are appropriate for the size of an individual. Published regressions of M-mode dimensions against body mass, however, might not agree with the visual interpretation of the cardiologist. Confidence intervals of these regressions ar...
Prolonged nontransmural ischemia was produced and the early and late effects of reperfusion were studied in 10 conscious dogs instrumented over the long term. Five hours of partial circumflex coronary artery-stenosis was produced with a hydraulic occluder, followed by gradual release over 20 min, with measurements of left ventricular pressure, regional myocardial function (systolic wall thickening by sonomicrometry), coronary blood flow velocity (pulsed Doppler), and myocardial blood flow (microspheres). During coronary stenosis the occluder was adjusted frequently to maintain a reduction of systolic wall thickening to 50% to 75% of control (average 62.6% of control). Myocardial blood flow in the ischemic area at 4 hr of partial coronary stenosis was reduced in the inner layers of the myocardium (subendocardium, from 0. 170-182, 1983. WITH the advent of surgical and nonsurgical revascularization of ischemic myocardium in man, coronary artery reperfusion has become an important therapeutic intervention. Many investigators" have reported the effects of reperfusion on ischemic myocardium after various periods of total coronary occlusion, but the value of this intervention remains controversial. The question of whether or not prolonged but revers- 170ible myocardial ischemic dysfunction can occur without coronary occlusion has also remained unexamined. In addition, despite recent clinical experience with coronary artery reperfusion by clot lysis or surgical means after acute myocardial infarction,9-there is little information on recovery of contractile function in zones that are partially perfused and exhibit nontransmural myocardial ischemia. In this study we investigated the effects of reperfusion on myocardial function and blood flow distribution over a 7 day period after 5 hr of partial coronary stenosis in conscious dogs instrumented over the long term. MethodsTen adult mongrel dogs weighing 22.1 to 39.6 kg (mean 28.4) were premedicated with acepromazine maleate (0.5 mg/ CIRCULATION
A novel method for quantitative echocardiographic interpretations is introduced based on the calculation of ratio indices in which each raw M-mode measurement is divided by the aortic root dimension (Ao). "Aorta-based" indices were calculated with the animal's measured aortic root dimension (Ao(m)) as the length standard. Conversely, "weight-based" indices employed an idealized estimate of aortic dimension (Ao(w)) with a weighted least squares linear regression against the cube root of body weight (Ao(w) = kW(1/3)). Use of these indices circumvented undesirable statistical characteristics inherent in linear regression of echocardiographic dimensions against body weight and, to a lesser extent, body surface area. Compared with the regressions, ratio indices resulted in substantial refinement of the predictive range for each M-mode measurement in dogs, particularly with decreasing body size. Weight-based indices outperformed aorta-based indices in this regard. To refine the predictive range, neither type of index was clearly advantageous in cats compared with the simple average method typically employed for that species. Several of the raw M-mode measurements, however, were correlated with body weight in cats and horses, indicating the need for an appropriate correction for body size in these species. The ratio index method was suitable for this purpose. Summary statistics derived from normal dogs (n = 53), cats (n = 32), and horses (n = 17) are presented for each index, including novel clinical indices calculated from area ratios. The latter were designed to represent body size-adjusted lett ventricular stroke area (ie, volume overload) and myocardial wall area (ie, hypertrophy).
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