Neurohormonal activation in canine degenerative mitral valve disease: implications on pathophysiology and treatment.

Neurohormonal systems play a critical role in canine degenerative mitral valve disease (DMVD). DMVD results in mitral regurgitation, which reduces forward cardiac output and increases intracardiac pressures. These changes trigger neurohormonal responses that ultimately result in maladaptive cardiac remodelling, congestion and heightened morbidity and mortality. Medical therapies such as ACE inhibitors and spironolactone derive their benefit by interrupting or suppressing these neurohormonal responses. Thus, knowledge of neurohormonal mechanisms can lead to a better understanding of how to treat DMVD.

The diagnostic and therapeutic approach to the patient in acute congestive heart failure.

The patient presented in acute congestive heart failure represents a diagnostic challenge. Life-threatening compromise of respiratory or cardiovascular function renders the patient vulnerable to the stresses associated with many diagnostic tests. Before risking any test in this situation, it is important to understand the information that each test will give, and how that will impact the diagnostic and therapeutic approach in this crucial early phase of patient management. This article describes the diagnostic tests commonly used in the evaluation of patients in acute heart failure and the information that each provides, and discusses how this information can be used to guide therapy. Pericardiocentesis is discussed in detail.

Metabolic findings in the erythrocytes of cardiopathic and anaemic dogs.

Few data are available on the activities of canine erythrocyte enzymes and on 2,3 diphosphoglycerate (2,3DPG) concentrations in pathological conditions other than heritable erythrocyte defects. Because some diseases might affect erythrocyte metabolism and oxygen transport, we evaluated these parameters in 10 healthy dogs and in dogs with symptomless dirofilariosis (n = 9), mild (n = 13) and severe (n = 8) cardiac failure, and haemolytic anaemia (n = 8). To evaluate possible membrane damage, the osmotic fragility of the red cells was measured. No haematological abnormalities were found in the dogs with mild cardiopathy or in those with symptomless dirofilariosis. Severe anaemia and neutrophilic leucocytosis were found in the dogs with haemolytic anaemia and, to a lesser degree, in those with severe heart failure. In dogs with these two diseases, elevated values obtained were, respectively: pyruvate kinase (PK) 17.5 +/- 10.3 U/g haemoglobin (Hb) (P < 0.001) and 11.6 +/- 7.5 U/g Hb (P < 0.01); glucose-6-phosphate dehydrogenase (G6PDH) 8.9 +/- 5.4 U/g Hb (P < 0.001) and 5.6 +/- 4.2 U/g Hb; 2,3DPG 21.8 +/- 4.9 U/g Hb (P < 0.001) and 22.5 +/- 4.1 U/g Hb (P < 0.001). The increased 2,3DPG concentrations may have been due to diminished oxygen availability but the observed enzymatic changes were attributed mainly to the presence of young red blood cells: there was a positive correlation between nucleated red blood cells and PK activity, G6PDH activity and 2,3DPG concentration and a negative correlation between mature erythrocytes and PK activity, G6PDH activity and 2,3DPG concentration. This was supported by the derivative curve of the fragiligram, which showed two or three peaks corresponding to different erythrocyte populations and by the negative correlation between the maximum haemolytic NaCl concentration and the reticulocyte number. The measurement of PK and G6PDH activity and of the 2,3PG concentration, together with information provided by the fragiligram, would seem to be of value in defining the clinico-haematological picture in clinical heart diseases and haemolytic anaemia.

Skeletal muscle extra-aortic counterpulsation in dogs with dilated cardiomyopathy.

Skeletal muscle extra-aortic counterpulsation was performed in seven dogs with dilated cardiomyopathy. A left latissimus dorsi dynamic descending thoracic aortomyoplasty was used as the autologous counterpulsator. Pulse train stimulation in diastole was used to initiate contraction and fibre type transformation. Two of the dogs died within 48 hours of surgery. The device was successfully activated in the five remaining dogs, but in one individual it failed within 48 hours of activation. Serial echocardiographic examinations of dogs in which the device functioned successfully (n = 4) showed trends towards the decrease in the left ventricular systolic internal dimension, left ventricular diastolic internal dimension, E-point to septal separation and left atrial diameter in systole seven to 14 days following the procedure, although these changes failed to persist in the long-term. The results suggest that skeletal muscle for cardiac assistances such as extra-aortic muscle counterpulsation, might be a therapeutic option for dogs with cardiac failure due to dilated cardiomyopathy.

The acute haemodynamic effects of captopril in dogs with heart failure.

The acute effects of three doses of captopril (12.5, 25, and 50 mg [approximately 0.5, 1.0, and 2.0 mg/kg]) on several haemodynamic variables and plasma aldosterone concentration were investigated in four dogs with experimentally produced heart failure (rapid ventricular pacing) and one dog with dilated cardiomyopathy. Haemodynamic variables were measured with a Swan-Ganz thermodilution catheter and an indwelling carotid artery catheter at baseline and 1, 2, and 4 h after drug administration. A statistically significant (P < 0.05) decrease in peripheral vascular resistance was observed 1 and 2 h following the 12.5 mg dose. A significant and large enough decrease in peripheral vascular resistance to produce a significant decrease in mean systemic arterial blood pressure was observed 1 and 2 h after administering 25 and 50 mg of captopril. A mild but significant increase in cardiac output was observed 1 h after each dose. The drug effect on systemic arterial blood pressure lasted less than 4 h. No statistically significant changes were observed for the group in pulmonary capillary wedge pressure, right atrial blood pressure, or plasma aldosterone concentration at any time. We conclude that the acute haemodynamic benefits provided by captopril administration were mild and due primarily to arteriolar dilation. Doses of approximately 1-2 mg/kg produced slightly greater arteriolar dilation than an approximate dose of 0.5 mg/kg. The drug effect was short-lived, lasting less than 4 h.

Changes in erythrocyte deformability in NaCl-induced right-sided cardiac failure in broiler chickens.

In this study, we tested the hypothesis that erythrocyte deformability is decreased in the development of cardiac failure induced by NaCl toxicosis. Deformability of erythrocytes and routine hematologic and biochemical variables were measured in 6 of 50 chickens that were given 5 g of NaCl/L in their drinking water from day 7 to day 42, and were compared with values in 6 of 50 healthy chickens given free access to tap water. Deformability was assessed by passing a 10% suspension of erythrocytes through a polycarbonate membrane with 5-microns pores. Chickens were euthanatized and heart and body weights were determined. Treatment with NaCl induced right-sided cardiac failure up to day 28. The ratios of heart weight to body weight were greater, for right ventricle by 20 to 64% and for left ventricle by 15 to 27%, attributable to NaCl treatment. Deformability of erythrocytes of NaCl-treated chickens was markedly decreased, in association with increased erythrocyte size and plasma Na+ concentration. However, only part of the decreased deformability could be explained by swelling of erythrocytes. Decreased deformability could not be explained by increased cell viscosity because mean corpuscular hemoglobin concentration, the primary determinant of erythrocyte viscosity, was decreased. Because decreased deformability of erythrocytes has been demonstrated previously to be associated with increased vascular resistance, decreased deformability may have contributed to the development of right-sided cardiac failure in these chickens.