The cardinal symptom of heartfailure, i.e., the dyspnea, is largely attributable to pulmonary hypertension (PH) and congestion in the pulmonary vasculature [ 1 ]. So it is crucial to emphasize the very important
Förhécz, Z., Gombos, T., Borgulya, G., et al.: Red cell distribution width in heartfailure: prediction of clinical events and relationship with markers of ineffective erythropoiesis, inflammation, renal function, and nutritional state. Am. Heart J., 2009
The most common causes of heart failure in dogs are valvular disease, predominantly endocardiosis, and myocardial disease, predominantly dilated cardiomyopathy. They are related to changes in the expression of several genes in the heart muscle and in peripheral blood nuclear cells which could be considered as prognostic or diagnostic markers of heart disease in dogs. Since many human genetic markers of heart failure have turned out to be useless in dogs, the screening for genomic markers of canine heart failure could give more insight into the molecular pathology of these diseases and aid the development of new treatment strategies.
Participation of apoptosis during the development of pacing-induced dilated cardiomyopathy is not fully understood. After 7 weeks rapid right ventricular pacing, gene expressions of Bax, Bcl-2 and Caspase-3 were measured by RTQ-PCR from interventricular septum biopsies that were taken weekly in 21 beagle dogs during the development of heart failure. We evaluated protein levels of these genes by Western blot and DNA fragmentation by TUNEL method from autopsy samples. Gene expression of Bax remained unchanged during the pacing period; Bcl-2 mRNA expression transiently decreased in moderate heart failure and their ratio (Bcl-2/Bax) was not significantly altered. Caspase-3 gene expression increased in heart failure. Compared to the control group, expression of Bax and Bcl-2 proteins and their ratio were increased in dogs only after 4 weeks of pacing. No band of activated Caspase was found in the normal nor in the paced myocardium. In the TUNEL assay there was no significant difference between numbers of apoptotic cells in any of the groups, although a few TUNEL-positive cells were detected in the paced groups. Our results are not in favour of apoptosis in the pathogenesis of heart failure in this model and may be it could be attributed to activation of other systems.
Aim: Ventricular remodeling causes left ventricular hypertrophy (LVH) in myocardial infarction patients. We hypothesized that LVH can be evaluated using isointegral body surface maps. Methods: Thirty-two patients with post-infarction stable chronic heart failure underwent a 64-electrode body surface mapping (isointegral QRS, QRST, ST and STT maps) and 2-D echocardiography. Results: LVH was present in 16 of them (50%) according to 2D-echocardiography. Isointegral maxima increased and the minima were more negative in patients with LVH, and the differences were statistically significant for: isointegral QRS maxima (35±16 versus 60±21 mV.ms, p=0.0085) and minima (25±15 versus 69±14 mV.ms, p=0.0067), isointegral maxima and minima in the second third of the QRS complex, isointegral QRST minima and isointegral ST minima (5±2 versus 10±4 mV.ms, p=0.0026). Isointegral multipolar maps prevalence was increased in patients with LVH (75% versus 50%). Isointegral QRS and QRST maxima correlated best with the left ventricular mass (r=0.73 and 0.81). Conclusion: Body surface mapping is a useful method for the evaluation of patients with left ventricular hypertrophy in post-infarction heart failure. The most sensitive parameters are: isointegral QRS maxima and minima, especially in the second third of the QRS complex, isointegral QRST maps (minima, maxima and multipolarity) and isointegral ST minima.