Extracorporeal life support (ECLS) is a treatment modality that provides prolonged blood circulation, gas exchange and can partially support or fully substitute functions of heart and lungs in patients with severe but potentially reversible cardiopulmonary failure refractory to conventional therapy. Due to high-volume bypass, the extracorporeal flow is interacting with native cardiac output. The pathophysiology of circulation and ECLS support reveals significant effects on arterial pressure waveforms, cardiac hemodynamics, and myocardial perfusion. Moreover, it is still subject of research, whether increasing stroke work caused by the extracorporeal flow is accompanied by adequate myocardial oxygen supply. The left ventricular (LV) pressure-volume mechanics are reflecting perfusion and loading conditions and these changes are dependent on the degree of the extracorporeal blood flow. By increasing the afterload, artificial circulation puts higher demands on heart work with increasing myocardial oxygen consumption. Further, this can lead to LV distention, pulmonary edema, and progression of heart failure. Multiple methods of LV decompression (atrial septostomy, active venting, intra-aortic balloon pump, pulsatility of flow) have been suggested to relieve LV overload but the main risk factors still remain unclear. In this context, it has been recommended to keep the rate of circulatory support as low as possible. Also, utilization of detailed hemodynamic monitoring has been suggested in order to avoid possible harm from excessive extracorporeal flow., Pavel Hála, Otomar Kittnar., and Obsahuje bibliografii
More than 50 % of end-stage renal disease (ESRD) patients treated by chronic hemodialysis die from cardiovascular diseases, including congestive heart failure (CHF). The incidence of CHF is rising in both general and ESRD population. However, the mechanisms, which lead to the development of CHF in dialyzed patients, differ considerably. First, there are several factors leading to increase of the left ventricular afterload: volume overload between dialyses, hypertension, increased arterial stiffness, anemia, vascular access flow (arteriovenous fistula) and sympathetic activation. Second, hypertension, left ventricular hypertrophy, anemia and frequently present coronary artery disease worsen myocardial oxygenation. The combination of these factors explains the high incidence of CHF in dialyzed patients and their roles are reviewed in this article., J. Malík ... [et al.]., and Obsahuje seznam literatury
The Spontaneously Hypertensive Heart Failure (SHHF) rat mimics the human progression of hypertension from hypertrophy to heart failure. However, it is unknown whether SHHF animals can exercise at sufficient levels to observe beneficial biochemical adaptations in skeletal muscle. Thirty-seven female SHHF and Wistar-Furth (WF) rats were randomized to sedentary (SHHFsed and WFsed) and exercise groups (SHHFex and WFex). The exercise groups had access to running wheels from 6-22 months of age. Hindlimb muscles were obtained for metabolic measures that included mitochondrial enzyme function and expression, and glycogen utilization. The SHHFex rats ran a greater distance and duration as compared to the WFex rats (P<0.05), but the WFex rats ran at a faster speed (P<0.05). Skeletal muscle citrate synthase and β-hydroxyacyl-CoA dehydrogenase enzyme activity was not altered in the SHHFex group, but was increased (P<0.05) in the WFex animals. Citrate synthase protein and gene expression were unchanged in SHHFex animals, but were increased in WFex rats (P<0.05). In the WFex animals muscle glycogen was significantly depleted after exercise (P<0.05), but not in the SHHFex group. We conclude that despite robust amounts of aerobic activity, voluntary wheel running exercise was not sufficiently intense to improve the oxidative capacity of skeletal muscle in adult SHHF animals, indicating an inability to compensate for declining heart function by improving peripheral oxidative adaptations in the skeletal muscle., R. L. Schultz, ... [et al.]., and Obsahuje seznam literatury
The acute effects of β-adrenergic stimulation on myocardial stiffness were evaluated. New-Ze aland white rabbits were treated with saline (control group) or do xorubicin to induce heart failure (HF) (DOXO-HF group). Effects of isoprenaline (10-10-10-5 M), a non-selective β-adrenergic agonist, were tested in papillary muscles from both groups. In the control group, the effects of isoprenaline were also evaluate d in the presence of a damaged endocardial endothelium, atenolol (β1-adrenoceptor antagonist), ICI-118551 (β2-adrenoceptor antagonist), KT-5720 (PKA inhibitor), L-NNA (NO-synthase inhibitor), or indomethacin (cyclooxygenase inhibitor). Passive length-tension relations were constructed before and after adding isoprenaline (10-5 M). In the control group, isoprenaline increased resting muscle length up to 1.017±0.006 L/Lmax. Correction of resting muscle length to its initial value resulted in a 28.5±3.1 % decrease of resting tension, indicating decreased muscle stiffness, as confirmed by the isoprenaline-induced right-downwa rd shift of the passive length- tension relation. These effects were modulated by β1- and β2-adrenoceptors and PKA. In DOXO-HF group, the effect on myocardial stiffness was significantly decreased. We conclude that β -adrenergic stimulation is a relevant mechanism of acute neurohumoral modulation of the diastolic function. Furthermore, this study clarifies the mechanisms by which myocardial stiffness is decreased., I. Falcão-Pires ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
The natriuretic peptides - atrial, brain and C-type - were discovered during the last tw enty years. Their effects on cardiovascular, renal, cerebral and other tissues through guanylyl cyclase were uncovered. Over the past decade natriuretic peptides (NPs) became a very useful tool in the management of heart failure patients. Results of many clinical trials have shown that BNP and NT-proBNP are helpful for diagnosis of heart failure. They are also independent markers of prognosis not only in heart failure patients but also in patients with other cardiovascular diseases. Recently published data document the utility of NPs in guiding treatment of heart failure patients. In this article, we focus on basic biochemical and physiological characteristics of NPs as well as on their significance in management of heart failure patients. Some limitations and pitfalls of NPs levels interpretation in diagnosing heart failure are also discussed., J. Krupička ... [et al.]., and Obsahuje seznam literatury
This study investigated whether endothelin (ET)-1-induced increase in myocardial distensibility is preserved in heart failure (HF) and whether it is modulated by nitric oxide (NO) and prostaglandins. New Zealand white rabbits were treated with doxorubicin (1 mg/kg, intravenously twice a week for 8 weeks, DOX-HF group) or saline (control group). Effects of ET-1 (0.1, 1, 10 nM) were tested in papillary muscles from the DOX-HF group and a control group in the presence of: i) intact endocardial endothelium (EE); ii) damaged EE; iii) NG-nitro-L-arginine (L-NNA; NO synthase inhibitor), and iv) indomethacin (INDO; cyclooxygenase inhibitor). In the presence of an intact EE, ET-1 promoted concentration-dependent positive inotropic and lusitropic effects that were maintained after damaging the EE, in the presence of L-NNA or INDO and in the DOX-HF Group. ET-1 reduced resting tension at the end of the isometric twitch (increased diastolic distensibility) by 3.2±1.3 %, 6.0±1.6 % and 8.8±2.7 % (at 0.1, 1 and 10 nM, respectively), in muscles with intact EE, effect that was completely abolished after damaging EE, in the presence of L-NNA or INDO or in the DOX-HF Group. This study demonstrated that the increase in myocardial distensibility induced by ET-1 is absent in HF and is dependent of NO and prostaglandin release., C. Brás-Silva, D. Monteiro-Sousa, A. J. Duarte, M. Guerra, A. P. Fontes-Sousa, C. Moura, J. C. Areias, A. F. Leite-Moreira., and Obsahuje bibliografii a bibliografické odkazy
Cardiac resynchronization therapy (CRT) has proven efficacious
in the treatment of patients with heart failure and
dyssynchronous activation. Currently, we select suitable CRT
candidates based on the QRS complex duration (QRSd) and
morphology with left bundle branch block being the optimal
substrate for resynchronization. To improve CRT response rates,
recommendations emphasize attention to electrical parameters
both before implant and after it. Therefore, we decided to study
activation times before and after CRT on the body surface
potential maps (BSPM) and to compare thus obtained results with
data from electroanatomical mapping using the CARTO system.
Total of 21 CRT recipients with symptomatic heart failure (NYHA
II-IV), sinus rhythm, and QRSd ≥150 ms and 7 healthy controls
were studied. The maximum QRSd and the longest and shortest
activation times (ATmax and ATmin) were set in the BSPM maps
and their locations on the chest were compared with CARTO
derived time interval and site of the latest (LATmax) and earliest
(LATmin) ventricular activation. In CRT patients, all these
parameters were measured during both spontaneous rhythm and
biventricular pacing (BVP) and compared with the findings during
the spontaneous sinus rhythm in the healthy controls. QRSd was
169.7±12.1 ms during spontaneous rhythm in the CRT group and
104.3±10.2 ms after CRT (p<0.01). In the control group the
QRSd was significantly shorter: 95.1±5.6 ms (p<0.01). There
was a good correlation between LATmin(CARTO) and
ATmin(BSPM). Both LATmin and ATmin were shorter in the
control group (LATmin(CARTO) 24.8±7.1 ms and ATmin(BSPM)
29.6±11.3 ms, NS) than in CRT group (LATmin(CARTO) was
48.1±6.8 ms and ATmin(BSPM) 51.6±10.1 ms, NS). BVP
produced shortening compared to the spontaneous rhythm of
CRT recipients (LATmin(CARTO) 31.6±5.3 ms and ATmin(BSPM)
35.2±12.6 ms; p<0.01 spontaneous rhythm versus BVP). ATmax
exhibited greater differences between both methods with higher
values in BSPM: in the control group LATmax(CARTO) was
72.0±4.1 ms and ATmax (BSPM) 92.5±9.4 ms (p<0.01), in the
CRT candidates LATmax(CARTO) reached only 106.1±6.8 ms
whereas ATmax(BSPM) 146.0±12.1 ms (p<0.05), and BVP paced
rhythm in CRT group produced improvement with
LATmax(CARTO) 92.2±7.1 ms and ATmax(BSPM) 130.9±11.0 ms
(p<0.01 before and during BVP). With regard to the propagation
of ATmin and ATmax on the body surface, earliest activation
projected most often frontally in all 3 groups, whereas projection
of ATmax on the body surface was more variable. Our results
suggest that compared to invasive electroanatomical mapping
BSPM reflects well time of the earliest activation, however
provides longer time-intervals for sites of late activation.
Projection of both early and late activated regions of the heart on
the body surface is more variable than expected, very likely due
to changed LV geometry and interposed tissues between the
heart and superficial ECG electrode.