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Myocardial Stretch (myocardial + stretch)
Selected AbstractsOpposite Effects of Myocardial Stretch and Verapamil on the Complexity of the Ventricular Fibrillatory Pattern: An Experimental StudyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2000FRANCISCO J. CHORRO CHORRO, F.J., et al.: Opposite Effects of Myocardial Stretch And Verapamil on The Complexity of The Ventricular Fibrillatory Pattern: An Experimental Study. An experimental model is used to analyze the effects of ventricular stretching and verapamil on the activation patterns during VF. Ten Langendorff-perfused rabbit hearts were used to record VF activity with an epicardial multiple electrode before, during, and after stretching with an intraventricular balloon, under both control conditions and during verapamil (Vp) infusion (0.4,0.8 ,mol). The analyzed parameters were dominant frequency (FrD) spectral analysis, the median (MN) of the VF intervals, and the type of activation maps during VF (I = one wavelet without block lines, II = two simultaneous wavelets with block lines, III = three or more wavelets with block lines). Stretch accelerates VF (FrD: 22.8 ± 6.4 vs 15.2 ± 1.0 Hz, P < 0.01; MN: 48 ± 13 vs 68 ± 6 ms, P < 0.01). On fitting the FrD time changes to an exponential model after applying and suppressing stretch, the time constants (stretch: 101.2 ± 19.6 s; stretch suppression: 97.8 ± 33.2 s) do not differ significantly. Stretching induces a significant variation in the complexity of the VF activation maps with type III increments and type I and II decrements (control: I = 17.5%, II = 50.5%, III = 32%; stretch: I = 7%, II = 36.5%, III = 56.5%, P < 0.001). Vp accelerates VF (FrD: 20.9 ± 1.9 Hz, P < 0.001 vs control; MN: 50 ± 5 ms, P < 0.001 vs control) and diminishes activation maps complexity (I = 25.5%, II = 60.5%, III = 14%, P < 0.001 vs control). On applying stretch during Vp perfusion, the fibrillatory process is not accelerated to any greater degree. However, type I and II map decrements and type III increments are recorded, though reaching percentages similar to control (I = 16.5%, II = 53%, III = 30.5%, NS vs control). The following conclusions were found: (1) myocardial stretching accelerates VF and increases the complexity of the VF activation pattern; (2) time changes in the FrD of VF during and upon suppressing stretch fit an exponential model with similar time constants; and (3) although stretching and verapamil accelerate the VF process, they exert opposite effects upon the complexity of the fibrillatory pattern. [source] Ventricular Fibrillation Induced by Stretch Pulse: Implications for Sudden Death Due to Commotio CordisJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2006FRANK BODE M.D. Introduction: Nonpenetrating chest wall impact (commotio cordis) may lead to sudden cardiac death due to the acute initiation of ventricular fibrillation (VF). VF may result from sudden stretch during a vulnerable window, which is determined by repolarization inhomogeneity. Methods: We examined action potential morphologies and VF inducibility in response to sudden myocardial stretch in the left ventricle (LV). In six Langendorff perfused rabbit hearts, the LV was instrumented with a fluid-filled balloon. Increasing volume and pressure pulses were applied at different times of the cardiac cycle. Monophasic action potentials (MAPs) were recorded simultaneously from five LV epicardial sites. Inter-site dispersion of repolarization was calculated in the time and voltage domains. Results: Sudden balloon inflation induced VF when pressure pulses of 208,289 mmHg were applied within a window of 35,88 msec after MAP upstroke, a period of intrinsic increase in repolarization dispersion. During the pressure pulse, MAPs revealed an additional increase in repolarization dispersion (time domain) by 9 ± 6 msec (P < 0.01). The maximal difference in repolarization levels (voltage domain) between sites increased from 19 ± 3% to 26 ± 3% (P < 0.05). Earliest stretch-induced activation was observed near a site with early repolarization, while sites with late repolarization showed delayed activation. Conclusions: Sudden myocardial stretch can elicit VF when it occurs during a vulnerable window that is based on repolarization inhomogeneity. Stretch pulses applied during this vulnerable window can lead to nonuniform activation. Repolarization dispersion might play a crucial role in the occurrence of fatal tachyarrhythmias during commotio cordis. [source] Hyper osmolality does not modulate natriuretic peptide concentration in patients after coronary artery surgeryACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2009E. L. HONKONEN Background: The heart secretes natriuretic peptides (NPs) in response to myocardial stretch. Measuring NP concentrations is a helpful tool in guiding treatment. It has been suggested that sodium ion and hyperosmolality could affect NP excretion. If this is true, peri-operative NP measurements could be inconsistent when hypertonic solutions are used. With different osmolalities but equal volumes of hydroxyethyl starch (HES) , and hypertonic saline (HS) , infusions, this double-blinded study tested the hypothesis that osmolality modulates the excretion of NPs. Methods: Fifty coronary surgery patients were randomized to receive within 30 min 4 ml/kg either HS or HES post-operatively. Samples for analysis of atrial NP (ANP), brain NP (BNP), plasma and urine sodium and osmolality and urine oxygen tension were obtained before and 60 min after starting the infusions and on the first post-operative morning. The haemodynamic parameters were measured at the same time points. Results: Plasma osmolality and sodium increased only in the HS group. Changes in plasma BNP and ANP levels did not differ between the groups (P=0.212 and 0.356). There were no correlations between NP levels and osmolality or sodium at any time point. In the HS group, urine volume was higher (3295 vs. 2644 ml; P<0.05) and the need for furosemide treatment was less (0.4 vs. 3.8 mg; P<0.01) than in the HES group. Conclusions: The absence of effects of plasma sodium content or hyperosmolality on NP release validates the value of NPs as a biomarker in peri-operative patients. [source] N-terminal pro-brain natriuretic peptide for detection of cardiovascular stress in patients with obstructive sleep apnea syndromeJOURNAL OF SLEEP RESEARCH, Issue 4 2006EDMOND VARTANY Summary Patients with obstructive sleep apnea syndrome (OSAS) have an elevated incidence of cardiovascular events that may be related to an increased ventricular load and hypoxemia caused by apneas and hypopneas. N-terminal pro-brain natriuretic peptide (NTproBNP) appears to be an excellent marker of myocardial stretch and could serve as an indicator of subclinical cardiac stress, thereby identifying a patient population at risk for cardiac effects from OSAS. Adult patients presenting with suspected OSAS and scheduled for nocturnal polysomnography were recruited. Patients with heart or renal failure or severe lung disease were excluded. NTproBNP was measured the evening before and the morning after sleep. Blood pressure (BP) was monitored intermittently throughout the night. Fifteen male and 15 female subjects with a mean ± SD body mass index of 38.2 ± 9.8 were studied. Mean Apnea,Hypopnea Index (AHI) was 38.4 ± 26, with 17 subjects having severe OSAS (AHI > 30). No subject had a significant rise in BP. NTproBNP values overnight decreased in 19 patients and rose in 11 (mean change 3.8 ± 33 pg mL,1), but only one patient had an abnormal morning value. Three patients had an abnormal NTproBNP value prior to sleep, but their levels decreased with sleep. No correlations were detected between the evening baseline or postsleep NTproBNP levels and OSAS. Monitoring pre- and postsleep NTproBNP levels revealed no association with the occurrence or degree of OSAS, making it unlikely that NTproBNP could serve as a marker of cardiac stress in OSAS patients with stable BP and without overt heart failure. [source] | ||||||||||