Electrophysiological delineation of the tachycardia circuit in atrioventricular nodal reentrant tachycardia.
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BACKGROUND: The exact boundaries of the reentry circuit in atrioventricular nodal reentrant tachycardia (AVNRT) have not been convincingly defined. METHODS AND RESULTS: To define the tachycardia circuit, single extrastimuli were delivered during AVNRT to 8 sites of the right intra-atrial septum: 3 arbitrarily divided sites of the AV junction extending from the His bundle (HB) site to the coronary sinus ostium (CSOS) (sites S, M, and I) and the superior (S-CSOS), inferior (I-CSOS), posterior (P-CSOS), and posteroinferior (PI-CSOS) portions of the CSOS and the CSOS in 18 patients. The mean tachycardia cycle length (TCL) was 368+/-52 ms. Retrograde earliest atrial activation was observed at the HB site in all patients. The longest coupling intervals of single extrastimuli that reset AVNRT at sites S, M, I, I-CSOS, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 356+/-51, 356+/-51, 355+/-52, 357+/-51, 318+/-47, 305+/-53, 311+/-56, and 312+/-56 ms, respectively, and the following return cycles at these sites were 368+/-52, 368+/-53, 367+/-53, 367+/-53, 407+/-66, 431+/-73, 415+/-55, and 412+/-56 ms, respectively. The longest coupling intervals at sites S, M, I, and I-CSOS did not differ from each other and were longer than those at CSOS and S-, P-, and PI-CSOS (P<0.0001). The return cycles at sites S, M, I, and I-CSOS did not differ from the TCL, whereas those at CSOS and S-, P-, and PI-CSOS were longer than the TCL (P<0.0001). CONCLUSIONS: The perinodal atrium extending from the HB site to I-CSOS was involved in the tachycardia circuit. I-CSOS was thought to be the entrance of the slow pathway. (+info)
Reflex control of sympathetic activity during simulated ventricular tachycardia in humans.
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BACKGROUND: Ventricular tachyarrhythmias present a unique set of stimuli to arterial and cardiopulmonary baroreceptors by increasing cardiac filling pressures and decreasing arterial pressure. The net effect on the control of sympathetic nerve activity (SNA) in humans is unknown. The purpose of this study was to determine the relative roles of cardiopulmonary and arterial baroreceptors in controlling SNA and arterial pressure during ventricular pacing in humans. METHODS AND RESULTS: Two experiments were performed in which SNA and hemodynamic responses to ventricular pacing were compared with nitroprusside infusion (NTP) in 12 patients and studied with and without head-up tilt or phenylephrine to normalize the stimuli to either the arterial or cardiopulmonary baroreceptors in 9 patients. In experiment 1, the slope of the relation between SNA and mean arterial pressure was greater during NTP (-4.7+/-1.4 U/mm Hg) than during ventricular pacing (-3.4+/-1.1 U/mm Hg). Comparison of NTP doses and ventricular pacing rates that produced comparable hypotension showed that SNA increased more during NTP (P=0.03). In experiment 2, normalization of arterial pressure during pacing resulted in SNA decreasing below baseline (P<0.05), whereas normalization of cardiac filling pressure resulted in a greater increase in SNA than pacing alone (212+/-35% versus 189+/-37%, P=0. 04). Conclusions--These data demonstrate that in humans arterial baroreflex control predominates in mediating sympathoexcitation during ventricular tachyarrhythmias and that cardiopulmonary baroreceptors contribute significant inhibitory modulation. (+info)
In vivo inhibition of elevated myocardial beta-adrenergic receptor kinase activity in hybrid transgenic mice restores normal beta-adrenergic signaling and function.
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BACKGROUND: The clinical syndrome of heart failure (HF) is characterized by an impaired cardiac beta-adrenergic receptor (betaAR) system, which is critical in the regulation of myocardial function. Expression of the betaAR kinase (betaARK1), which phosphorylates and uncouples betaARs, is elevated in human HF; this likely contributes to the abnormal betaAR responsiveness that occurs with beta-agonist administration. We previously showed that transgenic mice with increased myocardial betaARK1 expression had impaired cardiac function in vivo and that inhibiting endogenous betaARK1 activity in the heart led to enhanced myocardial function. METHODS AND RESULTS: We created hybrid transgenic mice with cardiac-specific concomitant overexpression of both betaARK1 and an inhibitor of betaARK1 activity to study the feasibility and functional consequences of the inhibition of elevated betaARK1 activity similar to that present in human HF. Transgenic mice with myocardial overexpression of betaARK1 (3 to 5-fold) have a blunted in vivo contractile response to isoproterenol when compared with non-transgenic control mice. In the hybrid transgenic mice, although myocardial betaARK1 levels remained elevated due to transgene expression, in vitro betaARK1 activity returned to control levels and the percentage of betaARs in the high-affinity state increased to normal wild-type levels. Furthermore, the in vivo left ventricular contractile response to betaAR stimulation was restored to normal in the hybrid double-transgenic mice. CONCLUSIONS: Novel hybrid transgenic mice can be created with concomitant cardiac-specific overexpression of 2 independent transgenes with opposing actions. Elevated myocardial betaARK1 in transgenic mouse hearts (to levels seen in human HF) can be inhibited in vivo by a peptide that can prevent agonist-stimulated desensitization of cardiac betaARs. This may represent a novel strategy to improve myocardial function in the setting of compromised heart function. (+info)
Measurement of myocardial glucose uptake in patients with ischemic cardiomyopathy: application of a new quantitative method using regional tracer kinetic information.
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Quantification of myocardial glucose uptake (MGU) by 18F-fluoro-2-deoxyglucose (FDG) using PET may be inaccurate, because the correction factor that relates myocardial FDG uptake to MGU, the lumped constant (LC), is not a true constant. Recent studies have shown that analysis of FDG time-activity curves allows determination of individual LCs and that variable LCs yield accurate determination of MGU. We compared the magnitude of the LC in different regions of the heart in patients with ischemic cardiomyopathy. METHODS: Twenty patients with ischemic cardiomyopathy and an average ejection fraction of 33% underwent dynamic 13N-ammonia and FDG PET. We determined myocardial perfusion and MGU in 177 regions classified as control (71 regions), mismatch (50 regions) and match (56 regions), according to findings on PET and echocardiography. Regional MGU was calculated with both regional LCs and a fixed LC of 0.67. RESULTS: All results were expressed as mean +/- SD. Myocardial perfusion was highest in control regions (0.52+/-0.18 mL/g/min), reduced in mismatch regions (0.43+/-0.19 mL/g/min; P < 0.05 versus control) and severely reduced in match regions (0.28+/-0.17 mL/g/min; P < 0.001 versus control and mismatch). Regional LCs ranged from 0.45 to 1.30 and differed between patients (P < 0.001). Regional LCs were similar in regions diagnosed as control (0.78+/-0.23), mismatch (0.80+/-0.24) and match (0.72+/-0.21). MGU (micromol/g/min) calculated by regional LCs was similar in control (0.52+/-0.16) and mismatch (0.49+/-0.19) regions and decreased in match regions (0.31+/-0.12, P < 0.001). The agreement between MGU calculated with variable and fixed LCs was poor. CONCLUSION: The LC used in the calculation of MGU was not affected by regional differences in the metabolic state of the myocardium. However, the LC varied substantially between patients in control, mismatch and match regions. These findings indicate that quantitative measurements of MGU using a fixed LC must be interpreted with caution. (+info)
Significance of increased right ventricular uptake on 99mTc-sestamibi SPECT in patients with coronary artery disease.
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The significance of increased right ventricular (RV) tracer uptake in patients with coronary artery disease (CAD) without pulmonary or valvular heart disease is unclear. METHODS: Forty consecutive patients with increased RV uptake on SPECT myocardial perfusion imaging and right heart catheterization within 4 wk were studied prospectively. Thirty-five individuals with very low likelihood of CAD served as controls. Rest and stress SPECT myocardial perfusion data were obtained using a standard 99mTc-sestamibi 1-d imaging protocol. A quick and simple RV-to-left ventricular (LV) myocardial uptake ratio was calculated from the maximum counts per pixel detected in the right and left ventricles using the reconstructed coronal slices. RV end-systolic pressure (RV-ESP), mean pulmonary artery pressure (PAP) and pulmonary capillary wedge pressure were obtained by standard techniques. RESULTS: The RV/LV uptake ratio in the controls was 0.31+/-0.05. Thirty-six of the 40 (90%) CAD patients with increased RV tracer uptake had increased RV-ESP, and 39 (97.5%) had increased PAP. Highly significant positive correlations between the RV/LV uptake ratio and RV-ESP and PAP were found (r = 0.45, P = 0.003; and r = 0.52, P < 0.001, respectively). CONCLUSION: Increased RV uptake, assessed from standard myocardial perfusion studies, can identify RV pressure overload among patients with CAD. In the absence of pulmonary or valvular heart disease, increased RV uptake (i.e., RV pressure overload) indicates significant backward failure, a variable with known significant negative prognostic implications. (+info)
Prognostic value of MIBG imaging in idiopathic dilated cardiomyopathy.
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Alterations of cardiac sympathetic innervation are likely to contribute to fatal outcomes in patients with heart failure. These alterations can be evaluated noninvasively by 123I-metaiodoben-zylguanidine (MIBG) imaging. METHODS: The hypothesis that impaired cardiac sympathetic innervation, as assessed using MIBG imaging, is related to adverse outcomes was tested in 112 patients with heart failure resulting from idiopathic cardiomyopathy. Main inclusion criteria were New York Heart Association classes II-IV and radionuclide left ventricular ejection fraction (LVEF) < 40%. Patients were assessed for cardiac MIBG uptake, circulating norepinephrine concentration, LVEF, peak Vo2, x-ray cardiothoracic ratio, M-mode echographic end-diastolic diameter and right-sided heart catheterization parameters. RESULTS: During a mean follow-up of 27 +/- 20 mo, 19 patients had transplants, 25 died of cardiac death (8 sudden deaths), 2 died of noncardiac death and 66 survived without transplantation. The only independent predictors for mortality were low MIBG uptake (P < 0.001) and LVEF (P = 0.02) when using multivariate discriminant analysis. Moreover, MIBG uptake (P < 0.001) and circulating norepinephrine concentration (P = 0.001) were the only independent predictors for life duration when using multivariate life table analysis. CONCLUSION: Impaired cardiac adrenergic innervation as assessed by MIBG imaging is strongly related to mortality. MIBG imaging may help risk stratify patients with heart failure resulting from idiopathic dilated cardiomyopathy. (+info)
Instantaneous pressure-flow velocity relations of systemic venous return in patients with univentricular circulation.
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OBJECTIVE: To assess the pressure and flow velocity relations and respiratory variability of the systemic venous and hepatic venous return in patients with univentricular circulation. PATIENTS: 15 selected patients who had undergone cavopulmonary anastomosis (10) or atriopulmonary anastomosis (5). Mean age at operation was 55.1 months (range 9 to 145). Studies were done at 75.5 (32.6) months (mean (SD)) after the operation. SETTING: Tertiary referral centre. METHODS: Patients were studied using simultaneous recordings of ECG, pressure trace, respirometer trace, and pulsed Doppler echocardiography. Mean systemic venous pressure and pulmonary vascular resistance did not differ significantly between the two patient groups. RESULTS: After total cavopulmonary anastomosis, systemic venous pressure tracings showed a flattened pressure curve without any dependence on cardiac or respiratory cycle. After atriopulmonary anastomosis, right atrial pressure tracings showed a significantly higher "a" wave corresponding to atrial contraction, without any respiratory variability. Pulsed Doppler examination of the superior and inferior caval vein and hepatic vein after total cavopulmonary anastomosis did not show a reverse flow after atrial contraction. The inspiratory to expiratory velocity ratio of antegrade flow revealed a significant dependence of flow on changes in intrathoracic pressure in the intra-atrial tunnel, caval veins, and hepatic vein. During expiration, decrease or cessation of antegrade hepatic venous flow was documented. After an atriopulmonary anastomosis, there was a biphasic antegrade venous flow pattern without significant respiratory variation. CONCLUSIONS: After total cavopulmonary anastomosis, there was marked respiratory dependence of systemic and hepatic venous return, whereas after an atriopulmonary anastomosis venous flow pattern varied according to cardiac cycle and pressure trace. The effects of total cavopulmonary anastomosis on venous return might counteract its other haemodynamic advantages. (+info)
Comparisons between hemodynamics, during and after bathing, and prognosis in patients with myocardial infarction.
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The purpose of this study was to establish the safest way to bathe patients with myocardial infarction (MI) through measuring the hemodynamics during and after bathing. Seventy patients with MI were bathed supine in a Hubbard tank filled with 42 degrees C tap water for 5 min. The subjects were divided into 2 groups depending on their hemodynamic values 10 min after bathing: pulmonary capillary wedge pressure unchanged even after bathing (group A), and decreased pressure after bathing (group B). The left ventricular ejection fraction of group B was significantly higher than that of group A: 53.6% vs. 39.7%, respectively (p<0.01). The physical work capacity of group B was significantly higher at 5.6 METs, than that of group A with 4.5 METs (p<0.05). During the average of their 37-month follow-up period, there were 3 cardiac events in group B and 6 in group A. There were 2 cardiac events during bathing, both of which occurred in group A. When patients with MI take a bath, it is essential to closely monitor them, especially to those patients with lower cardiac function, because they have a higher possibility of a cardiac event. (+info)