Slow rate during AF improves ventricular performance by reducing sensitivity to cycle length irregularity

2002 ◽  
Vol 283 (6) ◽  
pp. H2706-H2713 ◽  
Author(s):  
Zoran B. Popović ◽  
Kent A. Mowrey ◽  
Youhua Zhang ◽  
Shaowei Zhuang ◽  
Tomotsugu Tabata ◽  
...  
Keyword(s):  
Cycle Length ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Nonlinear Fitting ◽  
Beneficial Effects ◽  
Sinus Cycle Length ◽  
Cycle Lengths ◽  
Anesthetized Dogs ◽  
Heart Rate Slowing ◽  
The Impact

Atrial fibrillation (AF) is characterized by short and irregular ventricular cycle lengths (VCL). While the beneficial effects of heart rate slowing (i.e., the prolongation of VCL) in AF are well recognized, little is known about the impact of irregularity. In 10 anesthetized dogs, R-R intervals, left ventricular (LV) pressure, and aortic flow were collected for >500 beats during fast AF and when the average VCL was prolonged to 75%, 100%, and 125% of the intrinsic sinus cycle length by selective atrioventricular (AV) nodal vagal stimulation. We used the ratio of the preceding and prepreceding R-R intervals (RRp/RRpp) as an index of cycle length irregularity and assessed its effects on the maximum LV power, the minimum of the first derivative of LV pressure, and the time constant of relaxation by using nonlinear fitting with monoexponential functions. During prolongation of VCL, there was a pronounced decrease in curvature with the formation of a plateau, indicating a lesser dependence on RRp/RRpp. We conclude that prolongation of the VCL during AF reduces the sensitivity of the LV performance parameters to irregularity.

Effect of acute edema on left ventricular function and coronary vascular resistance in the isolated rat heart

1994 ◽  
Vol 267 (3) ◽  
pp. H1054-H1061 ◽  
Author(s):  
A. Rubboli ◽  
P. A. Sobotka ◽  
D. E. Euler
Keyword(s):  
Linear Relationship ◽  
Water Content ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Myocardial Edema ◽  
Left Ventricular ◽  
Coronary Vascular Resistance ◽  
Ventricular Performance ◽  
Developed Pressure ◽  
The Impact

The impact of acute myocardial edema on coronary flow and left ventricular performance was studied in isolated isovolumic rat hearts. After 15 min of aortic perfusion with Krebs-Henseleit buffer, hearts (10/group) were either removed for determination of water content or perfused for another 90 min. Three groups were perfused at a constant pressure of 60, 100, or 140 mmHg, and two groups were perfused at 60 or 140 mmHg with adenosine added. Compared with the 15-min group, there was a significant increase in water content in all groups except the 60-mmHg group (P < 0.005). There was a direct linear relationship between increases in coronary vascular resistance over time and water content (P < 0.0001). A decrease in developed pressure and peak +dP/dt was observed only in those groups that accumulated water. An inverse linear relationship was found between changes in developed pressure and water content (P = 0.0001). Water content had no effect on end-diastolic pressure below 5 ml/g; above 5 ml/g, a direct linear relationship was evident (P = 0.009). The results suggest that myocardial edema increases vascular resistance and decreases systolic performance. End-diastolic pressure is less influenced by edema than either systolic or coronary vascular function.

Effects of infarction, procainamide, coupling interval, and cycle length on refractoriness of extrastimuli

1985 ◽  
Vol 248 (5) ◽  
pp. H606-H613
Author(s):  
F. E. Marchlinski ◽  
M. E. Cain ◽  
R. A. Falcone ◽  
R. F. Corky ◽  
J. F. Spear ◽  
...  
Keyword(s):  
Refractory Period ◽  
Cycle Length ◽  
Narrow Range ◽  
Left Ventricular ◽  
Effective Refractory Period ◽  
Stimulation Site ◽  
Refractory Periods ◽  
Coupling Interval ◽  
Cycle Lengths ◽  
Site Of Stimulation

The effects of prematurity, cycle length, site of stimulation, and procainamide on ventricular refractoriness following an extrastimulus (S2) were assessed in 10 dogs with and 10 dogs without infarction. Extrastimuli were introduced at preselected coupling intervals (S1-S2) from normal right and left ventricular sites and from left ventricular sites of infarction during drive cycle lengths (S1-S1) of 350 and 250 ms. At each S1-S2 interval, the effective refractory period of S2 was determined by introducing a second extrastimulus (S3). At all stimulation sites, cycle lengths, and before and during infusion of procainamide (mean concn 18.6 +/- 3.5 micrograms/ml), shortening (greater than 10 ms change) in refractoriness was most marked over a narrow range of closely coupled S1-S2 intervals. Regardless of stimulation site, the effective refractory period of S2 was less during a cycle length of 250 ms compared with a cycle length of 350 ms. In dogs without infarction, the effective refractory periods of S2 from left ventricular sites tended to be longer than from right ventricular sites, particularly during procainamide administration. The refractory period of S2 at sites of infarction did not differ consistently from those at normal sites. Finally, at all stimulation sites and cycle lengths, procainamide prolonged refractoriness of S2 at each S1-S2 interval and blunted the total shortening in refractoriness in response to S2.

Haemodynamic insights into the effects of ischaemia and cycle length on tissue Doppler-derived mitral annulus diastolic velocities

2004 ◽  
Vol 106 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Sherif F. NAGUEH ◽  
Liyun RAO ◽  
Julia SOTO ◽  
Katherine J. MIDDLETON ◽  
Dirar S. KHOURY
Keyword(s):  
Cycle Length ◽  
Systolic Function ◽  
Vena Cava ◽  
Coronary Artery Occlusion ◽  
Mitral Annulus ◽  
Tissue Doppler ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Heart Catheterization ◽  
Cycle Lengths

In the present study, we performed simultaneous epicardial echocardiography and left heart catheterization on ten adult dogs to investigate the effects of ischaemia and tachycardia on the mitral annulus early (Ea) and late (Aa) diastolic velocities and the haemodynamic mechanisms involved. Left atrial pressure and left ventricular (LV) volumes and pressures were measured with 5 French Millar catheters. In each dog, inferior vena cava occlusion was used to alter preload and circumflex coronary artery occlusion was applied to induce ischaemia at two different cycle lengths: 450 and 550 ms. At both cycle lengths, ischaemia resulted in a reduction in LV relaxation, LV global and ipsilateral systolic function, transmitral pressure gradient (TMG), Ea and Aa (P<0.05). The shorter cycle length was associated with a shorter tau (time constant of LV relaxation), reduced TMG and reduced septal and lateral Ea (P<0.05 for all variables). Both septal and lateral Aa were significantly increased (P<0.05). Ischaemia influences Ea through changes in LV relaxation, global and regional systolic function and TMG. An increase in heart rate reduces Ea, but increases Aa.

Autonomic Balance in Cardiac Control

1958 ◽  
Vol 192 (3) ◽  
pp. 631-634 ◽  
Author(s):  
Robert F. Rushmer
Keyword(s):  
Heart Rate ◽  
Mechanical Performance ◽  
Stimulus Frequency ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Sympathetic Stimulation ◽  
Vagus Nerves ◽  
Ventricular Performance ◽  
Anesthetized Dogs ◽  
Stimulation Of

Stimulation of the sympathetic nerves to the heart in anesthetized dogs produced tachycardia and changes in left ventricular performance, including alterations in both pressures and dimensions. Stimulation of the vagus nerves in dogs predominately induced a bradycardia. When the heart rate was controlled by an artificial pacemaker, sympathetic stimulation produced changes in ventricular performance. By adjustments in stimulus frequency, the effects of vagal and sympathetic stimulation on heart rate could be balanced, but complete cancellation of effects was impossible because the vagus had a more powerful effect on heart rate and the sympathetic nerves had a greater influence on mechanical performance.

Effects of propafenone on sinus node function in the rabbit heart

1990 ◽  
Vol 68 (7) ◽  
pp. 851-855 ◽  
Author(s):  
Charles R. Kerr
Keyword(s):  
Cycle Length ◽  
Sinus Node ◽  
Rabbit Heart ◽  
Conduction Time ◽  
Supraventricular Arrhythmias ◽  
Sinus Cycle Length ◽  
Cycle Lengths ◽  
Dose Dependent ◽  
Control State

Propafenone is a type 1C antiarrhythmic drug with efficacy for both ventricular and supraventricular arrhythmias. We investigated the effects of propafenone on properties of sinus node function in an in vitro preparation of rabbit sinus node and surrounding atrium. Spontaneous sinus cycle length (SCL), atriosinus conduction time (ASCT), and sinus node effective refractory period (SNERP) at multiple pacing cycle lengths were measured in the control state and during superfusion with propafenone (2.3 μM). SNERP prolonged from 175 ± 25 ms in the control state to 220 ± 45 ms (p < 0.001) with propafenone. ASCT also prolonged significantly (p < 0.01) from 50 ± 20 to 65 ± 20 ms whereas SCL did not change. In four experiments, multiple concentrations of propafenone were utilized and there appeared to be a dose-dependent prolongation of SNERP. Thus, propafenone has a significant effect on SNERP and ASCT in an isolated rabbit sinus node preparation.Key words: propafenone, sinus node, atrium.

scholarly journals Left ventricular volume analysis as a basic tool to describe cardiac function

2018 ◽  
Vol 42 (1) ◽  
pp. 130-139 ◽  
Author(s):  
Peter L. M. Kerkhof ◽  
Tatiana Kuznetsova ◽  
Rania Ali ◽  
Neal Handly
Keyword(s):  
Cardiac Function ◽  
Volume Regulation ◽  
Function Analysis ◽  
Group Analysis ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Healthy Humans ◽  
End Diastolic Volume ◽  
The Impact

The heart is often regarded as a compression pump. Therefore, determination of pressure and volume is essential for cardiac function analysis. Traditionally, ventricular performance was described in terms of the Starling curve, i.e., output related to input. This view is based on two variables (namely, stroke volume and end-diastolic volume), often studied in the isolated (i.e., denervated) heart, and has dominated the interpretation of cardiac mechanics over the last century. The ratio of the prevailing coordinates within that paradigm is termed ejection fraction (EF), which is the popular metric routinely used in the clinic. Here we present an insightful alternative approach while describing volume regulation by relating end-systolic volume (ESV) to end-diastolic volume. This route obviates the undesired use of metrics derived from differences or ratios, as employed in previous models. We illustrate basic principles concerning ventricular volume regulation by data obtained from intact animal experiments and collected in healthy humans. Special attention is given to sex-specific differences. The method can be applied to the dynamics of a single heart and to an ensemble of individuals. Group analysis allows for stratification regarding sex, age, medication, and additional clinically relevant covariates. A straightforward procedure derives the relationship between EF and ESV and describes myocardial oxygen consumption in terms of ESV. This representation enhances insight and reduces the impact of the metric EF, in favor of the end-systolic elastance concept advanced 4 decades ago.

Anti-G suit effect of cardiovascular dynamic changes due to +GZ stress

1977 ◽  
Vol 43 (5) ◽  
pp. 765-769 ◽  
Author(s):  
D. F. Peterson ◽  
V. S. Bishop ◽  
H. H. Erickson
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Internal Diameter ◽  
Experimental Conditions ◽  
Beneficial Effects ◽  
Anesthetized Dogs ◽  
Acceleration Stress

Lightly anesthetized dogs underwent 1-min exposure to +Gz acceleration without and with a bladder-type anti-G suit. Prior chronic instrumentation permitted through evaluation of cardiac dynamics. During +3 Gz acceleration all recorded dynamic variables were lowered and transient tachycardia occurred. After acceleration ceases, all pressures and dP/dt exceeded control levels. Inflation of the anti-G suit during +3 Gz eliminated the dramatic effects observed during and after acceleration stress. During +6 Gz with the anti-G suit inflated, arterial pressure and dP/dt were maintained whereas left ventricular end-diastolic pressure and total peripheral resistance were much elevated and heart rate was lower. At the onset of G stress, internal diameter of the heart always fell transiently. Otherwise, diameter was not significantly affected by any of the experimental conditions. The results suggest that the anti-G suit maintains perfusion pressure at high sustained G; however, with the anti-G suit inflated at +6 Gz, central venous pressure is dramatically elevated and heart rate depressed. Thus, beneficial effects which provide tolerance to high G are accompanied by potentially detrimental effects.

Abstract 15316: Paradoxical Reduction in Myocardial Performance When Combining Two Independently Cardioprotective Agents: Mitochondrial-targeted Antioxidant MitoSNO and Adenosine Triphosphate-sensitive Potassium Channel Opener Diazoxide

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Jie Wang ◽  
Alex Suarez-Pierre ◽  
Natalie Gaughan ◽  
Rosmi Thomas ◽  
Krisztian Sebestyen ◽  
...  
Keyword(s):  
Adenosine Triphosphate ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Global Ischemia ◽  
Ros Production ◽  
Beneficial Effects ◽  
Channel Opener ◽  
The Impact

Introduction: Adenosine triphosphate-sensitive potassium (K ATP ) channel opener diazoxide (DZX) and Antioxidant MitoSNO are both independently cardioprotective in animal models. The cardioprotective mechanism of diazoxide is unknown, and involves a non-sarcolemmal location, requires the inhibition of succinate dehydrogenase, and the K ATP channel subunit SUR1. Mitochondrial - targeted Antioxidant MitoSNO is a S-nitrosylating agent that stalls complex 1, reduces ROS production and succinate accumulation. In an isolated myocyte model of stress due to hyperkalemic cardioplegia (CPG), that the combination of DZX and MitoSNO negated the beneficial effects of each alone. Hypothesis: We hypothesized that the combination of DZX and MitoSNO would negate the beneficial effects of each alone in an isolated heart model of global ischemia. Methods: Isolated mouse hearts underwent assessment of end diastolic pressure (EDP) and left ventricular developed pressure (LVDP) utilizing an LV balloon in a Langendorff model before and after 90 min of global ischemia. Hearts received test solution (CPG (9°C) or CPG±DZX (100μM) at onset of ischemia +/- MitoSNO (1μM/L) at end of ischemia), followed by 30 min reperfusion. LVDP and EDP were compared between groups utilizing a linear mixed model to assess the impact of treatment on the outcome, adjusting for baseline and balloon volume. Results: Similar to previous results, DZX improved LVDP and reduced EDP after ischemia compared to CPG (Figure). Similarly, MitoSNO improved LVDP and reduced EDP compared to CPG (Figure). The addition of MitoSNO with DZX was associated with the loss of cardioprotection observed with MitoSNO or DZX alone. Conclusions: Similar to data in a myocyte model, both MitoSNO and DZX provide cardioprotection that is lost with the combination of both, suggesting mutually exclusive mechanisms of action and that DZX’s mechanism requires a functional complex 1, ROS production, or succinate accumulation.

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