Relative Contributions of the Atrial Systole-Ventricular Systole Interval and of Patterns of Ventricular Activation to Ventricular Function during Electrical Pacing of the Dog Heart

Daggett, Willard M.; Bianco, Jesus A.; Powell, Wilson M.; Austen, William G.

doi:10.1161/01.res.27.1.69

Cited by 95 publications

(25 citation statements)

References 19 publications

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“…In patients, changing the AV interval from 100 to 130 to 0 ms decreased cardiac output by Ϸ20%. 12,28,29 In a separate series of experiments in 5 AV-blocked dogs, however, we found that switching the AV interval from 100 to 25 to 30 ms changed cardiac output only by Ϫ10 to 3% (M. Peschar, MSc, and F.W. Prinzen, PhD, unpublished data, 1997).…”

Section: Pump Functionmentioning

confidence: 96%

Asynchronous Electrical Activation Induces Asymmetrical Hypertrophy of the Left Ventricular Wall

et al. 1998

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Background-Asynchronous electrical activation, induced by ventricular pacing, causes regional differences in workload, which is lower in early-than in late-activated regions. Because the myocardium usually adapts its mass and structure to altered workload, we investigated whether ventricular pacing leads to inhomogeneous hypertrophy and whether such adaptation, if any, affects global left ventricular (LV) pump function. Methods and Results-Eight dogs were paced at physiological heart rate for 6 months (AV sequential, AV interval 25 ms, ventricular electrode at the base of the LV free wall). Five dogs were sham operated and served as controls. Ventricular pacing increased QRS duration from 47.2Ϯ10.6 to 113Ϯ16.5 ms acutely and to 133.8Ϯ25.2 ms after 6 months. Two-dimensional echocardiographic measurements showed that LV cavity and wall volume increased significantly by 27Ϯ15% and 15Ϯ17%, respectively. The early-activated LV free wall became significantly (17Ϯ17%) thinner, whereas the late-activated septum thickened significantly (23Ϯ12%). Calculated sector volume did not change in the LV free wall but increased significantly in the septum by 39Ϯ13%. In paced animals, cardiomyocyte diameter was significantly (18Ϯ7%) larger in septum than in LV free wall, whereas myocardial collagen fraction was unchanged in both areas. LV pressure-volume analysis showed that ventricular pacing reduced LV function to a similar extent after 15 minutes and 6 months of pacing. Conclusions-Asynchronous activation induces asymmetrical hypertrophy and LV dilatation. Cardiac pump function is not affected by the adaptational processes. These data indicate that local cardiac load regulates local cardiac mass of both myocytes and collagen. (Circulation. 1998;98:588-595.)

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Section: Pump Functionmentioning

confidence: 96%

Asynchronous Electrical Activation Induces Asymmetrical Hypertrophy of the Left Ventricular Wall

et al. 1998

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“…The right heart bypass preparation has been described in detail elsewhere (6). Briefly, mongrel dogs weighing 20-30 kg were anesthetized with thiamylal, 20 mg/kg, and alpha chloralose, 30 mg/kg, and ventilated with a volume ventilator.…”

Section: Methodsmentioning

confidence: 99%

Evidence of Incomplete Left Ventricular Relaxation in the Dog

Weisfeldt¹,

Frederiksen²,

Yin³

et al. 1978

J. Clin. Invest.

142

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A B S T R A C T Although it has been proposed that incomplete relaxation explains certain increases in left ventricular end diastolic pressure relative to volume, there has been no clear demonstration that incomplete relaxation occurs in the intact working ventricle. To identify incomplete relaxation, left ventricular pressure-dimension relationships were studied in 10 canine right heart bypass preparations during ventricular pacing. The fully relaxed, exponential diastolic pressuredimension line for each ventricle was first determined from pressure and dimension values at the end of prolonged diastoles after interruption of pacing. For 167 beats during pacing under widely varying hemodynamic conditions, diastolic pressure-dimension values encountered this line defining the fully relaxed state during the filling period indicating that relaxation was complete before end diastole. The time constant for isovolumic exponential pressure fall (T) was determined for all beats. For this exponential function, if no diastolic filling occurred, 97% of pressure fall would be complete by 3.5 T after maximal negative dPldt. For the 167 beats the fully relaxed pressure-dimension line was always encountered before 3.5 T.With very rapid pacing rates (170-200 beats/min) and(or) with pharmacologic prolongation of relaxation, incomplete relaxation occurred as evidenced by the fact that the line defining the fully relaxed state was never reached during diastole (n = 15). This evidence of incomplete relaxation occurred only when the subsequent

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“…The heart was exposed through a median sternotomy and heparin (3 mg/kg) administered i.v. This preparation has been described in detail previously (7). Briefly, venous return from the cannulated superior and inferior venae cavae was directed to a reservoir from which the blood was warmed, oxygenated, and returned to the arch of the aorta for retrograde coronary artery perfusion via a calibrated occlusive roller pump.…”

Section: Isozolumic Left Ventricle Fasting Adult Mongrel Dogsmentioning

confidence: 99%

Incomplete Relaxation between Beats after Myocardial Hypoxia and Ischemia

et al. 1974

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A B S T R A C T Recovery from hypoxia has been shown to prolong cardiac muscle contraction, particularly the relaxation phase. The present studies were designed to examine whether incomplete relaxation between beats can result from this prolongation of contraction and relaxation in isolated muscle after hypoxia and in the canine heart after both hypoxia and acute ischemia. The relationship between heart rate and the extent of incomplete relaxation is emphasized in view of the known enhancement of the velocity of contraction caused by increasing heart rate.The extent of incomplete relaxation during 10-s periods of pacing at increasing rates was examined before and after hypoxia in isometric cat right ventricular papillary muscle (12-120 beats/min) and in the canine isovolumic left ventricle (120-180 beats/min). Incomplete relaxation was quantified by measuring the difference between the lowest diastolic tension or pressure during pacing and the true resting tension or pressure determined by interruption of pacing at each rate. In eight cat papillary muscles (29°C), there was significantly greater incomplete relaxation 5 min after hypoxia at rates of 96 and 120 beats/min (P < 0.02 vs. before hypoxia). In seven canine isovolumic left ventricles, recovery from hypoxia and higher heart rates also resulted in incomplete relaxation. Incomplete relaxation before hypoxia at a rate of 180 beats/min was 0.8±0.5 cm H20 and at 5 min of recovery from hypoxia was 12.6±3.5 cm H20 (P < 0.01). 12 hearts were subjected to a 1.5-3-min period of acute ischemia and fibrillation. There was significant incomplete relaxation at a rate of 140 beats/ min for 5 min after defibrillation and reperfusion.This work was presented in part at the 44th Scientific Session of the American Heart Association, Anaheim, California, 1971.Dr. Daggett is an Established Investigator of the American Heart Association. These data indicate that incomplete relaxation is an important determinant of diastolic hemodynamics during recovery from ischemia or hypoxia. The extent of incomplete relaxation appears to be a function of the rate of normalization of the velocity of relaxation and tension development after ischemia or hypoxia, the heart rate, and the magnitude of developed tension or pressure.

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Relative Contributions of the Atrial Systole-Ventricular Systole Interval and of Patterns of Ventricular Activation to Ventricular Function during Electrical Pacing of the Dog Heart

Cited by 95 publications

References 19 publications

Asynchronous Electrical Activation Induces Asymmetrical Hypertrophy of the Left Ventricular Wall

Asynchronous Electrical Activation Induces Asymmetrical Hypertrophy of the Left Ventricular Wall

Evidence of Incomplete Left Ventricular Relaxation in the Dog

Incomplete Relaxation between Beats after Myocardial Hypoxia and Ischemia

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