Impaired left ventricular relaxation during pacing-induced ischemia

McLaurin, Lambert P.; Rolett, Ellis L.; Grossman, William

doi:10.1016/s0002-9149(73)80002-5

Cited by 320 publications

(81 citation statements)

References 22 publications

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“…At 6 weeks of age, each animal in which LVH was to be produced was anesthetized with sodium pentobarbital (20 to 25 mg/kg) and ventilated with a respirator, and a right thoracotomy was performed in the third intercostal space. A pericardial cradle was created and the ascending aorta, approximately 1.5 cm above the aortic valve, was dissected free from the surrounding fat and connective tissue.…”

Section: Methodsmentioning

confidence: 99%

Abnormalities in myocardial perfusion during tachycardia in dogs with left ventricular hypertrophy: metabolic evidence for myocardial ischemia.

et al. 1984

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This study tested the hypothesis that in the chronically hypertrophied left ventricle pacing stress may cause abnormalities of perfusion that result in myocardial ischemia. Left ventricular hypertrophy (LVH) was produced by banding the ascending aorta of 10 dogs at 6 weeks of age, and studies were carried out after the animals had reached adulthood and when mean left ventricular/body weight ratio was 74% greater than in eight control dogs. Myocardial blood flow was measured with microspheres during pacing at 100, 200, and 250 beats/min, while aortic and coronary sinus blood samples were obtained for determination of concentrations of lactate and the adenosine metabolites inosine and hypoxanthine. In the control dogs, increasing heart rates were associated with an increase in mean myocardial blood flow while subendocardial flow was maintained at a level equal to or greater than subepicardial flow. Myocardial lactate uptake ranged from + 60% to -5%, and adenosine metabolites were not detected in coronary sinus blood (<0.5 ,uM/l). In four dogs that underwent aortic banding no production of lactate or adenosine metabolites was observed at any heart rate; in these animals subendocardial flow was maintained at a level equal to or greater than subepicardial flow at all pacing rates. The remaining six dogs with LVH demonstrated net lactate production significantly greater than control during pacing at 250 beats/min; five of these six animals also produced adenosine metabolites. In these six animals mean myocardial blood flow failed to increase as the pacing rate was increased from 200 to 250 beats/min, and pacing at 250 beats/min was associated with a transmural redistribution of perfusion away from the subendocardium (subendocardial/subepicardial blood flow ratio = 0.50 + 0.05). These findings demonstrate that perfusion abnormalities may occur in the chronically hypertrophied heart during rapid cardiac pacing and that these result in myocardial ischemia.

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Section: Methodsmentioning

confidence: 99%

Abnormalities in myocardial perfusion during tachycardia in dogs with left ventricular hypertrophy: metabolic evidence for myocardial ischemia.

et al. 1984

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“…The left ventricular isovolumic relaxation period was assumed to be the period from peak negative dP/dt to the time at which left ventricular pressure fell to 5 mm Hg above left ventricular end-diastolic pressure (LVEDP). Using the method described by Weiss et al,22 a time constant of relaxation (T) was derived by computing a best exponential fit to the pressure data points during this isovolumic relaxation period: (2) where PE = left ventricular pressure (exponential fit pressure), PO = left ventricular pressure at the time of peak negative dP/dt, and t = time (sec).…”

Section: Methodsmentioning

confidence: 99%

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

Bourdillon¹,

Lorell²,

Mirsky³

et al. 1983

Circulation

168

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SUMMARY The left ventricular diastolic pressure-volume.relationship shifts upward during angina, but why this happens is not known. To assess regional myocardial stiffness, we studied 12 patients who.had coronary artery disease using simultaneous left ventricular micromanometer pressure recording and Mmode echocardiography before and during angina induced. by pacing tachycardia. All patients had two-or three-vessel coronary artery disease that involved the posterior left ventricular wall circulation and had positive pacing stress tests, i.e., development of angina and a postpacing rise in left ventricular end-diastolic pressure (15 3 to 31 6 mm Hg, p < 0.001). A marked upward shift in the relationship between the diastolic left ventricular pressure and the posterior wall thickness (h) occurred after pacing tachycardia, but the change in left ventricular posterior wall end-diastolic thickness was minimal (8.9 2.1 to 9.2 2.1 mm, NS). After pacing, the peak rate of left ventricular posterior wall thinning decreased (82 37 to 48 27 mm/sec, p < 0.005) and the time constant of relaxation derived from the best exponential fit to the isovolumic left ventricular pressure decay increased (49 5 to 58 7 msec,.p < 0.001). Diastolic active left ventricular pressure decay, extrapolated from the exponential fit, was subtracted from the measured left ventricular pressure (which is equal in magnitude but opposite in sign to the radial stress at the endocardium) to calculate residual left ventricular pressure (PR) and hence residual stress (6R = -PR). A radial stifiness modulus (ER) was determined by the slope of the PR VS log h plots before and after pacing. Over the same range of residual radial stress (aR), ER was always higher during pacing-induced angina, indicating increased residual myocardial stiffness. Increased myocardial stiffness in addition to a decreased rate of wall thinning and slow active pressure decay contribute to the upward shift in left ventricular pressure-wall thickness and pressure-volume relationships during pacing-induced angina.DURING pacing-induced angina in patients with coronary artery disease, the left ventricular pressure-volume relationships shift upward during diastole. 1-The mechanisms by which these acute changes take place are not well understood and have been the subject of controversy.8' 9 Potential mechanisms include changes in the heart's geometry, 1012 persistent interaction of some contractile elements within the ischemic myocardium throughout diastole,"3 interaction between the two ventricles,8 changes in intrapericardial pressure8 9 and alterations in passive myocardial properties.1418The or the right ventricle in causing these shifts seems unlikely. Also, recent evidence shows that in an isolated canine heart model, left ventricular diastolic pressures are significantly altered by changes in the right ventricle only at very high levels of right ventricular end-diastolic pressure.21The effects of dyssynergistic contraction on diastolic pressure might be expected only during the early p...

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“…Several experi-defect. 11 In another report,12 the left atrium was found at autopsy to have invaginated through the mitral orifice after severe hemorrhage, implying that the left ventricle had "sucked" the atrial wall through the mitral valve plane.…”

Section: Minimum Left Ventricular Pressure During J-adrenergic Stimulmentioning

confidence: 98%

Minimum left ventricular pressure during beta-adrenergic stimulation in human subjects. Evidence for elastic recoil and diastolic "suction" in the normal heart.

et al. 1990

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The influence of elastic recoil and restoring forces on diastolic left ventricular pressure decay and minimum left ventricular pressures has been demonstrated in animal models but has not been studied in the human heart. To investigate this issue in the normal human left ventricle, we studied eight patients with chest pain and normal coronary arteries with simultaneous measurement of left ventricular volume (by radionuclide angiography) and pressure (by micromanometer catheter) and coronary sinus blood flow. Electrocardiographic-gated data were obtained in the basal state, during rapid atrial pacing, and during isoproterenol infusion to a similar heart rate. Compared with pacing, isoproterenol increased ejection fraction and reduced end-systolic volume (p<0.005), end-systolic pressure (p<0.005), and the half-time of pressure decline after peak negative dP/dt (T1/2) (p<0.001). Negative diastolic pressure developed in seven of eight patients during isoproterenol (range, -0.5 to -2.4 mm Hg) but in only one of eight during pacing (-0.2 mm Hg). These reduced diastolic pressures during isoproterenol were accompanied by increased stroke volume (reflecting increased transmitral flow) and diminished pulmonary wedge pressure (reflecting left atrial pressure). The magnitude of reduction in minimum diastolic pressure during pacing and isoproterenol was related to the change in end-systolic volume (r=0.79,p<0.001), ejection fraction (r=-0.74,p<0.001), T1/2 (r=0.57, p<0.02), and coronary sinus flow (r=0.73, p<0.005). Stronger correlations were observed in analyzing changes during isoproterenol alone. From similar end-systolic volumes, T½/2 and the time constant tau were lower (both p<0.005), as was minimum diastolic pressure (p<0.05) during isoproterenol compared with pacing. Hence, isoproterenol infusion (simulating the catecholamine stimulation during exercise) significantly reduces minimum diastolic pressure in the normal human heart, resulting in the development of negative left ventricular pressures. The reduction in minimum left ventricular pressure is related to changes in left ventricular systolic volume, contractility, and coronary flow, and to the dynamics of isovolumic relaxation. This reduction in early diastolic pressure augments the left atrial-left ventricular pressure gradient during early diastole, enhancing the rate and magnitude of left ventricular filling required to maintain a high cardiac output at elevated heart rates. (Circulation 1990;82:1174-1182 It is generally accepted that left ventricular relaxation is an active, energy-requiring process, but some controversy exists as to whether the left ventricle is capable of generating a "suction" pressure, thus filling itself or aiding filling when faced with low pressure from the atrium. Several experimental studiest-6 have documented the existence of

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Impaired left ventricular relaxation during pacing-induced ischemia

Cited by 320 publications

References 22 publications

Abnormalities in myocardial perfusion during tachycardia in dogs with left ventricular hypertrophy: metabolic evidence for myocardial ischemia.

Abnormalities in myocardial perfusion during tachycardia in dogs with left ventricular hypertrophy: metabolic evidence for myocardial ischemia.

Increased regional myocardial stiffness of the left ventricle during pacing-induced angina in man.

Minimum left ventricular pressure during beta-adrenergic stimulation in human subjects. Evidence for elastic recoil and diastolic "suction" in the normal heart.

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