Analysis of left ventricular pressure during isovolumic relaxation in coronary artery disease.

Thompson, D S; Waldron, C B; Juul, S M; Naqvi, N; Swanton, R. H.; Coltart, D J; Jenkins, B S; Webb-Peploe, M M

doi:10.1161/01.cir.65.4.690

Cited by 95 publications

(25 citation statements)

References 14 publications

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“…Time to 50% pressure decline was not calculated, since this index is unreliable when developed pressure changes significantly (2). (10)(11)(12), large animal models (3), and isolated perfused hearts (7)(8)(9). However, previous studies in isolated perfused hearts studied only mild reductions of coronary flow to 50% (8) and 33% (7) cline.…”

Section: Methodsmentioning

confidence: 99%

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Ca2+ transient decline and myocardial relaxation are slowed during low flow ischemia in rat hearts.

et al. 1994

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The mechanisms that impair myocardial relaxation during ischemia are believed to involve abnormalities of calcium handling. However, there is little direct evidence to support this hypothesis. Therefore, we sought to determine whether the time constant of cytosolic calcium (ICa"2+I) decline (Tc,) was increased during low flow ischemia, and if there was a relationship between the time constant of left ventricular pressure decline (Tp) and Tc. Isolated perfused hearts were studied using indo-1 fluorescence ratio as an index of ICa2 "IcJ. Tp was used as an index of myocardial relaxation. The time constant of decline of the indo-1 ratio increased from 74±5 ms to 95±4, 144±10, and to 204±16 ms when coronary flow was reduced was reduced to 50, 20, and 10% of control, respectively. Indo-1 transients were calibrated to calculate Tc.a-Tc. increased from 67±6 ms to 108±9 and 158±19 ms when coronary flow was reduced to 20 and 10% of control, respectively. There was a linear relationship between rca and Tp (r = 0.82). These data support the hypothesis that during low flow ischemia, impaired myocardial relaxation may be caused by slowing of ICa2"Ic decline. (J.Clin. Invest. 1994.93:951-957.)

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Section: Methodsmentioning

confidence: 99%

“…The most reliable and least load-dependent index ofmyocardial relaxation is the time constant of left ventricular pressure decline (Tp)I (2)(3)(4). Several studies have documented an increase of rp during ischemia in a variety of experimental preparations (5)(6)(7)(8)(9) and patients with coronary artery disease (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Ca2+ transient decline and myocardial relaxation are slowed during low flow ischemia in rat hearts.

et al. 1994

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“…In their study, PB showed a significant change only in patients who developed myocardial ischemia with exercise. Thompson et al 42 showed a similar wide range of variation in resting values for PB and point out that the relevance of PB to diastolic relaxation after mitral valve opening is uncertain. Since the physiologic meaning of PB is unclear, we cannot interpret its failure to change consistently with milrinone in this study.…”

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confidence: 91%

Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone.

Monrad¹,

McKay²,

Baim³

et al. 1984

Circulation

186

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To elucidate the mechanisms by which the new bipyridine inotropic agent milrinone improves cardiac function, we examined multiple indexes of left ventricular diastolic function before and after administration of milrinone to patients with advanced (NYHA class III or IV) congestive heart failure. In 13 patients left ventricular pressure measurements were made with a micromanometer to permit assessment of peak negative dP/dt and the time constant of left ventricular isovolumic relaxation, T, before and after milrinone. In nine patients radionuclide ventriculographic studies were performed during left heart catheterization, allowing calculation of left ventricular peak filling rate, volumes, and the diastolic pressure-volume relationship before and after milrinone. After intravenous administration of milrinone, peak negative dP/dt increased ( + 18%; p < .01 ) and T decreased (-30%; p < .01), while heart rate increased by only 8% (87 + 12 to 94 + 15 beats/min; p < .01), left ventricular systolic pressure did not change, and mean aortic pressure fell by 11% (p < .01). Left ventricular peak filling rate increased (1.2 + 0.6 to 1.7 + 0.7 end-diastolic volumes/sec; p .02) despite a decrease in left ventricular filling pressure (mean pulmonary wedge pressure 27 ± 7 to 18 9 mm Hg; p < .01). There was a fall in left ventricular end-diastolic pressure (28.6 + 6 to 19 + 7 mm Hg; p ' .01), with no significant change in left ventricular end-diastolic volume. This was associated with a downward shift in the left ventricular diastolic pressure-volume relationship in most cases. These changes in parameters of left ventricular diastolic relaxation and chamber distensibility after administration of milrinone suggest that improved diastolic function may contribute to the beneficial hemodynamic effect of milrinone in patients with congestive heart failure. Circulation 70, No. 6, 1030-1037, 1984 MILRINONE, a derivative of the bipyridine inotrope amrinone, has previously been shown to have a profound effect on myocardial contractile function in isolated muscle' and animal preparations.2 The clinical response of patients with congestive heart failure who are treated with this agent has been ascribed to readily demonstrable improvements in indexes of left ventric- Received Feb. 22, 1984; revision accepted Sept. 6, 1984. Presented in part at the 56th Annual Scientific Sessions of the American Heart Association. Anaheim, November 1983. 1030 ular systolic function (including increases in peak positive dP/dt and in left ventricular ejection fraction) and concurrent arteriolar vasodilation.3However, possible effects of milrinone on ventricular diastolic function, which might also contribute to the hemodynamic response to this agent, have not been evaluated. In particular, improved diastolic relaxation and distensibility might lead to more effective sarcomere stretch within the ventricular myocardium and to better systolic performance.6 7 Thus it is possible that improved systolic pump function in patients with heart failure treate...

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“…We calculated the relaxation time constant with Thompson's method ( bf ) from exponential analysis [P(t) = (P0 -P∞) exp (-t / bf ) + P∞]. 19,20 Fitting was done from the time of the peak negative LV dP/dt to the time at which LV pressure had fallen to 5 mmHg above the succeeding end-diastolic pressure (EDP). Correlation coefficients of the exponential fittings of all the beats were more than 0.99 by this method in all the patients.…”

Section: Discussionmentioning

confidence: 99%

Left Ventricular Relaxation Abnormality Is Detectable by Analysis of the Relaxation Time Constant in Patients With Atrial Fibrillation

et al. 2001

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here has been increasing interest in atrial fibrillation (AF) in the fields of cardiology and cardiac surgery, 1 partly because of its high prevalence and partly because of the high morbidity associated with the risk of cerebral infarction. Unlike regular beats, indices of left ventricular (LV) contractility in arrhythmic beats, whether they may be load-dependent (peak LV dP/dt, the maximum rate of rise of LV pressure) 2 or load-independent (Emax), 3 have been shown to be constantly changing dependently on the force -interval relationship, 4 as well as on the FrankStarling relationship. 5 The force -interval relationships include the relations between indices of each beat and RR2 (the directly preceding RR intervals), which are referred to as mechanical restitution, and those between indices and RR1 (the pre-preceding RR intervals), which are referred to as postextrasystolic potentiation (PESP). 6-9 Moreover, Emax was shown to be reasonably predicted by RR2/RR1, 10 which combines mechanical restitution and PESP. In contrast, an earlier study suggested that LV relaxation abnormality could not be detected in patients with AF by means of analysis of the force -interval relationships. 11 Unfortunately, no information is currently available on LV relaxation in patients with both AF and impaired LV systolic function.Afterload-dependence of LV relaxation has been intensively investigated, 12-15 and accentuated afterload-dependence of the LV relaxation time constant ( ) has been attributed to one of the mechanisms underlying impaired LV relaxation observed in failing hearts. 16,17 Moreover, this method of analysis of LV relaxation was successfully applied to a tachycardia-induced heart failure model in dogs. 18 Therefore, in the present study we analyzed on a beat-to-beat basis in patients with both AF and impaired LV systolic function by means of the force (relaxation) -interval relationships, as well as afterload-dependence. To the best of our knowledge, this is the first report to study LV relaxation abnormality in such patients in detail. Methods PatientsOur subjects consisted of 7 men and 5 women with chronic AF, aged from 39 to 68 years old (mean, 53.7±2.5 years old), who had undergone diagnostic cardiac catheterization. Four patients had mitral stenosis, 6 had idiopathic dilated cardiomyopathy, 1 had a prosthetic mitral valve for mitral regurgitation, and 1 had no underlying disease except for AF. These patients were subdivided into 2 groups: group A (7 patients with LV ejection fraction [EF] <0.5) and group B (5 patients with LVEF ≥0.5). We excluded patients with mitral regurgitation that was more than mild because they had no isovolumic relaxation period. None of the patients had a history of angina or myocardial infarction, and all showed normal coronary angiograms. The investigation conformed with the principles outlined in the Declaration of Helsinki. Atsushi Yao, MD; Hiroshi Matsui, MD; Osami Kohmoto, MD*; Takashi Serizawa, MD**; Ryozo Nagai, MD; Toshiyuki Takahashi, MD Left ventricular (LV) contractility i...

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Analysis of left ventricular pressure during isovolumic relaxation in coronary artery disease.

Cited by 95 publications

References 14 publications

Ca2+ transient decline and myocardial relaxation are slowed during low flow ischemia in rat hearts.

Ca2+ transient decline and myocardial relaxation are slowed during low flow ischemia in rat hearts.

Improvement in indexes of diastolic performance in patients with congestive heart failure treated with milrinone.

Left Ventricular Relaxation Abnormality Is Detectable by Analysis of the Relaxation Time Constant in Patients With Atrial Fibrillation

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