Effects of coronary occlusion on early ventricular diastolic events in conscious dogs

Kumada, Toshiaki; Karliner, Joel S.; Pouleur, H.; Gallagher, Kim P.; Shirato, Kunio; Ross, John

doi:10.1152/ajpheart.1979.237.5.h542

Cited by 73 publications

(38 citation statements)

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“…Lesser amounts of each of these agents that were without effect upon systolic LV performance were also without discernable effect upon diastolic relaxation. By contrast, the intravenous infusion of the CEB pre-beta blockade in dosages that reduced arterial pressure equally (hereafter called equihypotensive) either substantially augmented ventricular relaxation (nifedipine) or produced no significant change in (-)dP/dt max or either measure of T (diltiazem and verapamil, (27). The dosages of the CEB employed for IC administration produced equivalent effects upon the rate of LV pressure development, extent of LV muscle shortening, and loading conditions.…”

Section: Discussionmentioning

confidence: 99%

“…Neither nifedipine nor diltiazem affected heart rate in these atropinized dogs, and yet each drug impaired LV relaxation. Mechanical dyssynchrony may also impair global ventricular pressure decay if delayed activation produces late regional contraction of a myocardial segment during isovolumic relaxation (27). Although we cannot entirely exclude temporal inhomogeneity of ventricular activation/deactivation as a contributory determinant of the impaired relaxation observed with circumflex intracoronary calcium entry blockade, such an effect seems unlikely since (a) minimum regional segment length always occurred before peak (-)dP/dt during calcium Figure 5.…”

Section: Discussionmentioning

confidence: 99%

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Direct and indirect effects of calcium entry blocking agents on isovolumic left ventricular relaxation in conscious dogs.

Walsh¹,

O’Rourke²

1985

J. Clin. Invest.

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To assess the direct and indirect effects of the commonly used calcium entry blockers (CEB) upon the major determinants of isovolumic left ventricular relaxation, we administered equidepressant intracoronary (IC, n = 7) and equihypotensive intravenous (n = 12) dosages of diltiazem (16±3 SE ,Ag/kg IC and 63±9 gg/kg i.v.), verapamil (10±2 and 57±5 Ag/kg), and nifedipine (1±0.1 and 8±0.3 ,g/kg) to preinstrumented awake dogs with normal ventricular function. The time constant of left ventricle (LV) relaxation, analyzed by two methods (T1, from the linear relation of the natural logarithm of LV pressure and time; T2, from the linear relation of LV pressure and negative high fidelity LV pressure), was significantly and equivalently prolonged by IC diltiazem (T, + 48%, P < 0.02), verapamil (T1 + 43%, P < 0.001), and nifedipine (T1 + 30%, P < 0.03). Lesser amounts of each CEB that did not affect rate of LV pressure development or extent of shortening produced no change in T1 or T2. By contrast, intravenous calcium entry blockade either produced no significant change (diltiazem and verapamil) or shortened (nifedipine T1 -18%, P < 0.01) LV isovolumic relaxation. However, after beta adrenergic blockade with propranolol (2 mg/kg i.v., n = 6) no change in ventricular relaxation was observed during nifedipine and the time constant was significantly prolonged by verapamil (T1 + 15%, P < 0.05).We conclude that calcium entry blockade directly impairs normal left ventricular relaxation: This effect is closely linked to the negative inotropic properties of these drugs. The prolongation of isovolumic relaxation produced by calcium blockade is attenuated or even reversed by reflex sympathetic stimulation and favorably altered loading conditions during systemic administration.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Direct and indirect effects of calcium entry blocking agents on isovolumic left ventricular relaxation in conscious dogs.

Walsh¹,

O’Rourke²

1985

J. Clin. Invest.

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“…The ischemic process impairs myocardial relaxation6' 7,[22][23][24][25][26] and results in asynchrony of left ventricular filling.7 27 When a filling pressure or a driving pressure increases, as indicated by an elevation in left ventricular end-diastolic pressure in our study, the peak rate of left ventricular filling should increase substantially. One of the factors that contributes to a blunting of the effect of an increase in a driving pressure on the left ventricular filling rate is impairment of myocardial distensibility with ischemia, which we have discussed above.…”

Section: Resultsmentioning

confidence: 73%

Effects of pacing-induced ischemia on early left ventricular filling and regional myocardial dynamics and their modification by nifedipine.

et al. 1987

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The effect of pacing-induced ischemia on early left ventricular filling and regional myocardial lengthening was studied in 11 patients with coronary artery disease (CAD) and six control patients with normal coronary arteriograms. All of the 11 patients with CAD developed typical anginal pain during pacing tachycardia, and in the postpacing beat, the left ventricular end-diastolic pressure (LVEDP) rose from 13 4 to 26 + 4 mm Hg (mean ± SD, p < .01), the relaxation time constant increased from 43 9 to 59 + 7 msec (p < .01), and the ejection fraction diminished from 62.1 + 6.7 to 51.6 + 10.6% (p < .01). However, the peak rate of early left ventricular filling (LVPF) obtained from frame-by-frame analysis of left ventriculograms and the LVPF normalized for the stroke volume and for the end-diastolic volume did not change significantly. In the ischemic segment, the peak rate of lengthening (PL) decreased by 45% with ischemia, and the PL normalized for the end-diastolic segment length decreased by 42%. However, the PL normalized for the extent of systolic shortening did not change. In the control segment there was a tendency for these three variables to increase, but the changes were not statistically significant. The time difference from the PL to the LVPF increased significantly in the ischemic segment (31 28 vs 75 + 48 msec, p < .05). Although the LVEDP rose slightly but significantly from 9 + 3 to 12 + 5 mm Hg (p < .05) in the control patients in the postpacing beat, the other global hemodynamic variables and the variables of regional myocardial dynamics did not change. The administration of nifedipine in six patients with CAD resulted in the disappearance or diminution of anginal pain even with the same duration and rate of pacing and was associated with restoration of global systolic function and regional myocardial shortening and lengthening in the ischemic segment. In the control segment, the three variables of segmental lengthening increased with administration of nifedipine. Thus, the segmental myocardial lengthening rate decreased with ischemia due to a decrease in segmental shortening and impairment of myocardial distensibility. The LVPF did not decrease with ischemia despite impairment in isovolumetric relaxation, accentuation of asynchrony in left ventricular filling, and a decrease in the PL in the ischemic segment because of an increase in the PL in the nonischemic segment secondary to an increase in left ventricular filling pressure. Administration of nifedipine resulted in improvement in segmental lengthening in the ischemic as well as in the control segment in the postpacing beat. Circulation 76, No. 6, 1232-1244, 1987 PREDOMINANT left ventricular filling occurs during so-called rapid ventricular filling in the early phase of diastole. Effective early ventricular filling is important for ventricular ejection, and the rate of early ventricular filling is thought to be influenced by left ventricular

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“…Alterations in LV relaxation have been shown to be an early manifestation of cardiac impairment often preceding abnormalities in ventricular systolic function (4,15,21,27). A slowed relaxation rate might result in incomplete relaxation and thereby in reduced early diastolic filling.…”

Section: Discussionmentioning

confidence: 99%

Left Ventricular Systolic and Diastolic Function during Coronary Arteriography before and after Acute Left Ventricular Failure in Dogs

Kløw¹,

Mortensen²,

Refsum³

1991

Acta Radiol

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Effects of coronary occlusion on early ventricular diastolic events in conscious dogs

Cited by 73 publications

References 0 publications

Direct and indirect effects of calcium entry blocking agents on isovolumic left ventricular relaxation in conscious dogs.

Direct and indirect effects of calcium entry blocking agents on isovolumic left ventricular relaxation in conscious dogs.

Effects of pacing-induced ischemia on early left ventricular filling and regional myocardial dynamics and their modification by nifedipine.

Left Ventricular Systolic and Diastolic Function during Coronary Arteriography before and after Acute Left Ventricular Failure in Dogs

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