Myocardial oxygen consumption in chronic heart disease: Role of wall stress, hypertrophy and coronary reserve

Strauer, B. E.

doi:10.1016/0002-9149(79)90295-9

Cited by 271 publications

(97 citation statements)

References 19 publications

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“…However, Strauer also reported normal CFR with haemodynamically compensated LVH. 12 In a work from Opherk et al 10 in subjects with arterial hypertension and without obstructive coronary lesions on angiogram, ECG-defined LVH was found to be associated with markedly reduced CFR measured by argon method without significant alteration of myocardial microvasculature in myocardial specimens showing insignificant interstitial fibrosis. Opherk et al 10 emphasized the role of coronary resistance and LV end-diastolic pressure as determinants of the reduced CFR associated with LVH.…”

Section: Discussionmentioning

confidence: 94%

“…With this regard, early experimental and clinical invasive studies reported association of LVH with reduced CFR. [6][7][8][9][10] However, others failed to find significant independent relationship between CFR and LVH, [11][12][13][14][15][16][17] and the independent relation between LVH and abnormal CFR remains disputed. In addition, LVH is independently associated with coronary artery disease, 18 which may confound the relation between LVH and CFR.…”

Section: Introductionmentioning

confidence: 99%

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Relations of left ventricular mass and systolic function to endothelial function and coronary flow reserve in healthy, new discovered hypertensive subjects

et al. 2005

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Left ventricular hypertrophy (LVH) is prognostically relevant, associated with major cardiovascular risk factors and with atherosclerosis. However, whether LVH is independently associated with impaired coronary flow reserve (CFR) and with endothelial dysfunction is disputed. We assessed the relationship of LV mass and systolic function to CFR and endothelial function in new discovered never treated subjects with essential arterial hypertension, but without coronary artery disease or microalbuminuria. LVH, ejection fraction (EF) and stress-corrected midwall shortening (MWS, a measure of myocardial contractility) were assessed by echocardiography. CFR was assessed by single-photon emission computed tomography and dipyridamole infusion. Endothelial function was evaluated by assessing 1-min postischaemic flow-mediated dilatation of the brachial artery (FMD); nitroglycerine-mediated dilatation (NMD) of the same brachial artery was used as measure of nonendothelium-dependent vasodilatation. In approximately 1 year, we enrolled 21 subjects who met stringent inclusion criteria (47710 years old, 26.672.8 kg/m 2 , 78% men). Five patients showed LVH. Multivariate analyses showed a significant negative correlation of LV mass index with FMD (b ¼ À0.61, Po0.05) but not with NMD, neither with CFR. Stress-corrected MWS showed independent correlation with CFR (b ¼ 0.51, Po0.05). Thus, in clinically healthy, new discovered hypertensive subjects, never treated and mostly in the early stage of arterial hypertension, LVH can be associated with endothelial dysfunction while maximal dipyridamoledependent CFR may be preserved; nevertheless, a cardiac phenotype presenting with tendency to impaired myocardial contractility, assessed by stress-corrected MWS, showed association with lower CFR in the early stage of arterial hypertension.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Relations of left ventricular mass and systolic function to endothelial function and coronary flow reserve in healthy, new discovered hypertensive subjects

et al. 2005

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“…The relationship between cardiac dysfunction and wall stress has been formerly recognized in different forms of cardiac disease, including HTN 18,30,33 and was corroborated by the strong inverse correlation found between fractional shortening and end-systolic stress. It is tempting to speculate that although coronary reserve impairment alone does not seem critical for cardiac decompensation, the imbalance between myocardial supply, represented by coronary reserve, and demand, represented by systolic wall stress, might perpetuate and/or aggravate cardiac dysfunction.…”

Section: Discussionmentioning

confidence: 72%

“…9,29 Apparently in contradiction with our results, coronary reserve impairment has been reported early in the development of human HTN 7 and has been implicated in subsequent cardiac dysfunction. 3,30 The disproportional growth of microvascular bed relative to myocardial mass during the development of hypertrophy may explain discrepant findings depending on the time point when the investigation is performed. 16 The premature changes in coronary flow are not necessarily related to hypertension but instead may result from concurrent unidentifiable causes of microvascular disease, particularly in the presence of chest pain.…”

Section: Discussionmentioning

confidence: 99%

The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension

Frimm¹,

Pereira²,

Rodrigues

et al. 2005

Clinical Cardiology

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SummaryBackground: The pathophysiologic role of coronary reserve impairment in hypertensive cardiac dysfunction is still debated. Previously, we demonstrated that satisfactory coronary vasodilatation may coexist with ventricular systolic dysfunction. It is conceivable that coronary reserve might otherwise be inappropriate for enhanced myocardial oxygen demand and may thus affect cardiac performance negatively.Hypothesis: Myocardial supply-demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN).Methods: Fractional shortening (%) and end-systolic stress (10 3 ·dyn·cm Ϫ2 ) were determined using echocardiography, and coronary reserve was calculated using transesophageal Doppler echocardiography. Coronary reserve/ stress (cm 2 ·dyn Ϫ1 ) was utilized as a measure of supply-demand. Groups NL (20 healthy subjects), HTN1 (15 patients, fractional shortening ≥ 30), HTN2 (19 patients, 20 ≤ fractional shortening < 30), and HTN3 (21 patients, fractional shortening < 20) were constituted.Results: Compared with NL and HTN1, groups HTN2 and HTN3 had significantly (p < 0.05) greater end-systolic stress (NL = 72 ± 16, HTN1 = 72 ± 23, HTN2 = 143 ± 32, HTN3 = 186 ± 70). Coronary reserve was impaired in HTN3 alone (NL = 3.5 ± 0.6, HTN1 = 3.4 ± 1.0, HTN2 = 3.1 ± 1.0, HTN3 = 2.6 ± 1.1), but coronary reserve/stress was reduced in both

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“…Publications up to the present have demonstrated that the contractile state of the hypertrophied myocardium remained unchanged in large animals, when pressureoverload was gradually applied (CARABELLO et al, 1981;SASAYAMA et al, 1976;WILLIAMS and POTTER, 1974;WISENBAUGH et a!., 1983). On the other hand, several investigators have indicated that concentric hypertrophy which occurred in the pressure-overload heart reduced the wall stress to the level of the normal ventricle and that the occurrence of hypertrophy was the mechanism of adaptation to the increased afterload (GROSSMAN et al, 1975;STRAUER, 1979). Little information is available, however, concerning the relationship between chamber geometry and ventricular function in the pressure-overload ventricle.…”

mentioning

confidence: 92%

Left ventricular function of concentric hypertrophied heart after chronic pressure overload as studied in the isolated canine heart preparation.

et al. 1984

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The function of the pressure-overload left ventricle was studied in relation to the chamber geometry of the isolated canine heart. The occurrence of concentric hypertrophy was confirmed in dogs with aortic constriction 40 weeks after operation. The effect of the concentric hypertrophy on left ventricular function was then studied in five pressure-overload dogs. The end-diastolic pressure of the preparation was preset at 20 mmHg. In the pressure-overload ventricle, the end-diastolic volume was smaller by 47% (p<0.01) and the peak systolic pressure was higher by 24% (p<0.01) than the control at isovolumic beats. Ejection pressure was controlled by our afterload controlling system at various levels and kept constant during the ejection phase. When ejection pressure was the same, the difference in stroke volume between the experimental and control groups was not significant. In the pressure-overload ventricle, the slope (the reciprocal is Emax) of the regression line of the end-systolic volume on ejection pressure decreased (p<0.01) to 0.095 ml/mmHg by 47% from 0.186 ml/mmHg in the control. The volume-axis intercept (Vd) of the line was reduced to 55 % of the control. A decrease in the regression line slope was in linear proportion to the degree of concentric hypertrophy, namely, to the change in chamber geometry. These results indicated that: (1) Despite reduction of the end-diastolic volume, the concentric hypertrophied ventricle showed no reduction in stroke volume at the same level of ejection pressure, because of its improved capability to generate pressure. (2) Ema$ was dependent on ventricular geometry.

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Myocardial oxygen consumption in chronic heart disease: Role of wall stress, hypertrophy and coronary reserve

Cited by 271 publications

References 19 publications

Relations of left ventricular mass and systolic function to endothelial function and coronary flow reserve in healthy, new discovered hypertensive subjects

Relations of left ventricular mass and systolic function to endothelial function and coronary flow reserve in healthy, new discovered hypertensive subjects

The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension

Left ventricular function of concentric hypertrophied heart after chronic pressure overload as studied in the isolated canine heart preparation.

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