Effects of Acute Regional Myocardial Ischemia on Left Ventricular Function in Dogs

Enright, Lee P.; Hannah, Hamner; Reis, Robert L.

doi:10.1161/01.res.26.3.307

Cited by 31 publications

(5 citation statements)

References 14 publications

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“…result in asynergy of the ischemic area. 25 With the functional loss of a portion of the ventricular muscle, ventricular ejection falls and an increase in residual volume occurs. Venous return and ventricular filling remain essentially unchanged, however, and thus left ventricular end-diastolic volume increases with an accompanying rise in left ventricular end-diastolic pressure.…”

Section: Discussionmentioning

confidence: 99%

Left Ventricular Pressure-Volume Relationships During Myocardial Ischemia in Man

McCans

Parker

1973

Circulation

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It has been shown in man that myocardial ischemia, whether precipitated by exercise or pacinginduced tachycardia, is associated with abnormalities of left ventricular end-diastolic pressure. There has been controversy as to whether this relationship is due to decreased myocardial compliance or to an increase in left ventricular volume as a manifestation of left ventricular failure. Simultaneous measurements of left ventricular pressure and left ventricular volume using ultrasonic techniques were carried out in five normal subjects and 21 patients with coronary artery disease. In the normal subjects a decrease in left ventricular end-diastolic pressure during pacing was associated with a decrease in left ventricular end-diastolic volume, and during interruption of pacing, pressures and volumes returned to normal. In nine patients with coronary artery disease who did not develop angina, a similar response was seen. In 12 patients with coronary artery disease who developed angina during pacing, the reduction in left ventricular end-diastolic volume during pacing was less marked than the other groups and during periods of interruption the increase in diastolic pressure to 26 mm Hg was accompanied by an increase in left ventricular end-diastolic volume to 24% above control values. The end-systolic volume showed a similar increase during myocardial ischemia.These data suggest that the changes in left ventricular filling pressure seen during myocardial ischemia are related to increase in left ventricular volume but do not exclude the possibility that there may be accompanying changes in left ventricular diastolic compliance.Additional Indexing Words: Left ventricular volume Left ventricular compliance T HE HEMODYNAMIC changes during myocardial ischemia have been examined intensively, and there is now general agreement as to the abnormalities that occur.1-9 Opinions differ however as to the pathophysiologic mechanisms involved. Some investigators interpret the elevation of left ventricular filling pressure seen during myocardial ischemia as evidence of a transient decrease in left ventricular compliance5 6, 10 while others consider that reversible left ventricular failure occurs with an associated increase in left ventricular volume.3 4 Only limited information is available in man concerning changes in left ventricular volume and compliance during myocardial ischemia.11-13 Until

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Section: Discussionmentioning

confidence: 99%

Left Ventricular Pressure-Volume Relationships During Myocardial Ischemia in Man

McCans

Parker

1973

Circulation

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“…Force-velocity relations were calculated as previously described (12,13). The ventricle was assumed to be a thickwalled sphere, and the total tangential force at the endocardial equator was calculated from a modification of the Laplace relation (14), where F = P <n r 2 .…”

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confidence: 99%

Effects of Coronary Blood Flow and Perfusion Pressure on Left Ventricular Contractility in Dogs

Abel

Reis

1970

Circulation Research

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101

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The effects of changes in coronary blood flow and coronary artery pressure on left ventricular (LV) contractility were determined in 18 animals. Dogs on cardiopulmonary bypass provided isovolumetric LV contractions during controlled perfusion of the coronary circulation. Coronary venous efflux, myocardial oxygen consumption, peak LV pressure, LV dp/dt, and the forcevelocity relations of the LV were determined at normal and at "supernormal" levels of flow and pressure. Coronary vasodilatation was obtained with nitroglycerine, permitting independent variation of flow and pressure. Augmenting flow by increasing pressure increased LV contractility, as reflected by increases in peak LV pressure, dp/dt max, peak wall tension, and maximal measured contractile element velocity. Increased contractility appeared to be primarily due to increased flow, rather than to pressure, as an increase in flow without an increase in pressure produced similar changes, and decreases in pressure at constant flow did not change maximal measured contractile element velocity or dp/dt max, although some decrease in peak LV pressure and wall tension did occur. These data suggest that coronary flow is an independent determinant of the contractile state of myocardium, and that an increase in flow in excess of that required to supply metabolic demands augments myocardial contractility. ADDITIONAL KEY WORDSmyocardial contractility nitroglycerine coronary vascular resistance myocardial oxygen consumption contractile element velocity force-velocity relations inotropic state ventricular compliance• The relationships between ventricular work, coronary blood flow and myocardial oxygen consumption (MVo 2 ) are well established (1). Ventricular contractility, as assessed by developed wall tension and the rate of contractile element shortening, has been shown to be an important determinant of MVo 2 and coronary vascular resistance (2, 3). The converse causal relationship (viz., coronary blood flow as a determinant of contractility), however, has not been established. Gregg (4, 5) observed that a change in left circumflex artery perfusion pressure caused directional changes in both coronary flow and MV02 without consistent changes in heartFrom the Clinic of Surgery, National Heart and Lung Institute, Bethesda, Maryland 20014.Received April 2, 1970; accepted for publication October 19, 1970. rate, cardiac output, aortic pressure, or left ventricular end-diastolic pressure (LV, EDP). "Gregg's phenomenon" or the suggestion that coronary flow and coronary artery pressure (CAP) were independent determinants of MV02 and ventricular contractility has been investigated in several laboratories by a variety of experimental methods (6-9). The results of these studies have been the subject of controversy possibly related to the variety of preparations utilized, amount of myocardial work generated in these studies and the failure to differentiate between the effects produced by changes in coronary flow versus coronary artery pressure. The present studies we...

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“…The fall in dP/dt during coronary occlusion can be explained by develop ment of a functional aneurysm, which significantly lengthens the period of intraventricular pressure rise. The isovolumetric phase of contraction must overcome the resistance of the dyskinetic part of the left ventricular wall, which has elastic [Enright et al, 1970] and contractile properties [H ood et al, 1969] different from those of the healthy myocardium. Thus, during the time of isovolumetric contraction, some blood flows into the aneurysm chamber, leading to a contraction which is neither fully isometric nor fully isotonic.…”

Section: Discussionmentioning

confidence: 99%

Role of Regional Changes in Ventricular Performance in the Hypodynamic State Induced hy Acute Coronary Occlusion

Zochowski¹,

Pieniak²

1973

Cardiology

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Short-term coronary ischemia was produced in dogs anesthetized with pentothal by ligating the left anterior descending coronary artery. The resulting changes in representative hemodynamic parameters and the patterns of segmental contraction within and outside the ischemic area were recorded. Two types of reaction to coronary ligation were obtained: in some animals the contractility of the ischemic area rapidly decreased, leading to ballooning of the cardiac wall, inversion of the segmental contraction trace, marked reduction in stroke volume, pronounced increase in ventricular end-diastolic volume, and significant reduction in rate of intra-ventricular pressure rise (dP/dt). In other animals there were no signs of functional ventricular aneurysm, the changes in ventricular end-diastolic volume were less marked, and dP/dt was not altered to a significant extent. These observations suggest that in these cases characterized by the development of a functional aneurysm, the decrease in stroke volume does not result solely from dilation of the entire left ventricle, but also from the increased requirement for systolic fiber shortening in the viable myocardium, which must compensate for the extra stretch in the aneurysmal portion of the ventricular wall. It is suggested that diminution of stroke volume is due not only to the increase in wall stress in the whole left ventricle; it owes also to the expending of contractile elements in the viable portion of the muscle to compensate for additional elasticity in the functional left ventricular aneurysm.

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Effects of Acute Regional Myocardial Ischemia on Left Ventricular Function in Dogs

Cited by 31 publications

References 14 publications

Left Ventricular Pressure-Volume Relationships During Myocardial Ischemia in Man

Left Ventricular Pressure-Volume Relationships During Myocardial Ischemia in Man

Effects of Coronary Blood Flow and Perfusion Pressure on Left Ventricular Contractility in Dogs

Role of Regional Changes in Ventricular Performance in the Hypodynamic State Induced hy Acute Coronary Occlusion

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