The pathophysiology of intramyocardial pressure and blood flow distribution—A surgical perspective

We critically evaluated the major techniques for measurement of intramyocardial pressure (IMP) (closed, perfusion, open, microtransducer). Each technique demonstrates a gradient in systolic IMP increasing with depth from the epicardium. The estimated magnitude of this gradient varies with the technique employed. Indirect methods (closed, perfusion) estimate a higher value for the systolic IMP gradient. The open and microtransducer methods, which measure a direct hydrostatic pressure within the myocardium, are less invasive and reflect more reliably the magnitude of IMP. The results for the open and microtransducer methods were comparable and indicate that normalized systolic IMP increases linearly from the epicardium. In the inner half of the myocardium systolic IMP approaches the level of systolic LVP and in the subendocardial layer it exceeds the systolic LVP by about 8%. A reverse IMP gradient occurred in late diastole ranging from 5 mmHg in the subendocardial region to 25 mmHg in the subepicardium.

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“…1-C) were employed in experiments performed by several investigators (11,14,15,5,6). A needle is placed at a specific depth within the LV wall.…”

Section: B) Perfusion Method: Various Modifications Of This Techniquementioning

confidence: 99%

Analysis of methodology for measurement of intramyocardial pressure

et al. 1984

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“…Since x is independent of peak pressure, the peak value of ENDO and EPI should not influence the calculated relax ation values. Measuring intramyocardial pressure is controversial since not all authors agree that ENDO exceeds LVP during systole [8,9,17], but all studies [8,9,19] ENDO to be higher than EPI during ejection and intramyocardial pressure to be well repro ducible using various measuring devices. The major critique on this method is that intro ducing any size transducer into the myocar dium causes tissue deformation and rear rangement of fibers.…”

Section: Discussionmentioning

confidence: 99%

Relaxation within the Left Ventricular Myocardial Wall

Aubert

Denys²,

Geest³

1994

Cardiology

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To evaluate relaxation mechanics in the wall of the left ventricle needle mounted miniature pressure transducers were inserted at the subendocardial (ENDO) and subepicardial (EPI) level of the anterior wall of the left ventricle during acute open-chest experiments in 10 mongrel dogs. Pressures were recorded during control, volume load and after verapamil administration. The relaxation time constant (τ) was determined by fitting a monoexponential with offset to the isovolumic relaxation period of the ENDO, EPI and left ventricular pressure (LVP) tracings: p = p₀e^-t/τ + p₁. Mean τ-values for LVP, ENDO and EPI during control were (mean ± 1 SD, ms): 38 ± 5, 60 ± 12, 83 ± 5; during volume overload: 55 ± 10, 72 ± 20, 85 ± 31 and after verapamil administration: 58 ± 13, 60 ± 17 and 73 ± 15, respectively. Relaxation time constants of ENDO and EPI were significantly longer than those of LVP during control and volume loading but not after verapamil when only EPI was significantly different from LVP. These results demonstrate that relaxation indices obtained from LVP may not always reflect intramyocardial mechanics.

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“…Although greater intramural forces in the subendocardium could influence the distribution of ischemic necrosis by increasing oxygen demand (21,59), it is currently assumed that they act by causing a relatively greater increase in the external impediment to coronary flow (extravascular resistance) in the deep myocardium (12,15,32,45). Although greater intramural forces in the subendocardium could influence the distribution of ischemic necrosis by increasing oxygen demand (21,59), it is currently assumed that they act by causing a relatively greater increase in the external impediment to coronary flow (extravascular resistance) in the deep myocardium (12,15,32,45).…”

Section: Introductionmentioning

confidence: 99%

Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia

Sêdek

Michalowski

1986

Basic Res Cardiol

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Verification of the current view that subendocardial preponderance of ischemia is due to greater forces generated in the deep myocardial layer during systole was undertaken. In anesthetized mongrel dogs transient ischemia was produced in two different situations of altered systolic forces. First, in order to remove that part of the systolic force which is related to intracavitary pressure, left ventricular bypass was created and the left ventricle vented. Second, in order to even out the transmural distribution of the remaining part of the forces, which is due directly to distortion and displacement of contracting fibers, ventricular fibrillation was induced in addition to venting under conditions of total cardiopulmonary bypass. In both series of experiments the ischemic area was then reperfused, normal circulation re-established and the animal allowed to survive for 3-5 days. After sacrifice, ischemic necrosis was found almost exclusively in the subendocardium. The persistence of subendocardial preponderance of ischemia under conditions of left ventricular venting and absence of coordinated contraction shows that uneven distribution of intramural forces generated during systole is not the primary cause of this preponderance.

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The pathophysiology of intramyocardial pressure and blood flow distribution—A surgical perspective

Cited by 7 publications

References 69 publications

Analysis of methodology for measurement of intramyocardial pressure

Analysis of methodology for measurement of intramyocardial pressure

Relaxation within the Left Ventricular Myocardial Wall

Evidence against systolic intramural forces as the primary cause of subendocardial preponderance of ischemia

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