Regional Myocardial Function in the Conscious Dog During Acute Coronary Occlusion and Responses to Morphine, Propranolol, Nitroglycerin, and Lidocaine

Théroux, Pierre; Ross, John; Franklin, Dean; Kemper, W S; Sasayama, S; Boulanger, M.

doi:10.1097/00132586-197612000-00009

Cited by 61 publications

(81 citation statements)

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“…In anesthetized dogs, using epicardial strain gauges and length gauges3 or intramyocardial ultrasonic segment length transducers,2 intravenous bolus injections of nitroglycerin improved segmental shortening of the ischemic border zone, and in the latter experiments slightly improved central ischemic zone shortening as well. Similar results were obtained in awake dogs.8 Theroux and coworkers concluded that nitroglycerin administration did result in improved myocardial shortening in border zones of ischemia, but they could not determine whether these effects were directly the result of improved myocardial performance, or whether they represented passive alterations in myocardial motion due to diminished preload and afterload.2, 8 In the present experiments, in contrast to those cited above, we found no improvement in ischemic wall thickness abnormalities in any location. Several possibilities might explain this discrepancy:…”

Section: Discussionsupporting

confidence: 67%

Effects of nitroglycerin on echocardiographic measurements of left ventricular wall thickness and regional myocardial performance during acute coronary ischemia.

Komer¹,

Edalji²,

Hood³

1979

Circulation

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The effects of nitroglycerin on regional left ventricular performance, assessed by echocardiographic techniques, were investigated in anesthetized, open-chest dogs during acute myocardial ischemia. During transient occlusion of the left anterior descending coronary artery, there was end-diastolic thinning and marked reduction in systolic thickening in the central ischemic zone. Similar changes of lesser degree were noted in the border zone. The normal zone was unaffected. Infusion of nitroglycerin during ischemia in dosages of 2.5--50 microgram/kg/min reduced left ventricular end-diastolic pressure without changing the abnormalities of systolic wall thickening. Effects of bolus injections of 20 and 50 microgram/kg of nitroglycerin were similar, although this also lowered aortic pressure. In a subgroup of animals in which nitroglycerin infusion was unaccompanied by tachycardia, there was also no evidence that ischemic dysfunction was altered. We conclude that nitroglycerin does not improve regional myocardial performance in acutely ischemic canine myocardium. The decrease in preload is probably entirely due to the peripheral effects of the agent.

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Section: Discussionsupporting

confidence: 67%

Effects of nitroglycerin on echocardiographic measurements of left ventricular wall thickness and regional myocardial performance during acute coronary ischemia.

Komer¹,

Edalji²,

Hood³

1979

Circulation

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“…A common finding in ischemic myocardium is postsystolic (postejection) shortening and consequently delayed onset of diastolic lengthening (8,16,17). Therefore, in the ischemic ventricle, there may be substantial regional asynchrony in the onset of myocardial diastolic lengthening, and this in turn may have an impact on intraventricular flow.…”

mentioning

confidence: 99%

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

Urheim¹,

Edvardsen²,

Steine³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Acute myocardial ischemia has been associated with abnormal filling patterns in the left ventricular (LV) apex. We hypothesized that this may in part be due to postsystolic shortening of ischemic apical segments, which leads to reversal of early diastolic apical flow. Fourteen open-chest anesthetized dogs were instrumented with micromanometers in the LV apex and left atrium and myocardial sonomicrometers in the anterior apical LV wall. Intraventricular filling by color Doppler and wall motion by strain Doppler echocardiography (SDE) were assessed from an apical view. Measurements were taken before and after 5 min of left anterior descending coronary artery (LAD) occlusion. In four dogs, we measured the pressure difference between the LV apex and outflow tract. At baseline, peak early diastolic flow velocities in the distal one-third of the LV were directed toward apex (9.2 Ϯ 1.6 cm/s). After LAD occlusion, the velocities reversed (Ϫ2.3 Ϯ 0.4 cm/s, P Ͻ 0.01), indicating that blood was ejected from the apex toward the base during early filling. This interpretation was confirmed by wall motion analysis, which showed postsystolic shortening of apical myocardial segments. The postsystolic shortening represented 9.7 Ϯ 1.7% (P Ͻ 0.01) and 14.2 Ϯ 2.4% (P Ͻ 0.01) of end-diastolic segment length by SDE and sonomicrometry, respectively. Consistent with the velocity changes, we found reversal of the early diastolic pressure gradient from the LV apex to outflow tract. In the present model, acute LAD occlusion resulted in reversal of early diastolic apical flow, and this was attributed to postsystolic shortening of dyskinetic apical segments. The clinical diagnostic importance of this finding remains to be determined. strain-Doppler echocardiography; two-dimensional color Doppler; myocardial ischemia; diastolic filling ASSESSMENT OF LEFT VENTRICULAR (LV) intracavitary filling by Doppler echocardiography is one of several noninvasive approaches for studying LV diastolic function. In the normal LV, the initial intraventricular filling wave propagates rapidly toward the apex, and, as demonstrated by color M-mode Doppler, there is near simultaneous onset of filling velocities along the entire LV inflow tract (7). However, in patients with reduced LV ejection fraction or impaired diastolic function, the early diastolic apical filling may be markedly delayed, and this can be measured as slowing of mitral-to-apical flow propagation (1, 13). This has been attributed to a decrease in rate of LV relaxation, which causes a decrease in the driving pressure for mitral-to-apical flow (1, 12, 13), to loss of "apical suction" (12), and enhanced vortex formations due to changes in LV and mitral valve geometry (10).There is, however, very limited insight into how regional wall motion interacts with intraventricular flow. A common finding in ischemic myocardium is postsystolic (postejection) shortening and consequently delayed onset of diastolic lengthening (8,16,17). Therefore, in the ischemic ventricle, there may be substantial regional async...

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“…[6][7][8][9][10] The changes are best characterized as a sequence that begins as late systolic outward motion and ends with total replacement of active shortening by passive expansion.4'5' Such a sequence is highly specific for regional ischemial 5 ' and invariably precedes electrocardiographic ST-segment shifts.4' It has been postulated4' 5that these alterations of regional function are directly analogous to qualitative angiographic contraction patterns such as "hypokinesis" and "dyskinesis.""' 12 If this is the case, clinical left ventriculography might be used as a quantitative measure of regional ischemia.…”

mentioning

confidence: 99%

Analysis of regional ischemic left ventricular dysfunction by quantitative cineangiography.

Tzivoni¹,

Diamond²,

Pichler³

et al. 1979

Circulation

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Regional Myocardial Function in the Conscious Dog During Acute Coronary Occlusion and Responses to Morphine, Propranolol, Nitroglycerin, and Lidocaine

Cited by 61 publications

References 0 publications

Effects of nitroglycerin on echocardiographic measurements of left ventricular wall thickness and regional myocardial performance during acute coronary ischemia.

Effects of nitroglycerin on echocardiographic measurements of left ventricular wall thickness and regional myocardial performance during acute coronary ischemia.

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

Analysis of regional ischemic left ventricular dysfunction by quantitative cineangiography.

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