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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regional myocardial blood flow during both control conditions and ischemia-induced vasodilatation was studied in eight chronically instrumented awake dogs. Seven of these animals had coarctation-banding of the ascending aorta performed at 6 wk of age, and the other dog had congenital subvalvular aortic stenosis. The mean left ventricular weight for the group was 157+/-7.6 g, and the left ventricular body weight ratio was 8.76+/-0.47 g/kg. None of the animals exhibited signs of congestive heart failure. During the control state, the mean left ventricular systolic pressure was 249+/-12 mm Hg and the left ventricular end-diastolic pressure was 11.5+/-0.5 mm Hg. The aortic diastolic pressure was 74+/-6 mm Hg. Mean left circumflex coronary artery blood flow was 71+/-6 cm(3)/min. In the animals with coarctation-banding, 52+/-6% of the flow occurred during systole. In the dog with congenital subvalvular aortic stenosis, 5% of the coronary flow was systolic. Mean transmural blood flow during resting conditions was 0.97+/-0.08 cm(3)/min per g, and the ratio of endocardial to epicardial flow (endo/epi) was 0.88+/-0.07. During reactive hyperemia, the mean transmural blood flow increased to 3.5+/-0.30 cm(3)/min per g; however, the endo/epi decreased to 0.52+/-0.06.THESE STUDIES DOCUMENT A DIFFERENCE IN TRANSMURAL BLOOD FLOW DISTRIBUTION BETWEEN THE NORMAL AND THE HYPERTROPHIED LEFT VENTRICLE: during resting conditions, in the normal ventricle, the highest flow occurs in the endocardial layer, whereas in the hypertrophied ventricle, the highest flow is in the middle layers with the endocardial flow less than the epicardial flow. During ischemia-induced vasodilatation, the abnormal endo/epi becomes accentuated markedly. These data demonstrate that, in situations requiring high flow, the endocardial layer of a heart with marked concentric left ventricular hypertrophy may not be perfused adequately.
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PMID:Myocardial blood flow distribution in concentric left ventricular hypertrophy. 14

Right ventricular hemodynamics were evaluated in 179 patients with coronary artery disease to determine the effects of chronic ischemia on right ventricular diastolic pressure. Abnormal right ventricular filling pressures occurred only in patients with an abnormal right ventricular systolic pressure or an abnormal left ventricular end-diastolic pressure. Of the 63 patients whose right ventricle was stressed by an increased systolic load secondary to passive pulmonary hypertension, 44 (72 percent) had an abnormal right ventricular end-diastolic pressure. In this group obstruction of vessels serving the right ventricular free wall or septum, or both, was almost universal (43 of 44, 98 percent) and a significantly increased incidence of inferior infarction (P less than 0.05) was noted. Such obstruction was significantly less frequent in patients with normal filling pressures (10 of 17, 59 percent; P less than 0.001). Compared with patients with coronary artery disease, patients with passive pulmonary hypertension due to aortic stenosis or mitral stenosis had significantly greater degrees of pulmonary hypertension (P less than 0.05) yet slightly lesser elevations of right ventricular end-diastolic pressure. These data suggest that in patients with ischemic heart disease the right ventricle exhibits diastolic dysfunction at lower levels of afterload stress than it would with normal coronary blood flow.
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PMID:Right ventricular diastolic pressure in coronary artery disease. 50 30

The records of 12 patients with aortic stenosis previously studied by Fallen et al. in 1967 before and after infusion of isoproterenol were reviewed to assess the value of hemodynamic indexes in predicting myocardial ischemia--defined as less than 5 percent transmyocardial lactate extraction or lactate production. Potential subendocardial blood supply was estimated from a diastolic pressure-time index (DPTI), calculated from the tension-time index (TTI). The ratio DPTI/TTI was used to estimate the supply/demand relation. Of eight patients with aortic stenosis but without associated coronary artery disease, four (Group A) metabolized lactate normally after administration of isoproterenol, and four (Group B) had biochemical evidence of ischemia. Three of four patients (Group C) with aortic stenosis and associated coronary artery disease had abnormal glycolysis after administration of isoproterenol. Calculated aortic valve areas were comparable in all groups. In patients with aortic stenosis alone, abnormal lactate metabolism occurred whenever DPTI/TTI was less than 0.30 (P smaller than 0.01) (Group B). Two of three patients with aortic stenosis and associated coronary artery disease (Group C) showed abnormal lactate metabolism when DPTI/TTI was greater than 0.6; this ratio was below 0.3 in the third patient. These results suggest that the supply/demand relation calculated from these readily obtained indexes may be useful (1) in predicting in which patients with aortic stenosis ischemia will develop, (2) in distinguishing the role played by associated coronary artery disease, and (3) as an adjunct to calculation of valve area since the quantitation of associated aortic regurgitation is not necessary.
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PMID:Ischemia in aortic stenosis: hemodynamic prediction. 113 Feb 86

We studied the interaction of tachycardia and aortic stenosis on the adequacy of subendocardial oxygen delivery. In 18 open-chest dogs with acute supravalvular aortic stenosis, we produced subendocardial ischemia by increasing either heart rate (artrial pacing) or the severity of aortic stenosis. Ischemia was determined from ST-elevation of the intracavitary electrocardiogram. Subendocardial oxygen supply was assessed by measuring subendocardial flow (radioactive microspheres, 8 to 10 microns) and arterial oxygen content, and related to simultaneous oxygen demand [estimated from the tension time index (TTI)]. The adequacy of the supply/demand relationship in the subendocardium was estimated from the ratio DPTI times 02 content (supply)/TTI (demand). Subendocardial ischemia occurred at aortic gradients ranging from 30 to 100 mm. Hg and heart rates from 120 to 180 beats per minute. Ischemic hearts were characterized by (1) redistribution of coronary flow away from the subendocardium (endo/epi flow ratio less than 1.0), (2) reduced subendocardial oxygen delivery per unit of demand (TTI) (p less than 0.01), (3) failure to lower left ventricular end-diastolic pressure with tachycardia, and (4) supply/demand ratios (DPTI times 02 content/TTI) below 15 ( less than 0.01). These findings suggest that (1) the principal determinant of subendocardial ischemia in aortic stenosis is the unfavorable alteration of the supply/demand relationship caused by the interaction between heart rate and severity of stenosis, rather than absolute heart rate or aortic gradient and (2) the adequacy of subendocardial oxygen delivery can be assessed from readily obtained measurements of blood pressure and oxygen content.
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PMID:Effects of tachycardia on the adequacy of subendocardial oxygen delivery in experimental aortic stenosis. 115 27

Intermittent murmurs of insufficiency (MI) associated with left atrial "V waves" often are ascribed to papillary muscle (PM) ischemia in coronary artery disease but their cause is not clear with unobstructed coronary arteries. In 49 open-chest dogs, left atrial, left ventricular, and aortic pressures and regional coronary flow (microsphere method) were measured. Subendocardial (SE) ischemia (endocardial/epicardial flow ratios less than 1.0, ischemic intracavitary electrocardiograms) was produced by lowering the SE supply/demand ratio (diastolic pressure time index times O2 content per tension time index) to below 12 with either arteriovenous fistulas, anemia, or aortic stenosis. In nonischemic hearts, O2 delivery to the PM was 20 percent more than to the SE (P less than 0.01) and rose with increasing demands. When ischemia occurred, O2 delivery per unit demand fell 35 percent (p less than 0.01) to the SE muscle, and PM O2 delivery decreased more strikingly (55 percent, p less than 0.01). This reduction in PM and SE O2 delivery often was associated with a "V wave" in the left atrium which disappeared when the intervention impairing the adequacy of O2 delivery was discontinued. We conclude that PM ischemia (1) is the probable cause of intermittent MI, and (2) can be predicted from readily obtained measurements of blood pressure and O2 content.
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PMID:Papillary muscle ischemia with patent coronary arteries. 116 9

Eighty-eight operations for correction of intracardiac congenital heart defects were performed using local cardiac hypothermia for protection of the ischemic myocardium. Twenty-six patients underwent repair of tetralogy of Fallot, 23 had patch closure of ventricular septal defect, 24 had correction of various types of congenital aortic stenosis, and 15 were operated upon for other complex lesions. The overall operative mortality was 5.6%. Ischemia times ranged from 9 to 119 minutes (mean, 48 minutes). Ischemic arrest protected by local cardiac hypothermia provides an optimal operative field, permitting repair of uncomplicated intracardiac defects in a precise, unhurried manner. No hemodynamic abnormalities attributable to the technique were encountered.
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PMID:Local cardiac hypothermia for myocardial protection during correction of congenital heart disease. 118 May 98

The hypertrophied left ventricle is at considerably greater risk for injury when subjected to global ischemia than is an otherwise normal heart. We evaluated the efficacy of verapamil, a calcium-channel blocking agent, as an adjunct to standard crystalloid cardioplegic solution in animals with left ventricular hypertrophy subjected to myocardial ischemia during cardiopulmonary bypass. Infracoronary aortic stenosis was produced in 15 mongrel puppies by plication of the noncoronary cusp of the aortic valve. Studies were conducted 3 to 4 months later. Left ventricular catheter-tip pressure transducers and major and minor axis ultrasonic dimension crystals were inserted, and the animals were then supported by cardiopulmonary bypass with 30 minutes of normothermic ischemia. Animals were randomized to receive either standard hyperkalemic crystalloid cardioplegic solution (n = 8) or the same solution with verapamil, 0.1 mg/kg (n = 7). After the 30 minutes of ischemia, the animals were supported on cardiopulmonary bypass for an additional 30 minutes and then separated from bypass. They were then studied for another 2 hours by measurement of myocardial adenosine triphosphate content, myocardial blood flow, systolic function with use of the end-systolic pressure/volume ratio, and compliance with use of the natural strain coefficient of the minor axis at 15 mm Hg end-diastolic pressure. There was a better recovery of systolic function in the animals treated with verapamil (89.2% versus 63.3%). The compliance as measured with use of the minor axis natural strain coefficient returned essentially to baseline in the group of animals treated with verapamil (0.236 +/- 0.038 before ischemia and 0.254 +/- 0.043 2 hours after ischemia), but it fell markedly in the control animals (0.219 +/- 0.027 before ischemia and 0.153 +/- 0.016 2 hours after ischemia). Myocardial adenosine triphosphate levels were not significantly different at any time during the study. Likewise, myocardial blood flow was not significantly different between groups. We conclude that the addition of verapamil to hyperkalemic cardioplegic solution improves recovery of both systolic and diastolic function after global ischemia in dogs with left ventricular hypertrophy resulting from aortic stenosis. The precise mechanism for this is unknown.
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PMID:Response of the hypertrophied left ventricle to global ischemia. Comparison of hyperkalemic cardioplegic solution with and without verapamil. 153 56

A case of aortic valve stenosis without coronary artery disease was confirmed to have diffuse subendocardial ischemia by exercise Thallium-201 myocardial single photon emission computed tomography. A 72-year-old woman, who had been diagnosed as aortic valve stenosis, was admitted because of chest pain during exercise. In cardiac catheterization findings, the patient angiographically had normal coronary arteries and no asynergy of left ventricular wall motion. The peak flow velocity in continuous wave Doppler echocardiography was about 5.0 m/sec at aortic valve level, providing a pressure drop of 100 mmHg across a stenotic valve with calculating on a modified Bernoulli equation (PG = 4V2). Thallium-201 myocardial SPECT images during exercise showed a transient "dilation and a widespread wall thinning" of left ventricle with apical perfusion defect. Simultaneous electrocardiogram showed further ST depression and the patient had chest pain. In 6 months after aortic valve replacement the patient no longer demonstrated both apical perfusion defect and "wall thinning" in postoperative thallium-201 myocardial SPECT images and also had neither ST depression nor chest pain. Thus; a transient "dilation and wall thinning" of left ventricle in this patient is suspected to be a sign of diffuse subendocardial ischemia.
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PMID:[Diffuse subendocardial ischemia in a patient with aortic valve stenosis without coronary artery disease by exercise 201Tl SPECT]. 157 26

The aim of this study was to determine the effect of low-pressure and high-pressure reperfusion, with and without ventricular fibrillation, on the recovery of hypertrophic and normal hearts after hypothermic cardioplegia. Fourteen hearts rendered hypertrophic by valvular aortic stenosis and 18 normal canine hearts were subjected to 1 hour of cardioplegic arrest at 28 degrees C during cardiopulmonary bypass. Each heart was then reperfused at a coronary pressure of either 40 mm Hg (low) or 80 mm Hg (high), initially in the empty beating state and then during ventricular fibrillation. Low-pressure reperfusion produced left ventricular subendocardial ischemia in hypertrophic and in normal hearts, shown by marked depression of subendocardial blood flow, myocardial pH, and myocardial oxygen consumption. In hypertrophic hearts the ischemia was more severe and resulted in a persistent depression of left ventricular function and myocardial oxygen consumption even when coronary pressure was returned to normal levels. High-pressure reperfusion was associated with rapid and complete recovery of myocardial metabolism and function in hypertrophic and in normal hearts. During low-pressure reperfusion, ventricular fibrillation exacerbated ischemia in hypertrophic and in normal hearts. During high-pressure reperfusion, a short period of ventricular fibrillation produced no adverse effects either in hypertrophic or in normal hearts. We conclude that low-pressure reperfusion produces subendocardial ischemia in normal and in hypertrophic hearts even in the empty beating state; in hypertrophic hearts it also impairs recovery of myocardial metabolism and function. The adverse effects of low-pressure reperfusion are exacerbated by ventricular fibrillation.
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PMID:Adverse effects of low-pressure reperfusion after hypothermic cardioplegia in normal and hypertrophic hearts. 183 91

Although the difficulty of preserving hypertrophied myocardium from induced arrest during aortic clamping has long been recognized, the difference of response to ischemia between the two types of hypertrophy induced by pressure-loading (P) and by volume overloading (V) has not been fully elucidated. In the present study, to assess the two types of hypertrophied myocardium we investigated the 44 patients undergoing valve replacement; the 23 patients of aortic stenosis (AS) without aortic regurgitation (AR), and the 21 patients of AR without AS. The patients of AS (group-P) were divided into two groups regarding the thickness of posterior wall of left ventricle; over 15 mm in P-1 and under 15 mm in P-2. The patients of AR (group-V) were also divided into two groups, which is, preoperative LVEDVI over 250 ml/m2 in V-I and under 250 ml/m2 in V-2. In all four groups myocardial temperature was kept about 5 degrees C with GIK and continuous cold blood coronary perfusion during aortic clamping time. There was no operative death. Postoperative serum enzymes (GOT and CPK) in P-1 were higher than in P-2. Per cent increase of LVEF in P-1 were greater than P-2 and V-1 greater than V-2, respectively. Postoperative catecholamines needed for P-1 was greater than P-2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Protection of the two types of severely hypertrophied myocardium induced by pressure-loading and by volume overloading]. 183 32


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