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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnostic accuracy of spin-echo Magnetic Resonance (MR) imaging in the detection and localization of a recent myocardial infarction (mean 4 days old) was compared to planar thallium-201 scintigraphy in 20 patients with a documented myocardial infarction. A control group of 10 subjects underwent a similar MR imaging procedure without thallium-201 scintigraphy. T1-weighted MR images (TE 30 msec) showed abnormal thinning of the infarcted left ventricular wall during systole (less than 50% of the opposite wall) in 11 patients (55%). On T2-weighted multi-echo MR images, (TE 30-60-90-120 msec) abnormally increased signal intensity was found in 17 patients and coincided with the location of the infarction. Thallium-201 scintigraphy detected the infarction in 18 patients. Comparison of T2-MR imaging and thallium-201 scintigraphy showed concordant findings in 82% of the left ventricular segments. In 9% of segments, thallium uptake was reduced with normal T2-MR and in 9% we found a normal thallium uptake with abnormal T2-MR findings. In all subjects of the control group, T1-MR images were normal, and only one subject showed increased signal intensity on T2-MR images. We conclude that the diagnostic accuracy of MR imaging in detecting a myocardial infarction is similar to that of T1-201 scintigraphy.
Cardiovasc Intervent Radiol
PMID:Value of magnetic resonance imaging in patients with a recent myocardial infarction: comparison with planar thallium-201 scintigraphy. 250 44

In each of 8 rabbits, a fiberoptic with a 1.5 mm diameter metal tip was inserted into the abdominal aorta. After preheating with 8-10 watts of argon laser energy, the metal tip was passed through the external iliac artery. Thermal injury was evaluated by histology and by measuring arterial contractions and wall mechanics. The contralateral iliac artery was used as a control. Laser thermal angioplasty (LTA) produced foci of coagulation necrosis, medial thinning, and wall rupture. Concomitantly, maximal arterial contractile force was reduced by 80% (p less than 0.01) and arterial wall stiffness was decreased (p less than 0.05). These changes may have clinical implications with regard to the incidence and severity of vasospasm and restenosis following angioplasty.
Cardiovasc Intervent Radiol
PMID:Effects of laser thermal angioplasty on arterial contractions and mechanics. 252 18

Some patients who undergo aortocoronary bypass develop lesions in the graft and recurrence of symptoms. Hydraulic distension is used for preparation of veins. We have studied properties of vein interstitium, before and after peroperative distension, in 30 consecutive unselected patients. Segments of vein were studied for water content, swelling behaviour, tracer distribution, and uronic acid content. Initial water content was the same in distended and undistended vein; initial uronic acid content was slightly lower in distended veins, 8.7 (SD = 2.3) micrograms/m, n = 4 vs 10.5 (SD = 5.1) micrograms/mg dry weight, n = 6, not significant. The initial ratio, uronate/hydroxyproline was less in distended veins, 0.14 (SD = 0.05) n = 4 vs 0.19 (SD = 0.07), n = 6 in controls, not significant. Distended veins swelled less during incubation in saline. Average weight gain/initial weight was 0.65 (SD = 0.45), n = 27, and 1.1 (SD = 0.66), n = 25 in controls (p less than 0.01); change in water content/dry weight was 1.2 (SD = 1.1), n = 22, and 1.7 (SD = 1), n = 23 (p less than 0.02), in controls. Distended veins desorbed less uronic acid into the bath; 0.40 (SD = 0.2) microgram/mg wet tissue, n = 26 and 0.59 (SD = 0.3), n = 25 in controls (p less than 0.01). The pattern of uptake of two tracers 125I Serum albumin and 51Cr EDTA, was similar in both groups. These findings suggest alteration of the interstitial matrix of veins during distension. Histologic examination of glutaraldehyde-fixed tissue by light and electron microscopy revealed mural thinning and endothelial cell damage in distended veins.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Surg (Torino)
PMID:Changes in vein interstitium following distension for aortocoronary bypass. 260 Jan 35

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used.(ABSTRACT TRUNCATED AT 400 WORDS)
Prog Cardiovasc Dis
PMID:Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts. 288 58

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic entity that involves principally the left ventricle and is caused by asymmetric or concentric hypertrophy of unknown cause. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the apex, at the midventricular level, or, rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by upper septal hypertrophy narrowing the outflow tract and setting the stage for Venturi forces to cause systolic anterior motion of the anterior or posterior mitral leaflets. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyotomy-myectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. This form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy available today. The extent of hypertrophy is believed to be the principal determinant of the impaired left ventricular relaxation and increased chambers stiffness (decreased compliance) that characterize diastole in hypertrophic cardiomyopathy. Relaxation is impaired by the contraction load (the obstruction), by a decrease in the principal relaxation loads, by a pathologic degree of nonuniformity of contraction and relaxation, and in all likelihood, by impaired inactivation of the biochemical processes responsible for contraction (? due to primary or ischemia-induced calcium overload). Calcium channel-blocking agents may dramatically improve left ventricular relaxation by speeding up the inactivation process, by decreasing the degree of nonuniformity, or by altering the contraction and relaxation loads in a favorable manner. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their occurrence also appears to depend on the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole as well as the disturbances of rhythm appear to be related to the site and/or extent of the hypertrophic process.(ABSTRACT TRUNCATED AT 400 WORDS)
Prog Cardiovasc Dis
PMID:Hypertrophic cardiomyopathy. The importance of the site and the extent of hypertrophy. A review. 316 67

Isolated rat heart preparations were studied to characterise the alterations in high energy phosphates that occur during reversible regional ischaemia and to determine whether pyruvate, as the sole exogenous energy substrate, would attenuate the ischaemia induced depletion of the nucleotide pool when compared with glucose. Using phosphorus-31 magnetic resonance spectroscopy baseline concentrations of adenosine triphosphate, phosphocreatine, inorganic phosphate, and intracellular pH were compared with values during 30 min of left coronary artery occlusion followed by 30 min of reperfusion. These variables were related to changes in developed pressure, coronary flow, and oxygen consumption. In addition, the total nucleotide pool was evaluated by biochemical analysis of myocardial tissue extracts and coronary effluent. The ischaemic region was characterised by a dye staining technique and cross sectional echocardiographic measurements of regional myocardial wall thinning. In both glucose and pyruvate perfused groups, coronary flow and oxygen consumption decreased to 50-60% of control within 1 min of ischaemia and returned to baseline values with reflow. Developed pressure decreased to 50(9) and 74(8)% (mean(SEM] of control after 30 min of ischaemia in glucose and pyruvate perfused groups respectively. Reperfusion resulted in complete recovery of developed pressure in hearts perfused with pyruvate but not in the glucose group. Glucose perfused hearts had a greater decrease in intracellular pH during ischaemia (7.07(0.01) to 6.36(0.1] than pyruvate perfused hearts (7.06(0.02) to 6.83(0.04]. Reperfusion resulted in a rapid return to baseline intracellular pH in both groups. During ischaemia, adenosine triphosphate values decreased to a greater degree in glucose than in pyruvate perfused hearts (57(4) and 79(5)% of baseline respectively). Thirty minutes of reperfusion did not significantly improve adenosine triphosphate concentrations in either group. Phosphocreatine concentrations decreased to 52(7) and 75(6)% of baseline in glucose and pyruvate perfused groups respectively after the ischaemic period. Reperfusion resulted in normalisation of phosphocreatine values in the pyruvate but not in the glucose perfused group. Biochemical analysis of myocardial tissue extracts confirmed the spectroscopy data and showed that pyruvate inhibits the efflux of adenine nucleotide derivatives. Tissue concentrations of adenosine monophosphate were three times greater and adenosine 50% less after 30 min of ischaemia in the pyruvate perfused group.(ABSTRACT TRUNCATED AT 400 WORDS)
Cardiovasc Res 1988 Mar
PMID:Substrate regulation of the nucleotide pool during regional ischaemia and reperfusion in an isolated rat heart preparation: a phosphorus-31 magnetic resonance spectroscopy analysis. 316 43

Regional diastolic wall motion was studied with sonomicrometry in 30 open chest anaesthetised dogs after left anterior descending stenosis or occlusion. Post-systolic shortening and thickening, defined as the magnitude of segment shortening or wall thickening that occurred after end systole, was measured in peripheral and central ischaemic segments. These post-systolic events developed concurrently with impaired systolic shortening or thickening, either immediately after acute coronary occlusion or during progressive stenosis, and persisted with the development of dyskinesis and during reperfusion. The magnitude of these events in dyskinetic segments of 24 dogs was considerable, reaching 50(2)% (mean(SEM)) and 33(3)% of shortening or thickening that was present before coronary occlusion. Post-systolic shortening and thickening were maximum at 100(2) ms after peak negative dP/dt. Significant correlations were found between systolic shortening or thickening before coronary occlusion and post-systolic shortening (r = 0.74, 56 segments) or thickening (r = 0.84, 19 segments) after occlusion, but there was no correlation between post-systolic shortening or thickening and dyskinetic lengthening or thinning. In seven dogs followed for 4 h after coronary occlusion post-systolic shortening fell by 15% in peripheral segments and by 70% in central segments (p less than 0.002). In 17 dogs reperfused after 60 (n = 9) or 90 (n = 8) min of coronary occlusion the maximal recovery of systolic shortening early after reperfusion was significantly related to the magnitude of post-systolic shortening immediately before reperfusion (60 min occlusion r = 0.84, 90 min occlusion r = 0.88). These data show that post-systolic shortening is a marker of potential for early recovery of function of acutely ischaemic myocardium and suggest that it is due, at least in part, to an active process.
Cardiovasc Res 1987 Oct
PMID:Post-systolic shortening: a marker of potential for early recovery of acutely ischaemic myocardium in the dog. 344 Feb 62

To investigate the mechanism of the depression of left ventricular (LV) peak negative dP/dt during acute regional ischemia, studies were performed in seven open-chest anesthetized dogs. Regional LV wall thickness was measured with ultrasonic crystals in both an ischemic and a normally perfused segment. Ischemia was produced by complete occlusion of the left anterior descending coronary artery for 30 seconds. Within 10 seconds of ischemia, premature thinning of the ischemic wall developed, which preceded thinning of the normal LV wall by 100 +/- 20 msec. Premature thinning of the ischemic segment was associated with 29% reduction of peak negative dP/dt, a 29% prolongation of LV isovolumic relaxation time, and a 15% reduction of the LV systolic ejection period. We offer the following explanation for the depression of LV peak negative dP/dt. 1. Peak negative dP/dt is depressed as a result of a prolongation of the isovolumic relaxation time. 2. The isovolumic relaxation time is prolonged as a result of shortening of the systolic ejection period. 3. Shortening of the systolic ejection period is mediated by an early fall of LV systolic pressure caused by inability of the LV to sustain systolic pressure. 4. Inability of the LV to sustain systolic pressure is caused by premature thinning of the ischemic region during late systole.
Cathet Cardiovasc Diagn 1986
PMID:Proposed mechanism for depression of maximal rate of left ventricular pressure fall (peak negative dP/dt) during regional myocardial ischemia. 373 Dec 66

To explore possible mechanisms of left ventricular early segmental relaxation, complete occlusion of the left anterior descending coronary artery (LAD) was produced in seven open-chest dogs and partial occlusion of the LAD was produced in six open-chest anesthetized dogs. Regional wall thickness was measured both in an ischemic and a normally perfused zone using implanted ultrasonic crystals. Two to three seconds following complete LAD occlusion, thinning of the ischemic wall occurred prematurely during isovolumic relaxation. The extent of premature thinning became more prominent 5 to 10 sec following LAD occlusion. Early thinning of the ischemic wall preceded thinning of the normally perfused wall by 110 +/- 10 msec. Partial occlusion of the LAD produced a 33 +/- 6% reduction of coronary flow and a 23 +/- 4% reduction of systolic wall thickening in the ischemic region. Systolic thickening of the nonischemic wall was unchanged relative to the preocclusion period. Premature early thinning of the mildly ischemic wall preceded thinning of the normally perfused segment by 90 +/- 8 msec. The observation that ischemia can produce segmental early thinning of the ventricular wall may have implications in understanding the mechanism of the angiographic observation of the segmental early relaxation phenomena in patients with coronary artery disease.
Cathet Cardiovasc Diagn 1983
PMID:Early segmental thinning of the left ventricular wall following regional ischemia. 664 Jun 63

The effects of step-wise reduction in left circumflex coronary blood flow on: 1) posteroinferior wall dynamics; 2) normally-perfused anterior wall dynamics; and 3) cavity function were assessed simultaneously by roentgen videometric analysis of left ventricular angiograms in open-chest dogs during normal and increased afterload. At control coronary flow with normal afterload, peak rates of systolic thickening and diastolic thinning of the posteroinferior and anterior walls were similar. Step-wise reduction in circumflex coronary flow resulted in a progressive fall in systolic and diastolic posteroinferior wall dynamics. Increased LV afterload resulted in a decrease in posteroinferior wall dynamics even at control coronary flow, and reduction in flow resulted in even greater deterioration than occurred with normal afterload. The decrease in posteroinferior wall dynamics with reduction in circumflex coronary flow was accompanied by an increase in peak rates of systolic thickening and diastolic thinning of the normally perfused anterior wall. The level of coronary blood flow at which this increase in anterior wall dynamics occurred, varied with LV loading conditions, occurring earlier when afterload was increased. There was no earlier or greater decrease in diastolic than systolic wall dynamics with progressive reduction in coronary flow with either normal or increased afterload. Left ventricular end-diastolic volume, end-diastolic pressure and ejection fraction changed little until coronary blood flow was reduced to 50% of control; by contrast, stroke-work was exquisitely sensitive to changes in coronary flow. There was no correlation between changes in regional and cavity systolic or diastolic function. The delay in onset of LV cavity dysfunction with ischemia may have been partly due to the "compensatory increase" in anterior wall dynamics, counterbalancing the impaired posteroinferior wall dynamics.
Cardiovasc Res 1982 Sep
PMID:Effects of progressive reduction in coronary blood flow on regional and global left ventricular contraction and relaxation during normal and increased afterload: a roentgen videometric study. 717 76


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